Adult Health Test 3

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Internal factors leading to CA: inherited genetic mutations, hormones, immune conditions, and mutations occurring from metabolism.
External factors leading to CA: Carcinogenic substances, etc...10 or more years pass before any signs of CA noted
Lifetime risk: The probablility that over the lifetime, a person will become diagnosed with CA
Viruses and bacteria linked to CA: HIV, HPV, HBV, and helicobacter
Carcinoma: Originates in surface of tissue or body organs. 80-90% of CA
Sarcoma: Originates in bone, cartilage, muscle, connective, fatty, or fibrous tissue
Myeloma: Originates in plasma cells of bone marrow
Lymphoma: Originates in lymph system (e.g. Hodgkin's dz)
Leukemia: Originates in blood forming tissue
Benign tumor char.: Encapsulated, differentiated, no metastasis, rare recurrence, slightly vascularized, resembles parent cell
Malignant tumor char.: Rarely encapsulated, poorly differentiated, freq. metastasis and recurrence, moder. to marked vascularity, abnormal appear.
Cancer staging: Number (bigger=worse), localization, metastasis, or recurrent
TNM Classification system: T: size of tumor
N: regional lymph node involvement
M:metastasis
Carcinoma in situ: CA has not spread to other cell layers
Invasive: CA has spread beyond original layer of cells
Freq. of CBE: Q3yrs. ages 20-39
qyr. 40+
Ductal carcinoma: (aka intraductal carcinoma)CA is in lining of milk ducts
Lobular carcinoma: CA in lobules of breast, at increased risk of developing invasive carcinoma
Adeno carcinoma: Develops in glandular tissue
DCIS: (Ductal carcinoma in situ) non-invasive neoplasm that can but not always progress to invasive ca. Ductal origin, picked up on mammogram
Fat and breast ca: Fat produces a stronger form of estrogen than ovaries, can lead to b. CA
ER/PR value: estrogen receptor/progesterone receptor. A low proliferative activity a good prognostic indicator
HER-2-NEU: overexpression of this gene occurs in 20% of b.CA, poor prognostic indicator
neo-adjuvant chemo: tx for very large tumors. Chemo to shrink tumor, surgical removal, then chemo again
Targeted therapy: Gene therapy for HER-2-NEU
Anti-estrogen therapy: (ER/PR positive) Tamoxifen (pre-menopausal) Arimidex and Femara (post-menopausal). Stop estrogen prod. in fat cells (aromatase inhibitors)
Prostate cancer: Most common non-skin CA in males, 2nd leading CA death in males, AA highest incidence rate worldwide
Risk factors for prostate CA: 75% dx in men aged 65+, ethinicity, family hx,diet high in sat. fats
Symptoms of prostate CA: Early dz: asymptomatic
Late stages: diff. urination, nocturia, hematurea
Metastasis: pain in lower back, pelvis and upper thighs
PSA: protein only secreted by prostate. Normal level 0-4 ng/ml. Can be elevated in benign and malignant tumors. Levels incr. w/ age and ethnicity
DRE: Digital rectal exam. Post. surface of prostate palpated. Yearly after age 50 unless AA or first degree fam. hx, then start at 45. Same w/ PSA. PSA must be drawn BEFORE DRE
TRUS: (trans-rectal ultrasound) determines density of prostate
Gleason's score: Two largest areas in biopsy sample graded from 1-5 (5 is worse) Added together to get score.
Tx for prostate ca: watchful waiting, surgical removal of prostate if confined to capsule, radiation if confined to prostate and surrounding area (good for poor surg. candid.), androgen blockade (dec.circulating testost.)
