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Path Block-3
Cardiovascular
| Question | Answer |
|---|---|
| when a blood vessel is damaged (ruptured or severed), hemostasis is achieved through these mechanisms: | vascular spasm, formation of a platelet plug, formation of a blood clot, clot organization |
| Vascular Spasm | contraction of vessel wall produced by autonomic reflexes, local spasm of vascular smooth muscle, local bioactive molecules (thromboxane A2 from platelets) |
| Formation of a platelet plug: endothelial cells | when damaged, they initiate thrombogenesis by exposure of subendothelial collagen which induces platelet adhesion (mediated by von Willebrand factor) |
| Patelet adhesion releases | ADP, histamine, seratonin, PDGF |
| Platelet aggregation to the endothelial-adhered platelets is due to: | ADP, thrombin, thromboxane A2, platelet activating factor |
| Platelet membrane phospholipase is activated with: | liberation of arachidonic acid which is metabolized via cyclo-oxygenase pathway to Thromboxane A2 to induce vasoconstriction and platelet aggregation |
| Activation of the coagulation cascade: | d/t exposure of phospholipid complex molecules in platelet membrane after adhesion; the platelet mass is stabilized by fibrin |
| Platelet cascade versus coagulation cascade | the platelet plug forms first, if the defect is small, the platelet plug is enough; if the damage is extensive, the clotting cascade is activated for fibrin stabilization |
| Activation of clotting cascade | endothelial release of bioactive substances; Platelet release of bioactive substances; Circulating coagulation proteins adhering to exposed collagen of vascular wall |
| Activation of the Extrinsic pathway of the clotting cascade is due to vascular injury | initiated by tissue factors from damaged vessels; tissue factors bind circulating factor VII forming activated complex; activated VIIa activates factors X and IX (intrinsic) |
| Activated factor X | the common final pathway that initiates: prothrombin (factor II) conversion to IIa w/help from activated co-factor V; thrombin converts fibrinogen to fibrin monomers ( w/factor XIII make fibrin) to stabilize platelet mass into a fxnl clot |
| Timing of clot formation | form in <1min; can occlude a med-sized vessel in <few min; after 20min, the clot contracts and closes the defect further; w/in a few hrs growth factors stimulate ingrowth of fibroblasts; in 10-14days the clot is completely fibrous |
| Pathophysiology of Shock (circulatory failure/hypotension) | compensation activated by baroreceptors in vessels/heart to stim sympathetics to inc BP and correct hypoxemia (inc HR, contractility, periph constrict, tachypnea); redistribute blood to brain/core; switch to anaerobic glycolysis (metab acidosis) |
| Traumatic blood loss | significantly dec volume; hypotension; tachycardic heart unable to maintain bp |
| Cardiogenic shock: pump failure | heart becomes an ineffective pump; significantly reduced cardiac output; unable to maintain bp |
| Neurogenic shock | usu a/w spinal cord injury; sudden loss of symp tone to systemic circulation (systemic vasodilation, peripheral blood pooling, dec return to heart); dec CO from LV and dec bp |
| Pulmonary Thromboembolism | sudden interruption of blood traversing the pulmonary vasculature; dec CO from LV, dec bp |
| Sequelae of prolonged HYPOtension | global cerebral hypoxia (brain damage/cerebral edema); global myocardial ischemia; acute respiratory distress syndrome (diffuse alveolar damage); acute tubular necrosis (kidney); centrilobular necrosis (liver); mesenteric bowel infarct |
| Pathophysiology of HYPERtension (sys >140 or dias >90) | usu either: 1. inc symp tone (vasoconstriction and inc CO) or 2. inc levels of renin-angiotensin-aldosterone (renin inc AT1 which ACE converts to AT2 for vasoconstriction, inc aldosterone (Na retention inc CO, periph bp) and stim symp (inc CO, vasoconst) |
| Increased sympathetics and increased renin levels lead to sustained bp elevations, which cause: | vascular damage in kidneys (a/w reduced renal blood flow; causes kidney to secrete more renin which elevates bp even more via effects on angiotensin and aldosterone) and other end organs |
| Pathophysiology of Secondary Hypertension | d/t: 1. Chronic renal failure (mc; dec renal fxn leads to inc plasma vol; dec renal blood flow elevates renin/angiotensin); 2. Renal artery stenosis (mc2; dec flow = inc renin/angiotensin); 3. Conn Syndrome (aka: primary hyperaldosteronism; inc plasma vol |
| Sequelae of Hypertension | Malignant hypertension (hypertensive encephalopathy/edema d/t vascular damage; intracerebral hemorrhage; renal failure (fibrinoid vascular necrosis in kidney; malignant nephrosclerosis); LVH & sudden death d/t dysrhythmia; CHF; accelerated atherosclerosis |
| More sequelae of hypertension | hyaline arteriosclerosis (brain infarction or nephrosclerosis from inc ECM production that thickens vessel wall); dec renal blood flow; inc renin; chronic renal failure; hyaline arteriosclerosis of retinal vessels and rupture w/bleeds; amblyopia |
| Cerebral Aneurysm: Saccular intracerebral | aka: berry aneurysm; usu young people; 1 in 20; usu >1; usu don't rupture; usu anterior cerebral circulation; rupture = subarachnoid bleed; death/morbidity |
| Risk factors for intracranial aneurysm formation | abnml/anomalous vessels; coarctation of aorta; polycystic kidney; fibromuscular dysplasia; CT disorder (Marfans; Ehlers-Danlos) |
| Pathophysiology of intracerebral aneurysm | origin, growth and configuration influenced by vascular and internal flow hemodynamics; usu at apex of vessel bifurcations; rounded outpouching dt local vascular wall degen or congenital defect in wall; involves only intima and adventitia (thru media) |
| Fusiform Intracerebral Aneurysm (atherosclerotic aneurysm) | older pts; vertebrobasilar system; telangiectasias occur; damage to media = arterial stretching over a length; intraluminal clots; thrombosis causes brainstem infarct & mass effect (compress brain/cranial n palsies) |
| Aortic aneurysm | d/t: arteriosclerosis (mc), infxn (mycotic aneurysm), aortitis (giant cell, lues (syphilis), A.I. dx), marfan/ehlers-danlos |
| Aortic aneurysm pathophysiology | d/t degeneration of tunica media of aorta causing slow and continuous dilation of aortic lumen; artherosclerosis (fibrosis, chronic inflam); elastic fiber fragmentation; cystic medial necrosis; Laplace's Law: luminal dilation results from inc wall tension |
| Aortic aneurysm pathology | AAAs are segmental dilations of aortic wall (>1.5x nml diameter); usu btw renal aa and iliac bifurcation; if >5cm in diameter there is a high risk for rupture; thoracic aortic aneurysm (3 grps); usu rupture/dissect |
| Thoracic aortic aneurysm | 1. ascending aorta (btw aortic valve and innominate artery); 2. aortic arch (btw innominate artery and subclavian artery); 3. descending aorta (btw L subclavian artery and diaphragm |
| Mitral valve stenosis | narrowing of inflow tract from LA to LV d/t: Rheumatic heart disease (mc); SLE, RA, infective valvulitis, congenital mitral stenosis |
| Pathophysiology of Mitral valve stenosis | ant/post leaflets; flow hindered at when area is red to 2cm (nml 4-6cm); LV filling red; to maintain CO, LA pressure inc; can cause regurgitation and pulmonary hypertension (dec pulm flow into LA/LV, if chronic: pulmonary edema/RHF (cor pulmonale) |
| Mitral valve stenosis pathology | valve leaflets thickened; valve commissures may or may not be fused; chordae tendineae are thickened and shortened; enlarged LA |
| Mitral valve stenosis: clinical synopsis | usu female; MV Triad: 1. loud S1; 2. mitral valve opening snap; 3. mid-diastolic murmur at apex d/t turbulant flow thru MV (diastolic and systolic murmur w/progression to stenosis and regurgitation) |
| Mitral valve stenosis: doppler flow findings | measurement of flow can estimate the pressure gradient (LA pressure minus LV pressure); Normal = 1-2mmHg, Mild stenosis = 5mmHg, Severe stenosis = 10+mmHg |
