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OPT Cardiac

vascular abnormalities cause disease by: 1. narrowing or obstructing the lumen 2. weakening of the walls
hypertension sustained systolic pressure of 140 or diastolic of 90
primary/essential hypertension idiopathic hypertension, 95% of cases
malignant hypertension rapidly rising BP, >200/120; leads to death in 1-2 years
hyaline arteriolosclerosis plasma components leak across endothelium and trigger excess CT production; walls thicken and lumen narrows
hyperplastic arteriolosclerosis vessels demonstrate 'onion-skin' laminations of replacement basement membrane material that encircles the vessel and narrows the lumen
arteriosclerosis "hardening of the arteries" but really thickening and inelasticity of arteries from pathologic process
atherosclerosis the most important pattern of arterial disease; thickening of arterial walls due to plaques involving large vessels
Mönckeberg medial calcific sclerosis calcific deposits in muscular arteries but do not encroach on the lumen so are benign
arteriolosclerosis thickening of vessel walls with resultant narrowing of the lumen
atheroma (atheromatous or atherosclerotic plaque) raised mass protruding to vessel lumen with soft core and dense cap; fundamental lesion of atherosclerosis and cause of lumen narrowing
rate of atherosclerosis has improved because: 1. altered lifestyle i.e. no smoking and better diets 2. improved therapies 3. prevention of recurrences
major risk factors for developing atherosclerosis: 1. hyperlipidemia 2. hypertension 3. cigarette smoking 4. diabetes mellitus
response-to-injury hypothesis for formation of atherosclerosis 1. focal areas of chronic endothelial injury or dysfunction 2. increased uptake and oxidation of LDL in areas of injury 3. intimal accumulation of macrophages and smooth muscle cells 4. proliferation of the smooth muscle cell in the fatty streak
2 main physical changes of ahterosclerosis 1. fatty streak 2. atheromas
fatty streak aggregate of lipid-containing and smooth muscle cells; can be converted to an {atheroma} by ECM production of smooth muscle cells
aneurysm congenital or acquired local dilation of blood vessels or heart in areas of weakness, more common in areas of higher pressure -can be spherical or fusiform
true aneurysm aneurysm that involve all 3 layers of the arterial wall
false aneurysm aneurysm that is a breach in the wall and leads to extravascular hematoma
arterial dissection blood spreading between layers of arterial wall
berry aneurysm congenital defect of intracranial arteries
abdominal aortic aneurysms aka atherosclerotic aneurysms; most common type of aneurysm in areas of severe atherosclerosis with damage to tunica media below the renal arteries
thoracic aortic aneurysms aka syphilitic aneurysms; associated with hypertension and Marfan syndrome, up in chest so have swallowing/breathing issues
aortic dissection intimal tears allow blood to enter wall and spread along the tunica media, usually within 10 cm of aortic valve
double-barreled aorta blood reenters aortic lumen through another tear distal to the first
cystic medial degeneration/necrosis elastin fragmentation with formation of cysts containing ECM; in people with CT disorders like Marfan's
vasculitis inflammation of vessels, usually immune-mediated or from an infection
systemic necrotizing vasculitides immunologic forms of vasculitis; includes Giant Cell arteritis, Kawasaki, Wegeners, and Buerger's
Giant Cell Arteritis most common arteritides; autoimmune reaction agains vessel wall antigen, especially in temporal arteries -centered around elastic membrane with multinucleated giant cells
Kawasaki disease aka mucocutaneous lymph node syndrome; in children with immunoregulatory defeat that triggers vasculitis after exposure to common infection -lymphadenopathy, erythema of palms and soles and {strawberry tongue}
Wegener granulomatosis cause unknown but possibly hypersensitivity to inhaled antigens; respiratory symptoms and bloody gingiva
ANCA; antineutrophil cytoplasmic autoantibodies lab test to detect the autoantibodies in systemic vasculitides
MPO-ANCA; anti-myeloperoxidase antineutrophil cytoplasmic autoantibodies seen in some autoimmune renal disorders
