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5242 Cards in this Set
- Front
- Back
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Common congenital malformations: Name 7 common congenital malformations
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(1) Heart Defects (congenital rubella) (2) Hypospadias (3) Cleft lip with or without cleft palate (4) congenital hip dislocation (5) spina bifida (6) anencephaly (7) pyloric stenosis (associated with polyhydramnios & projectile vomiting)
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Common congenital malformations: Name 2 neural tube defects (NTDs)
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Spina bifida and anencephaly
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Common congenital malformations: Name 2 diagnostic associations with NTDs during gestation
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increased serum and amniotic fluid levels of a-fetoprotein
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Common congenital malformations: How can the incidence of NTDs be reduced?
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Folate ingestion during pregnancy
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Congenital Heart Disease: What kind of shunts cause early cyanosis?
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R-to-L "blue babies"
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Congenital Heart Disease: What kind of shunts cause late cyanosis?
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L-to-R "blue kids"
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Congenital Heart Disease: Name 3 common R-to-L shunts.
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The 3 T's: Tetralogy of Fallot (most common cause of early cyanosis), Transposition of the great vessels, truncus arteriosus
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Congenital Heart Disease: What might you see children with a R-to-L shunt do to relieve discomfort?
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Squat to increase venous return
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Congenital Heart Disease: Name 3 common L-to-R shunts.
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VSD, ASD, PDA
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Congenital Heart Disease: Rank them in order of frequency
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VSD > ASD > PDA
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Congenital Heart Disease: What are the auscultatory signs of an Atrial Septal Defect?
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Loud S1; wide, fixed split S2
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Congenital Heart Disease: How do you treat PDA?
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Indomethacin
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Congenital Heart Disease: Name 3 sequelae of L-to-R shunts.
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1) Increased pulmonary resistance due to arteriolar thickening. 2) Progressive pulmonary HTN 3) R-to-L shunt (Eisenmenger's)
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Eisenmenger's Syndrome: What are signs/symptoms of Eisenmenger's?
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Late cyanosis, clubbing, polycythemia
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Tetrology of Fallot: What is the Tetrology?
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(1) Pulmonary Stenosis (2) RVH (3) Overriding aorta (4) VSD (mnemonic: PROVe)
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Tetrology of Fallot: What is the direction of the shunt in the tetralogy?
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right-to-left across the VSD
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Tetrology of Fallot: What is the x-ray finding on the tetralogy?
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Boot-shaped heart due to RVH
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Tetrology of Fallot: What is the embryological cause of the tetralogy?
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Anterosuperior displacement of the infundibular septum.
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Transposition of great vessels: The transposition occurs because of a failure of the --------------- --------- to -------
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failure of the aorticopulmonary septum to spiral
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Transposition of great vessels: In transposition of the great vessels, the aorta leaves ------------ and the pulmonary trunk leaves the ------------
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aorta leaves the RV (anterior) and the pulmonary trunk leaves the LV (posterior)
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Transposition of great vessels: How might transposition of the great vessels, be compatible with life?
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If a shunt (e.g. VSD, PDA or patent foramen ovale) exists, blood from the systemic and pulmonary circulations can mix. Clinicians use PGE to keep PDA open.
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Transposition of great vessels: Transposition of the great vessels is a common congenital heart disease in offspring of mothers with what disease?
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Diabetes
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Coarctation of aorta: Where is the aortic stenosis in the infantile type of coarctation?
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Preductal (proximal to insertion of ductus arteriosus) - INfantile (in close to heart)
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Coarctation of aorta: Where is the aortic stenosis in the adult type of coarctation?
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Postductal (distal to ductus arteriosus). - ADult (Distal to Ductus)
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Coarctation of aorta: Name 3 symptoms in adult type coarctation?
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(1) Notching of the ribs (2) HTN in uper extremities (3) Weak pulses in uper extremities
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Coarctation of aorta: What is the Male-to-Female ratio in coarctation?
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3-to-1
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Coarctation of aorta: What pulses should you check on physical exam?
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Femoral
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Patent ductus arteriosus: Which direction is the shunt in a neonate with PDA?
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Left-to-right
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Patent ductus arteriosus: What change occurs to the heart in PDA?
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RVH and failure
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Patent ductus arteriosus: What is the auscultatory finding in PDA?
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Continuous, "machine-like" murmur.
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Patent ductus arteriosus: How is patency maintained in PDA?
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prostaglandin (PGE) synthesis and low Oxygen tension.
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Patent ductus arteriosus: What drug is used to close a PDA?
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Indomethacin
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Patent ductus arteriosus: How is a PDA kept open?
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porstaglandin--PGE
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Patent ductus arteriosus: Why would you want to keep a PDA open?
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To sustain life in conditions such as transposition of the great vessels.
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Autosomal trisomies: What is the most common chromosomal disorder and cause of congenital mental retardation?
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Down Syndrome (trisomy 21), 1:700
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Autosomal trisomies: In Down syndrome, 4% of cases are due to ------- translocation, and 1% are due to -------- mosaicism
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Robertsonian; Down
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Autosomal trisomies: 95% of Down syndrome cases occur because of --------- --------- of homologous chromosomes
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meiotic nondisjunction
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Autosomal trisomies: What is the type and cause of the most common congenital heart malformation in Down syndrome?
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Septum-primum-type ASD due to endocardial cushion defects
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Autosomal trisomies: Name 8 findings in trisomy 21
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(1) mental retardation (2) flat facial profile (3) prominent epicanthal folds (4) simian crease (5) duodenal atresia (6) congenital heart disease (7) Alzheimer's in affected >35 yrs old (8) Increased risk of ALL
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Autosomal trisomies: Name a risk factor for Down Syndrome
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Advanced maternal age (1:500 < 20 yo; 1:25 > 45 yo)
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Autosomal trisomies: What is the name of the syndrome associated with trisomy 18?
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Edwards' syndrome (Election age = 18)
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Autosomal trisomies: Name 7 findings in trisomy 18
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(1) severe mental retardation (2) rocker bottom feet (3) low-set ears (4) microngathia (5) congenital heart dz (6) clenched hands (flexion of fingers) (7) prominent occiput
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Autosomal trisomies: What is the life expectancy in trisomy 18?
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Death usually w/in 1 year of birth
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Autosomal trisomies: What chromosomal anomaly is found in Patau's syndrome?
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trisomy 13 (1:6000)
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Autosomal trisomies: Name 7 findings in Patau's
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(1) severe mental retardation (2) microphthamlia (3) microcephaly (4) cleft lip/palate (5) abnormal forebrain structures (6) polydactyly (7) congenital heart dz
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Autosomal trisomies: What is the life expectancy in Patau's?
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Death usually w/in 1 year of birth
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Genetic gender disorders: What is the chromosomal anomaly in Klinefelter's syndrome?
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XXY (1:850) - male
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Genetic gender disorders: Name 5 characteristics of Klinefelter's syndrome
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(1) Testicular atrophy (2) Enuchoid body shape (3) Tall, long extremities (4) Gynecomastia (5) Female hair distribution
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Genetic gender disorders: What is a Barr body and is it found kin Klinefelter's syndrome?
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It is the inactivated X chromosome. Yes.
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Genetic gender disorders: What is the chromosomal anomaly in Turner's syndrome?
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Female XO; (1:3000)
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Genetic gender disorders: Name 4 characteristics of Turner's syndrome
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(1) Short stature (2) Ovarian dysgenesis (streak ovary) (3) Webbing of next (4) Coarctation of the aorta
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Genetic gender disorders: Turner's syndrome is the most common cause of primary ------------
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amenorrhea
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Genetic gender disorders: Is there a Barr body in Turner's syndrome?
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No
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Genetic gender disorders: Double Y males have what genotype?
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XYY (1:1000) - male
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Genetic gender disorders: What is the double Y phenotype?
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Normal phenotype, very tall, severe acne, antisocial behavior (seein in 1-2% of XYY males; seen increasingly among prison inmates)
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Muscular dystrophies: How are muscular dystrophies diagnosed?
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Elevated CPK and muscle biopsy
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Muscular dystrophies: What is the gene involved in muscular dystrophy?
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Dystrophin
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Muscular dystrophies: What is the mutation in Duchenne's MD?
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Frame-shift mutation - deletion of dystrophin gene - accelerated muscle breakdown.
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Muscular dystrophies: What is the age of onset in Duchenne's MD?
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Before 5 years
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Muscular dystrophies: In what muscles does weakness begin with Duchenne's MD?
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Pelvic girdle muscles and progresses superiorly
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Muscular dystrophies: Name 3 diagnostic characteristics of Duchenne MD.
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(1) Pseduohypertrophy of calf muscles due to fibrofatty replacement of muscle (2) Cardiac myopathy (3) Use of Gowers' maneuver, requiring assistance of uper extremities to stand up - indicates proximal lower limb weakness
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Muscular dystrophies: What distinguishes Becker's from Duchenne's MD?
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Less severe mutation in Becker's. Less debilitating.
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Pseudohermaphroditism: What is pseudohermaphroditism?
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Disagreement between the phenotypic (external genitalia) and gonadal (testes vs. ovaries) sex.
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Pseudohermaphroditism: A female pseudohermaphrodite has ------- present, but external genitalia are -------- or -----------.
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ovaries; virilized or ambiguous
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Pseudohermaphroditism: What causes female pseudohermaphroditism?
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Excessive and inapropraite exposure to androgenic steroids during early gestation (i.e.,congenital adrenal hyperplasia or exogenous administration of androgens suring pregnancy).
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Pseudohermaphroditism: What are the phenotypes in female and male pseudohermaphroditism?
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female - XX; male - XY
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Pseudohermaphroditism: A male pseudohermaphrodite has ------- present, but external genitalia are --------- or ---------.
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testes; female or ambiguous
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Pseudohermaphroditism: What is the most common form of male pseudohermaphroditism?
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Testicular feminization (androgen insensitivity), which results from a mutation in the androgen receptor gene (x-linked); blind-end vagina
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Pseudohermaphroditism: What determines gender identity?
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External genitalia and sex of upbringing.
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True Hermaphrodite (46,XX or 47, XXY): What is a true hermaphrodite?
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Both ovary and testicular tissue present; ambiguous genitalia.
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True Hermaphrodite (46,XX or 47, XXY): What are the genotypic possibilities for a true hermaphrodite?
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46,XX or 47,XXY
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Testicular Feminization syndrome (46, XY): What is the molecular defect in testicular feminization syndrome?
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Defect in DHT receptor resulting in normal-apearing female
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Testicular Feminization syndrome (46, XY): What genitalia are present in testicular feminization syndrome?
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female genitalia with rudimentary vagina; uterus and uterine tubes generally absent; develop testes (often found in labia majora; surgically removed to prevent malignancy)
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Testicular Feminization syndrome (46, XY): What are the genotype and horomone levels in testicular feminization syndrome?
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46, XY; levels of testosterone, estrogen and LH are all high
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5a-reductase deficiency: What is the biochemical consequence of 5a-reductase deficiency
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Unable to convert testosterone to DHT.
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5a-reductase deficiency: Describe genital development in 5a-reductase deficiency.
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Ambiguous genitalia until puberty, when increased testosterone causes masculinization of genitalia.
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5a-reductase deficiency: What are the hormone levels in 5a-reductase deficiency.
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Testosterone/estrogen levels are normal; LH is normal or elevated.
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Cri-du-chat syndrome: What is the mutation in Cri-du-chat syndrome?
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Congenital deletion of short arm of chromosome 5 (46,XX or XY, 5p-)
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Cri-du-chat syndrome: What are the findings in Cri-du-chat
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Microcephaly, severe mental retardation, high-pitched crying/mewing, epicanthal folds, cardiac abnormalities.
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Cri-du-chat syndrome: What does Cri-du-chat mean in english, which might help remember the symptoms?
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Cry of the cat.
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Fragile X syndrome: What is the 2nd most common cause of genetic mental retardation?
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Fragile X syndrome
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Fragile X syndrome: What genetic change is involved in Fragile X syndrome?
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x-linked defect affecting the methylation and expression of the FMR1 gene.
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Fragile X syndrome: Name 4 physical features associated with Fragile X syndrome?
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(1) macro-orchidism (enlarged testes) (2) Long face with a large jaw (3) large everted ears (4) autism
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Cystic Fibrosis (CF): What is the genetic defect in cystic fibrosis?
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Autosomal-recessive defect in CFTR gene on chromosome 7
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Cystic Fibrosis (CF): What is the molecular defect in CF?
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Defective Cl- channel
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Cystic Fibrosis (CF): What are the consequences of the defect in CF?
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The defective chloride channel causes secretion of abnormally thick mucus that plugs lungs, pancreas and liver, which leads to recurrent pulmonary infections (pseudomonas species and S. aureus), chronic bronchitis, bronchiectasis, pancreatic insufficiency (malabsorption and steatorrhea), meconium ileus in newborns.
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Cystic Fibrosis (CF): Name a diagnostic test for CF.
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Increased concentration of Cl- ions in sweat test.
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Cystic Fibrosis (CF): Why does CF cause infertility in males?
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Absent vas deferens.
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Cystic Fibrosis (CF): What vitamins are often deficient in CF?
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Fat-soluble - A,D,E,K
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Most common lethal genetic disease of Caucasians.
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Cystic Fibrosis
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Cystic Fibrosis (CF): What is the treatment for CF?
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N-acetylcysteine to loosen mucous plugs.
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Autosomal-dominant diseases: A patient presents with flank pain, hematuria, hypertension, progressive renal failure and has a mutation in one of his copies of APKD1 (chromosome 16); what is the diagnosis?
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Adult polycystic kidney disease. N.B. the juvenile form is recessive.
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Autosomal-dominant diseases: Name 2 other characteristics of adult polycystic kidney disease.
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(1) always bilateral, (2) massive enlargement of the kidneys due to multiple large cysts.
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Autosomal-dominant diseases: What sequelae are associated with adult polycystic kidney disease?
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(1) polycystic liver disease (2) berry aneurysms (3) mitral valve prolapse
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Autosomal-dominant diseases: What disease involves elevated LDL owing to defective or absent LDL receptor?
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Familial hypercholesterolemia (type IIA)
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Autosomal-dominant diseases: What are the average cholesterol levels in heterozygotes and homozygotes with familial hypercholesterolemia (tyype IIA)?
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heterozygotes (1:500) - 300 mg/dL homozygotes - 700+ mg/dL
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Autosomal-dominant diseases: What are 3 sequelae of familial hypercholesterolemia (type IIA)?
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(1) severe atherosclerotic disease early in life (2) tendon xanthomas (classically in the Achilles tendon) (3) MI may develop before age 20
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Autosomal-dominant diseases: What is the genetic defect in Marfan's syndrome?
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Fibrillin gene mutation leads to connective tissue disorders.
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Autosomal-dominant diseases: What are the skeletal abnormalities in Marfan's?
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tall with long exteremities, hyperextensive joints, and long, tapering fingers and toes.
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Autosomal-dominant diseases: What are the cardiovascular risks in Marfan's?
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cystic medial necrosis of aorta leads to aortic incompetence and dissecting aortic aneurysms; flopy mitral valve.
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Autosomal-dominant diseases: What are the ocular risks in Marfan's?
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Subluxation of lenses.
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Autosomal-dominant diseases: What is another name for Neurofibromatosis type 1?
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von Recklinghausen's disease
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Autosomal-dominant diseases: What chromosome is affected in NF type 1?
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Long arm of chromosome 17 (17 letters in von Recklinghasen's)
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Autosomal-dominant diseases: What are 5 classic characteristics of people with NF type 1?
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(1) café-au-lait spots (2) neural tumors (3) Lisch nodules (pigmented iris hamartomas) (4) skeletal disorders (e.g., scoliosis) (5) Increased tumor susceptibility
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Autosomal-dominant diseases: What disease is associated with bilateral acoustic neuroma?
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Neurofibromatosis type 2
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Autosomal-dominant diseases: What gene is affected in neurofibromatosis type 2?
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NF2 gene on chromosome 22; (type 2 = 22)
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Autosomal-dominant diseases: What is the genetic mutation in Von-Hippel-Lindau disease?
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Deletion of VHL gene (tumor supressor) on chromosome 3p. (Von Hipel-Lindau = 3 words for chromosome 3)
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Autosomal-dominant diseases: What are the clinical findings in Von-Hippel-Lindau disease?
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hemiangioblastomas of retina/cerebellum/medulla; about half of affected individuals develop multiple bilateral renal cell carcinomas and other tumors.
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Autosomal-dominant diseases: What is the diagnosis in a 20-50 year old person who presents with depression, progressive dementia, choreiform movements, caudate atrophy, and decreased levels of GABA and Ach in the brain?
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Huntington's disease
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Autosomal-dominant diseases: What chromosome holds the gene involved in Huntington's?
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Chromosome 4; triplet repeat disorder ("Hunting 4 food")
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Autosomal-dominant diseases: What disease is responsible for a colon that ecomes covered with adenomatous polyps after puberty?
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Familial adenomatous polyposis (FAP)
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Autosomal-dominant diseases: What is the progression in Familial adenomatous polyposis if colon not resected?
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Colon cancer
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Autosomal-dominant diseases: What is the genetic defect in Familial adenomatous polyposise?
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deletion on chromosome 5 - 5 letters in polyp
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Autosomal-dominant diseases: What are 3 characteristics of hereditary spherocytosis?
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(1) spheroid erythrocytes (2) hemolytic anemia (3) increased MCHC
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Autosomal-dominant diseases: What is the cure for hereditary spherocytosis?
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splenectomy
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Autosomal-dominant diseases: What is the genetic defect in achondroplasia?
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Autosomal dominant cell-signaling defect of fibroblast growth factor (FGF) receptor 3.
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Autosomal-dominant diseases: What are the physical characteristics of achondroplasia?
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Dwarfism, short limbs, but head and trunk are normal size.
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X-linked or AR:: Cystic fibrosis
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AR
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X-linked or AR:: albinism
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AR
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X-linked or AR:: Fragile X
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X-linked
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X-linked or AR:: Duchenne's muscular dystrophy
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X-linked
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X-linked or AR:: hemophilia A and B
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X-linked
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X-linked or AR:: a1-antitrypsin deficiency
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AR
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X-linked or AR:: Fabry's
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X-linked
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X-linked or AR:: G6PD deficiency
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X-linked
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X-linked or AR:: Hunter's syndrome
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X-linked
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X-linked or AR:: Phenylketonuria (PKU)
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AR
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X-linked or AR:: thalassemias
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AR
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X-linked or AR:: sickle cell anemias
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AR
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X-linked or AR:: ocular albinism
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X-linked
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X-linked or AR:: glycogen storage diseases
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AR
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X-linked or AR:: mucopolysaccharidoses (except Hunter's)
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AR
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X-linked or AR:: sphingolipidoses (except Fabry's)
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AR
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X-linked or AR:: infant polycystic kidney
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AR
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X-linked or AR:: Lesch-Nyhan syndrome
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X-linked
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X-linked or AR:: Bruton's agammaglobulinemia
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X-linked
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X-linked or AR:: hemochromatosis
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AR
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X-linked or AR:: Wiskott-Aldrich syndrome
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X-linked
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X-linked or AR:: What are femal carriers of x-linked recessive disorders rarely affected?
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Inactivation of X chromosomes in each cell
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Neural Tube Defects (NTD): Name two associations with neural tube defects during pregnancy.
|
(1) Low folic acid intake (2) Elevated a-fetoprotein in amniotic fluid
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Neural Tube Defects (NTD): What NTD is associated with failure of bony spinal canal to close, but no structural herniation?
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Spina bifida occulta
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Neural Tube Defects (NTD): Which NTD is involved with herniation of meninges through spinal canal defect?
|
Meningocele
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Neural Tube Defects (NTD): What is the NTD that involves herniation of meninges AND spinal cord through spinal canal defect?
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Meningomyelocele
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Neural Tube Defects (NTD): Which NTD is usually seen at lower vertebral levels?
|
Spina bifida occulta
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Neural Tube Defects (NTD): Take a look at the figures in the book for good visualization of the NTDs.
|
0
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Fetal Alcohol Syndrome: Who is at greatest risk of FAS?
|
Newborns of mothers who consumed significant amounts of alcohol (teratogen) during pregnancy (highest risk at 3-8 weeks).
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Fetal Alcohol Syndrome: Name 5 congenital abnormalities in FAS?
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(1) pre and postnatal developmental retardation (2) microcephaly (3) facial abnormalities (4) limb dislocation (5) heart and lung fistulas
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Fetal Alcohol Syndrome: How does FAS rank among congenital malformations in the U.S.?
|
It's number 1
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Fetal Alcohol Syndrome: What is the presumed mechanism of FAS?
|
Inhibition of cell migration?
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Fetal Alcohol Syndrome: AUTHOR
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Neha Pathak
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NEOPLASTIC PROGRESSION: when cells increase in number it is called?
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hyperplasia
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NEOPLASTIC PROGRESSION: what are two enzymes that allow neoplastic cells to invade th ebasement membrane?
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collagenase and hydrolase
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NEOPLASTIC PROGRESSION: when cells have an increased nulear to cytoplasmic ratio but have not invaded the basement membrane, it is called?
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carcinoma in situ
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_ -PLASIA DEFINITIONS: squamous _________ occurs in the trachea and bronchi of smokers
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metaplasia
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_ -PLASIA DEFINITIONS: what is it called when a cell has reversible preneoplastic changes with abnormal shape and size?
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dysplasia
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_ -PLASIA DEFINITIONS: abnormal cells that lack differentiation are called?
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anaplastic cells
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TUMOR STAGE VS. GRADE: staging of a tumor takes into account what factors?
|
TMN size of tumor, node involvment, metastases
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TUMOR STAGE VS. GRADE: histolgy of a tumor is used to determine?
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grade
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TUMOR STAGE VS. GRADE: what has more prognostic value? Grade or stage?
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stage
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TUMOR NOMENCLATURE: the term _________ implies epithelial origin, whereas _________ implies mesenchymal origin
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carcinoma, sarcoma
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TUMOR NOMENCLATURE: a tumor of blood vessels is called what when it is benign? When it is malignant?
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hemangioma, angiosarcoma
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TUMOR NOMENCLATURE: what is a benign tumor of skeletal muscle called?
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rhabdomyoma
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DISEASES ASSOCIATED WITH NEOPLASMS: Kaposi's sarcoma and aggressive malignant lymphomas are associated with what disease
|
AIDS
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DISEASES ASSOCIATED WITH NEOPLASMS: Actinic Keratosis predispose to what disease?
|
squamous cell carcinoma of skin
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DISEASES ASSOCIATED WITH NEOPLASMS: down syndrome is associated with what neoplasm?
|
ALL
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ONCOGENES: c-myc oncogenes are associated with what neoplasm?
|
burkitt's lymphoma
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ONCOGENES: breast, ovarian, and gastic carcinomas all have this oncogene mutation in common?
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erb B2
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ONCOGENES: MEN II and III are associated with what oncogenic mutation?
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ret
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TUMOR SUPRESSOR GENES: Name the associated tumor witht the following tumor supressor gene mutations: Rb, APC, WT1
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retinoma blastoma, colorectal cancer, wilms tumor
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TUMOR SUPRESSOR GENES: p53 is on what chromosome
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17p
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TUMOR SUPRESSOR GENES: osteosarcoma is associated with what tumor supressor gene mutation
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Rb
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TUMOR MARKERS: TRAP is a tumor marker for what neoplasm
|
hairy cell leukemia
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TUMOR MARKERS: what tumor marker is elevated in hyatidiform moles
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beta-HCG
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TUMOR MARKERS: ovarian tumors are associated with what tumor marker
|
CA-125
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ONCOGENIC VIRUSES: the virus associated with burkitts and nasopharyngeal cancer is?
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ebv
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ONCOGENIC VIRUSES: hpv is responsible for what cancers?
|
cervical, penile, and anal carcinoma
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ONCOGENIC VIRUSES: what virus is responsible for kaposis sarcoma?
|
hhv8
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CHEMICAL CARCINOGENS: aflatoxin, vinyl chloride and ccl4 damage what organ?
|
liver
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CHEMICAL CARCINOGENS: nitrosamines cause cancer in what organs?
|
esophagus or stomach
|
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CHEMICAL CARCINOGENS: asbestos causes what types of cancer?
|
bronchogenic and mesothelioma
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LOCAL EFFECTS OF TUMORS: When the following are obstructed, what can occur: bronchus? Biliary tree? Left colon?
|
pneumonia, jaundice, constipation
|
|
LOCAL EFFECTS OF TUMORS: tumor mass in the brain can cause the following
|
seizure, increased intracranial pressure, mass effect and herniation
|
|
LOCAL EFFECTS OF TUMORS: compression of the recurrent laryngeal nerve can cause what?
|
hoarseness
|
|
PROSTATIC ADENOCARCINOMA: what lobe/zone is most often involved in prostatic cancer?
|
posterior lobe, peripheral zone
|
|
PROSTATIC ADENOCARCINOMA: what is a common site of metastases for prostate cancer?
|
bone
|
|
PROSTATIC ADENOCARCINOMA: what are useful tumor markers for prostate CA
|
psa, and prostatic acid phosphatase
|
|
SKIN CANCER: this type of skin cancer has palisading nuclei
|
basal cell carcinoma
|
|
SKIN CANCER: dyplastic nevi are a precursor fot this type of cancer
|
melanoma
|
|
SKIN CANCER: this type of skin cancer is associated with keratin pearls
|
squamous cell carcinoma of skin
|
|
PRIMARY BONE TUMORS: the translocation 11;22 is associated with this cancer of the bone that occurs most commonly in young boys
|
ewing's sarcoma
|
|
PRIMARY BONE TUMORS: this tumor is characterized by a "double bubble" or "soap bubble" appearance
|
benign giant cell tumor
|
|
PRIMARY BONE TUMORS: this is the most common benign bone tumor, usually in men younger than 25, with a rare transformation to malignancy
|
osteochondroma
|
|
PRIMARY BONE TUMORS: AUTHOR
|
Gabe Pitta
|
|
Primary Brain Tumors-Adult peak incidence: Most common adult brain tumor?
|
Glioblastoma multiforme (grade IV astrocytoma) See pseudopalisading tumor cells, central necrosis and hemorrhage.
|
|
Primary Brain Tumors-Adult peak incidence: Second most common adult tumor?
|
Meningioma, occurring in convexities of hemispheres and parasagittal region. See psammoma bodies.
|
|
Primary Brain Tumors-Adult peak incidence: Benign, slow-growing tumor in frontal lobes?
|
Oligodendroglioma, look for fried egg apearance, often calcified.
|
|
Primary Brain Tumors-Adult peak incidence: Third most common tumor, often localized to CN8?
|
Schwannoma, see it in acoustic Schwannoma. Antoni A (compact) and Antoni B (loose) patterns.
|
|
Primary Brain Tumors-Adult peak incidence: Most common forms are prolactin-secreting?
|
Pituitary Adenoma, which derives from Rathke's Pouch and can produce secondary bitemporal hemianopsia and hypopituitarism
|
|
Primary Brain Tumors-Child Peak Incidence: Highly malignant cerebellar tumor?
|
Medulloblastoma, can compress 4th ventricle and cause hydrocephalus. See rosettes or pseudorosettes.
|
|
Primary Brain Tumors-Child Peak Incidence: Cerebellar tumor associated with von Hippel-Landau syndrome?
|
Hemangioblastoma, see foamy cells and high vascularity, can produce excess EPO-->polycythemia.
|
|
Primary Brain Tumors-Child Peak Incidence: Commonly found in fourth ventricle, causing hydrocephalus?
|
Ependyomomas, which have perivascular rosettes and rod-shaped blepharoblasts near nucleus on exam.
|
|
Primary Brain Tumors-Child Peak Incidence: Diffusely infiltrating glioma, usually found in posterior fossa?
|
Low-grade Astrocytoma
|
|
Primary Brain Tumors-Child Peak Incidence: Benign tumor often confused with pituitary adenoma?
|
Craniopharyngioma, which also is derived from Rathke's pouch, also presents with bitemporal hemianopsia, also calcified.
|
|
Common sites that receive metastatic tissue: To Brain?
|
Lung, Breast, Skin (melanoma), Kidney (renal cell carcinoma), GI. Lots of Bad Stuff Kills Glia. 50% of brain tumors are due to metastases.
|
|
Common sites that receive metastatic tissue: To liver?
|
Colon>Stomach>Pancreas>Breast>Lung. Cancer Sometimes Penetrates Benign Liver. Metastases much more common than primary liver tumors.
|
|
Common sites that receive metastatic tissue: To bone?
|
Breast, lung, thyroid, testes, kidney, prostate.=> "BLT with a Kosher Pickle."
|
|
Common sites that receive metastatic tissue: Most common organ receiving metastases?
|
Adrenal medulla, then cortex.
|
|
Common sites that receive metastatic tissue: Most common organ sending metastases?
|
Lung>Breast/Stomach
|
|
Paraneoplastic effects of tumors: Cushing's Syndrome
|
ACTH/ACTH-like peptide from small-cell lung CA
|
|
Paraneoplastic effects of tumors: SIADH
|
ADH/ANP from small cell lung CA and intracranial neoplasms.
|
|
Paraneoplastic effects of tumors: Hypercalcemia
|
PTH-related peptide/TGF-alpha/TNF-Alpha/IL-2 from squamous cell lung CA, renal cell CA, Breast CA, multiple myeloma, bone metastasis.
|
|
Paraneoplastic effects of tumors: Polycythemia
|
EPO from renal cell CA.
|
|
Paraneoplastic effects of tumors: Lambert-Eaton Syndrome
|
Antibodies against presynaptic Ca2+ channels at NMJ, generated by Thymomas and bronchogenic CA.
|
|
Paraneoplastic effects of tumors: Gout
|
Hyperuricemia due to excess nucleic acid turnover, found in various neoplasms.
|
|
Cancer Epidemiology: Male incidence?
|
Prostate(32%)>Lung(16%)>Colon and Rectum (12%)
|
|
Cancer Epidemiology: Male Mortality?
|
Lung(33%)>Prostate(13%)
|
|
Cancer Epidemiology: Female incidence?
|
Breast (32%)>Lung(13%)>Colorectal(13%)
|
|
Cancer Epidemiology: Female Mortality?
|
Lung(23%)>Breast(18%)
|
|
HEMATOLOGIC PATHOLOGY: Anemia
|
0
|
|
HEMATOLOGIC PATHOLOGY: Anemia presenting with increased TIBC, decreased ferritin, decreased serum iron.
|
Mycrocytic, Hypochromic, usually secondary to iron deficiency. Also seen with Thalassemia, lead poisoning
|
|
HEMATOLOGIC PATHOLOGY: Anemia in patients with B12/Folate deficiency
|
Macrocytic (MCV>100), presents with PMN hypersegmentation on blood smear. B12 deficiency presents with neuro effects, folate deficiency much easily reached through bad diet. Also seen in patients taking drugs blocking DNA synthesis (sulfa drugs, AZT)
|
|
HEMATOLOGIC PATHOLOGY: Anemia in patients with normocytic, normochromic smears?
|
Hemorrhagic, autoimmune hemolytic, enzyme defects (G6PD), bone marrow dz, anemia of chronic dz. Decreased serum haptoglobin and increased LDH indicate RBC hemolysis. Direct Coomb's test can show an immune-mediated process.
|
|
HEMATOLOGIC PATHOLOGY: Anemia in patients with a decreased TIBC, decreased serum iron, and decreased iron saturation?
|
Anemia of chronic disease
|
|
HEMATOLOGIC PATHOLOGY: Anemia in patients with an increased TIBC, decreased serum iron, and normal iron saturation?
|
Iron-deficiency anemia.
|
|
HEMATOLOGIC PATHOLOGY: Patient with normal TIBC, increased serum iron, and 100% iron saturation (normal is 20-50%)
|
Iron overload (hemosiderosis)
|
|
Aplastic Anemia: Patient presentation of Aplastic Anemia?
|
Patients with pancytopenia characterized by severe anemia, neutropenia, and thrombocytopenia caused by failure or destruction of multipotent myeloid stem cells.
|
|
Aplastic Anemia: What causes aplastic anemia?
|
Radiation, benzene, chloramphenicol, alkylating agents, antimetabolites, viral agents, Fanconi's anemia, idiopathic causes.
|
|
Aplastic Anemia: Common Sx?
|
Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection.
|
|
Aplastic Anemia: How do the blood smear and bone marrow aspirate appear?
|
Blood smear: pancytopenia with normal cell morphology. Aspirate:hypocellular marrow with fatty infiltration.
|
|
Aplastic Anemia: What's the treatment of aplastic anemia?
|
Withdraw offending agent, BMT, RBC/platelet transfusion, G-CSF or GM-CSF.
|
|
Hereditary Spherocytosis: How do patients with hereditary psherocytosis present (smear and labs)?
|
Smear shows microcytic RBCs that are small and round with no central pallor. The patients will have normal Hgb and MCV.
|
|
Hereditary Spherocytosis: What's the cause of hereditary spherocytosis?
|
Intravascular hemolysis due to spectrin defect.
|
|
Hereditary Spherocytosis: How is it confirmed and tested?
|
Will be Coombs' negative (unlike warm antibody hemolysis), can perform osmotic fragility test.
|
|
Hereditary Spherocytosis: What are some associated diseases?
|
Gallstones, splenomegaly, anemia, and jaundice.
|
|
Blood Dyscrasias-Sickle Cell Anemia: What is the HbS mutation?
|
Glutamate-->Valine in a Beta chain. Heterozygotes are usually malaria-resistant. *% of Af-Ams carry the HbS trait, 0.2% have the disease.
|
|
Blood Dyscrasias-Sickle Cell Anemia: What can precipitate sickling?
|
Low O2, dehydration.
|
|
Blood Dyscrasias-Sickle Cell Anemia: What are the common complications of HbS homozygotes?
|
aplastic crises from parvovirus infection, autosplenectomy, risk of encapsulated organism infection, salmonella osteomyelitis, vaso-occlusive pain crises, and splenic sequestration crises.
|
|
Blood Dyscrasias-Sickle Cell Anemia: What is the HbC defect?
|
Different Beta-chain mutation, the patients with HbC or HbSC have milder dz than HbSS patients.
|
|
Blood Dyscrasias-Sickle Cell Anemia: What are the treatment options?
|
Hydroxyurea (increased HbF) and bone marrow transplantation.
|
|
Blood Dyscrasias-Alpha-Thalassemia: What populations have the most prevalence?
|
Mediterranean populations. (thalaSEAmia)
|
|
Blood Dyscrasias-Alpha-Thalassemia: What is the etiology?
|
Underproduction of the alpha-globin chain, with no compensatory increase of any other chains. HbH has Beta-4 tetramers and lacks 3 alpha-globin genes.
|
|
Blood Dyscrasias-Alpha-Thalassemia: What is the presentation of a patient lacking all four alpha-globin genes?
|
hydrops fetalis and intrauterine fetal death.
|
|
Blood Dyscrasias-Beta-Thalassemia: Patient Presentation of Beta-Thalassemia major?
|
severe anemia requiring blood transfusion. Cardiac failure is often due to secondary hemochromatosis.
|
|
Blood Dyscrasias-Beta-Thalassemia: Etiology of Beta-Thalassemia major?
|
Beta chain is absent, fetal Hgb production is compensatorily increased but is inadequate.
|
|
Blood Dyscrasias-Beta-Thalassemia: Etiology of Beta-thalassemia minor?
|
The Beta chain is underproduced, again see fetal HgB compensatory increase. HbS/Beta-thalassemia heterozygote has mild to moderate disease.
|
|
DIC: What is the definition of DIC?
|
Activation of the coagulation cascade leading to microthrombi and global consumption of platelets, fibrin, and coagulation factors.
|
|
DIC: What causes DIC?
|
Obstetric complications (most common cause), gram-negative sepsis, transfusion, trauma, malignancy, acute pancreatitis, nephrotic syndrome.
|
|
DIC: What are the lab findings in DIC?
|
Increased PT, increased PTT, incrased fibrin split products (D-dimers), decreased platelet count.
|
|
Bleeding Disorders: What disorder type presents with mucous membrane bleeding, petechiae, purpura, and prolonged bleeding time?
|
Platelet abnormalities (microhemorrhages), which can be caused by ITP (antiplatelet antibodies and increased megakaryocytes), TTP (schistocytes), drugs, and DIC (increased fibrin split products).
|
|
Bleeding Disorders: What disorder type presents with hemarthroses (bleeding into joints), easy brusing, prolonged PT and/or PTT?
|
Coagulopathies (macrohemorrhages), which can be caused by Hemophilia A/B and von Willebrand's disease (most common)
|
|
Bleeding Disorders: What is the deficiency in Hemophilia A?
|
Factor VIII
|
|
Bleeding Disorders: What is the deficiency in Hemophilia B?
|
Factor IX
|
|
Bleeding Disorders: What is the deficiency in vW dz?
|
Deficiency of von Willebrand's antigen.
|
|
Bleeding Disorders: Which factors does the PT measure?
|
Extrinsic: Factors II, V, VII, and X.
|
|
Bleeding Disorders: Which factors does the PTT measure?
|
Intrinsic: All factors except VII and XIII.
|
|
Hemorrhagic disorders: What presents with increased bleeding time, normal platelet count, and normal PT/PTT and platelet count?
|
Qualitative platelet defects, can be Bernard Soulier disease (defect in adhesion) or Glanzmann's thrombasthenia (defect in aggregation). Can also see these labs in vascular bleeding.
|
|
Hemorrhagic disorders: What presents with decreased platelet count, increased bleeding time, and normal PT/PTT?
|
Thrombocytopenia
|
|
Hemorrhagic disorders: Which diseases present with increased PTT and normal PT, platelet count, and bleeding time?
|
Hemophilia A and B
|
|
Hemorrhagic disorders: What presents with a high PTT, normal PT, normal platelets, and increased bleeding time?
|
vW disease
|
|
Hemorrhagic disorders: What presents with increased Bleeding time/Pt/PTT and decreased platelet count?
|
DIC
|
|
Lymphomas: Hodgkin's Versus NHL: Which one presents with Reed-Sternberg cells?
|
Hodgkin's
|
|
Lymphomas: Hodgkin's Versus NHL: Which one is associated with HIV and immunosuppression?
|
NHL
|
|
Lymphomas: Hodgkin's Versus NHL: Which one involves multiple, peripheral nodes, with common extranodal involvement?
|
NHL
|
|
Lymphomas: Hodgkin's Versus NHL: Which one is localized to a single group of nodes, with contiguous spread and rare extranodal involvement?
|
HL
|
|
Lymphomas: Hodgkin's Versus NHL: Which one presents with constitutional signs/symptoms: low-grade fever, night sweats, weight loss?
|
HL (NHL has few signs/symptoms)
|
|
Lymphomas: Hodgkin's Versus NHL: Which one presents with mediastinal lymphadenopathy?
|
HL
|
|
Lymphomas: Hodgkin's Versus NHL: Which one involves mostly the B cells (except lymphoblastic origin)?
|
NHL
|
|
Lymphomas: Hodgkin's Versus NHL: Which one has hypergammaglobulinemia?
|
neither. Multiple Myeloma has hypergammaglobulinemia, where the excess B cells are in the resting state.
|
|
Lymphomas: Hodgkin's Versus NHL: Which one has a 50% association with EBV?
|
HL
|
|
Lymphomas: Hodgkin's Versus NHL: Which one has bimodal age distribution?
|
HL (NHL has peak incidence at 20-40 years old)
|
|
Lymphomas: Hodgkin's Versus NHL: Which one has more common male presentation?
|
HL
|
|
Hodgkin's: What factors denote a good prognosis?
|
Increased lymphocytes, decreased RS cells.
|
|
Hodgkin's: Which HL type has the best prognosis?
|
Nodular sclerosing (65-75%), which has least RS cells and lots of lymphocytes. Lymphocyte-predominant LH also has excellent prognosis.
|
|
Hodgkin's: Which HL type is the most common?
|
Nodular sclerosing, affecting women more than men and primarily young adults.
|
|
Hodgkin's: What is the prognosis of mixed cellular HL?
|
Intermediate. There are lots of lymphocytes but also lots of RS cells.
|
|
Hodgkin's: Which HL type has the worst prognosis?
|
Lymphocyte-depleted, which affects older males with disseminated disease.
|
|
Hodgkin's: Which HL type has the most RS cells?
|
Mixed cellular.
|
|
NHL: Which NHL type has only B cells?
|
Small Lymphocytic lymphoma, follicular lymphoma, Burkitt's
|
|
NHL: Which NHL type has a mix of B cells and T cells?
|
Diffuse large cell , occurring mostly in elderly but sometimes in children.
|
|
NHL: Which NHL type has only T cells?
|
Lymphoblastic Lymphoma, which has immature T cells. It is a very aggressive T-cell lymphoma.
|
|
NHL: Which type is associated with a t(8;14) c-myc gene mutation?
|
Burkitt's Lymphoma, occurring mostly in children. Has a high-grade "starry sky" apearance.
|
|
NHL: Which type is associated with a t(14;18) mutation and overexpression of bcl-2?
|
Follicular lymphoma, which is difficult to cure but has an indolent course.
|
|
NHL: Which type is associated with EBV infection and is endemic in africa?
|
Burkitt's
|
|
NHL: Which is the most common childhood NHL?
|
Lymphoblastic Lymphoma, which also presents with ALL and a mediastinal mass.
|
|
NHL: Which is the most common adult version of NHL?
|
Follicular lymphoma.
|
|
NHL: Which types occur in adults?
|
Small lymphocytic lymphoma, follicular lymphoma.
|
|
NHL: Which types occur in children?
|
Lymphoblastic lymphoma, Burkitt's lymphoma.
|
|
NHL: Which one has a distribution of 80% adults and 20% children?
|
Diffuse large cell lymphoma, which ALSO has an 80% B cells 20% T cell distribution.
|
|
NHL: Which low-grade NHL type presents like CLL?
|
Small Lymphocytic lymphoma.
|
|
NHL: AUTHOR
|
John Peoples
|
|
Leukemias: Peripheral and bone marrow characteristics
|
Increased circulating leukocytes, bone marrow infiltrates of leukemic cells
|
|
Leukemias: Consequences of marrrow failure
|
Anemia (dec. RBC's), infections (dec. WBC's), hemorrhage (dec. platelets)
|
|
Leukemias: Common organs of infiltration
|
Liver, spleen, lymph nodes
|
|
Leukemias: Characteristics of acute leukemias
|
Blasts predominate, children or elderly, short or drastic course
|
|
Leukemias: ALL characteristics (4)
|
Lympholasts (pre-B or pre-T), children, most responsive to therapy, associated with Down's Syndrome
|
|
Leukemias: AML characteristics
|
Myeloblasts, adults, auer rods
|
|
Leukemias: Characteristics of chronic leukemias
|
More mature cells, midlife age range, longer, less devastating course
|
|
Leukemias: CLL characteristics - cells
|
Lymphocytes, non-Ab producing B cells, increased smudge cells on peripheral blood smear
|
|
Leukemias: CLL - population
|
older adults
|
|
Leukemias: CLL - presentation and course
|
lymphadenopathy, hepatosplenomegaly, few sx., indolent course
|
|
Leukemias: CLL is similar to?
|
very similar to SLL (small lymphocytic lymphoma)
|
|
Leukemias: CLL is associated with what type of anemia?
|
warm antibody autoimmune hemolytic anemia
|
|
Leukemias: CML cell characteristics
|
Myeloid stem cells, increased neutrophils and metamyelocytes
|
|
Leukemias: CML translocation?
|
Ph Chromosome, t(9;22), bcr-abl
|
|
Leukemias: CML acute complications?
|
blast crisis (AML)
|
|
Chromosomal translocations - the following disorder is associated with what translocation?: CML
|
Ph chromosome, t(9;22), bcr-abl
|
|
Chromosomal translocations - the following disorder is associated with what translocation?: Burkitt's lymphoma
|
t(8;14), c-myc activation
|
|
Chromosomal translocations - the following disorder is associated with what translocation?: Follicular lymphomas
|
t(14;18), bcl-2 activation
|
|
Chromosomal translocations - the following disorder is associated with what translocation?: AML- M3 type
|
t(15;17), responsive to all-trans retinoic acid (ATRA)
|
|
Chromosomal translocations - the following disorder is associated with what translocation?: Ewing's sarcoma
|
t(11;22)
|
|
Chromosomal translocations - the following disorder is associated with what translocation?: Mantle cell lymphoma
|
t(11;14)
|
|
Lymphomas and Leukemias: What are the chronic leukemias associated with T-lymphoblasts?
|
Sezary Syndrome, CLL-T (both L2)
|
|
Lymphomas and Leukemias: What are the acute leukemias associated with T-lymphoblasts?
|
ALL-T (L2), ALL-null (L1), ALL-common(L1)
|
|
Lymphomas and Leukemias: What are the chronic leukemias associated with B-lymphoblasts?
|
CLL-B (L3)
|
|
Lymphomas and Leukemias: What are the acute leukemias associated with B-lymphoblasts?
|
ALL-B (L3)
|
|
Lymphomas and Leukemias: What are the chronic leukemias associated with monoblasts?
|
Chonic monocytic (M5), chronic myelomonocytic (M4)
|
|
Lymphomas and Leukemias: What are the acute leukemias associated with monoblasts?
|
Acute monocytic (M5), acute myelomonocytic (M5)
|
|
Lymphomas and Leukemias: What are the chronic leukemias associated with myeloblasts?
|
CML (M1, 2 and 3), Polycythemia rubra vera (M1), myelofibrosis (M1)
|
|
Lymphomas and Leukemias: What are the acute leukemias associated with myeloblasts?
|
AML (M2 and M1), Promyelocytic (M1)
|
|
Lymphomas and Leukemias: What are the chronic leukemias associated with eos-myeloblasts?
|
Eosinophilic (rare)
|
|
Lymphomas and Leukemias: What are the chronic leukemias associated with normoblasts?
|
Chronic erythroid (M6, rare)
|
|
Lymphomas and Leukemias: What are the acute leukemias associated with normoblasts?
|
acute erythroleukemia (M6)
|
|
Lymphomas and Leukemias: What are the chronic leukemias associated with megakaryoblasts?
|
Idiopathic thrombocytopenia (M7)
|
|
Lymphomas and Leukemias: What are the acute leukemias associated wwith megakaryoblasts?
|
acute megakaryocytic leukemias (M7)
|
|
Multiple Myeloma: What type of cell proliferates in MM, and what is its histologic appearance
|
Monoclonal plasma cell, fried egg apearance
|
|
Multiple Myeloma: Where does MM arise?
|
bone marrow
|
|
Multiple Myeloma: The 2 most common ab's, in order, are:
|
IgG (55%), IgA (25%)
|
|
Multiple Myeloma: Common symptoms are:
|
lytic bone lesions and hypercalcemia, renal insifficiency, increased suscpetibility to infection, anemia
|
|
Multiple Myeloma: This disease is associated with:
|
primary amyloidosis
|
|
Multiple Myeloma: Ig light chains are also called:
|
Bence Jones proteins
|
|
Multiple Myeloma: 3 key diagnostic features:
|
lytic bone lesions on x-ray, M-spike on serum protein electrophoresis, Bence-Jones proteins in urine
|
|
Multiple Myeloma: Red blood cell appearance on peripheral smear:
|
Rouleaux formation (poker chips)
|
|
Multiple Myeloma: What 2 differences are seen in Waldenstrom's macroglobulinemia?
|
M-spike is IgM, no lytic lesions
|
|
Achalasia: Achalasia results from:
|
failure of relaxation of lower esophogeal sphincter due to loss of the myenteric plexus (Aeurbach's). [A-chalasia = absence of relaxation]
|
|
Achalasia: Achalasia causes:
|
progressive dysphagia
|
|
Achalasia: Diagnosis is made by:
|
barium swallow showing "bird beak" dilated esophagus with distal stenosis.
|
|
Achalasia: Secondary achalasia may result from this protozoan disease:
|
Chagas disease (treponema cruzi)
|
|
Achalasia: Associated with increased risk of:
|
esophageal carcinoma
|
|
Barrett's esophagus: The distal esophageal colummnar epithelium is replaced with….
|
Gastric columnar epithelium
|
|
Barrett's esophagus: Barrett's results from:
|
Reflux
|
|
Barrett's esophagus: Barrett's can progress to:
|
adenocarcinoma
|
|
Esophageal Cancer: Risk factors are (ABCDEF):
|
achalasia, barrett's esophagus, corrosive esophagitis/cigarettes, diverticuli (e.g. zenker's), esophogeal web/EtOH, familial
|
|
Esophageal Cancer: The most common esophageal cancer in the world is:
|
squamous cell carcinoma
|
|
Esophageal Cancer: The most common esophageal cancer in the US is:
|
equal between squamous cell and adenocarcinoma (decreased cigarette use).
|
|
Esophageal Cancer: Esophageal Adenocarcinoma is found where?
|
lower third
|
|
Esophageal Cancer: Esophageal squamous cell carcinoma is found where?
|
uper 2/3
|
|
Congenital Pyloric Stenosis: What does this cause in infant?
|
Projectile vomiting at aproximately 2 weeks of age
|
|
Congenital Pyloric Stenosis: Treatment entails:
|
surgery
|
|
Malabsorption syndromes: Autoantibodies are seen to what in Celiac Sprue?
|
Gluten (gliaden) in wheat and other grains
|
|
Malabsorption syndromes: The histologic appearance of celiac sprue:
|
villous flattening, lymphocytic infiltrate
|
|
Malabsorption syndromes: Tropical sprue is due to what type of agent?
|
Infectious, treated with Antibiotics
|
|
Malabsorption syndromes: What are you infected with if you have Whipple's Disease?
|
Tropheryma whipelli
|
|
Malabsorption syndromes: Histologic cell type seen in Whipple's disease:
|
PAS+ macrophages
|
|
Malabsorption syndromes: What is the most common disaccharide deficiency leading to malabsorption?
|
lactase => milk intolerance
|
|
Chronic Gastritis: Fundal gastritis (type A) is characterized by 4 A's, what are they?
|
Autoimmune disorder with Autoantibodies to parietal cells, pernicious Anemia, Achlorydia
|
|
Chronic Gastritis: Antral gastritis (Type B) is caused by:
|
a Bug, H. Pylori infection
|
|
Chronic Gastritis: Both forms of gastritis carry an increased risk of what?
|
Gastric carinoma
|
|
Peptic Ulcer Disease: 2 etiologic agents underlying gastric ulcers are:
|
H. pylori (70%) and NSAID's
|
|
Peptic Ulcer Disease: Degeneration of what leads to gastric ulcers?
|
Gastric mucosal protection v. gastric acid
|
|
Peptic Ulcer Disease: Does the pain of a gastric ulcer increase or decrease with meals?
|
Increases => weight loss
|
|
Peptic Ulcer Disease: One etiologic agent underlies duodenal ulcers - what is it?
|
H. pylori (100%)
|
|
Peptic Ulcer Disease: 2 pathogenic mechanisms are thought to lead to development of duodenal ulcer - what are they?
|
Increased gastric acid secretion and decreased mucosal protection
|
|
Peptic Ulcer Disease: What tends to hypertrophy with duodenal ulcers?
|
Bruenner's glands
|
|
Peptic Ulcer Disease: The margins of a doudenal ulcer are:
|
clean and punched out
|
|
Peptic Ulcer Disease: The 4 common complications of of duodenal ulcers are:
|
bleeding, penetration, perforation, and obstruction (not necessarily pre-cancerous)
|
|
Peptic Ulcer Disease: Does the pain of a duodenal ulcer increase or decrease with meals?
|
Decreases => weight gain
|
|
Peptic Ulcer Disease: How is H.pylori infection treated?
|
triple therapy (metronidazole, bismuth salicylate, amoxocillin or tetracycline) with or without proton pump inhibitor
|
|
Peptic Ulcer Disease: Does smoking effect peptic ulcer development?
|
Yes, it is 2x as common in smokers
|
|
IBD: The possible etiology of Crohn's disease is:
|
Infectious
|
|
IBD: The location and lesion type of Crohn's disease is:
|
Skip lesions in any portion of GI tract, usually terminal ileum, SI, and colon. Rectal sparing.
|
|
IBD: Gross Morphological features (6) of Crohn's disease are:
|
Transmural inflammation, cobblestone mucosa, creeping fat, bowel wall tickening (string sign on x-ray), linear ulcers, and fissure. (FAT OLD CRONE SKIpING DOWN A COBBLESTONE ROAD)
|
|
IBD: The microscopic morphological features of Crohn's disease are:
|
non-caseating granulomas
|
|
IBD: The four major complications of Crohn's disease are:
|
Strictures, fistulas, perianal diease, malabsorption leading to nutritional depletion.
|
|
IBD: Two major extraintestinal manifestations associated with Chron's disease are:
|
migratory polyarthritis and erythema nodosum
|
|
IBD: The possible etiology of UC is:
|
autoimmune
|
|
IBD: Location and lesion type of UC is:
|
continuous lesions of colon with rectal involvement
|
|
IBD: The two gross morphological features of UC are:
|
mucosal inflammation, friable mucosal pseudopolyps with freely hanging mesentery.
|
|
IBD: The microscopic morphological features of UC are:
|
crypt abcesses, ulcers
|
|
IBD: 3 severe complications of UC are:
|
severe stenosis, toxic megacolon, and colorectal carcinoma
|
|
IBD: Two major extraintestinal manifestations associated with UC are:
|
pyoderma gangrenosum, sclerosing cholangitis
|
|
Diverticular Disease: Diverticuli are blind pouches found in the:
|
alimentary tract
|
|
Diverticular Disease: Diverticuli are lined by (3 layers):
|
Mucosa, muscularis, and serosa
|
|
Diverticular Disease: The 4 GI tract locations of diverticuli are:
|
esophagus, stomach, duodenum and colon
|
|
Diverticular Disease: Why are most diverticuli termed false?
|
They lack or have an attenuated muscularis mucosa.
|
|
Diverticular Disease: Percent of older patients likely to get diverticulosis (many diverticula):
|
50% of patients >60
|
|
Diverticular Disease: The reasons for increasing number of diverticula with age are:
|
Increased intraluminal pressure and focal weaknes in the colonic wall.
|
|
Diverticular Disease: What type of diet is diverticulosis associated with?
|
low-fiber
|
|
Diverticular Disease: Sx of diverticulosis?
|
usually asymptomatic, sometimes vague discomfort.
|
|
Diverticular Disease: Diverticulitis commonly presents with pain where?
|
LLQ
|
|
Diverticular Disease: Complications of diverticulitis include:
|
perforation, peritonitis, abcess formation, bowel stenosis
|
|
Intussusception and Volvulus: What is intussuception?
|
telecoping of 1 bowel segment into distal segment.
|
|
Intussusception and Volvulus: Complication of intussusception is:
|
compromised blood suply.
|
|
Intussusception and Volvulus: What is volvulus?
|
Twisting of portion of the bowel around its mesentery.
|
|
Intussusception and Volvulus: What volvulus lead to?
|
obstruction.
|
|
Stomach Cancer: What is the most common type of stomach cancer?
