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CV-McCance
Ch 30
| Question | Answer |
|---|---|
| intermittent claudication | obstructive blood flow in iliofemoral vessels causing pain when ambulate |
| Buerger Disease | inflammatory peripheral artery disease, male smokers. pain and tenderness, rubor cyanosis,thin shiny skin-no hair. Gangrene possible |
| arteriosclerosis | hardening & thickening of arteries |
| atherosclerosis | arteriosclerosis with plaque formation |
| cytokines | tumor necrosis factor-alpha, interferon-gamma, interleukin-1; proinflammatory. released by foam cells. |
| foam cell | macrophage filled with oxidized LDL |
| fatty streak | accumulation of foam cells, begin in youth |
| fibrous plaque | smooth muscle proliferation over fatty streak, from cytokines-may calcify and protrude into vessel-cause obstruction=angina or intermittent claudication |
| complicated plaque | ruptured plaque, cause thrombus formation=ischemia(unstable angina) or infarction |
| ischemia | diminished blood supply to coronary ateries, myocardium is alive but not functioning normally, lead to infarction if persist. |
| infarction | occlusion of coronary artery, irreversible myocardium damage |
| nonmodifiable, conventional risk factors for CAD | male, women after menopause, family history, advanced age. |
| modifiable conventional risk factors | hyperlipidemia, htn, smoking, diabetes-insulin resistance, obesity, sedentary lifestyle, atherogenic diet |
| chylomicrons | dietary fat particles in small intestine; triglycerides |
| desirable lipid profile | cholesterol <200, LDL < 100, HDL >60, triglycerides <150. |
| secondary causes of dyslipidemia | diabetes, hypothyroidism, pancreatitis, renal nephrosis; betablockers, glucocorticoids, interferons, antiretrovirals |
| HDL protecting role | (HDL-2)reverse cholesterol transporter to liver so that excess cholesterol can be eliminated as bile or converted to cholesterol containing steroids. repairs endothelium and decreases thrombosis. |
| what can increase HDL | exercise, wt loss, fish oil, moderate alcohol, niacins, fibrates, statins. |
| hyperhomocysteinemia | lack of enzyme to break down homocysteine or nutritional deficit of folate, B12, B6 |
| causes of plaque disruption | shear force, inflammation with release of inflammatory mediators, macrophage-derived degradative enzyme release, apoptosis of cells at edge of lesion. |
| vasoconstrictors | thromboxane A2, endothelin |
| Angiotensin II | released during ischemia; increase myocardial workload. cause release of catecholamine and spasm |
| myocardial stunning | temporary loss of contractile function |
| hibernating myocardium | persistent ischemia, adaptation to prolong myocyte survival |
| myocardial remodeling | hypertrophy and loss of contractile function mediated by angiontensin II, aldosterone, catecholamines, adenosine, cytokines--can be limited by rapid reperfusion, ACE inhibitors, beta-blockers after MI. |
| acute pericarditis | coxsackievirus, influenza, hepatitis, measles, mumps, varicella, HIV. fever, myalgia, malaise and sudden onset of chest pain worsen with respirations & lying down. pericardia friction rub-ST segment elevation that is concave without Q wave |
| serosanguineous pericardia effusion | TB, neoplasm, uremia, radiation |
| frank blood pericardia | aneurysm, trauma, coag defects. |
| chyle pericardia effusion | cholesterol pericarditis |
| Cardiac tamponade | r-sided heart failure sx. JVD, edema, hepatomegaly. dyspnea, pulsus paradoxus |
| tricuspid valve | between right atrium & right ventricle |
| pulmonic valve | semilunar, between right ventricle & pulmonary circulation |
| mitral valve | between left atrium & left ventricle. mitral stenosis (from rheumatic fever) or mitral regurgitation (prolapse from rheumatic, myxomatous degernation) can cause PAH, co pulmonale. |
| aortic valve | left ventricle & aorta. aortic stenosis (common over 65-age related degeneration; congenital; rheumatic)cause left sided heart failure. aortic regurgitation(connective tissue dx, appetite meds, atheroscleosis, trauma) left sided heart failure |
| diastole | myocardium relax, chamber fill with blood; coronary perfusion occurs at this time, < in tachycardia. |
| systole | myocardium contracts |
| p wave | atrial depolarization |
| QRS | ventricular depolarization |
| Preload | pressure generated in ventricles at end of diastole, depends on volume in ventricles. Contractility depends on preload. |
| Afterload | resistance to ejection of blood from ventricles, depends on pressure in aorta |
| Frank-Starling law | myocardium stretch determine force of myocardial contraction. |
| Laplace Law | amount of contractile force generated depends on radius of the chamber and thickness of the wall. smaller the radius & thicker the wall-greater the force of cnt. |
| 3 layers of vessel walls | 1)tunica intima-inner layer 2) tunica media-middle 3) tunica externa-outer layer |
| Virchow triad | venous stasis hypercoagulability injury to epithelial cells |
| Primary hypertension | genetic interaction with environment, neurohormonal response > BP |
| Secondary htn | caused by another disease; renal, endocrine, vascular, neurologic, PIH, stress, drugs |
| Systolic heart failure | inability of heart to generate adequate CO to perfuse tissue. > LVEDV. assoc w/hypothyroidism |
| Diastolic heart failure | pulmonary congestion with normal SV/CO. normal LVEDV with > LVEDP |
| Right sided heart failure | inability of right ventricle to provide adequate blood flow to pulmonary circulation. Often from LV systolic HF, or pulmonary disease (COPD) |
| High Output heart failure | inaabilty of heart to adequately supply body with oxygen despite adequate volume/cnt. anemia, hyperthyroidism, sepsis |