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235 Cards in this Set
- Front
- Back
UTERINE FIBROIDS
|
benign tumors in the
uterine corpus that may appear on the broad ligament or cervix. They may be related to levels of estrogen & HGH. |
|
UTERINE FIBROIDS/Signs
& symptoms - |
hypermenorrhea,
(dysmenorrhea or leukorrhea may occur) pain, backache, constipation, urinary frequency or urgency or intestinal obstruction |
|
UTERINE FIBROIDS Diagnosis-
|
blood tests,
palpation of the tumor, laparoscopy or D & C. Treatment- observation, blood transfusion or hysterectomy. |
|
GESTATIONAL TROPHOBLASTIC DISEASE
|
(hydatiform mole)-developmental anomaly
of the placenta. The chorionic villi convert into a mass of clear vesicles. (chorionic tumor) |
|
GESTATIONAL TROPHOBLASTIC DISEASE
Signs & symptoms |
- rapid growth of
the uterus, vaginal bleeding & cramping. Diagnosis- HCG levels are extremely high for early pregnancy. Ultrasound fails to reveal a fetal skeleton. |
|
GESTATIONAL TROPHOBLASTIC DISEASE
Treatment |
includes
D & C, weekly monitoring of HCG until they remain normal for 3 consecutive weeks. Periodic follow-up for 1 to 2 years because of increased risk of neoplasm. Emphasize contraception for a patient following removal of a gestational trophoblastic neoplasm until HCG is normal (may take as long as 2 years). |
|
GESTATIONAL TROPHOBLASTIC DISEASE Drug used
|
Methotrexate prophylactically is the drug
of choice for choriocarcinoma. |
|
FIBROCYSTIC DISEASE OF THE BREAST
|
overgrowths
of fibrous tissue in the area of the ducts forming small cysts that develop & disappear quickly. Common between ages of 30-50. Cysts have no malignant potential however breasts that have cysts are more prone to develop cancer. |
|
Treatment-FIBROCYSTIC DISEASE OF THE BREAST
|
aspiration of fluid, medication
(Danocrine), analgesics for pain. |
|
PYLORIC STENOSIS-
|
hyperplasia &
hypertrophy of the circular muscle at the pylorus narrows the pyloric canal. Defect is common in male infants between ages 1-6 months. |
|
PYLORIC STENOSIS-Signs & symptoms
|
projectile
vomiting, visible reverse peristaltic waves, weight loss, constipation & a hypertrophied sphincter, the size of an olive can be felt in the abdomen. Dehydration is common & metabolic alkalosis will occur without rapid intervention. |
|
PYLORIC STENOSIS- Treatment
|
Treatment- surgical
intervention (pyloromyotomy performed by laparoscopy). |
|
PROSTATIC HYPERPLASIA
|
PROSTATIC HYPERPLASIA-considered normal
result of aging. |
|
PROSTATIC HYPERPLASIA Signs & symptoms -
|
reduced stream force & caliber of urine, a
feeling of not emptying the bladder, urinary retention. |
|
PROSTATIC HYPERPLASIA Diagnosis-
|
rectal digital
exam of the prostate, intravenous pyelography, elevated BUN & Creatinine levels, UA & urine culture. Treatmentprostate massage, fluid restriction, sitz baths, regular sexual intercourse to relieve prostatic congestion. TURP (transurethral resection of the prostate). |
|
PROSTATIC HYPERPLASIA . Nursing
interventions |
Nursing
interventions include continuous irrigation to prevent clotting & maintain patency |
|
Chest Tumors
|
- benign or malignant –
malignant tumor can be primary, arising within the lung, chest wall, or mediastinum or a metastasis form a primary tumor elsewhere in the body. Bronchogenic Carcinoma – arise from a single transformed epithelial cell in the tracheobronchial airway. Tumors of the mediastinum – neurogenic, thymus, lymphomas, germ cell, cysts & mesenchymal tumors. More common in men, has a poor prognosis & is largely preventable. Types include squamous, oat-cell, adeno & large-cell (anaplastic) carcinoma. |
|
Lung Cancers –
|
Bronchogenic Carcinoma –
arise from a single transformed epithelial cell in the tracheobronchial airway. Tumors of the mediastinum – neurogenic, thymus, lymphomas, germ cell, cysts & mesenchymal tumors. More common in men, has a poor prognosis & is largely preventable. Types include squamous, oat-cell, adeno & large-cell (anaplastic) carcinoma.______ |
|
Lung Cancers – Chest Tumors s/s
|
Signs & symptoms - smoker’s
cough, wheezing, hemoptysis, dyspnea, & chest pain. Diagnosis- chest x-ray, sputum for cytology, bronchoscopy, needle biopsy of the lungs, tissue biopsy & thoracentesis. Treatment includes pneumonectomy, lobectomy, or wedge resection, radiation & chemotherapy. ___________________________________________________ |
|
Cancer of the lip-
|
occurs most often in men. Risk
factors include smoking, sun & wind exposure. Prognosis is good if the lesion is localized & totally excised. |
|
Cancer of the tongue- and treatment
|
common in men
related to persistent irritation caused by tobacco use, food, chronic alcoholism, or poorly aligned teeth. Treatment radiation & surgical removal of the lesion (may include removal of part or all of the tongue) |
|
Cancer of the mouth-
|
usually occurs in
middle-aged adults. Excision is treatment of choice. It affects speech, nutrition, facial features, & swallowing |
|
Parenteral Nutrition -Total parenteral nutrition (IV
hyperalimentation) is |
the IV
administration of carbs (high concentration of dextrose), protein (amino acids), electrolytes, vitamins, minerals, & fat emulsions. Usually admin through subclavian vein through a central venous catheter (triple-lumen to also permit meds, intralipid, or blood) |
|
Parenteral Nutrition - Solutions
|
Solution: 500mL 50% dextrose, 500mL of
8.5% amino acid, electrolytes, minerals, vitamins Always use infusion pump – discontinue gradually allowing pt to adjust to ↓ levels of glucose |
|
Parenteral Nutrition - Solutions Complications
|
Pneumothorax, air
embolism, clotted or displaced cath, sepsis, hyperglycemia, rebound hypoglycemia, fluid volume excess /overload; long-term use can lead to gallstone formation & liver disease |
|
Parenteral Nutrition - Nursing Diagnoses include:
|
Altered
nutrition, less than body requirements; Risk for infection related to contamination of central cath site; Risk for fluid volume excess (FVE) or deficit (FVD |
|
STOMACH CANCER-
|
caused by
degenerative changes in gastric ulcers. Men 2 times more frequently than women. Middle-aged adults in the low socioeconomic group are common because of a diet high in starch, with few fresh vegetables & fruits. |
|
STOMACH CANCER-Diagnosis-
|
Diagnosis- x-ray
exam, gastric analysis & biopsy via gastroscopy. Poor prognosis. Increased incidence of stomach cancer in Japanese. Cancer of the esophagus- epidermoid carcinoma is rare & affects people over the age of 60 |
|
STOMACH CANCER/ caused by
|
STOMACH CANCER-caused by
degenerative changes in gastric ulcers. Men 2 times more frequently than women. Middle-aged adults in the low socioeconomic group are common because of a diet high in starch, with few fresh vegetables & fruits. |
|
STOMACH CANCER Diagnosis
|
Diagnosis- x-ray
exam, gastric analysis & biopsy via gastroscopy. Poor prognosis. Increased incidence of stomach cancer in Japanese. Cancer of the esophagus- epidermoid carcinoma is rare & affects people over the age of 60. |
|
INTESTINAL OBSTRUCTION
|
85% of obstructions occur in small
intestine, adhesions are most common cause, 15% in large bowel – most often in sigmoid colon due to carcinoma, diverticulitis, IBS, benign tumors. o Mechanical – intraluminal or mural obstruction from pressure on the intestinal walls – polypoid tumors, neoplasms, stenosis, strictures, adhesions, hernias, abscesses. o Functional – intestinal musculature cannot propel contents – amyloidosis, muscular dystrophy, diabetes, Parkinson’s – can be temporary due to surgery |
|
COLORECTAL CANCER- Age, diet Hx of
|
COLORECTAL CANCER- Occurs in middleaged
adults, with low-residue diets of refined carbohydrates & fats, incidence increases with age – highest in ↑ age 85. History of ulcerative colitis; diverticulitis & polyps have been implicated in malignant changes. Diagnosis- guaiac stool tests, digital rectal exam & sigmoidoscopy. CEA antigen (unreliable, can be elevated in inflammation & other diseases). A CEA titer less than 5 ng is considered normal. A CEA greater than 10 ng must be investigated. Treatment- surgery, radiation & chemotherapy. 3 out of 4 people could be saved by early diagnosis |
|
COLORECTAL CANCE DX & treatment
|
Diagnosis- guaiac stool tests,
digital rectal exam & sigmoidoscopy. CEA antigen (unreliable, can be elevated in inflammation & other diseases). A CEA titer less than 5 ng is considered normal. A CEA greater than 10 ng must be investigated. Treatment- surgery, radiation & chemotherapy. 3 out of 4 people could be saved by early diagnosis |
|
RENAL TUMORS-highest in what sex, most common kind, early sign
|
Cancer of the kidney
accounts for approx. 2% of all cancers in adults in the USA & affects 2x more men then women. – Most common is renaladenocarcinoma – may metastasize early to the lungs, bone, liver, brain & contralateral kidney. – Usual sign that 1st calls attention to the tumor is painless Hematuria. |
|
BLADDER CANCER-more common in , age group, risk linked to ,
|
more common in men,
than in women. Occurs after age 50. Increased risk linked to occupations like cable workers, petroleum workers, hairdressers, weavers, aniline dye workers, rubber workers, spray painters, & leather finishers. |
|
BLADDER CANCER- s/s DX, treatment
|
Signs & symptoms - intermittent
hematuria, clots in the urine, pain after voiding, bladder irritability, nocturia, dribbling & urinary frequency. Diagnosis cystoscopy & biopsy. treatment- includes cystoscope resection if the tumor is well localized, radical cystectomy &urethrectomy with permanent ileal conduit (male impotence & permanent sterility) |
|
URINARY DIVERSION
|
procedures
performed to divert urine form the bladder to a new3 exit site – usually through a stoma |
|
URINARY DIVERSION types 4 ,
|
Cutaneous Urinary Diversion – Ileal
Conduit ((Ileal Loop) – oldest procedure – low # of complications. o Cutaneous Ureterostomy – ureters directed thru abdominal wall & attached to stoma – used for pts with advanced pelvic cancer, poor risk pts. o Continent Ileal Urinary Reservoir (Indiana Pouch) – for pts whose bladder has been removed or no longer functions o Ureterosigmoidostomy – implantation of the ureters into the sigmoid colon |
|
CERVICAL CANCER age group, Risk factors, s.s DX
|
Squamous cell cancer