|
adenocarcinoma
|
|
Stomach Cancer: Is this cancer aggresive?
|
Yes, it has early aggressive local spread and node/liver mets
|
|
Stomach Cancer: Stomach Cancer is associated with what 3 etiologic factors?
|
dietary nitrosamines, achlorhydria, chronic gastritis
|
|
Stomach Cancer: What is stomach cancer termed when it is diffusely infiltrative with thickened and rigid appearance?
|
Linitis plastica
|
|
Stomach Cancer: What does Virchow's node signify?
|
involvement of supraclavicular node by stomach mets
|
|
Stomach Cancer: What is Krukenberg's tumor?
|
bilateral stomach cancer mets to the ovary
|
|
Stomach Cancer: What are characteristics of Krukenberg's tumor?
|
Abundant mucus, "signet ring" cells
|
|
Hirschprung's Disease: What is Hirschprung's diease?
|
congential megacolon
|
|
Hirschprung's Disease: What is missing?
|
enteric nerve plexus (both Auerbach's and Meissner's). Seen on biopsy
|
|
Hirschprung's Disease: What is the cause of this disease?
|
failure of neural crest migration.
|
|
Hirschprung's Disease: How does this disease present?
|
Chronic constipation early in life.
|
|
Hirschprung's Disease: Which part of the colon is dilated?
|
That part proximal to the aganglionic segment - aganglionic portion is constricted.
|
|
Colorectal cancer risk factors: The risk factors are:
|
colorectal villous adenoma, IBD, low-fiber diet, age, FAP, HNPCC, personal and family hx. of colon cancer.
|
|
Colorectal cancer risk factors: What is Peutz-Jeghers, and does it lead to colorectal cancer?
|
It is a benign polyposis syndrome which is not a risk factor.
|
|
Colorectal cancer risk factors: Who schould be screened for colorectal cancer and how?
|
People over age 50, screen with stool occult blood test.
|
|
Cirrhosis/Portal HT: Cirrho in Greek means:
|
tawny yellow
|
|
Cirrhosis/Portal HT: Cirrhosis is:
|
diffuse fibrosis of the liver with destruction of norml architecture, nodular regeneration.
|
|
Cirrhosis/Portal HT: Cause of micronodular cirrhosis (nodules <3mm, uniform in size) is:
|
metabolic insult
|
|
Cirrhosis/Portal HT: Causes of macronodular cirrhosis (nodules >3mm, varied in size) are?
|
Significant liver injury leading to hepatic necrosis (post-infectious, drug-induced hepatitis)
|
|
Cirrhosis/Portal HT: Cirrhosis is assocated with what type of cancer?
|
hepatocellular carcinoma
|
|
Cirrhosis/Portal HT: The effects of portal hypertension are:
|
esophageal varices (hemetemesis, melena), peptic ulceration (melena), splenomegaly, caput medusae, ascites, hemmorhoids, and testicular atrophy
|
|
Cirrhosis/Portal HT: Portal hypertension may be relieved by what method?
|
Portacaval shunt between splenic vein ad left renal vein.
|
|
Cirrhosis/Portal HT: What are the effects of liver cell failure?
|
Coma, scleral icterus, fetor hepaticus (breath smells like a freshly opened corpse), spider nevi, gynecomastia, jaundice, loss of sexual hair, asterixis, bleeding tendency, anemia, ankle edema
|
|
Alcoholic Hepatitis: Hepatocytes in alcoholic hepatitis are:
|
swollen and necrotic
|
|
Alcoholic Hepatitis: Other histologic changes seen in aloholic hepatitis are:
|
neutrophil infiltration, mallory bodies (hyaline), fatty change, and sclerosis areound central vein
|
|
Alcoholic Hepatitis: SGOT (AST):SGPT (ALT) ratio is:
|
usually more than 1.5 (A Scotch and Tonic: AST elevated)
|
|
Budd Chiari Syndrome: What is Budd-Chiari Syndrome?
|
Occlusion of the IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease
|
|
Budd Chiari Syndrome: The features of congestive liver disease are:
|
hepatomegaly, ascites, abdominal pain, and eventual liver failure
|
|
Budd Chiari Syndrome: Budd-Chiari Syndrome is associated with what 3 conditions:
|
polycythemia vera, pregnancy, hepatocellular carcinoma
|
|
Wilson's Disease: Wilson's disease is?
|
Coper accumulation, especially in liver, brain and cornea
|
|
Wilson's Disease: It is due to what?
|
failure of coper to enter circulation in the form of ceruloplasmin
|
|
Wilson's Disease: What is another name for Wilson's Disease?
|
Hepatolenticular degeneration
|
|
Wilson's Disease: What are the symptoms of Wilson's Disease? (A,B,C-6,D)
|
Asterixis, basal ganglia degeneration (parkinsonian symptoms), Ceruloplasmin decrease, cirrhosis, corneal deposits (kayser-fleischer rings), coper accumulation, carcinoma (hepatocellular), choreiform movements, Dementia
|
|
Hemochromatosis: What is hemosiderosis?
|
Deposit of iron (hemosiderin) - this causes hemochromatosis
|
|
Hemochromatosis: The traid of sx. are?
|
micronodular cirrhosis, pancreatic fibrosis, and skin pigmentation ("bronze" diabetes)
|
|
Hemochromatosis: Possible complications include?
|
CHF, increased risk of hepatocellular carcinoma
|
|
Hemochromatosis: What is primary form?
|
inherited, Autosomal recessive
|
|
Hemochromatosis: What is secondary form due to?
|
chronic transfusion therapy
|
|
Hemochromatosis: What are ferritin, iron, TIBC and transferrin saturation levels?
|
Ferritin increased, iron increased, TIBC decreased => transferrin saturation is increased
|
|
Hemochromatosis: How much iron may the body contain?
|
As much as 50g, enough to set off airport metal detectors
|
|
Hemochromatosis: How is this condition treated?
|
Phlebotomy, deferoxamine
|
|
Hemochromatosis: AUTHOR
|
Tzevan Poon
|
|
Jaundice: bacteria convert conjugated bilirubin into what? what happens to some of this?
|
urobilinogen --> some which is reabsorbed, some which is excreted. (urobilinogen that's reabsorbed is converted to urobilin= yellow pigment in urine)
|
|
Jaundice: which is soluble in water/urine: conjugated or unconjugated bilirubin?
|
conjugted of course!
|
|
Jaundice: check out the 3 jaundice types: what are they? ***cover up the various parts of the chart in the text and test yourself.
|
heptocellular vs. obstructive vs. hemolytic jaundice
|
|
Heriditary hyper-bilirubinemias: What is the biochemical disorder in GILBERTS SYNDROME?
|
mild ↓ in UDP-glucuronyl transferase (this is key enzyme in conjugation of bilirubin)
|
|
Heriditary hyper-bilirubinemias: what are the symptoms?
|
asymptomatic
|
|
Heriditary hyper-bilirubinemias: what type of bilirubin is seen upon the lab findings? Do you have do you have major hemolysis?
|
unconjugated bilirubin is elevated w/o overt hemolysis
|
|
Heriditary hyper-bilirubinemias: What is the syndrome called when you have an ABSENCE of UDP-glc-ur-transferase?
|
Crigler-Najjar (CN) syndrome type 1 (type 2 is LESS severe)
|
|
Heriditary hyper-bilirubinemias: when does it present in life? What is the prognosis?
|
presents early in life: pts die in a few years.
|
|
Heriditary hyper-bilirubinemias: name 3 findings of C-N syndrome?
|
jaundice, kernicterus, ↑ unconjugated bilirubin
|
|
Heriditary hyper-bilirubinemias: type 2 is more sever or less severe? What do you treat it with?
|
less severe than type 1; treat type 2 with phenobarbital.
|
|
Heriditary hyper-bilirubinemias: what do you treat type 1 with (name 2)?
|
plasmapheresis + phototherapy (breaks down unconj. Bilirubin)
|
|
Heriditary hyper-bilirubinemias: What is Dubin Johnson syndrome?
|
↑↑ hyperbilirubin (conjugated) due to defective liver EXCRETION
|
|
Heriditary hyper-bilirubinemias: what does the liver look on gross exam?
|
black liver grossly
|
|
Heriditary hyper-bilirubinemias: what is the name of the less severe syndrome akin to Dubin Johnson?
|
Rotor's syndrome: also no black liver.
|
|
Heriditary hyper-bilirubinemias: see drawing: it's nice.
|
0
|
|
Primary sclerosing cholangitis: what is the pathophysiology
|
segmental inflammation and fibrosis of bile ducts: unaffected parts are dilated.
|
|
Primary sclerosing cholangitis: what test do you do to see this stricture/dilating/beading pattern?
|
ERCP
|
|
Primary sclerosing cholangitis: what disease is this associated with?
|
Ulcerative Colitis
|
|
Primary sclerosing cholangitis: What can prim. Scl. Cholangitis lead to?
|
2° biliary cirrhosis/sclerosis
|
|
Biliary sclerosis : what is the cause of Primary Biliary Sclerosis (PBS)? (compare the name/disease of PBS vs. PSC: primary sclerosing cholangitis)
|
autoimmune disorder with antimitochondrial antibodies
|
|
Biliary sclerosis : name 3 signs associated with PBS:
|
1) severe obstructive jaundice 2) itching 3) hypercholesterolemia (xanthoma)
|
|
Biliary sclerosis : What is the cause of SBS: secondary biliary sclerosis?
|
EXTRA-hepatic biliary obstruction → ↑ pressure in INTRA-hepatic ducts → ↑ injury/sclerosis
|
|
Biliary sclerosis : what is 2° biliary sclerosis associated with (name 3 things)?
|
ascending cholangitis (bacterial infection), bile stasis, and bile lakes
|
|
Heptocellular carcinoma = hepatoma: in liver cancers, is this common?
|
yes, #1 most common!
|
|
Heptocellular carcinoma = hepatoma: there is an ↑ incidence of hepatoma due to what diseases/exposures (name 7)
|
1) hep B, 2) hep C, 3) Wilson's disease, 4) hemochromatosis, 5) a-antitrypsin def 6) EtOH cirrhosis 6) carcinogens (e.g. aflatoxin B1)
|
|
Heptocellular carcinoma = hepatoma: How do hepatomas spread? How does this differ with renal cell ca. spread?
|
They BOTH commonly spread hematogenously!
|
|
Heptocellular carcinoma = hepatoma: What is major lab finding with hepatocelluar ca?
|
↑ AFP (alpha fetoprotein)
|
|
Reye's syndrome = rare!!! But…: What is this syndrome?
|
Hepato-encephalopathy: fatal: occurs in childhood
|
|
Reye's syndrome = rare!!! But…: name 3 findings:
|
1) fatty liver w/ microvesicular fatty change 2) hypoglycemia, 3) coma
|
|
Reye's syndrome = rare!!! But…: is this associated with any outside factors/triggering factors?
|
yes: 1) viral infection (esp. VZV or influenza B) 2) salicylates!!!
|
|
Reye's syndrome = rare!!! But…: if baby/child has fever what do you use in place of aspirin?
|
use acetaminophen (but with caution): i.e. acetaminophen OD hepato-toxicity
|
|
Gallstones: name 3 types of stones and tell me how they show up on CT scan:
|
1) cholesterol stone (radiolucent but 10-20% opaque due to calcification) 2) mixed stone = cholesterol + pigment (radiolucent) 3) pigment stone (radio-opaque)
|
|
Gallstones: Which is the most common type of gall stone?
|
mixed stone
|
|
Gallstones: name at least 5 out 9 risk factors for Cholesterol stones: is there a mnemonic?
|
1) obesity 2) Crohn's D 3) Cystic fibrosis 4) elderly 5) clofibrate 6) estrogens 7) multiparity 8) rapid weight loss 9) native American origin mnemonic = 4 F's fat, female….
|
|
Gallstones: name 4 risk factors for pigment stones:
|
1) pts with chronic RBC hemolysis 2) alcoholic cirrhosis 3) elderly 4) biliary infection
|
|
Gallstones: What is a good way to diagnosis stones?
|
ultrasound
|
|
Gallstones: What is CHARCOT'S TRIAD
|
1) epigastric/RUQ pain 2)fever 3) jaundice
|
|
Acute pancreatitis: this is what our US attorney general had. : pathophysiology mechanism?
|
activation and thus autodigestion by pancreatic enzymes
|
|
Acute pancreatitis: this is what our US attorney general had. : Causes? (good mnemonic)
|
Get Smashed (EtOH will can lead to AP) = 1) Gallstones 2) EtOH 3) Trauma 4) Steroids 5) Mumps 6) autoimmune disease 7) scorpion sting of all things! 8) hyperlipidemia 9) drugs
|
|
Acute pancreatitis: this is what our US attorney general had. : clinically presents with?
|
intense epigastric pain radiating to back
|
|
Acute pancreatitis: this is what our US attorney general had. : labs(name 2): which of the two has a higher specificity?
|
↑ amylase + ↑lipase (higher specificity) "li is hi"
|
|
Acute pancreatitis: this is what our US attorney general had. : Name 5 nasty complications that can result from AP?
|
1) DIC 2) ARDS 3) diffuse fat necrosis 4) hypocalcemia 5) pseudocyst formation
|
|
Acute pancreatitis: this is what our US attorney general had. : if you have CHRONIC pancreatitis: what do we think of your life habits?
|
Chronic Pancr. Is strongly associated w/ alcoholism
|
|
Pancreatic cancer: what is a common and fatal pancreatic cancer?
|
pancreatic adenocarcinoma
|
|
Pancreatic cancer: what is the prognosis?
|
6 months: very aggressive: usually has mets when pt. presents
|
|
Pancreatic cancer: where are tumors most commonly located? And what does this lead to?
|
pancreatic head → obstructive jaundice.
|
|
Pancreatic cancer: PATHOLOGY-RESPIRATORY SECTION
|
0
|
|
COPD = also known as OLD: obstructive lung disease: why is it called obstructive?
|
obstruction of AIR FLOW → air traping in lungs
|
|
COPD = also known as OLD: obstructive lung disease: what is the major PFT finding?
|
FEV1 / FVC ration is ↓ (hallmark finding)
|
|
COPD = also known as OLD: obstructive lung disease: name the 4 types of COPD
|
1) Chronic Bronchitis (Blue Bloater) 2) emphysema (pink puffer) 3) asthma 4) bronchietasis
|
|
COPD = also known as OLD: obstructive lung disease: what is the definition of Chronic Bronchitis
|
productive cough for >3 consecutive months in two or more years.
|
|
COPD = also known as OLD: obstructive lung disease: what do you expect on lung histology?
|
hypertrophy of mucus-secreting glands in the bronchioles (Reid index of >50%)
|
|
COPD = also known as OLD: obstructive lung disease: leading cause is smoking: what are the physical findings for Chronic Bronchitis? (name 3)
|
1)cyanosis 2) wheezing 3) crackles
|
|
COPD = also known as OLD: obstructive lung disease: what is the pathophysiological mechanism of EMPHYSEMA?
|
destruction of fibrous septa/alveolar walls → enlargement of air space and ↓ total surface area for gas exchange
|
|
COPD = also known as OLD: obstructive lung disease: if the cause is smoking, what kind of emphysema would you see on histo slide?
|
centri-acinar emphysema
|
|
COPD = also known as OLD: obstructive lung disease: what else can cause emphysema: (also may work synergistically with smoking): What kind of findings do you see in lung histo and name another organ affected?
|
alpha 1-antitrypsin deficiency → panacinar emphysema + liver cirrhosis
|
|
COPD = also known as OLD: obstructive lung disease: what causes the emphysema in this disorder?
|
↑ elastase activity to damage lung tissue.
|
|
COPD = also known as OLD: obstructive lung disease: name 4 findings of emphysema (in general)
|
1) dyspnea; 2) ↓ breath sounds 3) tachycardia 4) ↓ I/E ratio
|
|
COPD = also known as OLD: obstructive lung disease: What is mechanism of asthma
|
BRONCHIAL hypersensitivity/hyperresponsiveness → REVERSIBLE bronchoconstriction
|
|
COPD = also known as OLD: obstructive lung disease: name 3 common triggers
|
1) viral URI 2) allergens 3) stress!!
|
|
COPD = also known as OLD: obstructive lung disease: name 7 findings
|
1) cough 2) wheezing 3) dyspnea 4) hypoxemia 5)↓ I/E ratio 6) tachypnea 7) pulsus paradoxus
|
|
COPD = also known as OLD: obstructive lung disease: BRONCHIECTASIS: what is its mechanism??
|
chronic necrotizing infection of BRONCHI → dilated airways, purulent sputum, recurrent infections, hemoptysis (see Robbins for a good discussion of this)
|
|
COPD = also known as OLD: obstructive lung disease: what disorders is bronchietasis commonly associated with?
|
1) bronchial obstruction 2) cystic fibrosis 3) poor ciliary motility
|
|
Restrictive Lung Disease (RLD): What are classic PFT findings for RLD?
|
↓ VC ↓TLC ; FEV1/FVC ration > 80%
|
|
Restrictive Lung Disease (RLD): Name the two MAJOR types of RLD
|
1) poor breathing mechanics (EXTRA-pulmonary) 2) Interstitial lung diseases
|
|
Restrictive Lung Disease (RLD): cover up various parts of the text/table/outline to test yourself on the following: 1) 2 types of poor breathing mechanics 2) 8 types of interstitial disease that give you a restrictive picture.
|
0
|
|
Lung Physical Findings: cover up parts of the very good table to test yourself on various findings.
|
0
|
|
Lung Physical Findings: Obstructive vs. Restrictive findings
|
0
|
|
Lung Physical Findings: Name 3 lung volumes that are increased in COPD
|
↑TLC, ↑FRC, ↑RV
|
|
Lung Physical Findings: What 2 values are BOTH reduced in COPD and RLD?
|
1) FEV1 and 2) FVC (think FEV1/FVC ratio) NOTE! in COPD, FEV1 is more dramatically reduced and thus the FEV1/FVC ratio is ↓
|
|
Asbestosis = long latency = think shipbuilders and plumbers: what is the main pathology resulting from asbestosis?
|
DIFFUSE, interstitial fibrosis caused by inhaled asbestos Fibers.
|
|
Asbestosis = long latency = think shipbuilders and plumbers: What cancers are increased in pts with asbestosis?
|
1) pleural mesothelioma 2) bronchogenic carcinoma (BC)
|
|
Asbestosis = long latency = think shipbuilders and plumbers: Major finding in lung?
|
Ferruginous bodies: asbestos fibers coated with hemosiderin also 2) ivory white pleural plaques
|
|
Neonatal respiratory distress syndrome: What is the main cause
|
surfactant deficiency --> to increased surface tension --> alveolar collapse
|
|
Neonatal respiratory distress syndrome: surfactant is made by which cells? After when?
|
type 2 pneumocytes after 35th gestational week
|
|
Neonatal respiratory distress syndrome: what do you measure? Where do you get this fluid?
|
lecithin-to-sphingomyelin ratio in the amniotic fluid = measure of lung maturation <1.5 in neonatal distress syndrome
|
|
Neonatal respiratory distress syndrome: what is surfactant made of (chemical name)
|
dipalmitoyl phosph-tidyl-choline (DP-PTC)
|
|
Neonatal respiratory distress syndrome: treatment for poor maturation of lungs
|
1) before birth = maternal steroids 2) after= artificial surfactant
|
|
Karta-gener's syndrome: what is this?
|
immotile cilia due to dynein arm defect
|
|
Karta-gener's syndrome: results in what in female and male? (4 things)
|
1) sterility (in male sperm also immotile) 2)bronchietasis 3)recurrent sinusitis (bacteria & particles not pushed out) 4) associated with situs inversus (e.g. dextro-cardia)
|
|
Lung Cancer: name the 3 main classes of cancers that affect parts of the lung
|
1) bronchogenic carcinoma (with different subtypes) 2) carcinoid tumor 3) metastasis
|
|
Lung Cancer: list the 5 types of major bronchogenic carcinomas
|
CENTRAL 1) squamous cell ca 2)small cell ca PERIPHERAL 3) adenocarcinoma 4) bronchoalveolar ca 5) large cell ca
|
|
Lung Cancer: mnemonic: what is meant by SPHERE of symptoms?
|
S= superior vena cava syndrome; P= pancoast tumor; H= Horner's syndrome; E= Endocrine (paraneoplastic); Recurrent laryngeal / hoarseness; E = Effusions (pleural OR pericardial)
|
|
Lung Cancer: What can a CARCINOID tumor cause?
|
Carcinoid Syndrome = flushing, diarrhea, wheezing, and salivation
|
|
Lung Cancer: Metastases to lung is very common, LUNG cancer also prone to metastasize to what other parts?
|
1) brain (epilepsy) 2) bone (fracture) 3)liver (jaundice + hepatomegaly)
|
|
Pancoast tumor: What is it?
|
it's a carcinoma of the apex of lung
|
|
Pancoast tumor: what may it affect?
|
may affect CSP= cervical sympathetic plexus causing Horner's syndrome
|
|
Pancoast tumor: what is Horner's syndrome?
|
P.A.M. is Horny = Ptosis, Anhydrosis, Miosis
|
|
Pneumonia: 1st AID breaks it down into TYPE/ ORGANISM/ CHARACTERISTICS = cover parts of this table and fill in the blanks
|
0
|
|
Pneumonia: Lobar Pneumonia; Organism(s) and characteristics
|
Pneumococcus; intraalveolar exudate -> consolidation, may involve entire lung
|
|
Pneumonia: Bronchopneumonia: Organism and characteristics
|
S aureus, H flu, Klebsiella, S pyogenes; Acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving >= 1 lobes
|
|
Pneumonia: Interstitial pneumonia; Organism(s) and characteristics
|
Viruses, mycoplasma, legionella; diffuse patchy inflammation localized to interstitial areas at alvolar walls; distribution involving >= 1 lobes
|
|
Pneumonia: PATHOLOGY - NEUROLOGIC
|
0
|
|
Degenerative diseases: name two diseases that affect the CEREBRAL CORTEX
|
1) Alzheimer's disease 2) Pick's disease
|
|
Degenerative diseases: name two diseases that affect BASAL GANGLIA & BRAIN STEM:
|
1) Huntington's disease 2) Parkinson disease
|
|
Degenerative diseases: name 5 diseases that affect SPINOCEREBELLAR MOTOR NEURON
|
1) Olivo-ponto-cerebellar atrophy 2) Friedreich's ataxia 3)ALS = amyotrophic lateral sclerosis 4)Werdnig-Hoffmann disease 5) Polio
|
|
Degenerative diseases: what is the most common cause of elderly dementia?
|
Alzheimer's
|
|
Degenerative diseases: name two pathological findings characteristic of Alzheimer's
|
1) senile plaques = intracytoplasmic inclusion bodies 2) neurofibrillary tangles (abnormally phosphorylated tau protein)
|
|
Degenerative diseases: what is the 2nd most common cause of dementia in elderly?
|
multi-infarct dementia in elderly\\
|
|
Degenerative diseases: How can Alzheimer also affect intracranial vasculature?
|
amyloid angiopathy --> intracranial hemorrhage
|
|
Degenerative diseases: The familial form of Alzheimer's is associated with what chromosomes (name 4) and (name the allele's name in 2 of the 4)
|
chromosome 1, 14, 19 (APO-E4 allele), 21 (p-Ap gene)
|
|
Degenerative diseases: What is pathognemomic with Pick's disease upon histology?
|
Pick bodies = intra-cytoplasmic inclusion bodies
|
|
Degenerative diseases: What cortical areas does Pick's disease affect
|
Frontal and temporal lobes (remember; sharp, atrophic apearance of gross specimen)
|
|
Degenerative diseases: What is the inheritance pattern of Huntington's
|
Auto Dominant
|
|
Degenerative diseases: What are some symptoms?
|
1) chorea 2) dementia
|
|
Degenerative diseases: Huntington's is due to atrophy of _____ what? Loss of ___ ergic neurons.
|
atrophy of caudate nucleus = loss of GABA-nergic neurons
|
|
Degenerative diseases: what is the genetic abnormality of Huntington's?
|
1) Chr. 4 - expansion of CAG repeats
|
|
Degenerative diseases: Parkinson disease is associated with what pathology findings?
|
1) Lewy bodies 2) depigmentation of substantia nigra (loss of dopaminergic neurons)
|
|
Degenerative diseases: rare cases of Parkinson's have been linked to what contaminant of certain illicit drugs?
|
MPTP = contaminant to street drug
|
|
Degenerative diseases: Parkinson's can make you feel in a "TRAP" = ?
|
T = tremor at rest; R = cogwheel rigidity; A = akinesia ; Postural instability
|
|
Degenerative diseases: ALS = Lou Gehrig's disease (the Iron Horse of the Yankees, hero of Joe DiMaggio) = what signs is ALS associated with?
|
Both UMN and LMN deficits
|
|
Degenerative diseases: Werdnig-Hoffman disease - presents as birth as?
|
1) flopy baby syndrome 2) note tongue fasciculations as well (also seen in ALS)
|
|
Degenerative diseases: for Polio, what kind of signs to you see?
|
predominantly LMN deficits.
|
|
Intracranial Hemorrhage/Hemotomas: name 4 types of cranial related hemorrhages (think of layers that could possibly be involved)
|
1) epidural hemorrhage 2) subdural h 3) subarachnoid h 4) parenchymal h
|
|
Intracranial Hemorrhage/Hemotomas: what is a common site of epidural hematoma/hemorrhage
|
1) rupture of MMA: middle meningeal artery, often 2ndary to fracture of temporal bone
|
|
Intracranial Hemorrhage/Hemotomas: what does CT show for epidural h?
|
biconcave disc NOT crossing suture lines
|
|
Intracranial Hemorrhage/Hemotomas: what else do you see?
|
lucid interval
|
|
Intracranial Hemorrhage/Hemotomas: How do subdural h. most often occur?
|
rupture of bridging veins (think, elderly being jolted in roller coaster)
|
|
Intracranial Hemorrhage/Hemotomas: this is venous bleeding so how would this influence symptomatic findings?
|
venous = less pressure = delayed onset of symptoms
|
|
Intracranial Hemorrhage/Hemotomas: what types of people do you see subdural h.?
|
1) elderly, 2) alcoholics 3) blunt trauma/sudden change in velocity injuries
|
|
Intracranial Hemorrhage/Hemotomas: for SUBDURALs what do you see upon CT?
|
1) crescent-shaped hemorrhage instead 2) YES IT does cross the suture lines
|
|
Intracranial Hemorrhage/Hemotomas: subarachnoid hemorrhage is often seen where (name 2 types
|
rupture of 1) aneurysm (usually Berry aneurysm) or an 2)AVM
|
|
Intracranial Hemorrhage/Hemotomas: symptoms?
|
the worst headache of my life
|
|
Intracranial Hemorrhage/Hemotomas: since its subarachnoid, what do you see on what test?
|
bloody or xanthochromic CSF on spinal tap
|
|
Intracranial Hemorrhage/Hemotomas: name 4 risk factors for parenchymal hematoma
|
1) HTN 2) amyloid angiopathy 3) diabetes mellitus 4) tumor
|
|
Intracranial Hemorrhage/Hemotomas: AUTHOR
|
Hilcias Duran
|
|
Berry aneurysms: most common site for Berry aneurysms
|
bifurcation of the anterior communicating artery (Circle of Willis)
|
|
Berry aneurysms: berry aneurysms are associated with
|
adult polycystic disease, Ehlers-Danlos s., and marfan's
|
|
Berry aneurysms: Classic triad of Multiple Sclerosis
|
SIN: Scanning speech, intention tremor, nystagmus (affect woman 20-30s)
|
|
Berry aneurysms: Prevalence of MS
|
increase prevalence w/ increased distance from the equator
|
|
Berry aneurysms: Clinical s/s of MS
|
periventricular plaques, preservation of axons, loss of oligodentrocytes, reactive astrocystic gliosis, increased protein in csf(IgG) in CSF, relapsing course, optic neuritis, MLF syndrome, hemiparesis, bladder/bowel incontinence)
|
|
Berry aneurysms: Progressive multifocal leukoencephalopathy (PML) is associated w/
|
JC virus and seen in 2-4 % of AIDS pts (reactivation or latent infect)
|
|
Berry aneurysms: pathogenesis of Guillian-Barre syndrome
|
Inflammation and demyelination of peripheral nerves and motor fibers of the ventral roots (sensory effec less severe than motor)
|
|
Berry aneurysms: s/s of Guillian-Barre syndrome
|
symmetrical ascending muscle weakness beginning in the distal lower extremities. Autonomic fxn may be severely affected (eg. Cardiac irregularities, HTN, or hypoTN) Findings: inc. csf protein w/ normal cell count ("albumino-cytologic dissociation") elevated protein may lead to papilledema
|
|
Berry aneurysms: association between G-B syndrome and…
|
herpesvirus or camplobacter jejuni infection, inoculations, and stress but no definitive link to a pathogen
|
|
Poliomyelitis: organism causing polio and mechanism of action
|
poliovirus, transmitted via fecal oral route and enters blood stream then into CNS where it causes destruction of the anterior horn of S.C. leading in turn to LMN destruction
|
|
Poliomyelitis: s/s of polio
|
malaise, HA, fever, nausea, abd. Pain, sore throats, signs of LMN signs
|
|
Poliomyelitis: finding of polio
|
csf w/ lymphocytic pleocytosis w/ slight elevation of protein, virus recovered from stool or throat
|
|
Aphasia : describe Broca's (expressive) aphasia
|
confluent aphasia w/ intact comprehension broca's is broken speech
|
|
Aphasia : describe Wernicke's (aphasia)
|
Fluent aphasia w/ impaired concentration Wernick's ="What?" W area located in superior temperal gyrus
|
|
seizures : describe two types of partial seizures
|
1.simple partial (awareness is intact)--motor, sensory, autonomic, psychic 2.Complex partial (impaired awareness)
|
|
seizures : describe types of Generalized seizure ( diffuse)
|
1.absence- blank stare (petit mal) 2.myoclonic- quick repetitive jerks 3.tonic-clonic- alternating stiffening and mvmt (grand mal) 4. Tonic- stiffening 5.atonic-"drop" seizures
|
|
seizures : what are the causes of seizures in children?
|
genetic, infection, trauma, congenital, metabolic
|
|
seizures : adults?
|
tumors, trauma, stroke, infection
|
|
seizures : elderly?
|
stroke, tumor, trauma, metabolic, infection
|
|
Horner's syndrome: what is Horner's syndrome?
|
sympathectomy of face (lesion above T1) 1.Ptosis 2.anhidrosis and flushing of affected side 3.miosis [PAM is horny]
|
|
Horner's syndrome: Horner's syndrome is associated w/ what type of tumor?
|
pancoast tumor
|
|
syringomyelia: what is syringomyelia?
|
enlargement of the central canal of the S.C. Crossing fibers of spinothalamic tract are damaged.
|
|
syringomyelia: what are the s/s of syringomyelia?
|
b/l loss of pain and temp sensation in the uper extremities w/ the touch sensation. Most common at C8-T1
|
|
syringomyelia: commonly seen in what pts?
|
pts w/ Arnold-Chiari malformation
|
|
Tabes dorsalis : what infection is tabes dorsalis associated w/?
|
teriary syphilis
|
|
Tabes dorsalis : what happens in the CNS?
|
degeneration of dorsal columns and dorsal root
|
|
Tabes dorsalis : dorsalis also is associated with what s/s?
|
charcot's joint, shooting (lightning) pain, Argyll Robertson pupils, and absence of DTRs
|
|
Osteoarthritis : what occurs in OA?
|
mechanical wear and tear of the joints, leads to destruction of the articular cartilage, subchondral bone formation, sclerosis, osteophytes, eburnation, Herberden's nodes (DIP), and Bouchard's nodes (PIP)
|
|
Osteoarthritis : classical presentation of OA?
|
pain in weight bearing joints after use (worse at the end of the day0 improves w/ rest. No systemic symptoms
|
|
Rheumatoid Arthritis : what happens in in RA?
|
autoimmune inflammatory proccess which affects synovial joints, w/ pannus formation in joints (MCP, PIP), S-Q rheumatoid nodules, ulnar deviation,subluxation
|
|
Rheumatoid Arthritis : classical presentation of RA?
|
female, 80% pts Rf positive (anti-IgG Ab) morning stiffness improving w/ use, symmetrical joint involvement, and systemic symptoms (fever, fatigue, pleurtis, pericarditis)
|
|
Rheumatoid Arthritis : AUTHOR
|
Jason Portnof
|
|
Sjogren's Syndrome: What is the classic triad of Sjogren’s syndrome?
|
dry eyes (conjunctivitis, xeropthalmia), dry mouth (dysphagia, xerostomia), arthritis
|
|
Sjogren's Syndrome: What is SICCA syndrome?
|
dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis
|
|
Sjogren's Syndrome: T/F Sjogren’s syndrome predominantly affects males between 40 and 60 years of age.
|
False. Females between 40 and 60 y.o are predominantly affected in Sjogren’s syndrome.
|
|
Gout: T/F Gout is the precipitation of monosodium urate crystals into joints due to hyperuricemia.
|
TRUE
|
|
Gout: What is the favored manifestation of gout?
|
Podagra. (painful MTP joint)
|
|
Gout: The crystals of gout are:
|
needle shaped and negatively bifringent
|
|
Pseudogout: T/F Pseudogout is the precipitation of calcium pyrophosphate crystals within the joint space.
|
TRUE
|
|
Pseudogout: The crystals of psuedogout are:
|
basophilic, rhomboid crystals
|
|
Pseudogout: Psudogout usually affects:
|
Large joints (classically the knee)
|
|
Pseudogout: T/F Both gout and psuedogout predominantly affect men.
|
False. Gout is more common in men. Pseudogout affects both sexes equally, most pts are >50 years old.
|
|
Pseudogout: T/F The treatment for both pseudogout and gout is allopurinol, probenecid, colchicines, and NSAIDS.
|
False. That is the tx for gout. However, there is no tx for pseudogout.
|
|
Celiac sprue: Celiac sprue is the autoimmune-mediated intolerance of what substance, leading to steatorrhea?
|
gliadin (wheat)
|
|
Celiac sprue: T/F Findings in Celiac sprue include blunting of villi, neutrophils in the lamina propria, and abnormal D-xylose test.
|
False. lymphocytes, not neutrophils are found in the lamina propria.
|
|
Systemic Lupus Erythematosus: What drugs can produce a SLE-like syndrome that is commonly reversible?
|
HIp: Hydralazine, INH, Phenytoin, Procainamide
|
|
Systemic Lupus Erythematosus: SLE causes LSE. What is LSE?
|
Libman Sacks Endocarditis. Valvular vegetations found on both sides of valve (Mitral Valve Stenosis) and do not embolize.
|
|
Systemic Lupus Erythematosus: T/F 90% Systemic lupus erythematousus pts are female between ages 14 and 45. SLE is most common and severe in black females.
|
Both statements are true
|
|
Systemic Lupus Erythematosus: What are 4 lab tests in SLE? Which test, when positive is predictive of a poor prognosis?
|
1. ANA (antinuclear antibodies)- sensitive, not specific for SLE, 2. anti-ds DNA (antibodies to double stranded DNA)- very specific, poor prognosis, 3. Anti-Smith antibodies (anti-Sm)- very specific, but not prognostic, 4. Antihistone antibodies- drug induced lupus
|
|
Systemic Lupus Erythematosus: In what organ are wire loop lesions found in SLE?
|
kidney (with immune complex deposition and nephrotic syndrome)
|
|
Systemic Lupus Erythematosus: What causes death commonly in SLE?
|
Renal failures and infections
|
|
Systemic Lupus Erythematosus: What are symptoms of SLE?
|
fever, fatigue, wt loss, joint pain, malar rash, photosensitivity. Also: pleuritis, pericarditis, nonbacterial verrucous endocarditis, Raynaud’s phenomenon
|
|
Sarcoidosis: What disease is characterized by gamaglobulinemia, rheumatoid arthritis, ace increase, interstitial fibrosis, and noncaseating granulomas?
|
Sarcoidosis
|
|
Seronegative spondyloarthropathies: Name 2 seronegative spondyloarthropathies.
|
ankylosing spondylitis, reiters’ syndrome
|
|
Seronegative spondyloarthropathies: What is a seronegative spondyloarthropathy?
|
Arthritis without rheumatoid factor (no anti-IgG Ab). Strong association with HLA-B27 (gene that codes for HLA MHC1)
|
|
Seronegative spondyloarthropathies: T/F seronegative spondyloarthropahties occur more often in males
|
TRUE
|
|
Seronegative spondyloarthropathies: What is the classic triad for Reiter’s syndrome?
|
Urethritis, conjunctivitis and anterior uveitis, arthritis. “Can’t see, can’t pee, can’t climb a tree”
|
|
Seronegative spondyloarthropathies: T/F reiter’s syndrome occurs commonly post respiratory or chlamydia infections.
|
False. Post-GI or chlamydia infections
|
|
Seronegative spondyloarthropathies: Describe ankylosing spondylitis
|
Chronic inflammatory disease of spine and sacroiliac joints. Ankylosis (stiff spine), uveitis and aortic regurg.
|
|
Scleroderma: T/F Crest syndrome is wider-spread than diffuse scleroderma.
|
False. Diffuse scleroderma has widespread skin involvement, rapid progression, early visceral involvement. CREST syndrome has limited skin involvement, often confined to fingers and face. More benign clinical course.
|
|
Scleroderma: T/F Crest syndrome occurs in male pts that have allergic rxn to toothpaste.
|
False. CREST= calcinosis, raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia.
|
|
Scleroderma: What antibodies are associated with scleroderma (progressive systemic sclerosis- PSS)?
|
"diffuse scleroderma- anti-Scl-70 antibody, Crest syndrome- anticentromere antibody
|
|
Skin disorders: T/F Pemphigus vulgaris is described as an autoimmune disorder with IgG antibody against epidural basement membrane (linear immunofluorescence). Affects skin but spares oral mucosa.
|
False. That description is for Bullous pemphigoid (less severe disease than Pemphigus vulgaris). Pemphigus vulgaris is a potentially fatal autoimmune skin disorder. Intradermal bullae involve the oral mucosa and skin. Findings include acantholysis, IgG ab against epidermal cell surface.
|
|
Skin disorders: T/F Dermatitis is a group of inflammatory pruritic skin disorders. The etiology is allergy (usually type IV hypersensitivity), chemical injury, or infection.
|
TRUE
|
|
Skin disorders: What HLA groups are associated with psoriasis?
|
HLA-B27, HLA-13, HLA-17
|
|
Skin disorders: What is psoriasis? Where is it most commonly found?
|
Psoriasis is nonpruritic chronic inflammation of the skin, particularly on the knees and elbows.
|
|
Goodpasture's: T/F Goodpasture’s syndrome affects the lungs and liver.
|
False. Lungs and Kidneys. (Pulmonary hemorrhagesĂ hemoptysis, renal lesionsĂ hematuria, anemia, crescentic glomerulonephritis)
|
|
Goodpasture's: What type of Abs are associated with Goodpastures?
|
anti-glomerular basement membrane abs produce linear staining on immunofluorescence.
|
|
Goodpasture's: Who commonly gets Goodpastures?
|
Men between 20-40 years.
|
|
Cushing's syndrome: What are etiologies of Cushing’s syndrome? Is ACTH always elevated?
|
increased cortisol due to:, 1. Cushing’s disease (primary pituitary adenoma) increased ACTH, 2. Primary adrenal (hyperplasia/neoplasia) decreased ACTH, 3. Ectopic ACTH production (ie- small cell lung ca) increased ACTH, 4. Iatrogenic, decreased ACTH
|
|
Cushing's syndrome: Describe the clinical picture of Cushings.
|
HTN, wt gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin change (thinning, striae), osteoporosis, immune supression
|
|
Hyperaldosteronism: T/F Conn’s syndrome is secondary hyperaldosteronism.
|
False. Conn’s syndrome is primary hyperaldosteronism, caused by an aldosterone-secreting tumor. Results in HTN, hypokalemia, metabolic alkalosis, low plasma renin.
|
|
Hyperaldosteronism: Which hyperaldosteronism is associated with high plasma renin?
|
Secondary hyperaldosteronism. It is due to renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome. Kidney perception of low intravascular volume results in an overactive renin-angiotensin sysem.
|
|
Hyperaldosteronism: What is the tx for hyperaldosteronism?
|
Spironolactone, a diuretic that works by acting as a aldosterone antagonist.
|
|
Addison's Disease: What characterizes addison’s disease? (which hormones are elevated or deficient)? Is it associated with HTN or hypotension?
|
Primary deficiency of aldosterone and cortisol due to adrenal atrophy, causing hypotension and skin hyperpigmentation. Adrenal atrophy, absence of hormone production, involves all 3 cortical divisions.
|
|
Addison's Disease: T/F In primary insufficiency decreased pituitary ACTH production is characterized by skin hyperpigmentation.
|
False: increased ACTH causes MSH activity & hyperpigmentation
|
|
Tumors of adrenal medulla: T/F Neuroblastoma is the most common tumor of adrenal medulla in adults.
|
False. Pheochromocytoma is the most common tumor of adrenal medulla in adults. It is derived from chromaffin cells (arise from neural crest). It is associated with neurofibromatosis MEN types II and III.
|
|
Tumors of adrenal medulla: Where does neuroblastoma occur?
|
Neuroblastoma is the most common tumor of adrenal medulla in children. It can occur anywhere along the sympathetic chain.
|
|
Tumors of adrenal medulla: AUTHOR
|
Jason Lee
|
|
Pheochromocytoma: secrete combination of two molecules
|
epinephrine and norepinephrine
|
|
Pheochromocytoma: epidemiology (rule of 10's)
|
10% malignant, 10% bilateral, 10% extra-adrenal, 10% calcify, 10% kids, 10% familial
|
|
Pheochromocytoma: symptoms - 5 P's
|
(elevated blood) Pressure, Pain (headache), Perspiration, Palpitations, Pallor/diaphoresis --> relapsing and remittant
|
|
Pheochromocytoma: elevations in two lab values
|
urinary VMA and serum catecholamines
|
|
Pheochromocytoma: association with two other endocrine diseases
|
MEN II and III
|
|
Pheochromocytoma: treatment
|
alpha-antagonists
|
|
Multiple Endocrine Neoplasia: type I (Wermer's syndrome) - 3 P's
|
Pancreas, Pituitary, and Parathyroid tumors
|
|
Multiple Endocrine Neoplasia: type II (Sipple's syndrome)
|
medullary carcinoma of thyroid, pheochromocytoma, parathyroid tumor, or adenoma
|
|
Multiple Endocrine Neoplasia: type III
|
medullary carcinoma of thyroid, pheochromocytoma, oral/intestinal ganglioneuromatosis
|
|
Hypothyroidism and hyperthyroidism: myxedema is prominent in which one
|
hypothyroidism
|
|
Hypothyroidism and hyperthyroidism: chest pain, palpitations, arrhythmias
|
hyperthyroidism
|
|
Hypothyroidism and hyperthyroidism: TSH is (increased/decreased) in primary hyperthyroidism? In primary hypothyroidism?
|
hyper - decreased, hypo - increased
|
|
Hypothyroidism and hyperthyroidism: Graves' disease involves autoantibodies with what mechanism of action?
|
stimulation of TSH receptors
|
|
Hypothyroidism and hyperthyroidism: three symptoms of Graves'
|
ophthalmopathy, pretibial myxedema, diffuse goiter
|
|
Hypothyroidism and hyperthyroidism: Graves' is a type __ hypersensitivity
|
type II
|
|
Hashimoto's thyroiditis: thyroid is (enlarged/not enlarged) and (tender/nontender)
|
enlarged, nontender
|
|
Hashimoto's thyroiditis: autoimmune antibodies directed against ---
|
microsomes
|
|
Hashimoto's thyroiditis: histology shows (type of cell) infiltrate
|
lymphocytes (with germinal centers)
|
|
Subacute thyroiditis (de Quervain's): self-limited (hyper/hypo)thyroidism following ---
|
hypothyroidism following flu-like illness
|
|
Subacute thyroiditis (de Quervain's): symptoms include
|
jaw pain, tender thyroid gland, early hyperthyroidism
|
|
Thyroid cancer: most common, good prognosis, "ground glass" nuclei, psammoma bodies
|
papillary carcinoma
|
|
Thyroid cancer: poor prognosis, uniform follicles
|
follicular carcinoma
|
|
Thyroid cancer: calcitonin producing (C cells), sheets of cells
|
medullary carcinoma (MEN II and III)
|
|
Thyroid cancer: older patients, horrible prognosis
|
undifferentiated/anaplastic
|
|
Cretinism: caused by a lack of dietary --- or defect in --- formation
|
iodine (endemic), T4 (sporadic)
|
|
Cretinism: symptoms include
|
pot-belly, paleness, puffy face, protuberant tongue, protruding umbilicus
|
|
Acromegaly: caused by excess --- in adults
|
growth hormone
|
|
Acromegaly: symptoms include
|
large furrowed tongue, deep voice, large hands and feet, coarse facial features
|
|
Acromegaly: in children, leads to ---
|
gigantism
|
|
Diabetes mellitus: acute symptoms common to both types
|
polydipsia, polyuria, polyphagia, weight loss
|
|
Diabetes mellitus: match: (DKA/hyperosmolar coma) with (type I/type II)
|
DKA=type I, hyperosmolar coma=type II
|
|
Diabetes mellitus: effects (increased/decreased) of insulin deficiency and glucagon excess on 1) glucose uptake, 2) protein catabolism, 3) lipolysis
|
1) decreased, 2) increased, 3) increased
|
|
Diabetes mellitus: increased plasma free fatty acids leads to
|
ketogenesis
|
|
Diabetes mellitus: hyperglycemia has what effect on blood volume and electrolytes
|
decreased volume (osmotic diuresis), electrolyte depletion
|
|
Diabetes mellitus: three chronic manifestations
|
retinopathy (hemorrhage, exudate, microaneurysm), nephropathy (nodular sclerosis), neuropathy (sensory, motor, autonomic)
|
|
Diabetes mellitus: sorbitol accumulation leads to what sequelae in the eye
|
cataracts, glaucoma
|
|
Diabetes mellitus: three tests - what are they? which one measures long-term glucose control?
|
fasting glucose, glucose tolerance test, HbA1c
|
|
Diabetes mellitus: AUTHOR
|
Jacob Pugsley
|
|
Type 1 - juvenile onset: % of diabetes
|
0.15
|
|
Type 1 - juvenile onset: Insulin necessary in treatment
|
Always
|
|
Type 1 - juvenile onset: Age
|
<30
|
|
Type 1 - juvenile onset: Association with obesity
|
No
|
|
Type 1 - juvenile onset: Genetic predisposition
|
weak, polygenic
|
|
Type 1 - juvenile onset: Association with HLA system
|
Yes (HLA-DR3 & 4)
|
|
Type 1 - juvenile onset: Glucose intolerance
|
Severe
|
|
Type 1 - juvenile onset: Ketoacidosis
|
Common
|
|
Type 1 - juvenile onset: B-cell numbers in the islets
|
decreased
|
|
Type 1 - juvenile onset: Serum insulin levels
|
decreased
|
|
Type 1 - juvenile onset: Classic symptoms of polyuria, polydipsia, thirst, weight loss
|
Common
|
|
Type 1 - juvenile onset: Theorized cause
|
viral or immune destruction of B cells
|
|
Type 2 - adult onset: % of diabetes
|
0.85
|
|
Type 2 - adult onset: Insulin necessary in treatment
|
Sometimes
|
|
Type 2 - adult onset: Age
|
>40
|
|
Type 2 - adult onset: Association with obesity
|
Yes
|
|
Type 2 - adult onset: Genetic predisposition
|
Strong, polygenic
|
|
Type 2 - adult onset: Association with HLA system
|
No
|
|
Type 2 - adult onset: Glucose intolerance
|
mild to moderate
|
|
Type 2 - adult onset: Ketoacidosis
|
Rare
|
|
Type 2 - adult onset: B-cell numbers in the islets
|
Variable
|
|
Type 2 - adult onset: Serum insulin levels
|
Variable
|
|
Type 2 - adult onset: Classic symptoms of polyuria, polydipsia, thirst, weight loss
|
Sometimes
|
|
Type 2 - adult onset: Theorized cause
|
increased resistance to insulin
|
|
Diabetic Ketoacidosis (type 1): What precipitates this
|
Increase in insulin requirements from increase in stress (e.g. infection)
|
|
Diabetic Ketoacidosis (type 1): Ketone bodies from where
|
Excess fat breakdown, increase ketogenesis from increased free fatty acids which are made into ketone bodies
|
|
Diabetic Ketoacidosis (type 1): Signs/Symptoms
|
Kussmaul respirations (rapid/deep breathing), hyperthermia, nausea/vomiting, abdominal pain, psychosis/dementia, dehydration, fruity breath odor
|
|
Diabetic Ketoacidosis (type 1): Labs
|
Hyperglycemia, high H+, low HCO3- (anion gap metabolic acidosis), high blood ketone levels, leukocytosis
|
|
Diabetic Ketoacidosis (type 1): Complications
|
Life threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythimias, heart failure
|
|
Diabetic Ketoacidosis (type 1): Treatment
|
Fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia.
|
|
Diabetes insipidus: summary
|
intensive thirst, polyuria, inability to concentrate urine with fluid constriction owing to lack of ADH (central DI) or to lack of renal response to ADH (nephrogenic DI). Caused by lithium or demeclocycline
|
|
Diabetes insipidus: Findings
|
Urine specific gravity < 1.006; serum osmolality > 290 mOsm/L
|
|
Diabetes insipidus: Treatment
|
adequate fluid intake; Central DI - intranasal desmopressin (ADH analog); nephrogenic DI - hydrochlorothiazide, indomethacin, or amiloride
|
|
SIADH: what does it stand for
|
Syndrome of inapropriate ADH
|
|
SIADH: finds
|
1) excess water retention 2) hyponatremia [may lead to seizures - correct slowly] 3) urine osmolarity > serum osmolarity
|
|
SIADH: causes
|
1) Ectopic ADH [small cell lung cancer] 2) CNS disorders/head trauma 3) pulmonary disease 4) Drugs
|
|
Hyperparathyroidism: What causes primary hyperparathyroidism?
|
Usually an adenoma
|
|
Hyperparathyroidism: What are the findings of primary disease?
|
hypercalcemia, hypercalciuria, hypophosphatemia, high parathyroid hormone, high cAMP in urine; often asymptomatic, may present with weakness and constipation
|
|
Hyperparathyroidism: what is osteitis fibrosa cystica? (von Recklinghausen's syndrome)
|
cystic bone spaces filled with non-neoplastic fibrous tissue
|
|
Hyperparathyroidism: What causes secondary hyperparathyroidism?
|
low serum Ca++, most often chronic renal disease.
|
|
Hyperparathyroidism: What are the findings of secondary hyperparathyroidism?
|
hypocalcemia, hyperphosphatemia, high parathyroid hormone
|
|
Hypoparathyroidism: findings
|
hypocalcemia, tetany.
|
|
Hypoparathyroidism: causes
|
accidental surgical excision (thyroid surgery) or DiGeorge syndrome
|
|
Hypoparathyroidism: note: pseudohypoparathyroidism
|
autosomal recessive kidney unresponsiveness to PTH. Hypocalcemia, shortened 4th/5th digits, short stature
|
|
Carcinoid syndrome: frequency
|
rare
|
|
Carcinoid syndrome: cause
|
carcinoid tumors (neuroendocrine cells), especially those of the small bowel; they secrete high levels of serotonin (5-HT) that does not get metabolized by the liver due to liver metastases.
|
|
Carcinoid syndrome: symptoms
|
recurrent diarhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease.
|
|
Carcinoid syndrome: most common tumor of what?
|
apendix
|
|
Carcinoid syndrome: lab
|
high 5-HIAA in urine
|
|
Carcinoid syndrome: Rule of 1/3s:
|
1/3 metastasize; 1/3 present with second malignancy; 1/3 multiple
|
|
Carcinoid syndrome: Treatment?
|
Octreotide
|
|
Carcinoid syndrome: What is this medication?
|
synthetic octapeptide analog of somatostatin (growth hormone-inhibiting hormone)
|
|
Zollinger-Ellison syndrome: What kind of tumor causes this?
|
Gastrin secreting tumor (usually) of the pancreas
|
|
Zollinger-Ellison syndrome: what does it cause?
|
recurrent ulcers
|
|
Zollinger-Ellison syndrome: may be associated with what?
|
MEN type I
|
|
Osteoporosis: what is this?
|
reduction in bone mass in spite of normal bone mineralization
|
|
Osteoporosis: what characterizes type 1?
|
Postmenopausal (10-15 years after menopause); increased bone reabsorption due to low estrogen levels. Treated with estrogen replacement
|
|
Osteoporosis: what characterizes type 2?
|
Senile osteoporosis - affects men and women > 70 y/o
|
|
Osteoporosis: what races are affected most?
|
whites>blacks>asians
|
|
Osteoporosis: symptoms of vertebral crush fractures
|
acute back pain, loss of height, kyphosis
|
|
Osteoporosis: other
|
distal radius (Colles') fracures, vertebral wedge fracures.
|
|
Osteoporosis: see picure
|
0
|
|
Osteoporosis: PATHOLOGY - REPRODUCTIVE
|
(end of endocrine)
|
|
Benign prostatic hyperplasia: who gets BPH?
|
common in men > 50 y/o
|
|
Benign prostatic hyperplasia: what might cause it?
|
may be due to age-related increase in estradiol with possible sensitization of the prostate to the growth promoting effects of DHT.
|
|
Benign prostatic hyperplasia: findings
|
nodular enlargement of the periurethral (lateral and middle) lobes of the prostate gland, compressing the urethra to a vertical slit.
|
|
Benign prostatic hyperplasia: symptoms
|
increased frequency of urination, nocturia, difficulty in starting and stoping the stream of urine, dysuria.
|
|
Benign prostatic hyperplasia: complications
|
may lead to distention and hypertrophy of the bladder, hydronephrosis, UTIs
|
|
Benign prostatic hyperplasia: premalignant lesion?
|
No
|
|
Hydatidiform mole: What is it?
|
pathologic ovum (empty egg - ovum with no DNA) resulting in a cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast).
|
|
Hydatidiform mole: Most common precursor of what?
|
choriocarcinoma
|
|
Hydatidiform mole: what happens to B-hCG?
|
elevated
|
|
Hydatidiform mole: findings
|
honeycombed uterus, cluster of grapes apearance
|
|
Hydatidiform mole: genotype
|
complete mole is 46,xx and is completely paternal in origin (no maternal chromosomes); no associated fetus. PARTial mole is made up of 3 or more PARTS (triploid or tetraploid)
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): what is the triad?
|
hypertension, proteinuria, edema
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): what makes it eclampsia?
|
addition of seizures to the triad
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): what % of pregnant women?
|
0.07
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): when does it present?
|
20 weeks gestation to 6 weeks postpartum
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): what increases the likelihood?
|
preexisting hypertension, diabetes, chronic renal disease, autoimmune disorders
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): what is HELLP syndrome?