| Mitral valve stenosis: Clinical course and sequelae | Chronic atrial fib (dec CO by 15-20%); Spontaneous LA mural thrombosis (systemic thromboembolism); Pulmonary HT (R-side failure); Infective mitral valvulitis (aggressive antibiotics/prophylaxis); Combo stenosis/regurg; Dec lifespan w/o valve surgery |
| Mitral Valve Regurgitation | backwards leak during systole d/t: Papillary dysfxn d/t ischemic heart dx (mc); Mitral valve prolapse d/t myxomatous degen of MV (mc2); Senile degen (fibrocalcification); Rheumatic HD; (uncommon: tendinous cord rupture, infective valvulitis, post-balloon |
| Mitral valve regurgitation: Pathophysiology | during systole, a large portion of CO is directed back thru mitral valve into left atrium; enlarged LA, CO mildly red (inc HR/strength); larger vol enters LV in diastole causing LV dilation/inc LV end-diastolic vol/pressure; CHF; pulm edema; R-heart fails |
| Mitral valve regurgitation: clinical synopsis, course, sequelae | dyspnea on exertion, nocturnal dyspnea, orthopnea, chronic fatigue, holosystolic murmur at apex; chronic atrial fibrillation, recurrent pulmonary edema, congestive heart failure |
| Aortic valve stenosis | d/t: Senile fibrocalcific degen (mc); congen bicuspid aortic valve; Rheum HD; infective aortic valvulitis |
| Aortic valve stenosis: pathophysiology | nml area: 3-4cm; blood flow red w/area of 1.5cm; LV ejection pressure inc to maintain CO; LV outflow tract obstruction; dilated/hypertrophied LV; LV failure |
| Aortic valve stenosis: pathology | valve thickening and distrotion d/t fibrocalcification; only 2 leaflets (bicuspid) rather than 3; cusp fusion usu only if d/t rheum HD or other inflam etiologies |
| Aortic valve stenosis: clinical synopsis, course, sequelae | effort angina; syncope on effort; dyspnea; fatigue; systolic murmur; delayed S2; GI bleed; recurrent pulmonary edema; CHF |
| Aortic Valve Regurgitation | d/t: Degen of aorta leading to valve annulu expansion (idiopathic, atherosclerosis, lues, giant cell, CT dx); RheumHD; infxn; Uncommon: (severe HTN, bicuspid aorta, dissection, AI dx, quadricuspid aorta, myxomatous degen (rare)) |
| Aortic valve regurgitation: pathophysiology | if wall dilates, the valve annulus dilates = valve incompetency; blood pumped out LV flows back across aortic valve into LV; dilated/hypertrophied LV; cardiomegaly; inc LV pressure --> LA --> pulm circulation |
| Aortic valve regurgitation: pathology | stiffening of valve leaflets; fusion of cusps; thickening and retraction of cusps; commonly a/w markedly enlarged heart (cor bovinum) |
| Aortic valve regurgitation: clinical synopsis, course, sequelae | usu clinically silent for yrs; effort dyspnea, angina pectoris; chronic fatigue; pandiastolic murmur; slightly dec diastolic bp; laterally displaced apicul impulse; congestive heart failure w/recurrent pulmonary edema |
| Tricuspid valve stenosis | Very RARE; d/t RheumHD (mc, a/w MV stenosis); infective valvulitis; blood cannot get thru 1st valve of R heart; dec pulm blood flow; dec CO; (if w/MV stenosis, effects of pulm HTN and R-side failure are reduced) |
| Tricuspid valve stenosis: pathology, clinical synopsis, DDx, clinical course, sequelae | enlarged RA, valve thickening, shrinkage, deformity; fatigue, peripheral edema, ascites, hepatomegaly, anasarca, acrocyanosis; chronically dec CO and systemic hypoxemia (FTT in peds); chronic hepatic congestion --> hepatic cirrhosis ("cardiac cirrhosis") |
| Tricuspid Valve Regurgitation | Very RARE; d/t: congen dysplasia, infxn valvulitis, mysomatous degen, pulm valve stenosis, pulm HTN, primary cardiomyopathy; RV SV only partly sent to pulm circulation (d/t backflow thru incompetent valves); thick, shrunk retracted leaflets |
| Tricuspid valve regurgitation: clinical synopsis, course, sequelae | fatigue, dec CO, acrocyanosis, hepatomegaly, ascites, anasarca, systolic murmur; progressive RV dilation/hypertrophy leading to RV failure |
| Pulmonary valve stenosis | isolated is 2nd mc congenital heart defect; (others: non-syndromatic heart defects; Noonan syndrome; Tetralogy; congen rubella; williams syndrome); RheumHD |
| Pulmonary valve stenosis: pathophysiology | causes RV outflow obstruction leading to: inc RV pressures, RV dilation/hypertrophy; dec pulm blood flow leads to: red CO, systemic hypoxia |
| Pulmonary valve stenosis: pathology | failure in development of leaflets/separation of commissures leading to dysplastic dome-shaped valve (may have fusion or dysplasia); bicuspid valve is more fxnl; severe stenosis = RV dilation, RVH, RA dilation, tricuspid insufficiency |
| Pulmonary valve stenosis: clinical synopsis | pts w/mild or moderate stenosis will be relatively asymptomatic; exertional dyspnea; easy fatigability; acrocyanosis, hepatomegaly, ascites, anasarca, systolic murmur; if pressure gradient across valve is >40mmHg, surgery is needed (RVH/lifespan ok after) |
| Pulmonary valve stenosis: Clinico-pathological typology | Valvular (mc); Subvalvular/Infundibular (usu occurs w/VSD, noonan syndrome or tetralogy); Supravalvular (usu a/w congen rubella or williams syndrome) |
| Pulmonary valve regurgitation | Senile (trace PV regurgitation); Primary, Secondary (mc); d/t: dilation of pulmonic valve ring, congen malformation of valve (tetralogy), congen absence of PV, acquired PV dx (bacterial, RheumHD, etc); senile d/t structural deterioration of thin valve; |
| Pulmonary valve regurgitation: pathology | valve dysplasia (Primary PV regurg); Fenestrations in leaflets (congen or acquired d/t bacterial endocarditis d/t IVDA, immune defic, dysplastic valve); RVH |
| Pulmonary valve regurgitation: Clinical synopsis | easy fatigue, dizziness, light-headed, syncope, peripheral edema, chest pain, palpitations, ascites, diastolic murmur, hepatomegaly d/t chronic hepatic congestion, inc jugular venous pressure; inc RV end-diastolic vol/pressure; |
| Pulmonary valve regurgitation: common causes of secondary | CHF d/t primary cardiomyopathy; pulm HTN; bacterial valvulitis, RheumHD; carcinoid heart disease; marfans (d/t dilated PV ring); |
| Pulmonary valve regurgitation: clinical course and sequelae | highly variable based on cause of regurgitation; pts w/pulm HTN or congen absence of PV have worse prognosis d/t rapid development of RVH and RV failure |
| Mitral valve prolapse | idiopathic (mc); marfan or ehler's danlos syndromes; d/t MV regurgitation (CO returns to LA ; LA hypertrophy; pulm HTN; pulm edema; R-heart failure; inc vol entering LV = dilation; CHF) |
| Mitral valve prolapse: pathology and clinical course | myxomatous (mucoid degeneration) of valve leaflets; grossly thickened and expanded like a balloon; tendinous cords are thickened and fused; cardiac dysrhythmias, mitral valve regurgitation and complications, sudden death (rare) |
| Venous thromboembolism | if inflammation is present, it is called thrombophlebitis; if infection is also present, it is called pyelothrombosis; originates in deep vv of limbs (DVT); mc d/t bed rest or prolonged inactivity; pelvic vv postpartum; usu embolizes to pulm circulation |
| Pulmonary embolism | acute decrease in pulmonary blood flow and oxygenated blood to left heart (acute dec CO and generalized hypoxemia); acute inc in pulm artery pressure (acute RHF) |
| Arterial Thromboembolism | originates in arterial system (mc from endocardial surface of heart d/t atrial fib, MI, infective endocarditis); ruptured/ulcerated atherosclerotic plaque in large vessel (aorta, common carotid at jxn, iliac aa) |
| Arterial thromboembolism: embolization sites | brain (middle cerebral a infarct), internal organs (mesenteric a small bowel infarct OR renal a wedge-shaped cortical infarct), extremities (gangrene digits) |
| Arterial thromboembolism: clinical course, sequelae | Dissolution (fibrinolytic system); Partial dissolution (recanalization in coronary aa); Tissue/organ infarction (infarct size depends on size of thromboembolism and presence of collateral circulation); Sudden death (if large embolism in brain or lungs) |
| Monckeberg Arteriosclerosis | idiopathic (mc), metabolic bone dx (1* or 2*-CCsteroid), diabetes mellitus; areas of necrosis/dystrophic calcification of tunica media (small-med aa in lower leg; NOT tunica intima); usu asymptomatic; dysfxn rare (chronic distal ischemia &/or thrombosis) |