(10% are adenocarcinomas) – occurs most commonly in women aged 30-45, but can occur as young as 18. Risk factors – multiple sex partners, smoking, chronic cervical infection – usual asymptomatic until well advanced. Diagnosis with Pap smear, flowed by biopsy – HPV infections are usually implicated. |
|
HYDATIFORM MOLE S/s and treatment
|
HYDATIFORM MOLE - Placenta
abnormality, S/sx Uterine growth, bleeding, cramping. Can’t see the baby on a normal ultrasound, treatment C&D, monitor until HCG levels stable for 3 weeks, emphasize the importance of contraception. |
|
UTERINE CANCER-most common in age, s/s and treatment
|
common in
postmenopausal women aged 50-60. Signs & symptoms - abnormal uterine bleeding, anovulation obesity, hypertension, & familial tendency. Increased risk in a history of uterine polyps or endometriosis. Can NOT be Diagnosis from Pap smear. Biopsy of endometrial endocervical or cervical tissue. Schiller’s test: (staining of the vagina with iodine, health tissue turns brown, malignant tissue cannot absorb the stain. This is a definitive test for uterine cancer. Treatment- surgical intervention ranging from hysterectomy to pelvic exenteration, chemotherapy, radiation & hormonal therapy. |
|
CANCER OF THE VULVA, age, risk
|
3-5% of all GYN
malignancies; seen mostly in postmenopausal women, although incidence in younger women is increasing. Median age is 44 for cancer limited to the vulva, 61 for invasive vulvar cancer. Increased Incidence with HTN, obesity, diabetes, more whites than nonwhites |
|
VAGINAL CANCER result from
|
VAGINAL CANCER – usually results from
metastasized choriocarcinoma or cancer of the cervix or adjacent organs. |
|
rare & least
common genital cancer. |
CANCER OF FALLOPIAN TUBES
|
|
OVARIAN CANCER most common cancer, lowest in what country, s.s risk
|
Ovary is common site
of primary & metastatic lesion from other cancers – asymptomatic until well advanced, incidence is highest in industrialized countries, except Japan; 4 times increased risk of breast cancer. |
|
Radiations thearapy TBI
|
Total body
irradiation (TBI) is a radiotherapy technique used to prepare the body to receive a bone marrow transplant. |
|
Radiotherapy has a few
applications in non-malignant conditions, such as the treatment of |
trigeminal
neuralgia, severe thyroid eye disease, pterygium, prevention of keloid scar growth, & prevention of heterotopic bone formation. The use of radiotherapy in nonmalignant conditions is limited partly by worries about the risk of radiation-induced cancers The precise treatment intent (curative, adjuvant, neoadjuvant, therapeutic, or palliative) will depend on the tumor type, location, & stage, as well as the general health of the patient. |
|
most common
malignancy of women, |
BREAST CANCER- most common
malignancy of women, usually occurs after age 35. Risk factors include family history, long menstrual cycles, early menses, late menopause, constant stress, first pregnancy after age 35 |
|
Breast cancer
|
Commonly
metastases to lung, liver, bone, kidneys, brain & adrenal glands. Signs & symptoms - lump or mass, change in breast size or symmetry, thickening, dimpling of skin, unusual nipple discharge. Treatmentbased on stage of disease. Lumpectomy, modified radical mastectomy, radical mastectomy, chemotherapy & radiation. TNM staging system: Tumor size, Nodal involvement, Metastatic Progress |
|
PROSTATE CANCER-, TX<DX,S/s
|
bone metastasis is
common. Signs & symptoms - usually asymptomatic, urinary retention, dribbling, difficulty starting the stream & cystitis are late symptoms. Diagnosis- biopsy. Treatment- surgical intervention, chemotherapy, & radiation |
|
TESTICULAR CANCER
|
most common among males aged 15-
40; most common among Caucasians & rare among African Americans |
|
Testis cancer TX, risk
|
A major risk
factor for the development of testis cancer is cryptorchidism. The three basic types of treatment are surgery, radiation therapy, & chemotherapy; one of the highest cure rates of all cancers: (stage I can have a success rate of >95%) when detected early, recommend regular monthly |
|
Testicle examine s/s of cancer
|
lump in one testis or a hardening of
one of the testicles pain & tenderness in the testicles loss of sexual activity Copyright 2007 MyStudyGroup101 build-up of fluid in the scrotum Copyright 2007 MyStudyGroup101 a dull ache in the lower abdomen or groin Copyright 2007 MyStudyGroup101 an increase, or significant decrease, in the size of one testis blood in semen |
|
Testicular test to DX
|
DX by scrotal ultrasound & CT scans. Blood tests
are used to identify & measure tumor markers. The diagnosis is made by performing an orchiectomy, surgical excision of the entire testis along with attached structures epididymis & spermatic cord; A biopsy should not be performed, as it raises the risk of migrating cancer cells into the scrotum |
|
Basal cell epithelioma, common in , risk factors and type of
|
most commonly
occurs in adults after age 40 in blond, fairskinned, Caucasian males. Prolonged sun exposure is the largest risk factor. Lesions usually occur on the face. They are small, smooth, pink, translucent papules that progress to firm raised bordered lesions with depressed centers. |
|
Superficial basal cell epithelioma Risk and TX
|
epitheliomacommonly
found on the chest & back. It is an oval or irregular shaped lesion, slightly elevated & lightly pigmented. The lesion appears scaly & may resemble eczema or psoriasis. Risk factors for this lesion include arsenic ingestion. Treatmentchemotherapy (5-fluororacil), surgical excision, radiation or chemosurgery. Interventions include high protein diet; avoid sun exposure & tender skin care to prevent bleeding |
|
Squamous cell carcinoma- DX, TX and risk factors area of body
|
occurs in
Caucasian males over age 60 from sun, exposure. Other risk factors include x-ray therapy, arsenic ingestion (think gardener using herbicides), carcinogen exposure (tar, oil), & chronic skin inflammation & irritation. Lesions of the lower lip & ears have a poor prognosis but others have a good prognosis. Diagnosis- by biopsy. Treatment- chemosurgery, radiation, electrodessication & curettage & excision |
|
Malignant melanoma-TX, RISK FACTORS, LOCATION
|
more common in
women than men, ages 50-70. Very rare in children. Risk factors include sun exposure, fair skin type, pregnancy (hormones increase both growth & incidence), family history. Common locations are the head, neck, legs, & back. All moles (nevi) that change in color, size, texture, have drainage or bleed should be investigated. Diagnosis- biopsy. Treatment- surgical tumor removal with wide resection, lymphadenectomy, chemotherapy & radiation. |
|
Ocular Cancer
Conjunctival nevus |
a congenital benign
neoplasm is a flat slightly elevated brown spot that becomes pigmented during late childhood. Cop |
|
Rhabdomyosarcoma
|
is the most common
malignant primary orbital tumor in childhood, but can also develop in the elderly. Copyright 2007 MyStudyGroup101 |
|
1. bASAL CELL IS
2. CONJUNCTIVAL CARCINOMA 3. OCULAR MELANOMA 4.ENUCLEATION |
Basal cell is the most common malignant
tumor of the eyelid. Conjunctival carcinoma - grows in exposed areas of conjunctiva Ocular Melanoma – very rare – usually discovered on retinal exam. Enucleation – removal of the entire eye & part of the optic nerve |
|
BRAIN TUMORS
|
localized intracranial lesion
that occupies space in the skull. Secondary brain tumors develop from metastasized structures outside the brain & occur in 20- 40% of all cancer pts; incidence is higher with age 50s, 60s & 70s slightly higher in men then women. |
|
-GLIOMAS
-PITUITARY ADENOMAS- -ANGIOMAS -ACOUSTIC NEUROMAS -MENINGIOMAS |
Gliomas – most common neoplasm –
45% of all brain tumors. o Pituitary adenomas – 8-12% of all brain tumors – symptoms caused as a result of pressure on adjacent structures. Copyright 2007 MyStudyGroup101 o Angiomas – mass of abnormal blood vessels Copyright 2007 MyStudyGroup101 o Acoustic Neuromas-tumor of the eighth cranial nerve. o Meningiomas – common benign encapsulated tumor on the meninges – 15-20% of all brain tumors; slow growing, occurring most often in middle age more often in women |
|
BONE TUMORS
|
osteogenic,
chondrogenic, fibrogenic, muscle & marrow cell tumors as well as nerve, vascular & fatty cell tumors. Metastatic tumors are more common then primary |
|
bONE TUMORS BENIGN
OSTEOCHONDROMA ECCHONDROMA ANEURYSMAL UNICAMERAL |
Osteochondroma is the most
common – usually occurring as large projection of bone at the end of long bonds. Ecchondroma is common tumor of the hyaline cartilage Aneurysmal bone cysts seen in young adults – painful palpable mass of the long bones, vertebrae or flat bond. Unicameral bone cysts occur in children & cause mild discomfort |
|
Malignant - Osteogenic sarcoma, AGE GROUP, RISK FACTOR
|
is the
most common & most often fatal primary bone tumor; occurs more frequently. In males aged 10-25 & in older people with Paget’s due to radiation exposure. Chondrosarcomas – malignant tumors of the hyaline cartilage |
|
CHILDREN MOST FREQUENT CANCER 2 TYPES
|
2 types that account for 85%
of all primary malignant tumors are osteogenic sarcoma & Ewing Sarcoma. |
|
Osteogenic Sarcoma
|
most frequent
bone cancer in children – between 10- 25 years. – Primary sites are the metaphysic of long bones of lower extremitie |
|
Ewing Sarcoma
|
arises in the marrow
spaces of bone – principal sites of origin are shafts of long bones, trunk bones, & skull – almost exclusively in individuals under age 30, most occurrences age 4-25. |
|
Rhabdomyosarcoma –
|
soft tissue
sarcomas in muscles, tendons, bursae & fascia or from such cells in fibrous, connective, lymphatic or vascular tissue. – The 4th most common type of solid tumor in children |
|
Wilms Tumor s/S AND TREATMENT DX
|
5th most common
childhood tumor, tumor of the kidney with good prognosis if treated. Familial link. Signs & symptoms - palpable, firm, smooth mass in the abdomen, hypertension, vomiting. Diagnosisurine collection of catecholamines, presence rules out (r/o) tumor. Treatment includes radical nephrectomy, radiation, & chemotherapy. Palpation is contraindicated because it could cause rupture & seeding, dissemination of the tumor |
|
LIVER CANCER-RISK, S/S, TX
|
risk factors include cirrhosis.
