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CV-McCance

Ch 30

QuestionAnswer
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
Created by: Sniffen group