Lung cancer: #1 cause of ca deaths in men and women
Clinical features of lung CA: Change in cough, chest pain, recurrent bronchitis/pneumonia, dyspnea, wheezing, hepoptysis, weight loss, dysphagia
Small cell lung ca: 25%, dev. around mainstem bronchus, smokers, shorter doubling time, advanced when pt. presents
Non-small cell lung CA: Squamous cell:30%, adenocarcinoma(most common in non-smokers), large cell (least common)
Combined modality therapy: Chemo and XRT given conjunctively (XRT=radiation)
s/s of Colon CA in different colon regions: Ascending colon: fatigue, iron defecient anemia, palpitations
Transverse colon: alternating constip.and diarrhea
Descending colon: melena, abd. pain, hematochezia
Screening for Colon CA: Fecal occult test, flexible sigmoidoscopy q5y, colonoscopy q10y
Duke's classification: For colon CA, measures prognosis
A: 80-90% survival rate
B: 60%
C:25-45%
D: 5%
Anal: 48-68%
S/E of XRT: Fatigue, skin changes (dry and moist desquamation), stomatitis, esophagitis, low blood counts, n/v, diarrhea,cough
S/E of Chemo: n/v, diarrhea, constipation, stomatitis, neurotoxicity (tingling in fingers), cardiac toxicity, fatigue, low blood counts
ANC: Absolute neutrophil count. Pt. at risk for sepsis if less than 500.
Thrombocytopenia: Decr. plt. count
Triad for venous thrombosis: Venous stasis (bedridden, stroke, paraplegia, travel), hypercoagulability(genetic, protein C, chemo, estrogen tx,CA, sepsis, antithrombin), and injury to vessel wall (surgery, lines, contrast x-ray)
Thrombophlebitis: Thrombis w/ inflammation, venous thrombosis
Phlebothrombosis: Thrombis w/o inflammation
Intrinsic pathway: initiated by damage to vessel, septic shock, MI w/ partial occlusion, stress, anxiety, fear
Extrinsic pathway: initiated by external factors that damage b.v.
Obstruction of venous return leads to...: Edema, pain, compartment syndrome, critical limb ischemia
Postthrombotic syndrome: Recurrent DVT w/in one yr, impaired venous circulation, damaged valves, shiny skin, ulcers, venous claudication, swelling, stasis pigmentation,
S/s of venous htn: dilated veins, fluid leaking from vessel, impaired oxygen transport, ischemia, fat necrosis, skin pigmentation and ulceration
Pulmonary embolism: Dislodges from thrombus to R heart to pulm. artery. Gets stuck. Atelectasis b/c affected alveoli collapse. Incr. in pulmonary artery pressure and vascular resistance
Symptoms of PE: dyspnea, tachypnea, tachycardia, retrosternal chest pain, apprehension, hypotension, shock
Venous ultrasonography: DVT (NOT PE), more accurate than other indirect methods of measuring blood flow. Non-invasive, not effective in detective pelvis/iliac vein clot, operator dependant
V/Q scan: Compares ventilation w/ perfusion, for PE, no complications, only available at certain times, takes a long time to get images, no definitive answers just high or low probability
CT scan angiogram: incl. pelvis, thighs, and knees, used for DVT and PE, very accurate, takes seconds, requires monitoring, high flow iv, contrast, lg. dose of ionizing radiation. COMPLICATIONS: anaphylaxis, renal toxicity, infiltration of contrast
Contrast venogram: Direct injection of contrast, into foot or leg veins. If a clot, filling defects in lumen, must have radiologist, can induce phlebitis or cause a DVT, NPO 4h a procedure, if allergic to shellfish, need to give benadryl or Epi a injecting dye, difficult to inject if bad edema. Immediate results
Nursing Implications for contrast venogram: NPO 4h before, if allergic to dye, give benadryl or epi, monitor 4-6 h after procedure for allergic rxn, renal failure. Stop following meds 48 h before procedure: glucophage (causes acidosis), c/i w/ creatinine >2 and renal failure. Can cause n/v, flushing
Prophylaxis hep therapy dosage: 5000 u sq q12h (or q8h if high risk), 1/2 life of 60 minutes
LMWH dosage: Lovonox: sq q12h
Arixtra: sq qd
*don't give if pt. has spinal hematoma-use heparin)
*dosage based on pts. weight
What drug do you use if pt. develops HIT?: Arixtra sq qd
*If can't have hep, use Argatroban, hematologist prescribes, IV, hemoccult x3
Continuous drip hep: 1000 u/hr, ptt in 6h, q6h after that until therapeutic, then once more in 6h, then daily.
