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275 Cards in this Set
- Front
- Back
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What is the antidote:
Acetaminophen |
N-acetylcysteine
|
|
What is the antidote:
Anticholinergics |
Physostigmine
|
|
What is the antidote:
Benzodiazepines |
Flumazenil
|
|
What is the antidote:
Beta Blockers |
Glucagon and calcium
|
|
What is the antidote:
Carbon Monoxide |
Oxygen
|
|
What is the antidote:
Cyanide |
Amyl nitrate
|
|
What is the antidote:
Digoxin |
Anti-digoxin Fab antibodies
|
|
What is the antidote:
Ethylene Glycol |
Ethanol
|
|
What is the antidote:
Heparin |
Protamine
|
|
What is the antidote:
Iron |
Deferoxamine
|
|
What is the antidote:
Isoniazid |
Pyridoxine
|
|
What is the antidote:
Lead |
EDTA or BAL
|
|
What is the antidote:
Methanol |
Ethanol
|
|
What is the antidote:
Opioids |
Naloxone
|
|
What is the antidote:
Warfarin |
Vitamin K
|
|
What is the antidote:
Organophosphates |
Atropine or Pralidoxime (2-PAM)
|
|
What are the symptoms of anticholinergic overdose?
|
Anhidrosis
Fever Delirium Mydriasis "Dry as a bone, Mad as a hatter, Blind as a bat, Hot as a hare" |
|
What are the symptoms of opiate overdose?
|
Miosis
Out of it (sedation) Respiratory depression Pneumonia (aspiration) Hypotension Infrequency (constipation, urinary retention) Nausea Emesis MORPHINE |
|
What is benzodiazepine used for?
|
Sedative/Tranquilizer
Antidote to alcohol withdrawal |
|
What does an overdose of acetominophen do?
|
Liver failure
|
|
What does an overdose of benzodiazepines cause?
|
Sedation
Respiratory depression (life threatening) |
|
What does methanol ingestion cause?
|
Severe abdominal pain
Blindness (can be permanent) Found in antifreeze, "wood alcohol," improperly fermented alcohol |
|
What does ethylene glycol ingestion cause?
|
Renal failure
|
|
What is the cause of death in carbon monoxide poisioning?
|
Directly inhibits electron transport chain (respiration) in mitochondria by binding to hemoglobin with greater affinity than oxygen
|
|
What is the effect of cyanide ingestion?
|
Symptoms:
Drowsiness Tachycardia Coma Reacts with and inactivates respiratory enzymes, preventing production of ATP |
|
What are the symptoms of cholinergic overdose? (organophosphates)
|
Salivation
Lacrimation Urination Defecation GI upset Emesis SLUDGE |
|
Mechanism of Action:
Penicillins and Cephalosporins |
Inhibit peptide cell wall synthesis
|
|
Mechanism of Action:
Aminoglycosides |
Inhibit initiation of translation
Only kill aerobic gram neg bacteria Ototoxic - risk increased with use of loop diuretics |
|
List some aminoglycosides
|
Gentamicin
Amikacin Neomycin Streptomycin Tobramycin |
|
Mechanism of Action:
Vancomycin (glycopeptide antibiotic) |
Inhibits phospholipid plasma membrane synthesis and peptidoglycan polymerization
Inhibits cell membrane and cell wall synthesis |
|
Mechanism of Action:
Quinolones |
Inhibit Topoisomerase
Inhibit bacterial ability to use its own DNA |
|
What are the adverse effects of quinolones?
|
Contraindicated under age 16 (effects on cartilage in joints)
Use with caution over age 60 (increased risk of tendinopathy, rupture) Prolong QT interval |
|
Mechanism of Action:
Chloramphenicol |
Inhibits peptidyl transferase
Inhibits protein synthesis |
|
Mechanism of Action:
Macrolides (Erythromycin class) |
Inhibit protein synthesis
|
|
Mechanism of Action:
Tetracyclines |
Inhibit tRNA binding
Inhibit protein synthesis |
|
Name some tetracyclines
|
Doxycycline
Tetracycline Minocycline Tigecycline |
|
Mechanism of Action:
Sulfonamides |
Inhibit folate synthesis
|
|
Mechanism of Action:
Trimethoprim |
Inhibits folate use
|
|
Mechanism of Action:
Bacitracin |
Inhibits cell wall synthesis
|
|
How is bacitracin used?
|
Only topical
Very nephrotoxic |
|
What is polymyxin used for?
|
Antipseudomonal
Only topical, usually ophthalmic |
|
Mechanism of Action:
Carbapenems |
Inhibit cell wall synthesis (very powerful)
Effective against most gram pos and many gram neg, aerobic and anaerobic |
|
Name some carbapenems
|
Doripenem
Ertapenem Imipenem Meropenem |
|
Mechanism of Action:
Glycopeptides |
Inhibit cell wall synthesis
Teicoplanin and Vancomycin Only gram pos, usually reserved for serious infections |
|
Mechanism of Action:
Clindamycin |
Inhibits protein synthesis
|
|
Mechanism of Action:
Metronidazole |
Activates mechanisms that destroy microbial DNA
Anaerobic bacteria and protozoa |
|
Mechanism of Action:
Nitrofurantoin (nitrofuran) |
Inhibits bacterial enzyme systems
Accumulates in urine - used for UTI |
|
What are the most common bleeding disorders?