| Arteriosclerosis | obstruction of blood flow leading to end-organ ischemia & infarction; usu tunica intima; d/t HTN w/intimal hyalinization, medial hypertrophy, endothelial hyperplasia; kidneys (a/w generalized glomerular sclerosis/CRF); Brain (sm infarcts in basal ganglia) |
| Arteriosclerosis: clinical course and sequelae | increased incidence of chronic renal failure and cerebrovascular accident (aka: stroke) |
| Hyperplastic arteriosclerosis | fibrointimal proliferation creating "onion skin" appearance; common in kidneys; usu a/w severe chronic HTN or malignant HTN; inc incidence of chronic renal failure |
| Atherosclerosis | mc type of arteriosclerosis; Risks (male, age, postmenopausal, fam hx, smokers, HTN, diabetes mellitus, high LDL, high homocysteine, overweight, sedentary, high TGs) |
| Atherosclerosis: pathophysiology | inflam disease; degeneration of med-large muscular aa (tunica INTIMA); "response to injury theory" - endothelial dysfxn allows lipids/WBCs into subendothelial space (inc permeability of lipoptns, dec NO prod, inc leukocyte migration/adhesion) |
| Artherosclerosis: "Response to Injury" theory: 1 | endothelial injury (infection) is initiating event, mild predisposition to occur at anatomical branching pts in med-sized vessels (vulnerability of these areas d/t variations in shear stress and blood flow) |
| Artherosclerosis: "Response to Injury" theory: 2 | infiltration by inflam and phagocytic cells; deposition of LDL (oxidized by free radicals from inflam; ox LDL is tissue toxic, more inflam; phagocytosis by MQs produce "foam cell" fatty streak), cholesterol, calcium, cell debris w/in intima; |
| Artherosclerosis: "Response to Injury" theory: 3 | chronic/progressive inflam; repair initiated as fibroepithelial prolif and fibrosis; final lesion is combo of fibrosis and lipid ("Atheroma"); elevated homocysteine promotes atherosclerosis (coverted to reactive sulfur compound; promotes LDL chol deposit) |
| Atherosclerosis and the Positive Repair Reaction | intramural plaque growth buldges wall outward rather than in; usu does not cause angina (a/w progressive growth over yrs which finally causes luminal narrowing); accounts for most vulnerable plaques (more prone to result in plaque rupture and thrombosis) |
| Atherosclerosis and C-Reactive Protein | undergoes 100x increase during acute inflammation; pts w/ >1mg/dL have slight inc risk of atherosclerosis; those w/ levels >3mg/dL exhibit significant inc risk of atherosclerosis-related complications (AMI, mortality rate, dec response to statins) |
| Atherosclerosis: clinical synopsis 1 | Coronary aa (angina pectoris; begins w/exertion, a/w dyspnea, blood flow to aa red 30% to cause pain; at rest w/high-grade stenotic lesion; AMI, chronic ischemia leads to ischemic cardiomyopathy); Aorta (wall weakens/aneurysm; distal infarct d/t rupture) |
| Atherosclerosis: clinical synopsis 2 | Ilio-femoral aa (ischemia, fatigue, aches w/exertion d/t intermittant claudication; chronic ischemia (thin skin, hair loss, atrophy, distal infarction); Subclavian aa (ischemia on exertion, tiredness, aching in extremity, skin/hair/muscle change, infarct) |
| Atherosclerosis: clinical synopsis 3 | CVA (stroke; d/t either luminal narrowing/dec blood flow OR plaque thrombosis and acute dec in flow, OR plaque rupture/embolism & distal infarct (single or many)) |
| Atherosclerosis: clinical synopsis 4 | Renal aa (usu unilat dec blood flow/chronic renin elevation and renovascular HTN; unilat chronic ischemia leading to atrophy of kidney; Renal infarct (plaque thrombosis/acute blood flow red OR plaque rupture/embolism and distal infarction) |
| Coronary artherosclerosis: modifiable risk factors | smoking, dyslipidemia (HDL <35, LDL >160, TGs >250), HTN, obesity, physical inactivity, elevated circulating homocysteine, diabetes mellitus, heavy ethanol use |
| Pathophysiology of Coronary Atherosclerosis in Cigarette Smoking | exact mechinism unknown, but likely d/t injury to endothelium by carbon monoxide and/or nicotine; altered platelet adhesion properties; altered LDL chemistry (inc ability to become oxidized) |
| Pathophysiology of Homocysteinemia and Coronary Atherosclerosis | homocysteine converted to very reactive sulfur that reacts w/ LDL-C; promoting LDL-C deposition in vessel wall; also inc circulating LDL levels, inc angiotensin II levels (inc systemic vasoconstriction), inc platelet adhesiveness (thrombogenesis) |
| Pathophysiology of Hyperlipidemia and Coronary Atherosclerosis; the anti-atherosclerotic effects of HDL are exerted by | prevent/correct endothelial dysfxn (endothelial prolif & dec apoptosis); promote vasodilation d/t release of NO and prostacyclin thru expression of endothelial NO synthase & coupling COX2 w/prostacyclin synth; dec platelet adhesion, inc antiox activity |
| Clinical Synopsis of Coronary Atherosclerosis Lesions | dx is progressive thru life & most pts are asymptomatic (esp if diabetic b/c cardiac sensory nn are damaged); angina pectoris/SOB on exertion, dec exertional capacity, abnml fatigue, dizziness, palpitations (inc PVCs) |
| Clinical Course and Sequelae of Coronary Atherosclerosis Lesions | plaques grow slowly over 10-15yrs; distribution of lipid/CT determines stability/risk of rupture, thrombosis, and sequlae; "vulnerable plaques" w/thin fibrous cap will rupture and thrombose; |
| Thrombogenesis in atheroma | denudation of overlying endothelium or rupture of fibrous cap d/t chronic inflam results in exposure of thrombogenic contents, platelet adhesion, activation of clotting cascade, thrombosis (occlusive and non); 48% of AMI/CAD occur w/nml cholesterol levels |
| Blood supply to SA node in right atrium | either the left coronary artery soley, the right coronary artery soley, or a combo of both |
| blood supply to the AV node | supplied by the right coronary artery in most people |
| FLAP gene | mutations result in higher chronic levels of circulating leukotrienes; significantly increases risk of AMI |
| Acute Myocardial Infarction: risk factors | same as atherosclerosis; positive fam Hx (any 1st degree male relative <45yo or female <55yo who had AMI; diabetes mellitus (esp type I: IDDM); hypercholesterolemia; chronic stumulant use (cocaine, meth) |
| Pathogenesis of Myocardial Infarction | plaque rupture triggers event; usu from an area of atherosclerosis with <50% occlusion; leads to embolization of fragments, distal occlusion and subsequent infarct; thrombosis leads to coronary a occlusion and infarct |
| Pathophysiology of Myocardial Infarction 1 | heart m has no glycogen stores; after occlusion anaerobic glycolysis generates only sm amt of ATP; intracellular ATP creatine-P levels drop w/in min; interaction btw actin&myosin w/Ca influx is altered; ischemic area stops contracting d/t no mitoch oxphos |
| Pathophysiology of Myocardial Infarction 2 | Cardiocytes in ischemic area have hydropic change and Na/Ca enter cell; myocardium becomes pale; ejection fraction dec proportional to infarct area; electrical instability of heart = risk for re-entry impulses/dysrhythmias |
| Pathophysiology of Myocardial Infarction 3 | contraction band necrosis (if present, d/t re-O2 in reversible injury causing extreme contraction); coagulative necrosis of coronary aa, neutrophil infiltration 8-12hrs, MQs w/in days; repair begins at 7th day (fibroblasts, angiogen); non-contractile scar |
| Pathophysiology of Myocardial Infarction 4: enzymes released during necrosis | troponin I, troponin T, creatine phosphokinase (CPK), lactic dehydrogenase (LDH), aspartate aminotransferase (AST) |
| Myocardial Infarction: Subendothelial | located only in subendothelial area (interior 33% of LV wall thickness); area is most vulnerable d/t lack of blood supply (furthest distance from coronary aa and prolonged compression during systolic contraction) |
| Myocardial Infarction: Transmural | full thickness of the myocardium (from endocardium to epicardium) |