Commonly found in middle-aged to older males. Diagnosis- liver function studies, biopsy & scan of liver. Treatment- surgical removal of the liver. (Up to 90% of the liver can be removed with no loss of function, the liver can regenerate.) |
|
PANCREATIC CANCER-TX, DX, S/S, WHIPPLE PROCEDURE?
|
positive correlation
between alcoholism & cancer of the pancreas. Most common in older males. Signs/symptoms- weight loss, anorexia, weakness, nausea, jaundice & a palpable abdominal mass. Recent onset of diabetes mellitus. Diagnosis- liver function studies, x-rays, scans, biopsy & elevated fasting blood sugar. Treatment- “Whipple procedure”- surgical removal of the head of the pancreas, the common bile duct, the distal part of the stomach, & duodenum. Long, extensive surgery with risks associated with long anesthesia time & long exposure of the internal viscera |
|
LEUKEMIA-ALL, CML, AML, S/S.DX,TX
|
malignant proliferation of blast
cells (pre-WBC). ALL (acute lymphoblastic leukemia), common in young children, reasonably good prognosis. AML (acute myeloblastic leukemia) common in all ages. CML ( chronic myelogenous leukemia) uncommon before age 20. Signs/symptoms- high fever, abnormal bleeding, chills, pallor, recurrent infection, & prolonged weakness. Diagnosis- bone marrow aspirate with a large component of immature WBCs. Treatmentchemotherapy, bone marrow transplant |
|
SARCOMAS-DX, TX, RISK FACTORS
|
malignant tumor of bone
more common in males, most frequently children & adolescents. Signs/symptomsrapid growth (tall for age). Diagnosisbiopsy, bone scans & x-rays. Treatmentamputation & radiation. Chemotherapy, immunotherapy & bone transplants may also be combined. |
|
SARCOMAS, NURSING INTERVENTIONS
|
Nursing interventions
include teaching about phantom pain, psychological support for alteration in body image, proper body alignment & positioning Adriamycin, Cytoxan, vincristine (Oncovin), & prednisone. It has been effective in producing a prolonged remission |
|
Alkylating agents:
|
react with DNA to inhibit
cell division/growth. Busulfan, carboplatin, cisplatin, cyclophosphamide, ifosfamide, melphalan, nitrogen mustard & thiotepa. S/E- renal toxicity. |
|
Nitrosoureas:
|
cross blood-brain barrier to
react with DNA to inhibit cell division/growth. BCNU (carmustine), CCNU (lomustine), methyl CCNU (semustine), & streptozocin. S/E- myelosuppression, especially thrombocytopenia. |
|
Ribonucleotide Reductase Inhibitors
|
Hydroxyurea (Hydrea), trimetrexate
glucoronate (Neutrexin), 2- deoxycoformycin (Pentostatin, Nipent, DCF) |
|
Enzyme Inhibitors
|
pentostatin (Nipent
|
|
Mitotic Inhibitors
|
vinca alkaloids,
vinblastine sulfate (Velban, Oncovin, Vincasar), vincristine (Liposomal, Marqibo), vinorelbine (Navelbine |
|
Antimicrotubule or Taxanes
|
docetaxel
(Taxotere), paclitaxel (Taxol) |
|
Antitumor antibiotics:
|
interfere with DNAdependent
RNA synthesis & bind with DNA to block cell growth. Adriamycin, bleomycin, dactinomycin, daunorubicin, mithramycin, mitomycin, mitoxantrone. S/E- cardiac toxicity. Targeted Therapies – Topoisomerase I Inhibitors, Topoisomerase II Inhibitors, Tyrosine Kinase Inhibitors, Proteasome Inhibitors, Monoclonal Antibodies, Angiogenesis Inhibitors, Tetanoids |
|
Alkyl Sulfonates
|
busulfan (Myleran
|
|
Antimetabolites:
|
folic acid antagonist -
compete with metabolites during nucleic acid production which prevents cell growth. Methotrexate (MTX, amethopterin, Folex, Mexate) |
|
Pyrimidine Analogues
|
capecitabine
(Xeloda, cytarabine HCl (Cytosar-U, ARAC) floxuridine (FUDR), 5-fluorouracil (5-FU, Adrucil), gemcitabine HCl (Gemzar), procarbazine HCL (Matulane) |
|
Purine Analogues
|
cladribine (Leustatin),
fludarabine (Fludara), 6-mercaptopurine (6-MP, Purinethol, thioguanine (Lanvis |
|
Hormones, Hormonal Antagonists &
Enzymes: |
change the chemical
environment by binding to hormone receptor sites which prohibits the growth of tumors susceptible to hormones. Tamoxifen, androgens, anti-estrogens, estrogens, progesterone & steroids |
|
Targeted Therapies
|
Topoisomerase I Inhibitors, Topoisomerase II
Inhibitors, Tyrosine Kinase Inhibitors, Proteasome Inhibitors, Monoclonal Antibodies, Angiogenesis Inhibitors, Tetanoids |
|
Biologic Response Modifiers
|
class of agents used to enhance the body’s immune system. Interferon,
colony-stimulating factors, interleukins, tumor necrosis factor, monoclonal antibodies. Herbal preps are generally not recommended for clients receiving BRMs |
|
Incidence of breast, bladder, prostate, & colon cancer increase with age. Prevention includes
|
eating a high-residue diet, increased intake of cruciferous vegetables, vitamins A, D, & E,
carotene |
|
Alternative/complementary treatments
|
include hypnosis, acupressure, acupuncture, Reiki
therapy, guided imager, therapeutic touch, homeopathy, vitamins A, E, & B complex |
|
Seven Warning Signs of Cancer (American Cancer Society)
|
1. Changes in bladder or bowel habits
2. A sore that does not heal Copyright 2007 MyStudyGroup101 3. Unusual discharge or bleeding Copyright 2007 MyStudyGroup101 4. Thickening or lump in the breast or elsewhere Copyright 2007 MyStudyGroup101 5. Indigestion or difficulty swallowing Copyright 2007 MyStudyGroup101 6. Obvious change in a mole or wart Copyright 2007 MyStudyGroup101 7. Nagging cough or hoarseness |
|
Terms to know:
Hypertrophy- Atrophy- Hyperplasia- Neoplasia- Metaplasia- Dysplasia- |
Terms to know:
Hypertrophy- enlargement of an organ or part due to ↑ in the size or number of cells. Atrophy- normal in aging. Decrease in size or number of cells. Hyperplasia- ↑ in new cells that results from a stimulus, reversible once the stimulus is removed. Neoplasia- Malignant growth of new cells that doesn’t remove when the stimulus is removed. Metaplasia- conversion of a cell from highly specialized to less specialized. Dysplasia- bizarre cell growth that causes cells to be different in shape, size or arrangement than cells from the same type of tissue. May be reversible. |
|
Primary hypertension
Secondary hypertension |
Primary hypertension, or essential
hypertension, develops without apparent cause; • Secondary hypertension develops as a result of another illness or condition. |
|
Blood pressure s/s
|
Often the
client with hypertension will have no symptoms at all or might complain of an early morning headache and fatigueMedications such as oral contraceptives and bronchodilators can also cause elevations in blood pressure |
|
Malignant hypertension is managed with
administration of Hypertensive crises is Hypertensive crises exist when the diastolic blood pressure reaches 140 |
IV Nitropress, Nitroglycerine,
Nipride, Lasix, and other potent vasodilators such as Procardia. |
|
The atrioventricular
(AV) node is located in the interventricular septum and receives the impulse |
septum and receives the impulse and transmits
it on to the Bundle of His, which extends down through the ventricular septum and merges with the Purkinje fibers in the lower portion of the ventricles. |
|
SA node
|
The normal conduction system of the heart is
comprised of the sinoatrial (SA) node located Life Span 1 © 2008 – 2013 MyStudyGroup101 LLC – All rights reserved. 5 at the junction of the right atrium and the superior vena cava. This node is considered to be the main pacer of the heart rate. This area contains the pacing cells that initiate the contraction of the heart. |
|
Heart block can occur as a result of
|
structural
changes in the conduction system, such as tumors, myocardial infarctions, coronary artery disease, infections of the heart, or toxic effects of drugs such as Digitalis. Heart block occurs when there is a problem with the conduction system of the heart |
|
First-degree AV block
occurs when |
the SA node continues to
function normally but transmission of the impulse fails. Because of the conduction dysfunction and ventricular depolarization, the heart beats irregularly. These clients are usually asymptomatic and all impulses eventually reach the ventricles |
|
Second-degree heartblock is a block in which impulses
|
reach the
ventricles but others do not. |
|
third-degree
heart block or complete heart, |
none of the
sinus impulses reach the ventricle. This results in erratic heart rates where the sinus node and the atrioventricular nodes are beating independently. The result of this type of heart block can be hypotension, seizures, cerebral ischemia, or cardiac arrest. Detection of a heart block is made by assessing the electrocardiogram |
|
Toxicity to Medications
Toxicity to medications, such as ----------------causes heart blocks |
Digitalis, can
be associated with heart block. Clients taking Digitalis should be taught to check their pulse rate and to return to the physician for regular evaluation of their Digitalis level. The therapeutic level for Digitalis is 0.9–1.2 ng/ml. Digitalis exceeds 2.0 ng/mL, the client is considered to be toxic. Clients with Digitalis toxicity often complain of nausea, vomiting, and seeing halos around lights. |
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Digitalis toxicity includes
|
Digitalis toxicity includes
checking the potassium level because hypokalemia can contribute to Digitalis toxicity. The physician often will order potassium be given IV or orally and that the Digitalis be held until serum levels return to normal. Other medications, such as Isuprel or Atropine, and Digibind are frequently ordered to increase the heart rate. A high fiber diet will also be ordered because constipation contributes to Digitalis toxicity. |
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pacemakers concerns
|
avoid direct contact with electrical equipment.ä Wear a medic alert
• Take pulse for 1 full minute • Avoid applying pressure over the pacemaker. . • Inform the dentis • Avoid having a magnetic resonance imaging (MRI). detectors, and welding equipment because they can interfere with conduction. • Be careful when using microwaves. stand approximately 5 feet away from the device while cooking. • Report fever, redness, swelling, or soreness at the implantation site. • If beeping tones are heard coming from the internal defibrillator, immediately move away from any electromagnetic source. Stand clear from other people because shock can affect anyone touching the client during defibrillation. • Report dizziness, fainting, weakness, blackouts, or a rapid pulse rate. • The client will most likely be told not to drive a car for approximately 6 months blackouts, or a rapid pulse rate. • The client will most likely be told not to drive a car for approximately 6 months after the internal defibrillator is inserted to evaluate any dysrhythmias. • Report persistent hiccupping because this can indicate misfiring |
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Myocardial Infarction
|
When there is a disruption in blood supply to
the myocardium, the client is considered to have had a myocardial infarction. Factors contributing to diminished blood flow to the heart include arteriosclerosis, emboli, thrombus, shock, and hemorrhage. If circulation is not quickly restored to the heart, the muscle becomes necrotic. Hypoxia from ischemia can lead to vasodilation of blood vessels. Acidosis associated with electrolyte imbalances often occurs, and the client can slip into cardiogenic shock. The most common site for a myocardial infarction is the left ventricle. |
|
Myocardial Infarction The most commonly reported signs and