|
Inherited: VonWillebrand's
Acquired: Vitamin K deficiency |
|
Von Willebrand Disease
|
Lack of factor VIII-R
Features: aPTT prolonged Bleeding time prolonged |
|
Hemophilia A
|
Lack of factor VIII
Features: aPTT prolonged Normal bleeding time |
|
Hemophilia B
|
Lack of factor IX
Features: aPTT prolonged Normal bleeding time |
|
Vitamin K deficiency
|
Affects factors II, V, VII, IX, X
Features: PT prolonged Fat malabsorption |
|
Idiopathic Thrombocytic Purpura (ITP)
|
Features:
Immune mediated Usu. follows viral infection in children, can be chronic in adults |
|
Thromotic Thrombocytic Purpura (TTP)
|
Features:
Usu. young women Microthrombi Fragmented RBCs (helmet cells) |
|
What does bleeding time test?
|
platelet function
|
|
What does PT test?
|
Extrinsic and Common pathways
|
|
What does aPTT test?
|
Intrinsic and Common pathways
|
|
What does TT test?
|
Common pathway only
|
|
Spherocytosis
|
Autosomal Dominant hemolytic anemia
Features: Defective spectrin Splenomegaly |
|
G6PD Deficiency
|
Hemolytic anemia caused by hemolysis due to oxidative stress (reaction to viral infection, fava beans, sulfa drugs, quinine, nitrofurantoin)
Features: Heinz bodies (hemoglobin degradation products) |
|
Sickle Cell Anemia
|
HbS (2 alpha, 2 beta S)
Sickling triggered by: hypoxia, dehydration, acidosis Can cause vaso-occlusive crisis, aplastic crisis, sequestration crisis (splenomegaly), autosplenectomy |
|
alpha-Thalassemias
|
HbH (4 beta)
Common in Southeast Asia Features: Hypochromic cells Target cells |
|
beta-Thalassemias
|
HbA2 (2 alpha, 2 delta) and HbF (2 alpha, 2 gamma)
Common in Mediterranean and US Features: Hypochromic cells Target cells Homozygous = major, heterozygous = minor |
|
Immune Mediated Hemolytic Anemia with Warm Antibodies
|
Usually IgG
Active at 37 degrees C Drugs Malignancies SLE |
|
Immune Mediated Hemolytic Anemia with Cold Antibodies
|
Usually IgM
Most active at 0-4 degrees C Mycoplasma pneumonia Mononucleosis Lymphoma Agglutination occurs in peripheral (cool) parts of body - causes vascular obstruction (Raynaud's phenomenon) |
|
What is the Coombs test?
|
Direct: Mix patient's RBCs with anti-IgG
Detects cell bound antibodies Indirect: Mix patient's plasma with normal RBCs Detects free antibodies |
|
Megaloblastic Anemia
|
Features:
Hypochromic, macrocytic RBCs Hypersegmented neutrophils Caused by Folate deficiency: anemia only Caused by B12 deficiency: anemia PLUS neurological symptoms |
|
Iron Deficiency Anemia
|
Usu. from chronic blood loss (in elderly pts, suspect colorectal malignancy)
Features: Hypochromic, microcytic RBCs |
|
Aplastic Anemia
|
Caused by bone marrow failure due to viral infections, toxins, drugs (alkylating agents, chloramphenicol)
|
|
Plummer-Vinson Syndrome
|
Anemia
Atrophic glossitis Esophageal webs (cause dysphagia) |
|
Fanconi Anemia
|
Autosomal Recessive
Hypoplastic thumbs Absent radii Aplastic anemia Bone marrow DNA more susceptible to radiation and alkylating agents |
|
Special Feature of RBC:
Heinz Bodies |
Denatured hemoglobin
G6PD deficiency |
|
Special Feature of RBC:
Howell-Jolly Bodies |
Nuclear fragments
Post-splenectomy |
|
Special Feature of RBC:
Basophil Stippling |
Small dots on periphery of RBC - accumulations of rRNA
Lead poisoning |
|
Special Feature of RBC:
Siderocytes (Pappenheimer Bodies) |
Dense purple-blue granules within RBC
Iron overload |
|
Special Feature of RBC:
Reticulocytes |
Remains of ribosomal RNA
Increased production/release of RBCs Recovery from hemorrhage |
|
What is the reticulocyte index?
|
Relate reticulocyte count to hematocrit to correct for blood loss
Important following acute blood loss - reticulocyte count can double in first 24hrs, so important to correct |
|
Which drugs cause most drug induced neutropenia?