PR3-ANCA; antiproteinase-3 antineutrophil cytoplasmic autoantibodies detected in Wegener granulomatosis
thromboangiitis obliterans aka Buerger disease leads to clots of radial and tibial arteries, related to tobacco use; preceded by Raynaud's and pain in foot instep
Raynaud phenomenon exaggerated vasoconstriction of digits and cyanosis of acral parts; red>white>blue -primary in otherwise healthy people, secondary if systemic disorder
varicose veins dilated, tortuous veins from high pressure and loss of wall support -hemorrhoids and esophageal varices
phlebothrombosis/ thrombophlebitis thrombus formation in veins; associated with Trousseau sign/migratory thrombophlebitis
lymphangitis acute inflammation of lymphatics, can spread to lymph nodes and then become bacteremia
lymphedema accumulation of interstitial fluid from lymphatic occlusion
peau d'orange persistent lymphedema can thicken skin and give orange peel appearance
chylous ascites interstitial fluid in peritoneal cavity
chylothorax interstitial fluid in chest cavity
chylopericardium interstitial fluid in cardiac cavity
primary lymphedema accumulation of interstitial fluid as a congenital defect {simple congenital lymphedema} or familial origin {Milroy disease}; most commonly seen in legs
secondary lymphedema arises secondary to processes that disrupt lymphatic drainage i.e. scarring, neoplasms, surgery, filariasis
hemangioma benign tumor or blood vessel endothelium; capillary or cavernous depending on size
lymphangioma benign tumor of lymphatics
angiosarcoma malignant tumors of blood vessels and lymphatic vessels (lymphagiosarcoma) most common after radical mastectomy
Kaposi sarcoma low-grade malignancy of vascular endothelium in AIDS patients with HHV-8
congestive heart failure heart can no longer eject the blood delivered by the venous system so blood backs up
left-sided heart failure from ischemic heart disease, aortic and mitral valve issues, hypertension; creates lung, kidney and brain problems -decrease in renal perfusion but increase in total blood volume
dyspnea breathlessness
orthopnea dyspnea when reclining
paroxysmal nocturnal dyspnea extreme dyspnea that wakes up from sleep
prerenal azotemia decrease in renal filtration leads to increase in nitrogenous products
hypoxic encephalopathy hypoxia of brain from poor perfusion; irritability, restlessness, and coma
right-sided heart failure usually secondary to left-sided heart failure; primary from right-to-left shunts, cor pulmonale and tricuspid valve disease -liver issues and peripheral edema (ascites, anasarca)
cor pulmonale right ventricular strain from intrinsic lung disease; causes systemic venous congestion -affects liver, spleen and kidneys
nutmeg liver congestion of sinusoids of venous system creates this pattern in the liver
central hemorrhagic necrosis rupture of liver sinusoids from engorgement
centrilobular necrosis hepatocytes around the central vein undergo necrosis due to hypoxia
left-to-right shunts most common congenital heart problem; patients not cyanotic at birth but increase in pressure leads to reversal of flow -blood goes through lungs again
Eisenmenger syndrome the increase in pressure of the pulmonary circulation and the right side of the heart leads to the reversal of left-to-right shunts
tardive cyanosis late cyanosis in left-to-right shunts from pulmonary hypertension
atrial septal defects failure of closure of foramen ovale during intrauterine life -left-to-right shunt
ventricular septal defects usually close spontaneously but increased risk for endocarditis -left-to-right shunt
patent ductus arteriosus channel between pulmonary artery and aorta remains open after birth -left-to-right shunt
right-to-left cyanotic shunts cyanotic at birth with unoxygenated blood in systemic circulation -blood skips the lungs
paradoxical embolism emboli in veins bypass the filtration in the lungs and end up in peripheral circulation
hypertrophic osteoarthropathy clubbing of fingertips from long-standing cyanosis
Tetralogy of Fallot 1. ventricular septal defect 2. dextraposed aorta 3. right ventricular obstruction 4. right ventricular hypertrophy
transposition of the great arteries when aorta comes off the right ventricle instead of the left; can only survive if have a left-to-right shunt