Warfarin: Start tx while on hep; takes 3-5 days to become therapeutic, monitor INR (2-3), STOP 4-5 days before a procedure, reverse w/ Vit. K (10 mg SLOWLY in ER), c/i in first trimester
Heparin reversal: Protamine sulfate
Throbolytics: dissolve thrombus, severe problem with bleeding, streptokinase can only be used once (must pre-medicate)
Non-pharmacologic interventions for DVT/PE: Catheter based: mechanical dissolution or suction of clot
Surgical: removal of clot in extremity or pulm. artery
Vena cava interruption: umbrella inserted through jugular or femoral veins
PE s/s: hemoptysis, tachycardia, EKG changes, crackles, dyspnea, pleuritic chest pain, apprehension, diaphoresis, S3 or S4
ABG changes w/ PE: Increased CO2
Decreased O2 and sats
dx of PE: chest x-ray, ABGs, V/Q lung scan, pulmonary angiogram and CT scan.

Spiral CT scan BEST
Tx of PE: anticoagulants, thrombolytics, O2, monitoring, IV positive inotropics, tx anxiety, teach
Prevention of PE: active and passive ROM in bed-ridden pts, ambulate and SCDs post-op, avoid tight clothes and pressure under popliteal area
Acute coronary syndrome: The spectrum of clinical syndromes (unstable angina, MI, sudden death) representing coronary occlusion.
Causes of ACS: Unstable plaque, plaque rupture, unstable angina, microemboli, occlusive thrombus
New markers for CAD: 1. hs-CRP (highly sensitive C-reactive protein), shows systemic endothelial inflamm., predicts future CV events
2. Leukocyte count: inflammation, twice the risk for CAD, CVA, and MI, inexpensive.
3. Homocysteine level: strong independ. factor for CAD, PVD, and cerebral. Elevated in progression of atherosclerosis. c/i in renal dz
4. Traditional lipid panel
5. LDL-C: seven diff. particles, smallest 300% inc. chance of CAD
Tx for hypercholesterolemia: Statins-block prod. of hepatic HMG-CoA
Bile acid binding resins
Nicotinic acid-B3, inhibits lipoprotein synthesis
Fibric Acid derivatives
Intestinal absorp. blockers
Stable angina: Pain precipitated by exertion but relieved w/ rest. Resting EKG may be no change or T-wave inversion
S/s of stable angina in men: Retrosternal pain, heaviness, pressure radiates to back
s/s of stable angina in women: Epigastric or back discomfort
s/s of stable angina in diabetics: No typical pain but may have nausea, fatigue, diaphoretic
Mgt. of stable angina: Treat risk factors (htn, smoking, diet), decr. myocardial demand, drug therapy
Unstable angina: Angina of new onset at rest or w/ minimum exertion, inr. freq., severity, or duration.
Tx of unstable angina: Hospitalization, ASA therapy, LMWH, plavix, GP IIb/IIIa receptor antagonists, antianginal therapy (IV NTG or b-blockers) invasive strategy
Acute MI based on these findings:: Clinical presentation, serial EKG (x3), lab findings (CKMB, troponin->markers in bloodwork that say MI)
Clinical presentation for Male having MI: Severe unrelieved chest pain, may radiate to back, neck, shoulder, arm, atypical chest, stomach, back or abd. pain, n/v, dizziness, SOB, anxiety, palpations, cold sweat
Clinical manifestation of diabetic having MI: Silent MI, n, fatigue, SOB
Clinical manifestation of female having MI: Don't always have typical chest pain, Jaw, shoulder, upper back pain, abd. pain, SOB, fatigue, syncope, weakness, dizziness, n, cold sweats
EKG changes w/ ischemia: Inverted or peaked T-wave, elevated Q wave, elevated ST segment
Lab values for MI: Serum creatine kinase (CK-MB) isoenzyme, elevated 3-6h after, peaks 12-18.