|
Hemolysis, Elevated LFTs, Low Platelets
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): Clinical features
|
headache, blurred vision, abdominal pain, edema of face and extremeties, altered mentation, hyperreflexia
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): Lab findings
|
thrombocytopenia, hyperuricemia
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): Treatment
|
Delivery of fetus as soon as viable. Otherwise, bedrest, salt restriction, monitoring and treatment of hypertension
|
|
Pregnancy-induced hypertension (preeclampsia-eclampsia): Treatment for eclampsia (a medical emergency)
|
IV Magnesium sulfate, diazepam
|
|
Pregnancy complications: Abruptio placentae
|
premature separation of the placenta. Painful uterine bleeding (usually 3rd trimester). Fetal death. May be associated with DIC
|
|
Pregnancy complications: Placenta accreta
|
defective decidual layer allows placenta to attach directly to myometrium. Predisposed by prior C-section or inflamation. May have massive hemorrhage after delivery.
|
|
Pregnancy complications: Placenta previa
|
attachment of the placenta to lower uterine segment. May occlude cervical os. Painless bleeding in any trimester.
|
|
Pregnancy complications: Ectopic pregnancy
|
most often in fallopian tubes, predisposed by salpingitis (PID).
|
|
Cervical Pathology: Dysplasia and carcinoma in situ
|
Disordered epithelial growth; begins at basal layer and extends outward. Classified as CIN 1, CIN 2, or CIN 3 (carcinoma in situ), depending on extent of dysplasia. Associated with HPV. May progress to invasive carcinoma.
|
|
Cervical Pathology: Invasive carcinoma
|
Often squamous cell carcinoma. Pap smears can catch cervical dysplasia (koilocytes) before it progresses to invasive carcinoma.
|
|
Cervical Pathology: AUTHOR
|
Gabi Rizzuto
|
|
Uterine pathology: most common tumor in female (hint - has increased incidence in blacks)? Do they progress to malignancy?
|
leiomyoma; no.
|
|
Uterine pathology: endometriosis - most common site?
|
ovary
|
|
Uterine pathology: endometriosis in the myometrium = ?
|
adenomyosis
|
|
Uterine pathology: most common gyn malignancy? (hint - causes vaginal bleeding in a postmenopausal women)
|
endometrial carcinoma
|
|
Uterine pathology: Leiomyosarcoma: does it arise de novo or from leiomyoma?
|
de novo
|
|
PCOS (Stein-Leventhal syndrome): Major clinical manifestations include: amenorrhea, infertility, obesity, and ----?
|
hirsutism
|
|
Ovarian cysts: the four types of ovarian cysts
|
follicular, corpus luteum, theca-lutein, chocolate
|
|
Ovarian cysts: blood containing cyst from ovarian endometriosis
|
chocolate cyst
|
|
Ovarian cysts: cyst that is associated with choriocarcinoma and moles
|
theca-lutein cyst
|
|
Ovarian cysts: cyst defined by hemorrhage into persistent corpus luteum
|
corpus luteum cyst
|
|
Ovarian cysts: cyst defined by distention of unruptured graafian follicle
|
follicular cyst
|
|
Ovarian germ cell tumors : that which is analagous to male seminoma
|
dysgerminoma
|
|
Ovarian germ cell tumors : produces alpha-fetoprotein
|
yolk sac tumor
|
|
Ovarian germ cell tumors : associated with elevated hCG
|
choriocarcinoma
|
|
Ovarian germ cell tumors : monodermal teratoma made up of only thyroid tissue
|
struma ovarii
|
|
Ovarian germ cell tumors : most common germ cell tumor of ovary (90%)
|
teratoma
|
|
Ovarian germ cell tumors : True or False: immature teratomas are benign
|
False. Mature ("dermoid cyst") ones are benign, immature ones are aggressively malignant
|
|
Ovarian non-germ cell tumors: bilateral non germ cell tumor with fallopian tube like epithelium
|
serous cystadenoma
|
|
Ovarian non-germ cell tumors: Pseudomyxoma peritonei (intraperitoneal accumulation of mucinous material) may be a consequence of which ovarian non germ cell tumor?
|
mucinous cystadenocarcinoma
|
|
Ovarian non-germ cell tumors: tumor resembling bladder epithelium
|
brenner tumor
|
|
Ovarian non-germ cell tumors: triad of ovarian fibroma, ascites, and hydrothorax = ?
|
Meigs' syndrome
|
|
Ovarian non-germ cell tumors: Pathology term for the small follicles filled with eosinophilic secretions that are seen in granulosa cell tumors
|
Call-Exner bodies
|
|
Breast disease: Which one of the following does NOT put an individual at increased risk for breast disease? Gender, age, early 1st menarche, late 1st pregnancy, late menopause, family history, fibroadenoma/non-hyperplastic cysts
|
fibroadenoma/hyperplastic cysts
|
|
Breast disease: Eczematous patches on the nipple w/ corresponding large cell's with clear halo on histology are indicative of --?
|
Paget's disease & most likely an underlying ductal carcinoma
|
|
Breast disease: Fibrosis, cystic, sclerosing, & epithelial hyperplasia are all histologic subtypes of what breast disease?
|
Fibrocystic disease (note: no increase risk of developing carcinoma)
|
|
Breast disease: Most common breast tumor in women < 25 years of age? is it malignant or a precursor to malignancy?
|
Fibroadenoma. No, no.
|
|
Breast disease: A benign tumor of the breast that presents with nipple discharge
|
Intraductal papilloma
|
|
Breast disease: Are malignant breast tumors more common pre or post menopause
|
post
|
|
Hypertension: True of false: 50% is classified as secondary HTN (usually resulting from renal disease)
|
false. (90% essential/primary, 10% secondary)
|
|
Hypertension: "read the questioner's mind": HTN predisposes individuals to this disease (the one John Ritter died of)
|
aortic dissection
|
|
Hypertension: Pathology changes associated with HTN
|
hyaline thickening & atherosclerosis
|
|
Arteriosclerosis: This awful term refers to a stiffening of the arteries that invovles the media. Particularly likely to occur at the radial & ulnar arteries.
|
Monckeberg arteriosclerosis
|
|
Atherosclerosis: True or false: atherosclerosis is a disease of small sized arteries
|
false. affects elastic, large & medium muscular arteries.
|
|
Atherosclerosis: Earliest sign of atherosclerotic disease
|
fatty streak
|
|
Atherosclerosis: most likely location
|
abdominal aorta. (then coronary artery, popliteal artery, and carotid artery)
|
|
Ischemic heart disease: Type of angina resulting from coronary artery spasm
|
Prinzmetal's variant
|
|
Ischemic heart disease: This coronary artery branch is most commonly implicated in myocardial infarction
|
LAD (left anterior descending)
|
|
Ischemic heart disease: most common cause of sudden cardiac death
|
(lethal) arrhythmia
|
|
Infarcts: red vs. pale: Solid tissues like the heart, brain, kidney and spleen have only a single blood supply (not so good collaterals). Therefore infarcts are more likely to be --?
|
pale
|
|
Infarcts: red vs. pale: 2 instances where red infarct is likely
|
(1) reperfusion (2) loose tissues with good collaterals - like the lungs or intestine
|
|
Evolution of MI: Rank the following vessels from most to least commonly occluded: RCA, LAD, circumflex
|
LAD>RCA>circumflex
|
|
Evolution of MI: Histologic changes on day 1 of an MI?
|
pallor of infarcted area; coagulative necrosis
|
|
Evolution of MI: days 2-4?
|
dilated vessels (hyperemia); neutrophil invasion; extensive coagulative necrosis
|
|
Evolution of MI: days 5-10?
|
yellow-brown softening of infarcted region; macrophages present; granulation tissue begins to grow in
|
|
Evolution of MI: after 7 weeks?
|
infarct is gray-white; scar complete
|
|
Diagnosis of MI: True or false: ECG is not diagnostic during the first 6 hours following an MI
|
False; it is the gold standard within this time period
|
|
Diagnosis of MI: What is the test of choice within the first 24 hours?
|
CK-MB
|
|
Diagnosis of MI: This enzyme is elevated from 4 hours up to 10 days after an MI and is the most specific protein marker
|
cardiac troponin I
|
|
Diagnosis of MI: on ecg, transmural infarction causes ______
|
ST elevation, Q wave changes
|
|
MI complications: Most common (90% of patients)
|
arryhthmias, esp. 2 days after infarct
|
|
MI complications: automimmune phenomen several weeks post-MI that results in fibrinous pericarditis
|
Dressler's syndrome
|
|
MI complications: high risk of mortality
|
cardiogenic shock (large infarcts)
|
|
MI complications: seen about a week after the infarction
|
rupture of ventricular wall, septum, or papillary muscle
|
|
Cardiomyopathies: Most common
|
dilated (congestive) cardiomyopathy; heart looks like a ballon on X-ray
|
|
Cardiomyopathies: True or False: substance abuse is a common cause of dilated cardiomyopathy
|
True; cocaine and alcohol especially
|
|
Cardiomyopathies: These two infectious diseases are associated with dilated myopathy
|
coxsackievirus B and Chagas' disease
|
|
Cardiomyopathies: True or false: hypertrophic cardiomyopathy causes systolic dysfunction
|
False; dilated myopathy causes systolic dysfunction, hypertrophic causes diastolic
|
|
Cardiomyopathies: Half of hypertrophic myopathies are inherited as an _________ trait (x-linked, dominant, etc.)
|
autosomal dominant; major cause of sudden death in young athletes
|
|
Cardiomyopathies: On echo in hypertrophic disease, the LV thickens and the chamber looks how?
|
like a banana
|
|
Cardiomyopathies: These "-osis" diseases are major causes of restrictive/obliterative cardiomyopathy
|
sarcoidosis, amyloidosis, hemochromatosis, endocardial fibroelastosis, endomyocardial (Loffler's) fibrosis….also, scleroderma but it's not an -osis
|
|
Heart murmurs: Name two causes of holosystolic murmurs
|
1) VSD, 2) mitral regurg, and 3) tricuspid regurg
|
|
Heart murmurs: Widened pulse pressure seen with this diastolic murmur
|
aortic regurg
|
|
Heart murmurs: Describe the murmur associated with the most common valvular lesion
|
Mitral prolapse; late systolic murmur following mid-systolic click
|
|
Heart murmurs: True or false: aortic stenosis causes a decrescendo-crescendo murmur following an ejection click
|
False; ejection click is followed by a crescendo-decrescendo systolic murmur
|
|
Heart murmurs: cause of a continuous murmur loudest at time of S2?
|
patent ductus artieriosis
|
|
Heart murmurs: opening snap followed by late diastolic rumbling?
|
mitral stenosis
|
|
Cardiac tumors: most common heart tumor?
|
metastasis
|
|
Cardiac tumors: primary cardiac tumor in 1) adults and 2) children
|
adults=myxoma (almost always in left atrium); children=rhabdomyoma
|
|
CHF: fun gross pathologic term for changes in liver with CHF?
|
nutmeg
|
|
CHF: what are "heart failure cells"?
|
hemosiderin-laden macrophages in lung
|
|
CHF: dyspnea on exertion, pulmonary edema, and paroxysmal nocturnal dyspnea are symptoms of?
|
left heart failure
|
|
CHF: patient says "I have to sleep upright." the clinical term for this is?
|
orthopnea
|
|
embolus types: most pulmonary emboli arise from?
|
DVT
|
|
embolus types: True or false: Amniotic fluid can lead to DIC
|
TRUE
|
|
deep vein thrombosis: what are the component of virchow's triad?
|
stasis, hypercoagulability, endothelial damage
|
|
cardiac tamponade: what is pulsus paradoxus?
|
greater than 10 mmHg drop in systolic on inspiration
|
|
cardiac tamponade: what is electrical alternans?
|
characteristic of tamponade on ECG in which QRS complex height varies beat-to-beat
|
|
cardiac tamponade: AUTHOR
|
James Rosoff / Flora Waples-Trefil
|
|
Bacterial Endocarditis: What valve is usually involved in endocarditis?
|
Mitral
|
|
Bacterial Endocarditis: What valve indicated drug use if it is involved?
|
Tricuspid
|
|
Bacterial Endocarditis: Can endocarditis be non-bacterial?
|
Yes. It can be secondary to metastasis, renal failure (maranctic or thrombotic), fungal
|
|
Bacterial Endocarditis: What type of endocarditis does s. Aureus cause?
|
rapid onset, high virulence, tends to occur secondary to infection elsewhere
|
|
Bacterial Endocarditis: What do the vegetations look like
|
Large.
|
|
Bacterial Endocarditis: What type of endocarditis does s. viridians cause?
|
subacute. Tends to have smaller vegetations.
|
|
Bacterial Endocarditis: What predisposes you to s.viridins endocarditis?
|
tends to occur on previously damaged valves, so rheumatic fever. It is commonly seen after dental work.
|
|
Bacterial Endocarditis: What are the 8 sings of endocarditis?
|
JR=NO FAME Janeway lesions, Roth's spots, Nail-bed hemorrhages, Osler's nodes, Fever, Anemia, Murmur (new), Emboli
|
|
Bacterial Endocarditis: What do Janeway Lesions look like?
|
multiple small flat erythematous lesions on palms and soles
|
|
Bacterial Endocarditis: What are roth spots?
|
round white spots on the retina surrounded by hemorrhage.
|
|
Bacterial Endocarditis: What are osler's nodes?
|
Tender raised lesions on the fingers and toes.
|
|
Bacterial Endocarditis: What is the etiology of these lesions?
|
Bacterial vegetations fliping off the heart valve and lodging in the periphery.
|
|
Rheumatic Fever/Rheumatic Heart Disease: What type of bacteria causes rheumatic fever?
|
Group A beta-hemolytic strep
|
|
Rheumatic Fever/Rheumatic Heart Disease: when does it occur?
|
Children 5-15 years, four weeks after a bacterial infection
|
|
Rheumatic Fever/Rheumatic Heart Disease: Is the bacteria responsible for the symptoms?
|
No. RF is an autoimmune reaction of a cross-reactive protein that is found in the initial bacterial infection.
|
|
Rheumatic Fever/Rheumatic Heart Disease: What are the non cardiac clinical signs of rheumatic fever?
|
FEVERSS - Fever, Erythema marginatum, valve damage, Elevated ESR, Red-hot joints (migratory polyarthritis), Subcutaneous nodules, and St. Vitus dance (chorea)
|
|
Rheumatic Fever/Rheumatic Heart Disease: What hear valves are effected?
|
Mitral (most frequent), Aortic, Tricuspid (5%) - high pressure valves mainly.
|
|
Rheumatic Fever/Rheumatic Heart Disease: What is an Aschoff body?
|
classic histological sign of RF, found in the myocardium, contained fibrinoid material, fragmented collages, surrounded by giant cells.
|
|
Rheumatic Fever/Rheumatic Heart Disease: What are the cardiac signs of RF?
|
Verrucious vegetations on the valve, pancarditis, possible pericardial effusions and myocarditis (most common cause of death)
|
|
Pericarditis: Name four causes of serous pericarditis.
|
RAIL - Rheumatic Arthritis, Infection, Lupus, and Uremia
|
|
Pericarditis: What is serous pericarditis?
|
straw colored, protein rich exudates - non-purulent, and acute
|
|
Pericarditis: What are three causes of fibirnous exudates?
|
MI, Rheumatic fever, and Uremia
|
|
Pericarditis: Cloudy pericardial exudates indicated what?
|
Bacterial infection
|
|
Pericarditis: What are two causes of Hemorrhagic pericarditis?
|
malignancy and TB
|
|
Pericarditis: What is hemorrhagic pericarditis?
|
Bloody and inflammatory exudates
|
|
Pericarditis: What are the clinical signs of pericardial exudates?
|
pericardial pain, friction rub, decreased heart sounds, ST elevation throughout, and pulses paradoxes (like cardiac tamponade)
|
|
Pericarditis: What are the long term sequela of pericarditis?
|
chronic adhesive or constrictive pericarditis
|
|
Pericarditis: What is constiricit pericadritis
|
Fibrous scarring in the pericardium obliterates the space and constrict the right side of the heart (because it is less able to withstand the pressure)
|
|
Pericarditis: What types of pericaditis lead to this?
|
TB and pyrogenic staph infections
|
|
Syphilitic Heart Disease: What part of the heart does syphilis damage?
|
The vaso vasorum of the aorta
|
|
Syphilitic Heart Disease: What does this lead to?
|
Dilation of the aorta and valve ring
|
|
Syphilitic Heart Disease: What clinical results does this have?
|
it can cause an aortic aneurysm or valvular incompetence
|
|
Syphilitic Heart Disease: What parts of the aorta are effected
|
ascending and arch
|
|
Syphilitic Heart Disease: What is the appearance or the aorta?
|
Called a "tree-bark" apearance.
|
|
Buerger's Disease: Buerger's disease is also known as?
|
smoker's disease, thromboangiitis obliterans
|
|
Buerger's Disease: What are the Sx (5)?
|
intermittent claudication, superficial nodular phlebitis, cold sensitivity, severe pain in affected part, may lead to gangrene
|
|
Buerger's Disease: What is the Tx?
|
Quit smokng
|
|
Takayasu's arteritits: Also known as ?
|
pulseless disease
|
|
Takayasu's arteritits: What is it?
|
thickening of aortic arch and/or proximal great vessels
|
|
Takayasu's arteritits: ESR elevated?
|
yes
|
|
Takayasu's arteritits: Primarily affects whom?
|
Young Asian Females
|
|
Takayasu's arteritits: Mnemomic
|
FAN MY SKIN On Wednesday
|
|
Takayasu's arteritits: Sx (7)
|
Fever, Arthritis, Night Sweats, Myalgia, Ocular Disturbances, Weak pulses in uper extremities (FAN MY SKIN On Wednesday)
|
|
Temporal Arteritis: Also known as?
|
Giant Cell Arteritis
|
|
Temporal Arteritis: Affects what vessels?
|
medium and small arteries (usually carotid branches)
|
|
Temporal Arteritis: ESR elevated?
|
yes
|
|
Temporal Arteritis: Primarily affects whom?
|
Elderly Females
|
|
Temporal Arteritis: Sx (3)
|
Unilateral Headache, Jaw claudication, impaired vision
|
|
Temporal Arteritis: Many patients are also affected with this syndrome
|
Polymalgia Rheumatica
|
|
Temporal Arteritis: Tx (?)
|
Steroids
|
|
Polyarteritis Nodosa: How would you describe the inflammation in this disease?
|
necrotizing, caused by immune complex deposition
|
|
Polyarteritis Nodosa: In which vessels?
|
small to medium-sized muscular arteries, renal and visceral vessels
|
|
Polyarteritis Nodosa: ESR elevated?
|
yes
|
|
Polyarteritis Nodosa: Sx (7) … and they are SO specific
|
fever,weight loss,malaise,abdominal pain,headache ,myalgia,hypertension
|
|
Polyarteritis Nodosa: Other findings
|
cotton-wool spots, microaneurysms, pericarditis, myocarditis, palpable purpura
|
|
Polyarteritis Nodosa: What viral infection is found in 30% of PN patients?
|
Hepatitis B
|
|
Polyarteritis Nodosa: what antibody is associated with this disease?
|
P-ANCA
|
|
Polyarteritis Nodosa: What two ways can you remember the assoc Ab?
|
P-ANCA --> PAN (PolyArteritis Nodosa)
|
|
Polyarteritis Nodosa: What does P-ANCA refer to?
|
Perinuclear pattern of Antineutrophil Cytoplasmic Antibodies
|
|
Polyarteritis Nodosa: Primarily affects whom?
|
Young males
|
|
Polyarteritis Nodosa: Tx
|
Corticosteroids, Azathioprine, Cyclophosphamide
|
|
Wegener's Granulomatosis: What are three major findings (hint: they are necrotizing)
|
Focal Necrotizing Vasculitis, Necrotizing granulomas of the lung and uper airway, Necrotizing glomerulonephritis
|
|
Wegener's Granulomatosis: Sx (7)
|
Perforated nasal septum, Chronic Sinusitis, Otitis Media, Mastoiditis, Cough , Dyspnea, Hemoptysis
|
|
Wegener's Granulomatosis: What antibody is associated with this disease
|
C-ANCA
|
|
Wegener's Granulomatosis: What should you look for on CXR?
|
large nodular densities
|
|
Wegener's Granulomatosis: Tx
|
Corticosteroids, Azathioprine, Methotrexate
|
|
Kawasaki Disease: Who gets it?
|
infants, kids
|
|
Kawasaki Disease: What is the disease course?
|
acute, self-limiting
|
|
Kawasaki Disease: What vessels are involved?
|
small and medium sized
|
|
Kawasaki Disease: What does CRASH stand for
|
Conjunctivitis, Rash (truncal), Aneurysms of Coronary Arteries, Strawberry tongue, changes in lips/oral mucosa, Hands and Feet show induration and desquamation
|
|
Kawasaki Disease: Glomerular Pathology
|
275
|
|
Kawasaki Disease: What is prerenal azotemia?
|
selective rise in BUN during early renal failure
|
|
Kawasaki Disease: Define segmental.
|
involving part of the glomerular tuft
|
|
Kawasaki Disease: Nephritic Syndrome
|
0
|
|
Kawasaki Disease: hematuria, hypertension, oliguria, azotemia = ?
|
Nephritic Syndrome, "I" = inflammation
|
|
Kawasaki Disease: LM findings in post-strep glomerulonephritis?
|
lumpy bumpy and hypercellular w/ neutrophils
|
|
Kawasaki Disease: EM findings in post-strep glomerulonephritis?
|
subepithelial humps (from deposition of cationic antigen)
|
|
Kawasaki Disease: IF findings in post-strep glomerulonephritis?
|
granular
|
|
Kawasaki Disease: Goodpasture's is what type of hypersensistivity?
|
type II (IgG binding directly to BM)
|
|
Kawasaki Disease: Goodpasture's IF?
|
linear
|
|
Kawasaki Disease: Symptoms of Goodpasture's?
|
hemoptysis, hematuria
|
|
Kawasaki Disease: Membranoproliferative glomerulonephritis EM?
|
subendothelial humps; "tram track"
|
|
Kawasaki Disease: Course of crescentic glomerulonephritis?
|
rapid (the Red Crescent is the Islamic Red Cross, an organization that provides relief during emergencies, like crescentic glomerulonephritis)
|
|
Kawasaki Disease: Course of Membranoproliferative glomerulonephritis?
|
slow
|
|
Kawasaki Disease: IgA nephropathy IF and EM?
|
mesangial deposits of IgA (Mes"A"ngium)
|
|
Kawasaki Disease: Which can be post infectious, IgA nephropathy or Goodpasture's?
|
IgA nephropathy
|
|
Kawasaki Disease: Nephrotic Syndrome
|
0
|
|
Kawasaki Disease: Signs of nephrotic syndrome?
|
massive proteinuria, hypoalbuminemia, generalized edema, hyperlipidemia (think "erotic" = an erection(edema) and ejaculate(massive proteinuria)
|
|
Kawasaki Disease: LM of membranous glomerulonephritis?
|
diffuse capillary and basement membrane thickening
|
|
Kawasaki Disease: IF of membranous glomerulonephritis?
|
granular
|
|
Kawasaki Disease: EM of membranous glomerulonephritis?
|
spike and dome ("if you have a spike in your dome, you must be insane in the "membran"e," -Chirag)
|
|
Kawasaki Disease: Minimal change disease EM?
|
foot process effacement
|
|
Kawasaki Disease: Most common cause of childhood nephrotic syndrome?
|
minimal change disease
|
|
Kawasaki Disease: Focal segmental glomerular sclerosis LM?
|
segmental sclerosis and hyalinosis
|
|
Kawasaki Disease: Diabetic nephropathy LM?
|
Kimmelstiel-Wilson lesions
|
|
Kawasaki Disease: SLE (5 patterns of renal involvement) LM?
|
wire-loop apearance w/ extensive granular BM depsits in membranous glomerulonephritis pattern
|
|
Kidney Stones: What is the most common kidney stone?
|
Calcium (with either oxalate of phosphate)
|
|
Kidney Stones: What kidney stone is associated with a bacterial infection?
|
Ammonium magnesium phosphate (struivte) stones are associated with urase positive bugs that make ammonium
|
|
Kidney Stones: What are the two most common stone-forming bacteria?
|
proteus vulgaris and Staph.
|
|
Kidney Stones: What stones are associated with gout?
|
Uric acid stones
|
|
Kidney Stones: What else can cause uric acid stones?
|
Any disease with high cell turnover (remember that uric acid is a by-product of DNA formation), so leukemia and myeloproliferative disease
|
|
Kidney Stones: What stones are associated with cystineuria?
|
cystine stones
|
|
Kidney Stones: What two stones are radiolucent?
|
Uric acid and cystine (the two purely metabolic causes)
|
|
Kidney Stones: What are the complications of stones?
|
Hydronephrosis and pyelonephritis
|
|
Kidney Stones: What causes calcium stones?
|
Anything that increases calcium in the blood, so high PTH, malignancy (bone breakdown, PTH production), vitamin D overdose.
|
|
Renal Cell Carcinoma: Is this a common renal cancer?
|
Yes, the most common
|
|
Renal Cell Carcinoma: Who is prone to this?
|
males, ages 50-70, smokers, gene deletions on chromosome 3
|
|
Renal Cell Carcinoma: This is a cancer of what cell type?
|
renal tubule cells, histologically they apear clear.
|
|
Renal Cell Carcinoma: What are the clinical signs of this cancer?
|
flank pain, fever, hematuria, palpable mass, secondary polycythemia
|
|
Renal Cell Carcinoma: How does it spread?
|
It invades the renal veins and IVC, to spread hematogenously
|
|
Renal Cell Carcinoma: What hormones can it produce?
|
ACTH, prolactin, Parathyroid-like hormone, gonadotropins and renin.
|
|
Wilm's Tumor: Who gets this cancer?
|
Children 2-4 years
|
|
Wilm's Tumor: Is it common?
|
The most common renal cancer in children
|
|
Wilm's Tumor: What is the chromosomal abnormality that leads to this?
|
deletion of tumor supressor gene WT1 on chromosome 11
|
|
Wilm's Tumor: What tetrad is it associated with?
|
WAGR - Wilm's, Anirida (lack of an iris), Genitourinary malformation, and Retardation
|
|
Wilm's Tumor: How does it present?
|
huge palpable mass and hemihypertrophy
|
|
Wilm's Tumor: What is the histological appearance?
|
mixed - with stromal, mesenchymal, tubular, glomerular and fibrous elements
|
|
Transitional Cell Carcinoma: Where does this cancer occur?
|
Urinary spaces (tract, calyces, pelvis, bladder)
|
|
Transitional Cell Carcinoma: Does it recur?
|
yes, often
|
|
Transitional Cell Carcinoma: How does it spread?
|
Local invasion
|
|
Transitional Cell Carcinoma: What can predispose you to it?
|
Pee SAC toxins - Phenacetin, Smoking, Aniline dye (benezenes), and Cyclophsophimide.
|
|
Transitional Cell Carcinoma: How does it present?
|
Hematuria
|
|
Acid-Base Physiology: What is the primary disturbance in Metabolic acidosis?
|
a decrease in bicarbonate
|
|
Acid-Base Physiology: What is the compensation?
|
A drop in CO2 by hyperventilation
|
|
Acid-Base Physiology: What are common causes?
|
diabetic ketoacidosis (production of ketone acids), diarrhea (loss of GI bicarb), salisylate overdose, acetazoleamide (diuretic) OD, lactic acidosis, renal failure (can't excrete organic acids), ethylene glycol ingestion
|
|
Acid-Base Physiology: What is the primary disturbance in respiratory acidosis?
|
A build-up in CO2
|
|
Acid-Base Physiology: What is the compensation?
|
Increased bicarb reabosrobtion from the kidney
|
|
Acid-Base Physiology: What are some common causes?
|
COPD, airway obstruction, opiates and sedatives, guillan-barr or ALS,
|
|
Acid-Base Physiology: What is the primary disturbance in metabolic alkalosis?
|
increased bicarbonate
|
|
Acid-Base Physiology: What is the compensation?
|
Increased CO2 by decreased respiration
|
|
Acid-Base Physiology: What are some common causes?
|
Vomiting, hyperaldosteronism (increased H+ secretion), loop or thiazide diuretics (volume contraction)
|
|
Acid-Base Physiology: What is the primary disturbance in respiratory alkalosis?
|
A drop in CO2
|
|
Acid-Base Physiology: What is the compensation?
|
increased excretion of bicarb by the kidney
|
|
Acid-Base Physiology: What are some common causes?
|
hyperventilation, high altitude, pneumonia and pulmonary embolus (hypoxemia causes hyperventilation_
|
|
Acid-Base Physiology: What is the Henderson Haselbach equation?
|
pH = pKa + Log (HCO3-)/(.03*pCO2)
|
|
Acid Base Nomogram: Is there an awesome graph on page 277 that you should know?
|
Yes
|
|
Acid Base Nomogram: basically four cases
|
0
|
|
Acid Base Nomogram: Low pH, low pCO2 (low HCO3-)
|
metabolic acidosis
|
|
Acid Base Nomogram: Low pH, high pCO2 (high HCO3-)
|
chronic respiratory acidosis
|
|
Acid Base Nomogram: High pH, low pC02 (low HC03-)
|
acute respiratory alkalosis
|
|
Acid Base Nomogram: High pH, high pCO2 (high HCO3-)
|
metabolic alkalosis
|
|
Acidosis/Alkalosis: Check arterial pH
|
0
|
|
Acidosis/Alkalosis: pH < 7.4
|
acidosis
|
|
Acidosis/Alkalosis: pH > 7.4
|
alkalosis
|
|
acidosis: P (CO2) > 40
|
Respiratory acidosis
|
|
acidosis: P (CO2) > 40, Hypoventilation or Hyperventilation
|
HYPO
|
|
acidosis: Causes
|
Acute lung disesae, chronic lung disease, Drugs (opioids, narcotics, sedatives), Weakening of Resp. muscles
|
|
acidosis: P (CO2) < 40
|
0
|
|
acidosis: What should you do next?
|
Check Anion Gap
|
|
acidosis: What is the normal anion gap?
|
8-12 mEq/L
|
|
acidosis: Increased Anion Gap - 4 Causes
|
Renal Failure, lactic acidosis, ketoacidosis, aspirin ingestions
|
|
acidosis: Normal anion gap metabolic acidosis (4)
|
Diarrhea, sniffin glue, renal tubular acidosis, hyperchloremia
|
|
acidosis: pH > 7.4
|
alkalosis
|
|
acidosis: pCO2 < 40
|
Respiratory alkalosis
|
|
acidosis: respiratory acidosis Causes (2)
|
HYPERventilation, aspirin ingestion (early)
|
|
acidosis: pCO2 > 40
|
metabolic alkalosis w/ compensation
|
|
acidosis: metabolic alkalosis Causes (4)
|
vomiting, diuretic use, antacids, hyperaldosteronism
|
|
Anion gap acidosis: How do you calculate it
|
Na - Cl - HCO3
|
|
Anion gap acidosis: What is normal?
|
8-12 mEq/L
|
|
Anion gap acidosis, MUDPILES: M
|
Methanol
|
|
Anion gap acidosis, MUDPILES: U
|
Uremia
|
|
Anion gap acidosis, MUDPILES: D
|
DKA
|
|
Anion gap acidosis, MUDPILES: P
|
Paraldehyde or Phenformin
|
|
Anion gap acidosis, MUDPILES: I
|
Iron tablets or INH
|
|
Anion gap acidosis, MUDPILES: L
|
Lactic Acidosis
|
|
Anion gap acidosis, MUDPILES: E
|
Ethanol, Ethylene Glycol
|
|
Anion gap acidosis, MUDPILES: S
|
Salicylates
|
|
Acid Base Compensations: Metabolic acidosis
|
pCO2 = 1.5(HCO3) + 8 +/- 2
|
|
Acid Base Compensations: Metabolic alkalosis
|
pCO2 increases 0.7 mm Hg per 1 mEq/L HCO3 increase
|
|
Acid Base Compensations: Respiratory acidosis (acute)
|
HCO3 increases by 1 mEq/L for every 10 mmHg increase of pCO2
|
|
Acid Base Compensations: Respiratory acidosis (chronic)
|
HCO3 increases by 3.5 mEq/L for every 10 mmHg increase of pCO2
|
|
Acid Base Compensations: Respiratory alkalosis (acute)
|
HCO3 decreases by 2 mEq/L for every 10 mmHg decrease of pCO2
|
|
Acid Base Compensations: Respiratory alkalosis (chronic)
|
HCO3 decreases by 5 mEq/L for every 10 mmHg decrease of pCO2
|
|
Acute Pyelonephritis: Affects _______ of kidney
|
cortex
|
|
Acute Pyelonephritis: Spares ____________
|
glomeruli/vessels
|
|
Acute Pyelonephritis: _______ _______ in urine are pathognomonic
|
WBC casts
|
|
Chronic Pyelonephritis: Tubules may contain __________ casts
|
Eosinophilic
|
|
Chronic Pyelonephritis: Coarse ________, _________ scarring
|
Asymmetric corticomedullary
|
|
Diffuse Cortical Necrosis: infarction of _________ of both kidneys
|
cortex (cortices)
|
|
Diffuse Cortical Necrosis: due to combination of _________ and _________
|
vasospasm and DIC
|
|
Diffuse Cortical Necrosis: associated with _________ and _________
|
obstetric catastrophes and septic shock
|
|
Acute Tubular Necrosis: Most common cause of
|
renal failure
|
|
Acute Tubular Necrosis: reversible or irreversible
|
reversible
|
|
Acute Tubular Necrosis: fatal or non-fatal
|
fatal, if left untreated
|
|
Acute Tubular Necrosis: associated with (3)
|
renal ischemia (shock), crush injury (myoglobulinuria), toxins
|
|
Acute Tubular Necrosis: Death occurs most often during initial oliguric phase; T or F
|
TRUE
|
|
Renal Papillary Necrosis: Associated with (3)
|
Diabetes mellitus, Acute pyelonephritis, Chronic phenacetin use
|
|
Acute Renal Failure: Definition
|
abrupt decline in renal function over a period of days
|
|
Acute Renal Failure: Will see increase in _______ & _______
|
BUN & Creatinine
|
|
Acute Renal Failure: Prerenal is due to decreased ______
|
RBF
|
|
Acute Renal Failure: Renal is due to
|
ATN, Ischemia, toxins
|
|
Acute Renal Failure: Post renal is due to
|
outflow obstruction
|
|
Acute Renal Failure: 3 causes of above
|
renal stones, BPH, neoplasia
|
|
Acute Renal Failure: bilateral or unilateral
|
bilateral
|
|
Pre or post renal failure: Urine osmolality > 500
|
prerenal
|
|
Pre or post renal failure: Urine osmolality < 350
|
renal or postrenal
|
|
Pre or post renal failure: urine Na < 10
|
prerenal
|
|
Pre or post renal failure: urine Na > 40
|
postrenal
|
|
Pre or post renal failure: urine Na > 20
|
renal
|
|
Pre or post renal failure: FE(Na) >4%
|
postrenal
|
|
Pre or post renal failure: FE(Na) <1%
|
prerenal
|
|
Pre or post renal failure: FE(Na) >2%
|
renal
|
|
Pre or post renal failure: BUN/Cr ratio <15
|
renal
|
|
Pre or post renal failure: BUN/Cr ratio >15
|
postrenal
|
|
Pre or post renal failure: BUN/Cr ratio > 20
|
prerenal
|
|
Pre or post renal failure: Chronic renal failure due to (2)
|
diabetes, hypertension
|
|
Pre or post renal failure: Consequences of Renal Failure (8) p.279
|
Why?
|
|
Pre or post renal failure: Anemia
|
lack of EPO
|
|
Pre or post renal failure: Renal osteodystrophy
|
lack of active Vit D
|
|
Pre or post renal failure: Arrythmia
|
hyperkalemia
|
|
Pre or post renal failure: Metabolic acidosis
|
decreased acid secretion
|
|
Pre or post renal failure: Uremia
|
increase in BUN and Cr
|
|
Pre or post renal failure: CHF/Pulmonary Edema
|
retention of Na and H20
|
|
Pre or post renal failure: Chronic Pyelonephritis
|
0
|
|
Pre or post renal failure: Hypertension
|
0
|
|
Pre or post renal failure: AUTHOR
|
Aaron Goldberg
|
|
Alcoholism: tremor, tachcardia, hypertension, malaise, nausea, delirium tremens are symtpoms of what?
|
alcohol withdrawal
|
|
Alcoholism: when do you get symptoms of alcohol withdrawal?
|
in case of physiological tolerance and dependence when intake is interrupted
|
|
Alcoholism: what is disulfiram and how does it work?
|
disulfiram is a pharmacological treatment of alcoholism - negatively conditions patient against EtOH
|
|
Alcoholism: a good possible referral to sustain EtOH abstinence in alcoholics
|
Alcoholics Anonymous and other peer groups
|
|
Alcoholism: 3 mechanisms of EtOH action
|
1) interpolates into membranes --> toxic effects, partic. in brain 2) alcohol dehydrogenase converts EtOH to acetaldehyde, forms adducts with proteins and nucleic acids, converted to acetate, Ac-CoA, FA synthesis, fatty liver 3) increased NADH/NAD ratio
|
|
Complications of alcoholism: Condition in which these are seen: hepatitis and cirrhosis, pancreatitis, dilated cardiomyopathy, peripheral neuropathy, cerebellar degeneration, Wernicke-Korsakoff syndrome, testicular atrophy and hyperestrinism, and Mallory-Weiss syndrome
|
alcoholism
|
|
Complications of alcoholism: name histological type of cirrhosis in alcoholism
|
micronodular cirrhosis
|
|
Complications of alcoholism: accompanying symptoms of alcoholic cirrhosis
|
jaundice, hypoalbuminemia, coagulation factor deficiences, portal hypertension
|
|
Complications of alcoholism: list clinical findings in alcoholic cirrhosis besides jaundice
|
peripheral edema and ascites, encephalopathy, neurologic manifestations (asterixis, flaping tremor of hands)
|
|
Complications of alcoholism: What is the cause of Wernicke-Korsakoff syndrome?
|
thiamine (B1) deficiency, particularly in alcoholics
|
|
Complications of alcoholism: what is the presenting triad of Wernicke's encephalopathy?
|
psychosis, ophthalmoplegia, and ataxia
|
|
Complications of alcoholism: distinguishing features of Korsakoff's from Wernicke's
|
in Korsakoff, also *memory loss*, confabulation,confusion.
|
|
Complications of alcoholism: is Korsakoff's syndrome reversible?
|
No.
|
|
Complications of alcoholism: Tx for Wernicke-Korsakoff syndrome
|
IV Vitamin B1 (thiamine)
|
|
Complications of alcoholism: What is Mallory-Weiss syndrome?
|
longitudinal lacerations at the gastroesophageal junction caused by excessive vomiting (for ex., in alcoholism) with failure of LES relaxation that could lead to fatal hematemesis
|
|
Argyll Robertson pupil: name for a pupil that constricts with accomodation but is not reactive to light, and what is it pathognomonic for?
|
Argyll Robertson pupil. Pathognomonic for 3' syphilis. "Prostitute's pupil" accomodates but does not react.
|
|
Amyloidosis: detect what using apple green biorefringence on Conco red stain?
|
amyloid
|
|
Amyloidosis: most common cause of amyloidosis?
|
primary light chain deposition seen with multiple myeloma.
|
|
Amyloidosis: another cause of primary amyloidosis?
|
Waldenstrom's macroglobulinemia.
|
|
Amyloidosis: Secondary amyloidosis can cause what in the kidney?
|
nephrotic syndrome
|
|
Amyloidosis: disease associated with beta amyloid deposition in cerebral cortex
|
Alzheimer's
|
|
Amyloidosis: islet cell amyloid deposition characteristic of what
|
diabetes mellitus type 2
|
|
Aschoff body: "-------- body" found in rheumatic heart disease
|
Aschoff body (granuloma with giant cells)
|
|
Aschoff body: "------- cells" found in rheumatic heart disease
|
Anitschkow's cells (activated histiocytes) "Aschoff and Anitschow" -- two RHussians with RHeumatic heart disease
|
|
Auer bodies (rods): peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts, name and primary association
|
Auer rods; primarily seen in acute promyelocytic leukemia (M3)
|
|
Auer bodies (rods): treatment of AML M3 can release what, leading to what?
|
release Auer rods, leading to DIC
|
|
Casts: RBC casts indicate
|
glomerular inflammation (nephritic syndromes), ischemia, or malignant hypertension
|
|
Casts: how to determine if hematuria/pyuria is of renal origin
|
presence of casts
|
|
Casts: WBC casts indicate
|
inflammation in renal interstitium, tubules, and glomeruli
|
|
Casts: casts often seen in normal urine
|
hyaline casts
|
|
Casts: casts seen in chronic renal failure
|
waxy casts
|
|
Erythrocyte sedimentation rate: ESR elevated in
|
dramatically in infection, malignancy, connective tissue disease; also in pregnancy, inflammatory disease, and anemia
|
|
Erythrocyte sedimentation rate: ESR lowered in
|
sickle cell anemia, CHF, and polycythemia
|
|
Erythrocyte sedimentation rate: Should ESR be used for asymptomatic screening
|
No
|
|
Erythrocyte sedimentation rate: ESR used to monitor course of -----
|
temporal arteritis and polymyalgia rheumatica
|
|
Erythrocyte sedimentation rate: ESR is expensive and specific. T/F
|
false. Cheap and nonspecific.
|
|
Ghon complex: indicates TB granulomas with lobar or perihilar lymph node involvement
|
Ghon focus and lymph node involvement, Ghon complex.
|
|
Ghon complex: Does a Ghon complex reflect primary or secondary TB?
|
primary.
|
|
Hyperlipidemia signs: plaque in blood vessel wall
|
atheromata
|
|
Hyperlipidemia signs: plaque or nodule composed of lipid-laden histiocytes in skin, especially eyelids
|
xanthoma
|
|
Hyperlipidemia signs: lipid deposit in tendon, especially Achilles
|
tendinous xanthoma
|
|
Hyperlipidemia signs: lipid deposit in cornea, nonspecific (arcus senilis)
|
corneal arcus
|
|
Psammoma bodies: laminated, concentric, calcific spherules in tumor
|
Psammoma bodies
|
|
Psammoma bodies: Psammoma bodies seen in:
|
1. papillary adenocarcinoma of thyroid 2. serous papillary cystadenoma of ovary 3. meningioma 4. malignant mesothelioma "PSaMMoma" Papillary (thyroid), Serous (ovary), Meningioma, Mesothelioma
|
|
RBC forms: Biconcave RBC
|
normal
|
|
RBC forms: Spherocytes
|
hereditary spherocytosis, autoimmmune hemolysis
|
|
RBC forms: Elliptocyte
|
hereditary elliptocytosis
|
|
RBC forms: Macro-ovalocyte
|
megaloblastic anemia, marrow failure
|
|
RBC forms: Helmet cell, schistocyte
|
DIC, traumatic hemolysis
|
|
RBC forms: Sickle cell
|
obviously sickle cell anemia
|
|
RBC forms: Teardrop cell
|
myeloid metaplasia with myelofibroblasts
|
|
RBC forms: Acanthocyte
|
spiny apearance in abetalipoproteinemia
|
|
RBC forms: Target cell
|
Thalassemia, liver disease, HbC
|
|
RBC forms: Poikilocyte
|
Nonuniform shapes in TTP/HUS, microvascular damage, DIC
|
|
RBC forms: Burr cell
|
TTP/HUS
|
|
HLA subtypes!: HLA B27
|
Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter's syndrome ("PAIR")
|
|
HLA subtypes!: HLA 13,17
|
Psoriasis
|
|
HLA subtypes!: HLA DR2
|
Multiple sclerosis, hay fever
|
|
HLA subtypes!: HLA DR3, DR4
|
Diabetes mellitus type I
|
|
HLA subtypes!: HLA DR5
|
Pernicious anemia -- B12 deficiency
|
|
HLA subtypes!: HLA DR7
|
Steroid-responsive nephrotic syndrome
|
|
Reed-Sternberg cells: Distinctive giant cell in blood; binucleate or bilobed with 2 halves as mirror images ("owl's eyes"); name and disease association
|
Reed-Sternberg cells, necessary but not sufficient for dx of Hodgkin's disease. Variants include lacunar cells in nodular sclerosis variant.
|
|
Reed-Sternberg cells: How many types of Hodgkin's disease?
|
4 - see also p. 241
|
|
Reed-Sternberg cells: Only variant of Hodgkin's seen more in women than men
|
nodular sclerosis
|
|
Reed-Sternberg cells: prognosis of nodular sclerosis variant of Hodgkin's
|
excellent
|
|
Virchow's (sentinel) node: firm supraclavicular lymph node, often on left side, easily palpable (ie, by medical students), also known as "jugular gland" - name and association
|
Virchow's node - presumptive evidence of malignant visceral neoplasm (classically stomach)
|
|
Peripheral blood smears: most common cause of microcytic hypochromic anemia
|
iron deficiency
|
|
Peripheral blood smears: ferritin levels in microcytic hypochromic anemia
|
low
|
|
Peripheral blood smears: serum iron-binding capacity in microcytic hypochromic anemia
|
elevated
|
|
Peripheral blood smears: lead poisoning gives what appearance on peripheral smear
|
microcytic hypochromic
|
|
Peripheral blood smears: causes of megaloblastic anemia
|
folate or B12 deficiency
|
|
Peripheral blood smears: 5-7 lobes (hypersegmented) PMNs in
|
megaloblastic anemia
|
|
Peripheral blood smears: large RBCs (MCV >100) in
|
megaloblastic anemia
|
|
Peripheral blood smears: do you give folate to pt. deficient in B12?
|
Never
|
|
Peripheral blood smears: autoimmune disease that causes B12 deficiency; what does it deplete?
|
pernicious anemia, depletes intrinsic factor
|
|
Peripheral blood smears: where is B12 absorbed in gut?
|
terminal ileum, with intrinsic factor from stomach
|
|
Peripheral blood smears: Target cells mnemonic
|
HALT (Hemoglobin C disease, Asplenia, Liver disease, Thalassemia)
|
|
Peripheral blood smears: Hemoglobin SS in what disease?
|
sickle cell anemia
|
|
Peripheral blood smears: molecular change B-globin GLU->VAL at #6
|
HbS
|
|
Peripheral blood smears: 8% of US african-americans carry what Hb
|
HbS
|
|
Peripheral blood smears: conditions in which HbSS cells sickle
|
hypoxia, dehydration, increased blood viscosity
|
|
Peripheral blood smears: vaso-occlusive crises with chest pain in young african-americanl; consider
|
sickle cell anemia
|
|
Peripheral blood smears: aplastic crises in sickle cell anemia associated with which virus
|
B19 virus
|
|
Peripheral blood smears: manifestation of sickle cell anemia in spleen
|
splenic sequestration crisis
|
|
Peripheral blood smears: increased risk of CVA in sickle cell anemia?
|
yes
|
|
Enzyme markers: AST or ALT used for MI?
|
AST only
|
|
Enzyme markers: AST or ALT more elevated in viral hepatitis
|
ALT>AST in viral hepatitis ("virALT")
|
|
Enzyme markers: AST or ALT more elevated in alcholic hepatitis
|
AST>ALT in alcoholic hepatitis ("ToAST")
|
|
Enzyme markers: Amylase elevation
|
acute pancreatitis, mumps
|
|
Enzyme markers: Low ceruloplasmin
|
Wilson's disease
|
|
Enzyme markers: Creatine phosphokinase elevated in
|
muscle disorders (Duchenne's muscular dystrophy), and MI
|
|
Enzyme markers: subtype of CPK elevated in MI
|
CPK-MB
|
|
Enzyme markers: GGT stands for and elevated in
|
gamma glutamyl transferase, various liver diseases
|
|
Enzyme markers: Lipase elevated in
|
acute pancreatitis
|
|
Enzyme markers: Alkaline phosphatase elevated in
|
Bone disease (Paget's disease of bone), obstructive liver disease (hepatocellular carcinoma)
|
|
Immunohistochemical stains: Vimentin stains what
|
connective tissue
|
|
Immunohistochemical stains: Desmin stains what
|
muscle
|
|
Immunohistochemical stains: Cytokeratin stains what
|
epithelial cells
|
|
Immunohistochemical stains: Glial fibrillary acid proteins (GFAP) stains what
|
neuroglia
|
|
Immunohistochemical stains: Neurofilament stains what
|
neurons
|
|
Immunohistochemical stains: AUTHOR
|
Shailen Sehgal
|
|
Enzyme Kinetics: _______ is elevated in a myocardial infarction. (AST, ALT, or both)
|
AST
|
|
Enzyme Kinetics: In viral hepatitis, is ALT or AST more elevated?
|
ALT
|
|
Enzyme Kinetics: In alcoholic hepatitis, is ALT or AST more elevated?
|
AST
|
|
Enzyme Kinetics: ________ can be elevated in mumps or acute pancreatitis, while _________ elevation is more specific for acute pancreatitis.
|
amylase, lipase
|
|
Enzyme Kinetics: What enzyme is elevated in Duchenne's muscular dystrophy, and after a myocardial infarction?
|
CPK
|
|
Enzyme Kinetics: _______ can be elevated in Paget's disease and hepatocellular carcinoma.
|
alkaline phosphatase
|
|
Enzyme Kinetics: Elevated GGT is seen in various diseases of which organ?
|
liver
|
|
Enzyme Kinetics: True or False? In a myocardial infarction, serum LDH-1>LDH-2
|
TRUE
|
|
Enzyme Kinetics: Decreased serum ceruloplasmin is seen in _______
|
Wilson's Disease
|
|
Immunohistochemical Stain Corresponding cell type: (Match the stain with the corresponding cell type)
|
0
|
|
Immunohistochemical Stain Corresponding cell type: Vimentin
|
connective tissue
|
|
Immunohistochemical Stain Corresponding cell type: Cytokeratin
|
Epithelial cells
|
|
Immunohistochemical Stain Corresponding cell type: Neurofilaments
|
neurons
|
|
Immunohistochemical Stain Corresponding cell type: Glial Fibrillary acid proteins (GFAP)
|
neuroglia
|
|
Immunohistochemical Stain Corresponding cell type: Desmin
|
muscle
|
|
Pharmacokinetics: amount of drug in body/_______ = Vd
|
plasma drug concentration (note: Vd is Volume of Distribution)
|
|
Pharmacokinetics: rate of elimination of drug/[plasma drug] = ?
|
CL (Clearance)
|
|
Pharmacokinetics: (.7)(Vd)/CL = ?
|
T 1/2
|
|
Pharmacokinetics: A drug infused at a constant rate reaches about 94% of steady state after _______ t 1/2s.
|
4
|
|
Dosage Calculations: A loading dose is calculated using this formula.
|
(Cp)(Vd)/F (note: Cp = target plasma concentration, and F = bioavailability)
|
|
Dosage Calculations: A maintenance dose is calculated using this formula.
|
(Cp)(CL)/F
|
|
Elimination of Drugs: Rate of elimination is proportional to _______ ______ in 1st order elimination.
|
drug concentration
|
|
Elimination of Drugs: In the case of EtOH, which is elimated by _____ order elimination, a constant amount of drug is eliminated per unit time.
|
zero
|
|
Phase I vs. Phase II metabolism: Phase ____ (I or II) reactions yield slightly polar metabolites that are often _____ (active or inactive)
|
I, active
|
|
Phase I vs. Phase II metabolism: Phase ____ (I or II) reactions yield very polar metabolites that are often _____ (active or inactive) and are excreted by the _______.
|
II, inactive, kidney
|
|
Phase I vs. Phase II metabolism: Phase II reactions are often of this type.
|
conjugation
|
|
Phase I vs. Phase II metabolism: Cytochrome P-450 is involved in _____ phase (I or II) reactions.
|
I
|
|
Drug Development: A patent lasts for _____ years after filing for application.
|
20
|
|
Drug Development: How many phases are there in drug development?
|
4
|
|
Drug Development: Drugs are first tested in patients in phase _____ of clinical testing, pharmacokinetic safety is determined in phase ______ of clinical testing, double blind tests are done in phase ____ and post-market surveillance is done in phase _____.
|
2,1,3,4
|
|
Pharmacodynamics: In a dose response curve, a competitive antagonist shifts the curve _____, while a non-competitive antagonist shifts the curve ______.
|
right, down
|
|
Pharmacodynamics: AUTHOR
|
HiralShah
|
|
Pharmacodynamics (continued): What pharmacologic relationship would determine the existence of spare receptors?
|
EC50 < Kd
|
|
Pharmacodynamics (continued): What does it mean if EC50 and Kd are equal?
|
The system does not have spare receptors
|
|
Pharmacodynamics (continued): A partial agonist acts on the same receptor system as a full agonist? T/F
|
TRUE
|
|
Pharmacodynamics (continued): What's the main difference between a partial agonist and a full agonist?
|
A partial agonist has a lower maximal efficacy.
|
|
Pharmacodynamics (continued): Is a partial agonist less potent than a full agonist?
|
Not necessarily. It can be less, more or equally potent as a full agonist.
|
|
Antimicrobial Tx -- Mechanism of Action: The penicillin type drugs work by blocking ------ synthesis, specifically by inhibiting this molecule from cross-linking?
|
blocks bacterial cell wall synthesis by inhibition of peptidoglycan synthesis.
|
|
Antimicrobial Tx -- Mechanism of Action: Which other drugs (aside from penicillin) have this same mechanism of action?
|
Imipenem, aztreonam and cephalosporins
|
|
Antimicrobial Tx -- Mechanism of Action: Bacitracin, vancomycin and cycloserine block the synthesis of this molecule, preventing cell wall synthesis
|
peptidoglycans
|
|
Antimicrobial Tx -- Mechanism of Action: These drugs block the 50s ribosomal subunit
|
clindamycin, chloramphenicol, erythromycin, lincomycin, linezolid, streptogramins "Buy AT 30, CELL at 50"
|
|
Antimicrobial Tx -- Mechanism of Action: These drugs block the 30s ribosomal subunit
|
Aminoglycosides and tetracyclines "Buy AT 30, CELL at 50"
|
|
Antimicrobial Tx -- Mechanism of Action: These drugs block nucleotide synthesis by interfering with the folate pathway
|
Sulfonamides (e.g. Bactrim), trimethoprim
|
|
Antimicrobial Tx -- Mechanism of Action: These drugs block DNA topoisomerases
|
Quinolones (e.g. Cipro)
|
|
Antimicrobial Tx -- Mechanism of Action: Which drug blocks mRNA synthesis
|
rifampin
|
|
Antimicrobial Tx -- Mechanism of Action: Which are the bacteriacidal Abx
|
Penicillin, cephalosporin, vancomycin, aminoglycosides, fluoroquinolones, metronidazole
|
|
Antimicrobial Tx -- Mechanism of Action: These drugs disrupt the bacterial/fungal cell membranes
|
polymyxins
|
|
Antimicrobial Tx -- Mechanism of Action: These specific disrupt fungal cell membranes
|
amphotericin B, nystatin, fluconazole/azoles (FAN the fungal cell membranes)
|
|
Antimicrobial Tx -- Mechanism of Action: What is the mechanism of action of Pentamidine
|
Unknown
|
|
Penicillin: Which is the IV form and which is the oral form
|
G = IV, V=oral
|
|
Penicillin: Which of these is not a mechanism of penicillin action: (1) binds penicillin-binding protein, (2) blocks peptidoglycan synthesis, (3) blocks transpeptidase catalyzed cross-linking of cell wall and (4) activates autolytic enzymes
|
Penicillin does not block peptioglycan synthesis, bacitracin, vancomycin and cycloserine do that
|
|
Penicillin: T or F: penicillin is effective against gram pos and gram neg rods
|
False: penicillin is used to treat common streptococci (but not staph), meningococci, gram pos bacilli and spirochetes (i.e. syphilis, treponema). Not used to treat gram neg rods.