symptoms associated with myocardial infarction include |
Only 10% of
clients report the classic symptoms of a myocardial infarction. Women often fail to report chest pain and, if they do, they might tell the nurse that the pain is beneath the shoulder or in the back. Clients with diabetes have fewer pain receptors and might report little or no pain. Substernal pain or pain over the precordium of a duration greater than 15 minutes • Pain that is described as heavy, viselike, and radiating down the left arm • Pain that begins spontaneously and is not relieved by nitroglycerin or rest • Pain that radiates to the jaw and neck • Pain that is accompanied by shortness of breath, pallor, diaphoresis, dizziness, nausea, and vomiting • Increased heart rate, decreased blood pressure, increased temperature, and increased respiratory rate |
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Myocardial Infarction DX
|
diagnostic tools for determining the type and
severity of the attack: • Electrocardiogram (ECG), which frequently shows dysrhythmias • Serum enzymes and isoenzyme tests that are useful in providing a complete picture of the client’s condition are white blood cell count (WBC), sedimentations rate, and blood urea nitrogen (BUN |
|
Angina pectoris
Nitro ASA |
occurs when there are
vasospasms. This pain is relieved by nitroglycerine take one every 5 mins, no more than 3 at a time The client should be taught to replenish his supply every 6 months and protect the pills from light by leaving them in the brown bottle. The cotton should be removed from the bottle because it will decrease the tablets’ effectiveness. one 365 mg aspirin at the first sign of chest pain. Aspirin has an anticoagulant effect and decreases the clotting associated with heart attacks. The nurse must always wear gloves when applying nitroglycerine cream or patches to the client. Clip hair with scissors or shave, but do not abrade area. |
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Tropon 1,"", CRP, LDH
|
The Troponin T and 1 are specific
to striated muscle and are often used to determine the severity of the attack. Creactive protein (CRP) levels are used with the CK-MB to determine whether the client has had an acute MI and the severity of the attack. Lactic acid dehydrogenase (LDH) is a nonspecific enzyme that is elevated with any muscle trauma. |
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Ventricular tachycardia
|
is a rapid irregular
rhythm absence of a p-wave. Usually the rate exceeds 140–180 bpm. The SA node continues to discharge in-dependently of the ventricle |
|
Ventricular tachycardia is often associated
with |
valvular heart disease, heart failure,
hypomagnesium, hypotension, and ventricular aneurysms. |
|
Ventricular tachycardia
|
Ventricular tachycardia is treated
with oxygen and medication. Amiodarone (Cordarone), procainamide (Pronestyl), or magnesium sulfate is given to slow the rate and stabilize the rhythm. Lidocaine has long been established for the treatment of ventricular tachycardia; however, it should not be used in an acute MI client. Heparin is also ordered to prevent further thrombus formation but is not generally ordered with clients taking streptokinase. |
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Ventricular fibrillation (V-fib)
|
(V-fib) is the primary
mechanism associated with sudden cardiac arrest. This disorganized chaotic rhythm results in a lack of pumping activity of the heart. Without effective pumping, no oxygen is sent to the brain and other vital organs |
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Ventricular fibrillation (V-fib) s/s
|
The client quickly becomes
faint, loses consciousness, and becomes pulseless. Hypotension or a lack of blood pressure and heart sounds are present |
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Ventricular fibrillation (V-fib) TX
|
Three quick, successive shocks Administration of oxygen and
antidysrhythmic medications such as epinephrine, amiodarone, procainamide, lidocaine, or magnesium sulfate are ordered. If cardiac arrest occurs, the nurse should initiate cardiopulmonary resuscitation and be ready to administer first-line drugs such as epinephrine Cardiac catheterization is used to detect blockages associated with myocardial infarctions and dysthymias. |
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percutaneous
transluminal coronary angioplasty. Prior to and following this the nurse should |
catheterization, as with any other dye
procedure, requires a permit. This procedure can also accompany percutaneous transluminal coronary angioplasty. Prior to and following this procedure, the nurse should • Assess for allergy to iodine or shell fish. • Maintain the client on bed rest with the leg straight. • Maintain pressure on the access site for at least 5 minutes or until no signs of bleeding are noted. |
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Angio Seal is and the nursing interventions are
|
Angio
Seals to prevent bleeding at the insertion site. The device creates a mechanical seal anchoring a collagen sponge to the site. The sponge absorbs in 60–90 days. • Use pressure dressing and/or ice packs to control bleeding. • Check distal pulses because diminished pulses can indicate a hematoma and should be reported immediately. • Force fluids to clear dye from the body |
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Coronary artery bypass graft
|
The family should be instructed that
the client will return to the intensive care unit with several tubes and monitors. The client will have chest tubes and a mediastinal tube to drain fluid and to reinflate the lungs. If the client is bleeding and blood is not drained from the mediastinal area, fluid accumulates around the heart. This is known as cardiac tamponade. |
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Coronary artery bypass graft treatment afterward
|
A Swan-Ganz catheter for monitoring central venous
pressure, pulmonary artery wedge pressure monitor, and radial arterial blood pressure monitor is inserted to measure vital changes in the client’s condition. An ECG monitor and oxygen saturation monitor are also used. Other tubes include a nasogastric tube to decompress the stomach, a endotracheal tube to assist in ventilation, and a Foley catheter to measure hourly output. The client should be given small, frequent meals. The diet should be low in sodium, fat, and cholesterol. Adequate amounts of fluid and fiber are encouraged to prevent constipation, and stool softeners are also ordered. Post-MI teaching should stress the importance of a regular program of exercise, stress reduction, and cessation of smoking |
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Coronary artery bypass graft teaching
|
The client should be given small, frequent
meals. The diet should be low in sodium, fat, and cholesterol. Adequate amounts of fluid and fiber are encouraged to prevent constipation, and stool softeners are also ordered. Post-MI teaching should stress the importance of a regular program of exercise, stress reduction, and cessation of smoking Because caffeine causes vasoconstriction, caffeine intake should be limited. The client can resume sexual activity in 6 weeks or when he is able to climb a flight of stairs without experiencing chest pain. Medications such as Viagra are discouraged and should not be taken within 24 hours of taking a nitrite. Clients should be taught not to perform Valsalva maneuver or bending at the waist to retrieve items from the floor. Placing items in top drawers helps to prevent increased intrathoracic pressure. The client will probably be discharged on an anticoagulant such as enoxaparin (Lovenox) or sodium warfarin (Coumadin). |
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Anticoagulants such as heparin,the therapeutic range, test and antidote
|
The
nurse should check the partial thromboplastin time (PTT). The normal control level is approximately 30–60 seconds. The therapeutic bleeding time should be from one and a half to two times the control. The medication should be injected in the abdomen 2'' from the umbilicus using a tuberculin syringe. Do not aspirate or massage. The antidote for heparin derivatives is protamine sulfate. |
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Coumadin, the therapeutic range, test and antidote
|
If Coumadin
(sodium warfarin) is ordered, the nurse should check the PT or pro-time. The control level for a pro-time is 10–12 seconds. The therapeutic level for Coumadin should be from one and a half to two times the control. The antidote for Coumadin is vitamin K. The international normalizing ratio (INR) is done for oral anticoagulants. The therapeutic range is 2–3. If the level exceeds 7, watch for spontaneous bleeding |
|
Buerger’s Disease
|
Buerger’s Disease
Buerger’s disease (thromboangiitis obliterans) results when spasms of the arteries and veins occur primarily in the lower extremities. These spasms result in blood clot formations and eventually destruction of the vessels. |
|
Buerger’s Disease s/s
|
Symptoms
associates with Buerger’s include pallor of the extremities progressing to cyanosis, pain, and paresthesia. As time progresses, tophic changes occur in the extremities |
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Buerger’s Disease TX
|
Management of the client with Buerger’s
involves the use of Buerger-Allen exercises, vasodilators, and oxygenation. The client should be encouraged to stop smoking. |
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Thrombophlebitis
|
occurs when an inflammation
of a vein with formation of a clot occurs. Most thrombophlebitis occurs in the lower extremities, with the saphenous vein being the most common vein affected |
|
Thrombophlebitis TX s/s
|
Homan’s sign is
an assessment tool used for many years by healthcare workers to detect deep vein thrombi. It is considered positive if the client complains of pain on dorsiflexion of the foot. Homan’s sign should not be performed routinely because it can cause a clot to be dislodged and lead to pulmonary emboli. If a diagnosis of thrombophlebitis is made, the client should be placed on bed rest with warm, moist compresses to the leg. An anticoagulant is ordered, and the client is monitored for complications such as cellulitis. If cellulitis is present, antibiotics are ordered. |
|
Anti-thrombolytic stockings or compression
devices are ordered |
Anti-thrombolytic stockings or compression
devices are ordered to prevent venous stasis. When anti-thrombolytic stockings are applied, the client should be in bed for a minimum of 30 minutes prior to applying the stockings. The circumference and length of the extremity should be measured to prevent rolling |
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Raynaud’s Syndrome
|
Raynaud’s Syndrome occurs when there are
vascular vasospasms brought on by exposure to cold.causing discoloration of the fingers, toes, and occasionally other areas The most commonly effected areas are the hands, nose, and ears. Management includes preventing exposure, stopping smoking, and using vasodilators. The client should be encouraged to wear mittens when outside in cold weather. |
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An aneurysm
|
is a ballooning of an artery. The
greatest risk for these clients is rupture and hemorrhage. Aneurysms can occur in any artery in the body and can be due to congenital malformations or arteriosclerosis or be secondary to hypertension. |
