clinical med heart

aorta and beginnings of branches

the thick and smoooth muscles of the tunica media

they do autonomic blood flow regulation

ferwer than 5

accumulation of cholesterol-rich fat (plaques) in the intima of the large and medium sized arteries

• ischemic heart disease
• myocardial infarction
• strocke
• gangrene of extremities

• 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

ocular fundus

• has receptors for LDL
• can get into intima thru holes in internal elastic membrane

• hypertension - systolic > 160 mmHG and/or diasolic > 90 mmHG
• it's a consequence of arteriosclerosis

• cardiac output (pressure, venous return)
• renal function (renin-angiotensin-aldosterone)
• peripheral resistance (artieriosclerosis)
• sodium homeostasis (diet, 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

• 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

• 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

• 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

develops in the first few decades of life, may be related to the dev of atheroma

a zone of: fatty, necrotic, and partly calcified debris full of elongated smooth muscle cells, fibroblasts, and macrophages

• can lead to embolization (atheroembolism)
• that embolization can lead a naked non-endothelialized surface, which is a great site for thrombosis

the tunica media

formation of atherosclerotic aneurism - fusiform or sacular

• congenital
• infection
• trauma

movement of blood from one side of heart to the other

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

• type A - involves ascending part of aorta
• B - involves descending part

injury to arterial wall allows escape of blood to form a hematoma which is confined by arterial adventitia - usually result of a penetrating trauma

• thrombus formation in deep veins (usually in legs)
• often associated w prolonged bed rest
• can be deadly if embolizes to the lungs

• raynaud's
• polyarteritis nodosa
• thromboangiitis obliterans - Buerger disease

• a type of vasculits
• small and med sized arteries become swollen and damaged

• aka thromboangiitis obliterans
• a type of vasculitis
• inflam and thrombosis of small and med arteries and veins in hands and feet

• benign tumor of blood vessel, usually in skin, but can be in internal organs
• composed of masses of capillary like channels filled w blood

rare, highly malignant tumor that begins a sa small painless red nodule on skin or liver

• 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

• 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

chest pain, buring, tight, radiating to jaw or left arm

caused by imbalance between myocardial O2 supply and demand

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

• 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)

• 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

• ischemic heart disease where the necrosis is only partial thickness
• not associated w regional thrombosis

aka non-Q-wave infarction

• 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

• 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)