|
|
Penicillin: What should you watch out for when giving penicillin?
|
Hypersensitivity rxn (urticaria,severe pruritus) and hemolytic anemia
|
|
Methicillin, nafcillin, dicloxacillin: These drugs are used mainly for what type of infection
|
Staphlococcal infection (hence very narrow spectrum)
|
|
Methicillin, nafcillin, dicloxacillin: T or F: these drugs have the same mechanism of action as penicillin
|
TRUE
|
|
Methicillin, nafcillin, dicloxacillin: Are these drugs penicillinase resistant? If so why?
|
Bulkier R group makes these drugs resistant to penicillinase
|
|
Methicillin, nafcillin, dicloxacillin: What should you watch out for when giving these drugs?
|
Hypersensitivity rxn (urticaria,severe pruritus); methicillin can cuase interstitial nephritis
|
|
Ampicillin and amoxicillin: T or F: these drugs have the same mechanism of action as penicillin
|
TRUE
|
|
Ampicillin and amoxicillin: Which has greater oral bioavailability?
|
amOxicillin (O for Oral)
|
|
Ampicillin and amoxicillin: What do you use these for?
|
Ampicillin/amoxicillin HELPS to kill enterococci (H. influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella)
|
|
Ampicillin and amoxicillin: Can penicillinase effect these drugs efficacy?
|
Yes, they are penicillinase sensitive
|
|
Ampicillin and amoxicillin: Why not give these drugs with a penicillinase inhibitor. Name one.
|
clavulanic acid
|
|
Ampicillin and amoxicillin: What should you watch out for when giving these drugs?
|
Hypersensitivity rxn (ampicillin rash), pseudomembranous colitis
|
|
Carbenicillin, piperacillin, ticarcillin: Why are these considered to have an extended spectrum?
|
Because they are effective against pseudomonas and other gram neg rods (enterobacter and some species of klebsiella)
|
|
Carbenicillin, piperacillin, ticarcillin: What should you watch out for when giving these drugs?
|
Hypersensitivity rxn
|
|
Carbenicillin, piperacillin, ticarcillin: Why does concomitant administration with clavulanic acid increase the efficacy of these drugs?
|
Because they are penicillinase sensitive. (only piperacillin and ticarcillin)
|
|
Cephalosporins: What is the mechanism of action of Cephalosporins?
|
inhibit cell wall synthesis
|
|
Cephalosporins: How are they similar/different from penicillin?
|
both have a beta-lactam ring structure but cephalosporins are less susceptible to penicillinases
|
|
Cephalosporins: What are the main similarities/difference between 1st and 2nd generation cephalosporins?
|
2nd gen has extensive gram neg coverage but weaker gram pos coverage
|
|
Cephalosporins: 1st gen covers what bugs?
|
gram positives (staph and strep), Proteus mirabilis, E. coli, Klebsiella (PEcK)
|
|
Cephalosporins: 2nd gen covers what bugs?
|
gram positives (staph and strep) though less so, H. influenzae, Enterobacter aerogenes, Neisseria, Proteus mirabilis, E. coli, Klebsiella (HEN PEcK)
|
|
Cephalosporins: What can 3rd generation drugs do that 1st and 2nd generation can't?
|
Cross the blood brain barrier
|
|
Cephalosporins: What are some other benefits of 3rd gen?
|
better activity against gram neg bugs resistant to beta-lactam drugs. Ceftazidime for Pseudomonas and ceftriaxone for N. gonorrhea
|
|
Cephalosporins: What are the benefits of 4th gen (e.g. Cefipime)?
|
increased activity against Pseudomonas, gram pos organisms and more beta-lactamase resistant (i.e. 4th gen combines 1st gen and 3rd gen characteristics into super drug)
|
|
Cephalosporins: What drugs should you avoid taking with cephalosporins?
|
Aminoglycosides (increases nephrotoxicity) and ethanol (causes a disulfiram-like rxn -- headache, nausea, flushing, hypotension)
|
|
Aztreonam: When would you use aztreonam?
|
Only to treat Klebsiella, Pseudomonas and Serratia sp.
|
|
Aztreonam: Is it beta-lactamase resistant?
|
Yes, this is one of the huge benefits of the drug, and it is not cross-reactive with PCN!
|
|
Aztreonam: Which population of pt. is this drug good for?
|
The PCN-allergic patient that can't take aminoglycosides b/c of renal insufficiency
|
|
Aztreonam: Are there any toxicity issues with this drug?
|
Not really. Generally well tolerated with occasional GI upset. Vertigo, Headache and rare hepatotoxicity have been reported.
|
|
Imipenem/cilastatin: What is imipenem?
|
broad spectrum beta-lactamase-resistant abx
|
|
Imipenem/cilastatin: What do you always administer it with and why?
|
cilastatin -- it decreases inactivation of imipenem in renal tubules
|
|
Imipenem/cilastatin: What do you use it for?
|
Gram pos cocci, gram neg rods and anaerobes (broad spectrum)
|
|
Imipenem/cilastatin: What bug is it the drug of choice for?
|
Enterobacter
|
|
Imipenem/cilastatin: What are its side-effects
|
GI distress, skin rash, seizures at high conc.
|
|
Vancomycin: Is it bactericidal or bacteriastatic and why?
|
Bactericidal because it blocks cross linkage and elongation of peptidoglycan by binding D-ala D-ala protion of cell wall.
|
|
Vancomycin: How does resistance to Vanco occur?
|
D-ala D-ala is replaced with D-ala D-lactate which vanco does not block
|
|
Vancomycin: What is it used for?
|
Used for serious infection that is resistant to other drugs (e.g. gram pos multi-drug resistant organisms like S. aureus and C. difficile, methicillin resistant staph (MRSA))
|
|
Vancomycin: What are the important toxicities of vanco?
|
generally NOT many problems except, Nephrotoxicity, Ototoxicity and Thrombophlebitis
|
|
Vancomycin: What can happen with rapid infusion of vanco?
|
Red man's syndrome. Diffuse flushing which can be controlled by pretreatment with anti-histamines and with slow infusion rate
|
|
Protein Synthesis Inhibitors: Which drugs target bacterial protein synthesis by blocking the 30S unit vs 50S unit?
|
Buy AT 30, CELL at 50
|
|
Protein Synthesis Inhibitors: What does AT stand for?
|
A = Aminoglycosides (streptomycin, gentamicin, tobramycin an damikacin. And T = Tetracyclines
|
|
Protein Synthesis Inhibitors: What does CELL stand for?
|
C = Chloramphenicol, E= Erythromycin, L= Lincomycin and L= cLindamycin
|
|
Protein Synthesis Inhibitors: Which of the above are bactericidal?
|
Only the aminoglycosides are, the rest are bacteriostatic
|
|
Aminoglycosides: Name some aminoglycosides?
|
Gentamicin, neomycin, amikacin, tobramycin and streptomycin
|
|
Aminoglycosides: How do these drugs work?
|
They inhibit formation of the initiation complex in mRNA translation
|
|
Aminoglycosides: Why are they ineffective against anaerobes?
|
They require oxygen for uptake into bacteria
|
|
Aminoglycosides: When would you use aminoglycosides?
|
against severe gram-negative rod infections
|
|
Aminoglycosides: What drugs can you use aminoglycosides with for synergy?
|
the drugs that inhibit cell wall synthesis (e.g. penicillin and cephalosporins -- the beta-lactam antibiotics). Presumably this allows the drug to get in with out reliance on oxygen transport
|
|
Aminoglycosides: What drug in this class is commonly used for bowel surgery?
|
Neomycin
|
|
Aminoglycosides: What are the two major toxicities?
|
Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp. when used with loop diuretics). amiNOglycosides
|
|
Tetracyclines: Name some tetracylcines
|
Tetracycline, doxycycline, demeclocycline, minocycline
|
|
Tetracyclines: How does it work?
|
Blocks t-RNA attachment to 30S subunit
|
|
Tetracyclines: Which tetracycline can you use in patients with renal failure and why?
|
Can use doxycycline because its elimination is fecal
|
|
Tetracyclines: Should you take these drugs with a glass of milk?
|
NO, because it intereferes with absorption in the gut as does antacids and iron-containing preparations
|
|
Tetracyclines: What are tetracyclines used for?
|
VACUUM your Bed Room -- Vibrio cholerae, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi, Rickettsia, tularemia
|
|
Tetracyclines: What are the common toxicities
|
GI distress, teeth discoloration, inhibition of bone growth in children, Fanconi's syndrome and photosensitivity
|
|
Macrolides: Name some macrolides?
|
Erythromycin, azithromycin, clarithromycin
|
|
Macrolides: How do these drugs work?
|
inhibit protein synthesis
|
|
Macrolides: What are they used for?
|
URIs, pneumonias, STDs -- gram pos cocci in patients that are allergic to PNC --- Mycoplasm, Legionella, Chlamydia, Neisseria.
|
|
Macrolides: Pneumonic for macrolide use?
|
Eryc's Niple is at his Mid Clavicular Line (Eryc is brand name for erythromycin). Mycoplasm, Legionella, Chlamydia, Neisseria.
|
|
Macrolides: What are the major toxicities?
|
GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes
|
|
Macrolides: What is the most common cause for non-compliance to macrolides?
|
GI discomfort
|
|
Chloramphenicol: How does this drug work?
|
inhibits 50S peptidyltransferase
|
|
Chloramphenicol: Main use?
|
Meningitis (H. influenzae, N. meningitides, S. pneumo). Used conservatively b/c of toxicity
|
|
Chloramphenicol: What are the main toxicities?
|
Anemia and aplastic anemia (both dose dependent), gray baby syndrome (in premes b/c they lack UDP-glucoronyl transferase)
|
|
Clindamycin: How does it work?
|
blocks peptide bond formation at 50S
|
|
Clindamycin: When do you use it?
|
Anaerobic infections (e.g. Bacteroides fragilis and C.perfringens)
|
|
Clindamycin: Toxicities?
|
Pseudomembranous colitis, fever, diarrhea
|
|
Sulfonamides: Name some sulfonamides
|
Sulfamethoxazole (SMX), sulfisoxazole, triple sulfa and sulfadiazine
|
|
Sulfonamides: How does it work?
|
Inhibits bacterial folic acid synthesis from PABA by blocking dihydropteroate synthase.
|
|
Sulfonamides: What are its uses?
|
Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas and SMX for simple UTIs
|
|
Sulfonamides: Toxicities?
|
hypersensitivity rxn, hemolysis if G6PD deficient, nephorotoxicity (tubulointerstitial nephritis), kernicterus in infants, displace other drugs from albumin (e.g. warfarin)
|
|
Trimethoprim: How does it work?
|
inhibits folic acid pathway by blocking dihydrofolate reductase which humans have as well
|
|
Trimethoprim: What are its uses?
|
used in combo with Sulfamethoxazole (TMP-SMX) causing a sequential block of folate synthesis. Used for recurrent UTIs, Shigella, Salmonella, and prophylaxis for PCP in AIDS patients
|
|
Trimethoprim: Toxicities?
|
Megaloblastic anemia, pancytopenia (may be alleviated with suplemental folinic acid)
|
|
Fluoroquinolones: What the most famous floroquinolone?
|
Ciprfloxacin (treatment for Anthrax)
|
|
Fluoroquinolones: How does it work?
|
inhibits DNA gyrase (topoisomerase II)
|
|
Fluoroquinolones: What are its uses?
|
Gram neg rods or urinary and GI tract (incl. pseudomonas), Neisseria, some gram pos sp
|
|
Fluoroquinolones: What population is contraindicated for use?
|
pregnancy and children
|
|
Fluoroquinolones: What are its toxicities?
|
GI upset, superinfection, skin rashes, headache, dizziness and tendonitis and tendon rupture in adults. FluoroquinoLONES hurt attachment to BONES.
|
|
Metronidazole: How does it work?
|
forms toxic metabolites in the bacteria. Bactericidal.
|
|
Metronidazole: What are its uses?
|
anti-protozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, anaerobes (bacteroides, clostridium)
|
|
Metronidazole: What is the role of Metronidazole in H. pylori infection?
|
Used as part of triple therapy: bismuth, amoxicillin and metronidazole
|
|
Metronidazole: Main toxicity?
|
disulfiram-like (antabuse) reaction to alcohol and headache
|
|
Metronidazole: Which drug do you use to treat anaerobic infections above the diaphram and below the diaphram
|
anaerobes above diaphram: Clindamycin, and anaerobes below diaphram: metronidazole
|
|
Polymyxins: How does it work?
|
disrupts osmotic properties of bacteria, acts like a detergent
|
|
Polymyxins: What is it used for?
|
resistant gram negative infections
|
|
Polymyxins: Toxicities?
|
neurotoxicity, ATN
|
|
Isoniazid: How does it work?
|
decreases synthesis of mycolic acid
|
|
Isoniazid: What is it used for?
|
MTB (mycobacterium tuberculosis). The only agent used as solo prophylaxis against TB
|
|
Isoniazid: Toxicities?
|
Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicitiy, drug induced SLE. INH, Injures Neurons and Hepatocytes
|
|
Isoniazid: What vitamin prevents neurotoxicity
|
Vitamin B6 (pyridoxine)
|
|
Isoniazid: Why are toxicities particularly important to monitor in patients taking INH?
|
INH half-lives are different in fast versus slow acetylators!
|
|
Rifampin: How does it work?
|
inhibits DNA-dependent RNA polymerase
|
|
Rifampin: What is it used for?
|
MTB, meningococcal prophylaxis
|
|
Rifampin: Toxicities?
|
Minor hepatotoxicity and increases P-450
|
|
Rifampin: How can it be used for leprosy?
|
rifampin delays resistance to dapsone when used for leprosy
|
|
Rifampin: What would happen if you used rifampin alone?
|
get rapid resistance
|
|
Rifampin: What does it do to bodily fluids?
|
makes them red/orange in color
|
|
Rifampin: What are the 4 R's of Rifampin
|
RNA polymerase inhibitor, Revs up microsomal p-450, Red/Orange body fluids, Resistance is rapid
|
|
Anti-TB Drugs: What are the anti-TB drugs?
|
Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH) -- RESPIre
|
|
Anti-TB Drugs: What do you use for TB prophylaxis?
|
INH
|
|
Anti-TB Drugs: What toxicity is common to all?
|
hepatotoxicity
|
|
Anti-TB Drugs: AUTHOR
|
Michael Shino
|
|
Resistance mechanisms for various antibiotics: Most common resistance mechanism for penicillins / cephalosporins.
|
Beta-lactamase cleavage of beta-lactam ring.
|
|
Resistance mechanisms for various antibiotics: Most common resistance mechanism for aminoglycosides.
|
Modification via acetylation, adenylation, or phosphorylation.
|
|
Resistance mechanisms for various antibiotics: Most common resistance mechanism for vancomycin.
|
Terminal D-ala of cell wall component replaced with D-lac; decrease affinity.
|
|
Resistance mechanisms for various antibiotics: Most common resistance mechanism for Chlorampenicol.
|
Modification via acetylation.
|
|
Resistance mechanisms for various antibiotics: Most common resistance mechanism for macrolides.
|
Methylation of rRNA near erythromycin's ribosome-binding site.
|
|
Resistance mechanisms for various antibiotics: Most common resistance mechanism for tetracycline.
|
Decrease uptake or increase transport out of cell.
|
|
Resistance mechanisms for various antibiotics: Most common resistance mechanism for sulfonamides.
|
Altered enzyme (bacterial dihydropteroate synthetase), decrease uptake, or increase PABA synthesis.
|
|
Nonsurgical antimicrobial prophylaxis: Drug of choice for meningococcal infection.
|
Rifampin (drug of choice), minocycline.
|
|
Nonsurgical antimicrobial prophylaxis: Drug of choice for gonorrhea.
|
Cefriaxone.
|
|
Nonsurgical antimicrobial prophylaxis: Drug of choice for syphilis.
|
Benzathine penicillin G.
|
|
Nonsurgical antimicrobial prophylaxis: Drug of choice for history of recurrent UTIs.
|
TMP-SMX.
|
|
Nonsurgical antimicrobial prophylaxis: Drug of choice for Pneumocystis carinii pneumonia.
|
TMP-SMX (drug of choice), aerosolized pentamindine.
|
|
Anti-fungal therapy: Mechanism of action of the anti-fungal therapy polyenes.
|
Form artificial pores in the cytoplasmic membrane.
|
|
Anti-fungal therapy: Mechanism of action of the anti-fungal therapies terbinafine and azoles.
|
Terbinafine blocks the conversion of squalene to lanosterol. Azoles block the conversion of lanosterol to ergosterol.
|
|
Anti-fungal therapy: Mechanism of action of the anti-fungal therapy flucytosine.
|
Blocks the production of purines from the precurors.
|
|
Anti-fungal therapy: Mechanism of action of the anti-fungal therapy griseofulvin.
|
Disrupts microtubles.
|
|
Amphotericin B: Mechanism of action of Amphotericin B.
|
Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes and disrupt homeostasis. "Amphotericin 'tears' holes in the fungal membrane by forming pores."
|
|
Amphotericin B: Clinical uses of Amphotericin B.
|
Used for a wide spectrum of sytemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier.
|
|
Amphotericin B: Symptoms of Amphotericin B toxicity.
|
Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias ("amphoterrible").
|
|
Nystatin: Mechanism of action of Nystatin.
|
Binds to ergosterol, disrupting fungal membranes.
|
|
Nystatin: Clinical use of Nystatin.
|
Swish and swallow for oral candidiasis (thrush).
|
|
Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Mechanism of action for fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
|
Inhibits fungal steroid (ergosterol) synthesis.
|
|
Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Clinical uses of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
|
Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, coccidioides, Histoplasma, Candida albicans; hypercortisolism.
|
|
Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Symptoms of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole toxicity.
|
Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills.
|
|
Flucytosine: Mechanism of action of Flucytosine.
|
Inhibits DNA synthesis byconversion to fluorouracil, which competes with uracil.
|
|
Flucytosine: Clinical uses of Flucytosine.
|
Used in sytemic fungal infections (e.g. Candida, Cryptococcus).
|
|
Flucytosine: Symptoms of Flucytosine toxicity.
|
Nausea, vomitting, diarrhea, bone marrow supression.
|
|
Caspofungin: Mechanism of action for Caspofungin.
|
Inhibits cell wall synthesis.
|
|
Caspofungin: Clinical use of Caspofungin.
|
Invasive aepergillosis.
|
|
Caspofungin: Symptoms of Caspofungin toxicity.
|
GI upset, flushing.
|
|
Terbinafine: Mechanism of action of Terbinafine.
|
Inhibits the fungal enzyme squalene epoxidase.
|
|
Terbinafine: Clinical use of Terbinafinel.
|
Used to treat dermatophytoses (especially onychomycosis).
|
|
Griseofulvin: Mechanism of action of Griseofulvin.
|
Interfers with microtubule function; disrupts mitosis. Deposits in keratin-contianing tissues (e.g. nails).
|
|
Griseofulvin: Clinical use of Griseofulvin.
|
Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).
|
|
Griseofulvin: Symptoms of Griseofulvin toxicity.
|
Teratogenic, carcinogenic, confusion, headaches, increase warfarin metabolism.
|
|
Antiviral chemotherapy: Viral adsorption and penetration into the cell is blocked by ---------.
|
Gama-globulins (non-specific).
|
|
Antiviral chemotherapy: Uncoating of the virus after its penetration into the cell is blocked by --------.
|
Amantadine (influenza A).
|
|
Antiviral chemotherapy: Early viral protein synthesis is blocked by --------.
|
Fomivirsen (CMV).
|
|
Antiviral chemotherapy: Viral nuclei acid synthesis is blocked by --------.
|
Purine, pyrimidine analogs; reverse transcriptase inhibitors.
|
|
Antiviral chemotherapy: Late viral protein synthesis and processing is blocked by --------.
|
Methimazole (variola); protease inhibitors.
|
|
Antiviral chemotherapy: Packaging and assembly of new viron is blocked by --------.
|
Rifampin (vaccinia).
|
|
Amantadine: Mechanism of action of Amantadine.
|
Blocks viral penetration/uncoating; may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals. "Amantadine blocks influenza A and rubellA and causes problems with the cerebellA."
|
|
Amantadine: Clinical uses of Amantadine.
|
Prophylaxis for influenza A; Parkinson's disease.
|
|
Amantadine: Symptoms of Amantadine toxicity.
|
Ataxia, dizziness, slurred speech. (Rimantidine is a derivative with fewer CNS side effects.)
|
|
Zanamivir: Mechanism of action of Zanamivir.
|
Inhibits influenza neuraminidase.
|
|
Zanamivir: Clinical use of Zanamivir.
|
Both influenza A and B.
|
|
Ribavirin: Mechanism of action of Ribavirin.
|
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
|
|
Ribavirin: Clinical use of Ribavirin.
|
RSV (respiratory syncytial virus).
|
|
Ribavirin: Symptoms of Ribavirin toxicity.
|
Hemolytic anemia. Severe teratogen.
|
|
Acyclovir: Mechanism of aciton of Acyclovir.
|
Perferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.
|
|
Acyclovir: Clinical use of Acyclovir.
|
HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in immunocompromised patients.
|
|
Acyclovir: Symptoms of Acyclovir toxicity.
|
Delirium, tremor, nephrotoxicity.
|
|
Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Mechanism of action of Ganciclovir.
|
Phosphorlation by viral kinase; perferentially inhibits CMV DNA polymerase.
|
|
Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Clinical use of Ganciclovir.
|
CMV, especially in immunocompromised patients.
|
|
Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Symptoms of Ganciclovir toxicity.
|
Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.
|
|
Foscarnet: Mechanism of action of Foscarnet.
|
Viral DNA polymerase inhibitor that binds to the pyrophophate binding site of the enzyme. Does not require activation by viral kinase. "FOScarnet = pyroFOSphate analog."
|
|
Foscarnet: Clinical use of Foscarnet.
|
CMV retinitis in immunocompromised patients when ganciclovir fails.
|
|
Foscarnet: Symptoms of Foscarnet toxicity.
|
Nephrotoxicity.
|
|
HIV therapy: Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are example of this type of anti-HIV drug.
|
Protease inhibitor.
|
|
HIV therapy: Mechanism of action of protease inhibitors.
|
Inhibit assembly of new virus by blocking protease enzyme.
|
|
HIV therapy: Symptoms of protease inhibitor toxicity.
|
GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities, thrombocytopenia (indinavir).
|
|
HIV therapy: Reverse transcriptase inhibitors:
|
0
|
|
HIV therapy: Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC), stavudine (d4T), lamivudine (3TC), and abacavir are examples of --------- reverse transcriptase inhibitors.
|
Nucleoside.
|
|
HIV therapy: Nevirapine, delavirdine, and efavirenz are examples of --------- reverse transcriptase inhibitors.
|
Non-nucleoside.
|
|
HIV therapy: Mechanism of action of reverse transcriptase inhibitors.
|
Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of viral genome into host DNA.
|
|
HIV therapy: Symptoms of reverse transcriptase inhibitor toxicity.
|
Bone marrow supression (neutropenia, anemia), periphral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).
|
|
HIV therapy: Highly active antiretroviral therapy (HAART) generally entails combination therapy with ---------- and -----------.
|
Protease inhibitors, reverse transcriptase inhibitors.
|
|
HIV therapy: When should HIV therapy be initiated?
|
When patients have low CD4 counts (<500 cells/mm3) or high viral load.
|
|
HIV therapy: -------- is used during pregnancy to reduce risk of fetal transmission.
|
AZT.
|
|
Interferons: Mechanism of action of Interferons.
|
Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis.
|
|
Interferons: Clinical use of Interferons.
|
Chronic hepatitis B and C, Kaposi's sarcoma.
|
|
Interferons: Symptoms of Interferon toxicity.
|
Neutropenia.
|
|
Antiparasitic drugs: Clinical uses of Ivermectin.
|
Onchocerciasis "rIVER blindness treated with IVERmectin".
|
|
Antiparasitic drugs: Clinical uses of Mebendazole / thiabendazole.
|
Nematode/roundworm (e.g., pinworm, whipworm) infections.
|
|
Antiparasitic drugs: Clinical uses of Pyrantel pamoate.
|
Giant roundworm (Ascaris), hookworm (Necator/Ancylostoma), pinworm (Enterobius).
|
|
Antiparasitic drugs: Clinical uses of Praziquantel.
|
Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis) and cysticercosis.
|
|
Antiparasitic drugs: Clinical uss of Niclosamide
|
Cestode/tapeworm (e.g., Diphyllobothrium latum, Taenia species) infections except cysticercosis.
|
|
Antiparasitic drugs: Clinical uses of Pentavalent antimony.
|
Leishmaniasis.
|
|
Antiparasitic drugs: Clinical uses of Chloroquine, quinine, mefloquine, atovaquone, proguanil.
|
Malaria.
|
|
Antiparasitic drugs: Clinical uses of Primaquine.
|
Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P.ovale).
|
|
Antiparasitic drugs: Clinical uses of Metronidazole.
|
Giardiasis, amebic dysentery (Entamoeba histolytica), bacterial vaginitis (Gardnerella vaginalis), Trichomonas.
|
|
Antiparasitic drugs: Clinical uses of Pentamidine.
|
Pneumocystis carinii pneumonia prophylaxis.
|
|
Antiparasitic drugs: Clinical uses of Nifurtimox.
|
Chagas' disease, American trypanosomiasis (Trypanosoma cruzi).
|
|
Antiparasitic drugs: Clinical uses of Suramin.
|
African trypanosomiasis (sleeping sickness).
|
|
Pharmacology - CNS / Neurologic drugs: Parasympathetic preganglionic neurons release the neurotransmitter -------- which act on -------- receptors.
|
Ach, nicotinic.
|
|
Pharmacology - CNS / Neurologic drugs: Parasympathetic postganglionic neurons release the neurotransmitter -------- which act on ------- receptors.
|
Ach, muscarinic.
|
|
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.
|
Ach, nicotinic.
|
|
Pharmacology - CNS / Neurologic drugs: Sympathetic postganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.
|
Ach, muscarinic.
|
|
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to glands, cardiac and smooth muscles release the neurotransmitter ------- which act on ------- receptors.
|
Ach, nicotinic.
|
|
Pharmacology - CNS / Neurologic drugs: Sympathetic postganglionic neurons to glands, cardiac and smooth muscles release the neurotransmitter ------- which act on ------- receptors.
|
NE, alpha and beta
|
|
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to renal vascular smooth muscle release the neurotransmitter ------- which act on ------- receptors.
|
Ach, nicotinic.
|
|
Pharmacology - CNS / Neurologic drugs: Sympathetic postganglionic neurons to renal vascular smooth muscle release the neurotransmitter ------- which act on ------- receptors.
|
Dopamine, D1
|
|
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to the adrenal medulla release the neurotransmitter ------- which act on ------- receptors.
|
Ach, nicotinic.
|
|
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to the adrenal medulla synapse directly on ------- cells of the adrenal medulla.
|
Chromaffin.
|
|
Pharmacology - CNS / Neurologic drugs: Somatic neurons synapse directly on -------- muscle and release the neurotransmitter ------- which act on ------- receptors.
|
skeletal muscle, Ach, nicotinic.
|
|
Autonomic drugs: Cholinergic:
|
0
|
|
Autonomic drugs: Ach is synthesized from acetyl-CoA and choline by the enzyme ---------.
|
Choline acetyltransferase.
|
|
Autonomic drugs: The transport of choline into the nerve terminal can be inhibited by --------.
|
Hemicholinium.
|
|
Autonomic drugs: The release of transmitter from vesicles in the nerve ending require the entry of ------ into the neuron.
|
Calcium.
|
|
Autonomic drugs: --------- inhibits the release of the stored Ach.
|
Botulinum toxin.
|
|
Autonomic drugs: The action of Ach in the synapse is terminated by its metabolism to acetate and choline by the enzyme ---------.
|
Acetylcholinesterase.
|
|
Noradrenergic:: In the noradrenergic nerve terminal, tyrosine is hydroxylated to -------, which is decarboxylated to --------, which is finally hydroxylated to NE.
|
DOPA, dopamine.
|
|
Noradrenergic:: Dopamine is transported into vesicles for hydroxylation to NE. This transport can be blocked by the drug --------.
|
Reserpine.
|
|
Noradrenergic:: The action of NE and DA is terminated by --------- and ----------.
|
Reuptake, diffusion (different than for Ach).
|
|
Noradrenergic:: --------- inhibits the release of the stored NE.
|
Guanethidine.
|
|
Noradrenergic:: The --------- drugs promote catecholamine release.
|
Amphetamine.
|
|
Noradrenergic:: The drugs --------- and ---------- inhibit the reuptake of NE.
|
Cocaine, TCA.
|
|
Noradrenergic:: The release of NE from a sympathetic nerve ending is modulated by ---------, --------- and ---------.
|
NE, Ach, angiotensin II.
|
|
Noradrenergic:: NE inhibits its own release at the noradrenergic nerve terminal through --------- receptors.
|
Alpha 2.
|
|
Noradrenergic:: Angiotensin II --------- (inhibits / stimulates) the release of NE from the noradrenergic nerve terminal.
|
Stimulates.
|
|
Noradrenergic:: Ach inhibits the release of NE from the noradrenergic nerve terminal by binding to --------- receptors.
|
M1.
|
|
Direct agonists:: Clinical application and action of Bethanechol.
|
Postoperative and neurogenic ileus and urinary retention. / Activates bowel and bladder smooth muscle.
|
|
Direct agonists:: Clinical application and action of Carbachol and Pilocarpine.
|
Glaucoma. / Activates ciliary muscle of eye (open angle), pupillary sphincter (narrow angle).
|
|
Indirect agonists (anticholinesterases):: Clinical application / action of Neostigmine.
|
Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative). / Increase endogenous Ach.
|
|
Indirect agonists (anticholinesterases):: Clinical application / action of Pyridostigmine.
|
Myasthenia gravis. / Increase Ach; increase strength.
|
|
Indirect agonists (anticholinesterases):: Clinical application / action of Edrophonium.
|
Diagnosis of myasthenia gravis (extremely short acting). / Increase endogenous Ach.
|
|
Indirect agonists (anticholinesterases):: Clinical application / action of Physostigmine.
|
Glaucoma (crosses blood-brain barrier) and atropine overdose. / Increase endogenous Ach.
|
|
Indirect agonists (anticholinesterases):: Clinical application / action of Echothiophate.
|
Glaucoma. / Increase endogenous Ach.
|
|
Indirect agonists (anticholinesterases):: Symptoms of cholinesterase inhibitor poisoning.
|
Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, Salivation (also abdominal cramping). "DUMBBELSS".
|
|
Indirect agonists (anticholinesterases):: Cholinesterase inhibitor poisoning may be caused by ---------.
|
Parathion and other organophosphates.
|
|
Indirect agonists (anticholinesterases):: The cholinesterase regenerator ------- can be used as an antidote for cholinesterase inhibitor poisoning.
|
Pralidoxime.
|
|
Indirect agonists (anticholinesterases):: Mechanism of action of Pralidoxime.
|
Regenerates active cholinesterase, chemical antagonist, used to treat organophosphate exposure.
|
|
Cholinoreceptor blockers:: Clinical uses of the muscarinic antagonist Atropine.
|
Dilate pupils, decrease acid secretion in peptic ulcer disease, decrease urgency in mild cystitis, decrease GI motility, reduce airway secretions, and treat organophosphate poisoning. "Blocks SLUD: Salivation, Lacrimation, Urination, Defecation."
|
|
Cholinoreceptor blockers:: Side effects of Atropine.
|
Increase body temp, rapid pulse, dry mouth, dry/flushed skin, disorientation, mydriasis with cycloplegia, and constipation. "Atropine parasympathetic block side effects: Blind as bat, Red as a beet, Mad as a hatter, Hot as a hare, Dry as a bone."
|
|
Cholinoreceptor blockers:: Hexamethonium (ganglionic blocker) blocks -------- receptors.
|
Nicotinic.
|
|
Cholinoreceptor blockers:: AUTHOR
|
Tzivia Moreen
|
|
antimuscarinic drugs: "tropi" are anti-muscarinic
|
while vacationing in the tropics you lie on a beach and your muscles waste away!
|
|
antimuscarinic drugs: benztropine is used to treat
|
Parkinson's disease
|
|
antimuscarinic drugs: scopolamine is used to treat
|
motion sickness
|
|
antimuscarinic drugs: scopolamine is an antimuscarinic that does not convert to the mnemonic!
|
0
|
|
antimuscarinic drugs: name 2 antimuscarinic drugs that act on the CNS
|
benztropine, scopolamine
|
|
antimuscarinic drugs: name a muscarinic used to treat motion sickness
|
scopolamine
|
|
antimuscarinic drugs: name a muscarinic used to treat Parkinson's disease
|
benztropine
|
|
antimuscarinic drugs: mechanism of action of benztropine
|
antimuscarinic
|
|
antimuscarinic drugs: mechanism of action of scopolamine
|
antimuscarinic
|
|
antimuscarinic drugs: name three antimuscarinics that act on eye
|
atropine, homatropine, tropicamide
|
|
antimuscarinic drugs: the action of atropine is ______
|
produce mydriasis, cycloplegia
|
|
antimuscarinic drugs: mechanism of atropine is
|
antimuscarinic
|
|
antimuscarinic drugs: the action of homatropine is ______
|
produce mydriasis, cycloplegia
|
|
antimuscarinic drugs: mechanism of homatropine is
|
antimuscarinic
|
|
antimuscarinic drugs: the action of tropicamide is
|
produce mydriasis, cycloplegia
|
|
antimuscarinic drugs: mechanism of tropicamide is
|
antimuscarinic
|
|
antimuscarinic drugs: ipatropium is used to treat
|
asthma, COPD
|
|
antimuscarinic drugs: mechanism of ipatropium is
|
antimuscarinic
|
|
antimuscarinic drugs: name an antimuscarinic used to treat asthma and COPD
|
ipatropium
|
|
neuromuscular blocking drugs: neuromuscular blocking drugs are used for
|
muscle paralysis in surgery or mechanical ventilation
|
|
neuromuscular blocking drugs: name a depolarising neurmuscular blocking drug
|
succinylcholine
|
|
neuromuscular blocking drugs: name 6 nondepolarizing neuromuscular blocking drugs
|
tubocurarine
|
|
neuromuscular blocking drugs: *mnemonic -- the "cur" drugs are nondepolarizing neuromuscular blocking agents
|
atracurium
|
|
neuromuscular blocking drugs: is succinylcholine depolarizing or nondepolarizing?
|
depolarizing
|
|
neuromuscular blocking drugs: is tubocurarine depolarizing or nondepolarizing?
|
nondepolarizing
|
|
neuromuscular blocking drugs: is atracurium depolarizing or nondepolarizing?
|
nondepolarizing
|
|
neuromuscular blocking drugs: is mivacurium depolarizing or nondepolarizing?
|
nondepolarizing
|
|
neuromuscular blocking drugs: is pancuronium depolarizing or nondepolarizing?
|
nondepolarizing
|
|
neuromuscular blocking drugs: is vacuronium depolarizing or nondepolarizing?
|
nondepolarizing
|
|
neuromuscular blocking drugs: is rapacuronium depolarizing or nondepolarizing?
|
nondepolarizing
|
|
neuromuscular blocking drugs: what is tubocurarine used for
|
nondepolarizing neuromuscular blockade
|
|
neuromuscular blocking drugs: what agents are used to reverse neuromuscular blockade by succinylcholine?
|
cholinesterase inhibitors in phase II (ex -- neostigmine)
|
|
neuromuscular blocking drugs: what phase of succinylcholine neuomuscular bloackade is reversible?
|
phase II (repolarized but blocked)
|
|
neuromuscular blocking drugs: what agents are used to reverse pahse I neuromuscular blockade by succinylcholine?
|
phase I Succinylcholine neuromuscular blockade cannot be reversed
|
|
neuromuscular blocking drugs: what phase of succinylcholine neuomuscular bloackade is irreversible?
|
phase I Succinylcholine neuromuscular blockade cannot be reversed
|
|
neuromuscular blocking drugs: what is atracurium used for
|
nondepolarizing neuromuscular blockade
|
|
neuromuscular blocking drugs: what is the effect of cholinesterase inhibitors on succinylcholine neuromuscular blockade?
|
phase I: cholinesterase inhibitors potentiates the blockade phase II: cholinesterase inhibitors reverse the blockade
|
|
neuromuscular blocking drugs: what cholinesterase inhibitor is used to reverse phase II of succinylcholine neuromuscular blockade?
|
neostigmine
|
|
neuromuscular blocking drugs: what is mivacurium used for
|
nondepolarizing neuromuscular blockade
|
|
Dantrolene: what is dantrolene used for
|
treat malignant hyperthermia
|
|
Dantrolene: what causes malignant hyperthermia
|
use inhalation anesthetics and succinylcholine together
|
|
Dantrolene: what inhalation anesthetic DOES NOT cause malignanat hyperthermia?
|
N2O
|
|
Dantrolene: what is dantrolene used for
|
neuroleptic malignant syndrome
|
|
Dantrolene: what is neuroleptic malignant syndrome
|
a toxicity of antipsychotic drugs
|
|
Dantrolene: what drug is used to treat malignant hyperthermia
|
dantrolene
|
|
Dantrolene: what is the mechanism of dantrolene
|
prevents release of Ca++ from saarcoplasmic reticulum of skeletal muscle
|
|
Sympathomimetics: epinephrine, NE, isoproterenol, dopamine, and dobutamine are all________________
|
catecholamines
|
|
Sympathomimetics: catecholamines are_____________________
|
sympathomimetics
|
|
Sympathomimetics: name 5 catecholamines
|
EPI, NE, Isoproterenol, dopamine, dobutamine
|
|
Sympathomimetics: what receptors does epinephrine act on?
|
alpha-1, alpha-2, beta-1, beta-2 adrenergics
|
|
Sympathomimetics: what receptors does NE work on?
|
alpha-1, alpha-2, beta-1 adrenergics
|
|
Sympathomimetics: what receptors does isoproterenol work on?
|
beta-1 = beta-2 adrenergics
|
|
Sympathomimetics: what receptors does dopamine work on?
|
D1 = D2, D1 and D2 more than beta, beta more than alpha
|
|
Sympathomimetics: what receptors does dobutamine work on?
|
beta-1 > beta-2
|
|
Sympathomimetics: which catecholamines are agonists to alpha-adrenergic receptors
|
EPI, NE > dopamine
|
|
Sympathomimetics: which catecholamines are agonists to beta-1 adrenergic receptors
|
EPI, NE, Isoproterenol, dopamine, dobutamine
|
|
Sympathomimetics: which catecholamines are agonists to beta-2 adrenergic receptors
|
EPI, isoproterenol, dopamine and dobutamine (less)
|
|
Sympathomimetics: what is epinephrine used to treat?
|
anaphylaxis, open-angle glaucoma, asthma, hypotension
|
|
Sympathomimetics: what is norepinephrine used to treat?
|
hypotension (but decreases renal perfusion)
|
|
Sympathomimetics: what is isoproterenol used to treat?
|
AV block
|
|
Sympathomimetics: what is dopamine used to treat
|
shock with renal failure, heart failure
|
|
Sympathomimetics: what is dobutamine used to treat
|
shock, heart failure
|
|
Sympathomimetics: what catecholamine is used to treat anaphylaxis
|
epinephrine ("EPI-pen")
|
|
Sympathomimetics: what catecholamines are used to treat hypotension
|
EPI, NE
|
|
Sympathomimetics: what catecholamine is used to treat asthma
|
epinephrine
|
|
Sympathomimetics: what catecholamine is used to treat AV block
|
isoproterenol
|
|
Sympathomimetics: what catecholamines are used to treat shock
|
doapmine, dobutamine
|
|
Sympathomimetics: what is the action of amphetamine
|
indirect general adrenergic agonist, releases stored catecholamines
|
|
Sympathomimetics: what is the action of ephedrine
|
indirect general adrenergic agonist, releases stored catecholamines
|
|
Sympathomimetics: what is amphetamine used to treat
|
narcolepsy, obesity, attention deficit disorder
|
|
Sympathomimetics: what is ephedrine used to treat
|
nasal decongestion, urinary incontinence, hypotension
|
|
Sympathomimetics: name three sympathomimetic drugs used to treat hypotension
|
epinephrine, norepinephrin, ephedrine
|
|
Sympathomimetics: what is the action of phenylephrine
|
adrenergic agonist, alpha-1 > alpha-2
|
|
Sympathomimetics: what is the action of albuterol
|
adrenergic agonist, beta-2 >beta-1
|
|
Sympathomimetics: what is the action of terbutaline
|
adrenergic agonist, beta-2 >beta-2
|
|
Sympathomimetics: what is phenylephrine used for?
|
pupil dilator, vasoconstriction, nasal decongestion
|
|
Sympathomimetics: what sympathomimetics are used to treat nasal congestion
|
ephedrine, phenylephrine
|
|
Sympathomimetics: what is the mechanism of cocaine
|
indirect general adrenergic agonist, catecholamine uptake inhibitor
|
|
Sympathomimetics: what is the action of cocaine
|
vasoconstriction, local anesthesia
|
|
Sympathomimetics: what is the mechanism of clonidine
|
centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow
|
|
Sympathomimetics: what drug has the same mechanism as amphetamine
|
ephedrine
|
|
Sympathomimetics: what is the mechanism of alpha-methyldopa
|
centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow
|
|
Sympathomimetics: what drug has the same mechanism as clonidine
|
alpha-methyldopa
|
|
Sympathomimetics: what are clonidine and alpha-methyldopa used to treat
|
hypertension, especially in renal disease because they do not decreased blood flow to the kidney
|
|
Sympathomimetics: what sympathomimetic is used to treat urinary incontinence
|
ephedrine
|
|
Sympathomimetics: what sympathomimetic is used to treat attention deficit disorder
|
amphetamine
|
|
Sympathomimetics: what sympathomimetic is used to treat narcolepsy
|
amphetamine
|
|
alpha-blockers: name a nonselective irreversible alpha blocker
|
phenoxybenzamine
|
|
alpha-blockers: name a nonselective reversible alpha blocker
|
phentolamine
|
|
alpha-blockers: what is the mechanism of phenoxybenzamine
|
nonselective irreversible alpha blocker
|
|
alpha-blockers: what is the mechanism of phentolamine
|
nonselective reversible alpha blocker
|
|
alpha-blockers: what are phenoxybenzamine and phentolamine used for
|
pheochromocytoma
|
|
alpha-blockers: what are the side effects of nonselective alpha blockers
|
orthostatic hypotension, reflex tachycardia
|
|
alpha-blockers: name 3 alpha-1 selective adrenergic blockers
|
prazosin, terazosin, doxazosin
|
|
alpha-blockers: what is the mechanism of prazosin
|
alpha-1 selective adrenergic blocker
|
|
alpha-blockers: what is the mechanism of terazosin
|
alpha-1 selective adrenergic blocker
|
|
alpha-blockers: what is the mechanism of doxazosin
|
alpha-1 selective adrenergic blocker
|
|
alpha-blockers: what are alpha-1 selective adrenergic alpha blockers used for
|
hypertension, urinary retention in BPH
|
|
alpha-blockers: what are the side effects of alpha-1 blockers
|
orthostatic hypotension, dizziness, headache
|
|
alpha-blockers: what is prazosin used for?
|
hypertension, urinary retention in BPH
|
|
alpha-blockers: what drugs have the same action as prazosin
|
terazosin, doxazosin
|
|
alpha-blockers: what are the side effects of terazosin?
