Bio 669 Quiz 4 Graded A+

Bio 669 Quiz 4 Graded A+ 3 types of myocardial ischemia stable angina-specific amount of exercise ppl can do before noticing chest pain, chronic, know how far they can go before symptoms start. tx w/NTG to vasodilate -prizmetal angina-occurs unpredictably & at rest, while sleeping. transient ischemia that doesn't follow any pattern -silent iscemia-have ischemia w/out the detectable symptoms like angina acute & chronic orthostatic hypotension acute=elderly at increased risk b/d decreased thrist mechanisms. causes=drugs, prolonged immoblilty, starvation, exhaustion, dehydration/volume depletion, venous pooling chronic-causes=DM, endocrine d/o, metabolic d/o, CNS or PNS d/o, cerebral infarcts, parkinsons, autonomic neuropathy=most common cause acute coronary syndromes include unstable & stable angina, transient ischemia, sustained ischemia, MI, myocardial inflammation & necrosis acute pericarditis acute inflammation of pericardium -occurs w/anything that increases friction like an increase in proteins, transudate, or anything that causes inflammation of pericardial fluid -leads to friction rubs anaphylactic shock exposure to antigen/allergen results in antibody formation causing histamine/cytokine/prostaglandins released from mast cells causing vasodilation, increased permeability, GI cramps, constriction of smooth muscle leading to decreased SVR, edema, hypovolemia, decreased cardiac output & tissue perfusion aneurysm localized dilation or outpouching of a vessel wall or cardiac chamber -can be thoracic or abdominal or can occur in cerebral circle of willis -most common=abdominal causes=atherosclerosis or HTN -can lead to aortic dissection or rupture aortic regurgitation aortic valve leaflets don't close during diastole so blood backflows from aorta to ventricles causing increased LV, increased preload, & increased stroke volume to maintain cardiac output -will see a widened pulse pressure from increased SV & diastolic backflow aortic stenosis narrowing of semilunar valves which increases the workload of LV to push thru narrowing into systemic circulation resulting in hypertrophy atherosclerosis thickening & hardening of vessel wall caused by accumulation of lipid-laden macrophages in arterial wall which leads to plaque development risk factors=smoking, DM, HTN, hyperlipidemia atherosclerosis progression inflammation of endothelium-cellular proliferation-macrophage migration & adherence to DAMPs- LDL oxidation(adding oxygen)- LDLs are engulfed & called foam cells-accumulated foam cells=fatty streak-collagen produced & causes fibrous plaque which obstructs blood flow -leads to inadequate tissue perfusion, ischemia, necrosis