|
Alkylating agents
Chloramphenicol Chlorpromazine Sulfonamides Phenylbutazone |
|
Leukocytosis:
Neutrophils |
Acute infections
Stress |
|
Leukocytosis:
Eosinophils |
Allergy
Asthma Parasitic infections |
|
Leukocytosis:
Lymphocytes |
Tuberculosis
Viral infections |
|
Leukocytosis:
Monocytes |
Tuberculosis
Malaria Rickettsia |
|
Acute Lymphoblastic Leukemia (ALL)
|
Children
Fever Petechiae Ecchymoses CNS infiltrate Lymphoblasts Prognosis: Good |
|
Acute Myeloid Leukemia (AML)
|
Any age
Fever Petechiae Ecchymoses Lymphadenopathy Splenomegaly Auer rods in myeloblasts Prognosis: depends on type |
|
Chronic Myelogenous Leukemia (CML)
|
Young adults
Fever Night sweats Splenomegaly * Philadelphia chromosome Prognosis: Poor |
|
Chronic Lymphocytic Leukemia (CLL)
|
Elderly
Insidious Few symptoms Low Ig levels Infections Lymphocytes predominate Prognosis: Fair |
|
Hairy Cell Leukemia
|
Hepatomegaly
Splenomegaly Pancytopenia TRAP stain Prognosis: Poor |
|
What is the Philadelphia chromosome?
|
c-abl proto-oncogene on chromosome 9 when translocated to the bcr region of chromosome 22 to form a fusion gene bcr/abl
Encodes protein with high tyrosine kinase activity If present, better prognosis for CML |
|
What is Trousseau's Sign?
|
Migratory venous thrombosis
Associated with neoplasms |
|
What are the key features of atherosclerosis?
|
In large to medium arteries
Fatty streaks Atheromas |
|
What are the key features of Monckeberg's Arteriosclerosis?
|
Calcific stenosis of the media
"Gooseneck" lumps In small to medium arteries Asymptomatic |
|
What are the key features of hyperplastic arteriosclerosis?
|
Fibrinoid necrosis
Malignant hypertension "Onion skin" hyperplasia |
|
What are the key features of hyaline arteriosclerosis?
|
Diabetes mellitus
Thickened basement membrane |
|
Describe the pathogenesis of arteriosclerosis.
|
Vascular epithelium is injured
Lipids and platelets adhere to injured surface Leukocytes and platelets release growth factors, triggering smooth muscle proliferation Macrophages become foam cells Foam cells aggregate to form fatty streaks, the beginning formation of an atherosclerotic plaque |
|
What are the key features of hypersensitivity arteritis?
|
In small vessels
Lesions all at same stage Cryoglobulins Associated with Henoch-Schonlein Purpura |
|
What are the key features of polyarteritis nodosa?
|
In small to medium vessels
Kidneys, heart, muscles, skin Can be fatal but responds well to steroid treatment |
|
What are the key features of thromboangiitis obliterans (Buerger's)?
|
In small to medium vessels
Smokers |
|
What are the key features of giant cell arteritis?
|
Temporal Artery:
Sudden blindness Female > Male Associated with polymyalgia rheumatica |
|
What are the key features of Wegener's?
|
Upper respiratory vasculitis
Lower respiratory vasculitis Glomerulonephritis |
|
What are the key features of Takayasu?
|
"Pulseless Disease"
In aorta or large arteries Asian females |
|
What are the key features of Kawasaki?
|
Mucouctaneous lymph node syndrome
Coronary artery aneurysms Fever, conjunctivitis, maculopapular rash Japanese children |
|
What are the key features of atherosclerotic aneurysms?
|
Fusiform
In abdominal aorta Hypertension |
|
What are the key features of syphilitic aneurysms?
|
Saccular
In ascending aorta Associated with aortic insufficiency |
|
What are the key features of dissecting aneurysms?
|
In aorta (ascending or descending)
Hypertension Marfan syndrome Not a true aneurysm |
|
What are the key features of berry aneurysms?
|
Congenital
In circle of Willis Associated with polycystic kidney disease (adult form) |
|
What are the key features of micro aneurysms?
|
Cerebral - Hypertension
Retinal - Diabetes |
|
Heart Sounds:
Mitral Valve Prolaps |
Midsystolic click
Occurs in young women, Marfan syndrome |
|
Heart Sounds:
Mitral Stenosis |
Diastolic rumble
Occurs in rheumatic heart disease, atrial fibrillation |
|
Heart Sounds:
Mitral Regurgitation |
Holosystolic murmur
Transmitted to axilla Occurs in MI of papillary muscle, acute rheumatic fever, endocarditis |
|
Heart Sounds:
Aortic Stenosis |
Systolic murmur
Transmitted to carotid arteries Pulsus tardus Can be congenital or caused by degenerative calcifications |
|
Heart Sounds:
Aortic Regurgitation |
Diastolic murmur
"Pistol shots" in femoral artery "Water hammer" pulse |
|
Heart Sounds:
Patent Ductus Arteriosus |
Continuous murmur
"Machine like" |
|
What are the acyanotic heart defects?
