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81 Cards in this Set
- Front
- Back
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Cardiac Structure
A. myocardium: structures B. valves: pathologic changes C. Conduction system D. bloodsupply |
A. sacromere = contractile unit wiht regulatory protein troponin and tropomyosin
- atrial myocytes have specific atrial granules with ANP B. leaflets (tricuspid/mitral) vs cusps (aortic/pulmonary) - damage to collagen (MVP), nodular clacification, fibrotic thickening (rheumatic heart dz) C. SA node (atria, SVC) --> AV --> bundle of His D. oxidative phosphorylation. LAD, LCX, RCA |
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Heart Failure = Congestive Heart Failure
A. def B. adaptation C types |
A. heart unable to pump blood to meet metabolic demands
B. Frank-Starling mehcanism - myocardial adaption (hypertrophy, dilation) - activation o fneurohumoral system (NOEPI, RAAAR) C. cardiac hypertrophy (compensatory response of myocardium to incr mechanical work) - Righ sided heart failure - left sided heart failure |
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Cardiac hypertrophy
A. types B. progression to failure C. types of cardiac dysfxn |
A. pressure overload hypertrophy: concentric incr
- volume-overload hypertrophy: dilation B. incr in myocyte size not accompanied by pincr in capillaries --> decompensation, fibrosis, induction of fetal gene program C. arrhythmias, heart failure, neurohumoral stimulation |
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Left-sided heart failure
A. morphology conseq of heart B. "" of lungs C. clinical sx |
A. LV hypertrophied
- LA dilation = risk of atrial fibrillation + thrombus form B. pulmonary congestion + edema - heart failure cells = hemosiderin-laden macrophages C. cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea |
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Left-sided HF
A. types B. misc consequences |
A. Systolif failure: pump failure
- diastolic failure: LV stiff = unable to incr output in response to demand (exercise) -> flash pulmonary edema B. decr in renal perfusion --> RAAS --> RETENTION OF SALT/WATER = worsen pulmonary edema - in sever hypoperfusion, azotemia (impaired nitrogenous waste excretion) + hypoxic encephalopathy |
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Right-sided heart failure
A. etiology B. morphologic changes in heart C. "" in liver/portal system |
A. caused by left-sided HF
- cor pulmonale: pure right HF caused by parenchymal lung dz B. hypertorphy + dilation of RA + RV C. congestive hepatomegaly sec to pasive congestion in central veins = "nutmeg liver" - long-term --> cardiac sclerosis (fibrotic) + centrilobular necrosis --> cardiac cirrhosis |
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Right-sided HF
A. morphologic changes in spaces B. "" in subcutaneous tissues C. morphology summary |
A. fluid accumation
B. ankle and pretibial edema = hallmark C. pulmonary congestion mini but systemic and portal venous sytsem pronounced. congestion of kidne more marked, and more azotemia |
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Heart failure
A. pharm treatments |
- fluid overload (diuretics
- block RAAAS (angiotensin converting enzyme inhibitors) - lower adrenergic tone (beta-1-adrenergic blockers |
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cardiac Development
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1. 3 sources: 1st and 2nd heart field from lateral mesoderm
2. FHF = crscent shape in anterior; SHF dorsal to FHF 3. SHF migrate into anterior and posterior ends of tube = RV, conotruncus and part of atria 4. FHf = LV 5. rightward looping of heart tube 6. cardiac neural crest migrate in outflow tract = septate outflow tract and pattern symmetic aortic arch arteries 7. note ECM underlying the AV caal and outlfow tract produce endocardial cushions |
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Congential Heart Disease
A. right-to-left shunts B. obstructive C. Left-to-right shunt D. define atresia |
A. TOF, transposition of great arteries, persistant truncus arteriosus, tricuspid atresia and TAPVC
B. coarctation, pulmonary stenosis/atresia, aortic stenosis/atresia C. ASD, VSD, patent ductus arteriosus D. complete obstruction |
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A. Right-to-Left Shunts consequences
B. left-to-right shunt consequences |
A. emboli bypass lungs and enter systemic = paradoxical embolism = brain infarction
- hypertrophic osteoarthropathy = clubbing of fingers/toes - polythemia B. incr pulmonary blood flow (no cyanosis) - RV hypertrophy and atherosclerosis of pulmonary vasculaure (vasoconstriction and medial hypertrophy) - eisenmenger syndrome |
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Atrial septal defect
A. most common type B. murmur C. clinical presentation |
