clinical med heart

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clinical med heart
2012-05-20 19:20:19
clinical med heart

clinical med heart
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  1. which arteries are elastic?
    aorta and beginnings of branches
  2. when are arteries muscular?
    the thick and smoooth muscles of the tunica media
  3. tell me about small arteries
    they do autonomic blood flow regulation
  4. how many layers of muscles in arterioles?
    ferwer than 5
  5. atheroschlerosis (#1 killer in US) is a response to injury featuring...?
    accumulation of cholesterol-rich fat (plaques) in the intima of the large and medium sized arteries
  6. when plaques occlude arteries (in atherosclerosis) this can cause what 4 things?
    • ischemic heart disease
    • myocardial infarction
    • strocke
    • gangrene of extremities
  7. 7 risk factors for atherosclerosis
    • high LDL level - result of heredity, diet, exercise
    • smoking - bc smoke oxidizes LDL
    • high blood pressure - causes intima damage
    • lack of exercise - change in lipoprotein receptor count
    • heredity - familial hypercholesterolemia
    • low HDL levels - bc HDL keeps LDL from binding to plaques
  8. examinatin of the ___ is important for monitoring any pt at risk of arteriosclerosis
    ocular fundus
  9. why is vascular smoth muscle an important factor in atherosclerosis
    • has receptors for LDL
    • can get into intima thru holes in internal elastic membrane
  10. hypertesion def in terms of bp
    rel to ateriosclerosis
    • hypertension - systolic > 160 mmHG and/or diasolic > 90 mmHG
    • it's a consequence of arteriosclerosis
  11. hypertension resluts form an imbalance in waht 4 things?
    • cardiac output (pressure, venous return)
    • renal function (renin-angiotensin-aldosterone)
    • peripheral resistance (artieriosclerosis)
    • sodium homeostasis (diet, pheochromocytoma)
  12. pheochromocytoma
    it's a tumor that's related somehow to increased secretion of nor/epinephrine and to the sodeum homeostasis problme that can lead to hypertension
  13. aneurism
    • outpoaching of weak arterial wall
    • most common spot is in aorta below the artery renalis -- this is where it's going thru the abdomen, so rupture here = big trouble
  14. 3 phases of atherosclerosis deve
    • 1 - early lesion of endothelial surface of large arteries (lesion here is a. fatty streaks or b. diffuse intimal fibrosis)
    • 2 - a specific lesion occurs as fibrolipd plaque, and now intimal changes are irreversible (the fibrous cap encloses a zone of fatty, necrotic, and partly calcified debris full of elongated smoth muscle cells, fibroblasts, and macrophages)
    • 3 - formation of complicated plaque - this is what causes signs and symptoms of the disease
  15. fatty streaks (early lesions seen in the first stage of atherosclorosis)
    • lesions that begin in kids in all populations
    • collection s of foamy lipid-laden macrophages and smooth muscle cells just beneath the intimal surface of the arteries
  16. diffuse intimal fibrosis (early lesions seen in first stage of atherosclerosis)
    develops in the first few decades of life, may be related to the dev of atheroma
  17. in the second phase of arteriosclerosis you the intimal surface shows a layer of fibrosis, a "fibrous cap" which encloses what?
    a zone of: fatty, necrotic, and partly calcified debris full of elongated smooth muscle cells, fibroblasts, and macrophages
  18. the perils of ulcerated plaque
    • can lead to embolization (atheroembolism)
    • that embolization can lead a naked non-endothelialized surface, which is a great site for thrombosis
  19. as plaque expands, the internal layer of intima may become broken up, and the lesion will induce pressure changes on...?
    the tunica media
  20. damage to tunica media (resulting from plaque expansion breaking up the internal layer, putting pressure on the tunica media) can lead to ...
    formation of atherosclerotic aneurism - fusiform or sacular
  21. 3 real basic causes of aneurisms
    • congenital
    • infection
    • trauma
  22. shunt
    movement of blood from one side of heart to the other
  23. dissecint aneurism
    a lesion that occurs when blood is forced thru an intimal defect into wall of an artery under arterial pressure ---> estension of column of blood traveling along the arterial tunica media, seperating the wall into two planes