| Myocardial Infarction: Clinical Synopsis | acute chest pressure/squeezing discomfort (anterior precordium, radiates to jaw, neck, arms (L>R), back, epigastrium); actue SOB, nausea or epigstric pain (a/w inf or post wall infarcts); syncope, diaphoresis; no symptoms if diabetic or old |
| Myocardial Infarction: Laboratory Diagnosis of Serum Markers | Specific: Creatine phosphokinase (elevated total CPK w/specific elevation in MB fraction; 4hrs after injury, peak 24hrs, nml 72hrs); Troponin-I (3-4hrs after injury, nml w/in wks); Troponin-T (onset after troponin-I); Non-specific (myoglobin, LDH) |
| Myocardial Infarction: Clinical Course and Sequelae: Early | Cardiac arrhythmias (mc; PVCs, supraventricular tach, bradycardia (post wall infarct; AV node is supplied by R), v-tach, v-fib); Acute mitral regurgitation (ant papillary m ruptur/infarct); Cardiogenic shock (pump failure d/t large LV infarct) |
| Myocardial Infarction: Clinical Course and Sequelae: Late | Ventricular aneurysm (d/t transmural infarcts, wall replace w/fibrous tissue); LV wall rupture (a/w transmural w/in 4-7d; necrotic wall can't withstand LV pressure; acute tamponade d/t hemopericardium); 30% mortality (rest have dec life expectancy) |
| Myocardial Infarction: Clinical Course and Sequelae: uncommon | infarction of mitral valve papillary m (MV incompetence); Endocardial (mural) thrombosis at site of infarction (may impede LV filling and dec CO); IV septum rupture (acute L--> R shunt, dec CO, acute RVF, acute pulm HTN) |
| Non-atherosclerosis-related Myocardial Infarction | d/t: severe LVH (asymmetric, aortic stenosis); Hypoxia (COPD); Microvascular MI; Coronary a. spasm (Prinzmetal's angina; cocaine, meth); Coronary a emboli (mycotic, aneurysm-related, atherosclerotic); Vasculitis (kawasaki, polyarteritis nodosa); dissectio |
| Non- atherosclerosis-related Myocardial Infarction: Pathophysiology | coronary aa have minimal or absence atherosclerosis; myocardial O2 demands temporarily exceed supply of coronary aa leading to necrosis of portions of myocardium (commonly subendocardial) |
| Causes of ischemic heart disease | mc: coronary artery atherosclerosis; coronary artery spasm (aka: Prinzmetal's angina); chronic anemia; chronic hypoxemia d/t chronic lung dx; valvular heart dx; cardiomyopathy |
| Ischemic heart disease: Pathophysiology | imbalance btw blood/O2 requirements of heart & coronary aa ability to meet it (dysfxn begins in 1min of dec; 1sec if obstructed; cell death w/in 30min) |
| Factors INCREASING the blood/oxygen demands of the myocardium | systemic HTN, LV hypertrophy; inc HR; LV outflow obstruction; inc LV end-diastolic blood vol |
| Factors DECREASING the blood/oxygen supply to the myocardium | narrowing of coronary aa; valvular heart dx; cardiac dysrhythmias; systemic HTN; chronic anemia; chronic hypoxia d/t chronic lung dx |
| Cocaine-induced myocardial ischemia: Pathophysiology | cocain induces coronary artery spasm which is especially harmful if coronary artery disease is also present; chronic use is a/w accelerated coronary artery atherosclerosis and chronic myocarditis (followed by myocardial fibrosis) |
| Cocaine-induced myocardial ischemia: clinical course/sequelae | inc bp/hr, chest pain; inc risk of AMI, cardiac dysrhythmia and sudden cardiac death |
| Prinzmetal's Angina | myocardial ischemia unrelated d/t spont coronary a. spasm; polymorphisms in stromelysin-1 5A/6A gene = impaired NO synth, dec availability, inc basal vascular tone, spont vasospasm, platelet activ/thrombosis, inc thromboxane A2 & other vasoconstrictor |
| Prinzmetal's Angina: pathophysiology | elevated LDL chol (esp in oxid form) inhibit NO synthase and inc free O2-radical prod which inactivates NO; genetic polymorphs (common in Japanese) dec NO levels; spasm usu occurs in areas where atherosclerosis has begun d/t higher LDL levels; M8x>W |
| Prinzmetal's Angina: clinical synopsis, course, sequelae | inc incidence of AMI, inc incidence of dysrhythmias, inc incidence of sudden cardiac death |
| Microvascular Angina | presence of angina pectoris, ischemic changes on ECG during stress testing, but arteriographically normal arteries; usu post-menopausal women; related to DM, chronic HBP, systemic inflam dx (SLE, polyarteritis nodosa, etc) |
| Microvascular Angina: Pathophysiology | unknown etiology; ;poor coronary vasodilatory response; inc sensitivity of microcirculation to vasoconstrictor stimuli a/w abnml smooth muscle; dec flow d/t narrowing of intramyocard vessels; LVH inc intramyocard resistance; hypersensitive to heart pain |
| Microvascular Angina: Clinical synopsis, coarse, sequelae | chest pain on effort or at rest; poor response to sublingual nitroglycerin; prognosis better than coronary artery atherosclerosis (only a minority suffer progressive myocardial ischemia or AMI); **not a/w inc risk of arrhythmia or sudden cardiac death** |
| Hereditary Homocystinuria: Genetics of Classic Type | auto rec; clinical variability d/t multiple genes and mutational polymorphs; classic d/t def of cystathionine synthase (21q22.3); heterozygoes have mildly elevated homocysteine, but usu asymptomatic till late childhood |
| Hereditary Homocystinuria: Genetics of other types | mehtylene tetrahydrofolate reductase (MTHFR) on 1q36.3 (normally involved in methionine met and single-carbon transfer); C677T homo (1 in 11 people w/dec MTHFR activity); C677T/A1298C hetero (1 in 6 people; dec MRHFR activity) |
| Hereditary Homocystinuria: General Pathophysiology | hyperhomocysteinemia is atherogenic & thrombogenic d/t effects on vasclar endothelium (free-radical chronic damage/dec NO levels); highly reactive sulfur promotes LDL deposition; also interferes w/collagen x-linking in soft tissue |
| Hereditary Homocystinuria: Pathophysiology of Cystathionine Synthase | def leads to a block in the metabolic path for homocysteine leading to elevated circulating levels of homocysteine |
| Hereditary Homocystinuria: Pathophysilogy of MTHFR deficiency | dec MTHFR activity leads to chronically low folate levels and chronically elevated homocysteine (hyperhomocysteinemia) |
| Hereditary Homocystinuria: Clinical synopsis | symptoms present over time; Marfanoid habitus (dolichocephalia, arachnodactyly, kyphoscoliosis, eye lens dislocation); pale skin (dec melanin formation); mild cognitive defect w/behav & psych probs (autistic-like) |
| Hereditary Homocystinuria: Lab diagnosis | positive urine cyanide-nitroprusside rxn (homocysteine reacts = red/purple color); elevated serum: methionine, homocysteine, and dec cystathionine synthase in cultured fibroblasts or hepatocytes |
| Hereditary Homocystinuria: DDx, clinical course and sequelae | Marfan syndrome; generally dec lifespan d/t thromboembolic complications; inc incidence of: pancreatitis, atherosclerosis, and spont thrombosis (CVA, PE, AMI) |
| Thromboangiitis Obliterans (Buerger's Disease) | non-atherosclerotic segmental inflam vasoocclusive disease that affects sm-med sized vessels in upper and lower extremities (mc in lower); d/t smoking or chewing tobacco or pot |
| Thromboangiitis Obliterans: Pathophysiology | tobacco-related antigen provoke immunopath rxn & vascular injury, spasm, thrombosis; autoantibodies detected against: type I & III collagen, elastin; *integrity of vessel wall incl elastic lamina is maintained - diff from atherosclerosis & vasculitis* |
| Thromboangiitis Obliterans: Acute phase | occlusive inflam thrombosis w/min inflam in vessel walls; PMNs form microabscess w/dep of IgG, IgM, IgA, C3d, C4d in inner aspect of internal elastic membrane |
| Thromboangiitis Obliterans: Subacute phase | intraluminal thrombosis organizes; vascular recanulization |
| Thromboangiitis Obliterans: End-stage | vascular fibrosis and lumen obliteration; **pathologic characteristics of atherosclerosis (foam cells, chol clefts, fibrous intimal prolif, hyaline degen, calcification) are ABSENT** |
| Thromboangiitis Obliterans: Lab diagnosis | elevated ESR, elevated CRP, red levels of total complement and C3 |
| Thromboangiitis Obliterans: Clinical course and sequelae | most develop ischemia of extremities leading to skin ulceration, "spontaneous gangrene" and surgical amputation; coronary artery narrowing leads to myocardial infarction |