A. secundum ASD
B. pulmonary valve b/c xcessive flow - systolic ejection murmur mid-left SB + ULSB - fixed split S2 - diastolic rumble LLSB C. well tolerated, asym, pulmonary HTN unsusual |
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Patent Foramen Ovale
A. change from fetus B. clinical scenerio |
A. in fetus, right to left shunt
B. opens even in transient incr in R pressures = bowel mvmt, coughing, sneezing |
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Ventricular septal defect
A. most common location B. murmur |
A. membranous interventricular septum
B. smaller the VSD the more thrill the murmur - holosystolic murmur LLSB - diastolic rumble at apex if pulmoanry flow high |
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Patent Ductus Arteriosus
A. murmur |
- continuous at ULSB (machine-like)
- brisk pulses |
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AV septal defect
A. etiology B. pathophsio |
A. failure of superior & inferior endocardial cusio nof AV canal to fuse
B. malformation of tricuspid and mitral valves - incomplete AV septum - all 4 cardiac chambers freely communicate = volume hypertrophy in all (Down syn) |
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Tetralogy of Fallot
A x-ray image B. cardinal features C. murmur |
A. boot-shaped
B. VSD, subpulmonary stenosis, overriding aorta from VSD, RV hypertrophy C. systolic ejection murmur of pulmonary stenosis |
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Tetralogy of Fallot
A. pathogenesis |
- subpulmonic stenosis --> pulmonary arteries hypoplastic(= RV failure rare) --> aorta larger
- child grows --> pulmonic orific e no expand = obstruciton worse |
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Transposition of great arteries
A. physiology B. murmur |
A. RV hypertorphy; LV atrophic
B. no murmur; single S2 |
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Persistent Truncus Arteriosus
A. pathophysio B. murmur |
A. failure separation of aorta & pulmonary --> systemic cyanosis + incr pulmonary blood flow
B. single S2 - systolic ejection murmur along LSB - diastolic murmur at apex |
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Tricuspid Atresia
A. pathophysio B. murmur |
A. no tricuspid --> RV hypoplasia --> cyanosis (VSD)
B. no murmur - signle S2 if no VSD - if VSD, systolic murmur like VSD |
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Total Anomalous Pulmonary Venous Connection
A. pathophysio B. murmur |
A. PV not join LA --> volume/pressure hypertrophy & dilation of right side
- dilation of plumonary trunk - RA hypoplastic (ASD must) but nl LV B. pulmonaryejection murmur along left sternal border |
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Coarctation of Aorta
A. types B. association C. exam findings |
A. infantile form = proxima
= adult form = folding opposite ductus arteriosus distal to arch B. Turner syndrom, bicuspid aortic valve C. only in those w/o patent ductus arteriosus: - elevated BP (right arm) - reduced BP in legs - dampened/delayed femoral pulse - bruit left upper back - rib notching = collateral arteries |
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Coarctation of aorta
- sx FOR W/ PATENT DUCTUS ARTERIOSUS |
- bad prognosis
- delivery of unsat blood through patent ducts arteriosus = cyanosis localized to lower half of body |
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pulmonary stenosis/atresia
A. physio consequences B. murmur |
A. RV hypertrophy
- poststenotic dilation of pulmonary artery b/c jetting of blood - if completely atretic = ASD, hypoplastic RV = blood reac through PDA B. ejection click - systolic ejection murmur at ULSB |
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Aortic Stenosis
A. hypoplastic left heart syndrome B. subartic stenosis C. supravlvular aortic stenosis |
A. hypoplasia of LV and ascending aorta
- ductus open to allow blood flow to aorta and coronaries B. thickened ring or colar of dense endocardial fibrous tissue below cusp C. ascending aortic wall thickened = luminal constriction |
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Aortic stenosis
A. murmur |
- ejectionclick
- systolic ejection murmur at base with radiation to URSB, apex, suprasternal notch and cortids - thrill URSB and suprsternal notch |
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Ischemic Heart Disease
A. vs hypoxia B. another name C. consequences of myocadia ischemia |
A. hypoxia more tolerated b/c ischemia also reduce nutrients delivery
B. coronary artery disease C. stable angina, unstable angina (plaque rupture) -myocardial infarction - sudden cardiac death (disrupted plaque -> regional myocardial ischemia -> ventricular arrhythmia |
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Angina pectoris
A. clinical sx B. types |
A. constricting, squeezing, knife-like chest discomfort