|
Left to Right
VSD (most common) ASD PDA |
|
What are the cyanotic heart defects?
|
Right to Left
Tetralogy of Fallot (most common) Transposition of the great vessels Persistent truncus arteriosus Eisenmenger (reversal of L to R shunt due to pulmonary hypertension) |
|
What are the obstructive heart defects?
|
Coarctation of the aorta (preductal in infants, postductal in adults)
Pulmonary stenosis or atresia Aortic stenosis or atresia |
|
What is TORCH?
|
Toxoplasmosis
Rubella CMV Herpes |
|
Common Congenital Defects:
Fetal Alcohol Syndrome |
Cardiac defect
Microcephaly Short upturned nose with long philtrum |
|
Common Congenital Defects:
Fetal Hydantoin Syndrome |
Cardiac defect
Microcephaly Nail hypoplasia |
|
Common Congenital Defects:
Isotretinoin (vitamin A) |
Cardiac defect
Hydrocephalus Cleft palate |
|
Common Congenital Defects:
TORCH (intrauterine infection) |
Cardiac defect
Microcephaly Auditory and visual defects |
|
Common Congenital Defects:
Syphilis |
Cardiac defect
Bullous skin lesions (palms, soles) Hutchinson's teeth (serrated-looking edges) Saber shins |
|
What is the Tetralogy of Fallot?
|
Pulmonary artery stenosis
Overriding aorta VSD Right ventricular hypertrophy |
|
Signs and Treatment:
Stable Angina |
Triggered by exercise/exertion
ST depression Relieved by rest TX: Nitroglycerin |
|
Signs and Treatment:
Unstable Angina |
Occurs at rest
Crescendo like Often leads to MI Unresponsive to nitroglycerin |
|
Signs and Treatment:
Prinzmetal's Angina |
Occurs at rest
ST elevation TX: Calcium antagonists |
|
Signs and Treatment:
Myocardial Infarction |
Occurs during exercise/exertion or REM sleep
ST elevation T inversion TX: Nitroglycerin, morphine, lidocaine |
|
Gross and Microscopic Changes After MI:
30 min |
Gross: none
Micro: mitochondrial swelling |
|
Gross and Microscopic Changes After MI:
4-12 hours |
Gross: none
Micro: edema hemorrhage |
|
Gross and Microscopic Changes After MI:
18-24 hours |
Gross: pallor
Micro: neutrophilic infiltrate |
|
Gross and Microscopic Changes After MI:
24-72 hours |
Gross: pallor
Micro: coagulation necrosis loss of nuclei heavy neutrophil infiltrate |
|
Gross and Microscopic Changes After MI:
3-7 days |
Gross: central softening
hyperemic borders Micro: resorption of dead myofibers |
|
Gross and Microscopic Changes After MI:
10 days |
Gross: soft and yellow hyperemic borders
Micro: granulation tissue |
|
Gross and Microscopic Changes After MI:
8 weeks |
Gross: gray and firm scar
Micro: scar |
|
What is the most common causes of death in the first hours after an MI?
|
Arrhythmia (most common)
Congestive heart failure Cardiogenic shock Muscle rupture (least common, highest risk 1-2 weeks after MI) |
|
What are the causes of left sided heart failure? The consequences?
|
Causes:
Ischemic heart disease Arterial hypertension Valvular disease Consequences: Pulmonary congestion (dyspnea, orthopnea) Renal hypertension (salt retention) |
|
What are the causes of right sided heart failure? The consequences?
|
Causes:
Left sided heart failure Lung disease Primary pulmonary hypertension Consequences: Increased venous pressure leads to: Edema Liver congestion Ascites |
|
Key Features Of:
Acute Endocarditis (Infective) |
Caused by Staph aureus, Strep
Previously normal valves Janeway lesions (non-tender macular patches on palms and soles - septic emboli) High fever, chills, hematuria |
|
Key Features Of:
Subacute Endocarditis (Infective) |
Caused by Strep viridans, gram neg bacilli
Previously abnormal valves Roth spots (oval retinal hemorrhages with pale center) Osler nodes (red tender lesions on finger and toe pulps) Low grade fever |
|
Key Features Of:
Marantic Endocarditis (Noninfective) |
Associated with chronic illnesses
Thrombotic |
|
Key Features Of:
Libman Sacks Endocarditis (Noninfective) |
Associated with SLE
Verrucous lesions on both sides of valve leaflets |
|
Key Features Of:
Fibrinous Pericarditis |
Transmural myocardial infarction
Dressler Syndrome (delayed pericarditis 2-10 wks after MI, due to autoantibodies - responds well to corticosteroids) "Bread and butter" appearance |
|
Key Features Of:
Serous Pericarditis |
Viral infections (often Coxsackie)
Uremia |
|
Key Features Of:
Suppurative Pericarditis |
Bacterial infections
Fungal infections Parasitic infections |
|
What are the clinical signs of pericarditis?