|
orthostatic hypotension, dizziness, headache
|
|
alpha-blockers: what selective alpha blockers cause orthostatic hypotension
|
phenoxybenzamine, phentolamine, terazosin, prazosin, doxazosin
|
|
alpha-blockers: name an alpha-2 selective adrenergic blocker
|
yohimbine
|
|
alpha-blockers: what is yohimbine used for
|
impotence (effectiveness controversial)
|
|
alpha-blockers: what alpha blockers are used to treat pheochromocytoma
|
phenoxybenzamine, phentolamine
|
|
beta-blockers ("lol"s): name some beta-blockers
|
propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol, labetalol
|
|
beta-blockers ("lol"s): what is the mechanism of propanolol
|
selective beta-adrenergic blocker
|
|
beta-blockers ("lol"s): what is the mechanism of metoprolol
|
selective beta-adrenergic blocker
|
|
beta-blockers ("lol"s): what is the mechanism of esmolol
|
selective beta-adrenergic blocker
|
|
beta-blockers ("lol"s): what is the mechanism of pindolol
|
selective beta-adrenergic blocker
|
|
beta-blockers ("lol"s): what are beta-blockers used to treat
|
hypertension, angina, MI, SVT, CHF, glaucoma
|
|
beta-blockers ("lol"s): how do beta blockers treat hypertension
|
decrease cardiac output, decrease renin secretion
|
|
beta-blockers ("lol"s): how do beta blockers treat angina
|
decrease heart rate, decrease cardiac contractility, decreased O2 consumption
|
|
beta-blockers ("lol"s): why are beta blockers used to treat MI
|
decrease MI mortality
|
|
beta-blockers ("lol"s): which beta blockers are used to treat SVT
|
propanolol, esmolol
|
|
beta-blockers ("lol"s): how do propanolol and esmolol treat SVT
|
decrease AV conduction velocity
|
|
beta-blockers ("lol"s): how do beta blockers treat CHF
|
slow progression of chronic failure
|
|
beta-blockers ("lol"s): which beta blocker is used to treat glaucoma
|
timolol
|
|
beta-blockers ("lol"s): what is timolol used to treat glaucoma
|
decrease secretion of aqueous humor
|
|
beta-blockers ("lol"s): what are the toxic effects of beta blockers
|
impotence, exacerbation of asthma, caution in diabetes
|
|
beta-blockers ("lol"s): what are the cardiovascular toxic effects of beta blockers
|
bradychardia, AV block, CHF
|
|
beta-blockers ("lol"s): what are the CNS adverse effects of beta blockers
|
sedation, sleep alterations
|
|
beta-blockers ("lol"s): which beta blockers are beta-1 selective
|
acebutolol, betaxolol, esmolol, atenolol, metaprolol (A BEAM of beta-1 blockers)
|
|
beta-blockers ("lol"s): which beta-1 blocker is short-acting
|
esmolol
|
|
beta-blockers ("lol"s): which beta blockers are non-selective
|
propanolol, timolol, pindolol, nadolol, labetalol
|
|
beta-blockers ("lol"s): which beta blocker also blocks alpha receptors
|
labetalol (all others are spelled "olol")
|
|
glaucoma drugs: which alpha agonists are used to treat glaucoma
|
epinephrine, brimonidine
|
|
glaucoma drugs: which beta blockers are used to treat glaucoma
|
timolol, betxolol, carteolol
|
|
glaucoma drugs: which cholinomimetics are used to treat glaucoma
|
pilocarpine, carbachol, physostigmine, echothiophate
|
|
glaucoma drugs: which diuretics are used to treat glaucoma
|
acetazolamide, dorzolamide, brinzolamide
|
|
glaucoma drugs: which prostaglandin is used to treat glaucoma
|
latanoprost
|
|
glaucoma drugs: what classes of drugs are used to treat glaucoma
|
alpha agonists, beta blockers, cholinomimetics, diuretics, prostaglandins (*mnemonic -- treating glaucoma is easy as ABCD)
|
|
glaucoma drugs: what is the effect of epinephrine in glaucoma
|
increase outflow of aqueous humor
|
|
glaucoma drugs: what are the side effects of epinephrine treatment in glaucoma
|
mydriasis, stinging
|
|
glaucoma drugs: what glaucoma should epinephrine NOT be used for
|
closed-angle glaucoma
|
|
glaucoma drugs: what is the effect of brimonidine in glaucoma
|
decreased aqueous humor synthesis
|
|
glaucoma drugs: what are the side effects of brimonidine treatment in glaucoma
|
no pupillary or vision changes
|
|
glaucoma drugs: what is the effect of beta-blocker treatment in glaucoma
|
decrease aqueous humor secretion
|
|
glaucoma drugs: what are the side effects of beta blocker treatment in glauzoma
|
no pupillary or vision changes
|
|
glaucoma drugs: what is the effect of cholinomimetics in glaucoma
|
ciliary muscle contraction, opening of trabecular meshwork, increase outflow of aqueous humor
|
|
glaucoma drugs: what are the side effects of cholinomimetics in glaucoma
|
miosis, cyclospasm
|
|
glaucoma drugs: what is the effect of diuretic treatment in glaucoma
|
inhibition of carbonic anhydrase --> decrease HCO3 secretion --> decrease aqueous humor secretion
|
|
glaucoma drugs: what are the side effects of diuretics in glaucoma
|
no pupillary or vision changes
|
|
glaucoma drugs: what is the effect of prostaglandin (latanoprost) treatment in glaucoma
|
increase outflow of aqueous humor
|
|
glaucoma drugs: what is the side effect of prostaglandin treatment in glaucoma
|
darkens color of iris (browning)
|
|
glaucoma drugs: which drugs used to treat glaucoma increase outflow of aqueous humor
|
cholinomimetics, prostaglandin, epinephrine
|
|
glaucoma drugs: can you use epinephrine in closed-angle glaucoma
|
NO
|
|
glaucoma drugs: brimonidine is used to treat what eye disease
|
glaucoma
|
|
glaucoma drugs: what kind of drug is latanoprost
|
prostaglandin
|
|
glaucoma drugs: latanoprost is used to treat what eye disease
|
glaucoma
|
|
glaucoma drugs: which glaucoma drugs decrease aqueous secretion
|
beta blockers, diuretics
|
|
L-dopa/carbidopa: what does L-dopa stand for
|
levodopa
|
|
L-dopa/carbidopa: what is the mechanism of action of L-dopa/carbidopa
|
increase dopamine level in brain
|
|
L-dopa/carbidopa: what is L-dopa/carbidopa used to treat
|
Parkinson's disease
|
|
L-dopa/carbidopa: how is L-dopa different from dopamine
|
L-dopa can cross the blood-brain barrier, dopamine cannot
|
|
L-dopa/carbidopa: what happens to L-dopa after it crosses the BBB
|
converted to dopamine by dopa decarboxylase
|
|
L-dopa/carbidopa: what enzyme convertes L-dopa to dopamine
|
dopa decarboxylase
|
|
L-dopa/carbidopa: what is the function of carbidopa
|
peripheral decarboxylase inhibitor
|
|
L-dopa/carbidopa: why is carbidopa given with L-dopa
|
increase L-dopa availability in CNS by inhibiting decarboxylase in periphery, also limits peripheral side effects
|
|
L-dopa/carbidopa: what are the side effects of L-dopa.carbidopa treatment
|
arrhythmias, dyskinesias
|
|
L-dopa/carbidopa: why do patients taking L-dopa get arrhythmias
|
peripheral effects of dopamine
|
|
L-dopa/carbidopa: why do patients taking L-dopa get dyskinesias
|
excess dopamine stimulation in CNS
|
|
Parkinson's disease drugs: what drugs are used to treat Parkinson's disease
|
dopamine agonists, MAO inhibitors, antimuscarinics
|
|
Parkinson's disease drugs: specifically, which drugs are used to treat Parkinson's
|
Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics (BALSA)
|
|
Parkinson's disease drugs: which dopamine agosts are used to treat Parkinson's
|
L-dopa/carbidopa, bromocriptine, pramipexole, ropinirole, amantadine
|
|
Parkinson's disease drugs: what is the action of bromocriptine in Parkinson's
|
ergot alkaloid, partial dopamine agonist
|
|
Parkinson's disease drugs: what is the action of amantadine in Parkinson's
|
enhances dopamine release
|
|
Parkinson's disease drugs: what MAOI is used to treat Parkinson's
|
selegiline
|
|
Parkinson's disease drugs: what is the mechanism of selegiline
|
selective MAO type B inhibitor
|
|
Parkinson's disease drugs: what antimuscarinic is used to treat Parkinson's
|
benztropine
|
|
Parkinson's disease drugs: what is the effect of benztropine in Parkinson's
|
improves tremor, rigidity, little effect on bradykinesia
|
|
Sumatriptan: what is sumatriptan used for
|
acute migraine, cluster headache attacks
|
|
Sumatriptan: what is the mechanism of sumatriptan
|
5-HT1D agonist
|
|
Sumatriptan: what is the half life of sumatriptan
|
less than 2 hours
|
|
Sumatriptan: what are the side effects of sumatriptan
|
chest discomfort, mild tingling
|
|
Sumatriptan: what are the contraindications for sumatriptan
|
patients with CAD or Prinzmetal's angina
|
|
Epilepsy drugs: which drugs are used for simple and complex partial seizures
|
phenytoin, carbamazapine, lamotrigine, gabapentin, topiramate, phenobarbital
|
|
Epilepsy drugs: what types of seizures is phenytoin indicated for
|
simple and complex partial, tonic-clonic, status epilepticus
|
|
Epilepsy drugs: what types of seizures is carbamazepine indicated for
|
simple and complex partial, tonic-clonic
|
|
Epilepsy drugs: what types of seizures is lamotrigine indicated for
|
simple and complex partial, tonic-clonic
|
|
Epilepsy drugs: what types of seizures is gabapentin indicated for
|
simple and complex partial, tonic-clonic
|
|
Epilepsy drugs: what types of seizures is topiramate indicated for
|
simple and complex partial
|
|
Epilepsy drugs: what types of seizures is phenobarbital indicated for
|
simple and complex partial, tonic-clonic
|
|
Epilepsy drugs: what drugs can be used for tonic-clonic seizures
|
phenytoin, carbamazapine, lamotrigine, gabapentin, phenobarbital, valproate
|
|
Epilepsy drugs: what drugs can be used for absence seizures
|
valproate, ethosuximide
|
|
Epilepsy drugs: what drugs can be used for status epilepticus
|
phenytoin, benzodiazapines (diazepam, lorazepam)
|
|
Epilepsy drugs: what types of seizure is valproate indicated for
|
tonic-clonic, absence
|
|
Epilepsy drugs: what types of seizure is ethosuximide inidcated for
|
absence
|
|
Epilepsy drugs: what type of seizure are benzodiazepines indicated for
|
status epilepticus
|
|
Epilepsy drugs: other than anti-seizure, what else is phenytoin used for
|
class 1B anti-arrhythmic
|
|
Epilepsy drugs: how should a patient taking carbamazepine be followed
|
monitor LFT's weekly
|
|
Epilepsy drugs: which seizure drugs have adjunct use
|
gabapentin, topiramate
|
|
Epilepsy drugs: which seizure drug is safest in pregnant women
|
phenobarbital
|
|
Epilepsy drugs: which seizure drug is used in Crigler-Najjar II
|
phenobarbital
|
|
Epilepsy drugs: what are the advantages of phenobarbital
|
can be used in pregnant women, Crigler Najjar II
|
|
Epilepsy drug toxicities: what are the side effects of benzodiazepines
|
sedation, tolerance, dependence
|
|
Epilepsy drug toxicities: what are the side effects of carbamazepine
|
diplopia, ataxia, CYP induction, blood dyscrasias, liver toxicity
|
|
Epilepsy drug toxicities: what are the side effects of ethosuximide
|
GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome
|
|
Epilepsy drug toxicities: what are the side effects of phenobarbital
|
sedation, CYP induction, tolerance, dependence
|
|
Epilepsy drug toxicities: what are the side effects of phenytoin
|
nystagmus, diplopia, ataxia, sedation, ginigival hyperplasia, hirsutism, anemias, teratogenic
|
|
Epilepsy drug toxicities: what are the side effects of valproate
|
GI distress, rare by fatal hepatotoxicity, neural tube defects (spina bifida)
|
|
Epilepsy drug toxicities: what are the side effects of lamotrigine
|
life-threatening rash, Stevens-Johnson syndrome
|
|
Epilepsy drug toxicities: what are the side effects of gabapentin
|
sedation, movement disorders
|
|
Epilepsy drug toxicities: what are the side effects of topiramate
|
sedation, mental dulling, kidney stones, weight loss
|
|
Epilepsy drug toxicities: which anti-epileptic drug is teratogenic
|
phenytoin
|
|
Epilepsy drug toxicities: which anti-epileptic drug can cause dependence
|
benzodiazepines, phenobarbital
|
|
Epilepsy drug toxicities: which anti-epileptic drug can cause neural tube defects
|
valproate
|
|
Epilepsy drug toxicities: which anti-epileptic drugs can cause GI distress
|
valproate, ethosuximide
|
|
Epilepsy drug toxicities: it is necessary to check LFT's with which anti-epileptic drugs
|
carbamazepine, valproate
|
|
Epilepsy drug toxicities: which anti-epileptic drugs cause CYP induction
|
phenobarbital, carbamazepine
|
|
Epilepsy drug toxicities: which anti-epileptic drugs can cause blood problems
|
carbamazepine, phenytoin
|
|
Epilepsy drug toxicities: which anti-epileptic drugs can cause Stevens-Johnson syndrome
|
lamotrigine, ethosuximide
|
|
Epilepsy drug toxicities: which anti-epileptic drugs can cause diplopia
|
carbamazepine, phenytoin
|
|
Phenytoin: what is the mechanism of phenytoin action
|
use-dependent blockade of Na+ channels
|
|
Phenytoin: what is the clinical application of phenytoin
|
grand mal seizures
|
|
Phenytoin: what are the toxicities of phenytoin
|
nystagmus, ataxia, diplopia, lethargy
|
|
Phenytoin: what are the chronic toxicities of phenytoin
|
gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia, malignant hyperthermia (rare)
|
|
Phenytoin: should pregnant women take phenytoin
|
NO -- teratogenic
|
|
Phenytoin: why does phenytoin cause megaloblastic anemia
|
causes decreased vitamin B-12
|
|
Barbiturates: name 4 barbiturates
|
phenobarbital, pentobarbital, thiopental, secobarbital
|
|
Barbiturates: what is the mechanism of barbiturate action
|
increase duration of Cl channel opening --> decreased neuron firing --> facilitate GABA-A action
|
|
Barbiturates: how do barbiturates facilitate GABA-A action
|
increase duration of Cl channel opening which decreases neuron firing (Barbidurate increases duration
|
|
Barbiturates: is barbiturate action on the CNS stimulatory or inhibitory
|
inhibitory
|
|
Barbiturates: what is the clinical application of barbiturates
|
sedative for anxiety, seizures, insomnia, anesthesia induction (thiopental)
|
|
Barbiturates: which barbiturate is used for anesthesia induction
|
thiopental
|
|
Barbiturates: what are the side effects of barbiturates
|
dependence, additive CNS depression effects with alcohol, respiratory or CV depression (death), drug interactions due to CYP induction
|
|
Barbiturates: what should you find out before giving a patient barbiturates
|
what other medications they take, because of CYP induction and many drug interactions
|
|
Barbiturates: what happens if you give barbiturates to a patient in alcohol-induced coma or DT's
|
they might DIE!! Because of additive effect of barbiturates and alcohol --> respiratory depression
|
|
Barbiturates: when are barbiturates contra-indicated
|
porphyria
|
|
Barbiturates: can barbiturates cause dependence
|
YES
|
|
Barbiturates: My friend Barb was very anxious so her doctor gave her barbiturates to increase the duration of the time she could speak in public without freaking out and having a seizure. She became so dependent on it that she recommended it to her friend Portia who couldn't take it because of porphyria. One day Barb drank too much alcohol and took her barbiturates and never woke up! THE END
|
clinical pharmacology made ridiculous. Period
|
|
Benzodiazepines: name a bunch of benzodiazepines
|
diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide (all have ZZZ in them)
|
|
Benzodiazepines: what is the mechanism of benzodiazepines
|
increase frequency of Cl channel opening --> facilitate GABA-A action (Frenzodiazepines increase frequency)
|
|
Benzodiazepines: which GABA receptors are facilitated by barbiturates and bezodiazepines
|
GABA-A
|
|
Benzodiazepines: what are the clinical applications of benzodiazepines
|
anxiety, spasticity, status epilepticus (diazepam), detoxification (alcohol withdrawal, DT's)
|
|
Benzodiazepines: which benzodiazepine can be used for status epilepticus
|
diazepam
|
|
Benzodiazepines: what drugs can be used to treat alcohol withdrawal
|
benzodiazepines
|
|
Benzodiazepines: which benzodiazepines are short-acting
|
TOM thumb: Triazolam, Oxazepam, Midazolam
|
|
Benzodiazepines: what are the toxic effects of benzos
|
dependence, additive CNS depression effects with alcohol
|
|
Benzodiazepines: how are benzos better than barbiturates
|
less respiratory depression and coma risk
|
|
Benzodiazepines: how do you treat benzo overdose
|
flumazenil
|
|
Benzodiazepines: what is flumzenil used for
|
benzo overdose
|
|
Benzodiazepines: how does flumazenil work
|
competitive antagonist at GABA receptor
|
|
Benzodiazepines: can a patient become benzodiazepine dependent
|
YES
|
|
Benzodiazepines: are barbiturates or benzodiazepines used for alcohol withdrawal
|
benzodiazepines
|
|
Antipsychotics (neuroleptics): what is another name for antipsychotics
|
neuroleptics
|
|
Antipsychotics (neuroleptics): name 4 antipsychotic drugs
|
thioridazine, haloperidol, fluphenazine, chlorpromazine
|
|
Antipsychotics (neuroleptics): how do you keep benzos straight from antipsychotics
|
Benzos help 3rd year Jon Kazam be less anxious around patients: Shazam Kazam! Without antipsychotics patients talk like a crazy 'zine (well, not perfect, but I'm working on it)
|
|
Antipsychotics (neuroleptics): what is the mechanism of most antipsychotics
|
block dopamine D2 receptors
|
|
Antipsychotics (neuroleptics): what is the clinical application of antipsychotics
|
schizophrenia, psychosis
|
|
Antipsychotics (neuroleptics): what are the side effects of antipsychotics
|
extrapyramidal side effects (EPS), sedation, endocrine, muscarinic blockade, alpha blockade, histamine blockade
|
|
Antipsychotics (neuroleptics): what is a long-term effect of antipsychotic use
|
tardive dyskinesia
|
|
Antipsychotics (neuroleptics): what is neuroleptic malignant syndrome
|
a side effect of antipsychotics; rigidity, autonomic instability, hyperpyrexia
|
|
Antipsychotics (neuroleptics): how do you treat neuroleptic malignant syndrome
|
dantrolene, dopamine agonists
|
|
Antipsychotics (neuroleptics): what is tardive dyskinesia
|
side effect of neuroleptics; stereotypic oral-facial movements, may be due to dopamine receptor sensitization
|
|
Antipsychotics (neuroleptics): what is the "rule of 4" with EPS side effects from antipsychotic drugs
|
evolution of EPS side effects: 4 hours -- acite dystonia, 4 days -- akinesia, 4 weeks -- akasthesia, 4 months -- tardvie dyskinesia
|
|
Antipsychotics (neuroleptics): is tardvie dyskinesia reversible
|
often irreversible
|
|
Antipsychotics (neuroleptics): what is fluphenazine used for
|
schizophrenia, psychosis
|
|
Atypical antipsychotics: name 3 atypical antipsychotics
|
clozapine, olanzapine, risperidone
|
|
Atypical antipsychotics: what type of antipsychotic is clozapine
|
atypical
|
|
Atypical antipsychotics: what type of antipsychotic is olanzapine
|
atypical
|
|
Atypical antipsychotics: what type of antipsychotic is risperidone
|
atypical
|
|
Atypical antipsychotics: what is the mechanism of atypical antipsychotics
|
block 5-HT2 and dopamine receptors
|
|
Atypical antipsychotics: what is the mechanism of clozapine
|
block 5-HT2 and dopamine receptors
|
|
Atypical antipsychotics: what is the mechanism of olanzapine
|
block 5-HT2 and dopamine receptors
|
|
Atypical antipsychotics: what is the mechanism of risperidone
|
block 5-HT2 and dopamine receptors
|
|
Atypical antipsychotics: what is the clinical application of clozapine
|
schizophrenia positive and negative symptoms
|
|
Atypical antipsychotics: what is the clinical application of olanzapine
|
schizophrenia positive and negative symptoms, OCD, anxiety disorder, depression
|
|
Atypical antipsychotics: what is the clinical application of risperidone
|
schizophrenia positive and negative symptoms
|
|
Atypical antipsychotics: how are atypical antipsychotics different from classic ones
|
atypicals treat positive and negative symptoms of schizophrenia, fewer extrapyramidal and anticholinergic side effects than classic antipsychotics
|
|
Atypical antipsychotics: which antipsychotics should be used to treat positive and negative symptoms of schizophrenia
|
atypical ones -- clozapine, olanzapine, risperidone
|
|
Atypical antipsychotics: which antipsychotics should be used for fewer side effects
|
atypical ones -- clozapine, olanzapine, risperidone
|
|
Atypical antipsychotics: what is a potential toxicity of clozapine
|
agranulocytosis
|
|
Atypical antipsychotics: which antipsychotic drug can cause agranulocytosis
|
clozapine
|
|
Atypical antipsychotics: what test must be done weekly on patients taking clozapine
|
WBC count because of potential agranulocytosis
|
|
Lithium: what is the mechanism of action of lithium
|
unknown; may be related to inhibition of phosphoinositol cascade
|
|
Lithium: what is the clinical application of lithium
|
mood stabilizer for bipolar disorder
|
|
Lithium: how does lithium help people with bipolar disorder
|
prevents relapse and acute manic episodes
|
|
Lithium: what are the side effects of lithium
|
tremor, hypothyroidism, polyuria, teratogenic
|
|
Lithium: is it OK for women taking lithium to get pregnant
|
NO -- teratogenic
|
|
Lithium: what does lithium cause polyuria
|
ADH antagonist --> nephrogenic diabetes insipidus
|
|
Lithium: AUTHOR
|
Hina Talib
|
|
Antidepressants: What do the following drugs inhibit: 1. MAO inhibitors, 2. Desipramine/maprotilline, 3. Mirtazapine and 4. Fluoxetine/trazodone?
|
1. MAO 2. NE reuptake 3. Alpha 2-R 4. 5HT reuptake
|
|
Antidepressants: All of the above actions are ------synaptic
|
PRE
|
|
List the Tricyclic Antidepressants: What are the three C's of their toxicity?
|
Convulsions, Coma, Cardiotoxicity (arrythmias). Also respiratory depression, hypyrexia.
|
|
List the Tricyclic Antidepressants: How about toxicity in the eldery?
|
confusion and hallucinations due to anticholinergic SE
|
|
List the Tricyclic Antidepressants: What is the mechanism of TCA?
|
block reuptake of NE and 5HT
|
|
List the Tricyclic Antidepressants: What is the clinical uses of TCAs?
|
Endogenous depresion. Bed wetting - imipramine. OCD- clomipramine.
|
|
List the Tricyclic Antidepressants: How are tertiary TCA's different than secondary in terms of side effects?
|
Amitriptyline (tertiary) has more anti-cholinergic effects than do secondary (nortriptyline). Desipramine is the least sedating.
|
|
List the Tricyclic Antidepressants: what are the SE of TCAs?
|
sedation, alpha blocking effects, atropine-like anti cholinergic side effects (tachycardia, urinary retention)
|
|
List the Tricyclic Antidepressants: Fluoxetine, sertraline, paroxetine, citalopram are what class of drugs?
|
pg 311 SSRI's for endogenous depression
|
|
List the Tricyclic Antidepressants: How long does it take an anti-depressant to have an effect?
|
2-3weeks
|
|
List the Tricyclic Antidepressants: How does the toxicity differ fromTCA's and what are they?
|
Fewer than TCA's. CNS stimulation - anxiety, insomnia, tremor, anorexia, nausea, and vomiting.
|
|
List the Tricyclic Antidepressants: What toxicity happens with SSRI's and MAO inhibitors given together?
|
Seratonin Syndrome! Hyperthermia, muscle rigidity, cardiovascular collapse
|
|
List the Tricyclic Antidepressants: What are heterocyclics?
|
pg 312 2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used major depression.
|
|
List the Tricyclic Antidepressants: Examples of heterocyclics?
|
trazodone, buproprion, venlafaxine, mirtazapine, maprotiline
|
|
List the Tricyclic Antidepressants: Which one is used for smoking cessation?
|
Buproprion. Mechanism not known. Toxicity - stimulant effects, dry mouth, aggrevation of pyschosis
|
|
List the Tricyclic Antidepressants: Which one used in GAD?
|
Venlafaxine - inhibits 5HT and DA reuptake. Toxicity - stimulant effects
|
|
List the Tricyclic Antidepressants: which one blocks NE reuptake
|
maprotiline
|
|
List the Tricyclic Antidepressants: Which one increases release of NE and 5HT via alpha 2 antagonism?
|
mirtazapine. Also potent 5HT Rantagonist. Toxicity - sedation, increase serum cholesterol, increase apetite
|
|
List the Tricyclic Antidepressants: What is trazodone and it' SE?
|
primarily inhibits seratonin reuptake. Toxicity - sedation, nausea, priapism, postural hypotension
|
|
Give 2 examples of MAO: Mechanism and Clinical Uses?
|
non selevtive MAO inhibition. Atypical antidepressant, anxiety, hypochondriasis
|
|
Give 2 examples of MAO: What is the toxicity with tyramine ingestion (in foods) and meperidine?
|
Hypertensive crisis
|
|
Give 2 examples of MAO: Other toxicities?
|
CNS stimulation, contraindicated with SSRI's or B-agonists
|
|
What is the mechanims of selgiline (deprenyl)?: what is the clinical use and toxicity?
|
adjunctive agent to L-dopa for Parkinsons. May enhance adverse effects of L-dopa
|
|
General principles: What is the significance of drugs with decreased solubility in blood?
|
rapid induction and recovery times . Ie. N20
|
|
General principles: What is the significance of drugs with increased solubility in blood?
|
increased potency = I/ MAC. Ie. Halothane
|
|
Inhaled Anesthetics: list them
|
halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
|
|
Inhaled Anesthetics: What is good about lower solubility?
|
the quicker the anesthetic response, and the quicker the recovery
|
|
Inhaled Anesthetics: What are these drug's effects?
|
myocardial depression, respiratory depression, nausea/emesis, increase cerebral blood flow
|
|
Inhaled Anesthetics: What toxicity mactches the following drugs 1. Halothane 2. Methoxyflurane 3. Enflurane 4. Rare
|
1. Hepatotoxcity 2. Nephrotoxicty 3. Proconvulsant 4. Malignant hyperthermia
|
|
IV anesthetics: What do barbituates, benzodiazepines, arylcyclohexylamines and narcotic analgesics have in common?
|
they are IV anesthetics
|
|
IV anesthetics: What the pharmacokinetics and uses of thiopental?
|
high lipid solubility, rapid entry into brain. Used for induction of anesthesia for short surgical procedures. Terminated by redistribution from brain. Decreased cerebral blood flow
|
|
IV anesthetics: Give an example of a benzo and what is this class's shortcoming?
|
midazolam used for endoscopy. Used with gaseous anesthetics and narcotics. May cause severe post-op respiratory depressio and amnesia
|
|
IV anesthetics: What does Ketamine (PCP analog and an arylcyclohexylamine) do?
|
dissociative anesthetic. Cardiovascular stimulant. Causes disorientation, hallucination, bad dreams. Increases cerebral blood flow.
|
|
IV anesthetics: How are narcotic analgesics used? Examples?
|
Morphone and fentanyl are used with CNS depressant during general anesthesia.
|
|
IV anesthetics: What is the advantage of propofol
|
used for rapid anesthesia induction and short procedures. Less post-op nausea than thiopental
|
|
Local anesthetics: Name some esters?
|
procaine, cocaine, tetracaine,
|
|
Local anesthetics: Name some amides?
|
lidocaine, bupivacaine, (amides have two I's in name!)
|
|
Local anesthetics: What is the mechanism and clinical use?
|
bind receptor and block Na channels. Tertiary amine local anesthetics penetrate membrane in uncharge form, then bind charged form. Use for minor surgical procedures, spinal anesthesia.
|
|
Local anesthetics: How do you decide to use ester or amides?
|
if allergic to esters, give amides
|
|
Local anesthetics: what is the toxicity
|
CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, arrhythmias (cocaine)
|
|
Local anesthetics: In infected ________ tissue, anesthetics are charged and cannot penetrate membrane. Therefore, ______ anesthetics are needed.
|
acidic; more
|
|
Local anesthetics: What is the order of nerve blockade for size and myelination? Which factor predominates?
|
small diameter> large diameter. Myelinated fibers> unmyelinated fibers. Size factor predominates
|
|
Local anesthetics: what is the order of loss of sensation?
|
pain first, then temp, then touch, then pressure
|
|
Local anesthetics: Why would you give these drugs with vasoconstrictors?
|
to enhance local action
|
|
Opiod analgesics: List as many as you can.
|
morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan
|
|
Opiod analgesics: Mechanism: They act as _____ for opiod receptors to modulate synaptic transmission
|
agonists
|
|
Opiod analgesics: which drugs act at the mu, delta, kappa receptors?
|
morphine enkephalin, dynorphin
|
|
Opiod analgesics: Clinical use?
|
pain, cough supression (dex), diarrhea (loperamide), acute pulmonary edema, methadone maintenance programs
|
|
Opiod analgesics: What are the major toxicities?
|
addiction, respiratory depression, constipation, miosis, additive CNS depression wth other drugs
|
|
Opiod analgesics: Tolerance does not develop to __________and ______
|
miosis and constipation
|
|
Opiod analgesics: How would you treat toxicity?
|
naloxone, naltrexone (opiod R antagonist)
|
|
Other NSAIDS: List three NSAIDS?
|
ibuprofen, naproxen, indomethacin
|
|
Other NSAIDS: What is their mechanism?
|
reversibly inhibit COX 1 and 2. Blocks PG synthesis
|
|
Other NSAIDS: What is their clinical use (3As)?
|
Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.
|
|
Other NSAIDS: What are common toxicities?
|
renal damage, aplastic anemia, GI distress, ulcers
|
|
COX 2 Inhibitors: Where is cox2 found?
|
in inflammatory cells and mediates inflammation and pain
|
|
COX 2 Inhibitors: Why is cox2 inhibition better than cox1?
|
cox1 helps to maintain gastric mucosa, thus, should not have the corrosive effects of other NSAIDs on the GI lining (less incidence of ulcers and bleeding)
|
|
COX 2 Inhibitors: Clinical Use?
|
RA and osteoarthritis
|
|
Acetaminophen: What is its mechanism and where does it work?
|
reversibly inhibits cox, mostly in CNS. Inactivated peripherally.
|
|
Acetaminophen: What are its 2 As?
|
antipyretic, analgesic but NOT anti-inflammatory.
|
|
Acetaminophen: Overdose effects?
|
hepatic necrosis, acetaminophen metabolites depletes glutathine and forms toxic tissue adducts in the liver
|
|
cardiovascular therapy: Changes in CO affect two major pathways?
|
1. Carotid sinus firing, sympa discharge 2. Renal blood flow, renin-ang pathway
|
|
cardiovascular therapy: What is the effect of the following drugs: 1. Positive inotropic drugs 2. Beta blockers 3. Ace inhibitors 4. AII antagonists 5. Vasodilators and 6. Diuretics
|
1. Increases cardiac output. 2. Inhibit renin release. 3. Inhibit ACE 4. Inhibits effects of AngII including increasing the preload, increasing the afterload and remodelling. 5. Decrease the preload and afterload. 6. Decrease the preload and afterload
|
|
antihypertensive drugs: What are the adverse effects of these two diueretics: hydrochlorothiazide, loop diuretics
|
1. Hypokalemia, hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia 2. Hypokalemia, met alk, hypotension, ototoxicity
|
|
antihypertensive drugs: These are wahat class of drugs: clonidine, methyldopa, ganglionic blockers, reserpine, guanethidine, prazosin, beta blockers?
|
sympathoplegics
|
|
antihypertensive drugs: Adverse effects of clonidine?
|
dry mouth, sedation, severe rebound HTN
|
|
antihypertensive drugs: Adverse effects of methyldopa?
|
sedation, positive coombs test
|
|
antihypertensive drugs: Adverse effects of ganglionic blockers?
|
orthostatic HTN, blurred vision, constitpation, sexual dysfuncction
|
|
antihypertensive drugs: Adverse effects of reserpine?
|
sedation, depression, nasal stuffiness, diarrhea
|
|
antihypertensive drugs: adverse effects of beta blockers?
|
impotence, asthma, cardiovascular, cns
|
|
antihypertensive drugs: Adverse effects of guanethidine?
|
orthostatic and exercise Hypotension, sex dysfxn, diarrhea
|
|
antihypertensive drugs: Adverse effects of prazosin?
|
1st dose orthostatic hypotension, dizzy, headache
|
|
antihypertensive drugs: The following are what class: hydralazine, minoxidil, nifedipine, verapamil, nitroprusside
|
vasodilators
|
|
antihypertensive drugs: which one causes lupus like syndrome? Other toxicities?
|
hydralazine, nausea, headache, reflex tachycardia, angina, salt retention
|
|
antihypertensive drugs: adverse effets of minoxidil?
|
hypertrichosis (hair growth - think Rogaine with minoxidil!), pericardial effusion, reflex tachycardia, angina, salt retention
|
|
antihypertensive drugs: Side effects of nifedipine, verapamil?
|
dizziness, flushing, constipation, nausea
|
|
antihypertensive drugs: which one causes cynide toxicity?
|
nitroprusside
|
|
antihypertensive drugs: Adverse effects of ACE-I Captorpil? Think CAPTOPRIL
|
C: cough, A: angioedema, P: proteinuria, T: taste changes, O: hypOtension, P: pregnancy problems like fetal renal damage, R: rash, I: increased renin, L: lower angiotensin. Also hyperkalemia.
|
|
antihypertensive drugs: Losartan is a ----------- R-Inhibitor? With ____-toxicity and ____kalemia
|
angiotensin II, fetal renal, hyper
|
|
Hydralizine: Which two anti-htn drugs do you use with B blockers to prevent reflex tachycardia, diuretic to block salt retention?
|
hydralizine, minoxidil
|
|
Hydralizine: What is hydralizine's mechanims and clinical use?
|
increase cGMP --> smooth muscle relaxation. Vasodilates arteries > veins. Reduces afterload. Used for severe HTN or CHF
|
|
Calcium channel blockers, name three: Mechanism: block _____ chanels of cardiac and smooth muscles to reduce contractility
|
voltage dependednt L type Ca
|
|
Calcium channel blockers, name three: Rank their effects on vascular smooth muscle ad on the heart.
|
smooth muscle nifed> diltia > verapamil heart: vera> diltia> nifedepine
|
|
Calcium channel blockers, name three: What is the calcium channel blockers use?
|
HTN, angina, arrythmias (not nifedipine)
|
|
Calcium channel blockers, name three: ACE -I, name three
|
captopril, enalapril, lisinopril
|
|
Calcium channel blockers, name three: Mechanim considering bradykinin and renin release?
|
reduce lvels of ang II, prevent inactivation of bradykinin, renin release is increased to to loss of feedback inhibition
|
|
Calcium channel blockers, name three: what is the clinical use of these?
|
HTN, CHF, diabetic renal disease
|
|
Diuretics- site of action: What is the site of action of 1. Acetazolamide, 2. Osmotic agents, 3. Loop agents, 4. Thiazides, 5. Potassium sparing, 6. ADH antagonists
|
1. PCT 2. PCT, thin desc limb, CD 3. Thick ascending limb 4. Distal conv tubule 5. DCT a bit later 6. CD in inner medulla
|
|
Diuretics- site of action: How does mannitol an osmotic diuretic work?
|
increase tubular fluid osmolarity, producing increased urine flow
|
|
Diuretics- site of action: what is the use and toxicity?
|
Use: shock, drug overdose, decrease intracranial pressure. Toxicity - pulmonary edema, dehydration. Contraindicated in anuria, CHF
|
|
Acetazolamide: Is a ______inhibitor. Causes ______diuresis and _____ in total body HC03 stores.
|
Carbonic anhydrase, self-limited NaHCO3, reduction.
|
|
Acetazolamide: What electrolye disturbace does it treat? Does it cause?
|
treats met alk, causes in toxicity hyperchloremic met acidosis. ACIDazolamide caues ACIDosis.
|
|
Acetazolamide: Other toxicity?
|
neuropathy, NH3 toxicity, sulfa allergy
|
|
Acetazolamide: uses?
|
glaucoma, urinary alk, met alk, altitude sickeness
|
|
Furosemide: This sulfonamide loop diuretic inhibits _______cotransport
|
NA, K, 2CL
|
|
Furosemide: Furosemide also works by?
|
abolishes hypertonicit y of medulla, prevent concentration of urine. Increase Caexcertion. Loops Lose calcium
|
|
Furosemide: The three uses for this loop diuretic?
|
edematous states, htn, hypercalcemia
|
|
Furosemide: Toxicity using the OH DANG?
|
ototoxicity, hypokalemia, dehydration, allergy, nephritis interstitial, gout
|
|
Ethacrynic Acid: How is this drug different from furosemide? And how does that affect its use?
|
Although both have the same action, ethacrynic is a phenoxyacetic acid derivative not a sulfonamide. Therefore use this drug when you are allergic to sulfa.
|
|
Ethacrynic Acid: What drug can be used to treat acute gout?
|
ethacrynic acid
|
|
Ethacrynic Acid: AUTHOR
|
Stacy Ugras
|
|
Hydrochlorothiazide: Hydrochlorothiazide is a thiazide diuretic that inhibits the reabsorption of ----- in the ---- tubule
|
NaCl; early distal tubule
|
|
Hydrochlorothiazide: Does hydrochlorothiazide increase or decrease the excretion of calcium ion?
|
decrease
|
|
Hydrochlorothiazide: A toxic dose of hydrochlorathiazide will do what to the blood levels of these electrolites: potassium, sodium, glucose, lipid, uric acid, calcium
|
hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC)
|
|
K+-sparing diuretics: Spironolactone is a competitive antagonist to the --- receptor in the ---- tubule
|
aldosterone; cortical collecting tubule
|
|
K+-sparing diuretics: Name two K+-sparing diuretics that block Na+ channels in the cortical collecting duct
|
Triamterine and amiloride
|
|
K+-sparing diuretics: Besides causing hyperkalemia, a toxic dose of spironolactone will cause this endocrine effect
|
Gynecomastia (antiandrogen effect)
|
|
K+-sparing diuretics: Name three K+-sparing diuretics
|
Spironolactone, Triamterene, Amiloride (The K+ STAys.)
|
|
Diuretics: electrolye exchange: Diuretics are classified as carbonic anhydrase inhibitors, loop diuretics, thiazides, and K+-sparing diuretics. Which of these causes in increase in urine NaCl?
|
All of them!
|
|
Diuretics: electrolye exchange: Which types of diuretucs increase urine K+?
|
All except K+-sparing diuretics. Carbonic anhydrase inhibitors, loop diuretics, thiazides.
|
|
Diuretics: electrolye exchange: Do carbonic anhydrase inhibitors increase or decrease blood pH?
|
Decrease, cause acidosis
|
|
Diuretics: electrolye exchange: Do K+-sparing diuretics cause acidosis or alkalosis?
|
Acidosis, decreases pH
|
|
Diuretics: electrolye exchange: Do loop diuretics cause acidosis or alkalosis?
|
Alkalosis, increases pH
|
|
Diuretics: electrolye exchange: Do thiazide diuretics cause an increase or decrease in blood pH?
|
Increase, cause alkalosis
|
|
Diuretics: electrolye exchange: Do loop diuretics increase or decrease levels of urine calcium ion?
|
Increase
|
|
Diuretics: electrolye exchange: Do thiazide diuretics increase or decrease levels of urine calcium ion?
|
Decrease
|
|
Antianginal therapy: Name four determinants of the level of myocardial oxygen consumption
|
There are five: end diastolic volume, blood pressure, heart rate, contractility, ejection time
|
|
Antianginal therapy: Do nitrates affect preload or afterload?
|
preload
|
|
Antianginal therapy: Do Beta-blockers affect preload or afterload?
|
afterload
|
|
Antianginal therapy: What is the effect of nitrates on: diastolic volume, blood pressure, contractility, heart rate, ejection time?
|
decrease EDV, decrease BP, increase contractility (reflex response), increase HR (reflex response), decrease ejection time
|
|
Antianginal therapy: What is the effect of Beta-blockers on: diastolic volume, blood pressure, contractility, heart rate, ejection time?
|
increase EDV, decrease BP, decrease contractility, decreased HR, increase ejection time
|
|
Antianginal therapy: The effects of using nitrates and Beta-blockers together will: a) decrease myocardial oxygen demands by the same amount as using either alone, b) decrease myocardial oxygen demands by an amount greater than if each were used alone, or c) have no effect on myocardial oxygen demand
|
b) Decrease myocardial oxygen demands by an amount greater that if each were used alone
|
|
Antianginal therapy: Nifedipine blocks -- channels
|
calcium
|
|
Antianginal therapy: In its effects on myocardial oxygen consumption, is Nifedipine similar to Nitrates or B-blockers?
|
Nitrates (Nifedipine is similar to Nitrates)
|
|
Antianginal therapy: In its effects on myocardial oxygen consumption, is Verapamil similar to Nitrates or B-blockers?
|
B-blockers
|
|
Nitroglycerine, isosorbide dinitrate: Dose nitroglycerin dilate arteries or veins more?
|
Veins>>arteries
|
|
Nitroglycerine, isosorbide dinitrate: Does nitroglycerin increase or decrease cGMP in smooth muscle?
|
Increase
|
|
Nitroglycerine, isosorbide dinitrate: In industrial exposure to nitroglycerine, weekend withdrawal is characterized by which three symptoms?
|
Tachycardia, dizziness , and headache ("Monday disease")
|
|
Nitroglycerine, isosorbide dinitrate: Toxic dosage of nitroglycerine causes which three symptoms?
|
Tachycardia, hypotension, headache
|
|
Cardiac drugs: sites of action: Digitalis has its action on which cell membrane transporter?
|
Na/K ATPase
|
|
Cardiac drugs: sites of action: Ryanodine has its action on which channel?
|
Calcium release channel in the sarcoplasmic receptor
|
|
Cardiac drugs: sites of action: Calcium enters cardiac cells through which channel?
|
Voltage-gated calcium channel
|
|
Cardiac drugs: sites of action: Cytoplasmic calcium concentrations in cardiac cells can be decreased by sequestering calcium in the sarcoplasmic reticulum. Calcium enters the SR through which transporter?
|
Calcium pump in the wall of the SR
|
|
Cardiac drugs: sites of action: Calcium channel blockers have their effect on which calcium transporters?
|
Voltage-gated calcium channel
|
|
Cardiac Glycosides: What is digoxin's effect on the intracellular Na+ level?
|
Increase
|
|
Cardiac Glycosides: What is digoxin's effect on the intracellular calcium level?
|
Increase
|
|
Cardiac Glycosides: Name two ECG changes ellicited by digoxin administration
|
There are 4: increase PR, decrease QT, scooping of ST segment, T-wave inversion
|
|
Cardiac Glycosides: Name three symptoms of digoxin toxicity
|
Nausea, vomiting, diarrhea, blurry vision, arrhythmia
|
|
Cardiac Glycosides: Which potentiates the effects of digoxin- hypo- or hyperkalemia?
|
hypokalemia
|
|
Antiarrhythmics- Na+ channel blockers (classI): Which phase of the cardiac action potential do antiarrhythmics decrease the slope of?
|
Phase 4 depolarization
|
|
Antiarrhythmics- Na+ channel blockers (classI): What type of antiarrhythmic is Amiodarone?
|
Class 1A (Class 1A includes Quinidine, Amiodarone, Procainamide, Disopyramide, "Queen Amy Proclaims Diso's pyramid."
|
|
Antiarrhythmics- Na+ channel blockers (classI): Do class 1A antiarrhythmics increase or decrease the effective refractory period, AP duration, and QT interval?
|
Increase ERP, increase AP duration, increase QT interval
|
|
Antiarrhythmics- Na+ channel blockers (classI): What do class 1B antiarrhythmics do to the AP duration?
|
Decrease AP duration
|
|
Antiarrhythmics- Na+ channel blockers (classI): What type of antiarrhythmic is mexiletine?
|
Class 1B (includes Lidocaine, mexiletine, tocainide)
|
|
Antiarrhythmics- Na+ channel blockers (classI): What type of antiarrhythmic is encainide?
|
Class IC (includes flecainide, encainide, propafenone)
|
|
Antiarrhythmics- Na+ channel blockers (classI): What effect do class 1C antiarrhythmics have on the AP duration?
|
No effect!
|
|
Antiarrhythmics- Beta-blockers (classII): What does esmolol do to the cAMP in cardiac cells?
|
decreases cAMP (a beta-blocker)
|
|
Antiarrhythmics- Beta-blockers (classII): What does atenolol do the calcium currents in cardiac cells?
|
decreases calcium current (beta-blocker)
|
|
Antiarrhythmics- Beta-blockers (classII): Timolol decreases the slope of which phase of the cardiac AP cycle?
|
Phase 4 (a beta-blocker)
|
|
Antiarrhythmics- Beta-blockers (classII): What does propanolol do the the PR interval?
|
Increases interval (beta-blocker)
|
|
Antiarrhythmics- Beta-blockers (classII): Is esmolol a short- or long-acting beta blocker?
|
short-acting
|
|
Antiarrhythmics- K+ channel blockers (class III): Does amiodarone increase or decrease AP duration?
|
Increase (K+ channel blocker)
|
|
Antiarrhythmics- K+ channel blockers (class III): Does sotalol increase or decrease the effective refractory period?
|
Increase (K+ channel blocker)
|
|
Antiarrhythmics- K+ channel blockers (class III): Does bretylium increase or decrease the QT interval?
|
Increase (K+ channel blocker)
|
|
Antiarrhythmics- K+ channel blockers (class III): Name a symptom of sotalol toxicity.
|
Torsades de pointes (K+ channel blocker)
|
|
Antiarrhythmics- K+ channel blockers (class III): Name three of the symptoms of amiodarone toxicity.
|
Pulmonary fibrosis, corneal deposits, hepatoxicity, skin deposits resulting in photodermatitis, neurologic effects, constipation, bradychardia, heart block, CHF, hypothyroidism/hyperthyroidism. (Therefore, should check PFTs, LFTs, and TFTs)
|
|
Antiarrhythmics- Ca2+ channel blockers (class IV): Does verapamil increase or decrease the conduction velocity of the AV nodal cells?
|
Decrease (calcium channel blocker)
|
|
Antiarrhythmics- Ca2+ channel blockers (class IV): How does diltiazem affect the effective refractory period and the PR interval?
|
Increases ERP, increases PR (calcium channel blocker)
|
|
Other antiarrhythmics: Name a potential use of Mg+ to treat arrhythmias.
|
To treat torsades de pointes and digoxin toxicity
|
|
Other antiarrhythmics: Name a potential use of K+ to treat arrhythmias.
|
Depress ectopic pacemakers, especially in digoxin toxicity
|
|
Other antiarrhythmics: Name a use of adenosine in treating arrhythmias.
|
To diagnose and abolish AV nodal arrhythmias.
|
|
Lipid-lowering agents: What is the effect of cholestyramine on the serum triglyceride level?
|
Slight increase (cholestyramine is a bile acid resin)
|
|
Lipid-lowering agents: What is the effect of colestipol on HDL?
|
No effect! (colestipol is a bile acid resin)
|
|
Lipid-lowering agents: What is the effect of lovastatin on HDL?
|
Increase (lovastatin is an HMG-CoA reductase inhibitor)
|
|
Lipid-lowering agents: Name 2 side effects of pravastatin.
|
Increase LFTs and cause myositis (prevastatin is an HMG-CoA reductase inhibitor)
|
|
Lipid-lowering agents: What is the effect of Niacin on HDL?
|
Increase
|
|
Lipid-lowering agents: What are the side effects of clofibrate?
|
Incease LFTs and cause myositis (Clofibrate is a "Fibrate")
|
|
Lipid-lowering agents: Which increases HDL most: simvastatin, niacin, or gemfibrozil?
|
Niacin
|
|
Lipid-lowering agents: Which decreases triglyceride level most: colestipol, Atorvastatin, niacin, or bezafibrate?
|
Bezafibrate
|
|
Lipid-lowering agents: What is the main effect of ezetimibe?
|
decrease serum LDL (a cholesterol absorption inhibitor)
|
|
Lipid-lowering agents: Gemfibrozil increases the activity of which enzyme?
|
Lipoprotein lipase (which converts VLDL to IDL)
|
|
Lipid-lowering agents: AUTHOR
|
Rafael Vazquez
|
|
Arachidonic acid products: What enzyme breaks down membrane lipid into arachidonic acid?
|
Phospholipase A2
|
|
Arachidonic acid products: What two enzymes are responsible for the production of Hydroperoxides (HPETEs) and Endoperoxidases, respectively from arachidonate?
|
Lipoxygenase= HPETE, Cyclooxygenases=endoperoxidases
|
|
Arachidonic acid products: What major class of products do HPETEs give rise to?
|
Leukotrienes
|
|
Arachidonic acid products: What are the 3 major products of Endoperoxidases?
|
Prostacyclin (PGI), Prostaglandins (PGE, PGF), Thromboxane (TXA)
|
|
Arachidonic acid products: In general what effect do leukotrienes have on bronchial tone?
|
Leukotrienes in general increase bronchial tone
|
|
Arachidonic acid products: In the arachodonic acid pathway, what two enzymes do corticosteroids block?
|
Phospholipase A2, COX-2
|
|
Arachidonic acid products: NSAIDs, Acetaminophen and COX-2 inhibitors block which arachadonic acid pathway enzymes
|
NSAIDs-non-selectively block COX-1 and COX-2, acetaminophen doesn't block COX-1 or COX-2, but instead it may block COX-3 in found in the brain, COX-2 inhibitors block COX-2
|
|
Arachidonic acid products: What are the 4 major effects of Prostacyclin
|
decrease platelet aggregation, decrease vascular tone, decrease bronchial tone, decrease uterine tone
|
|
Arachidonic acid products: What are the 3 major effects of Prostaglandins
|
increased uterine tone, decrease vascular tone, decrease bronchial tone
|
|
Arachidonic acid products: What are the 3 major effects of Thromboxane
|
increase platelet aggregation, increase vascular tone, increase bronchial tone
|
|
Arachidonic acid products: Zileuton is a ________ pathway inhibitor?
|
Lipoxygenase
|
|
Arachidonic acid products: Zariflukast is associated with what enzymes?
|
Lekukotrienes
|
|
Asthma drugs: Bronchodilation is mediated by what molecule
|
cAMP
|
|
Asthma drugs: Bronchoconstriction is mediated by _________ and ___________
|
Ach and adenosine
|
|
Asthma drugs: How many asthma drug categories are there?
|
7- (1) nonspecific B-agonists, (2) B2 agonists, (3) Methylxanthines, (4) muscarinic antagonist, (5) cromolyn, (6) corticosteroids, (7) Antileukotrienes
|
|
Asthma drugs: What is the only nonspecific B-agonist drug and what are its effects?
|
Isoprotenerol-relaxes bronchial smooth muscle (B2) and tachycardia (B1) (adverse effect).
|
|
Asthma drugs: What are the two B2 selective agonist asthma drugs?
|
Albuterol- relaxes bronchial smooth muscle (B2), Salmetrol
|
|
Asthma drugs: What are the indications for Albuterol and Salmetrol, respectively?
|
Albuterol- use during acute exarcebation, Salmetrol- long-acting agent for prophylaxis
|
|
Asthma drugs: what are the notable adverse effects of B2 agonist?
|
arythmias and tremor
|
|
Asthma drugs: B2-agonists activate this enzyme in bronchial smooth muscle that leads to an increase in ________ = bronchodilation
|
B2 agonists activate adenylate cyclase and increase conversion of ATP to cAMP
|
|
Asthma drugs: What are the likely mechanism of action theophylline?
|
bronchodialation by inhibition phosphodiesterase (PDE), decreasing cAMP hydrolysis and antagnonizing adenosine action
|
|
Asthma drugs: Why is usage of theophylline limited?
|
limited b/c narrow therapeutic index (cardiotoxicity, neurotxicity)
|
|
Asthma drugs: What kind of drug is Ipratropium?
|
muscarinic antagonist
|
|
Asthma drugs: How does mechanism of action of Ipratropium?
|
competitive block of muscarinic receptors= prevention of bronchoconstriction
|
|
Asthma drugs: cromolyn works by inhibiting the release of _______ from ______ cell?
|
prevents release of medicators from mast cells
|
|
Asthma drugs: Cromolyn is mainly used for the ______ of athsma and it is not indicated for _______ treatment of athsma?
|
Used only for prophylaxis, not effective during acute episode. Also, toxicity rare
|
|
Asthma drugs: __________and ________ are two major corticosteroids used for treatment of what kind of asthma?
|
Beclomethasone and prednisone are 1st line therapy for chronic asthma
|
|
Asthma drugs: What is the mechanism of action of corticosteroids?
|
inhibits the synthesis of virtually of cytokines-->inactivates NF-KB, the transcription factor that induces the production of TNF-a, amonth other inflammatory agents.
|
|
Asthma drugs: Zileuton blocks the conversion of _______ to ________.
|
zileuton is a 5-lipoxygenase pathway inhibitior. Blocks the conversion of arachidonic acti to leukotrienes
|
|
Asthma drugs: Zafirlukast works by_______ ________ ________
|
bloking leukotriene receptors
|
|
Asthma drugs: What the most basic asthma treatment strategy?
|
avoidance of exposure to antingen (dust, pollen, etc)
|
|
Asthma drugs: After exposure to antigen crosslinks IgE on mast cells. This is prevented by the following drugs: _________ and ________
|
cromolyn and steroids
|
|
Asthma drugs: Following allergen exposure mediators are released (ex. _______ and _________). This triggers an ______ asthmatic response characterized by ________ and may be treated with the following 3 asthmatic drug categories to treat the symptoms.
|
examples of mediators are leukotrienes and histamine. Following allergen exposure an early asthmatic response characterized by bronchoconstriction that can be treated with B-agonsists, methylxanthines, and muscarinic antagonists.
|
|
Asthma drugs: Also, mediators elicit a ________ response is which leads to bronchial __________ and is treated with __________.
|
mediators elicit a late response and this leads to bronchial hyperactivity. This is best treated with steroids.
|
|
GI therapy: the following questions are from the diagram at the top of the page
|
0
|
|
GI therapy: _____ cells are predominatly found in the antrum and _________ cells are predominatly found in the fundus.
|
Gastrin cells are predominant in the antrum and parietal cells are predominant in the fundus.
|
|
GI therapy: What are the 3 main stimuli of acid secretion?
|
Ach, histamine, gastrin
|
|
GI therapy: Gastrin stimulates the ECL cells to secrete histamine that stimulates ______ cells. Gastrin also activate the ______ cells to increase expression of _______ that increases ______secretion.
|
Gastrin stimulates the ECL cells to secrese histamine that stimulates parietal cells. Parietal cells are also activated by gastrin to increase the expression of the H,K ATPase that increases acid secretion.
|
|
GI therapy: This type of drug acts by inhibiting M1 and M3 receptors on ECL cells and Parietal cells, respectively.
|
muscarinic antagonists block M1 receptors in ECL cells and M3 receptors in parietal cells.
|
|
GI therapy: This type of drug inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the _____ receptor.
|
H2 blocker inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the parietal H2 receptor.
|
|
GI therapy: The most direct way of inhibiting acid secretion is by using this type of drug which acts on this enzyme.
|
the most direct way of inhibiting acid secretion is by using proton pump blockers which inhibit the H,K ATPase on parietal cells.
|
|
GI therapy: ____________ acts by binding to the ulcer and increasing its healing. It may interfere with drug absorption in the stomach.
|
sucralfate binds to the ulcer base and provides physical protection. It allows HCO3- secretion to reestablish pH gradient in the mucus layer.
|
|
GI therapy: What hormone binds ECL cells and decreases acid secretion?
|
somatostatin
|
|
GI therapy: These type of drugs used to decrease pH in the stomach.
|
antacids….duh….jk. (I was instructed to make a question of every word)
|
|
GI therapy: questions not from the diagram
|
0
|
|
GI therapy: ____________, ___________, ___________, and ___________ are examples of H2 blockers and they act by (reversibly/irreversibly)
|
cimetedine, ranitidine, famotidine, nizatidine reversilbly block H2 receptors.
|
|
GI therapy: This H2 blocker is the only one that has many side effects which include potent inhibition of ______, _____ effects, and _____ renal excretion of creatinine.
|
cimetedine is a potent inhibitor of P450, it has antiandrogenic effect and decrease renal excretion of creatinine. Other H2 blockers are relatively free of these effects.
|
|
GI therapy: _________ and _________ (reversibly/irreversibly) inhibit the H/K ATPase in the stomach _______cells.
|
Omeprazole and Iansoprazole irreversibly inhibit the H/K ATPase in stomach parietal cells
|
|
GI therapy: Proton pump inhibitors are indicated for peptic ulcer, ________, _______, and _________ syndrome
|
peptic ulcer, gastritis, esophageal reflux, and Zollinger-Ellison syndrome
|
|
GI therapy: T/F: Bismuth and sucralfate allow HCO3- secretion.
|
True: bismuth and sucralfate bind to ulcer base and provide physical protection, and allow HCO3- secretion to reestablish pH gradient in the mucus layer=increased ulcer healing
|
|
GI therapy: T/F: misoprostol is a PGE2 analog and increases the production and secretion of gastric mucous barrier.
|
False: misoprostol is a PGE1 analog and it increases the production and secretion of gastric mucous barrier.
|
|
GI therapy: What are the 3 indications for misoprosol?
|
prevention of NSAID-induced peptic ulcers, maintains a PDA and used to induce labor
|
|
GI therapy: In what population is misoprostol contraindicated?
|
women of childbearing potential (abortifacient). It also casues diarrhea
|
|
GI therapy: Infliximab is ___________ against ______.
|
monoclonal antibody to TNFa
|
|
GI therapy: The clinical indication for Infliximab is:
|
Crohn's, along with fistula healing
|
|
GI therapy: T/F: Infliximab can cause respiratory infection, fever, hypotension
|
TRUE
|
|
GI Drugs (cont.): This drug offers both anitbacterial action and anti-inflamatory effects. It is used for 2 inflammatory GI diseases ______ and _______.
|
sulfasalazine: combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory effects). It is used for Ulcerative colitis and remission of Crohn's.
|
|
GI Drugs (cont.): T/F: Side effects of the above include: malaise, sulfonamide toxicity, neutropenia
|
false: side effects: malaise, nausea, sulfonamide toxicity
|
|
GI Drugs (cont.): ___________ is a powerful central-acting antiemetic. It acts by antagonizing the______ receptor.
|
Ondansetron: is a powerful antiemetic. Think: you will not vomit with ondansetron, so you can go on dancing.
|
|
GI Drugs (cont.): T/F used to treat vomiting preoperatively and for cancer chemo therapy pts.
|
False: it is used to treat vomiting postoperatively.
|
|
GI Drugs (cont.): Headache and __________ are side effects
|
constipation (can't vomit or poop)
|
|
GI Drugs (cont.): Antacid overuse can affect:_________, __________, or ______ excretion of other drugs by altering ______ and ______ pH or by delaying gastric _________.
|
Antacid overuse can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
|
|
GI Drugs (cont.): Constipation and (hypo/hyper) phosphatemia is seen with overuse of ________________
|
aluminum hydroxide - Aluminimum amt. of feces
|
|
GI Drugs (cont.): Magnesium hydroxide overuse = ___________
|
diarhea; Mg = Must go to the bathroom
|
|
GI Drugs (cont.): Calicium carbonate= hypercalcemia and (increase/decreased) acid
|
causes hypercalcemia and increased acid.
|
|
GI Drugs (cont.): T/F: hyperkalemia can be seen with AlOH, MgOH, CaCO2
|
False! hypokalemia
|
|
heparin: Catalyzes activation of ____________, decreases ________ and __________. It has a ____t1/2. check PTT
|
catalyzes the activation of antithrombin III, decreases thrombin and Xa. It has a short t1/2
|
|
heparin: It is used for immediated anticoagulation for pulmonary embolism,_______, _______, MI, and ________. Follow PTT
|
used for pulmonary embolism, stroke, angina, MI, and DVT.
|
|
heparin: T/F: Is used during pregnancy
|
true: it is used during pregnancy because it does not cross the placenta.
|
|
heparin: It can cause bleeding,___________, and drug-drug interactions.
|
thrombocytopenia
|
|
heparin: ___________ is used for rapid reversal of heparization (it is a _______ charged molecule that binds the ________ charged heparin)
|
protamine sulfate is used for rapid reversal of heparinization (it is a positively charged molecule that binds the negatively charged heparin).
|
|
heparin: Newer________________ (enoxaparin) act more on _____, have better bioavailability and 2-4 times longer t1/2. Can be administered subcut and (with/without) lab monitoring.
|
lower-molecular-weight heparins (enoxaparin) act more on Xa, have better bioavailabitlity and 2-4 times longer half-life. Can be adm. Subcut and without lab monitoring.
|
|
warfirin (coumandin): Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent factors ___, ___, ___, and ___, also, ___ and ___ via ______ antagonism.
|
Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X, protein C and S via vitamin K antagonism.
|
|
warfirin (coumandin): t1/2 (short/long)
|
long
|
|
warfirin (coumandin): Used for _______ anticoagulation. Follow PT
|
WEPT - Warfirin affects the Extrinsic pathway and prolongs PT
|
|
warfirin (coumandin): T/F: is used during pregnacy
|
False! (warfarin, unlike heparin, can cross the placenta).
|
|
warfirin (coumandin): Toxicity: bleeding, _________, drug-drug interactions
|
teratogenic
|
|
heparin vs. warfarin: Heparin is a (large/small) _____charged acicid polymer while Warfarin is (large/small) (charged/neutral) molecule
|
Heparin is a large negatively charged acidic polymer while Warfarin is a small neutral charged lipid-soluble molecule
|
|
heparin vs. warfarin: T/F: Heparin is given orally while warfarin is given SC/IV
|
False! Heparin is given IV/SC and warfarin is give oral
|
|
heparin vs. warfarin: Site of action: heparin _________, warfarin ______
|
heparin's site of action is the blood; warfarin's site of action is the liver (synthesises clotting factors)
|
|
heparin vs. warfarin: Onset of action of _________ is slow; the onset of action of ______ is rapid
|
onset of action of heparin is rapid (secs) and the onset of action of warfarin is slow, limitd by t1/2 of normal clotting factors.
|
|
heparin vs. warfarin: Warfarin works by imparing the synthesis of _______ dependent factors __, ___, ___, and ___ also _____, and ____; heparin activates _____, ____ and ___
|
Warfarin works by imparing the synthesis of vitamin K dependent factors II, VII, IX, and X also protein S and protein C; heparin activates ATIII, Iia (thrombin) and Xa.
|
|
heparin vs. warfarin: Heparin 's duration of action is (acute/chronic); warfarin's duration of action is (actue/chronic)
|
Heparin's duration of action is actute and warfarin's duration of action is chronic.
|
|
heparin vs. warfarin: Tx of acute OD: Heparin = _________; warfarin=______
|
Tx of heparin OD is protamine sulfate; Tx of warfarin= IV vit. K and fresh frozen plasma.
|
|
heparin vs. warfarin: Warfarin is monitored by _________ while Heparin is monitored by ___________.
|
Warfrin is monitored by PT (extrinsic pathway) (WEPT) and heparin is monitored by PTT (intrinsic pathway)
|
|
Thrombolytics: questions from diagram at bottom of page
|
0
|
|
Thrombolytics: plasmin is the major ___________ enzyme. It breaks down both _______ and _______
|
fibrinolytic enzyme. It accelerates breaks down of both fribin and fibrinogen yielding fibrin splip products and degradation products, respectively.
|
|
Thrombolytics: Fibrinogen is converted to fibrin by _________
|
thrombin
|
|
Thrombolytics: tPA and urokinase promote the converson of ______ to ________ thereby increasing fibrinolysis.
|
plasminogen to plasmin
|
|
Thrombolytics: Various stimuli activate a blood proactivator to a blood activator that promotes conversion of _________ to blank thereby increasing fibrinolysis
|
plasminogen to plasmin
|
|
Thrombolytics: Streptokinase and anistreplase both activate and Activator that increases convesion of plasminogen to plasmin.
|
0
|
|
Thrombolytics: Aminocaproic acid:____________ fibrinolysis.
|
inhibits fibrinolysis by inhibition of plasminogen conversion to plasmin.
|
|
Thrombolytics: 4 examples of thrombolytics include: ________, _________, _____________, and ___________
|
Streptokinase, urokinase, tPA(altepalse), APSAC (anistreplase)
|
|
Thrombolytics: work by directly or indirectly aiding the conversion of ___________ to __________, which cleaves ______ and ________ clots. tPA specifically coverts _______________ to plasmin
|
Directly or indirectly aid conversion of plaminogen to plasmin, which cleaves thrombin and fribrin clots. It is claimed that tPA specifically coverts fribrin-bound plasminogen to plasmin.