B. stable angina: imbalance in coronary perfusion relative to myocardial demand. tx = nitroglycerin vasodilator - prinzmetal variant angina: coronary artery spasm unrelated to physical activity. tx: nitroglycerin, Ca blocker - unstable angina: incr freq pain during exercise/rest caused by disruption of atherosclerotic plaque with superimposed mural thrombosis |
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Myocardial infarction
A pathogenesis (coronary arterial occlusion) |
1. intraplaque hemorrhage
2. platelets adhere, release granules and form microthrombi 3. vasospasm by mediators from platelets 4. tissue factor activates coagulation pathway = enlarge thrombus that occlude vessels |
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MI
A. acute changes after MI B. irrev change |
A. no aerobic = no ATP = acute HF + myocardial cell death
- hallmark: loss integrity of sarcolemmal membrane B. only after 2-4 hrs - first in subendocardial zone (1/3 - 1/2 myocardial wall) = non-ST elevation infarct - transmural infarct = ST elevation infarcts |
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MI
A. supply of LAD B. supply of LCX C. supply of RCA |
A. apex, anterior wall of LV, anterior 2/3 of vent septum
B. lateral wall of LV C. entire RV, posterobasal of LV and posterior 1/3 of V septum |
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MI Morphology
A. 2-3 hrs B. 6-12 hrs C. 1-3 days |
A. use triphenyltetrazolium chloride
- nl tissue has dehydrogenase = red color - infarct tissue leaked dehydrogenase = unstained pale B. wavy fibers = forceful systolic tugs of viable fibers on dead fibers - myocytolysis: vacuolar degen = large vacuolar spaces within cells C. acute inflammation, macrophages remove necrosis |
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MI morphology
A. 7- 10 days B. extension morphology |
A. ingrowth of granulation tissue at periphery
B. repetivitive necrosis of adjacent regions - central zone of healing more advanced than perihery |
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MI - reperfusion
A. consequencies |
- arrhythmias
- myocardial hemorhag ew/ contraction bands = eosinophilic intracellular strips of packed sarcomeres from xagerrated contraciton of myofibers when perfusion established - microvascular injury: hemorrahge + endothelial swelling that further occludes capillaries - myocardial stunning: prolonged ischemic dysfxn |
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MI
A. clinical sx B. lab dx |
A. rapid, weak pulse + profuse sweating (diaphoresis)
- dypnea (pulm congestion from decr heart contraction) B. myoglobin first --> CK-MB (sensitive but no specific b/c elevated in skeletal injury) - troponin and CK-MB peak earlier in pts with hearts reperfused b/c washe dout necrotic tissue - troponin persist longer - most sensitive nad specific = troponin I and T |
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MI
- medications |
- aspirin, heparin to prevent thrombosis
- oxygen - nitrates (vasodilation and reverse vasospasm) - beta adrenergic inhibitors - beta-blockers (dim cardiac O2 demand and decr arrythmias) - ACE inhibitors to limit ventricular dilation |
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Mi
- complications |
- myocardial rupture
- arrhythmias - pericarditis - infarct expansion/extension - mural thrombus - ventricular aneurysm - anterior transmural infarcts = risk for free-wall rupture, mural thrombi, aneurysm - posterior transmural infact cause conduciton blocks |
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Chronic IHD = ischemic cardiomyopathy
A. def B. mrophology macro C. micro morphology |
A. HF as conseq of ischemic myocardial damage
B. LV hypertrophy, mural thrombi C. subendo vacuolization, fibrosis |
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Sudden cardiac death
A. common cause B. predispositions |
A. arrhythmias (ventricular fibrillation)
B. long QT syndrome, Wolff-Parkinson-White, - channelopathies (KCNQ1 gene mutation = K channel) |
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Hypertensive Heard Disease
A. 2 types |
1. Systemic (left-sided) HHD: LV hypertrpy (concentric) in absence of cardio pathology + hx of HTN
2. Cor Pulmonale (pulmonary HHD): pressure overload of RV = LV hypertrophy/dilation - acute cor pulmonale: dilation of RV w/o hypertrophy - chronic: RV hypertrophy --> fat in wall disappears and myoctyes aligned circumferentially instead of haphazardly |
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Valvular Heart disease
A. 2 types and causes B. MCC aortic stenosis C. MCC aortic insuf D. MCC mitral stenosis E. MCC mitral insufficiency |
A. stenosis = impedes forward flow --> pressure overload
insuf --> volume overload = regurgitation functional regurg: stem from abnl structure B. calcifcation or congenital bicuspid valve C. dilation of acendign aorta related to HTN/age D. rheumatic heart disease E. myxomatous (tumor of conn tissue) degen (MVP) |