| Dilated Cardiomyopathies: General Pathophysiology | dep systolic fxn and systolic pump failure; dec LV contractile forces = dec CO & inc residual vol in end-systole/end-diastole; low CO upreg SNS & RAA-axis, releasing ADH & ANP to inc vol, but vasoconstriction further dec CO...vicious cycle! |
| Pathophysiology & Pathology of Idiopathic Dilated Cardiomyopathy | unknown etiology w/inc genetic association; cardiomegaly - LV wall thickness, mitral valve regurg &/or tricuspid (d/t chamber dilation) & valve leaflet thickening; mitral regurg leads to more LV overload...vicious cycle! |
| Dilated cardiomyopathy: Clinical synopsis | dyspnea on exertion, exercise intolerance, fatigue, chronic tachycardia (compensatory tachycardia to maintain CO); *systolic heart murmur (usu d/t mitral valve regurgitation)* |
| Dilated cardiomyopathy: Lab diagnosis | hypernatremia (d/t hyperaldosteronism) OR hyponatremia (d/t plasma vol expansion) may be present; *elevated serum B-type natriuretic peptide (BNP) --> most sensitive indicator of natriuretic peptides for CHF* |
| Common causes of secondary dilated cardiomyopathy | chronic HTN, ischemia, chronic alcoholism, cocaine, meth, mitral/aortic valve dx; post-viral myocarditis, chaga's, anemia, sarcoidosis, drug-related (doxorubicin), peripartum CM, thyrotoxicosis, amyloidosis, GSDs, Muscular dystrophy, thiamine def |
| Dilated cardiomyopathy: Clinical course | most progress to chronic CHF; inc incidence of sudden cardiac death d/t dysrhythmia; 5YS 50% (better prognosis for women) |
| Dilated cardiomyopathy: Variants - Familial | aka; hereditary DC; may account for 40% of all idiopathic dilated cardiomyopathies; may be sporadic, auto dom, auto rec, or X-linked |
| Hypertrophic Cardiomyopathy: Genetics | most auto dom w/variable expressivity; some sporatic; heterogenous w/>6genes on 4 chromosomes (sarcomeric ptns - myosin heavy beta chains, actin, tropomyosin) |
| Hypertrophic Cardiomyopathy: General Pathophysiology | several mechanisms; diastolic dysfxn d/t impaired LV filling; systolic dysfxn d/t abnml Ca kinetics & subendocardial ischemia; asymmetric septal hypertrophy a/w LV outflow obstruction & dec CO |
| Hypertrophic Cardiomyopathy: General Pathology | disorganized cardiocytes & myocardial muscle bundles (whorled pattern); interstitial/myocardial fibrosis; abnml intramural coronary aa w/dec lumen & thickening of vessel wall (intramyocardial sm vessel dx; usu ventricular septum a/w myocardial fibrosis) |
| Hypertrophic Cardiomyopathy: clinical course and sequelae | inc risk of death d/t strenuous exercise; **mc cause of sudden cardiac death in kids/teens*; CHF, chronic cardiac dysrhytmia |
| Hypertrophic Cardiomyopathy: variants - obstructive primary HCM | (aka: asymmetric septal hypertrophy, idiopathic subaortic stenosis, idiopathic hypertrophic subaortic stenosis); **systolic dysfxn predominates (LV outlfow obstruction dec CO, abnml Ca kinetics, subendocardial ischemia)*; diastolic dysfxn w/dec LV filling |
| Hypertrophic Cardiomyopathy: variants - Non-obstructive Primary HCM | (aka: concentric hypertrophic cardiomyopathy); more common than obstructive HCM; **predominately a diastolic dysfxn d/t impaired LV filling** |
| Secondary Hypertrophic Cardiomyopathy: common causes, course, sequelae | athletic training, hypertension, coarctation of aorta, aortic stenosis; course is similar to primary HCM (sudden cardiac death, CHF, dysrhytmia); changes d/t training are physiologic and will return to nml if training stops |
| Restrictive cardiomyopathy: common causes | idiopathic (primary); Acute/chronic myocarditis (idiopathic, infectious - chagas; sarcoidosis, loeffler's endomyocarditis); LVH; LV infiltrative disease (amyloidosis, glycogen storage dx, hemochromatosis); endocardial fibroelastosis |
| Restrictive cardiomyopathy: Pathophysiology | excessive rigidity of LV walls resulting in inability of LV to stretch during diastole leading to dysfxn in contraction & dec CO; bilat dilation; endomyocardial Bx shows thick endomyocardial fibroelastosis, chronic myocarditis or non-specific fibrosis |
| Restrictive cardiomyopathy: Clinical course and sequelae | progressive cardiac dysfxn ending in CHF (more rapid in younger pts); inc incidence of thromboembolic events in pts w/significant endomyocardial pathology; 5YS ~25% |
| Restrictive cardiomyopathy:Pathophysiology | replacement of portions of myocardial wall usu RV by fibrofatty tissue w/loss of cardiocytes; pulm circulation maintained by RA contraction (aka: Fontan heart); electrical instability, V-arrhythmias (PVCs, V-tach, V-fib) |
| Restrictive cardiomyopathy: Pathology | very characteristic gross features: large areas of RV wall are thinned and replaced w/pale, yellow-white fibroadipose tissue ("parchment change"); areas of smooth muscle may also be present in the areas of dysplastic myocardium; mc in RV (rare in LV) |
| Restrictive cardiomyopathy: Clinical synopsis and course | onset of symptoms usu in teens/young adult; palpitations, syncope, inverted T waves in anterior chest leads over RV; most pts (if they live thru abnml heart rhythms) develop various degrees of heart failure; inc incidence of tricuspid regurgitation |
| WHO Criteria for Obesity: Grade I | overweight; BMI: 25-29.9kg/m2 |
| WHO Criteria for Obesity: Grade 2 | obesity; BMI of 30-39.9kg/m2 |
| WHO Criteria for Obesity: Grade 3 | severe morbid obesity; BMI >40kg/m2 |
| Obesity Cardiomyopathy: Pathophysiology | probably related to elevated metabolic requirements and inc blood volume; possible mechanism for chronic hypoxia d/t chronic respiratory insufficiency d/t inhibition of respiratory movement from obesity (Pickwickian syndrome) |
| Obesity Cardiomyopathy: Pathology and Clinical course | cardiomegaly, LVH, dilated ventricular chambers, may be a/w fibrofatty change in SAN and AVN; inc incidence of primary cardiomyopathy, CHF, sudden cardiac death |
| Peripartum Cardiomyopathy | dilated cardiomyopathy leading to symptomatic systolic dysfxn in 3rd trimester of pregnancy or immediately postpartum w/o evidence of other caue; may occur in 1/1500 pregnancies; usu >30yo, inc in blacks; a/w *systolic dysfxn* |
| Peripartum Cardiomyopathy: Clinical course and sequelae | inc incidence of CHF d/t uterine contraction of 3-500mL blood into circulation; sudden cardiac death d/t dysrhythmia, thromboembolism d/t myocarditis & hypercoagulable blood; 40% return to nml; 1YS 60%; **avoid future pregnancy** |
| Common causes of Congestive Heart Failure | mc: coronary artery disease/ischemic cardiomyopathy; HTN (mc2); cardiomyopathy, aortic stenosis, coarctation of aorta, primary pulmonary HTN, pulm valve stenosis, myocarditis, cardiac dysrhythmia (atrial fib (mc)); anemia |
| Cardiac output and compensatory mechanism: Sympathetic Nervous System | inc HR (chronotropic) - inc CO; inc contractile strength (inotropic) - inc SV d/t inc shortening of myofibrils; stim peripheral vasculature (aa vasoconstrict in skin, skeletal mm, bowel, kidneys to shift blood to CNS, heart, lungs) & vv constrict to heart |
| Cardiac output and compensatory mechanism: Inc levels of circulating catecholamines | inc HR, inc contractility of heart, systemic vasoconstriction |
| Cardiac output and compensatory mechanism: Activation of renin-angiotensin-aldosterone system | effects of angiotensin II: vasoconstriction inc BP & slightly inc peripheral resistance; inc circulating aldosterone (causes kidneys to retain Na & water to expand blood plasma/vol) |
| Cardiac output and compensatory mechanism: Net result | increase CO back to normal; BUT...in diseased heart these mechanisms need to work on a min-min basis to maintain CO; they inc the heart's workload which is detrimental and produces further heart failure |
| Pathophysiology of the Compensatory Mechanisms in Heart Failure: effects of chonically elevated catecholamines and SNS stimulation | chronic vasoconstriction (chronic inc total peripheral resistance and elevated afterload; LVH); alteration in Ca metabolism in myocardium (depressed contractility, inability of myocardium to relax during diastole) |