|
|
Thrombolytics: T/F: clinical use is for DVTs
|
False: used for early MI
|
|
Thrombolytics: pts. receiving this medication are at most risk for: ______
|
bleeding
|
|
Hematologic Drugs: mechanism of antiplatelet interaction
|
0
|
|
Hematologic Drugs: questions from diagram at top of page
|
0
|
|
Hematologic Drugs: When a break in the endothelium occurs _________ and _________ are exposed.
|
collagen and vWF
|
|
Hematologic Drugs: Platelets are activated by binding to the above macromolecules. The two structures expressed by the platelets involved in this process are __________ and _________ and they bind to _________ and __________, repectively
|
Platelets bind to collagen and vWF. The two structures expressed by platelets that are involved in this process are GP 1a and GP 1b. GP 1a and GP 1b bind to collagen and vWF, respectively.
|
|
Hematologic Drugs: After platelet activation _________ is expressed on their surface. What is the role of this structure?
|
after platelets are activated they express GP IIb/IIIa. This molecule is important in platlelet-platelet aggregation.
|
|
Hematologic Drugs: _________ and _________ interaction is needed in order for platelet aggregation to occur.
|
GP IIb/IIIa and fribinogen
|
|
Hematologic Drugs: 5-HT, _______, and ________ are molecules that play a role in the glycoprotein expression of activated platelets.
|
5-HT, ADP, and TxA2 are molecules that play a role in the glycoprotein expression of activated platelets.
|
|
Hematologic Drugs: Aspirin acts by inhibiting production of ________ that in turn inhibits glycoprotein expression in activated platelets.
|
TxA2
|
|
Hematologic Drugs: ADP production is inhibited by the drug _________.
|
ticlopidine
|
|
Hematologic Drugs: This antibody drug targets the _______ on platelets.
|
Abciximab
|
|
Copidogrel, ticlopidine: T/F: inhibits platele aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen
|
TRUE
|
|
Copidogrel, ticlopidine: It is used for ______ ________ syndrome, coronary _______, and it has been shown to decrease the incidence or recurrence of___ ____.
|
it is used for acute coronary syndrome, coronary stenting. Decreases incidence or recurrence of thrombotic stroke
|
|
Copidogrel, ticlopidine: Ticlopidine is associated with_________ as a side effect.
|
Ticlopidine causes neutropenia and it is reserved for those who cannot tolerate aspirin.
|
|
Abciximab: This drug binds to __________ on activated platelets.
|
gp IIb/Iia
|
|
Abciximab: It is used for ___________ and ________ _________ ___________ ___________
|
acute coronary syndromes and percutanous transluminal coronary angioplasty
|
|
Abciximab: toxiciites are _______ and ________
|
bleeding and thrombocytopenia
|
|
Aspirin: It ________ and (reversibly/irreversibly) inhibits COX1 and COX2 to prevent the conversion of _______ to prostaglandins.
|
acetilates and irreversably inhibits COX-1 and COX-2
|
|
Aspirin: T/F: aspirin has an effect of PT, PTT
|
false it has no effect
|
|
Aspirin: What are the 4 A's of aspirin and NSAIDS in general
|
Antipyretic, Analgesic, Anti-inflam, antiplatelet
|
|
Aspirin: Important toxicities include _________, bleeding, hyperventilation, __________- in children, and CN ____ toxicity
|
gastric ulceration, bleeding, hyperventilation, Reyes syndrome and tinnitus (CNVIII).
|
|
diabetes drugs: AUTHOR
|
Marc Waase
|
|
Endocrine Drugs: Hydrocortisone, prednisone, triamcinolone, dexamtasone, bleclomethasone are examples of what kind of drugs?
|
Glucocorticoid
|
|
Endocrine Drugs: Glucocorticoids decrease the production of ___ and ____
|
Leukotrienes and prostanglandins
|
|
Endocrine Drugs: To treat Addison's disease, inflammation, immune suppression, asthma, use ____
|
Glucocorticoids
|
|
Endocrine Drugs: An important side-effect of Glucocortioid usage is ____
|
Iatrogenic Cushing's Syndrome
|
|
Endocrine Drugs: Buffalo hump, moon facies, truncal obesity, muscles wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers characterize what syndrome?
|
Cushing's Syndrome
|
|
Reproductive Drugs: Which two drugs inhibit cGMP phosphodiesterase, leading to smooth muscle relaxation in the corpus cavernosum and penile erection?
|
Sildenafil and Verdenafil --they fill the penis
|
|
Reproductive Drugs: What class of drugs are used tto treat erectile dysfunction
|
cGMP Inhibitors
|
|
Reproductive Drugs: CGMP inibitors taken with ____have a high risk of liofe-threeatening hypotension
|
nitrates
|
|
Reproductive Drugs: Which drugs is a partial agonist of estrogen recpetors in the pituitary gland, stimulating increase in LH and FSH, which stimulates ovulation to treat infertility
|
clomiphene
|
|
Reproductive Drugs: Clomiphene's side effects include:
|
Hotflashes, ovarian enlargment, multiple simultaneous pregnancies, visual disturbances
|
|
Reproductive Drugs: What abortifacient is a competitite inhibitor of preogestins at progesterone recpetor and may lead to heavy menstrual-like bleeding?
|
Mifepristone (RU486)
|
|
Reproductive Drugs: The advantage of this drug is that it is reliable, decreases incidence of ectopic pregnancy, decreases risk of pelvic infections, and regulates menses; however it also puts you in a hypercoagulable stat and may increase your trigylcerides, weight, and blood pressure
|
Oral Contracpetices - syntheitc progestins/estrogen
|
|
Rheumatologic Drugs: ____is converted to uric acid which leads to gout
|
Xanthine (converted from excess purines)
|
|
Rheumatologic Drugs: This drug depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation, and used to treat acute gout
|
Colchicine
|
|
Rheumatologic Drugs: This drugs inhibits reabsorption of uric acid and used to treat chronic gout
|
Probenecid
|
|
Rheumatologic Drugs: This drug is used to treat chronic gout, but also inhbits secretion of penicillin
|
Probenecid
|
|
Rheumatologic Drugs: This drugs inhibits xanthine oxidase decreasing the conversion fo xanthine to uric acid
|
Allopurinol
|
|
Oncologic Drugs: What are the cell cycle specific oncologic drugs
|
antimetabolites, plant alkaloids, stroid hormones, bleomycin, paclitaxel, etoposide
|
|
Oncologic Drugs: What are the cell cycle Nonspecific oncologic drugs?
|
alkylating agents and antibiotics
|
|
Oncologic Drugs: ____is an S-phase-specific anti-metabolite that is an folic acid analog that inhibits dihydrofolate reducate decreasing dTMP(thymidine and purines) and decreaing DNA/prtein synthesis.
|
Methotrexate
|
|
Oncologic Drugs: ____is an S-phase-specific anti-metabolite that is a pyrmidine analog which complexed to folic acid, inhibiting thymidylate synthase, decreasing dTMP and decreasing DNA/protein synthesis
|
5-Fluorouracil (5-FU)
|
|
Oncologic Drugs: Myelosuppression by methotrxate is reversible with ____
|
leucovorin (folinic acid) rescue
|
|
Oncologic Drugs: Which drug blocks purine synthesis and is used to treat leukemias, lymphomas (not CLL or Hodgkins)
|
6-mercaptopurine (6-MP)
|
|
Oncologic Drugs: Which drug alkylates DNA and is used to treat CML?
|
Busulfan
|
|
Oncologic Drugs: Which drug inhibits DNA polymerase and is used to treat AML?
|
cytarabine
|
|
Oncologic Drugs: This drug used to treat Leukemias and Lymphomas is metaboilized by xanthine oxidase
|
6-mercaptopurine (6-MP)
|
|
Oncologic Drugs: Used to treat leukemias, lymphomas, choricarcinoma, sacromas, rheumatoid arthritis, psoriasis, and can be an abortifacient; it may lead to myelosuppression
|
Methotrexate
|
|
Oncologic Drugs: Used to treat colon cancer and other solid tumors, basal cell carcinoma (topically)
|
5-Fluorouracil (5-FU)
|
|
Oncologic Drugs: Myelosuppression by 5-FU is ______
|
Not reversible
|
|
Oncologic Drugs: This drug used to treat AML may lead to leukopenia, thrombocytopenia, megaloblastic anemia?
|
cytarabine
|
|
Oncologic Drugs: This drugs used to treat CML may lead to pulmonary fibrosis and hyperpigmentation?
|
Busulfan
|
|
Oncologic Drugs: ____is an alkylating agent acivated by liver that covalently x-links DNA at guanine N-7, and is used to treat non-hodgkin's lymphoma, breast/ovarian carcinomas
|
cyclophosphamides
|
|
Oncologic Drugs: ____ alkylates DNA after bioactivation and can cross the BBB and treats brain tumors (glioblastoma multiforme)
|
Nitrosoureas (Carmustine, lomustine, semustine, streptozocin)
|
|
Oncologic Drugs: ____acts like an alkylating agent, x-linking via hyrdolysis of Cl and platinum; used to treat testicular, bladder, lung carcinomas
|
Cisplatin
|
|
Oncologic Drugs: This alkylating agent can cause myelosuppression and hemorhagic cystitis
|
cyclophosphamides
|
|
Oncologic Drugs: This combination of drugs is used to treat Hodgkin's and myelomas, sarcomas, and solid tumors (breast, ovary, lung)
|
ABVD: Adriamycin, Bleomycin, Vinblastine, Dacarbazine
|
|
Oncologic Drugs: ____noncovalently intercalates in DNA, creating breaks to decrease replication and transcription
|
Doxorubicin (adriamycin)
|
|
Oncologic Drugs: ____intercalates DNA strands and induces free radical fromation which causes strand breaks
|
Bleomycin, Dactinomycin
|
|
Oncologic Drugs: Which drugs causes cardiotoxicity, alopecia, and myelosuppression?
|
Doxorubicin (adriamycin)
|
|
Oncologic Drugs: Which drug is used to trat oat cell carcinoma of the lung and prostate/testicular carcinoma?
|
Etoposide
|
|
Oncologic Drugs: This combination of drugs is used to treat lymphoma, CLL, Hodgkin's, Wilm's tumor, choriocarcinoma
|
MOp (Mustargen, Oncovin (Vincristine), Procarbazine (Matulane), Prednisone)
|
|
Oncologic Drugs: Which glucocorticoid may trigger apoptosis and may even work on nondividing cells
|
Prednisone
|
|
Oncologic Drugs: This drug is a G2-phase specific inhibitor of Topisiomerase II, leaving double strand breaks in DNA following DNA replication
|
Etoposide
|
|
Oncologic Drugs: This drug used to treat testicular cancer and lymphomas may cayse pulmonary fibrosis, skin chnages, and myelosuppression
|
Bleomycin, Dactinomycin
|
|
Oncologic Drugs: This drugs used as an immunosuppressant and in lymphomas may cause acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis?
|
Prednisone
|
|
Oncologic Drugs: ____is an estrogen receptor mixed agonist/antagonist that blocks the binding of estrogen to ER+ cells.
|
Tomoxifen/Raloxifene
|
|
Oncologic Drugs: ____is n M-phase-specific alkaloid that binds to tubulin and blocks polymerization of microtubules, preventing spindle formation
|
Vincristine and Vinblastine
|
|
Oncologic Drugs: ____is an M-phase-specific agen that binds to tubulin and hyperstabilizes the polymerized microtubules, so that the mitotic spindle cannot break down
|
Paclitaxel
|
|
Oncologic Drugs: What drugs is used to treat breast cancer, but may increas the risk of endometrial carcinomas and hot flashes
|
Tomoxifen
|
|
Oncologic Drugs: Side-effects of Vinblastine include….
|
VinBASTine BLASTs Bone Morraow, causing myelosupression, as well as neurotoxicity and paralutic ileus.
|
|
Oncologic Drugs: Side effects of Paclitaxel include….
|
Myelosupression and hypersensitivity
|
|
Immunosuppressants and Cytokine Therapy: This drug binds to cyclophilins, blocking differentiation and activation of T cells mainly by inhibiting IL2 production
|
cyclosporine
|
|
Immunosuppressants and Cytokine Therapy: This antimetabolite derivative of 6-mercaptopurine interferes with the metabolism and synthesis of nucleic acid, therefore toxic to proliferating lymphocytes
|
azathioprine
|
|
Immunosuppressants and Cytokine Therapy: This potent immunosuppressive drug binds to the FK-binding protein and inhibits secretion of IL2 and other cytokines
|
tacrolimus (FK506)
|
|
Immunosuppressants and Cytokine Therapy: This drug is used to suppress organ rejection after transplantation, but may predispose patient to viral infections and lymphoma
|
cyclosporine
|
|
Immunosuppressants and Cytokine Therapy: Azaothioprine is used to in what setting?
|
Kidney transplants, autoimmune disorders (glomerulonephritis, hemolytic anemia)
|
|
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- Aldesleukin (interleukin-2) is used for?
|
Renal cell carcinoma, metastatic melanoma
|
|
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- Erythropoietin (epoetin) is used for?
|
anemia
|
|
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- Filgrastim is used for?
|
Recovery of Bone Marrow; it is a granulocyte colony stimulating factor
|
|
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- alpha interferon is used for?
|
Hep B/C, Kaposi's sarcoma, leukemia, malgnant melanoma
|
|
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- beta interferon is used for?
|
Multiple Sclerosis
|
|
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- gamma interferon is used for?
|
Chronic Granulomatous disease
|
|
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- oprelvekin (interleukin2) is used for?
|
Thrombocytopenia
|
|
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- sargamostim is used for?
|
Recovery of Bone Marrow (it is a granulocyte-macrophage colony stimulating factor)
|
|
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- thrombopoietin is used for?
|
Thrombocytopenia
|
|
Toxicology: What is the antidote for acetaminophen toxicity/overdose
|
N-acetylcysteine
|
|
Toxicology: What is the antidote for salicylates toxicity/overdose
|
Alkanize urine/dialysis
|
|
Toxicology: What is the antidote for antichoinesterase toxicity/overdose
|
Atropine, pralidoxime
|
|
Toxicology: What is the antidote for antimuscarinic/anticholinergic agents toxicity/overdose
|
physostigimine salicylate
|
|
Toxicology: What is the antidote for Beta-blockers toxicity/overdose
|
glucagon
|
|
Toxicology: What is the antidote fordigitalis toxicity/overdose
|
Stop digitalis, Normalize K+, lodpcaine, anti-digitialis Fab Fragments, Magnesium
|
|
Toxicology: What is the antidote for lead toxicity/overdose
|
CaEDTA, dimercaprol, succimer, penicillamine
|
|
Toxicology: What is the antidote for iron toxicity/overdose
|
Deferoxamine
|
|
Toxicology: What is the antidote for aresnic/mercury/gold toxicity/overdose
|
Dimercaprol (BAL), succimer
|
|
Toxicology: What is the antidote for copper, arsenic, gold toxicity/overdose
|
Penicillamine
|
|
Toxicology: What is the antidote N-acetylcysteine used to treat?
|
Acetaminophen toxicity/overdose
|
|
Toxicology: What is the antidote for cyanide toxicity/overdose
|
nitrite, hydroxocobalamin, thiosoulfate
|
|
Toxicology: What is the antidote for methemoglobin toxicity/overdose
|
methylene blue
|
|
Toxicology: What is the antidote glucagon used to treat?
|
Beta-blocker toxicity/overdose
|
|
Toxicology: What is the antidote for carbon monoxide toxicity/overdose
|
100% oxygen, hyperbaric oxygen
|
|
Toxicology: What is the antidote atropine used to treat?
|
anticholinesterase toxicity/overdose
|
|
Toxicology: What is the antidote for methanol toxicity/overdose
|
Ethanol, dialusis, fomepizole
|
|
Toxicology: What is the antidote for opiods toxicity/overdose
|
Nalozone/naltrexone
|
|
Toxicology: What is the antidote for ethylene glycol toxicity/overdose
|
Ethanol, dialusis, fomepizole
|
|
Toxicology: What is the antidote for benzodiazepines toxicity/overdose
|
Flumazenil
|
|
Toxicology: What is the antidote for (TCA) Tricyclic Antidepressants toxicity/overdose
|
NaHCO3
|
|
Toxicology: What is the antidote for Heparin toxicity/overdose
|
Protamine
|
|
Toxicology: What is the antidote Deferoxamine used to treat?
|
Iron toxicity/overdose
|
|
Toxicology: What is the antidote for warfarin toxicity/overdose
|
vitamin K, fresh frozen plasma
|
|
Toxicology: What is the antidote Naloxone/naltrexone used to treat?
|
opioid toxicity/overdose
|
|
Toxicology: What is the antidote for tPA/streptokinase toxicity/overdose
|
aminocaproic acid
|
|
Toxicology: What is the antidote Physostigmine salicylate used to treat?
|
Antimuscarinic/anticholinergic agents toxicity/overdose
|
|
Toxicology: What is the antidote Flumazenil used to treat?
|
Benzodiazepine toxicity/overdose
|
|
Toxicology: What is the antidote Protamine used to treat
|
Heparin toxicity/overdose
|
|
Toxicology: Children living in old houses might eat the paint chips which could cause ____
|
Lead Poisoning
|
|
Toxicology: Signs of Lead poisoning include:
|
Lead Lines on gingivae and epiphyses of Long bones, Encephalopathy and Erythrocyte Basophilic stipling, Abdominal colic and sideroblastic Anemia, Wrist and Foot Drop
|
|
Toxicology: 1st line of Treatment for Lead Poisoning include
|
Dimercaprol and EDTA
|
|
Toxicology: Weak acids, such as phenobarbitol, methotreaxate, aspirin, alkanize urine with ____ to increase clearance
|
bicarbonate
|
|
Toxicology: Weak bases, such as amphetamines, acidify urine with NH4Cl to ____ clearance
|
increase
|
|
Toxicology: AUTHOR
|
Lakshmi Swamy
|
|
Drug reactions: For each drug reaction, give the pharmacological agents responsible. The number of drugs you should list are given in parentheses. You could also quiz yourself in reverse by going down the list of drugs on the right.
|
0
|
|
Drug reactions: Pulmonary fibrosis (3)
|
bleomycin, amiodarone, busulfan
|
|
Drug reactions: Hepatitis (2)
|
isoniazid, halothane
|
|
Drug reactions: Focal to massive hepatic necrosis (4)
|
halothane, valproic acid, acetaminophen, amanita phalloides
|
|
Drug reactions: Anaphylaxis (1)
|
penicillin
|
|
Drug reactions: SLE-like syndrome (4). [mnemonic: it's not HIPP to have lupus]
|
hydralazine, INH, procainamide, phenytoin
|
|
Drug reactions: Hemolysis in G6PD-deficient patients (8)
|
sulfonamides, INH, aspirin, ibuprofen, primaquine, nitrofurantoin, pyrimethamine, chloramphenicol
|
|
Drug reactions: Thrombotic complications (1 class)
|
OCPs (e.g. estrogens and progestins)
|
|
Drug reactions: Adrenocortical insufficiency (withdrawal of what class of drugs causes adrenocortical insufficiency?)
|
withdrawal of glucocorticoids causes hypothalamic-pituitary-axis supression
|
|
Drug reactions: Photosensitivity reactions (3) [mnemonic: SAT for a photo]
|
Sulfonamides, amiodarone, tetracycline
|
|
Drug reactions: Induce P-450 system (6)
|
barbiturates, phenytoin, carbamazepine, rifampin, griseofulvin, quinidine
|
|
Drug reactions: Inhibit P-450 system (6, including one fruit)
|
cimetidine, ketoconazole, grapefruit, erythromycin, INH, sulfonamides
|
|
Drug reactions: Tubulointerstitial nephritis (5)
|
sulfonamides, furosemide, methicillin, rifampin, NSAIDs (except aspirin)
|
|
Drug reactions: Hot flashes (1)
|
Tamoxifen
|
|
Drug reactions: Cutaneous flushing (4)
|
niacin, Ca++ channel blockers, adenosine, vancomycin
|
|
Drug reactions: Cardiac toxicity (2)
|
doxorubicin (adriamycin), daunorubicin
|
|
Drug reactions: Agranulocytosis (3, all start with letter C)
|
clozapine, carbamazepine, colchicine
|
|
Drug reactions: Stevens-Johnson syndrome (3)
|
ethosuximide, sulfonamides, lamotrigine
|
|
Drug reactions: Cinchonism (2)
|
quinidine, quinine
|
|
Drug reactions: Tendonitis, tendon rupture and cartilage damage (kids) (1)
|
fluoroquinolones
|
|
Drug reactions: Disulfiram-like reaction (4)
|
metronidazole, certain cephalosporins, procarbazine, sulfonylureas
|
|
Drug reactions: Otoxicity and nephrotoxicity (3)
|
aminoglycosides, loop diuretics, cisplatin
|
|
Drug reactions: Drug-induced Parkinson's (4)
|
haloperidol, chlorpromazine, resperine, MPTP
|
|
Drug reactions: Torsades de pointes (two subclasses of antiarrhythmics)
|
Class III (sotalol), class IA (quinidine) antiarrhythmics
|
|
Drug reactions: Aplastic anemia (3)
|
chloramphenicol, benzene, NSAIDs
|
|
Drug reactions: Neuro/nephrotoxicity (1)
|
polymyxins
|
|
Drug reactions: Pseudomembranous colitis (2)
|
clindamycin, ampicillin
|
|
Drug reactions: Gynecomastia (5) [mnemonic: Some Drugs Create Awesome Knockers]
|
spironolactone, digitalis, cimetidine, chronic Alcohol use, estrogens, ketoconazole
|
|
Drug reactions: Atropine-like side effects (1)
|
tricyclics
|
|
Drug reactions: Cough (1)
|
ACE inhibitors (losartan --> no cough)
|
|
Drug reactions: Gingival hyperplasia (1)
|
phenytoin
|
|
Drug reactions: Diabetes insipidus (1)
|
lithium
|
|
Drug reactions: Tardive dyskinesia (1)
|
antipsychotics
|
|
Drug reactions: Fanconi's syndrome (1)
|
tetracycline
|
|
Drug reactions: Gray baby syndrome (1)
|
chloramphenicol
|
|
Drug reactions: Extrapyramidal side effects (3)
|
chlorpromazine, thioridazine, haloperidol
|
|
Drug reactions: Osteoporosis (2)
|
corticosteroids, heparin
|
|
Alcohol toxicity: Ethylene glycol is converted to ------- ------ by alcohol dehydrogenase. This product can lead to acidosis and nephrotoxicity.
|
oxalic acid.
|
|
Alcohol toxicity: Alcohol dehyrogenase also converts methanol to formaldehyde and formic acid, which can cause severe ----- and damage to the -------.
|
acidosis. retina
|
|
Alcohol toxicity: Ethanol competes with ethylene glycol and methanol (if present) for alcohol dehydrogenase. ADH action on EtOH produces -------.
|
acetaldehyde
|
|
Alcohol toxicity: What symptoms does acetaldehyde cause?
|
nausea, vomiting, headache, hypotension
|
|
Alcohol toxicity: Acetaldehyde itself can be metabolized by acetaldehyde dehydrogenase to ----- -----.
|
acetic acid.
|
|
Alcohol toxicity: Acetaldehyde dehydrogenase is inhibited by what drug?
|
disulfiram.
|
|
Herbal agents: Give the clinical uses for the following herbal agents.
|
0
|
|
Herbal agents: echinacea clinical use
|
common cold
|
|
Herbal agents: ephedra clinical use
|
as for ephedrine
|
|
Herbal agents: feverfew clinical use
|
migraine
|
|
Herbal agents: ginko clinical use
|
intermittent claudication
|
|
Herbal agents: kava clinical use
|
chronic anxiety
|
|
Herbal agents: milk thistle clinical use
|
viral hepatitis
|
|
Herbal agents: saw palmetto clinical use
|
benign prostatic hyperplasia
|
|
Herbal agents: St. John's wort clinical use
|
mild to moderate depression
|
|
Herbal agents: dehyroepiandrosterone clinical use
|
symptomatic improvement in females with SLE or AIDS
|
|
Herbal agents: Melatonin clinical use
|
jet lag, insomnia
|
|
Herbal agents: Give the toxicities for the following herbal agents.
|
0
|
|
Herbal agents: echinacea toxicity
|
GI distress, dizziness, and headache
|
|
Herbal agents: ephedra toxicity
|
CNS and cardiovascular stimulation; arrhythmias, stroke and seizures at high doses.
|
|
Herbal agents: feverfew toxicity
|
GI distress, mouth ulcers, antiplatelet actions
|
|
Herbal agents: ginko toxicity
|
GI distress, anxiety, insomnia, headache, and antiplatelet actions
|
|
Herbal agents: kava toxicity
|
GI distress, sedation, ataxia, hepatotoxicity, phototoxicity, dermatotoxicity
|
|
Herbal agents: milk thistle toxicity
|
loose stools
|
|
Herbal agents: saw palmetto toxicity
|
GI distress, decreased libido, hypertension
|
|
Herbal agents: St. John's wort toxicity
|
GI distress and phototoxicity; serotonin syndrome with SSRIs
|
|
Herbal agents: dehyroepiandrosterone toxicity
|
Androgenization (premenopausal women), estrogenic effects (postmenopausal), feminization (young men)
|
|
Herbal agents: Melatonin toxicity
|
Sedation, supresses midcycle LH, hypoprolactinemia
|
|
Drug category: For each drug name ending, give the general category of drug it indicates and an example of a drug in that category.
|
0
|
|
Drug category: -ane
|
inhalational general anesthetic. Halothane
|
|
Drug category: -azepam
|
benzodiazepine. Diazepam
|
|
Drug category: -azine
|
phenothiazine (neuroleptic, antiemetic). Chlorpromazine
|
|
Drug category: -azole
|
antifungal. Ketoconazole
|
|
Drug category: -barbital
|
barbiturate. Phenobarbital
|
|
Drug category: -caine
|
local anesthetic. Lidocaine
|
|
Drug category: -cillin
|
penicillin. Methicillin
|
|
Drug category: -cycline
|
antibiotic, protein synthesis inhibitor. Tetracycline
|
|
Drug category: -ipramine
|
tricyclic antidepressant. Imipramine
|
|
Drug category: -navir
|
protease inhibitor. Saquinavir
|
|
Drug category: -olol
|
beta antagonist. Propranolol
|
|
Drug category: -operidol
|
butyrophenone (neuroleptic). Haloperidol
|
|
Drug category: -oxin
|
cardiac glycoside (inotropic agent). Digoxin
|
|
Drug category: -phylline
|
methylxanthine. Theophylline
|
|
Drug category: -pril
|
ACE inhibitor. Captopril
|
|
Drug category: -terol
|
beta-2 agonist. Albuterol
|
|
Drug category: -tidine
|
H2 antagonist. Cimetidine
|
|
Drug category: -triptyline
|
tricyclic antidepressant. Amitriptyline
|
|
Drug category: -tropin
|
pituitary hormone. Somatotropin
|
|
Drug category: -zosin
|
alpha-1 antagonist. Prazosin
|
|
Drug category: AUTHOR
|
Lakshmi Swamy
|
|
Drug category: PHYSIOLOGY
|
0
|
|
Bacterial Strucutre & Cell Walls: Where is beta-lactamase in bacteria? What does it do?
|
Beta-lactamases are found in the periplasm of gram negative bacteria. The enzyme hydrolyzes beta-lactam antibiotics, conferring resistance.
|
|
Bacterial Strucutre & Cell Walls: Which gram-positive organism lacks a polysaccharide capsule and has a capsule made of something else?
|
Bacillus anthracis - has D-glutamate instead of polysaccharide
|
|
Bacterial Strucutre & Cell Walls: What are spores made of and what do they do?
|
Keratin-like coat, dipicolinic acid. Provide resistanceto dehydration, heat and chemicals
|
|
Bacterial Strucutre & Cell Walls: What helps organisms adhere to indwelling catheters?
|
The glycocalyx (composed of polysaccharide)
|
|
Bacterial Strucutre & Cell Walls: What is the major surface antigen of gram-positive cell walls and what does it do?
|
Teichoic acid - unique to gram-positive bacteria. Induces TNF and IL-1
|
|
Bacterial Strucutre & Cell Walls: What is specific to gram-negative bacterial cell membranes?
|
Endotoxin/LPS (lipopolysaccharide)
|
|
Bacterial Growth Curve: Describe the four phases of bacterial growth.
|
1) Lag phase of metabolic activity without division. 2) Log phase of rapid cell division. 3) Stationary phase in which nutrient depletion slows growth. 4) Death due to prolonged nutrient depletion and buildup of waste products.
|
|
Main Exotoxin and Endotoxin Features: What are exotoxins and endotoxin chemically?
|
Exotoxins are polypeptides, while endotoxins are lipopolysaccharides.
|
|
Main Exotoxin and Endotoxin Features: Where do bacteria keep their exotoxin or endotoxin genes?
|
Exotoxin genes on plasmids or bacteriophages; endotoxin genes on bacterial chromosomes.
|
|
Main Exotoxin and Endotoxin Features: Which is more fatal – exotoxin or endotoxin?
|
Exotoxin is highly fatal (~1 microgram), while you need 100’s of micrograms for endotoxin to prove lethal.
|
|
Main Exotoxin and Endotoxin Features: Which has greater heat stability – endotoxin or exotoxin?
|
Endotoxin – stable at 100°C for 1 hour, while endotoxin is rapidly destroyed at 60°C (EXCEPT Staph enterotoxin)
|
|
Main Exotoxin and Endotoxin Features: True or False: We can vaccinate against exotoxins and endotoxins.
|
False: We do have toxoids vaccines against exotoxins for diseases like tetanus, botulism and diphtheria, but there are no vaccines against endotoxins.
|
|
Bugs with Exotoxins: Which bugs have Exotoxin that acts by ADP ribosylation?
|
Corynebacterium diphtheriae (which then inactivates EF-2). Also Escherichia coli, Vibrio cholerae, and Bordetalla pertussis (all these then stimulate adenylate cyclase).
|
|
Bugs with Exotoxins: Which bug has exotoxin that blocks the release of acetylcholine? What symptoms does that cause?
|
Clostridium botulinum. Anticholinergic symptoms, CNS paralysis, flopy baby, and a wrinkle-free forehead if injected!!
|
|
Bugs with Exotoxins: Which bug has exotoxin that blocks glycine release? What does that cause?
|
Clostridium tetani. Causes “lockjaw”.
|
|
Bugs with Exotoxins: How does Staph aureus cause toxic shock syndrome?
|
The toxin is a superantigen that binds to MHC II protein and T-cell receptor Ă induces IL-1 and IL-2 Ă TSS
|
|
Endotoxin (especially lipid A): How could bacterial infection cause disseminated intravascular coagulation?
|
Endotoxin can activate Hageman factor --> initiates coagulation cascade --> DIC
|
|
Endotoxin (especially lipid A): How could bacterial infection cause hypotension?
|
Endotoxin activates macrophages to release nitric oxide (--> vasodilationĂ hypotension); can also activate alternate complement pathway C3a, --> hypotension (N.B. also edema).
|
|
Endotoxin (especially lipid A): How does bacterial infection cause fever?
|
Endotoxin activates macrophages to release IL-1 and TNF --> fever.
|
|
Gram Stain Limitations: --- are too thin to be visualized. Use darkfield microscopy and fluorescent antibody staining instead.
|
Treponema
|
|
Gram Stain Limitations: --- lack a cell wall
|
Mycoplasma
|
|
Gram Stain Limitations: --- stain with silver
|
Legionella pneumophila
|
|
Fermentation patterns of Neisseria: What are the two Neisseria species?
|
N. meningitidis, N. gonorrhoeae
|
|
Fermentation patterns of Neisseria: How are the Neisseria species differentiated?
|
MeninGococci ferment Maltose & Glucose; Gonococci ferment only Glucose
|
|
Pigment-producing Bacteria: --- produces a yellow pigment
|
Staphylococcus aureus (Latin aureus = gold)
|
|
Pigment-producing Bacteria: --- produces a blue-green pigment
|
Pseudomonas aeruginosa
|
|
Pigment-producing Bacteria: --- produces a red pigment
|
Serratia marcescens (think red marachino cherry)
|
|
IgA Proteases: IgA proteases allow organisms to…
|
… colonize mucosal surfaces
|
|
IgA Proteases: Name 4 organisms with IgA proteases
|
Strep pneumoniae, N. meningitidis, N. gonorhoeae, H. influenzae
|
|
Gram-positive Lab Algorithm: What are the lab steps for ID'ing Staphylococcus aureus?
|
1st gram stain --> get purple/blue cocci (= positive); 2nd catalase test --> positive (staphylococcus clusters); 3rd coagulase test --> positive (differentiates S. aureus from the coagulase-negative S. epidermidis and S. saprophyticus)
|
|
Gram-positive Lab Algorithm: What are the 4 types of gram-postive rods?
|
Corynebacterium, Listeria, Bacillus, Clostridium
|
|
Gram-positive Lab Algorithm: When do you test for bacitracin sensitivity or resistance?
|
For beta-hemolytic strep. Bacitracin-sensitive --> Group A beta-hemolytic Strep pyogenes. Bacitracin-resistant --> Group B (Bad!) beta-hemolytic Strep agalactiae
|
|
Gram-positive Lab Algorithm: Name 4 laboratory features of Streptococcus pneumoniae
|
alpha hemolytic (green – partial hemolysis), positive Quellung reaction, optochin-sensitive, and bile-soluble
|
|
Gram-positive Lab Algorithm: When would you do the optochin test?
|
When you have alpha hemolytic strep
|
|
Gram-negative Lab Algorithm: Once you see gram-negative rods under the microscope, what is your next diagnostic test?
|
test lactose fermentation
|
|
Gram-negative Lab Algorithm: What are the 3 fast lactose fermenters:
|
Klebsiella, E. coli, and Enterobacter
|
|
Gram-negative Lab Algorithm: How do you distinguish among lactose non-fermenters?
|
Perform an oxidase test
|
|
Gram-negative Lab Algorithm: Which are oxidase-positive?
|
Pseudomonas
|
|
Gram-negative Lab Algorithm: Which are oxidase-negative?
|
Shigella, Salmonella, or Proteus
|
|
Gram-negative Lab Algorithm: What are the gram-negative cocci?
|
Neisseria
|
|
Gram-negative Lab Algorithm: What are the gram-negative coccoid rods?
|
H. influenzae, Pasteurella, Brucella, Bordetella pertussis
|
|
Gram-negative Lab Algorithm: Which gram negative coccoid requires factors V and X for growth?
|
H. flu
|
|
Special Culture Requirements: Use chocolate agar and factors V & X for ---
|
Hemophilus influenzae
|
|
Special Culture Requirements: Factor V has --- and Factor X has ---
|
NAD, hematin
|
|
Special Culture Requirements: Thayer-Martin (VCN) media to culture ---
|
Neisseria gonorrhoeae
|
|
Special Culture Requirements: Bordet-Gengou (potato) agar to culture ---
|
Bordetella pertussis
|
|
Special Culture Requirements: Tellurite plate, Loffler's medium, blood agar for ---
|
Corynebacterium diphtheriae
|
|
Special Culture Requirements: Lowenstein-Jensen agar for growing ---
|
Mycobacterium tuberculosis
|
|
Special Culture Requirements: Pink colonies on MacConkey's agar are ---
|
Lactose-fermenting enterics (Klebsiella, Eschericihia, or Enterobacter
|
|
Special Culture Requirements: Charcoal yeast extract agar buffered with increased iron and cysteine to grow ---
|
Legionella pneumophila
|
|
Special Culture Requirements: Sabouraud's agar to culture ---
|
Fungi
|
|
Stains: Stain used to diagnose Whipple's disease
|
PAS (Periodic Acid Schiff)
|
|
Stains: PAS stains ---
|
glycogen, mucopolysaccharides
|
|
Stains: Ziehl-Neelsen stains ---
|
Acid-fast bacteria
|
|
Stains: India ink stains ---
|
Cryptococcus neoformans
|
|
Stains: Congo red stains -- and exhibits ---
|
Amyloid, aple-green birefringence in polarized light
|
|
Stains: Giemsa's stains what 4 organisms?
|
Borrelia, Plasmodium, trypanosomes, Chlamydia (intracellular inclusions on Giemsa)
|
|
Conjugation, Transduction, Transformation: Which process can involve eukaryotic DNA?
|
Transformation
|
|
Conjugation, Transduction, Transformation: DNA transferred from 1 bacterium to another through a sex pilus is
|
Conjugation
|
|
Conjugation, Transduction, Transformation: DNA transferred by a virus from 1 cell to another
|
Transduction
|
|
Conjugation, Transduction, Transformation: Generalized transduction can transfer --
|
Any gene
|
|
Conjugation, Transduction, Transformation: Specialized transduction transfers ---
|
only certain genes (that's why it's special!)
|
|
Obligate Aerobes: "Nagging Pests Must Breathe" helps you remember what?
|
obligate aerobes: Nocardia, Pseudomonas aeruginosa, Mycobacterium tuberculosis, Bacillus
|
|
Obligate Aerobes: Aerobic bacteria commonly found in burn wounds, nosocomial pneumonia, and pneumonias in cystic fibrosis patients?
|
Pseudomonas aeruginosa (an obligate aerobe)
|
|
Obligate Aerobes: What bug likes the lungs’ apices and why?
|
Mycobacterium tuberculosis – because the apices have the highest partial pressure of oxygen
|
|
Obligate Anaerobes: If you hear crepitus, indicating gas in tissue, what type of infection do you suspect?
|
Anaerobic bacterial infection, such as Clostridium, Bacteroides, or Actinomyces (CBA)
|
|
Obligate Anaerobes: Which bugs are anaerobic and why?
|
Clostridium, Bacteroides, and Actinomyces. Air causes them oxidative damage, because they lack catalase and/or superoxide dismutase.
|
|
Obligate Anaerobes: Why are aminoglycoside antibiotics ineffective against anerobic bacteria?
|
AminO2glycosides require O2 to enter into bacterial cells; anaerobic bacteria aren't where the oxygen is
|
|
Intracellular Bugs: Name the 2 obligate intracellular organisms
|
Rickettsia, Chlamydia - "They stay inside (cells) when it's Really Cold"
|
|
Intracellular Bugs: Why do they need the host's cell?
|
They can't make ATP
|
|
Intracellular Bugs: Name 7 facultative intracellular organisms
|
Mycobacterium, Brucella, Francisella, Listeria, Yersinia, Legionella, Salmonella
|
|
Intracellular Bugs: AUTHOR
|
Olga Kulinets
|
|
Encapsulated Bacteria: List 4 examples of encapsulated bacteria
|
Streptococcus Pneumoniae, Haemophilus influenzae, Neisseria meningitidis, Klebsiella pneumoniae
|
|
Encapsulated Bacteria: What is the main virulence factor of encapsulated bacteria and why?
|
Polysacharide capsule is antiphagocytic
|
|
Encapsulated Bacteria: What is a necessary component of humoral immune response to encaps. Bacteria?
|
IgG2
|
|
Encapsulated Bacteria: What vaccines are available for encapsulated bacteria?
|
Pneumovax, H. influenzae, meningococcal
|
|
Encapsulated Bacteria: What serves as vaccine antigen?
|
Capsule
|
|
Encapsulated Bacteria: What laboratory test can be used to detect the presence of encapsulated bacteria?
|
Quellung reaction - capsule swells when specific anticapsular antisera are added - "Quellung = capsular swellung"
|
|
Encapsulated Bacteria: What complications/clinical signs is pneumococcus associated with?
|
Rusty sputum, sepsis in sickle cell anemia, and splenectomy
|
|
Spores: Bacterial: What kind of bacteria form spores and when?
|
Certain gram-positive rods when nutrients are limited
|
|
Spores: Bacterial: Name 3 spore-formers
|
Bacillus anthracis, C. perfringens, C. tetani = gram positive soil bugs
|
|
Spores: Bacterial: T or F: Spores are highly resistant to destruction by heat and chemicals
|
TRUE
|
|
Spores: Bacterial: Spores have ___ acid in their core
|
dipicolinic
|
|
Spores: Bacterial: T or F: Spores are metabolically active
|
False. Spores have no metabolic activity
|
|
Spores: Bacterial: What disinfecting procedure kills spores?
|
Autoclaving (ex/ surgical equipment)
|
|
Alpha-hemolytic Bacteria: What organisms are alpha-hemolytic?
|
Pneumococci, viridans strep
|
|
Alpha-hemolytic Bacteria: Pneumococci are catalase ___ and optochin ___
|
Pneumococci are catalase negative and optochin sensitive
|
|
Alpha-hemolytic Bacteria: Viridans strep are catalase ___ and optochin ___
|
Viridans strep are catalase sensitive and optochin resistant
|
|
Beta-hemolytic Bacteria: What organisms are beta-hemolytic?
|
Staph aureus, strep pyogenes, strep agalactiae, lysteria monocytogenes
|
|
Beta-hemolytic Bacteria: Staph aureus is catalase ___ and coagulase ___
|
Positive, positive
|
|
Beta-hemolytic Bacteria: Strep pyogenes is catalase ___ and bacitracin __
|
negative, sensitive
|
|
Beta-hemolytic Bacteria: Strep agalactiae is catalase __ and bacitracin__
|
negative, resistant
|
|
Beta-hemolytic Bacteria: Where is Lysteria monocytogenes found, and what is its characteristic pathology and laboratory appearance?
|
Unpausterized milk, miningitis in newborns, tumbling motility
|
|
Catalase/Coagulase: What are catalase and coagulase tests used for?
|
Catalase is used to distinguish staph (+) from strep (-), coagulase is used to distinguish S. aureus (+) from S. epidermis (-) and S. saprophyticus(-)
|
|
Catalase/Coagulase: How is catalase a virulence factor?
|
It degrades H2O2, an antimicrobial product of PMNs that is a substrate for myeloperoxidase
|
|
Staph aureus: What is the function of protein A?
|
Virulence factor - binds to Fc-IgG and inhibits complement fixation and phagocytosis
|
|
Staph aureus: TSST is a ___ (type of virulence factor) that binds to ___ (2 types of receptor) and causes ___ of ___ (type of cells) leading to ___ (disease)
|
TSST is a superantigen that binds to MHC II and T-cell receptor and causes polyclonal activation of T-cells leading to toxic shock syndrome
|
|
Staph aureus: 3 toxins of S. aureus and a syndrome caused by each
|
TSST- 1 - toxic shock syndrome, exfoliative toxin - scalded skin syndrome, enterotoxins - rapid-onset food poisoning
|
|
Staph aureus: T/F - S. aureus causes acute bacterial endocarditis
|
TRUE
|
|
Staph aureus: T/F - S. aureus causes skin disease and organ abscesses, but not pneumonia
|
False - causes all 3
|
|
Staph aureus: T/F - S. aureus food poisoning is due to bacterial infiltration of the intestinal wall
|
False - it is due to ingestion of preformed enterotoxin
|
|
Strep Pyogenes: T/F: strep pyogenes is catalase negative and bacitracin sensitive
|
TRUE
|
|
Strep Pyogenes: 3 pyogenic manifestations of strep pyogenes
|
pharyngitis, cellulitis, impetigo
|
|
Strep Pyogenes: Which is not a toxigenic manifestation of strep pyogenes: scarlet fever, rheumatic fever, TSS, acute glomerulonephritis
|
Rheumatic fever and acute glomerulonephritis are immune-mediated
|
|
Strep Pyogenes: List 5 signs and symptoms characteristic of rheumatic fever
|
PECCS: polyarthritis, erythema marginatum, chorea, carditis, subcutaneous nodules
|
|
Enterococci: T/F: Enterococci are penicillin G sensitive and show variable hemolysis
|
F - they are resistant, but do have variable hemolysis
|
|
Enterococci: Lancefield group D includes ___ and ___, which can be differentiated through ___ (lab test)
|
Enterococci and non-enterococcal Group D strep. Enterococci can grow on 6.5% NaCl, and non-enterococci cannot.
|
|
Enterococci: Lancefield grouping is based on ___ on the bacterial cell wall
|
C carbohydrate
|
|
Viridans Strep: Viridans Strep are ___ hemolytic
|
alpha
|
|
Viridans Strep: Strep mutans causes ___
|
dental caries
|
|
Viridans Strep: S. sanguis causes ___
|
bacterial endocarditis
|
|
Viridans Strep: How do you differentiate viridans strep from S. pneumoniae in the laboratory?
|
Both are alpha-hemolytic, but viridans strep is resistant to optochin (live in the mouth, not afraid of-the-chin)
|
|
Clostridia: T/F: Clostridia are gram-positive, spore-forming, microaerophilic bacteria
|
False - they are obligate anaerobes
|
|
Clostridia: Name 4 types of Clostridia and disease caused by each
|
Tetanus - tetanic paralysis, Botulinum - flaccid paralysis, Perfringens - gangrene, Difficile - diarrhea
|
|
Clostridia: How does Clostridia cause tetanic paralysis?
|
Exotoxin blocks glycine (inhibitory neurotransmitter) release from Renshaw cells in spinal chord leading to tetanic paralysis
|
|
Clostridia: How does C. botulinum cause flaccid paralysis?
|
Preformed, heat - labile toxin inhibits ACh release
|
|
Clostridia: T/F: C. perfringens produces alpha-toxin, a globulin that causes myonecrosis, gas gangrene, or hemolysis
|
False - alpha-toxin is a lecithinase
|
|
Clostridia: What causes pseudomembranous colitis? How is it treated?
|
Cytotoxin, an alpha toxin produced by C. diff, usu after antibiotic use (clindamycin ar ampicillin). Treat with metronidazole.
|
|
Diphtheria: Exotoxin is encoded by ___ and ihibits ___ by ADP-ribosylation of ___
|
beta-prophaage, protein synthesis, EF-2
|
|
Diphtheria: T/F: Symptoms of diphtheria include pseudomembranous pharyngitis, lymphadenopathy, and hematuria
|
Does not cause hematuria
|
|
Diphtheria: Lab tests for Diphtheria
|
Gram-positive, club-shaped rods with metachromatic granules; grow on tellurite agar
|
|
Diphtheria: ABCDEFG of diphtheria
|
ADP ribosylation, Beta-prophage, Corynebacterium, Diphtheriae, EF-2, Granules
|
|
Anthrax: Anthrax is caused by ___ (bacteria)
|
Bacillus anthracis
|
|
Anthrax: T/F: Bacillus anthracis is spore-forning and gram negative rod
|
FALSE - it is a gram-positive rod
|
|
Anthrax: What is the progression of anthrax?
|
Contact leads to malignant pustule (painless ulcer) which can progress to bacteremia and death
|
|
Anthrax: What is woolsorter's disease?
|
Life-threatening pneumonia caused by inhalation of spores
|
|
Anthrax: Characteristic lesion of anthrax
|
Black skin lesions - vesicular papules covered by black eschar
|
|
Actinomycis Vs. Nocardia: Actinomycis, Nocardia are gram___ rods that form long-branching filaments resembling fungi
|
positive
|
|
Actinomycis Vs. Nocardia: What air requirement do actinomysis and nocardia have?
|
Actinomyces is an anaerobe and nocardia is an aerobe
|
|
Actinomycis Vs. Nocardia: A vs. N (pick one): pulmonary infection in immunocompromized
|
nocardia
|
|
Actinomycis Vs. Nocardia: A vs. N (pick one): oral/facial abscess with sulfur granules that may drain through sinus tracts in skin
|
actinomyces
|
|
Actinomycis Vs. Nocardia: A vs. N (pick one): Normal oral flora
|
actinomyces
|
|
Actinomycis Vs. Nocardia: A vs. N (pick one): Weakly acid fast
|
nocardia
|
|
Actinomycis Vs. Nocardia: What treatment do you use for actinomycis? For nocardia?
|
SNAP - sulpha for nocardia; actinomyces use penicillin
|
|
Penicillin and gram-neg bacteria: Gram negative bugs are ___ to benzyl penicillin G and ____ to penicillin derivatives such as ampicillin
|
resistant, may be susceptible
|
|
Penicillin and gram-neg bacteria: T/F: Vancomycin can enter gram-negative bacteria
|
False - gram-negative outer membrane layer inhibits entry of penicillin G and vancomycin
|
|
Name bacteria associated with food poisoning from the following sources:: Reheated rice
|
Bacillus cereus
|
|
Name bacteria associated with food poisoning from the following sources:: Contaminated seafood
|
Vibrio parahemolyticus and vulnificus
|
|
Name bacteria associated with food poisoning from the following sources:: Meats, mayonaise, custard
|
S. aureus
|
|
Name bacteria associated with food poisoning from the following sources:: Reheater meat dishes
|
C. perfringens
|
|
Name bacteria associated with food poisoning from the following sources:: Improperly canned food
|
C. botulinum
|
|
Name bacteria associated with food poisoning from the following sources:: Undercooked meat
|
E. coli 0157:H7
|
|
Name bacteria associated with food poisoning from the following sources:: Poultry, meat, eggs
|
Salmonella
|
|
Name diarrheal organism associated with the following:: Ferments lactose and causes non-bloody diarrhea
|
enterotoxigenic E. coli
|
|
Name diarrheal organism associated with the following:: Comma-shaped organism
|
Vibrio cholerae
|
|
Name diarrheal organism associated with the following:: Does not ferment lactose, motile, bloody diarrhea
|
Salmonella
|
|
Name diarrheal organism associated with the following:: Does not ferment lactose, nonmotile, very low ID50, bloody diarrhea
|
Shigella
|
|
Name diarrheal organism associated with the following:: Comma or S-shaped, growth at 42 degrees, bloody diarrhea
|
Campylobaxter jejuni
|
|
Name diarrheal organism associated with the following:: Transmitted by seafood
|
Vibrio parahemolyticus
|
|
Name diarrheal organism associated with the following:: Transmitted through pet feces (puppies), bloody diarrhea
|
Yersenia enterocolitica
|
|
Name diarrheal organism associated with the following:: Rice-water stools
|
Vibrio cholerae
|
|
Name diarrheal organism associated with the following:: 4 non-bacterial causes of non-bloody diarrhea
|
Virus - rotavirus, norwalk virus; protozoan - Cryptosporidium and Giardia
|
|
Name diarrheal organism associated with the following:: Ferments lactose and causes bloody diarrhea
|
E. coli 0157:H7
|
|
Name diarrheal organism associated with the following:: Protozoan cause of bloody diarrhea
|
Entamoeba histolytica
|
|
Enterobacteriaceae: Lab tests for enterobacteriaceae
|
Ferment glucose, oxidase negative
|
|
Enterobacteriaceae: T/F: Enterobacteriaceae includes E.coli, Salmonella, Klebsiella, Enterobacter, Serratia, Proteus, and Pseudomonas
|
False - does not include Pseudomona
|
|
Enterobacteriaceae: Describe O, K, and H antigens
|
O - somatic, polysacharide of endotoxin; K - capsular, related to virulence; H - flagellar, found in motile species
|
|
Haemophilus Influenzae: Name 4 diseases caused by H. influenzae
|
epiglottitis, meningitis, otitis media, pneumonia
|
|
Haemophilus Influenzae: T/F - H. influenzae is a large gram-negative rod
|
False - it is a small (coccobacillary) gram-negative rod
|
|
Haemophilus Influenzae: H. influenzae is transmitted by ____ and invasive disease is caused by capsular type ___. It produces ___ protease.
|
aerosol, B, IgA
|
|
Haemophilus Influenzae: Culture on ___ agar requires ___ and ___
|
Chocolate agar, Factor V (NAD), X (hematin)
|
|
Haemophilus Influenzae: T/F: H. influenzae causes the flu.
|
False - influenza virus causes flue
|
|
Haemophilus Influenzae: Use ___ to treat H. influenzae meningitis and ___ for prophylaxis of close contacts.
|
Ceftriaxone, rifampin
|
|
Haemophilus Influenzae: T/F: H. influenzae vaccine contains type D capsular polysacharide conjugated to enterotoxin
|
False: vaccine contains type B capsular polysacharide conjugated to diphtheria toxoid or other protein
|
|
Haemophilus Influenzae: When is the H. influenzae vaccine given?
|
Btw 2 and 18 months of age
|
|
Legionella Pneumophilia: Legionella Pneumophilia is a gram___ rod
|
negative
|
|
Legionella Pneumophilia: It will grow on ___ yeast extract with ___ and ___, and should be treated with ___
|
Charcoal, iron, cysteine, erythromycin
|
|
Legionella Pneumophilia: T/F: Legionella pneumophilia is transmitted through environmental water source habitat.
|
TRUE
|
|
Legionella Pneumophilia: T/F: Legionella is transmitted person to person.
|
False - no person to person transmission
|
|
Pseudomonas Aerugenosa: T/F: Pseudomonas Aerugenosa is anaerobic gram-negative rod found in water sources
|
False - it is AERobic (AERuginosa)
|
|
Pseudomonas Aerugenosa: Name 5 infections commonly caused by Pseudomonas
|
Pneumonia (esp. in CF), sepsis, external otitis, UTI, hot tub folliculitis
|
|
Pseudomonas Aerugenosa: T/F: Pseudomonas Aerugenosa ferments lactose and is oxidase-negative
|
False - P. Aurugenosa does not ferment lactose and is oxidase negative
|
|
Pseudomonas Aerugenosa: Blue-green pigment produced by P. Aerugenosa
|
pyocyanin
|
|
Pseudomonas Aerugenosa: What 2 toxins does P. Aerugenosa produce?
|
Endotoxin (causes fever and shock), exotoxin A (inactivated EF-2)
|
|
Pseudomonas Aerugenosa: What is the treatment for P. aeruginosa
|
Aminoglycoside plus extended-spectrum penicillin (piperacillin, ticarcillin)
|
|
Pseudomonas Aerugenosa: What kind of injury makes a person especially susceptible to P. aeruginosa infection?
|
Burns
|
|
Helicobacter Pylori: What conditions does H. pylori cause and is a risk factor for?
|
Causes gastriti and 90% of duodenal ulcers, risk of peptic ulcer, gastric carcinoma
|
|
Helicobacter Pylori: T/F: H. pylori is a gram-negative rod that creates an alkaline environment
|
TRUE
|
|
Helicobacter Pylori: What is a test for H. pylori?
|
Urease breath test
|
|
Helicobacter Pylori: What is the treatment for H. pylori?
|
Triple therapy - bismuth, metronidazole, and tetracycline or amoxicyclin OR more expensive metronidazole, omeprazole, and clarithromycin
|
|
Helicobacter Pylori: What 2 bacteria are urease positive?
|
H. pylori and Proteus
|
|
Lactose - fermenting enteric bacteria: What culture technique differentiates lactose fermenting from non-fermenting bacteria?
