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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 |