| Pathophysiology of the Compensatory Mechanisms in Heart Failure: effects of chronic Renin-Angiotensin-Aldosterone Stimulation | chronic vasoconstriction (inc TPR afterload, LVH (dec angiogenesis, loss of cardiocites/gain of fibrosis; dysrhytmias: atrial-fib); Chonic inc blood vol (inc preload, inc TPR, inc afterload, LVH) |
| Pathophysiology of the Compensatory Mechanisms in Heart Failure: Effects of Left Ventricular Hypertrophy | failure of capillary ingrowth to support hypertrophied heart, leads to dec cardiocytes and inc fibrosis; predisposition to cardiac dysrhythmias (atrial-fibrillation) |
| Congestive Heart Failure: Clinical Synopsis | Dyspnea on exertion that can progress to dyspnea at rest; exercise intolerance, fatigue, chronic tachycardia to maintain CO, angina pectoris, peripheral edema |
| Congestive Heart Failure: Lab diagnosis | hypernatremia d/t hyperaldosteronism (more common than hyponatremia which is d/t volume expansion); elevated serum B-type natriuretic peptide (BNP); CXR: cardiomegaly; Echocardiography: dilated LV & LA, LV wall dysfxn, dec LV ejection fraction (<50%) |
| Congestive Heart Failure: Clinical course and sequelae | progressive debility leading to inability to walk or exercise; inc incidence of cardiac dysrhythmias, inc incidence od sudden cardiac death, 5YS 50% |
| Cor pulmonale | alteration in structure and fxn of RV d/t primary disorder of the respiratory system (ex: COPD (mc); pulmonary interstitial fibrosis, chronic bronchial asthma) |
| Cor pulmonale: Pathophysiology | elevated pulm arterial pressure (pulm HTN) leads to chronically inc work for RV, leading to RVH; progressive inc in pulm circulation pressures, RV fails d/t dec pulm blood flow, dec CO, systemic hypoxia, systemic edema) |
| Cor pulmonale: pathology and clinical synopsis | RVH, w/ or w/o RV dilation; excessive fatigue, SOB on exertion, near-syncope or syncope, ankle/pedal edema; hepatomegaly, *split S2, JVD, (uncommon: pleural effusions, ascites) |
| Cor pulmonale: Lab findings | EKG (RVH, P-pulmonale enlarged P wave d/t RA dilation); CXR (prominent hilar vessels-pulm aa; cardiomegaly; RV shadow); 2-D echocardiogram (RVH, paradoxical motion if IV septum - buldge into LV during sytole; doppler - inc R IV/pulm outlfow press, RV dil) |
| Cor pulmonale: clinical course and sequelae | dec RV cardiac output leads to dec pulm blood flow & systemic hypoxia; Inc systemic venous pressure leads to ascites, chronic passive liver congestion, cardiac cirrhosis; peripheral edema; 5YS 30% |
| Dysrhythmias: common causes | hypoxia, ischemia, electrolyte imbalances, drug side effects |
| Disorders of impuls origination: Common Causes of Ectopic Pacemakers | damaged/dysfxnl sinus node; emergence of excitable focus in atria or ventricles (PVCs, PACs, premature nodal contractions); HTN, hypoxia, electrolye imbalance (K, Ca, Na, Mg), drug-related |
| Pathophysiology of sinus node dysfxn | usu d/t ageing or atherosclerosis of nodal artery; if sinus node is damaged, the AV node (40-60bpm) or Purkinje fibers (15-40bpm) take over; these escape rhythms are slower and lead to dec CO |
| Pathophysiology of ectopic foci | enhanced or localized depolarization of segments of conduction system or myocardium; ectopic beats (atrial or ventricular) are common and alone do not imply underlying disease; inc risk of initiating sustained re-entry tachycardias |
| Disorders of Impulse Conduction: Pre-excitation syndromes | Wolf-Parkinson-White: 1 in 400; accessory tract links atria w/ventricles (Kent/Mahaim fibers) bypasses AV node w/diff conduction properties & refractory periods, facilitates reentry; abnml tahyarrhythmias d/t dual conduction; *recurrent A-fib, A-flutter* |
| Disorders of Impulse Conduction: Common Causes of Re-entry Dysrhytmias | ischemic heart disease (mc); cardiomyopathy w/cardiomegaly; electrolyte imbalances, drug effect; *loss of atrial contribution to ventricular filling, dec ventricular filling, dec CO* |
| Disorders of Impulse Conduction: Pathophysiology of Re-entry Dysrhythmias | d/t circular electrical impulse w/in heart; conduction system is slow & part of impuls arrives late so heart treats it as new impulse that spreads abnml paths, leading to re-entry circuits; originate from border zone btw scarred & active myocardial tissue |
| Disorders of Impulse Conduction: Clinical Course of Re-entry Dysrhythmias - Atrial Fibrillation | loss of 15% of diastolic filling of ventricles d/t loss of atrial contraction; has a propensity to from atrial thrombosis that embolizes in pulmonary or systemic circulation |
| Disorders of Impulse Conduction: Clinical Course of Re-entry Dysrhythmias - Ventricular Tachycardia and V-Fib | lack of an "atrial kick"; dec CO, often degenerates to ventricular fibrillation (the complete absence of cardiac output) |
| Thrombophlebitis: Risk Factors | prolonged bed rest, vascular injury (IV cannulation, IV diagnostic procedures, traumatic injury, IVDA); Malignancy (lung, ovary, brain); Thrombophilia (Factor V Leiden, Antithrombin III Def, Ptn C or Ptn S Def) |
| Thrombophlebitis: General Pathophysiology | "Virchow's Triad" - flow stasis, hypercoagulability, vessel wall injury; w/o endothelial injury it will rarely occur; endothelial injury initiates inflam and platelet adhesion; pts w/superficial thrombophlebitis often have deep vein too |
| Superficial Venous Thrombophlebitis | most have associated deep vein thrombophlebitis; leg pain, localized erythema and edema a/w palpable venous induration |
| Deep Vein Thrombophlebitis - Clinical synopsis | low grade fever, unilat leg edema, soft tissue tenderness, Homan's Sign (tenderness w/dorsiflexion of foot); superficial thrombophlebitis |
| Deep Vein Thrombophlebitis - Lab findings and clinical course | elevated serum D-dimer (fibrin degredation product indicating active thrombolysis); few calf vein infxns progress to DVTs of upper leg; 1 in 6 pts w/DVT of upper leg veins develop pulmonary thromboembolism |
| Deep vein thrombophlebitis: Sequelae | 1. Pulm embolism does NOT occur w/superficial cases; 2. Postphlebitis Syndrome - occurs in 50%, valvular damage in vv causes peripheral venous insufficiency (chronic edema, discoloration, ulceration) |
| Venous Thromboembolism: Pathophysiology | originates in deep vv of lower extremities; mc d/t bed rest or prolonged inactivity; pelvic vv - commonly postpartum; embolizes to pulmonary circulation |
| Venous Thromboembolism: Pathology | gritty, may or may not have lines of Zahn, adherent to luminal endothelium (esp if thrombophlebitis inflam is present); higher [ ] of RBCs than arterial thromboemboli (darker and more homogenous) |
| Arterial Thromboembolism: Pathophysiology | originates in arterial system on endocardial surfaces (atrial fibrillation, mitral stenosis, MI) or Luminal surfaces of carotid aa; embolize to middle cerebral a, mesenteric or renal aa, gangrene of digits |
| Arterial Thromboembolism: Pathology | lines of Zahn are common; adherent to luminal endothelium, gritty in consistency |
| Clinical Course and Sequelae of Thromboembolism | 1. dissolution (d/t fibrinolysis); 2. Partial dissolution, organization or recanulization (freq in coronary aa, new lumen is narrower); 3. Tissue/organ infarct (size of infarct depends on size of thromboembolus & collateral flow); 5. death (lung) or CVA |
| Paradoxical Thromboembolism | originates in venous (Right heart circulation) and embolizes thru a R-->L shunt (atrial septal defect (mc), or VSD) causing damage in systemic arterial circulation; (normally, thromboemboli originate in venous circulation and lodge in lungs as PE) |
| Atherosclerotic Plaque Embolism (cholesterol embolism syndrome): Common Causes | vascular diagnostic/surgical procedure (mc) (aortic aneurysm repair, carotid endarterectomy, diagnostic ateriography, coronary a. angioplasty, renal a. angioplasty); aortic aneurysm, aortic dissection |
| Atherosclerotic Plaque Embolism (cholesterol embolism syndrome): Pathophysiology | chol crystals break off from atherosclerotic plaques & enter downstream organs, occlude arterioles & sm arteries; induce inflam rxn, adventitial fibrosis that occludes lumen; local inflam rxn (vasospastiv mediators & tissue ischemia = organ damage/infarct |