Troponin T cardiac iso-enzyme: elevates w/in 3-6h after onset of pain, lasts 14-21days
Myoglobin: elevated w/in 2h but not MI specific
Troponin I more specific but takes 12h
Stress test and women: Give a false positive because not calibrated for women.
PTCA: Drug-coated stents.
MONA: Morphine
Oxygen
Nitro
Aspirin
Acute mgt. of MI: Relieve ischemic pain, provide O2, Manage hypotensn, pulmonary edema, & arrythmias. If 3 nitro patches and MSO4 don't work, hook up to nitro drip.
Management of ST elevation in MI: get to cath lab, STAT. No cath lab? Give thrombolytic or carbolytic
*Get lab values for cardiac enzymes, CBC, PT/PTT, CMP, lipids, EKG continuous, pulsox
Management of inverted T MI: MONA, have more time than ST elevation
Meds for MI: ASA: Non-enteric coated, 160-325 mg immediately
Hep: IV bolus, then line
B-blockers: IV loading dose, then PO
Nitro: SL 0.4mg
Morphine: if chest pain not relieved by NTG
Lethal rhythms: Pulseless vtach. and vfib
Tx of heart failure: ACE inhibitors, diuretic, digitalis, B-blockers, Aldosterone antagonists, and vasodilators
Nesiritide: synthetic B-type natriuretic peptide, promotes nomal cardiac function and fluid status. Give IV bolus then drip. Can use w/ renal pts, ACS, and diastolic dysfunction
Natrecor: improves hemodynamics and CHF symptoms (Dyspnea), increases urinary o, decreases diuretic need
CV effects of smoking: Incr. coronary vascular resistance, decr. blood flow in the absence of atherosclerosis, may cause sudden arterial constric. & angina, accelerates atherogenisis, thrombogenic state
Tx of uncomplicated htn: <65, diuretics, beta blockers
Tx of htn w/ DM: ACE inhibitors, ARBs
Stages of Htn: Normal 120/80
Pre-htn 139/89
Stage 1 159/99
Stage 2 >160/100
Complex htn pt.: Htn puls one or more additional risk factors: CAD, DM, metabolic syndrome, renal dz, AA, Hispanic
Tx of complex htn: Polytherapy (diuretic, B-blocker, ACE inhib, Ca channel blockers, ARBs) Use two or more
Hypertensive crisis: Diastolic >120-130, upper levels of Stage 3 htn, Optic disk edema, end-organ complications, HA, blurred vision, focal neurologic symptoms
Cardene: Ca channel blocker, continuous IV, tx htn emergencies
Sodium Nitroprusside: Immediate onset, allows for minute to minute titration of BP, goal DBP 110-120. Monitor for thiocyanate poisoning...metabolic acidosis, vomiting. Tx. w. Vit. B derivative to bind w/ cyanide
Severe asthma: Rapid onset attack, more from bronchospasm than inflammation, quickly reversed w/ bronchodilators, exposure to allergens, inhale a B-2 agonist, give anticholinergic (Atropine, atrovent), control inflammation, inhaled corticosteroids (prevent mast cell from emptying)
Clinical manifestations of emphysema: Enlarged resp. airspaces (blebs), destruction of alveolar septa, A-1 antitrypsin breaks down lungs, progressive dyspnea on exertion, dyspnea at rest, enlarged R-ventricle (cor pulmonale), cyanosis, clubbing, pitting peripheral edema, look dusty
Mgt. of COPD: Bronchodilation w/ Anticholinergic (Atrovent) and B-blockers (albuterol), inhaled steroids, combivent inhaler (atrovent and albuterol) more effective
Clinical manif. of pneumonia: Fever, chills, sweats, pleuritic pain, cough, sputum production, hemoptysis, ha, fatigue

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