coarctation of the aorta narrowing or constriction of the aorta proximal (symptomatic) or distal (asymptomatic) to the ligamentum arteriosum
ischemic heart disease imbalance between myocardial demand and supply of oxygen; leading cause of death in the US
acute plaque changes fissuring, hemorrhage, rupture, embolization into distal coronary arteries
coronary artery thrombosis arises from plaque rupture that exposes collagen to platelet aggregation and local coagulation
coronary artery vasospasm reduction of cardiac blood flow from unknown cause but possibly stress on top of preexisting atherosclerosis
angina pectoris intermittent chest pain from transient reversible myocardial ischemia without infarct
typical/stable angina associated with atherosclerosis; brought on by stress or exertion and relieved with rest or nitroglycerin
prinzmetal angina vasospasm but not with fixed stenosis; occurs at rest, even sleep, and relieved with nitroglycerin
unstable/crescendo angina from atherosclerotic stenosis and platelet aggregation; most intense and prolonged pain from exertion -warns of future MI aka {preinfarction angina}
myocardial infarction area of myocardial necrosis from local ischemia
subendocardial infarction inner 1/3 of ventricle wall where necrosis begins
transmural myocardial infarction necrosis of full thickness of ventricular wall
cardiac troponin I specific enzyme for contractile protein, remains elevated for days following an MI -other enzymes to test: creatine kinase and MB isoenzyme
intracoronary thrombolytic medications clot busters like tPA that can limit infarct
coronary artery bypass grafting (CABG) bypass with leg vein or mammary artery
transluminal angioplasty removes, destroys and compresses stenosing plaques
chronic ischemic heart disease (ischemic cardiomyopathy) slow development of CHF from longterm ischemia; causes arrhythmias (tachycardia, bradycardia, ventricular fibrillation and asystole)
sudden cardiac death unexpected death from cardiac disease, usually due to a lethal arrhythmia
systemic hypertensive heart disease combination of hypertension and left ventricular hypertrophy
pulmonary hypertensive heart disease (cor pulmonale) right ventricular enlargement secondary to pulmonary hypertension
acute cor pulmonale right ventricular dilation from pulmonary embolism
chronic cor pulmonale right ventricular hypertrophy from prolonged pressure overload
rheumatic fever acute autoimmune condition following group A strep; antigen cross reacts in heart and joints -get {arthritis} and {skin lesions}
acute rheumatic heart disease get carditis of all three layers {pancarditis}
Aschoff bodies collections of intramuscular inflammatory cells that form this pattern of myocarditis in rheumatic heart disease
Anitschkow cells large macrophages surrounding necrotic centers seen in rheumatic heart disease
vurrucae inflammatory vegetations on valve leaflets
chronic rheumatic heart disease secondary to fibrocalcific thickening of valves so get improper closure
infective endocarditis colonization of heart valves or wall by microorganisms; forms thrombotic masses {vegetations}
acute endocarditis secondary to highly virulent organisms on otherwise healthy hearts; usually Staph aureus
subacute endocarditis lower virulence microorganisms that colonize hearts that have had issues; usually Strep viridans in plaque
cardiomyopathy primary non-inflammatory disorder of myocardium
dilated cardiomyopathy dilated, hypocontracting hearts; requires transplant
hypertrophic cardiomyopathy heavy, hypercontracting heart with hyperplasia of left ventricle; ejection is strong but low volume -sudden, unexplained death in young athletes
restrictive cardiomyopathy decrease in ventricular flexibility
myocarditis inflammatory process that injures myocardium, usually from infection
pericarditis inflammation of pericardium secondary to myocardial or endocardial disease
pericardial effusion fluid accumulation in pericardial sac
constrictive pericarditis complete encasement of heart in fibrous CT
hemopericardium when pure blood fills pericardial sac
cardiac tamponade compression of the heart by fluid accumulation in pericardial sac
Created by: Alexandra Arnold Alexandra Arnold