| Atherosclerotic Plaque Embolism (cholesterol embolism syndrome): Clinical Triad | renal failure (or multi-organ dysfunction), HTN, distal ischemic injury (CVA, extremity ischemia (livedo reticularis on skin or focal gangrene) |
| Atherosclerotic Plaque Embolism (cholesterol embolism syndrome): Lab findings | peripheral blood eosinophilia; elevated BUN and creatinine, hematuria, dec total complement, elevated C-reactive ptn |
| Atherosclerotic Plaque Embolism (cholesterol embolism syndrome): Clinical course and sequelae | emboli don't reach lung, but inflam mediators released from ischemic tissue may result in acute lung injury causing Diffuse Alveolar Damage and manifestation of Acute Respiratory Distress Syndrome; mortality: 20-90% |
| Vasculitis: Polyarteritis Nodosa Pathophysiology | big inc circulating alpha-interferon & IL-2; mild inc TNF-a, IL-1b; 30% w/HBV, HCV Ab-Ag complexes; develops from immune complex deposition (type III hypersensitivity); few w/anti-ANCA (antineutrophil cytoplas); multiorgan dysfxn from systemic vasculitis |
| Organs affected by Polyarteritis Nodosa | renal system (60%) - progressive renal failure; Skin (40%) - purpura, nodules, cut infarcts, livido reticularis, non-spec rashes, Raynaud; CNS (25%) - vasculitis & CVA; CV system (25%) - myocarditis; Musculoskeletal system |
| Polyarteritis Nodosa: Clinical Synopsis, course, sequelae | fever, wt loss, diffuse myalgias, HTN, livedo reticularis, renal failure; Inc incidence of: med-large artery aneurysms, renal failure, CVA, bowel infarcts, myocardial infarct; mortality 25% w/aggressive Rx |
| Churg-Strauss Syndrome: Pathophysiology | pulm sm vessel inflam (vasculitis) a/w necrosis, granulomatous inflam in & around blood vessels & w/in lung parenchyma; inflam of sm-med non-pulm vessels (systemic vasculitis) esp in kidneys (glomerulonephritis) |
| Churg-Strauss Syndrome: Clinical synopsis, course, sequelae | fever, myalgias, wt loss, recurrent bronchospasm (asthma), chronic sinusitis, hemoptysis, renal failure, cut purpura, livedo reticularis; coronary arteritis in minority a/w AMI, high mortality w/o Tx; 5YS 65% w/Rx |
| Wegener Granulomatosis: Pathophysiology | autoimmune inflam w/anti-ANCA (antineutrophil cytoplasmic antibodies) directed at neutrophil proteinase 3 (PR-3); activated PMNs target endothelium, damage = inflam mediators, monocyte, Tcell recruitment and more damage |
| Wegener's Granulomatosis: Pathology | necrotizing granulomatous lesions of upper or lower respiratory tract; necrotizing vasculitis w/acute and chronic inflam cells and vessels destruction (sinuses, upper airways, necrotizing glomerulonephritis; pulm dx can occur w/o renal-"Regional Wegeners" |
| Wegener's Granulomatosis: Clinical Synopsis | fever, wt loss, arthralgias, chronic sinusitis, chronic nasal discharge, recurrent otitis media, recurrent oropharyngeal ulcerations, chronic cough, livedo reticularis, recurrent cut purpura/ulceration on lower extremities, renal failure |
| Wegener's Granulomatosis: Lab findings | anti-ANCA; elevated ESR, elevated BUN and creatinine; X-ray: pulmonary infiltrates and sinusitis |
| Wegener's Granulomatosis: Clinical course and sequelae | progressive renal failure, inc incidence of infectious pneumonia, inc incidence of tracheal stenosis d/t chronic inflam; w/o Tx 1YS 20%; immune suppressive Rx allows high 5YS |
| Wegener's Granulomatosis: On the Boards!! | Wegener granulomatosis, Churg-Strauss Syndrome and Microscopic Polyangiitis often manifest antibodies to neutrophil cytoplasmic antigens: ANCA |
| Temporal Arteritis: Pathophysiology | chronic inflam in temporal aa (other vessels such as aorta & intracerebral aa); mononuclear cell infiltration often a/w multi-nucleate giant cells; *thickening/sclerosis of tunica intima & media* d/t cell-mediated response to Ag near elastic arterial wall |
| Temporal Arteritis: Clinical Synopsis | unilat headache, onset of amblyopia w/compromise of ophthamlic a circulation; palpatory tenderness over temporal a; few have polymyalgia rheumatica as prodrome or associated disease |
| Temporal Arteritis: lab findings | markedly elevated ESR; elevated C-reactive ptn, elevated liver enzymes (ALT, AST) |
| Temporal Arteritis: Clinical course, sequelae | most develop visual loss w/o Rx; inc incidence of aortic aneurysm; inc incidence of CVA |
| Kawasaki's Disease: Pathophysiology | probably d/t infectious etiology d/t periodic epidemics w/geographic spread; systemic vasculitis of med sized arteries d/t immune system hyper-reaction (infiltrate of CD4 cells); proinflam cell-med rxn triggered by unknown antigen or superantigen |
| Kawasaki's Disease: Clinical synopsis | abrupt onset of fever, edematous and cracked lips, bilat conjunctivitis, exanthem & desquamation, cervical adenopathy, acral erythema and swelling |
| Kawasaki's Disease: Lab findings | elevated ESR, liver enzymes (ALT, AST), platelet count after several wks |
| Kawasaki's Disease: Clinical course, sequelae | most resolve spontaneously; 25% develop acquired heart disease (coronary artery aneurysm (mc); myocarditis, valvulitis); **it is the most common cause of acquired heart disease in children**; there in an inc incidence of chronic non-specific arthritis |
| Raynaud's Disease | (idiopathic or primary); recurrent vasospasm of sm arteries/arterioles followed by vasodilation; usu young women initiated by cold exposure; period of pallor/pain in digits followed by erythema |
| Raynaud's Phenomenon | secondary raynaud's disease; vasospasm/vasodilation of small arteries/arterioles; occurs in a/w underlying disease, usu autoimmune (SLE, Scleroderma (PSS)) |
| Immune Complex Vasculitis: Pathophysiology | type III immune complex deposition; vasculitis d/t deposition in sm vessels and capillaries (IgA and activated C3); >95% resolve spontaneously; few develop chronic renal failure d/t glomerulonephritis |
| Serum Sickness: common causes | meds (act ast haptens that bind to endogenous ptns which invoke antibody formation and immune complex deposition); IV antitoxin Rx (anti-rabies, anti-tetanus, anti-snake venom) |
| Serum sickness: Pathophysiology | antibodies bind to foreign ptns leading to immune complex formation; vascular deposition of immune complexes (type III hypersensitivity) leads to complement fixation, recruitment of PMNs, cytokine production, tissue damage from inflammtion |
| Serum sickness: clinical synopsis, course, sequelae | fever, urticaria, erythematous rash, generalized lymphadenopathy, arthritis, erythema multiforme, glomerulonephritis; almost all resolve spontaneously, inc incidence of renal failure d/t glomerulonephritis |
| Non-cyanotic Congenital Heart Disease | mc: aortic stenosis and coarctation of the aorta; no significant L-->R or R-->L shunts |
| Occurance of Congenital Heart Disease | Ventricular septal defect (40%); Patent Ductus Arteriosus (12%); Atrial Septal Defect Ostium Secundum type (8%); Atrial Septal Defect Ostium Primum type (8%); Coarctation of Aorta (8%); Aortic Stenosis (8%); Pulmonary Stenosis (8%) |
| Ventricular Septal Defect: Pathophysiology | any part of ventricular septum fails to close after 7th wk gestation; large or small; L-->R shunt may or may not present (CHF delayed to 2nd-3rd mo of life); Inc pressure in R heart/pulm vasculature R heart overload and pulm HTN; inc vol to LV & dec CO |
| Ventricular Septal Defect: Clinical Synopsis | symptoms depend on size of L-->R shunt; cyanosis depends on size of shunt; FTT; tachypnea; diaphroesis; dyspnea on exertion progressing to fatigue; *holosystolic murmur may not present if VSD is very large* |
| Ventricular Septal Defect: Clinical Course and Sequelae | inc incidence of pulm HTN leads to RV failure; Eisenmenger complex (acute onset of R-->L shunting; reversal of L-->R when pressure of pulm circulation excedes the LH pressure; acute systemic hypoxia & cyanosis d/t deO2 blood in LV); LHF; good Px w/surgery |