|
Lactose fermenters grow pink colonies on MacConkey's agar (Lactose is KEE)
|
|
For the following, state if they ferment lactose:: Klebsiella
|
Ferments lactose
|
|
For the following, state if they ferment lactose:: Salmonella
|
Does not ferment
|
|
For the following, state if they ferment lactose:: E.coli
|
Ferments lactose
|
|
For the following, state if they ferment lactose:: Staph Aureus
|
Does not ferment
|
|
For the following, state if they ferment lactose:: Enterobacter
|
Ferments lactose
|
|
For the following, state if they ferment lactose:: Citrobacter
|
Ferments lactose
|
|
Salmonella Vs. Shigella: Select salmonella, shigella, or both:
|
0
|
|
Salmonella Vs. Shigella: Non-lactose fermenter
|
both
|
|
Salmonella Vs. Shigella: Motile
|
SalMOnella
|
|
Salmonella Vs. Shigella: Invades futher, disseminates hematogenously
|
Samonella
|
|
Salmonella Vs. Shigella: More virulent
|
Shigella (10e1 innocumlum compared to 10e5 innoculum for Salmonella)
|
|
Salmonella Vs. Shigella: Symptoms prolonged with antibiotic treatment
|
Samonella
|
|
Salmonella Vs. Shigella: Has an animal resevoir
|
Samonella
|
|
Salmonella Vs. Shigella: Invade intestinal mucosa causing bloody diarrhea
|
both
|
|
Salmonella Vs. Shigella: What immune cell type predominantly responds to Salmonella?
|
Monocytes
|
|
Salmonella Vs. Shigella: How is Shigella transmitted?
|
4 f's: food, fingers, feces, and flies
|
|
Cholera and Pertussi toxins: How does Vibrio Cholerae toxin work?
|
Permanently activates Gs causing rice-water diarrhea
|
|
Cholera and Pertussi toxins: How does Pertussis toxin work?
|
Permanently disables Gi, causing whooping cough, also promotes lymphocytosis by inhibiting chemokine receptors
|
|
Cholera and Pertussi toxins: What do Pertussis toxin and Choleratoxin have in common?
|
Act via ADP ribosylation that permanently activates adenyl cyclase, resulting in increased cAMP
|
|
Zoonotic Bacteria: Name 5 common zoonotic bacteria
|
Bugs from your pet: Borrelia burgdorferi, Brucella, Francisella tularensis, Yersinia pestis, Pasteirella multocida
|
|
Name the disease, mode of transmission, and source associated with the following:: Borrelia burgdorferi
|
Lyme disease; tick bite; Ixodes ticks that live on deer and mice
|
|
Name the disease, mode of transmission, and source associated with the following:: Brucella
|
Brucellosis/undulant fever; dairy products, contact with animals -- "Undulate and Unpasteurized products give you Undulant fever"
|
|
Name the disease, mode of transmission, and source associated with the following:: Francisella tularensis
|
Tularemia; tick bite; rabbits, deer
|
|
Name the disease, mode of transmission, and source associated with the following:: Yersenia pestis
|
Plague, flea bite; rodents, esp. prarie dogs
|
|
Name the disease, mode of transmission, and source associated with the following:: Pasteurella multocida
|
Cellulitis; animal bite; cats, dogs
|
|
Gardnerella vaginalis: What symptoms are associated with G. vaginalis infection?
|
Vaginosis - greenish vaginal discharge, fishy smell, not painful
|
|
Gardnerella vaginalis: What is Mobiluncus?
|
An anaerobe commonly involved in G. vaginalis infections
|
|
Gardnerella vaginalis: G. vaginallis should be treated with ___
|
Metronidazole
|
|
Gardnerella vaginalis: What are the laboratory characteristics of G. vaginalis?
|
Pleiomorphic, gram-variable rod; clue cells - vaginal epithelial cells covered with bacteria are visible under a microscope
|
|
Identify as associated with Meningococci, Gonococci, or both:: Gram-negative cocci
|
both
|
|
Identify as associated with Meningococci, Gonococci, or both:: Polysacharide capsule
|
Meningococci
|
|
Identify as associated with Meningococci, Gonococci, or both:: Neonatal conjunctivitis
|
Gonococci
|
|
Identify as associated with Meningococci, Gonococci, or both:: Vaccine available
|
Meningococci
|
|
Identify as associated with Meningococci, Gonococci, or both:: Gonorrhea
|
Gonococci
|
|
Identify as associated with Meningococci, Gonococci, or both:: Meningitis w/ septicemia
|
Meningococci
|
|
Identify as associated with Meningococci, Gonococci, or both:: Waterhouse - Friederichsen syndrome
|
Meningococci
|
|
Identify as associated with Meningococci, Gonococci, or both:: Septic arthritis
|
Gonococci
|
|
Identify as associated with Meningococci, Gonococci, or both:: PID
|
Gonococci
|
|
Identify as associated with Meningococci, Gonococci, or both:: Maltose fermentation
|
Meningococci
|
|
Primary and Secondary TB (figure): What is primary TB?
|
Reponse to TB infection by a non-immune host, consists of hilar node involvement and Ghon focus
|
|
Primary and Secondary TB (figure): What are possible outcomes of primary TB?
|
Healing by fibrosis (characterized by hypersensitivity w/ pD+), progressive lung disease (ass. W/ HIV, malnutrition), severe bacteremia (leading to miliary TB and death), preallergic lymphatic or hematogenous dissemination (leads to dormant tubercle bacilli in several organs and reactivation in adult life)
|
|
Primary and Secondary TB (figure): What is secondary TB?
|
Response to reinfection by a partially immune hypersensitized host (usu adult) OR reactivation of dormant tubercle bacilli from primary infection -- consists of fibrocaseous cavitary lesion
|
|
Primary and Secondary TB (figure): What organs are commonly effected by extrapulmonary TB?
|
CNS (parenchymal tuberculoma or meningitis), vertebral body (Pott's disease), lymphadenitis, renal, GI
|
|
Mycobacteria: What are common symptoms of TB?
|
Fever, night sweats, weight loss, hemoptysis
|
|
Mycobacteria: T/F: All mycobacteria are acid-fast
|
TRUE
|
|
Mycobacteria: T/F: M. Tuberculosis and M. avium-intracellulare can be resistant to multiple drugs
|
TRUE
|
|
Mycobacteria: T/F: M. kansasii is asymptomatic
|
False: causes pulmonary TB-like symptoms
|
|
Mycobacteria: T/F: M. scrofulaceum commonly causes cervical lymphadenitis in the elderly
|
False: usually causes cervical lymphadenitis in kids
|
|
Leprosy (Hansen's disease): What organism causes leprosy?
|
Mycobacterium leprae
|
|
Leprosy (Hansen's disease): T/F: M. leprae is an acid-fast bacterium that grows well in vitro
|
False - M. leprae does not grow in vitro
|
|
Leprosy (Hansen's disease): M. leprae likes ___ temperatures and infects ___ and ___ (tissues)
|
cool, skin, superficial nerves
|
|
Leprosy (Hansen's disease): What are the two forms of Hansen's disease? Which form is worse?
|
Lepromatous and tuberculoid, tuberculoid is self-limited, lepromatous is worse (failed cell-mediated immunity) "LEpromatous = LEthal"
|
|
Leprosy (Hansen's disease): What is wrong with armadillos?
|
Resevoir of leprosy in U.S.
|
|
Leprosy (Hansen's disease): What is treatmet for leprosy and associated toxicities?
|
Long-term oral dapsone, toxicity = hemolysis and methemoglobinemia. Alternate treatments include rifampin and combination of clofazimine and dapsone.
|
|
Leprosy (Hansen's disease): AUTHOR
|
Adam Weitzman, et al.
|
|
Ricketsia: What is the classic triad of Rickettsial infection?
|
headache, fever, rash
|
|
Ricketsia: True/False: Ricketsia are facultative intracellular parasites
|
False, they are obligate parasites and need CoA and NAD
|
|
Ricketsia: Most Ricketsia are transmitted by what?
|
arthropod vector
|
|
Ricketsia: Why is Coxiella an atypical ricketsia?
|
It is transmitted by aerosol and causes pneumonia and no rash. Has negative Weil-Felix test.
|
|
Ricketsia: What is the treatment of choice for rickettsial infection?
|
Tetracycline
|
|
Rickettsial diseases and vectors: What bug causes Rocky Mountain spotted fever? What is the vector?
|
Rickettsia rickettsii, tick vector
|
|
Rickettsial diseases and vectors: What bug causes Endemic typhus? What is the vector?
|
Rickettsia typhi, flea vector
|
|
Rickettsial diseases and vectors: What bug causes Epidemic typhus? What is the vector?
|
Rickettsia prowazeckii, human body louse
|
|
Rickettsial diseases and vectors: What bug causes Q fever? What is the vector?
|
Coxiella burnetii, only rickettsial disease without a vector
|
|
Rocky Mountain spotted fever: What three diseases have characteristic palm and sole rash?
|
Rocky Mountain spotted fever, syphilis, and coxsackievirus A16 (hand, foot, and mouth disease)
|
|
Rocky Mountain spotted fever: How does the rash of Rocky Mountain spotted fever progress?
|
centripetally, starting on palms and soles, migrating to wrists/ankles, then trunk
|
|
Rocky Mountain spotted fever: What are the symptoms of Rocky Mountain spotted fever? What is the causative agent?
|
Classic triad of rickettsial disease-headache, fever, rash. Rickettsia rickettsii
|
|
Rocky Mountain spotted fever: Where is Rocky Mountain spotted fever common?
|
Endemic to EAST coast
|
|
Weil-Felix reaction: What does the Weil-Felix reaction assay for?
|
antirickettsial antibodies using cross reactivity with Proteus antigen.
|
|
Weil-Felix reaction: Which rickettsia test positive with Weil-Felix? Which test negative?
|
typhus (R. typhi and R. prowazekii) and Rockey Mountain spotted fever (R. rickettsii) are usually positive. Q fever (C. burnetii, the weird one) is usually negative.
|
|
Mycoplasma pneumonia: Mycoplasma pneumonia causes what type of infection? Describe the symptoms. Which age group is it most common in?
|
Classic cause of atypical "walking" pneumonia. Insidious onset, headache, nonproductive cough, diffuse interstitial infiltrate. More common in patients under 30.
|
|
Mycoplasma pneumonia: How does an X-ray appear in a Mycoplasma infection?
|
Streaky, much worse than the patient apears.
|
|
Mycoplasma pneumonia: What is special about the mycoplasma cell wall?
|
Only bacterial membrane containing cholesteral
|
|
Mycoplasma pneumonia: What can you test for in the blood of patient with Mycoplasma?
|
They have high titers of cold agglutinins (IgM)
|
|
Mycoplasma pneumonia: Why can't you treat Mycoplasma infection with penecillin? What can you use?
|
Mycoplasma has no cell wall. Use tetracycline or erythromycin
|
|
Mycoplasma pneumonia: What agar is Mycoplasma grown on?
|
Eaton's
|
|
Chlamydiae: True/False: Chlamydia is an obligate intracellular parasite.
|
TRUE
|
|
Chlamydiae: Chlamydiae infects which type of surface?
|
Mucosal
|
|
Chlamydiae: How many forms does Chlamydia have? Describe them.
|
Two: Elementary body, small/dense (Enters cell) and Initial/Reticulate body (Replicates by fusion)
|
|
Chlamydiae: What is unusual about Chlamydia's cell wall?
|
The peptidoglycan wall lacks muramic acid.
|
|
Chlamydiae: What 4 things does Chlamydia cause?
|
arthritis, conjunctivitis, pneumonia, and nongonococcal urethritis
|
|
Chlamydiae: How do you diagnose a chlamydial infection? How do you treat it?
|
cytoplasmic inclusions seen on Giemsa or fluorescent antibody-stained smear. Use erythromycin or tetracyclin
|
|
Chlamydiae: Why is Chlamydia psittaci notable?
|
Has an avian reservoir
|
|
Chlamydiae: What species of animals do Chlamydia trachomatis and Chlamydia pneumonia infect? What do they cause?
|
They only infect humans. C. trachomatis causes arthritis. C. pneumonia causes atypical pneumonia; transmitted by aerosol.
|
|
Chlamydia trachomatis serotypes: What are the serotypes of chlamydia?
|
A - K, L1 - 3
|
|
Chlamydia trachomatis serotypes: What do types A, B, C cause?
|
chronic infection; blindness in Africa (Africa/Blindness/Chronic infection
|
|
Chlamydia trachomatis serotypes: What do L1 - L3 cause?
|
L = Lymphogranuloma venereum (acute lymphadenitis - positive Frei test)
|
|
Chlamydia trachomatis serotypes: What do type D - K cause?
|
everything else!! --> urethritis/PID, ectopic pregnancy, neonatal pneumonia, or neonatal conjunctivitis
|
|
Chlamydia trachomatis serotypes: How is neonatal chlamydia aquired?
|
passage through infected birth canal
|
|
Chlamydia trachomatis serotypes: How is neonatal chlamydia treated?
|
erythromycin eye drops
|
|
Spirochetes: Describe the shape of a spirochete.
|
Spiral shaped bacteria with axial filaments
|
|
Spirochetes: Name the three major spirochetes.
|
Borrelia (big size), Leptospira, Treponema (BLT. B is Big)
|
|
Spirochetes: Which can be identified by light microscopy using aniline dyes (Wright or Giemsa)?
|
Borrelia (big size)
|
|
Spirochetes: How is Treponema visualized?
|
dark-field microscopy
|
|
Lyme disease: What is the classic symptom of Lyme dz and how is it characterized?
|
erythema chronicum migricans (an expanding "bull's eye" red rash with central clearing.
|
|
Lyme disease: What else does Lyme dz affect?
|
joints, CNS, heart
|
|
Lyme disease: What are the Sx of Stage 1 Lyme dz?
|
erythema chronicum migricans, flu-like sx
|
|
Lyme disease: What are the Sx of Stage 2 Lyme dz?
|
neurologic and cardiac manifestations
|
|
Lyme disease: What are the Sx of Stage 3 Lyme dz?
|
autoimmune migratory polyarthritis
|
|
Lyme disease: What causes Lyme disease and how is it transmitted?
|
Borrelia burgdorferi, by the Ixodes tick.
|
|
Lyme disease: What are important reservoirs?
|
Mice
|
|
Lyme disease: What animal is required for the life cycle?
|
Deer
|
|
Lyme disease: How do you treat Lyme disease?
|
Tetracycline
|
|
Lyme disease: Where in the US is Lyme disease common?
|
northeast (named after Lyme, Connecticut)
|
|
Lyme disease: During what time of year is transmission most common?
|
summer months
|
|
Treponemal disease: Treponemes are what type of organism?
|
spirochetes
|
|
Treponemal disease: What causes syphillis?
|
Treponema pallidum
|
|
Treponemal disease: What causes yaws?
|
Treponema pertenue
|
|
Treponemal disease: What is yaws?
|
a tropical infection that is not an STD (although, VDRL test is positive)
|
|
Syphilis: What causes syphilis?
|
Treponema pallidum, a spirochete
|
|
Syphilis: What is characteristic of primary syphilis?
|
A painless chancre (localized disease)
|
|
Syphilis: What is characteristic of secondary syphilis?
|
Constitutional symptoms, maculopapular rash, and condylomata lata.
|
|
Syphilis: What is characteristic of end state syphilis?
|
Gummas, aortitis, neurosyphilis (tabes dorsalis), Argyll Robertson pupil.
|
|
Syphilis: What do you treat syphilis with?
|
Penicillin G
|
|
VDRL vs. FTA-ABS: What do VDRL and FTA-ABS test for? Which is better and why?
|
treponemes (syphilis), FTA-ABS is more specific, turns positive earlier and stays positive longer.
|
|
VDRL false posititves: What does VDRL detect? What disease is it used for?
|
Nonspecific antibody that reacts with beef cardiolipin. Used for diagnosis of syphilis.
|
|
VDRL false posititves: What false positives are detected with VDRL?
|
viral infection (mononucleosis, hepatitis), some drugs, rheumatic fever, rheumatoid arthritis, SLE, and leprosy.
|
|
Spores: fungal: Most fungal spores are sexual or asexual?
|
asexual
|
|
Spores: fungal: How are coccidioidomycosis and histoplasmosis transmitted?
|
inhalation of asexual spores
|
|
Spores: fungal: What are asexual spores called?
|
conidia (e.g. blastoconidia, arthroconidia)
|
|
Candida albicans: Is c. albicans infection local, systemic, or both?
|
both
|
|
Candida albicans: What is the morphology of c. albicans in culture at 20 deg C?
|
budding yeast with pseudohyphae
|
|
Candida albicans: What is the morphology of c. albicans in culture at 37 deg C?
|
germ tubes
|
|
Candida albicans: What does "alba" mean?
|
White
|
|
Candida albicans: What disease does c. albicans cause in immunocompromised patients?
|
thrush in throat (neonates, steroids, diabetes, AIDS)
|
|
Candida albicans: What disease does c. albicans cause in IV drug users?
|
endocarditis
|
|
Candida albicans: What disease does c. albicans cause s/p antibiotic tx?
|
vaginitis
|
|
Candida albicans: What disease does c. albicans cause in people who wear diapers (i.e. babies)?
|
diaper rash
|
|
Candida albicans: What is the treatment for superficial c. albicans infection?
|
nystatin
|
|
Candida albicans: What is the treatment for serious systemic c. albicans infection?
|
amphotericin B
|
|
Systemic Mycoses: Name 4 types of systemic mycoses.
|
Coccidioidomycosis, Histoplasmosis, Paracoccidioidomycosis, Blastomycosis
|
|
Systemic Mycoses: Name the Endemic location of Coccidioidomycosis.
|
Southwestern United States, California.
|
|
Systemic Mycoses: Why is the disease caused by Coccidioidomycosis called “valley fever?”
|
Common in the San Joaquin Valley or desert (desert bumps) "valley fever"
|
|
Systemic Mycoses: Name the Endemic location of Histoplasmosis.
|
Mississipi and Ohio river valleys.
|
|
Systemic Mycoses: What is a common form of transmission of Histoplasmosis.?
|
Bird or bat dropings
|
|
Systemic Mycoses: Is Histoplasmosis found intracellularly or extracellularly?
|
Intracellular (frequently seen inside macrophages)
|
|
Systemic Mycoses: Name the Endemic location of Paracoccidioidomycosis.
|
Rural Latin America.
|
|
Systemic Mycoses: What is special about Paracoccidioidomycosis’ appearance?
|
Captain's wheel apearance.
|
|
Systemic Mycoses: Name the Endemic location of Blastomycosis.
|
States east of Mississipi River and Central America.
|
|
Systemic Mycoses: How does Blastomycosis reproduce?
|
Big, Broad-Based Budding.
|
|
Systemic Mycoses: What is a dimorphic fungus?
|
Mold in soil (at lower temperature) and yeast in tissue (at higher/body temperature: 37°C) Cold=Mold; Heat=Yeast
|
|
Systemic Mycoses: Which of the following are dimorphic: Coccidioidomycosis, Histoplasmosis, Paracoccidioidomycosis, Blastomycosis ?
|
All except coccidioidomycosis, which is a spherule in tissue.
|
|
Systemic Mycoses: What is the appropriate treatment for local infection with the systemic mycoses?
|
Treat with fluconazole or ketoconazole for local infection
|
|
Systemic Mycoses: What is the appropriate treatment for systemic infection with the systemic mycoses?
|
Treat with amphotericin B for systemic infection.
|
|
Systemic Mycoses: What acid fast bacterial disease can the systemic mycoses mimic?
|
TB (granuloma formation)
|
|
Systemic Mycoses: What is the appropriate agar to use for culturing of systemic mycoses?
|
Culture on Sabouraud's agar.
|
|
Cutaneous Mycoses: What organism causes Tinea versicolor?
|
Malassezia furfur. Causes hypopigmented skin lesions.
|
|
Cutaneous Mycoses: What organism causes Tinea nigra?
|
Cladosporium werneckii
|
|
Cutaneous Mycoses: How do you treat Tinea versicolor?
|
miconazole, selenium sulfide
|
|
Cutaneous Mycoses: What part of the skin is infected by tinea nigra and how does it present?
|
Infection of keratinized layers of skin. Apears as brownish spots
|
|
Cutaneous Mycoses: How do you treat tinea nigra?
|
sialicylic acid
|
|
Cutaneous Mycoses: Concerning Tinea pedis, cruris, corporis, capitis, what does the lesion look like?
|
Pruritic lesion wit central clearing resembling a ring.
|
|
Cutaneous Mycoses: What organisms cause Tinea pedis, cruris, corporis, & capitis?
|
Dermatophytes: Microsporum, Trichophyton, Epidermophyton
|
|
Cutaneous Mycoses: Concerning Tinea pedis, cruris, corporis, capitis, what do you see in a KOH prep?
|
Mold hyphae, not dimorphic
|
|
Cutaneous Mycoses: Concerning Microsporium, what is the reservoir for this organism
|
Pets
|
|
Cutaneous Mycoses: How is Microsporum infetction treated?
|
topical azoles
|
|
Opportunistic fungal infections: What organism is the cause of thrush in immunocomprornised?
|
Candida albicans
|
|
Opportunistic fungal infections: Other than thrush and vulvovaginitis, what other diseases can Candida albicans cause?
|
Disseminated candidiasis (to any organ) & chronic mucocutaneous candidiasis
|
|
Opportunistic fungal infections: What is the morphology of Candida albicans?
|
Pseudohyphae + budding yeasts or Germ tubes at 37 degrees C
|
|
Opportunistic fungal infections: What pulmonary disease is caused by Aspergillus fumigatus?
|
lung cavity aspergilloina ("fungus ball"), invasive aspergillosis.
|
|
Opportunistic fungal infections: What is the morphology of Aspergillus fumigatus?
|
Mold with septate hyphae that branch at a V-shaped (45°) angle.
|
|
Opportunistic fungal infections: Is Aspergillus fumigatus dimorphic?
|
NO
|
|
Opportunistic fungal infections: What diseases does the yeast Cryptocuccus neoformans cause?
|
Cryptococcal meningitis, cryptococcosis.
|
|
Opportunistic fungal infections: What is the morphology of Cryptocuccus neoformans?
|
Heavily encapsulated yeast.
|
|
Opportunistic fungal infections: Is Cryptocuccus neoformans dimorphic?
|
No
|
|
Opportunistic fungal infections: What type of budding pattern is seen in Cryptocuccus neoformans?
|
Narrow-based unequal budding
|
|
Opportunistic fungal infections: What natural environment is Cryptocuccus neoformans usually found?
|
Found in soil, pigeon dropings.
|
|
Opportunistic fungal infections: What do you culture Cryptocuccus neoformans on?
|
Culture on Sabouraud's agar.
|
|
Opportunistic fungal infections: What special stain is used for Cryptocuccus neoformans ?
|
Stains with India ink.
|
|
Opportunistic fungal infections: What special test does the capsule of Cryptocuccus neoformans allow you to do?
|
Latex agglutination test detects polysaccharide capsular antigen
|
|
Opportunistic fungal infections: What is the morphology of Mucor?
|
Mold with irregular nonseptate hyphae branching at wide angles (> 90°).
|
|
Opportunistic fungal infections: What immune modifying diseases (2) state is commonly associated with infection with Mucor?
|
Disease mostly in ketoacidotic diabetic and leukemic patients.
|
|
Opportunistic fungal infections: How does infection with Mucor lead to sympotms (pathogensis)?
|
Fungi proliferate in the walls of blood vessels and cause infarction of distal tissue.
|
|
Pneumocystis carinii: What disease does Pneumocystis carinii cause?
|
Causes pneumonia (PCP).
|
|
Pneumocystis carinii: What class of organism is Pneumocystis carinii?
|
Yeast (originally classified as protozoan)
|
|
Pneumocystis carinii: How is Pneumocystis carinii transmitted to caused disease?
|
Inhaled
|
|
Pneumocystis carinii: What predisposes to disease with Pneumocystis carinii?
|
Most infections asymptomatic. Immunosupression (e.g., AIDS) predisposes to disease.
|
|
Pneumocystis carinii: How do you stain for Pneumocystis carinii?
|
Silver stain of lung tissue.
|
|
Pneumocystis carinii: How do you treat infection with Pneumocystis carinii?
|
Treat with TMP-SMX, pentamidine.
|
|
Pneumocystis carinii: With regards to P. carinii, what should you do for an AIDS patient with CD4 below 200 cells/mL to prevent PCP?
|
Start prophylaxis when CD4 drops below 200 cells/mL in HIV patients.
|
|
Sporothrix schenckii: Where is Sporothrix schenckii normally found and how is it transmitted?
|
Found on vegetation and transmitted by trauma to the skin, typically by a thorn ("rose gardener's" disease)
|
|
Sporothrix schenckii: What are the symptoms of Sporcitrichosis?
|
Local pustule or ulcer with nodules along draining lymphatics. Little systemic illness.
|
|
Sporothrix schenckii: How do you treat Sporcitrichosis?
|
Treat with itraconazole or potassium iodide.
|
|
Entamoeba histolytica: What disease(s) does it cause?
|
Amebiasis: bloody diarrhea, (dysentery), liver abscess, RUQ pain
|
|
Entamoeba histolytica: How is it transmitted?
|
Cysts in water
|
|
Entamoeba histolytica: How is it diagnosed?
|
Serology and/or trophozoites or cysts in stool
|
|
Entamoeba histolytica: How it is treated?
|
Metronidazole and iodoquinol
|
|
Giardia lamblia: What disease(s) does it cause?
|
Giardiasis: bloating, flatulence, foul-smelling diarrhea
|
|
Giardia lamblia: How is it transmitted?
|
Cysts in water
|
|
Giardia lamblia: How is it diagnosed?
|
Trophozoites or cysts in stool
|
|
Giardia lamblia: How it is treated?
|
Metronidazole
|
|
Cryptosporidium: What disease(s) does it cause?
|
Severe diarrhea in AIDS. Mild disease (watery diarrhea) in non-HIV
|
|
Cryptosporidium: How is it transmitted?
|
Cysts in water
|
|
Cryptosporidium: How is it diagnosed?
|
Cysts in water
|
|
Cryptosporidium: How it is treated?
|
None
|
|
Toxoplasma: What disease(s) does it cause?
|
Brain abscess in HIV, birth defects
|
|
Toxoplasma: How is it transmitted?
|
Cysts in meat or cat feces
|
|
Toxoplasma: How is it diagnosed?
|
Serology, biopsy
|
|
Toxoplasma: How it is treated?
|
Sulfadiazine + pyrimethamine
|
|
What are the different species?: What disease(s) does it cause?
|
Malaria: cyclic fever, headache, anemia, splenomegaly; Malaria - severe (cerebral)
|
|
What are the different species?: How is it transmitted?
|
Mosquito (Anopheles)
|
|
What are the different species?: How is it diagnosed?
|
Blood smear
|
|
What are the different species?: How it is treated?
|
Chloroquine (primaquine for P. vivax, P. ovale), sulfadoxine + pyrimethamine, mefloquine, quinine
|
|
Trichomonas vaginalis: What disease(s) does it cause?
|
Vaginitis: foul-smelling, greenish discharge; itching and burning
|
|
Trichomonas vaginalis: How is it transmitted?
|
Sexual
|
|
Trichomonas vaginalis: How is it diagnosed?
|
Trophozoites on wet mount
|
|
Trichomonas vaginalis: How it is treated?
|
Metronidazole
|
|
Trypanosoma cruzi: What disease(s) does it cause?
|
Chagas' disease (heart disease)
|
|
Trypanosoma cruzi: How is it transmitted?
|
Reduviid bug
|
|
Trypanosoma cruzi: How is it diagnosed?
|
Blood smear
|
|
Trypanosoma cruzi: How it is treated?
|
Nifurtimox
|
|
Trypanosoma gambiense & rhodesiense: What disease(s) does it cause?
|
African sleeping sickness
|
|
Trypanosoma gambiense & rhodesiense: How is it transmitted?
|
Tsetse fly
|
|
Trypanosoma gambiense & rhodesiense: How is it diagnosed?
|
Blood smear
|
|
Trypanosoma gambiense & rhodesiense: How it is treated?
|
Suramin for blood-borne disease or melarsoprol for CNS penetration
|
|
Leishmania donovani: What disease(s) does it cause?
|
Visceral leishmaniasis (kala-azar)
|
|
Leishmania donovani: How is it transmitted?
|
Sandfly
|
|
Leishmania donovani: How is it diagnosed?
|
Macrophages containing amastigotes
|
|
Leishmania donovani: How it is treated?
|
Sodium stibogluconate
|
|
Babesia: What disease(s) does it cause?
|
Babesiosis
|
|
Babesia: How is it transmitted?
|
Ixodes tick
|
|
Babesia: How is it diagnosed?
|
Blood smear, no RBC pigment, apears as "maltese cross"
|
|
Babesia: How it is treated?
|
Quinine, clindamycin
|
|
Naegleria: What disease(s) does it cause?
|
Rapidly fatal meningoencephalitis
|
|
Naegleria: How is it transmitted?
|
Swimming in fresh water lakes
|
|
Naegleria: How is it diagnosed?
|
Amebas in spinal fluid
|
|
Naegleria: How it is treated?
|
None
|
|
Naegleria: AUTHOR
|
Nomi Levy
|
|
Medically important helminths: Which Cestode (tapeworm) can cause brain cysts and seizures?
|
Taenia solium
|
|
Medically important helminths: Echinococcus granulosus (a cestode) can cause cysts in the ____when ingested in dog feces; and _____ if antigens are released from cysts
|
liver, anaphylaxis
|
|
Medically important helminths: What is the standard treatment for trematodes (flukes)?
|
Praziquantel
|
|
Medically important helminths: Which fluke penetrates human skin, forming granulomas, fibrosis, and inflammation of the spleen & liver?
|
Schistosoma
|
|
Medically important helminths: Larvae of the nematode (roundworm) ___ are known to penetrate skin of feet & cause anemia if infect intestine.
|
Ancylostoma duodenale (hookworm)
|
|
Medically important helminths: Echinococcus granulosus (a cestode) can cause cysts in the ____when ingested in dog feces; and _____ if antigens are released from cysts.
|
liver, anaphylaxis
|
|
Medically important helminths: Which nematode causes anal pruritis?
|
Enterobius vermicularis (pinworm)
|
|
Medically important helminths: Lavae of the nematode ___ are found in the soil, penetrate the skin, and cause intestinal infection.
|
Strongyloides stercoralis
|
|
Medically important helminths: Trichinella spiralis (a nematode) is usually found in what food?
|
undercooked meat, usually pork
|
|
Medically important helminths: Which nematode can be seen crawling in the conjunctiva?
|
Loa loa
|
|
Medically important helminths: Treatment for river blindness, caused by onchocerca volvulus, is ___
|
Ivermectin
|
|
Medically important helminths: Wuchereria bancrofti cause blockage of lymphatic vessels in a condition known as:
|
elephantiasis
|
|
Medically important helminths: Three nematodes treated with Diethylcarbamazine:
|
Loa loa, Toxocara canis, and Wucheria bancrofti
|
|
Parasite hints: Perianal pruritis caused by:
|
Enterobius
|
|
Parasite hints: Microcytic anemia a result of infection with
|
Ancylostoma, Necator
|
|
Parasite hints: Schistosoma mansoni is known to result in
|
portal hypertension
|
|
Parasite hints: Schistosoma haematobium can cause ___ cancer and hematuria
|
bladder
|
|
Parasite hints: A trematode that causes hemoptysis is:
|
Paragonimus westernani
|
|
Parasite hints: Clonorchis sinensis causes disease in the:
|
biliary tract
|
|
Virology: All DNA viruses are dsDNA except:
|
parvoviridae
|
|
Virology: All DNA viruses are linear except these two:
|
papoviruses, hepadnavirus (circular)
|
|
Virology: All RNA viruses are ssRNA except
|
Reoviridae ("repeato-virus" (reovirus) is dsRNA)
|
|
Virology: Do hepadnavirus, herpesviruses, and poxvirus have an envelope?
|
Yes
|
|
Virology: Which virus is often responsible for "pink eye" (conjunctivitis)?
|
adenovirus
|
|
Virology: Which SS-linear(-) DNA virus is responsible for "slapped cheeks" rash?
|
Parvovirus
|
|
Virology: Which is the smallest DNA virus?
|
Parvovirus
|
|
Virology: Which DNA virus can cause aplastic crises in sickle cell disease?
|
Parvovirus (B19 virus)
|
|
Virology: Name 3 "naked" DNA virsuses (no envelope)
|
Parvo, Adeno, and Papovirus (you have to be naked for a PAP smear…)
|
|
Virology: The largest DNA virus, one which can cause "milkmaid's blisters" or molluscum contagiosum (and could be used in germ warfare), is:
|
poxvirus
|
|
DNA virus characteristics: Papovirus is not linear, but rather ____
|
circular, supercoiled
|
|
DNA virus characteristics: The only DNA virus that is not icosahedral is
|
Pox (complex)
|
|
DNA virus characteristics: All DNA viruses replicate in the nuclear except
|
Pox (carries own DNA-dependent RNA polymerase)
|
|
RNA viruses: Poliovirus, Echovirus,Rhinovirus, Coxsackievirus, and HAV are all members of which viral family?
|
Picornaviruses ("PERCH")
|
|
RNA viruses: Picorna-, Calci-, Flavi-, Toga-, Retro-, and Coronaviruses all share which RNA structure?
|
SS + linear
|
|
RNA viruses: Which SS-linear, nonsegmented RNA virus family is responsible for measles, mumps, and croup?
|
PaRaMyxovirus (Parainfluenza-croups; RSV-bronchiolitis in babies; Measles, Mumps)
|
|
RNA viruses: Hantavirus, Sanfly/Rift Valley fevers, and California encephalitis are all part of this SS-circular RNA viral family.
|
Bunyaviruses
|
|
RNA viruses: Orthomyxoviruses include which ubiquitous virus?
|
Influenza virus
|
|
RNA viruses: HIV and HTLV are both ____ with ____capsid symmetry.
|
retroviruses; icosahedral
|
|
RNA viruses: What is the #1 cause of fatal diarrhea in children?
|
Rotavirus (a reovirus)
|
|
RNA viruses: Rabies is caused by this viral family.
|
Rhabdoviruses
|
|
RNA viruses: Virus family credited with the "common cold"
|
Coronaviruses
|
|
RNA viruses: Ebola/Marburg hemorrhagic fever are caused by which viral family?
|
Filoviruses
|
|
More virology: Three naked (nonenveloped) RNA viruses are:
|
Calcivirus, Picornavirus, Reovirus (Naked CPR)
|
|
More virology: From where to herpesviruses aquire their envelopes?
|
nuclear membrane
|
|
More virology: From where do enveloped viruses usually acquire their envelopes?
|
plasma membranes
|
|
More virology: This is the only virus that is not haploid:
|
retrovirus (which has 2 identical ssRNA molecules, so considered diploid)
|
|
More virology: The only DNA viruses that does not replicate in the nucleus is:
|
poxvirus
|
|
More virology: The two RNA viruses which do not replicate in the cytoplasm are:
|
Influenza virus and retroviruses
|
|
Viral Vaccines: Live attenuated vaccines induce humoral and cell-mediated immunity, while killed viruses induce only ____ immunity.
|
humoral
|
|
Viral Vaccines: Are MMR (measles, mumps, rubella) vaccines live or killed?
|
Live attenuated
|
|
Viral Vaccines: Rabies, influenza, HAV, and Salk polio vaccines are of which type (live or killed)?
|
Killed (SalK=killed)
|
|
Viral Vaccines: A recombinant viral vaccine exists for which virus?
|
HBV (antigen=HBsAg)
|
|
Viral Vaccines: Worldwide pandemics of influenza virus are in part attributable to which type of viral genetics?
|
Reassortment (viruses with segmented genomes exchange segments)
|
|
Viral Pathogens: What structural similarity is shared by herpesviruses, HBV, and smallpox virus?
|
They are DNA enveloped viruses.
|
|
Viral Pathogens: RNA nucleocapsid enteroviruses include which pathogens?
|
poliovirus, coxsackievirus, echovirus, HAV
|
|
Viral Pathogens: The viral pathogens adenovirus, papillomaviruses, and parvoviruses are all what type of viral pathogens?
|
DNA nucleocapsid viruses
|
|
Viral Pathogens: Bunyaviruses, Orthomyxoviruses (influenza viruses), Arenaviruses, and Reoviruses are all what type of RNA virus?
|
segmented (BOAR)
|
|
Viral Pathogens: Aseptic (viral) meningitis can be caused by which small RNA viruses?
|
poliovirus, coxsackievirus, echovirus (and not by two other picoRNAviruses, rhinovirus and HIV)
|
|
Viral Pathogens: Reovirus considered the most important global cause of infantile gastroenteritis
|
Rotavirus (ROTA=Right Out The Anus)
|
|
Viral Pathogens: All paramyxoviruses have 1 serotype with this exception:
|
parainfluenza virus (4 serotypes)
|
|
Viral Pathogens: Parotitis can be caused by this paramyxovirus:
|
mumps virus ("mumps gives you bumps")
|
|
Viral Pathogens: Triad of mumps symptoms are:
|
asceptic Meningitis, Orchitis, and Parotitis (MOP)
|
|
Viral Pathogens: AUTHOR
|
Connie Chang
|
|
Measles virus: What virus type causes measles?
|
paramyxovirus
|
|
Measles virus: What bluish-gray spots on the buccal mucosa are diagnostic of measles
|
Koplik spots
|
|
Measles virus: 3 Cs of measles
|
Cough, Coryza, Conjunctivitis
|
|
Measles virus: 3 possible sequellae
|
SSPE, encephalitis, giant cell pneumonia. SSPE = subacute sclerosing panencephalitis
|
|
Influenza viruses: Five facts about Influenza: enveloped/nonenveloped, nuclear material, antigens, infection --> what risk?, protection.
|
1. Enveloped 2. ssRNA with segmented genome 3. Hemagglutinin and neuraminidase antigens 4. Risk of fatal bacterial superinfection 5. Protection = killed viral vaccine
|
|
Influenza viruses: Treatment for influenza A?
|
Amantadine, rimantadine, zanamivir, and oseltamivir
|
|
Influenza viruses: Treatment for influenza B?
|
Zanavir and oseltamivir (neuraminidase inhibitors)
|
|
Rabies virus: Rabies -- _______ (cytoplasmic inclusion) in _______(cell type)
|
Negri bodies in neurons
|
|
Rabies virus: Rabies -- incubation period
|
weeks to 3 months
|
|
Rabies virus: Rabies -- most common sources in US
|
bat, raccoon, skunk (>dog)
|
|
Rabies virus: Rabies travels to the CNS by…
|
retrograde migration up nerve axons
|
|
Rabies virus: Rabies - Si/Sx
|
hydrophobia and fatal encephalitis with seizures
|
|
Arboviruses: Arbovirus -- mode of transmission
|
Transmitted by arthropods (mosquitoes, ticks)
|
|
Arboviruses: Arbovirus -- classic illnesses
|
Dengue fever (in SE Asia = hemorrhagic shock syndrome) and yellow fever
|
|
Arboviruses: Arbovirus -- members of the family
|
flavivirus, togavirus, bunyavirus
|
|
Yellow fever: Yellow fever is transmitted by ____________
|
the Aedes mosquito (flavivirus)
|
|
Yellow fever: Symptoms of yellow fever
|
high fever, black vomitus, and jaundice.
|
|
Yellow fever: Yellow fever -- histology
|
Liver: councilman bodies (acidophilic inclusions)
|
|
Name the diseases caused by the following Herpesviridae:: HSV-1
|
Gingivostomatitis, keratoconjunctivitis, temporal lobe encephalitis, herpes labialitis
|
|
Name the diseases caused by the following Herpesviridae:: HSV-2
|
Herpes genitalis, neonatal herpes
|
|
Name the diseases caused by the following Herpesviridae:: VSV
|
Varicella-zoster (shingles), encephalitis, pneumonia
|
|
Name the diseases caused by the following Herpesviridae:: EBV
|
Infecious mononuelosis, Burkitt's lymphoma
|
|
Name the diseases caused by the following Herpesviridae:: CMV
|
Cogenital infection, mononucleosis, pneumonia
|
|
Name the diseases caused by the following Herpesviridae:: HHV-8
|
Karposi's sarcoma
|
|
Name the routes of transmission for the following Herpesviridae:: HSV-1
|
respiratory secretions and saliva
|
|
Name the routes of transmission for the following Herpesviridae:: HSV-2
|
sexual contact, perinatal
|
|
Name the routes of transmission for the following Herpesviridae:: VSV
|
respiratory secretions
|
|
Name the routes of transmission for the following Herpesviridae:: EBV
|
respiratory secretions, saliva
|
|
Name the routes of transmission for the following Herpesviridae:: CMV
|
congenital, transfusion, sexual contact, saliva, urine, transplant
|
|
Name the routes of transmission for the following Herpesviridae:: HHV-8
|
sexual contact
|
|
Mononucleosis: Mononucleosis is caused by _______
|
EBV
|
|
Mononucleosis: symptoms of mono
|
fever, hepatosplenomegaly, pharyngitis, and lymphadenopathy (esp posterior auricular nodes)
|
|
Mononucleosis: how do you test for mono?
|
heterophil antibody test
|
|
Mononucleosis: what do you see in the peripheral blood (mono)?
|
atypical lymphocytes (cytotoxic T cells)
|
|
Tzank test: What's a Tzanck test?
|
A smear of an opened skin vesicle to detect multinucleated giant cells (seen in HSV-1, HSV-2, VSV)
|
|
Hepatitis transmission: Name the type of nucleic acid and the virus type for the following hepatitis viruses:
|
0
|
|
Hepatitis transmission: Name the type of nucleic acid and the virus type for the following hepatitis viruses: Hepatitis A
|
RNA picornavirus
|
|
Hepatitis transmission: Name the type of nucleic acid and the virus type for the following hepatitis viruses: Hepatitis B
|
DNA hepadnavirus
|
|
Hepatitis transmission: Name the type of nucleic acid and the virus type for the following hepatitis viruses: Hepatitis C
|
RNA flavivirus
|
|
Hepatitis transmission: Name the type of nucleic acid and the virus type for the following hepatitis viruses: Hepatitis D
|
deta agent -- requires HBsAG as its envelope (coinfection only)
|
|
Hepatitis transmission: Name the type of nucleic acid and the virus type for the following hepatitis viruses: Hepatitis E
|
RNA calcivirus
|
|
Hepatitis transmission: Name the mode of transmission for the following hepatitis viruses
|
0
|
|
Hepatitis transmission: Mode of transmission: Hepatitis A
|
fecal-oral
|
|
Hepatitis transmission: Mode of transmission: Hepatitis B
|
parenteral, sexual, maternal-fetal
|
|
Hepatitis transmission: Mode of transmission: Hepatitis C
|
blood (IV drug users)
|
|
Hepatitis transmission: Mode of transmission: Hepatitis D
|
coinfection with HBV!
|
|
Hepatitis transmission: Mode of transmission: Hepatitis E
|
enterically; water-borne epidemics
|
|
Hepatitis transmission: which Hepatitis virus causes a high mortality rate in pregnant women?
|
E
|
|
Hepatitis transmission: which hepatitis virus has a short incubation period?
|
A (3 weeks)
|
|
Hepatitis transmission: which Hep virus has a long incubation period?
|
B (3 months)
|
|
Hepatitis transmission: which Hep virus has a DNA-dependent DNA polymerase?
|
B; reverse transcription also occurs
|
|
Hepatitis transmission: which pairs of viruses are similar in course, severity, and incubation?
|
HAV & HEV; HBV & HCV
|
|
Hepatitis transmission: Which virus type infection leads to chronic-carrier-status?
|
B, C, and D
|
|
Hepatitis serologic markers: If I got a Hepatitis B vaccine (no infection), for what Ab would I have a positive serology?
|
HBsAb
|
|
Hepatitis serologic markers: If I recently had a Hepatitis B infection, for what Ab would I have a positive serology
|
HBsAb and HBcAb (positive during window period)
|
|
Hepatitis serologic markers: What test tells you either that I have a current infection or that I am a chronic Hep B carrier?
|
HBsAg
|
|
Hepatitis serologic markers: What test demands that you(the doctor) to tell me to stop having sex with my spouse lest I give them Hep B?
|
HBeAg
|
|
Hepatitis serologic markers: What test tells you(the doctor) that I can resume sex with my spouse because I'm not likely to give them Hep B?
|
HBeAb (indicates low transmissibility)
|
|
Hepatitis serologic markers: What is the "window period"?
|
after the actue infection is cleared and before the humoral response produces lots and lots of Ab (HBsAg AND anti-HBs negative; HBcAb positive)
|
|
Hepatitis serologic markers: How big is the Hep B virus
|
42 nm
|
|
Hepatitis serologic markers: When can I detect HBV particles by DNA polymerase?
|
during the incubation period and the acute disease period
|
|
Hepatitis serologic markers: How can I distniguish between complete recovery from Hep B infection and the chronic carrier state?
|
Complete recovery: HBsAg-neg, HBsAb-pos; Chronic carrier: HBsAb-neg. HBsAb-pos; HBcAb is positive in BOTH states
|
|
HIV: HIV has a ________ genome with __<#>__ molecules of __<nucleic acid>____
|
HIV has a diploid genome with 2 molecules of RNA
|
|
HIV: name the "rectangular nucleocapsid protein": HIV: name the envelope proteins
|
gp41 and gp 120
|
|
HIV: name the matrix protein: HIV: what other important protein hangs out inside the nucleocapsid?
|
reverse transcriptase
|
|
HIV: name the matrix protein: Does HIV integrate into the host genome?
|
YES. HIV syntehsizes dsDNA from RNA and integrates the dsDNA into the host genome
|
|
HIV diagnosis: How do I make a diagnosis of HIV?
|
ELISA --> confirmed by Western blot
|
|
HIV diagnosis: T or F: HIV testing is always positive 1-2 weeks after infection
|
FALSE. ELISA/Western blot look for viral PROTEINS and can be falsely negative for the first 1-2 months of HIV infection
|
|
HIV diagnosis: How can I monitor the effect of HIV drug therapy?
|
HIV PCR/viral load
|
|
HIV immunity: Who is immune to HIV?
|
homozygous for CCR5 mutation
|
|
HIV immunity: What % of US caucasians have a slower course of HIV infection because of heterozygosity for the above allele?
|
0.2
|
|
HIV immunity: Persons with ______________ have a rapid progression to AIDS
|
CXCR1 mutation
|
|
Time course of HIV infection: HIV become symptomatic _____ after infection
|
3-10 years
|
|
Time course of HIV infection: Anti-p 24 and anti-gp120 increase between _______ after initial infection; after the onset of immunodeficiency, they ___________(increase or decrease)
|
1-2 months; decrease
|
|
Name the opportunistic infections seen in the following categories: (for AIDS patients): bacterial
|
TB, Mycobacterium avium-intercellulare complex
|
|
Name the opportunistic infections seen in the following categories: (for AIDS patients): viral
|
HSV, VAV, CMV, PML (JC virus)
|
|
Name the opportunistic infections seen in the following categories: (for AIDS patients): fungal
|
Thrush (Candida albicans), cryptococcosis (cryptococcal meningitis), histoplasmosis, Pneumocystis pneumonia
|
|
Name the opportunistic infections seen in the following categories: (for AIDS patients): protozoan
|
toxoplasmosis, cryptosporidiosis
|
|
Prions: Multiple choice: Prions are -- 1) infectious proteins ONLY 2) infectious RNA 3) infectious DNA 4) infectious proteins occasionally mixed with nucleic acids
|
1) infectious proteins
|
|
Prions: Name examples of prion diseases
|
CJD, kuru, scrapie, "mad cow"
|
|
Prions: Jeopardy style: pathologic prions take on this conformation
|
What is beta-pleated sheet
|
|
Prions: Prions are associated with ___________ encephalopathy
|
spongiform
|
|
Name the dominant normal flora in each of these areas:: skin
|
Staph epidermidis
|
|
Name the dominant normal flora in each of these areas:: nose
|
Staph aureus
|
|
Name the dominant normal flora in each of these areas:: oropharynx
|
Strep viridans
|
|
Name the dominant normal flora in each of these areas:: dental plaque
|
Strep mutans
|
|
Name the dominant normal flora in each of these areas:: colon
|
Bacteroides fragilis > E. coli
|
|
Name the dominant normal flora in each of these areas:: vagina
|
Lactobacillus, colonized by E. coli and group B strep
|
|
Common causes of pneumonia: Name the common causes of pneumonia in the following age groups:
|
0
|
|
Common causes of pneumonia: Name the common causes of pneumonia in the following age groups: Children (6 weeks to 18 yrs)
|
Virus (RSV), Mycoplasma, Chlamydia pneumoniae, Strep pneumoniae
|
|
Common causes of pneumonia: Name the common causes of pneumonia in the following age groups: Adults (18-40 yrs)
|
Mycoplasma, Chlamydia pneumoniae, Strep pneumoniae
|
|
Common causes of pneumonia: Name the common causes of pneumonia in the following age groups: Adults (40-65 yrs)
|
Strep pneumoniae, H. influenze, Anaerobes, Viruses, Mycoplasma
|
|
Common causes of pneumonia: Name the common causes of pneumonia in the following age groups: Elderly
|
Strep pneumoniae, viruses, anerobes, H. Influenzae, Gram-negative rods
|
|
Common causes of pneumonia: An AIDS patient comes into your office with symptoms of pneumonia. What organisms are you considering?
|
Staphylococcus, gram-negative rods, fungi, viruses, Pneumocystis carinii
|
|
Common causes of pneumonia: A patient in the CCU gets pneumonia. What organisms are you thinking?
|
Nosocomial infections are usually Staphylococcus and gram-negative rods
|
|
Common causes of pneumonia: The same patient also aspirated some peas prior to getting sick. What organisms do you add to your list?
|
Anaerobes
|
|
Common causes of pneumonia: His domineering wife of this same patient is mad because he also had a viral infection last week. What infectious agents would you now consider?
|
add H. influenzae; another common postviral pneumonia bug is Staph
|
|
Common causes of pneumonia: The wife is so distressed she goes into labor and gives birth to a 10 lb baby girl, who also gets pneumonia. Does she have the same bug as her dad in the CCU?
|
Neonatal pneumonia is usually due to Group B streptococci or E. coli -- the dad could have the latter.
|
|
Common causes of pneumonia: Of course, the wife get sick too, but her pneumonia is classified as "atypical." What might she have?
|
Mycoplasma, Legionella, Chlamydia
|
|
Name the causes of meningitis in the following age groups:: Newborn (0-6 months)
|
Group B strep, E. coli, Listeria
|
|
Name the causes of meningitis in the following age groups:: Children (6 mo to 6 years)
|
Strep pneumoniae, Neisseria meningitidis, Haemophilus influenze type B, Enteroviruses
|
|
Name the causes of meningitis in the following age groups:: 6-60 years
|
N. meningitidis, Enteroviruses, S. pneumoniae, HSV
|
|
Name the causes of meningitis in the following age groups:: 60+ years
|
Gram-negative rods, Listeria
|
|
Name the causes of meningitis in the following age groups:: An AIDS patient comes to you with high fevers, stiff neck, and mental status changes. What organisms might be causing his meningitis?
|
Cryptococcus, CMV, toxoplasmosis (brain abscess), JC virus (PML)
|
|
CSF findings in meningitis: You do a spinal tap on your patient. The CSF pressure appears to be increased. What type of infectious agent have you eliminated?
|
none. It could be bacterial, TB, fungal, or viral (in viral, CSF pressure is normal to increased)
|
|
CSF findings in meningitis: You do a quick smear of the spinal tap under the microscope and see increased polys. What type of infectious agent does this suggest?
|
bacterial. In fungal, TB, and viral, you see increased lymphocytes.
|
|
CSF findings in meningitis: The lab tests show an increase in protein and a decrease in sugar in the CSF. Does that confirm your previous guess or confuse you?
|
Confirms. These findings are seen in bacterial, fungal, and TB infections. In viral infections the protein and sugar concentrations of the CSF are normal.
|
|
Osteomyelitis: What population is most likely to get osteomyelitis?
|
children
|
|
Osteomyelitis: What lab test is elevated in osteomyelitis?
|
ESR
|
|
For each of the following groups of persons, name the organism that is most likely to cause osteomyelitis: Most people (nonspecific)
|
S aureus -- assume S aureus if no other information
|
|
For each of the following groups of persons, name the organism that is most likely to cause osteomyelitis: sexually active
|
Neisseria gonorrhea (rare -- septic arthritis is more common)
|
|
For each of the following groups of persons, name the organism that is most likely to cause osteomyelitis: drug addicts
|
Pseudomonas aeruginosa
|
|
For each of the following groups of persons, name the organism that is most likely to cause osteomyelitis: Sickle cell Px
|
Salmonella
|
|
For each of the following groups of persons, name the organism that is most likely to cause osteomyelitis: Prosthetic replacement
|
S. aureus and S. epidermidis
|
|
For each of the following groups of persons, name the organism that is most likely to cause osteomyelitis: Vertebral
|
Mycobacterium tuberculosis
|
|
Urinary tract infections: What 2 groups of males are likely to get UTIs?
|
old men with enlarged prostates and baby boys with congenital defects
|
|
Urinary tract infections: What are symptoms of pyelonephritis?
|
fever, chills, flank pain, CVA tenderness
|
|
Urinary tract infections: What are symptoms of a UTI?
|
dysuria, frequency, urgency, suprapubic pain
|
|
Urinary tract infections: The 2nd most common cause of UTI in young, ambulatory women is __________________
|
Staphylococcus saprophyticus
|
|
Urinary tract infections: Your patient gets a UTI while in the hospital. What organisms do you want to make sure his antibiotics cover while his urine culture is growing?
|
E. coli, Proteus, Klebsiella, Serratia, Pseudomonas
|
|
Urinary tract infections: What are predisposing factors for UTIs?
|
female gender (10:1; short urethra colonized by fecal flora), flow obstruction, kidney surgery, catheterization, gynecologic abnormalities, diabetes, pregnancy
|
|
Urinary tract infections: AUTHOR
|
Sharyn Miskovitz
|
|
UTI Bugs: Has a blue-green pigment and fruity odor
|
Pseudomonas aeruginosa
|
|
UTI Bugs: Two UTI bugs that are nosocomial and drug resistant
|
Pseudomonas aeruginosa and Serratia marcescens
|
|
UTI Bugs: Leading cause of UTIs
|
Escherichia coli
|
|
UTI Bugs: What does Proteus mirabilis produce?
|
Urease
|
|
UTI Bugs: Serratia marcescens produce what color pigment?
|
red
|
|
UTI Bugs: Large mucoid capsule and viscous colonies
|
Klebsiella pneumoniae
|
|
UTI Bugs: What do E. coli colonies show on EMB agar?
|
metallic sheen
|
|
UTI Bugs: 2nd leading cause of UTIs in sexually active women
|
Staphylococcus saprophyticus
|
|
UTI Bugs: Associated with struvite stones and swarming on agar
|
Proteus mirabilis
|
|
Sexually transmitted diseases: What are the three clinical stages of syphilis
|
1st degree, 2nd degree, and thrid degree
|
|
Sexually transmitted diseases: Lymphogranuloma venereum is caused by what organism?