|
types of aneurysms
|
Fusiform—This aneurysm affects the
entire circumference of the artery. • Saccular—This aneurysm is an outpouching affecting only one portion of the artery. • Dissecting—This aneurysm results in bleeding into the wall of the vessel. |
|
abdominal aortic
|
complains of feeling her heart
beating in her abdomen or lower back pain. Any such complaint should be further evaluated. On auscultation of the abdomen, a bruit can be heard. |
|
abdominal aortic DX and TX
|
Diagnosis can be made by
ultrasound, arteriogram, or abdominal x-rays. If the aneurysm is found to be 6 centimeters or more, surgery should be scheduled. During surgery the aorta is clamped above and below and a donor vessel is anastomosed in place. When the client returns from surgery, pulses distal to the site should be assessed and urinary output should be checked. Clients who are not candidates for surgery might elect to have stent placement to reinforce the weakened artery. These stents are threaded through an incision in the femoral artery, hold the artery open, and provide support for the weakened vessel |
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Congestive Heart Failure
|
When fluid accumulation occurs and the heart
is no longer able to pump in an efficient manner, blood can back up. Most heart failure occurs when the left ventricle fails. When this occurs, the fluid backs up into the lungs, causing pulmonary edema. |
|
Congestive Heart Failure left side, s/s of PE
|
The signs of
pulmonary edema are frothy, pink tinged sputum; shortness of breath; and orthopnea. Distended jugular veins might also be present. Crackles & wheezes Cough Grunting (infants) Dyspnea Nasal flaring Orthopnea Head bobbing (infants) Retractions Tachypnea Periods of cyanosis |
|
Congestive Heart Failure right-sided
|
right-sided congestive
heart failure occurs, the blood backs up into the periphery. The nurse might also note signs of pitting edema. Pitting can be evaluated by pressing on the extremities and noting the degree of pitting, how far up the extremity the pitting occurs, and how long it takes to return to the surface. Ascites Oliguria Hepatosplenomegaly Weight Gain Jugular vein distention Peripheral edema, especially dependent & periorbital edema |
|
Congestive Heart Failur RX
|
Treatment for congestive heart
failure includes use of diuretics, Natrecor, Primacor, and cardiotonics. Morphine might also be ordered to manage pain Diuretics • Cardiotonics • Antihypertensives • Anticoagulants • Thrombolytics |
|
Diagnostic Tests CHF
|
Arteriogram—Arteriography reveals the
presence of blockages and abnormalities in the vascular system. • Cardiac catheterization—A cardiac catheterization reveals blockages, turbulent flow, and arteriosclerotic heart disease. CBC • Chest x-ray— ekg |
|
Secondary hypertension Precipitating disorders or conditions
|
Precipitating disorders or conditions
a. Cardiovascular disorders b. Renal disorders c. Endocrine system disorders d. Pregnancy e. Medications (meds)e.g., estrogens, glucocorticoids, mineralocorticoids |
|
HTN Assesment
|
1. May be asymptomatic
2. Headache 3. Visual disturbances 4. Dizziness 5. Chest pain 6. Tinnitus 7. Flushed face 8. Epistaxis |
|
HTN interventions 14 of them
|
1. Goals
a. One treatment goal is to reduce the BP. b. Another treatment goal is to prevent or lessen the extent of organ damage. 2. Question the client regarding the signs & symptoms indicative of hypertension. 3. Obtain the BP two or more times on both arms, with the client supine & standing. 4. Compare the BP with prior documentation. 5. Determine family history of hypertension. 6. Identify current medication therapy. 7. Obtain weight. 8. Evaluate dietary patterns & sodium intake. 9. Assess for visual changes or retinal damage. 10. Assess for cardiovascular changes such as distended neck veins, increased heart rate, & dysrhythmias. 11. Evaluate chest x-ray for heart enlargement. 12. Assess the neurological system. 13. Evaluate renal function. 14. Evaluate results of diagnostic & laboratory studies |
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Nonpharmacological TX
|
Nonpharmacological interventions
1. Weight reduction, if necessary, or maintenance of ideal weight 2. Dietary sodium restriction to 2 g daily as pre-scribed 3. Moderate intake of alcohol & caffeinecontaining products 4. Initiation of a regular exercise program 5. Avoidance of smoking 6. Relaxation techniques & biofeedback therapy 7. Elimination of unnecessary meds that may contribute to the hypertension |
|
Step approach for HTN
|
Step 1: A single medication is prescribed, which may be a diuretic, b-blocker, calcium
channel blocker, angiotensin-converting enzyme inhibitor, or angiotensin II receptor blocker. Step 2: a. Step 1 therapy is evaluated after 1 to 3 months. b. If the response is not adequate, compliance is evaluated. c. The medication may be increased or a new medication may be prescribed or a second medication added the treatment plan. Step 3: a. Compliance is evaluated. b. Further evaluation of step 2. c. If a therapeutic response is not adequate, a second medication is substituted or a third medication is added to the treatment plan. Step 4: a. Compliance is evaluated. b. Careful assessment of factors limiting the antihypertensive response is done. c. A third or fourth medication may be added to the treatment plan. |
|
hypertensive crisis
|
A hypertensive crisis is any clinical
condition requiring immediate reduction in BP. 2. A hypertensive crisis is an acute & lifethreatening condition. 3. The accelerated hypertension requires emergency treatment because target organ damage (brain, heart, kidneys, retina of the eye) can occur quickly. 4. Death can be caused by stroke, renal failure, or cardiac disease |
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Hhypertensive crisis s/s
|
Assessment
• An extremely high BP; usually, the diastolic pressure is > 120 mm Hg • Headache • Drowsiness & confusion • Blurred vision • Changes in neurological status • Tachycardia & tachypnea • Dyspnea Cyanosis • Seizures |
|
hypertensive crisis intervention
|
Interventions
1. Maintain a patent airway. 2. Administer antihypertensive meds intravenously as prescribed, which may include nitroprusside (Nitropress), diazoxide (Hyperstat), nicardipine (Cardene), or labetalol (Trandate). 3. Monitor vital signs, assessing the BP every 5 minutes. 4. Assess for hypotension during the administration of antihypertensives; place the client in a supine position if hypotension occurs. 5. Have emergency meds & resuscitation equipment readily available. 6. Maintain bed rest, with the he Monitor IV therapy, assessing for fluid overload. 8. Monitor intake & output |
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Beta blockers
|
Propranolol (Inderal), atenolol (Tenormin), nadolol (Corgard
|
|
Diuretics
|
Thiazide: Chlorothiazide (Diuril), hydrochlorothiazide (Esidrix, HydroDIURIL)
Loop diuretics: Furosemide (Lasix), ethacrynic acid (Edecrin) Potassium sparing diuretics: Spironolactone (Aldactone), triamterene (Dyrenium) |
|
Calcium channel
blockers |
Nifedipine (Procardia), verapamil (Calan), diltiazem hydrochloride
(Cardizem) |
|
Angiotensin
converting |
Captopril (Capoten), enalapril (Vasotec), lisinopril enzyme inhibitors (Zestril,
Prinivil) |
|
Angiotensin receptor
|
Angiotensin receptor C andesartan (Atacand), losartan (Cozaar), telmisartan blockers (Micardis)
These drugs can be used alone or in conjunction with one another. Diuretics & vasodilators are often given in combination to lower BP through diuresis & vasodilation. Hypertensive crises exist when the diastolic BP reaches 140. Malignant hypertension is managed with administration of IV Nitropress, Nitroglycerine, Nipride, Lasix, & other potent vasodilators such as Procardia |
|
HTN drugs
|
Diuretics, beta blockers, calcium channel blockers, angiotensin converting, angiotensin recepor
|
|
PERIPHERAL VASCULAR DISEASE (PVD) S/S
|
Reduced blood flow through peripheral
blood vessels characterizes all peripheral vascular diseases. The physiologic effects of altered blood flow depend on the extent to which tissue demands exceed the supply of oxygen & nutrients available. If tissue needs are high, even modestly reduced blood flow may be inadequate to maintain tissue integrity. Tissues then fall prey to ischemia (deficient blood supply), become malnourished, & ultimately die if adequate blood flow is not restored. Although many types of peripheral vascular diseases exist, most result in ischemia & produce some of the same symptoms: pain, skin changes, diminished pulse, & possible edema. The type & severity of symptoms depend in part on the type, stage, & extent of the disease process & on the speed with which the disorder develops |
|
ARTERIOSCLEROTIC HEART DISEASE
|
Arteriosclerosis ("hardening of the arteries")
The process whereby abnormal deposits of lipids, cholesterol & plaque buildup, leading to narrowing or blockage in arteries taking blood to the hand, foot head or vital organs. |
|
Atherosclerosis
|
(fatty deposits
called plaque on inner lining of vessel walls). |
|
Calcific sclerosis (calcium
|
deposits on the middle layer of
the wall of the arteries |
|
Arteriolar sclerosis
|
a thickening
of the arterioles caused by hypertension) |
|
Coronary Artery Disease
(atherosclerosis/arteriosclerosis) |
A build-up
of fatty material in the wall of the coronary artery that causes narrowing of the artery is a narrowing of the small blood vessels that supply blood & oxygen to the heart. CHD is also called coronary artery disease or arteriosclerotic heart disease. |
|
CAUSES: of cad chd
|
Causes, incidence, & risk factors:
Coronary heart disease is usually caused by a condition called atherosclerosis, which occurs when fatty material & a substance called plaque buildup on the walls of your arteries. This causes them to get narrow. As the coronary arteries narrow, blood flow to the heart can slow down or stop. This can cause chest pain (stable angina), shortness of breath, heart attack, & other symptoms. CHD is the leading cause of death in the United States for men & women. |
|
risk
for heart disease: |
Men in their 40s have a higher risk of CHD
than women. But as women get older (especially after they reach menopause), their risk increases to almost equal that of a man's risk. • Bad genes (heredity) can increase your risk. You are more likely to develop the condition if someone in your family has had a history of heart disease -- especially if they had it before age 50. Your risk for CHD goes up the older you get. • Diabetes is a strong risk factor for heart disease High BP increases your risk of coronary artery disease & heart failure. • Abnormal cholesterol levels: your LDL ("bad") cholesterol should be as low as possible, & your HDL ("good") cholesterol should be as high as possible. • Metabolic syndrome refers to high triglyceride levels, high BP, excess body fat around the waist, & increased insulin levels. People with this group of problems have an increased chance of getting heart disease. • Smokers have a much higher risk of heart disease than nonsmokers. • Chronic kidney disease can increase risk. • Already having atherosclerosis or hardening of the arteries in another part of your body (examples are stroke & abdominal aortic aneurysm) increases your risk of having coronary disease. • Other risk factors including alcohol abuse, not getting enough exercise, & excessive amounts of stress. • Higher-than-normal levels of inflammationrelated substances, such as C-reactive protein & fibrinogen are being studied as possible indicators of an increased risk for heart disease. • Increased levels of a chemical called homocysteine, an amino acid, are also linked to an increased risk of a heart attack |
