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115 Cards in this Set

  • Front
  • Back
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
Originates in surface of tissue or body organs. 80-90% of CA
Originates in bone, cartilage, muscle, connective, fatty, or fibrous tissue
Originates in plasma cells of bone marrow
Originates in lymph system (e.g. Hodgkin's dz)
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
Carcinoma in situ
CA has not spread to other cell layers
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
(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
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
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
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
(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%
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
Absolute neutrophil count. Pt. at risk for sepsis if less than 500.
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)
Thrombis w/ inflammation, venous thrombosis
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.
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
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.
Drug-coated stents.
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
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
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
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