|
Chlamydia trachomatis
|
|
Sexually transmitted diseases: A painless chancre is a sign of what disease?
|
1st degree syphilis
|
|
Sexually transmitted diseases: What organism causes chlamydia?
|
Chlamydia trachomatis
|
|
Sexually transmitted diseases: What are the clinical features of Gonorrhea?
|
Urethritis, cervicitis, PID, prostatitis, epididymitis, arthritis
|
|
Sexually transmitted diseases: What serotypes of Chlamydia trachomatis cause chlamydia?
|
D-K
|
|
Sexually transmitted diseases: What are the features of AIDS?
|
Oportunistic infections, Kaposi's sarcoma, lymphoma
|
|
Sexually transmitted diseases: The clinical feature of Trichomoniasis is what?
|
Vaginitis
|
|
Sexually transmitted diseases: Chancroid is caused by what organism?
|
Haemophilus ducreyi
|
|
Sexually transmitted diseases: Gummas, tables dorsalis, general paresis, aortitis, Argyll Robertson pupil are clinical features of what STD?
|
3rd degree syphilis
|
|
Sexually transmitted diseases: HSV-2 causes what disease with what features?
|
Genital herpes with painful penile,vulvar, or cervical ulcers
|
|
Sexually transmitted diseases: Ulcers, lymphadenopathy, and rectal strictures are signs of what disease?
|
Lymphogranuloma venereum
|
|
Sexually transmitted diseases: Which organisms cause Condylomata acuminata?
|
HPV 6 and 11
|
|
Sexually transmitted diseases: Hepatitis B causes what clinical feature?
|
Jaundice
|
|
Sexually transmitted diseases: What are the clinical features of 2nd degree syphilis?
|
Fever, lymphadenopathy, skin rashes, condylomata lata
|
|
Sexually transmitted diseases: Chancroid has what clinical feature?
|
Painful genital ulcers
|
|
Sexually transmitted diseases: What serotypes of Chlamydia trachomatis cause Lymphogranuloma venereum?
|
L1-L3
|
|
Sexually transmitted diseases: Trichomonas vaginalis causes what disease?
|
Trichomoniasis
|
|
Sexually transmitted diseases: Urethritis, cervicitis, conjunctivities, Reiter's syndrome, and PID are features of what diesease?
|
Chlamydia
|
|
Sexually transmitted diseases: Koilocytes are characteristic of what diease?
|
Condylomata acuminata
|
|
Sexually transmitted diseases: What organism causes 1st, 2nd, and 3rd degree syphilis?
|
Treponema pallidum
|
|
Pelvic inflammatory disease: What are the top bugs that cause PID?
|
Chlamydia trachomatis (subacute, often undiagnosed), Neisseria gonorrheae (acute, high fever)
|
|
Pelvic inflammatory disease: What is a risk factor for ectopic pregnancy, infertility, chronic pelvic pain, and adhesions?
|
Salpingitis
|
|
Pelvic inflammatory disease: What is the most common STD in the US?
|
Chlamydia trachomatis (3-4 million cases per year)
|
|
Pelvic inflammatory disease: What type of abscesses can occur in PID?
|
Tubo-ovarian abscesses
|
|
Pelvic inflammatory disease: What does the chandelier sign test for?
|
Cervical motion tenderness
|
|
Pelvic inflammatory disease: What are some of the manifestations of PID?
|
Purulent cervical discharge, salpingitis, endometriosis, and hydrosalpinx
|
|
Pelvic inflammatory disease: What STDs other than C. trachomatis and N, gonorrhea cause PID?
|
Gardnerella (clue cells) and Trichomonas (motile on wet prep)
|
|
Nosocomial infections: What are 2 of the most common causes of nosocomial infections?
|
E. Coli (UTI) and S. aureus (wound infection)
|
|
Nosocomial infections: When in a renal dialysis unit which pathogen should you be concerned about?
|
HBV
|
|
Nosocomial infections: What is the most likely pathogen when a water source (water aerosols) is involved?
|
Legionella
|
|
Nosocomial infections: What pathogen is often found on respiratory therapy equiptment?
|
Pseudomonas aeruginosa (AIRuginosa when AIR or burns are involved?
|
|
Nosocomial infections: What are the two pathogens most commonly associated with urinary catheterization?
|
E. coli and Proteus mirabilis
|
|
Nosocomial infections: Being in a newborn nursery is a risk factor for what pathogens?
|
CMV and RSV
|
|
Nosocomial infections: Which pathogen would most associated with hyperalimentation (total parenteral nutrition)
|
Candida albicans
|
|
Infections dangerous in pregnancy: What are the organisms that can cross the blood-placenta barrier and be dangerous in pregnancy?
|
ToRCHcS=Toxoplasma, Rubella, CMV, HSV/HIV, Syphilis
|
|
Infections dangerous in pregnancy: Bug hints (if all else fails)
|
Name the associated bug
|
|
Infections dangerous in pregnancy: Branching rods in oral infection
|
Actinomyces israelii
|
|
Infections dangerous in pregnancy: Surgical wound
|
S. aureus
|
|
Infections dangerous in pregnancy: Pus, empyema, abscess
|
S. aureus
|
|
Infections dangerous in pregnancy: Pediatric Infection
|
Haemophilus influenzae (including epiglottis)
|
|
Infections dangerous in pregnancy: Sepsis/meningitis in newborn
|
Group B strep
|
|
Infections dangerous in pregnancy: Dog or cat bite
|
Pasteurella multocida
|
|
Infections dangerous in pregnancy: Pneumonia in cystic fibrosis, burn infection
|
Pseudomonas aeruginosa
|
|
Infections dangerous in pregnancy: Currant jelly sputum
|
Klebsiella
|
|
Infections dangerous in pregnancy: Traumatic open wound
|
Clostridium perfringens
|
|
Antibody structure and function: Which part of the light and heavy chain recognizes the antigen?
|
Variable part
|
|
Antibody structure and function: The interchain and intrachain bonds in the antibody are of what type?
|
Disulfide bonds
|
|
Antibody structure and function: What is the term called when the antibody prevents bacterial adherence?
|
Neutralization
|
|
Antibody structure and function: The amino terminal is part of which fragment of the antibody?
|
Fab fragment
|
|
Antibody structure and function: The fab fragment of the antibody is composed of which chain(s)?
|
Light and heavy chains
|
|
Antibody structure and function: Describe the Fc fraction of the B cell receptor.
|
Constant, Carboxy terminal, Complement-binding (IgG + IgM only), Carbohydrate side chains
|
|
Antibody structure and function: What is the purpose of opsonization?
|
The antibody promotes phagocytosis
|
|
Antibody structure and function: The hypervarible region is a compontent of which fragment of the antibody?
|
Fab fragment
|
|
Antibody structure and function: Only the heavy chain contributes to which fraction of the antibody?
|
Fc
|
|
Antibody structure and function: Why does an antibody activate complement?
|
To enhance opsonization and lysis
|
|
Antibody structure and function: The constant part of the heavy chain of IgM and IgG does what?
|
Fixes complement
|
|
Immunogloblulin isotypes: Which isotype has an unclear function?
|
IgD
|
|
Immunogloblulin isotypes: What is the main anitbody in a second response to an antigen?
|
IgG
|
|
Immunogloblulin isotypes: When is IgM produced?
|
Primary response to an antigen
|
|
Immunogloblulin isotypes: Which isotype induces the release of mediators from mast cells and basophils when exposed to an antigen?
|
IgE
|
|
Immunogloblulin isotypes: Where is IgD found?
|
On the surface of many B cells and in serum
|
|
Immunogloblulin isotypes: Which isotype fixes complement, crosses the placenta, opsonizes bacteria, and neutralizes bacterial toxins and viruses ?
|
IgG
|
|
Immunogloblulin isotypes: Which isotype that guards the mucous membranes from attachement of bacteria and viruses?
|
IgA
|
|
Immunogloblulin isotypes: IgE stimulates which type of hypersensitivity reaction?
|
Type I
|
|
Immunogloblulin isotypes: IgE mediates immunity to what?
|
Worms
|
|
Immunogloblulin isotypes: Which isotype fixes complement but does not cross the placenta?
|
IgM
|
|
Immunogloblulin isotypes: Which isotype has the lowest concentration in the serum?
|
IgE
|
|
Immunogloblulin isotypes: Which isotype found in secretions?
|
IgA
|
|
Immunogloblulin isotypes: Which isotype crosses the placenta?
|
IgG
|
|
Ig epitopes: Which Ig epitope is common to a single class of Ig (5 classes, determined by the heavy chain)?
|
Isotype (IgG, IgA, IgM, IgE, IgD) Isotype=iso (same). Common to same class.
|
|
Ig epitopes: Which Ig epitope is determined by antigen-binding site?
|
Idiotype (specific for a given antigen) Idiotype=idio (unique). Hypervariable region is unique.
|
|
Ig epitopes: Which Ig epitope differs among members of the same species and can be on the light or heavy chain?
|
Allotype (polymorphism)
|
|
MHC I and II: Antigen presenting cells have which type(s) of MHC protein?
|
MHC I and MHC II
|
|
MHC I and II: Which class MHC proteins is the main determinants of organ rejection?
|
MHC II
|
|
MHC I and II: How many class I genes does the MHC consist of?
|
3 (A, B, C)
|
|
MHC I and II: What class of MHC antigen loading occurs in acidified endosomes?
|
MHC II
|
|
MHC I and II: All nucleated cells have which type of MHC protein(s)?
|
MHC I
|
|
MHC I and II: Which class MHC protein has 1 polypeptide with beta 2 microglobin?
|
MHC I
|
|
MHC I and II: Where does MHC I antigen loading occur in the cell?
|
RER (viral antigens)
|
|
MHC I and II: What are the 3 MHC II genes?
|
DP, DQ, DR
|
|
MHC I and II: Which class MHC protein has 2 polypeptides and and alpha and beta chain?
|
MHC II
|
|
Differentiation of B and T cells: Which helper T cell is involved in antibody-mediated immunity?
|
Th2 cell
|
|
Differentiation of B and T cells: In an environment with a lot of IL-12, naĂŻve helper T cells will mature to which helper T cell?
|
Th1 cell
|
|
Differentiation of B and T cells: Why do Th2 cells produce IL-4 and IL-5?
|
To help B cells make antibody (B=2nd letter of alphabet)
|
|
Differentiation of B and T cells: Gamma interferon is secreted by what cell to activate macrophages?
|
Th1 cell
|
|
Differentiation of B and T cells: Which growth factor induces the maturation from naĂŻve helper T cell to Th2 cell?
|
IL-4
|
|
Differentiation of B and T cells: Th1 secretes what growth factor to activate CD8 cells?
|
IL-2
|
|
Differentiation of B and T cells: IL-4 and IL-5 are released from Th2 to activate what type of cell?
|
B cell
|
|
Differentiation of B and T cells: Why do Th1 cells produce IL-2 and gamma-interferon?
|
To activate macrophages (increase killing efficiency of intracellular bacteria) and CD8 cells
|
|
Differentiation of B and T cells: Which helper T cell is involved in cell-mediated immunity?
|
Th1 cell
|
|
Differentiation of B and T cells: Major function of B cells and T cells
|
Choose either B (antibody-mediated immunity) or T cell (cell-mediated immunity)
|
|
Differentiation of B and T cells: Allergy (hay fever)
|
B cell
|
|
Differentiation of B and T cells: Regulation of antibody response (help and suppression)
|
T cell
|
|
Differentiation of B and T cells: Autoimmunity
|
B cell
|
|
Differentiation of B and T cells: Allergy (poison oak)
|
T cell
|
|
Differentiation of B and T cells: Host defense against infection (opsonize bacteria, neutralize toxins and viruses)
|
B cell
|
|
Differentiation of B and T cells: Host defense against infection (especially Mycobacterium uberculosis, viruses, and fungi)
|
T cell
|
|
Differentiation of B and T cells: Graft and tumor rejection
|
T cell
|
|
Adjuvant definition: What is the short definition of an adjuvant?
|
That which aids another
|
|
Adjuvant definition: Human vaccines contain aluminum hydroxide or what?
|
Lipid adjuvants
|
|
Adjuvant definition: Adjuvants are ________ stimulators of the immune response but are not immunogenic by themselves.
|
Nonspecific
|
|
Adjuvant definition: What are adjuvants given with to enhance response?
|
Weak immunogen
|
|
T-cell glycoproteins: Cytotoxic T cells have which type of co-receptor?
|
CD8
|
|
T-cell glycoproteins: CD4 cell secretes which 3 cytokines to activate B cells?
|
IL-2, IL-4, IL-5
|
|
T-cell glycoproteins: What is the CD3 complex?
|
A cluster of polypeptides associated with a T-cell receptor. It is important in signal transduction
|
|
T-cell glycoproteins: When a cell first gets infected with a virus which three cells respond?
|
APC, B cell (through IgM BCR), and CD8 (through TCR and MHC I on infected cell)
|
|
T-cell glycoproteins: Name three antigen-presenting cells.
|
Macrophage, dendritic cell, and B cell
|
|
T-cell glycoproteins: CD4 are on which type of T cells?
|
Helper T cells
|
|
T-cell glycoproteins: CD4 cell secretes which growth factor to activate the CD8 cells?
|
IL-2
|
|
T-cell glycoproteins: CD4 on helper T cells bind to what?
|
MHC II on antigen-presenting cells. Product of CD and MHC=8
|
|
T-cell glycoproteins: CD8 on cytotoxic T cells bind to what?
|
MHC I on virus-infected cells. Product of CD and MHC=8
|
|
T cell activation: What recognizes the foreign antigen that is presented by MHC II?
|
TCR on the Th cell
|
|
T cell activation: IL-2 from the helper T cell activates which cell to kill virus-infected cells?
|
Cytotoxic T cell
|
|
T cell activation: A foreign body is phagocytosed by what type of cell?
|
APC
|
|
T cell activation: The helper T cell is activated to produce which two cytokines in cell-mediated immunity?
|
IL-2 and gamma-interferon
|
|
T cell activation: What recognizes endogenously synthesized (viral or self) proteins that are presented by MHC I?
|
TCR on cytotoxic T cell
|
|
T cell activation: What is the costimulatory signal needed for a helper T cell to be activated by MHC II on an APC?
|
B7 (protein on APC) and CD28 (receptor on helper T cell)
|
|
T cell activation: AUTHOR
|
Flora Waples-Trefil
|
|
Anergy: The state when an immune cell matures but does not respond to antigens, this process is called…..
|
Anergy
|
|
Anergy: Anergy in both T and B cells is caused by…
|
Their response to a self-antigen
|
|
Anergy: Where are B cells exposed to self-antigen
|
bone marrow
|
|
Anergy: Which type of cell is more sensitive to anergic stimulus?
|
T cells
|
|
Important Cytokines: What cytokine is an endogenous pyrogen?
|
IL-1
|
|
Important Cytokines: Which major cytokines are produced by Macrophages?
|
IL-1, IL-6, and TNF-alpha
|
|
Important Cytokines: What are the effects of the cytokines produced by macrophages?
|
(1) causes the liver to make more complement, (2) fever, (3) mobilizes neutrophils from bone marrow, (4)helpts T-cells migrate to lymph nodes and mature, therefore, helps acute phase reaction
|
|
Important Cytokines: IL-1 by itself causes what effects?
|
Fever, stimulates the growth and differentiation of T and B cells, neutrophils, fibroblasts and epithelial cells
|
|
Important Cytokines: What cytokine stimulates the growth of helper T and NK cells
|
IL-2
|
|
Important Cytokines: What cells secrete IL-2
|
Helper T cells
|
|
Important Cytokines: What cytokine has the same effect as GM-CSF
|
IL-3
|
|
Important Cytokines: What cytokines promote the growth and differentiation of B cells
|
IL-4, IL-5, TNF-alpha
|
|
Important Cytokines: What cytokine stimulates the synthesis of IgE and IgG?
|
IL-4
|
|
Important Cytokines: What cytokine stimulates eosinophil production?
|
IL-5
|
|
Important Cytokines: T-helper cells secrete which cytokines?
|
IL-2, IL-4, IL-5, gamma interferon
|
|
Important Cytokines: What cytokine stimulates the synthesis of IgA?
|
IL-5
|
|
Important Cytokines: What cytokine acts to attract neutrophils?
|
IL-8 (major) and TNF-alpha (minor)
|
|
Important Cytokines: What cytokine stimulates macrophages?
|
gamma-interferon
|
|
Important Cytokines: What is the difference between TNF-alpha and TNF-beta?
|
TNF-alpha is secreted by macrophages, and TNF-beta is secreted by T lymphocytes. Their functions are similar.
|
|
Important Cytokines: What do TNF-alpha and TNF-beta do?
|
increase IL-2 output and B-cell proliferation, attracts neutrophils
|
|
Cell Surface Proteins: What markers identify T cells
|
TCR and CD3
|
|
Cell Surface Proteins: what cells have receptors for MHC I
|
NK cells
|
|
Cell Surface Proteins: What does MHC I do?
|
presents self-antigens, in viral infections the molecules presented by MHC I will change, which is why NK cells respond to viral infections best.
|
|
Cell Surface Proteins: What cells have MHC I on their surface?
|
all cells except RBCs
|
|
Cell Surface Proteins: what does MHC II do?
|
Presents non-self antigens
|
|
Cell Surface Proteins: What cells have MHC II?
|
macrophages, monocytes, dendritic cells (called professional antigen presenting cells)
|
|
Cell Surface Proteins: What markers are specific for B cells?
|
CD20, CD19, IgM
|
|
Cell Surface Proteins: What marker disappears when B cells become anergic?
|
IgM is internalized in anergic cells
|
|
Cell Surface Proteins: What is a marker for Macrophages?
|
CD14
|
|
Cell Surface Proteins: What is a marker for NK cells?
|
receptors for MHC I, CD 16
|
|
Acute Phase Response: What cytokines are responsible for the Acute Phase Response?
|
IL-1, IL-6, TNF-alpha
|
|
Acute Phase Response: How does the acute Phase Reaction cause a fever?
|
IL-1 acts on the hypothalamus to increase body temp, fat is mobilized to increase energy, and muscle mass is used to create heat
|
|
Acute Phase Response: The Acute Phase Reaction involves the mobilization of which cells?
|
B cells, T cells, Neutrophils
|
|
Acute Phase Response: Why is fever useful in an infection?
|
Viruses and bacteria divide less in higher temperatures, it increases antigen production, and increases parts of the immunes response
|
|
Acute Phase Response: What does the liver do in the Acute Phase Reaction?
|
Creates acute phase proteins (ex: C-reactive) which then activate complement and help in opsinization
|
|
Acute Phase Response: What does bone marrow do in the Acute Phase Reaction?
|
Releases CSF which causes leukocytosis
|
|
Acute Phase Response: What do Dendritic cells do in the Acute Phase Reaction?
|
the Professional antibody presenting cells migrate to the lymph nodes to initiate the adaptive response.
|
|
Complement: What kind of bacteria does complement act against?
|
Gram negative
|
|
Complement: Why does complement act preferentially against gram - bacteria?
|
Complement initiators like to behind to carbohydrates, so gram- bacteria or noticed more than others.
|
|
Complement: The classic pathway is initiated by….?
|
IgM or IgG (remember, GM makes Classic cars) antibody-antigen complexes
|
|
Complement: The alternate pathway is initiated by….?
|
basically, everything else - endotoxins, microbial surfaces, IgA, etc.
|
|
Complement: C1, C2, C3, C4 do what?
|
Viral neutralization
|
|
Complement: C3b does what?
|
think B for Binding - anything that ends in b acts to opsinize bacteria
|
|
Complement: What does C3a do?
|
Think A for Inflame - anything that ends in a acts to increase the inflammatory response. C3a leads to anaphylaxis, along with C5a
|
|
Complement: What is MC5b6,7,8,9?
|
This is the name for the membrane attack complex that punches holes in membranes and actually kills the bacteria.
|
|
Complement: What does a lack of C1 esterase cause and why?
|
causes angioedema - which is basically overactive complement. This is because C1 is the initial step in the classic pathway, and if it cannot be limited, you over-react.
|
|
Complement: What does a lack of C3 cause?
|
sever and recurrent pyrogenic infections of the sinuses and UR tract, because C3 is the first common step in both pathways, and without it both pathways are cripled.
|
|
Complement: Lack of C6, C7, and C8 cause what?
|
Nisseria bacteremia. I have no idea why.
|
|
Complement: Lack of decay accelerating factor (DAF) leads to what?
|
Paroxysmal nocturnal hemaoglobinuria because the complement attacks the RBCs. DAF stops C3.
|
|
Complement: What is the first step in the complement cascade that combines the two pathways?
|
C3 activation
|
|
Complement: What is the first step to bind to the cell membrane?
|
C5a (after C5 is cleaved by C3 products)
|
|
Interferon Mechanism: What is the purpose of interferons?
|
Interferons interfere is viral infection of cells and replication. They also activate NK cells to kill infected cells
|
|
Interferon Mechanism: What do Alpha and beta interferon do?
|
degrade viral mRNA, thereby inhibiting viral protein synthesis.
|
|
Interferon Mechanism: what does gamma interferon do?
|
upregulates MHC I and II in all cells
|
|
Hypersensitivity: What is another name for Type I hypersensitivity
|
anaphylactic or atpoic
|
|
Hypersensitivity: What do type I, II, and III have in common?
|
they all use antibodies
|
|
Hypersensitivity: What cells are involved in Type I?
|
Mast cell and Basophils
|
|
Hypersensitivity: What Ig triggers Type one reactions?
|
IgE
|
|
Hypersensitivity: What molecule acts as a mediator of this reaction?
|
IgE causes the release of histamine. This is a very fast reaction. Think First is Fast.
|
|
Hypersensitivity: What are some examples of Type I reactions?
|
Anaphylactic shock, asthma, hives, local wheal and flare reactions.
|
|
Hypersensitivity: What is another name for Type II Hypersensitivity?
|
Cytotoxic (think Cy-2-toxic)
|
|
Hypersensitivity: What happens in this reaction?
|
antibodies bind to a perceived "enemy" cell and use complement and phagocytosis to kill it.
|
|
Hypersensitivity: What antibodies are common in this reaction?
|
IgM and IgG
|
|
Hypersensitivity: What are some examples of Type II reactions?
|
Goodpasture's, autoimmune hemolytic anemia, graves disease, rheumatic fever, etc.
|
|
Hypersensitivity: What do Type II and Type III have in common
|
They both use complement MAC (Membrane attack complexes) to do some of the work.
|
|
Hypersensitivity: What is different between Type II and Type III reactions
|
Type III reactions involve neutrophils and the release of a large number of cytokines and inflammatory mediators. Type II also hapens to specific cells or tissues, while type III is soluble.
|
|
Hypersensitivity: What is the mechanism of a Type III Hypersensitivity Reaction?
|
Soluble antibody-antigen complexes activate complement and attract inflammatory cells
|
|
Hypersensitivity: What are some examples of this?
|
SLE, rheumatoid arthritis, etc
|
|
Hypersensitivity: What is serum sickness
|
When you have a type III reaction to a foreign protein, such as an injected drug. It takes about 5-10 days, and you present with fever, utricara, arthralgia, and proteinuria
|
|
Hypersensitivity: What is Arthus Reaction?
|
A local, subacute reaction to injected antibodies. Hapens in the skin.
|
|
Hypersensitivity: Examples of the Arthus reaction?
|
hypersensitivity pnemonitis and thermophilic actinomycetes
|
|
Hypersensitivity: What is the mechanism of a Type IV reaction?
|
This is T-cell mediated and therefore delayed. Think that 4 is last.
|
|
Hypersensitivity: What are examples of this type of reaction?
|
TB skin test, poison ivy, transplant rejection
|
|
Immune Deficiencies: Lack of B cells lead to what kind of disorders?
|
Lack of Ig
|
|
Immune Deficiencies: Give two examples of this…..
|
Burton's Agammaglobulinemia, Selective Immunoglobin deficiency
|
|
Immune Deficiencies: Burton's agammaglobulinemia is caused by what?
|
X-linked defect that cause low levels in all Igs. Causes all kinds of bacterial infects. Think Boys and Bacteria for Burton's
|
|
Immune Deficiencies: At what age do the infections start in Burton's?
|
6 months, because that is when the maternal IgG declines.
|
|
Immune Deficiencies: What is the defect in Selective immunoglobulin deficiency?
|
A lack of a certain class of Ig, probably caused by a defect in iostype switching.
|
|
Immune Deficiencies: What Ig is most likely to be lacking?
|
IgA, which results in sinus and lung bacterial infections
|
|
Immune Deficiencies: What are three diseases that involve B and T cells?
|
Wiscott-Aldrich syndrome, and Ataxia-telangiactasia
|
|
Immune Deficiencies: What is SCID?
|
Stem cell defect (can be anything, no one gene), leads to total lack of an immune system.
|
|
Immune Deficiencies: How do the patients present?
|
patients present early with viral, bacterial, fungal, and protazoal infections
|
|
Immune Deficiencies: What is Wiskott-Aldritch Syndrome
|
an X-linked defect that results in depressed cellular immunity and IgM formation
|
|
Immune Deficiencies: How does it present?
|
Triad of Eczema, thrombocytopenia, and pyogenic infections. There is a specific inability to fight off encapsulated bacteria
|
|
Immune Deficiencies: What are the Ig titers in a patient like this?
|
IgA is elevated, IgE is normal, and IgM is depressed
|
|
Immune Deficiencies: What is ataxia-telangiactasia?
|
Defect in DNA repair that leads to neurologic problems (ataxia) and spider angiomas (telangiectasia) and IgA deficiency
|
|
Immune Deficiencies: Name six phagocytotic disorders.
|
Il-12 receptor deficiency, Hyper IgM syndrome, Job's syndrome, Chediak-Higashi disease, Chronic granulomatous disease, Leukocyte adhesion syndrome. (Use: In Heaven Jesus Can Contemplate Love, use Job to remember the biblical link)
|
|
Immune Deficiencies: What does Il-12 receptor deficiency cause?
|
Mycobacterial infections
|
|
Immune Deficiencies: What does Hyper IgM syndrome cause?
|
Because the cells can't class switch, you have only IgM, and nothing else, resulting is never pyogenic infections at 6 months
|
|
Immune Deficiencies: What will the titers look like in Hyper IgM?
|
High IgM, low IgA, IgE, and IgG
|
|
Immune Deficiencies: What causes Job's disease?
|
T-cells fail to make interferon gamma and therefore neutrophils are not attracted to sites of infection
|
|
Immune Deficiencies: What is the clinical picture in Job's disease?
|
recurrent "cold" staph abscesses, eczema, and high levels of IgE
|
|
Immune Deficiencies: What is Chronic Granulomatous Disease?
|
a group of disorders that result in impaired neutrophils function
|
|
Immune Deficiencies: How does CGD present?
|
multiple oportunistic infections with bacteria
|
|
Immune Deficiencies: What is the test for CGD?
|
negative nitoblue tertraolium dye reduction test
|
|
Immune Deficiencies: What is Chediak-Higashi disease?
|
autosomal recessive disease of microtubule dysfunction, leading to impaired phagocytosis
|
|
Immune Deficiencies: How does Chediak-Higashi disease present?
|
Multiple pyrogenic Staph and strep infections
|
|
Immune Deficiencies: What is Leukocyte Adhesions deficiency syndrome?
|
deficiency of LFA-1 in phagocytotic cells, presents with pyrogenic infections
|
|
Immune Deficiencies: Of the phagocytotic disorders, which two do not present with pyogenic bacterial infections?
|
Job's disease (no neutrophils action leads to "cold" abcesses) and IL-12 (mycobacterial infections)
|
|
Passive vs. Active Immunity: What is active immunity?
|
slow onset, leads to long-lasting memory, hapens after you are exposed to an antigen, basis for vaccines
|
|
Passive vs. Active Immunity: What is passive immunity?
|
When you receive pre-formed antibodies, limited by the lifespan of the antibodies, rapid onset
|
|
Passive vs. Active Immunity: What diseases are treated by using passive immunity?
|
Tetanus, Botulism, HBV, Rabies (To Be Healed Rapidly)
|
|
Passive vs. Active Immunity: What Igs are used for this treatment?
|
high-affinity IgA and IgG
|
|
Passive vs. Active Immunity: What is another scenario in which Igs are transferred from host to patient?
|
Maternal Igs are transferred to the infant.
|
|
Antigen Variation: What is antigenic variation?
|
When pathogens change their proteins (surface, flagellar, etc) so that they can escape the immune system's antibodies.
|
|
Antigen Variation: What are two mechanisms of antigenic shift?
|
DNA re-arrangement, and RNA segment re-arrangement
|
|
Antigen Variation: What type of antigenic shift does Borrelia have?
|
It changes it's surface proteins and causes relapsing fevers - each new fever corresponds to new growth of the bacteria due to new antigens.
|
|
Antigen Variation: What bacteria has antigenic shift in its flagella?
|
Salmonella has two types of flagella, and it can shift between them.
|
|
Antigen Variation: What type of shifting does n. Gonorrhea undergo?
|
There is DNA recombinations that cause its pillus to be hypervariable.
|
|
Antigen Variation: African sleeping sickness is caused by what bacteria?
|
Trypanosome gabiense and T. rhodesiense
|
|
Antigen Variation: What kind of antigen shift do Trypanosomes have?
|
The Trypanosomes shift the proteins on their membranes in a cyclic, pre-programmed manner, leading to cyclic fevers.
|
|
Antigen Variation: Influenza has both antigenic shift and antigenic drift. What is the difference between the two?
|
Drift is a minor change in surface glycoproteins that allows new stains of flu to avoid host defense. Shift is a major change where new surface proteins are created.
|
|
Antigen Variation: What is the mechanism of antigenic shift in influenza?
|
when two types of flu infect the same cell and trade pieces of RNA new proteins are made.
|
|
Autoantibodies: ANA is associated with?
|
SLE
|
|
Autoantibodies: What is specific for SLE
|
anti ds-DNA, anti-Smith
|
|
Autoantibodies: What is associated with drug-induced lupus?
|
antihistone
|
|
Autoantibodies: What is Rheumatoid Factor
|
anti-IgG, associated with Rhematoid arthritis
|
|
Autoantibodies: What is Anti-neutrophil associated with?
|
vasculitis
|
|
Autoantibodies: What indicates CREST scleroderma?
|
Anti-centromere antibody
|
|
Autoantibodies: what is anti-mitochondrial associated with?
|
primary billiary cirrhosis
|
|
Autoantibodies: What indicates celiac sprue?
|
anti-gliaden antibodies
|
|
Autoantibodies: What is anti-basement membrane associated with?
|
Goodpasture's syndrome
|
|
Autoantibodies: What indicates pemphigus vulgaris?
|
anti-epithelial antibodies
|
|
Autoantibodies: What is anti-microsomal associated with?
|
Hashimoto's thryroiditis
|
|
Transplant Rejection: What is hyperacute rejection?
|
This occurs when the host has pre-formed antibodies to the donor
|
|
Transplant Rejection: How fast does this occur?
|
Within minutes of the transplant
|
|
Transplant Rejection: Can it be controlled?
|
No. IT is innate because the antibodies are already into the blood.
|
|
Transplant Rejection: What is acute rejection?
|
a cell mediated type II cytotoxic response that occurs in the weeks following the rejection
|
|
Transplant Rejection: What molecule causes this reaction?
|
the foreign MHC on the transplant
|
|
Transplant Rejection: Is it reversible?
|
Yes, with immunosupressive drugs (cyclosporin, OKT3).
|
|
Transplant Rejection: What is chronic rejection?
|
Antibody mediated vascular necrosis that hapens over months/years
|
|
Transplant Rejection: Is it reversible?
|
No - the damage is permenant.
|
|
Transplant Rejection: What is graft-versus-host disease?
|
This occurs when graft T-cells proliferate in the immune-supressed host and attack the host cells as foreign.
|
|
Transplant Rejection: What are symptoms of GVHD?
|
maculopapular rash, jaundice, hepatosplenomegaly, diarrhea
|
|
Transplant Rejection: AUTHOR
|
Marc Otten
|
|
Blood Cell Differentiation: True/False: Myeloblast --> Promyelocyte --> Metamyelocyte --> Myelocyte --> Stab cell --> Neutrophil, Eosinophil or Basophil
|
False, Metamyelocyte is after myelocyte (Greek tip - 'meta' means after)
|
|
Blood Cell Differentiation: A megakaryoblast becomes a ------------- then ----------------
|
Megakaryocyte then platelet
|
|
Blood Cell Differentiation: A reticulocyte is an immature -------------
|
erythrocyte
|
|
Blood Cell Differentiation: Monoblasts are progenitors of
|
monocytes
|
|
Blood Cell Differentiation: What is the progenitor of plasma cells and active T cells?
|
Lymphoblasts
|
|
Erythrocyte: Describe the shape of rbc's
|
Anucleate, biconcave, large SA:V ratio
|
|
Erythrocyte: What is the rbc's source of energy?
|
C2
|
|
Erythrocyte: Why purpose does the large SA:V ratio serve in an rbc?
|
easy gas exchange of O2 and CO2
|
|
Erythrocyte: Define erythrocytosis
|
Increased number of red cells
|
|
Erythrocyte: Define poikilocytosis
|
Varying shapes
|
|
Erythrocyte: How is glucose metabolized in an rbc?
|
90% anaerobic and 10% HMP shunt
|
|
Erythrocyte: What is the lifetime of the rbc?
|
120 days
|
|
Erythrocyte: Importance of "physiologic chloride shift"?
|
Membrane contains chloride-bicarbonate antiport which allows rbc to transport CO2 from the periphery to the lungs for elimination
|
|
Leukocyte: Name three types of granulocytes
|
Neutrophils, eosinophils, basophils
|
|
Leukocyte: Name two mononuclear cells
|
lymphocytes and monocytes
|
|
Leukocyte: Purpose of leukocytes?
|
Defense against infections
|
|
Leukocyte: Normal levels of leukocytes?
|
4.000 - 10,000/ul
|
|
Basophil: What % of all leukocytes do basophils comprise?
|
<1%
|
|
Basophil: True/False: Nucleus of basophil is trilobed
|
False, bilobed
|
|
Basophil: Granules of a basophil are ------------ and stain with -------------- stains
|
basophilic, basic (wow, tough one)
|
|
Basophil: Granules of a basophil contain
|
heparin (anticoagulant), histamine (vasodilator), other vasoactive amines and SRS-A
|
|
Mast Cell: Function of mast cell?
|
Mediates allergic reactions
|
|
Mast Cell: Upon degranulation, mast cells release
|
histamine, heparin, and eosinophil chemotactic factors
|
|
Mast Cell: Mast cells bind which class of globulin
|
IgE
|
|
Mast Cell: True/False: Mast cells are the same cell type as basophils
|
False, they are the same structurally and functionally, but are not the same cell type
|
|
Mast Cell: Mast cells are involved in which type of hypersensitivity reactions?
|
Type 1
|
|
Mast Cell: Which pharmacologic agent is used to prevent mast cell degranulation and what is it used to treat?
|
Cromolyn sodium/asthma
|
|
Eosinophil: What % of all leukocytes do eosinophils comprise?
|
1-6%
|
|
Eosinophil: The nucleus of an eosinophil is ------------
|
bilobed
|
|
Eosinophil: Function of an eosinophil?
|
Defend against helminthic and protozoan infections
|
|
Eosinophil: Eosinophils are highly phagocytic for ---------------
|
Antigen-antibody complexes
|
|
Eosinophil: What are the causes of eosinophilia?
|
Neoplastic, Asthma, Allergic Processes, Collagen Vascular Diseases, Parasites (NAACP = mnemonic)
|
|
Eosinophil: What substances do eosinophils produce?
|
histaminase and arylsulfate
|
|
Neutrophil: Function of neutrophil?
|
Acute inflammatory response cell, phagocytosis
|
|
Neutrophil: What percentage of WBC's do neutrophils comprise?
|
40-75%
|
|
Neutrophil: Nucleus of a neutrophil is ----------------
|
multilobed
|
|
Neutrophil: Primary granules in a neutrophil are called -------------
|
lysosomes
|
|
Neutrophil: Describe primary granules of a neutrophil.
|
Large, spherical, azurophilic
|
|
Neutrophil: Primary granules in a neutrophil contain --------------
|
hydrolytic enzymes, lysozyme, myeloperoxidase and lactoferrin
|
|
Neutrophil: In what pathologic conditions do you see hypersegmented neutrophils?
|
B12/folate deficiency
|
|
Monocyte: Shape of monocyte nucleus
|
kidney shaped
|
|
Monocyte: Cytoplasm of monocyte looks like --------------
|
frosted glass
|
|
Monocyte: In the tissues, monocytes differentiate into --------------
|
macrophages
|
|
Monocyte: Monocytes comprise what percent of all leukocytes?
|
2-10%
|
|
Lymphocyte: Describe nucleus of lymphocyte
|
small, round, densely staining
|
|
Lymphocyte: True/False: A lymphocyte has a large amount of dark cytoplasm
|
False, small amount of pale cytoplasm
|
|
Lymphocyte: What to B lymphocytes produce?
|
antibodies
|
|
Lymphocyte: Function of T lymphocytes?
|
Cellular immune response and regulation of B lymphocytes and macrophages
|
|
B Lymphocyte: B lymphocytes are part of the -------------- immune response.
|
humoral
|
|
B Lymphocyte: Where do B lymphocytes mature?
|
Bone marrow (B = Bone marrow)
|
|
B Lymphocyte: What markers are present on B lymphocytes?
|
CD19 and CD20
|
|
B Lymphocyte: B lymphocytes migrate to
|
peripheral lymphoid tissue (follicles of lymph nodes, white pulp of spleen, unencapsulated lymphoid tissue)
|
|
B Lymphocyte: When B cells encounter antigen, they differentiate into --------- and produce ---------
|
plasma cells/antibodies
|
|
B Lymphocyte: B cells function as antigen presenting cells (APC) via ------------
|
MHC II
|
|
Plasma Cell: Nucleus of plasma cell is ----------- and has a -------------- chromatin distribution
|
off-center/clock-face
|
|
Plasma Cell: True/False: Plasma cells have abundant RER and well-developed Golgi apparatus
|
TRUE
|
|
Plasma Cell: Plasma cell neoplasm
|
multiple myeloma
|
|
Plasma Cell: Plama cells differentiate from --------- to produce large amounts of ---------- specific to a particular antigen
|
B cells/antibody
|
|
T Lymphocyte: Function of T cells?
|
Mediate cellular immune response
|
|
T Lymphocyte: T cells mature in the -------------
|
Thymus
|
|
T Lymphocyte: What does CD stand for?
|
Cluster of Differentiation
|
|
T Lymphocyte: Name four types of cells that T cells differentiate into?
|
cytotoxic, helper, supressor, delayed hypersensitivity
|
|
T Lymphocyte: Markers present on T helper cells?
|
CD3, CD4
|
|
T Lymphocyte: Markers present on cytotoxic T cells?
|
CD3, CD8
|
|
T Lymphocyte: Class ----- MHC molecules present antigen to CD--- positive T helper cells
|
2, 4
|
|
T Lymphocyte: Class ----- MHC molecules present antigen to CD--- positive cytotoxic T cells
|
1, 8
|
|
Macrophage: Function of macrophages
|
phagocytize bacteria, cell debris and senescent red cells, and scavenges damaged cells and tissues
|
|
Macrophage: Macrophages differentiate from circulating ---------------
|
monocytes
|
|
Macrophage: Macrophages are activated by
|
gamma interferon
|
|
Macrophage: Macrophages function as APC via ------------
|
MHC II
|
|
Airway cells: Ciliated cells extend to -------------------
|
respiratory bronchioles
|
|
Airway cells: Goblet cells extend to ------------------
|
terminal bronchioles
|
|
Airway cells: Type ----- cells line the alveoli and take up what % of the alveolar surface?
|
Type 1, 97%
|
|
Airway cells: Type ----- cells secrete pulmonary surfactant and take up what % of the alveolar surface?
|
Type 2, 3%
|
|
Airway cells: Pulmonary surfactant is made up of ----------------
|
dipalmitoylphosphatidylcholine
|
|
Airway cells: What is the purpose of pulmonary surfactant?
|
Decrease alveolar surface tension
|
|
Airway cells: Which type of cells serve as precursors to both type 1 and type 2 cells?
|
Type 2
|
|
Airway cells: In amniotic fluid, what ratio is indicative of fetal lung maturity?
|
lecithin:sphingomyelin ratio >2.0
|
|
Airway cells: Function of ciliated cells?
|
To sweep mucus secretions out of the lungs toward the mouth
|
|
Microglia: Microglia are CNS --------------
|
phagocytes
|
|
Microglia: Embryonic origin of microglia?
|
mesodermal
|
|
Microglia: True/False: Microglia are readily seen with Nissl stain
|
FALSE
|
|
Microglia: Describe nucleus and cytoplasm of microglia
|
small irregular nuclei, little cytoplasm
|
|
Microglia: In response to tissue damage, microglia transform into ------------
|
large, ameboid phagocytic cells
|
|
Microglia: HIV-infected microglia form ----------------------- in the CNS
|
multinucleated giant cells
|
|
Oligodendroglia: Function of oligodendroglia?
|
To myelinate multiple CNS axons
|
|
Oligodendroglia: In Nissl stain, oligodendroglia appear as -------------
|
small nuclei with dark chromatin and relatively little cytoplasm
|
|
Oligodendroglia: Oligodendroglia are the predominant type of glial cell in --------- matter
|
white
|
|
Oligodendroglia: Oligodendroglia are destroyed in --------------------
|
Multiple sclerosis
|
|
Schwann Cells: Each Schwann cell functions to myelinate how many PNS axons?
|
One
|
|
Schwann Cells: What is the function of Schwann cells?
|
To promote axonal regeneration
|
|
Schwann Cells: Name an example of a schwannoma
|
acoustic neuroma
|
|
Schwann Cells: Location of acoustic neuroma commonly associated with what anatomical landmark?
|
internal acoustic meatus (CN VII and CN VIII)
|
|
Gas Exchange Barrier: See p. 73 for Gas exchange barrier diagram
|
0
|
|
Fetal landmarks: Implantation of blastocyst is present in which week?
|
1
|
|
Fetal landmarks: The bilaminar disk is formed within which week?
|
2
|
|
Fetal landmarks: Gastrulation, primitive streak, notochord, neural plate begin to form
|
Within week 3
|
|
Fetal landmarks: Neural tube formed, organogenesis, extremely susceptible to teratogens
|
Weeks 3-8
|
|
Fetal landmarks: Heart begins to beat, Upper and lower limb buds begin to form
|
Week 4
|
|
Fetal landmarks: When do genitalia begin to have male/female characteristics?
|
Week 10
|
|
Fetal landmarks: From day 0 to implantation at end of week 1, name stages of embryogenesis
|
Fertilization (day 0), zygote (day 2), morula (day 3), blastocyst (day 5), implantation (day 6)
|
|
Teratogens: Example
|
Effect on fetus
|
|
Teratogens: ACE Inhibitors
|
Renal damage
|
|
Teratogens: Cocaine
|
Abnormal fetal development, fetal addiction
|
|
Teratogens: DES
|
vaginal clear cell adenocarcinoma
|
|
Teratogens: Iodide
|
congenital goiter or hypothyroidism
|
|
Teratogens: 13-cis-retinoic acid
|
extremely high risk for birth defects
|
|
Teratogens: thalidomide
|
limb defects ("fliper" limbs)
|
|
Teratogens: warfarin, x-rays
|
multiple anomalies
|
|
Teratogens: fetal infections
|
congenital malformations
|
|
Umbilical cord: how many umbilical arteries?
|
2
|
|
Umbilical cord: what kind of blood do the umbilical arteries carry?
|
deoxygenated blood from fetus
|
|
Umbilical cord: how many umbilical veins?
|
1
|
|
Umbilical cord: what kind of blood is carried by umbilical vein?
|
suplies oxygenated blood from placenta to the fetus
|
|
Umbilical cord: a single umbilical artery is associated with what anomalies?
|
congenital and chromosomal
|
|
Embryologic derivatives: surface ectoderm
|
adenohypophysis, lens of eye, epithelial linings, epidermis
|
|
Embryologic derivatives: neuroectoderm
|
neurohypophysis, CNS neurons, oligodendrocytes, astrocytes, pineal gland
|
|
Embryologic derivatives: neural crest
|
ANS, dorsal root ganglia, melanocytes, chromaffin cells of adrenal medulla, enterochromaffin cells, pia, celiac ganglion, Schwann cells, odontoblasts, parafollicular - C cells of thyroid, laryngeal cartilage
|
|
Embryologic derivatives: mesoderm
|
dura connective tissue, muscle, bone, cardiovascular structures, lymphatics, blood urogenital structures, serous linings of body cavities (peritoneal), spleen, adrenal cortex
|
|
Embryologic derivatives: endoderm
|
gut tube epithelium and derivatives (lungs, liver, pancreas, thymus, thyroud, parathyroid)
|
|
Embryologic derivatives: what induces ectoderm to form neuroectoderm (neural plate)?
|
notochord
|
|
Embryologic derivatives: what is the postnatal derivative of the notochord?
|
nucleus pulposus of the intervertebral disk
|
|
Early Develpoment: Name the precursor for the ectoderm and its purpose
|
epiblast, invaginates to form primitive streak
|
|
Early Develpoment: Cells from the primitive streak give rise to
|
intraembryonic mesoderm and endoderm
|
|
Early Develpoment: How many germ layers in second week and what are they?
|
2, epiblast and hypoblast (remember rule of 2's for second week)
|
|
Early Develpoment: How many cavities in second week and what are they?
|
2, amniotic cavity and yolk sac (remember rule of 2's for second week)
|
|
Early Develpoment: How many components to placenta in second week and what are they?
|
2, cytotrophoblast and syncytiotrophoblast (remember rule of 2's for second week)
|
|
Early Develpoment: How many germ layers in third week and what are they?
|
3, (gastrula): ectoderm, mesoderm, endoderm (Rule of 3's for third week)
|
|
Fetal Erythropoiesis: In the 3-8th weeks, fetal erythropoiesis occurs in
|
Yolk sac
|
|
Fetal Erythropoiesis: In the 6-30th weeks, fetal erythropoiesis occurs in
|
Liver
|
|
Fetal Erythropoiesis: In the 9-28th weeks, fetal erythropoiesis occurs in
|
Spleen
|
|
Fetal Erythropoiesis: Erythropoiesis occurs in the Bone marrow from the ---- week onward
|
28th
|
|
Fetal Erythropoiesis: Mnemonic for remembering fetal erythropoiesis?
|
Young Liver Synthesizes Blood
|
|
Heart Embryology: Embryonic structure
|
Gives rise to
|
|
Heart Embryology: Truncus arteriosus
|
Ascending aorta and pulmonary trunk
|
|
Heart Embryology: Bulbus cordis
|
Smooth parts of left and right ventricle
|
|
Heart Embryology: Primitive ventricle
|
trabeculated parts of left and right ventricle
|
|
Heart Embryology: Primitive atria
|
trabeculated left and right atrium
|
|
Heart Embryology: Left horn of sinus venosus (SV)
|
coronary sinus
|
|
Heart Embryology: Right horn of sinus venosus (SV)
|
smooth part of right atrium
|
|
Heart Embryology: Right common cardinal vein and right anterior cardinal vein
|
SVC
|
|
Twinning: Monozygotic twins have ---- amniotic sacs, ----- placentas, ---- chorions
|
2,1,1
|
|
Twinning: Dizygotic (fraternal) twins have ---- amniotic sacs, ----- placentas, ---- chorions
|
2,2,2
|
|
Twinning: AUTHOR
|
Alex Arriaga
|
|
Fetal Circulation: Do you want to see a high yield diagram?
|
Then go to page 76!
|
|
Fetal Circulation: Saturation level of blood in umbilical vein?
|
0.8
|
|
Fetal Circulation: Foramen ovale: its function in fetal circulation?
|
Most oxygenated blood reaching the heart via the IVC is diverted through the foramen ovale and pumped out the aorta to the head.
|
|
Fetal Circulation: Ductus Arteriosus: its function in fetal circulation?
|
Deoxygenated blood from the SVC is expelled into the pulmonary artery and ductus arteriosus to the lower body of the fetus.
|
|
Fetal Circulation: What happens at birth, when infant takes a breath?
|
Decreased resistance in pulmonary vasculature causes increased left atrial pressure vs right atrial pressure; foramen ovale closes; increase in O2 leads to decrease in prostaglandins, causing closure of ductus arteriosus.
|
|
Fetal Circulation: What drug can be given to close a patent ductus arteriosus?
|
Indomethacin
|
|
Fetal Circulation: What drug can be given to keep a patent ductus arteriosus open?
|
Prostaglandins
|
|
Fetal-postnatal derivatives: Umbilical vein becomes the:
|
ligamentum teres hepatis
|
|
Fetal-postnatal derivatives: umbilical arteries become the:
|
medial umbilical ligaments
|
|
Fetal-postnatal derivatives: ductus Arteriosus becomes the:
|
ligamentum arteriosum
|
|
Fetal-postnatal derivatives: ductus venosus becomes the:
|
ligamentum venosum
|
|
Fetal-postnatal derivatives: foramen ovale becomes the:
|
fossa ovalis
|
|
Fetal-postnatal derivatives: allantois - urachus becomes the:
|
median umbilical ligament
|
|
Fetal-postnatal derivatives: notochord becomes the:
|
nucleus pulposus
|
|
Fetal-postnatal derivatives: urachal cyst or sinus is a remnant of the:
|
allantois (urine drainage from the bladder)
|
|
Aortic Arch Derivatives: 1st arch:
|
part of maxillary artery (1st is MAXimal)
|
|
Aortic Arch Derivatives: 2nd arch:
|
stapedial artery and hyoid artery (Second = Stapedial)
|
|
Aortic Arch Derivatives: 3rd arch:
|
common Carotid artery and proximal part of internal carotid artery (C is the 3rd letter of the alphabet)
|
|
Aortic Arch Derivatives: 4th arch:
|
on left, aortic arch; on right, proximal part of right subclavian artery 4th arch (4 limbs) = systemic
|
|
Aortic Arch Derivatives: 6th arch:
|
proximal part of pulmonary arteries and (on left only) ductus arteriosus. 6th arch = pulmonary and the pulmonary-to-systemic shunt (ductus arteriosus)
|
|
Aortic Arch Derivatives: diagram of aortic arch derivatives:
|
see page 76!
|
|
Branchial apparatus: branchial clefts are dervied from:
|
ectoderm
|
|
Branchial apparatus: branchial arched are derived from:
|
mesoderm and neural crests
|
|
Branchial apparatus: branchial pouches are derived from:
|
endoderm
|
|
Branchial apparatus: mnemonic to remember branchial apparatus derivation:
|
CAP covers outside from inside (Clefts = ectoderm, Arches = mesoderm, Pouches = endoderm)
|
|
Branchial arch 1 derivatives: Meckel's cartilage:
|
Mandible, Malleus,incus,sphenoMandibular ligament
|
|
Branchial arch 1 derivatives: Muscles:
|
Muscles of Mastication (temporalis, Masseter, lateral and Medial pterygoids), Mylohyoid, anterior belly of digastric, tesnsor tympani, tensor veli palatini
|
|
Branchial arch 1 derivatives: Nerve:
|
CN V3
|
|
Branchial Arch 2 derivatives: Reichert's cartilage:
|
Stapes, Styloid process, lesser horn of hyoid, Stylohyoid ligament
|
|
Branchial Arch 2 derivatives: Muscles:
|
muscles of facial expression, Stapedius,Stylohyoid, posterior belly of digastric.
|
|
Branchial Arch 2 derivatives: Nerve:
|
CN VII
|
|
Branchial arch 3 derivatives: Cartilage:
|
greater horn of hyoid
|
|
Branchial arch 3 derivatives: Muscle:
|
stylopharyngeus (Think of pharnx: stylopharyngeus is innervated by glossopharyngeal nerve.
|
|
Branchial arch 3 derivatives: Nerve:
|
CN IX
|
|
Branchial arch 4 to 6 derivatives: Cartilages:
|
thyroid, cricoid, arytenoids, cornicuate, cuneiform
|
|
Branchial arch 4 to 6 derivatives: Muscles (4th arch):
|
mostly pharyngeal constrictors, cricothyroid, levator veli palatini.
|
|
Branchial arch 4 to 6 derivatives: 5th arch:
|
makes no major developmental contributions
|
|
Branchial arch 4 to 6 derivatives: Muscles (6th arch):
|
all intrinsic muscles of larynx except cricothyroid
|
|
Branchial arch 4 to 6 derivatives: Nerve (4th arch):
|
CN X
|
|
Branchial arch 4 to 6 derivatives: Nerve (6th arch):
|
CNX (recurrent laryngeal branch)
|
|
Branchial arch innervation: Arch 1 derviatives are supplied by:
|
CN V2 and V3
|
|
Branchial arch innervation: Arch 2 derivatives are supplied by:
|
CN VII
|
|
Branchial arch innervation: Arch 3 derivatives are supplied by:
|
CN IX
|
|
Branchial arch innervation: Arch 4 and 6 derivatives supplied by:
|
CNX
|
|
Branchial arch innervation: For diagram:
|
see p. 77
|
|
Branchial cleft derivatives: 1st cleft develops into
|
external auditory meatus
|
|
Branchial cleft derivatives: 2nd through 4th clefts form:
|
temporary cervical sinuses, which are obliterated by proliferation of 2nd arch mesenchyme.
|
|
Branchial cleft derivatives: Persistent cervial sinus can lead to a:
|
branchial cyst in the neck
|
|
Ear development:: Bone: Incus/Malleus come from:
|
1st arch
|
|
Ear development:: Bone: Stapes comes from:
|
2nd arch
|
|
Ear development:: Muscle: Tensor tympani (V3) comes from:
|
1st arch
|
|
Ear development:: Muscle: Stapedius (VII) comes from:
|
2nd arch
|
|
Ear development:: External auditory meatus comes from:
|
1st cleft
|
|
Ear development:: Eardrum, eustacian tube comes from:
|
1st pharyngeal membrane
|
|
Branchial pouch derviatives:: 1st pouch develops into:
|
middle ear cavity, eustacian tube, mastiod air cells (1st pouch contributes to endoderm-lined structures of ear)
|
|
Branchial pouch derviatives:: 2nd pouch develops into:
|
epithelial lining of palatine tonsil
|
|
Branchial pouch derviatives:: 3rd pouch (dorsal wings) develops into:
|
inferior parathyroids (3rd pouch contributes to 3 structures: thymus, left and right inferior parathyroids)
|
|
Branchial pouch derviatives:: 3rd pouch (ventral wings) develops into:
|
thymus
|
|
Branchial pouch derviatives:: 4th pouch develops into:
|
superior parathyroids
|
|
Branchial pouch derviatives:: Aberrant development of 3rd and 4th pouches -->
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DiGeorge's syndrome --> leads to T-cell deficiency (thymic hypoplasia) and hypocalcemia (parathyroid glands)
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Thymus: Site of:
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T-cell maturation
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Thymus: Encapsulated or une |