|
ANGINA PECTORIS
|
clinical syndrome usually
characterized by episodes or paroxysms of pain or pressure in the anterior chest. The cause is usually insufficient coronary blood flow. The insufficient flow results in a decreased oxygen supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress. |
|
Stable angina
Unstable angina (also called preinfarction or crescendo angina Intractable or refractory angina Variant angina (also called Prinzmetal’s angina): Silent ischemia: |
Stable angina: predictable & consistent
pain that occurs on exertion & is relieved by rest • Unstable angina (also called preinfarction or crescendo angina): symptoms occur more frequently & last longer than stable angina. Threshold for pain is lower, & pain may occur at rest. • Intractable or refractory angina: severe incapacitating chest pain • Variant angina (also called Prinzmetal’s angina): pain at rest with reversible STsegment elevation; thought to be caused by coronary artery vasospasm • Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress test), but patient reports no symptoms |
|
RX FOR ANGINA
|
Medications used to treat angina include
aspirin, beta blockers, nitroglycerin, & ACE inhibitors. Other meds that may be used to treat angina include calcium channel blockers to relax blood vessels, allowing greater blood flow to the heart & a lower BP; antihypertensive & lipid-lowering agents; & oral antiplatelets, such as clopidogrel bisulfate (Plavix), which stop platelets from clumping together to form clots |
|
MANAGEMENT OF ANGINA , WHAT TO WATCH FOR WITH THE RX
|
A
beta blocker dose may be withheld or decreased at the physician’s discretion if the heart rate is below 50 or 60 or if the patient becomes symptomatic. Both ACE inhibitors & beta blockers can lower BP & may need to be withheld if the systolic BP drops below 90. These parameters are often part of standing orders in the telemetry unit, Monitoring of vital signs is an important component of medication management |
|
gANGRENE, TYPES- DRY AND GAS AND WET
|
Wet gangrene (also called
moist gangrene)necrotizing fasciitis, or infection of the skin & tissues directly beneath the ski occurs when dry gangrene becomes infected, often due to injury, & the infection causes the tissue to die. Gas gangrene, the most serious form of wet gangrene, often is caused by Clostridium bacteria, which are normal inhabitants of the gastrointestinal, respiratory, & female genital tracts. Areas of either dry or moist gangrene are initially characterized by a red line on the skin that marks the border of the affected tissues. Dry gangrene occurs when a portion of bodily tissue dies because its blood supply has been decreased or completely cut off. This type of gangrene will not spread to other healthy tissue, & infection is not present. |
|
Some of
the most common causes of dry gangrene include: |
arterial obstruction, or occlusion of an
artery, caused by arteriosclerosis, diabetes mellitus, AIDS or blood clot • severe blunt trauma to a part of the body causing damage & therefore obstruction of an artery • frostbite, which occurs when tissue becomes so cold that it is literally deprived of blood & therefore oxygen, & dies • diseases that affect the blood vessels, & especially the arteries, such as Buerger's or Raynaud's disease • traumatic occurrences such as crushing injuries, fractures, burns, & even injections given into skin or muscle Causative organisms for wet gangrene infection include: • Streptococcus • Staphylococcus |
|
symptoms of gas
gangrene include |
edema, or swelling, at the injury site that
expands quickly • pain in the area surrounding the skin injury • crepitus, a bubbly, crackling sound often heard upon palpation • pallor at the injury site, then increasingly dusky discoloration • low-grade to moderate temperature elevation |
|
Myocarditis
|
Myocarditis describes any
inflammation that occurs within the heart muscle. It is induced by various infections which will include viruses like sarcoidosis, & distinct immune diseases. The most prevalent form of infection is the viral kind that assaults the heart muscle resulting in local inflammation. Once the infection subsides the immune response will still endure. Because of this, myocarditis will continue to plague the heart muscle long after the infection has ceased. |
|
Myocarditis s/s early and late
|
It is not unusual for the disease to
be completely asymptomatic. Pain in the chest is the most likely sign of myocarditis astringent instances the disease may progress into degeneration of the heart muscle. It is then unfortunately able to trigger heart failure with the associated symptoms: shortness of breath or difficulty breathing, edema or swelling of feet & ankles, fatigue among others. |
|
Myocarditis DX
|
ECG or electrocardiogram will be used to
detect deviations within the heartbeat. MRI or magnetic resonance imaging tests will be applied to reveal heart muscle peculiarities. Blood tests will be performed to search for any likely infection & also for the possible rise in level of heart muscle enzymes |
|
Myocarditis Prognosis
|
There is much uncertainty about
the likelihood of recovery in the early phases of the disease. A fair portion of individuals achieve total recovery while some may eventually be inflicted with chronic heart failure due to extravagant damage to the heart muscles. Infrequently a person may be struck with fulminant heart failure which will necessitate a heart transplant. If the degeneration of the muscle is enormous a defibrillator may be implanted to better the heart’s ability to function |
|
PERICARDITIS DEF AND RISK
|
Pericarditis is a disease that
causes inflammation of the pericardium. The pericardium is the fluid sac that envelopes the heart. It provides lubrication to the heart thus decreasing friction during activity & also firmly secures the heart to the surrounding walls within the cavity. The cause of pericarditis may possibly be unexplained however there are some factors that may induce the disease. These will include: • Some tumors & cancers • Specific metabolic disorders potentially hypothyroidism & uremia (kidney failure) • Infection with a virus or bacteria • Prior impairment to the heart, for example heart attack, trauma & heart surgery • An underlying connective tissue disease such as sarcoidosis & rheumatoid arthritis • An unexpected reaction to a particular type of medication |
|
PERICARDITIS S/S
|
pain when
swallowing.a slight fever,- The most defining symptom will be chest pain or angina pectoris that is generally expressed as a cutting, intense pain that migrates from the chest area to the shoulder blades, back & neck. It is also quite possible to experience pain near the diaphragm that extends to the back. When inhaling deeply the chest pain will become significantly worse. The pain is typically unbearable when lying flat but will be bettered by leaning forward. |
|
PERICARDITIS TX
|
The primary treatment is the
administering of anti-inflammatory meds,A narcotic pain medication,Pericardiocentesis may be applicable as a form of progressive treatment. It will remove excessive fluid from the sac & or will detect the pathogen of origin that may have induced the condition |
|
PERICARDITIS DX
|
Diagnosis will begin
with an assessment of the pain symptoms to distinguish it from pain associated with another condition. an ECG electrocardiogram, chest x-ray & ultrasound of the heart will be utilized. A blood test may be undertaken to detect any other underlying conditions that may have triggered the development of pericarditis, pericardial friction rub IS SIGN OF INFLAMMATION BUT NOT PERICARDITIS FOR SURE |
|
ENDOCARDITIS
|
Endocarditis is induced by an
infection of the endocardium or inner lining of the heart resulting in pronounced inflammation. It will present itself when pathogens from other regions of the body infect the bloodstream & affix to defective areas of the heart. If it is not treated speedily it may cause partial or complete damage to the heart valve or may develop into a life-threatening condition. It usually affects individuals who have an artificial heart valve in place or have suffered degeneration of a heart valve. Having a preexisting heart defect also increases the odds of developing the condition. It does not normally affect healthy people. |
|
ENDOCARDITISs/s risk
|
fairly long period of time or may manifest
quite suddenly corresponding heart defect or infection o Unexplained & sudden weight loss o Joint & muscular pain o Fever & chills o Visible purple or red spots exhibited in the mouth on the skin or on the whites of the eyes o Heart murmurs (irregular sounds arising from the heart) o Constant coughing o Blood in the urine o Edema or swelling of the feet & abdomen o Fatigue & unusual tiredness o Night sweats o Tenderness below the rib cage that is associated with the spleen o A pale complexion o Areas of red tender spots just below the skin of the fingers. o Shortness of breath or difficulty breathing/ people at risk are people with an artificial heart valve or heart condition and Intravenous drug users are at a greater risk of developing the condition because of needle sharing. The bacterium that may incite this condition is commonly harbored in contaminated needles |
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ENDOCARDITIS dx
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Diagnosis
• Blood tests will be applicable. They will discover the source of bacterial infection. • An echocardiogram will be employed to properly assess the heart’s condition. • An ECG or electrocardiogram & x-ray will also be used to confirm diagnosis. • MRI magnetic resonance or CT computerized tomography imaging scan will be used if it is believed the infection may have traveled to other areas of the body |
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ENDOCARDITIS tx
|
The main treatments are
antibiotics in less intense cases & possible surgery where damage is significantly compromising. |
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RHEUMATIC FEVER, HEART/ VALVE DISEASE
DX and test |
1. Rheumatic fever is an inflammatory
autoimmune disease that affects the connective tissues of the heart, joints, subcutaneous tissues, & blood vessels of the central nervous system. 2. The most serious complication is rheumatic heart disease, which affects the cardiac valves, particularly the mitral valve. 3. Rheumatic fever presents 2 to 6 weeks following an untreated or partially treated group A beta-hemolytic streptococcal infection of the upper respiratory tract. 4. Jones criteria are used to determine the diagnosis.,1. Fever: Low-grade fever that spikes in the late afternoon 2. Elevated antistreptolysin O titer 3. Elevated sedimentation rate 4. Elevated C-reactive protein level 5. Aschoff bodies (lesions): Found in the heart, blood vessels, brain, & serous surfaces of the joints & pleura |
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Interventions
RHEUMATIC FEVER, HEART/ VALVE DISEASE |
Assess vital signs.