|
Low grade fever
Pericardial friction rub Chest pain aggravated by movement of trunk Pulsus paradoxus (inspiratory fall of BP that is exaggerated) |
|
Who does rheumatic fever occur in?
|
School-age children with untreated Strep pharyngitis
|
|
Key Features Of:
Acute Rheumatic Fever |
1-4 wks after tonsillitis
Group A beta-hemolytic streptococci Children 5-15 yrs |
|
Key Features Of:
Rheumatic Heart Disease |
Occurs many years after rheumatic fever
Often asymptomatic Fibrotic, deformed calcified lines of closure on valve leaflets Mitral valve > Aortic valve |
|
What are the carditis of rheumatic fever?
|
Pericarditis (serous effusions)
Myocarditis (heart failure) Endocarditis (valve damage) |
|
What is an Aschoff Body?
|
Granuloma
Focal interstitial myocardial inflammation Found with enlarged macrophages (Anitschkow cells) |
|
What are the Major Jones Criteria?
|
For diagnosing rheumatic fever
Polyarthritis Erythema Subcutaneous nodules Chorea Carditis |
|
Key Features Of:
Emphysema |
Obstructive lung disease
"Pink puffers" Barrel chest Panacinar Centrilobular Associated with: Alpha-1 antitrypsin deficiency in lower lobes Smoking in upper lobes |
|
Key Features Of:
Chronic Bronchitis |
Obstructive lung disease
"Blue bloaters" Chronic irritation or infection Hypertrophy of submucosal glands |
|
Key Features Of:
Asthma |
Obstructive lung disease
Expiratory wheezing Types: Extrinsic - triggered by allergens Intrinsic - triggered by cold and exercise Aspirin induced |
|
Key Features Of:
Bronchiectasis |
Obstructive lung disease
Result of chronic infections Kartagener's - immotile cilia |
|
What characterizes obstructive lung disease?
|
Reduced airflow due to high resistance or low elastic recoil
FRC and TLC are high |
|
What is the REID Index?
|
Ratio between thickness of submucosal mucus secreting glands and wall thickness between epithelium and cartilage
Used for research and autopsy only (not for diagnosis) |
|
Key Features Of:
Adult ARDS |
Restrictive lung disease
Acute diffuse alveolar damage Caused by: Shock Sepsis Pancreatitis Toxins |
|
Key Features Of:
Neonatal ARDS |
Restrictive lung disease
Insufficient lecithin synthesis by type 2 pneumocytes |
|
Key Features Of:
Pneumoconiosis |
Restrictive lung disease
Caused by: Coal - "tattooing," black sputum Anthracosis - carbon dust Asbestosis - fibrous silicates, dry cough Berylliosis - type IV hypersensitivity |
|
What characterizes restrictive lung disease?
|
High elastic recoil of lungs
FRC, VC, TLC are low |
|
Key Features Of:
Hypersensitivity Pneumonitis |
Restrictive lung disease
Acute - type III - fever, cough, dyspnea, leukocytosis Chronic - type IV - peribronchial granulomas Farmer's lung, pigeon breeder's lung, etc |
|
Key Features Of:
Goodpasture Syndrome |
Restrictive lung disease
Type II hypersensitivity - antibodies against basal membrane Hemoptysis, rapidly progressive glomerulonephritis |
|
Key Features Of:
Pulmonary Hemosiderosis |
Restrictive lung disease
Type II hypersensitivity - antibodies against basal membrane Hemoptysis, no renal involvement |
|
Key Features Of:
Alveolar Proteinosis |
Restrictive lung disease
Overproduction of surfactant like material |
|
Key Features Of:
Eosinophilic Pneumonia |
Restrictive lung disease
Acute (Loffler's) - Type I hypersensitivity Chronic |
|
Key Features Of:
Diffuse Idiopathic Fibrosis |
Restrictive lung disease
Interstitial pneumonitis and fibrosis Hyperplasia of type II pneumocytes |
|
Key Features Of:
Collagen Vascular Disorders |
Restrictive lung disease
Scleroderma SLE Wegener's RA etc |
|
Where is the alar ligament?
|
Connects sides of odontoid process (on C2) to lateral aspects of foramen magnum
|
|
Where is the transverse ligament (cervical spine)?
|
Between C1 lateral masses - holds dens in place
Located posterior to dens |
|
What are the components of the cervical cruciform ligament?
|
Transverse ligament - across dens
Superior band - from transverse ligament to occiput Inferior band - from transverse ligament to body of C2 |
|
What is the tectorial membrane?
|
Superior continuation of posterior longitudinal ligament
Lies posterior to cruciform ligament Passes from C1 to internal surface of occipital bone |
|
Where are the anterior and posterior longitudinal ligaments?
|
Anterior - runs over anterior of spine
Posterior - runs over posterior of vertebral bodies, anterior to spinal cord |
|
What is the function of the scalene muscles?