| Patent Ductus Arteriosus: Pathophysiology | delay or failure in closure of ductus arteriosus; prolonged patency at higher altitudes and a/w congenital rubella infxn; few have L-->R shunt leading to: inc vol/pressure in RV & pulm circulation & inc vol to LV |
| Patent Ductus Arteriosus: Clinical Synopsis | varies w/size of L-->R shunt (few are asymptomatic); may be cyanotic depending on size of shunt; FTT, tachypnea, *continuous (machine-like) systolic murmur* that can involve diastole |
| Patent Ductus Arteriosus: CXR | prominence of pulmonary trunk; cardiomegaly |
| Patent Ductus Arteriosus: Clinical course, sequelae | inc incidence of pulm HTN leading to RVF; inc incidence of LVF; excellent Px w/surgery; significant morbidity and dec lifespan w/o surgery |
| Atrial Septal Defect: Pathophysiology | atrial setum forms btw 4th and 5th wk; w/any AST a L-->R shunt can develop d/t inc LA pressure as pulm resistance falls and RV becomes more compliant after birth; L-->R shunt presence depends on size of defect and may not show till 6-8wks old w/CHF |
| Atrial Septal Defect: Anatomic typology - Ostium Secundum | mc & least serious type; located in central portion of interarterial septum in area of fossa ovali; usu not a/w significant probs; most pts do not require surgery; can account for paradoxical embolization in adults |
| Atrial Septal Defect: Clinical Synopsis | most are asymptomatic; systolic ejection murmur may be present; if significant L-->R shunt pt may have: FTT, slowly progressive dyspnea --> pulm HTN and RV failure |
| Atrial Septal Defect: Clinical Course, Sequelae | 1 in 6 pts w/ ASD-OS undergo spontaneous closure by 5yo; inc incidence of cardiac dysrhythmias d/t abnml conduction system; few develop significant L-->R shunts w/progressive pulm HTN |
| Atrial Septal Defect: Note | in severe congenl heart defects, survival is dependent on open fossa ovalis (ASD, secundum) or ductus arteriosus (tricuspid atresia or mitral valve atresia); when both avenues of R-->L shunting are closed, the pt has sudden loss of CO & terminal hypoxemia |
| Coarctation of the Aorta: Pathophysiology | narrowing of aorta mc distal to L subclavian a (abnml development of L-4th/6th aortic arches); causes inc pressure for LV to pump against (inc afterload); dec flow to systemic circulation esp limbs; ductus arteriosus is bypass till closure/decompensation |
| Coarctation of the Aorta: Pathology | d/t marked ridgelike thickening of aortic wall media; opposite to insertion of PDA/ligamentum arteriosum (becomes obstruction when patent ductus involutes); defect in vessel media = posterior infold (post shelf) that may extend around entire aorta |
| Coarctation of the Aorta: Clinical Synopsis in Neonates | cyanosis depends on degree of stenosis (differential: upper limbs pink. lower blue); dec peripheral pulses; tachycardia; tachypnea; lethargy d/t hypoxemia; systolic ejection murmur in L chest area |
| Coarctation of the Aorta: Clinical Synopsis in Childhood | usu presents during childhood; dyspnea (during exertion if mild stenosis or at rest if severe); angina pectoris, chronic HTN, marked BP differences btw upper & lower limbs if coarcted segment is aortic arch; systolic ejection murmur diminishes w/LVF |
| Coarctation of the Aorta: Clinical Course, Sequelae | if prox to ductus arteriosus neonatal acute CHF w/closure; inc LHF & CHF; chronic systemic HTN (d/t RAA-activity d/t dec renal flow); inc aortic/cerebral aneurysm; inc spinal cord infarct/paraplegia; Turners; dec life w/o surgery; excellent w/surgery |
| Aortic Stenosis: Pathophysiolgoy | obstruction to LV outflow leading to low CO and dec perfusion thru coronary aa; enlargement d/t combo of dilation & compensatory LVH |
| Aortic Stenosis: Clinical Synopsis in Neonates | may be cyanotic depending on severity of stenosis; dec peripheral pulses; tachycardia; tachypnea; lethargy d/t hypoxemia; *systolic ejection murmur at L upper sternal border* |
| Aortic Stenosis: Clinical Synopsis in Childhood | usu presents in childhood; dyspnea on exertion or at rest depending on severity; angina pectoris; systolic ejection murmur at L upper sternal border dec w/development of LVF; CXR shows cardiomegaly |
| Aortic Stenosis: Clinical Course, Sequelae | if severe, CHF develops after birth when ductus arteriosus closes (leads to acute drop in blood reaching aorta); most progress to severe stenosis but depends on pressure gradient across aortic valve; inc incidence of sudden cardiac death |
| Pulmonary Stenosis: Pathophysiology/Pathology | valvular type (mc); d/t fusion of leaflet commissures = thick, domed valve; dec RV output to pulm circulation; inc RV pressure; RV dilation; RA dilation |
| Pulmonary Stenosis: Clinical Synopsis | **usu acyanotic** but can be cyanotic if stenosis is severe; dyspnea (depends on severity); systolic ejection murmur at L upper sternal border; CXR: prominent pulmonary trunk |
| Pulmonary Stenosis: Clinical Course, Sequelae | variable depending on pressure gradient across pulm valve (as measured via cardiac catheterization: No probs if <25mmHg; Unpredictable if 26-40mmHg; Progression to RVF if >41mmHg); excellent prognosis w/Rx |
| Eisenmenger's Syndrome | sudden change from a L-->R to a R-->L shunt; reversal thru a PDA, ASD or VSD d/t pathological changes of prolonged pulmonary hypertension |
| Genetic Diseases Commonly a/w Congenital Heart Defects | Trisomy 18, 13 and 21; Cri du chat syndrome (Chrom 5 deletion); Monosomy X (Turner); |
| Genetic Diseases and Congen Heart Defects: On the Boards!! | VSD is mc type of defect in genetic disease pts EXCEPT Turner, with is Coarctation of the Aorta!! |
| Pericardial Effusion: Hydropericardium | accum of serous fluid in pericardial sac d/t Transudate [(mc) low cell & ptn content; ultrafiltrate of plasma d/t imbalance of hydrostatic forces usu d/t CHF) or Exudates (high cell & ptn content; indicative of pericardial dx such as infxn, AI or cancer) |
| Pericardial Effusion: Hemopericardium | accumulation of blood in pericardial sac; d/t ventricular rupture (mc); aortic dissection, angioplasty; trauma; may progress to cardiac tamponade depending on volume of accumulation |
| Cardiac Tamponade: Pathophysiology | fluid fills pericardial sac; slow filling stretches sac to accomodate 12oz; pressure rises and constricts heart; impairs ventricular filling (dec CO, dec systemic BP, generalized hypoxia) |
| Cardiac Tamponade: Clinical Synopsis | Beck Triad (hypotension, inc JVD, diminished heart sounds); Pulsus Paradoxus (exaggerated, >12mmHg, of nml inspiratory dec in systolic bp); Kussmaul sign (inc JVD w/inspiration) |
| Cardiac Tamponade: Echocardiography Findings, Clinical Course, Sequelae | fluid distending the pericardial sac, collaps of ventricular walls during diastole; significant risk of sudden death unless pericadial fluid is removed! |
| Acute Pericarditis: Comon Causes | idiopathic (primary, mc); Uremia (mc2); metastatic (mc3); Infectious (mc4; bacterial, viral, TB, fungal, parasitic - protozoan/metazoan) |
| Acute Pericarditis: General Pathophysiology | commonly a/w hydropericardium (exudative type); rich in fibrin, ptn and inflam cells; (infrequently a/w hemorrhage) |
| Acute Pericarditis: Selected Pathophysiologies - Acute uremic Pericarditis | elevated levels of circulating urea cause an inflam pericarditis in addition to being toxic to other tissues |
| Acute Pericarditis: Selected Pathophysiologies - Acute Bacterial Pericarditis | usu lymphatic or hematogenous spread in the context of sepsis |
| Acute Pericarditis: Clinical synopsis, course, sequelae | chest pain, pericardial friction rub; most resolve spontaneously; few develop cardiac tamponade, few evolve into chronic pericarditis |
| Constrictive Pericarditis: Pathophysiology/Pathology | evolution of pericarditis from acute to chronic to constrictive; severe fibrous thickening of pericardium; venous return to heart is dec; dec diastolic filling, inc ventricular end-diastolic & pulm vascular pressure; dec CO (CHF d/t inability to inc SV) |
| Constrictive Pericarditis: Clinical Synopsis | elevated JVD, compensatory tachycardia; acral cyanosos (d/t low CO and chronic hypoxemia) |
Created by:
bscaryp