2. Control joint pain & inflammation with massage & alternating hot & cold applications as prescribed. 3. Provide bed rest during acute febrile phase. 4. Limit physical exercise in the child with carditis. 5. Administer antibiotics (penicillin) as prescribed. 6. Administer salicylates & anti-inflammatory agents (prednisone [Deltasone]) as prescribed; these meds should not be administered before the diagnosis is confirmed, because these meds mask the polyarthritis). 7. Initiate seizure precautions if the child is experiencing chorea. 8. Instruct the parents about the importance of follow-up & the need for antibiotic prophylaxis for dental work, infection, & invasive procedures. 9. Advise the child to inform the parents if anyone in school develops a streptococcal throat infection |
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KAWASAKI DISEASE DX
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1. Known as mucocutaneous lymph node
syndrome & is an acute systemic inflammatory illness. 2. The cause is unknown but may be associated with an infection from an organism or toxin. 3. Cardiac involvement is the most serious complication; aneurysms can develop. Assessment 1. Acute stage a. Fever b. Conjunctival hyperemia c. Red throat d. Swollen hands, rash, & enlargement of the cervical lymph nodes 2. Subacute stage a. Cracking lips & fissures b. Desquamation of the skin on the tips of the fingers & toes c. Joint pain d. Cardiac manifestations e. Thrombocytosis 3. Convalescent stage: Child appears normal but signs of inflammation may be present |
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KAWASAK INTERVENTIONS
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Interventions
1. Monitor temperature frequently. 2. Assess heart sounds, rate, & rhythm. 3. Assess extremities for edema, redness, & desquamation. 4. Examine eyes for conjunctivitis. 5. Monitor mucous membranes for inflammation. 6. Monitor strict intake & output. 7. Administer soft foods & liquids that are neither too hot nor too cold. 8. Weigh the child daily. 9. Provide passive range-of-motion exercises to facilitate joint movement. 10. Administer acetylsalicylic acid (aspirin) as prescribed for its antipyretic & antiplatelet effects. 11. Administer immune globulin intravenously as prescribed to reduce the duration of the fever & the incidence of coronary artery lesions & aneurysms; IV immune globulin (IVIG) is a blood product, so blood precautions when administering it are warranted. 12. Parent education |
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CHF IN CHILDREN
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2. In infants & children, inadequate cardiac
output most commonly is caused by congenital heart defects (shunt, obstruction, or a combination of both) that produce an excessive volume or pressure load on the myocardium. 3. In infants & children, a combination of leftsided & right-sided heart failure is usually present |
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CHF S/S EARLY SIGNS
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Assessment of early signs
1. Tachycardia, especially during rest & slight exertion 2. Tachypnea 3. Profuse scalp diaphoresis, especially in infants 4. Fatigue & irritability 5. Sudden weight gain 6. Respiratory distress |
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CHF INTERVENTIONS FOR CHILDREN
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2. Monitor for respiratory distress (count
respirations for 1 minute). 3. Monitor apical pulse (count pulse for 1 minute) & monitor for dysrhythmias. 4. Monitor temperature for hyperthermia & for other signs of infection, particularly respiratory infection. 5. Monitor strict intake & output. 6. Weigh diapers as appropriate. 7. Monitor daily weight to assess for fluid retention; a weight gain of 0.5 kg (1 lb) in 1 day is caused by the accumulation of fluid. 8. Monitor for facial or peripheral dependent edema, auscultate lung sounds, & report abnormal findings indicating excessive fluid in the body. 9. Elevate the head of the bed in a semi- Fowler's position. 10. Maintain a neutral thermal environment to prevent cold stress in infants. 11. Provide rest & decrease environmental stimuli. 12. Administer cool humidified oxygen as prescribed, using an oxygen hood for young infants & a nasal cannula or face mask for older infants & children. 13. Organize nursing activities to allow for uninterrupted sleep. 14. Maintain adequate nutritional status. 15. Feed when hungry & soon after awakening, conserving energy & oxygen supply. 16. Provide small, frequent feedings, conserving energy & oxygen supply. 17. Administer sedation as prescribed during the acute stage to promote rest. 18. Administer digoxin (Lanoxin) as prescribed a. Assess apical heart rate for 1 minute before administration b. Hold digoxin if pulse is < 90 beats/min in infants & young children & < 70 beats/min in older children, as prescribed c. Be aware that infants rarely receive more than 1 mL of digoxin in one dose 19. Monitor digoxin levels & for signs of digoxin toxicity, including bradycardia, headache, & vomiting. a. Normal digoxin level is 0.5 to 2.0 mg/dL b. Digoxin toxicity occurs when level is above 2.0 mg/dL 20. Administer angiotensin-converting enzyme inhibitors (captopril [Capoten] or enalapril [Vasotec]) as prescribed. a. Monitor for hypotension, renal dysfunction, & cough when angiotensin-converting enzyme inhibitors are administered. b. Assess the BP, serum protein, albumin, blood urea nitrogen, & creatinine levels, white blood cell count, urine output, urinary specific gravity, & urinary protein level. 21. Administer diuretics (furosemide [Lasix]) as prescribed a. Monitor for signs & symptoms of hypokalemia (serum potassium level < 3.5 mEq/L), including muscle weakness & cramping, confusion, irritability, restlessness, & inverted T wave on the electrocardiogram (ECG). b. If signs & symptoms of hypokalemia are present & the child is also being administered digoxin, then monitor closely for digoxin toxicity because hypokalemia potentiates digoxin toxicity. 22. Administer potassium supplements & provide dietary sources of potassium as prescribed. a. Supplemental potassium should only be given if indicated by potassium levels & i& if adequate renal function is evident, & is usually necessary when giving a non– potassium-sparing diuretic such as furosemide. b. Encourage foods that the child will eat that are high in potassium, as appropriate, such as bananas, baked potato skins, & peanut butter. 23. Monitor electrolyte levels, particularly the potassium level (normal level is 3.5-5.1 mEq/L). 24. Restrict fluid as prescribed in the acute stage. 25. Monitor for signs/symptoms of dehydration, including sunken fontanel, nonelastic skin turgor, dry mucous membranes, decreased tear production, decreased urine output, & concentrated urine. 26. Monitor sodium levels as prescribed. a. Normal level is 135 -145 mEq/L. b. Many infant formulas have slightly more sodium than breast milk. 27. Instruct the parents regarding the description of the diagnosis & administration of meds. 28. Instruct the parents in CPR. |
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NSR RATE
|
60 TO 100
|
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SINUS BRADY INTERVENTIONS
|
a. Attempt to determine the cause of
sinus bradycardia; if a medication is suspected of causing the bradycardia, hold the medication & notify the physician. b. Administer oxygen as prescribed. c. Administer atropine sulfate as prescribed to increase the heart rate to 60 beats/min. d. Be prepared to apply a noninvasive (transcutaneous) pacemaker initially as prescribed if the atropine sulfate does not increase the heart rate sufficiently. e. Avoid additional doses of atropine sulfate because this will induce tachycardia f. Monitor for hypotension & administer fluids intravenously as prescribed. g. Depending on the cause of the bradycardia, the client may need a permanent pacemaker |
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A FIB Description
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a. Multiple rapid impulses from many foci
depolarize in the atria in a totally disorganized manner at a rate of 350 to 600 times/min. b. The atria quiver, which can lead to the formation of thrombi. c. No definitive P wave can be observed, only fibrillatory waves before each QRS. |
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A-FIB
Interventions |
Administer oxygen.
b. Administer anticoagulants as prescribed because of the risk of emboli. c. Administer cardiac meds as prescribed to control the ventricular rhythm & assist in the maintenance of cardiac output. d. Prepare the client for cardioversion as prescribed. e. Instruct the client in the use of meds as prescribed to control the dysrhythmia |
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PVC'S INTERVENTIONS
|
a. Notify the physician if PVCs occur.
b. Identify the cause & treat based on the cause. c. Evaluate oxygen saturation to assess for hypoxemia, which can cause PVCs. d. Administer oxygen as prescribed. e. Evaluate electrolytes, particularly the potassium level, because hypokalemia can cause PVCs. f. Lidocaine may be prescribed. g. Notify the physician if the client complains of chest pain or if PVCs increase in frequency, are multifocal, occur on the T wave (R on T), or occur in runs of ventricular tachycardia. |
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VENTRICULAR TACHYCARDIA 140 TO 250
|
Ventricular tachycardia occurs
because of a repetitive firing of an irritable ventricular ectopic focus at a rate of 140 to 250 beats/min or more. |
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TREATMENT FOR STABLE AND UNSTABLE V=TACH
|
Stable client with sustained VT (with pulse
& no signs or symptoms of decreased cardiac output) a. Administer oxygen as prescribed. b. Administer antidysrhythmics, such as amiodarone (Cordarone), lidocaine (Xylocaine), or procainamide (Pronestyl) as prescribed. 3. Unstable client with VT (with pulse & signs & symptoms of decreased cardiac output) a. Administer oxygen & antidysrhythmic therapy as prescribed. b. Prepare for synchronized cardioversion if the client is unstable. c. Attempt 'cough' cardiopulmonary resuscitation (CPR) by asking the client to cough hard every 1 to 3 seconds. 4. Pulseless client with ventricular tachycardia: |
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VENTRICULAR FIBRILLATION DX AND TREATMENT
|
VF is fatal if not successfully terminated
within 3 to 5 minutes. d. Client lacks a pulse, BP, respirations, & heart sounds. 2. Interventions a. Defibrillate the client immediately, up to 3 times consecutively at 200, 300, & 360 joules (J). b. Initiate CPR. c. Administer oxygen as prescribed. d. Administer epinephrine or vasopressin & antidysrhythmic therapy with amiodarone or lidocaine as prescribed; other antidysrhythmics also may be prescribed |
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MI RX TX
|
Medical management includes betaadrenergic
blockers (propranolol-Inderal, Lopressor) * contraindicated if patient also has CHF, hypotension or bronchospasm. treatment: May be referred for immediate PTCA. Same meds as Pt with unstable angina with possible additions of thrombolytics, analgesics, & ACE Inhibitors. Thrombolytic therapy includes the use of Streptase, & Eminase. These are contraindicated if the patient has had recent surgery, or experienced a fall or head wound concurrent with the MI. |
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Mitral valve prolapse DX
|
is one or both valve
leaflets protruding into the left atrium. It has an unknown etiology. ECG shows prolapse of the mitral valve into the left atrium |
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Mitral stenosis -DX
|
obstructs blood flow from
the left atrium to the left ventricle. Can be caused by rheumatic fever. Diagnosiscardiac catheterization shows diastolic pressure gradient across the valve & elevated left atrial & pulmonary artery wedge pressures. Echocardiography shows thickened mitral valve leaflets. ECG shows left atrial hypertrophy & x-ray shows left atrial & ventricular enlargement. |
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Mitral Regurgitation
|
blood flowing back
from the left ventricle into the left atrium during systole. Often the margins of the mitral valve cannot close during systole. Left atrium stretches & eventually hypertrophies & dilates, diminishing volume of bloods flowing into the atrium form the lungs – lungs become congested adding extra strain on the right ventricle. Acute episode usually presents as severe CHF |
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Aortic Stenosis -
|
narrowing of the orifice
between the left vent. & aorta |
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Aortic Regurgitation – Aortic Insufficiency
|
results in blood flowing back into the left
ventricle during diastole (rest), creating fluid overload in the left atrium & pulmonary system. Causes include endocarditis, hypertension, rheumatic fever, & syphilis. Diagnosisechocardiography shows left ventricular enlargement, x-ray shows left ventricular enlargement & pulmonary vein congestion |
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CARDIOMYOPATHY CAUSES
|
increased muscle mass
to compensate for flabby L. ventricle, altering cardiac function & resulting in decreased cardiac output. Causes include alcoholism, infection, metabolic & immunologic disorders, pregnancy & postpartum disorders, hypertension, myeloidosis & cancer or other infiltrative disease. |
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CARDIOMYOPATHY S/S
|
Signs & symptoms -murmur
(S3, S4), dyspnea, cough, crackles, jugular vein distention, dependent pitting edema, fatigue. |
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CARDIOMYOPATHY DX
|
Diagnosis- echo indicates left ventricular
hypertrophy & nonspecific changes. TX- betaadrenergic blockers, calcium channel blockers, diuretics, inotropic drugs (dopamine), anticoagulants. Interventions include monitoring for arrhythmias & ischemia, monitor for hypokalemia (s/e of diuretics), monitor respiratory & cardiovascular status for signs of heart failure, & administer O2 & meds to improve oxygenation & cardiac output. |
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Shock can be classified by etiology & may be
described as 4 TYPES |
(1) hypovolemic shock, (2)
cardiogenic shock, or (3) circulatory or distributive shock. Some authors identify a fourth category, obstructive shock, that results from disorders that cause mechanical obstruction to blood flow through the central circulatory system despite normal myocardial function & intravascular volume |
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SHOCK RESULTS TO THE CELLS
|
produce energy through anaerobic
metabolism. This results in low energy yields from nutrients & an acidotic intracellular environment. Because of these changes, normal cell function ceases. The cell swells & the cell membrane becomes more permeable, allowing electrolytes & fluids to seep out of & into the cell. The sodiumpotassium pump becomes impaired; cell structures, primarily the mitochondria, are damaged; & death of the cell results. |
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In the
compensatory stage of shock, |
the
compensatory stage of shock, the patient’s blood pressure remains within normal limits. Vasoconstriction, increased heart rate, & increased contractility of the heart contribute to maintaining adequate cardiac output. This results from stimulation of the sympathetic nervous system & subsequent release of catecholamines (epinephrine & norepinephrine). The patient displays the often-described “fight or flight” response. The body shunts blood from organs such as the skin, kidneys, & gastrointestinal tract to the brain & heart to ensure adequate blood supply to these vital organs. As a result, the patient’s skin is cold & clammy, bowel sounds are hypoactive, & urine output decreases in response to the release of aldosterone & ADH Normalbp >100 bpm >20 breaths/min Cold, clammy Decreased URINARY OUTPUT Confusion Respiratory alkalosis |
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In the progressive
stage of shock, |
In the progressive
stage of shock, the mechanisms that regulate blood pressure can no longer compensate & the MAP falls below normal limits, with an average systolic blood pressure of less than 90 mm Hg Systolic <80–90 mm Hg >150 bpm Rapid, shallow respirations; crackles Mottled, petechiae 0.5 mL/kg/hr Lethargy Metabolic acidosis |
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The irreversible (or
refractory) stage of shock r |
represents the
point along the shock continuum at which organ damage is so severe that the patient does not respond to treatment & cannot survive. Despite treatment, blood pressure remains low. Complete renal & liver failure, compounded by the release of necrotic tissue toxins, creates an overwhelming metabolic acidosis. Anaerobic metabolism contributes to a worsening lactic acidosis. Reserves of ATP are almost totally depleted, & mechanisms for storing new supplies of energy have been destroyed. Multiple organ dysfunction progressing to complete organ failure has occurred, & death is imminent. Multiple organ dysfunction can occur as a progression along the shock continuum or as a syndrome unto itself Requires mechanical or pharmacologic support Erratic or asystole Requires intubation Jaundice Anuric, requires dialysis Unconscious Profound acidosis |
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THE MOST LIFE THREATENING SHOCK
|
Hypovolemic shock, the most common type of
shock, is characterized by a decreased intravascular volume. Body fluid is contained in the intracellular & extracellular compartments. Intracellular fluid accounts for about two thirds of the total body water. Hypovolemic shock occurs when there is a reduction in intravascular volume of 15% to 25%. This would represent a loss of 750 to 1,300 mL of blood in a 70-kg (154- lb) person. |
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HYPOVOLEMIC SHOCK- S.S
|
acute pancreatitis,
dehydration from excessive perspiration, intestinal obstruction, severe diarrhea, protracted vomiting, inadequate fluid intake & diuresis. Signs & symptoms - cold, pale, clammy skin, decreased sensorium, hypotension with narrowing pulse pressure, reduce urine output, tachycardia, rapid, shallow respirations. |
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HYPOVOLEMIC SHOCK DX
|
Blood tests (elevated K, serum
lactate, BUN urine specific gravity (greater than 1.020), ABG reveals metabolic acidosis (decreased pH) decreased PO2 & increased PCO2. treatment- blood & fluid replacement control of bleeding. |
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CARDIOGENIC SHOCK- CAUSES AND S/S
|
LIFE THREATENING!