|
Unilateral contraction - sidebend neck
Bilateral contraction - flex neck Anterior and middle - elevation of first rib in forced respiration Posterior - elevation of second rib in forced respiration |
|
What is the motion of the OA joint?
|
"Yes" joint
Flexion - Extension Rotation and sidebending opposite |
|
What is the motion of the AA joint?
|
"No" joint
Rotation Rotation and sidebending opposite |
|
What is the motion of the upper cervical spine?
|
Primarily rotation
Rotation and sidebending same |
|
What is the motion of the lower cervical spine?
|
Primarily sidebending
Rotation and sidebending same |
|
Autoantibody:
Autoimmune Hemolytic Anemia |
Anti-RBC
|
|
Autoantibody:
Bullous Pemphigoid |
Anti-epidermal basement membrane
|
|
Autoantibody:
Type I Diabetes Mellitus |
Anti-islet cell
|
|
Autoantibody:
Pemphigus |
Anti-keratinocyte junction
|
|
Autoantibody:
Pernicious Anemia |
Anti-intrinsic factor
Anti-parietal cell |
|
Autoantibody:
Microscopic Polyangiitis |
p-ANCA
|
|
Autoantibody:
Polymyositis |
Speckled ANA
20% have anti-Jo-1 |
|
Autoantibody:
Progressive Systemic Sclerosis |
Anti-Scl 70
|
|
Autoantibody:
Sjogren's Syndrome |
Anti-SS A (anti-Ro)
Anti-SS B (anti-La) |
|
Autoantibody:
Idiopathic Thrombocytopenic Purpura (adult form) |
Anti-structural platelet
|
|
Autoantibody:
Vitiligo |
Anti-melanocyte
|
|
Clinical Triad:
Autoimmune Hemolytic Disease |
2 types: warm antibody, cold antibody
Warm: Severe anemia Splenomegaly High MCHC Cold: Anemia Raynaud's syndrome Acrocyanosis |
|
Clinical Triad:
Bullous Pemphigoid |
Bullae
Pruritis Elderly |
|
Clinical Triad:
Type I Diabetes Mellitus |
Hyperglycemia
DKA risk Infections Long-term: Retinopathy Nephropathy Atherosclerosis |
|
Clinical Triad:
Pemphigus |
Nikolsky's sign (skin sloughs off easily)
Oral and skin erosions Older patients |
|
Clinical Triad:
Pernicious Anemia |
Megaloblastic anemia
Gastritis B12 deficiency |
|
Clinical Tetrad:
Polyarteritis Nodosa |
Fever
Hypertension Abdominal pain Renal disease without glomerulonephritis |
|
Clinical Triad:
Microscopic Polyangiitis |
Hemoptysis
Hematuria Palpable purpura With glomerulonephritis |
|
Clinical Triad:
Polymyositis |
Proximal muscle weakness
Elevated muscle enzymes Elevated myoglobin |
|
Clinical Triad:
Progressive Systemic Sclerosis |
Visceral organ fibrosis
Facial tightening Sclerodactyly |
|
Clinical Triad:
Sjogren's Syndrome |
Xerostomia (dry mouth)
Keratoconjuctivitis sicca Arthritis |
|
Clinical Triad:
Idiopathic Thrombocytopenic Purpura (adult form) |
Thrombocytopenia
Petechiae and purpura Mucosal bleeding |
|
Clinical Triad:
Vitiligo |
Hypopigmented areas of skin
White hair in areas of affected skin Sunburn risk |
|
Clinical Criteria:
Rheumatoid Arthritis |
Need 4 for diagnosis
Morning stiffness > 1 hr Arthritis in 3 or more joints simultaneously Arthritis in hand joints Symmetrical arthritis Rheumatoid nodules Serum rheumatoid factor Erosions or bony decalcification identifiable on X-ray |
|
Clinical Triad:
Systemic Lupus Erythematosus (SLE) |
Malar rash
Lupus nephropathy Arthritis |
|
Clinical Pentad:
CREST |
Calcinosis
Raynaud's Esophageal dysmotility Sclerodactyly Telangiectasia |
|
Clinical Triad:
Drug Induced Lupus |
Arthralgia
Fever Serositis |
|
Clinical Triad:
Myasthenia Gravis |
Post-use episodic muscle weakness
Ptosis Thymus gland pathologies |
|
Clinical Triad:
Graves' Disease |
Symptomatic hypothyroidism
Exophthalmos Pretibial myxedema |
|
Clinical Triad:
Hashimoto's Thyroiditis |
Nontender goiter
Typically female Hypothyroidism which becomes symptomatic |
|
Clinical Triad:
Wegener's Granulomatosis |
Sinusitis
Glomerulonephritis Lung lesions (cavitary) |
|
Clinical Triad:
Celiac Sprue |
Malabsorption (often with diarrhea)
Dermatitis herpetiformis (papular vesicular rash with pruritis and burning, presents symmetrically on body) Short stature |
|
Clinical Triad:
Primary Biliary Cirrhosis |
Pruritis
Female Jaundice |
|
Autoantibody:
Rheumatoid Arthritis |
Anti-IgG
|
|
Autoantibody:
Systemic Lupus Erythematosus (SLE) |
Anti-nuclear antibody (ANA) for screening
Anti-ds DNA for confirmation |
|
Autoantibody:
Drug Induced Lupus |
Anti-histone
|
|
Autoantibody:
CREST |
Anti-centromere
|
|
Autoantibody:
Myasthenia Gravis |
Anti-ACh receptor
|
|
Autoantibody:
Graves' Disease |
Anti-TSH receptor
|
|
Autoantibody:
Hashimoto's Thyroiditis |
Anti-microsomal
|
|
Autoantibody:
Wegener's Granulomatosis |
Anti-neutrophil cytoplasm (ANCA)
|
|
Autoantibody:
Celiac Sprue |
Anti-gliadin
|
|
Autoantibody:
Goodpasture's Syndrome |
Anti-glomerular basement membrane (anti-GBM)
|
|
Autoantibody:
Primary Biliary Cirrhosis |
Anti-mitochondrial
|
|
What is the mediator of Type I Hypersensitivity?