    associated w hypertensions bt may be result of arterial wall degen seen in cystic medial necrosis or Marfan's
  24. classifications of dissecint aneurisms
    • type A - involves ascending part of aorta
    • B - involves descending part
  25. pseudoaneurysm occurs when?
    injury to arterial wall allows escape of blood to form a hematoma which is confined by arterial adventitia - usually result of a penetrating trauma
  26. thrombophlebitis and phlebothrombosis describe what?
    • thrombus formation in deep veins (usually in legs)
    • often associated w prolonged bed rest
    • can be deadly if embolizes to the lungs
  27. 3 types of vasculitis (inflam and necrosis of blood vessels)
    • raynaud's
    • polyarteritis nodosa
    • thromboangiitis obliterans - Buerger disease
  28. polyarteritis nodosa
    • a type of vasculits
    • small and med sized arteries become swollen and damaged
  29. Buerger disease
    • aka thromboangiitis obliterans
    • a type of vasculitis
    • inflam and thrombosis of small and med arteries and veins in hands and feet
  30. hemangioma
    • benign tumor of blood vessel, usually in skin, but can be in internal organs
    • composed of masses of capillary like channels filled w blood
  31. hemangiosarcoma
    rare, highly malignant tumor that begins a sa small painless red nodule on skin or liver
  32. cor pumonale
    • syndrome of R ventricular enlargement and associated heart failure
    • it's secondary to pulm disease
    • acute: seen w acute pulm embolism
    • chronic - seen in COPD
  33. ischemic heart disease aka coronary heart disease describe a family of clinical syndromes:
    • angina pectoris
    • myocardial infarction
    • chronic ischemic heart disease
    • sudden death

    in these the underlying lesion is usually due to atherosclerotic stenosis or occlusion of coronary arteries
  34. angina pectoris basic def
    caused by
    chest pain, buring, tight, radiating to jaw or left arm

    caused by imbalance between myocardial O2 supply and demand
  35. stable vs variant (Prinzmetal's ischemai) vs unstable angina
    stable - most common - myocardial O2 demand greatly exceeds supply -- treat w beta blockers and organic nitrates or calcium channel blockers

    variant - O2 supply to myocardium decrease bc of coronary artery vasospasm - can occur when pt's at rest -- treat w calcium chanel blockers and long lasting nitrates for severe problems

    unstable - serious, life-threatening forms of myocardial ischemia associated w thromobsis in coronary arteries --- it's vasoconstriction + increased myocardial O2 demand (a combo of stable and variant) -- begin w minimal activity or at rest
  36. myocardial infarction def
    relatied to..?
    • necrosis of certain portion of heart muscles
    • rel to thromobosis of a coronary artery feeding the zone of ischemia, but on rare occasions cab be result of muscle ischemia produced by prolonged arterial spasm (arteritis)
  37. transmural infarcts (a category of myocardial infarction)
    • necrotic area goes thru full thickness of myocardium
    • almost always associated w history of thrombosis
    • usually develop from endocardium outwards (bc the endocardium is at the end of the arteries, so they're the first to be deprived of blood and O2 when things go wrong)
    • most common sites for thromobosis: L anterior descending artery, right coronary artery, left circumflex artery 3:2:1
    • aka q-wave infarction bc Q-waves are deeper and wider
  38. subendocardial infarct
    • ischemic heart disease where the necrosis is only partial thickness
    • not associated w regional thrombosis

    aka non-Q-wave infarction
  39. timeline of ischemic heart disease
    • first 6 hours: no visible changes
    • later: muscle fibers become omre intensely eosinophile and nuclei undergo pyknosis
    • 6-12 hours - coagulative necrosis begins
    • 12-24 h - infarct becomes infiltrated w neutrophils and muscles begin to lose their nuclei and cross striations
    • next several days - dead myocardial cells are replaced by macrophages and repartative proliferative fibroblasts (critical point for recovery bc wall has so little mechanical integrity and is prone to rupture)
    • next few months - resorption of necrotic muscle, replacement by fibrous tissue, myocardial scar is laid down
  40. complications of myocardial infarctions
    • cardiac arrhythmia (usually within first week - ex - lethal ventricular fibrillation and ventricular tachicardia)
    • left ventricular dysfunction (leads to congestive heart failure)
    • myocardial rupure (10-14 days post infarct involving L vent wall leading to cardiac tamponade)
    • cardiogenic shock
    • acute mitral insufficience iinvolving papillary muscles
    • ventricular aneurism (rel to mature myocardial scars)