Heart fails to adequately pump, reducing cardiac output & compromising tissue perfusion. Decreased stroke volume increases back volume in the left ventricle. Blood from the left ventricle backs up into the lungs creating pulmonary edema. Compensation for decreased CO is increased heart rate & contractility, increasing the need for O2. An imbalance between supply of O2 & demand for O2 increase myocardial ischemia further impairing the heart’s pumping action. Causes include MI, heart failure, Myocarditis, cardiomyopathy & advanced heart block. Signs & symptoms - cold, clammy skin, hypotension with a narrow pulse pressure, Oliguria (less than 30 ml/hr), S3 & S4 heart sounds, tachycardia, tachypnea, & weak, thready pulse. |
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CARDIOGENIC SHOCK- DX AND MEDS
|
EKG shows enlarged
Q wave, elevated ST segment (MI). Drug treatment includes adrenergic (epinephrine_, digoxin, dopamine, diuretics, vasodilators (Nitro-press) & vasopressors (norepinephrine). Interventions include NPO status to reduce risk of aspiration, administer meds, fluids, oxygen to maximize cardiac, pulmonary & renal Fx. Use of IABP (intra-aortic balloon pump) - an inflatable balloon is inserted through the femoral artery into the descending aorta. Coronary artery perfusion increases when the aortic valve closes & the balloon inflates during diastole (rest). It deflates during systole (squeeze) to reduce cardiac workload by reducing resistance to ejection. |
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CIRCULATORY SHOCK THREE TYPES, CAUSES
|
Circulatory or
distributive shock occurs when blood volume is abnormally displaced in the vasculature—for example, when blood volume pools in peripheral blood vessels. The displacement of blood volume causes a relative hypovolemia because not enough blood returns to the heart, which leads to subsequent inadequate tissue perfusion. The ability of the blood vessels to constrict helps return the blood to the heart. Thus, the vascular tone is determined both by central regulatory mechanisms, as in blood pressure regulation, & by local regulatory mechanisms, as in tissue demands for oxygen & nutrients. Therefore, circulatory shock can be caused either by a loss of sympathetic tone or by release of biochemical mediators from cells. The varied mechanisms leading to the initial vasodilation in circulatory shock further subdivide this classification of shock into three types: (1) septic shock, (2) neurogenic shock, & (3) anaphylactic shock. |
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SEPTIC SHOCK – CAUSED BY
|
Septic shock is the most
common type of circulatory shock & is caused by widespread infection. Despite the increased sophistication of antibiotic therapy, the incidence of septic shock has continued to rise during the past 60 years. IToxic shock syndrome is a specific form of septic shock |
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Septicemia
|
The presence of infective agents
or their toxins in the bloodstream. Septicemia is a serious infection & must be treated promptly; otherwise, the infection leads to circulatory collapse, profound shock, & death |
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NEUROGENIC SHOCK CAUSES S/S THAT DIFFER OF OTHER SHOCK
|
In neurogenic shock,
vasodilation occurs as a result of a loss of sympathetic tone. This can be caused by spinal cord injury, spinal anesthesia, or nervous system damage. It can also result from the depressant action of meds or lack of glucose (eg, insulin reaction or shock). Neurogenic shock may have a prolonged course (spinal cord injury) or a short one (syncope or fainting). It is characterized by dry, warm skin rather than the cool, moist skin seen in hypovolemic shock. Another characteristic is bradycardia, rather than the tachycardia that characterizes other forms of shock |
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ANAPHYLACTIC SHOCK
|
- ANAPHYLACTIC shock
is caused by a severe allergic reaction when a patient who has already produced antibodies to a foreign substance (antigen) develops a systemic antigen–antibody reaction. This process requires that the patient has previously been exposed to the substance. An antigen– antibody reaction provokes mast cells to release potent vasoactive substances, such as histamine or bradykinin that cause widespread vasodilation & capillary permeability. |
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Crystalloids
- 0.9% sodium chloride (normal saline solution) - Lactated Ringer’s - Hypertonic saline (3%, 5%, 7.5%) |
Widely available, inexpensive
- Lactate ion helps buffer metabolic acidosis - Small volume needed to restore intravascular volume Requires large volume of infusion; can cause pulmonary edema - Requires large volume of infusion; can cause pulmonary edema - Danger of hypernatremia |
|
Albumin (5%, 25%)
- Dextran (40, 70) - Hetastarch |
Rapidly expands plasma volume
- Synthetic plasma expander Synthetic; less expensive than albumin; effect lasts up to 36 h - Expensive; requires human donors; limited supply; can cause heart failure - Interferes with platelet aggregation; not Recommended for hemorrhagic shock - Prolongs bleeding & clotting times |
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ANEMIAS:
IRON DEFICIENCY ANEMIA- s/s and TX |
Signs & symptoms -
tongue that is red, smooth, & sore, pallor, & sensitivity to cold, weakness & fatigue. Diagnosis- decreased Hgb, HCT, & iron. treatment- diet high in iron, fiber, & protein with increased fluids. Avoid teas & coffee which reduce absorption of iron. Increase the intake of vitamin C |
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IRON DEFICIENCY ANEMIA interventions
|
include iron injection deep into the muscle
using Z-track technique to avoid subQ irritation & discoloration from leaking drug. IM B12. make sure infants have iron fortified cereals. |
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APLASTIC ANEMIA s/s dx tx
|
rare decrease of blood
cells from bone marrow failure, S&S are bleeding, bruises, fatigue, DX with bone marrow BX & may need a transplant |
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MEGALOBLASTIC ANEMIAS
|
an anemia (of
macrocytic classification) which results from a deficiency of vitamin B12 & folic acid; can be result of a lack of intrinsic factor; characterized by many large immature & dysfunctional red blood cells (megaloblasts) in the bone marrow; associated with pernicious anemia. |
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PERNICIOUS ANEMIA-
|
ANEMIA-chronic, progressive,
macrocytic anemia caused by a deficiency of intrinsic factor which prevents the absorption of dietary vitamin B12. Without intrinsic factor RBCs are defective as they mature. |
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PERNICIOUS ANEMIA-TX, DX, S/S
|
Signs & symptoms - tingling &
paresthesia of hands & feet, weight loss, anorexia, dyspepsia. Diagnosis- bone marrow aspiration shows increased megaloblasts, few maturing erythrocytes & defective leukocyte maturation. Peripheral blood smear reveals oval, macrocytic, hyperchromic erythrocytes. treatment- diet high in iron & protein & restricting highly seasoned or extremely hot foods. Vitamins especially B12 & B6, Vitamin C & folic acid. |
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MYELODYSPLASTIC SYNDROMES (MDS) formerly known as "preleukemia")
|
are a
diverse collection of hematological conditions united by ineffective production of blood cells & varying risks of transformation to acute myelogenous leukemia. Anemia requiring chronic blood transfusion is frequently present. Although not truly malignant, MDS is nevertheless classified within the hematological neoplasms. |
|
HEMOLYTIC ANEMIAS
|
anemia due to
hemolysis, the abnormal breakdown of red blood cells either in the blood vessels (intravascular hemolysis) or elsewhere in the body (extra vascular). It has numerous possible causes, ranging from relatively harmless to life-threatening. The general classification of hemolytic anemia is either acquired or inherited. Treatment depends on the cause & nature of the breakdown |
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.SICKLE CELL ANEMIA-
|
The RBCs are rigid & rough,
forming an elongated sickle shape & impairing circulation by “clumping” together. This happens during periods of hypoxia which can be provoked by strenuous exercise, high altitude, unpressurized aircraft, cold & vasoconstrictive drugs. |
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SICKLE CELL ANEMIA- S/S
|
aching bones, jaundice, pallor,
tachycardia, family history, frequent infections, joint swelling & leg ulcers, especially on ankles. Sickle cell crisis is very painful. |
|
SICKLE CELL ANEMIA-DX
|
Diagnosis- decreased RBC,
elevated WBC & platelet counts, decreased ESR. HB electrophoresis shows HbS. |
|
SICKLE CELL ANEMIA-TX
|
iron & folic acid supplements
prevent dehydration & analgesics for pain. Interventions during crisis include warm compresses to painful areas, (cold aggravates the condition) maintain bed rest to reduce workload on the heart & to reduce pain, encourages fluid intake to prevent dehydration, which can precipitate crisis |
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THALASSEMIA / THALASSEMIA MAJOR (Cooley’s
Anemia)- |
an group of inherited disorders
associated with defective hemoglobinchain syntheses; occurring worldwide, highest prevalence in people of Mediterranean, African & Southeast Asian ancestry. |