|
IgE
|
|
What are typical allergens/triggers of Type I Hypersensitivity?
|
Pollens
Drugs Foods Insect Venom Animal Dander |
|
What mediates Type II Hypersensitivity?
|
Antibodies
Cytotoxic |
|
What are the triggers for Type II Hypersensitivity?
|
Blood and Rh antigens
Drugs that attach to RBC membranes (penicillin, quinidine) Drugs that attach to platelet membranes (quinine) Drugs that change host tissues (hydralazine) Infectious agents - molecular mimicry (rheumatic fever) Autoimmunity |
|
What are some examples of Type II Hypersensitivity reactions?
|
Autoimmunity
Transfusion reactions Erythroblastosis fetalis Theumatic fever Drug-induced lupus |
|
What mediates Type III Hypersensitivity?
|
Immune complex deposition
|
|
What are the triggers for Type III Hypersensitivity?
|
Drugs
Vaccines* Inhaled antigens (ex: fungus) |
|
What are examples of Type III Hypersensitivity reactions?
|
Arthus reacition
Serum sickness |
|
What mediates Type IV Hypersensitivity?
|
Cell-mediated
|
|
What are examples of Type I Hypersensitivity reactions?
|
Allergic rhinitis
Systemic anaphylaxis Eczema Hives |
|
What are the triggers for Type IV Hypersensitivity?
|
Delayed type:
Poison ivy/oak Nickel Soaps Mycobacterial infection Transplanted tissue T-cell mediated Cytotoxicity: Transplanted cells Virus-infected cells/tissue Tumor cells |
|
What are examples of Type IV Hypersensitivity reactions?
|
Delayed type:
Contact dermatitis Acute graft rejection Positive PPD skin test T-cell mediated Cytotoxicity: Acute graft rejection Viral infection Neoplasia |
|
What makes Type IV Hypersensitivity unique from the other types of hypersensitivity?
|
No antibodies involved
Type I, II, III all involve antibodies in some way |
|
Mechanism of:
Hyperacute Transplant Rejection |
Type II Hypersensitivity
Preformed antibodies bind to antigen on tissues Onset: minutes to hours |
|
Mechanism of:
Acute Transplant Rejection |
Type IV Hypersensitivity - T cell mediated cytotoxicity
Memory T cells recognize antigen CD8 T cells destroy graft Onset: days to months |
|
Mechanism of:
Chronic Transplant Rejection |
Type II and III Hypersensitivity
Antibodies develop over time and damage graft vasculature Onset: months to years |
|
Mechanism of:
Graft vs. Host |
Type IV Hypersensitivity - T cell mediated cytotoxicity
T cells in transplanted tissue attack host Onset: days to weeks |
|
Oncogene:
c-myc |
Burkitt lymphoma
|
|
Oncogene:
c-abl |
Chronic myelogenous leukemia (CML)
|
|
Oncogene:
ras |
Colon carcinoma
|
|
Tumor Suppressor Gene:
BRCA-1 |
Breast cancer
Ovarian cancer |
|
Tumor Suppressor Gene:
p53 |
Breast cancer
Colon cancer Lung cancer (carcinomas) |
|
What is the difference between an onocogene and a tumor suppressor gene, with regard to contributing to the development of cancer?
|
Oncogene: when ACTIVE causes uncontrolled cell division
Tumor suppressor: when MUTATED or LOST allows uncontrolled cell division |
|
Tumor Marker:
Carcinoembryonic Antigen (CEA) |
Adenocarcinomas
|
|
Tumor Marker:
Alpha-fetoprotein (AFP) |
High:
Hepatoma Multiple gestation Neural tube defects (found in mother during pregnancy) Yolk sac tumor Endodermal sinus disease Low: Down's syndrome |
|
Tumor Marker:
Prostate Specific Antigen (PSA) |
Prostate cancer
|
|
Tumor Marker:
Acid Phosphatase |
Prostate cancer
|
|
Tumor Marker:
Alkaline Phosphatase |
Diagnose:
Non-neoplastic bone disease Non-neoplastic disease of biliary system Track: Bone cancers Renal cell carcinoma Normally produced in four places: Bone Kidney Placenta Biliary system |
|
Tumor Marker:
5'-HIAA (5'-hydroxyindole acetic acid) |
Carcinoid
|
|
Tumor Marker:
CA 19-9 |
Colon cancer
Pancreatic cancer Breast cancer |
|
Tumor Marker:
CA 125 |
Ovarian cancer
|
|
Tumor Marker:
CD 25 |
Hairy cell leukemia
Adult T-cell lymphoma |
|
Tumor Marker:
CD 30 |
Hodgkin's disease
|
|
Tumor Marker:
Neuron-specific Enolase |
Small cell lung cancer
Neuroblastoma |
|
Tumor Marker:
Human Chorionic Gonadotropin (beta-hCG) |
Pregnancy
Gestational trophoblastic disease (hydatidiform mole) Choriocarcinoma |
|
Most likely sites of metastasis:
Breast Cancer |
Bone > Brain
|
|
Most likely sites of metastasis:
Lung Cancer |
Brain > Bone
|
|
Key Facts:
Autosomal Dominant Inheritance |
Never skips generations
|
|
Key Facts:
X-Linked Dominant Inheritance |
No male to male transmission
Never skips generations |
|
Key Facts:
X-Linked Recessive Inheritance |
No male to male transmission
|
|
Key Facts:
Mitochondrial Inheritance |
Passed from mother to ALL children
Never passed from father to children Often variable penetrance |
|
Key Facts:
De Novo Mutation (Inheritance) |
Both parents healthy, but one progeny has mutation/disease
Will probably follow one of normal inheritance patterns in the mutated progeny's offspring |
|
What are the questions to ask when determining inheritance pattern?
|
1. Are any generations skipped? If yes, not dominant.
2. Is there any male to male transmission? If yes, not X-linked. |
|
Inheritance Pattern:
Hyperphosphatemic Rickets |
X-Linked dominant
Inherited vitamin D resistance Bowed legs |
|
Inheritance Pattern:
Incontinentia Pigmenti |
X-Linked dominant
Mini-teeth Patchy alopecia |
|
Inheritance Pattern:
Leber's Optic Neuropathy |
Mitochondrial
Bilateral blindness with onset sometime after 15 years of age (variable penetrance) |
|
Cystic Fibrosis
|
Most common lethal genetic disease of Caucasians
Autosomal Recessive inheritance Mutation in CFTR gene - defect in chloride transmembrane movement in epithelial cells Clinical Findings: Recurrent respiratory infections (Staph aureus first 6 mos, Pseudomonas aeruginosa 6 mos and older) Meconium ileus Viscous mucus High NaCl in sweat and tears (positive sweat test) Chronic pancreatitis Cholelithiasis Malnutrition due to poor bowel function |
|
Phenylketonuria
|
Autosomal Recessive inheritance
Unable to metabolize amino acid Phenylalanine Buildup of Phenylalanine brakdown products Inability to make melanin, norepinephrine, dopamine (lack phenylalanine hydroxylase) Neurotoxicity from phenylalanine breakdown products (phenylketones) Lighter complexion due to lack of melanin Mental retardation (preventable if stop intake of phenylalanine) |
|
Albinism
|
Autosomal Recessive inheritance
Inability to make melanin Lack tyrosinase (convert tyrosine to melanin) |
|
Alpha-1 Antitrypsin Deficiency
|
Autosomal Recessive inheritance
Loss of inhibition of elastase Liver destruction (liver makes alpha-1 antitrypsin but can't release it) Primarily destroys elastic tissue in lung Emphysema |
|
Thalassemias, Sickle Cell Anemia
|
Autosomal Recessive inheritance
Abnormally structured hemoglobin resulting in RBC defects that cause RBC destruction Microcytic anemia |
|
Glycogen Storage Diseases
|
vonGierke disease
Pompe disease McArdle disease Autosomal Recessive inheritance Inability to utilize glycogen stores normally |
|
Mucopolysaccharidoses
|
Lysosomal storage disease
Unable to metabolize GAGs (component of connective tissue) May or may not cause mental retardation or corneal clouding Gargoyle-like facies Hurler Scheie Autosomal Recessive inheritance Hunter X-Linked Recessive inheritance |
|
Sphingolipidoses
|
Lysosomal storage disease
Unable to metabolize sphingolipids (molecules involved with myelin and CNS) Niemann-Pick Gaucher's Krabbe's Tay-Sachs Metachromatic dystrophy Autosomal Recessive inheritance Cause serious CNS disorders Fabry X-linked Recessive inheritance Does not cause serious CNS disorders |