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Calcific Aortic stenosis
A. vs atherosclerosis B. morphology C. vs rheumatic aortic stenosis |
A. instead of SMC, valves contain osteoblasts that syn bone matrix for calcium salts
B. heaped-up calcified masses that protrud and prevent opening of cusps. free cusp edges not involved C. no commissural fusion and no mitral valve abnl |
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Calcific stenosis of bicuspid aortic valve
A. anatomy |
A. cusp of unequal size with larger cusp ahs midline raphe which is site of calcific deposits
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Mitral annular calcifcation
A. consequences |
- regug by interfer contraction of valve ring
- stenosis by impir opening of mitral leaflets - arrhythmias - site of thrombi that embolize = stroke - nidus for infective endocarditis |
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Mitral Valve Prolapse (myxomatous degen)
A. def B. morphology |
A. leaflets balloon back into left atrium in systole
B. attenuation of collagenous fibrosa layer of valve - marked thickening of spongiosa layer with deposition of myxomatous material |
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MVP
A. sx B. consequences |
A. midsystolic click
B. infectivce endocardiis - mitral insuf - stroke infarct from embolism - arrhythmias |
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Rheumatic fever
A. def |
A. immuno mediated inflammatory dz after GABHS pharygngitis
- rheumatic carditis during acute phase and progress to RHD |
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Rheumatic heart disease
A. morphology micro B. acute morphology C. chornic morphology |
A. aschoff bodies = foci of T cells
- anitschkow cells = abundat cytplasm with chromatin in slener, wavy ribbon "catepillar cells" B. pancarditis (peri, myo-endo) - verrucae = necrotic foci vegetation along lies of closure - MacCallum plaques - in LA, subendocardial lesions by regurgitant jets C. leaflet thickening - commissural fusion "buttonhole" stenosis - RV hypertrophy, pulmonary vascular congestion - diffuse fibrosis/neovascu that obliterate layered and avascular architecture - thickening and fusion of tendinous cords |
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Rheumatic heart disease
A. pathogenesis B. sx |
A. I against M proteins of step cross-react self antigen in heart
B. migratory polyarthritis of large joints - pancarditis - subcutaneous nodules - erythema marginatum of skin - sydenham chorea |
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Infective endocarditis
A. types B. pathogenesis C. morphology |
A. acute: infxn of normal valve by highly virulent organism
subacute: organisms of lower virulence B. colonization of invasion of valve --> vegetations of thrombotic debris and organisms C. friable vegetations of fibrin and bacteria of aortic/mitral valves - ring abscess: when vegetations errod myocardium - septic infarcts: emboli from vegetations |
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Infective endocarditis
A. risk factors B. etiology bacterial |
A. MVP, bicuspid aortic valve, prostheitc valve, congenital defects
B. strep viridans (oral), S. aureus (IV drug) - HACEK (H. flu, actinobacillus, cardiobacterium, ekenella, kingella) - staph. epidermidis (prosthetics) |
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Infective endocarditis
- sx |
- fever, weakness, lassitude
- glomerulonephritis - Janeway lesions: erythematous nontender lesion on palms/soles - Osler (subcutaneous nodules in pulp of digts) - Roth spots (retinal hemorrhage) |
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Noninfected vengetations
A. types |
1. nonbacterial thrombotic endocarditis: deposition of small sterille thrombi = source of systemic emboli
- Libman - Sacks disease: mitral/tricuspid valvulitis - vegetation of finely fibrinous eosinophilic mateiral with hematoxylin bodies |
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Carcinoid heart disease
A. region affected B. associated C. morphology |
A. right sided valves
B. carcinoid syndrome: episodic flushing of skin, cramps, nausea, vomting and diarrhea C. firm plaquelike endocardial firbous thickening on inside surface and right sided valves |
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Carcinoid heart disease
- etilogy |
- gut carcinoid turmos relaease mediators into portal circuation = metabolized by liver so do not reach heart unless extensive hepatic metastases into interior vena cava
- carcinoid tumors outsid eof poart system that empty directly into IVC = induce syndrome (ovary and lung) |
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Cardiomyopathies
A. dilated: causes B. hypertrophic C. restrictive |
A. contracitly impair (systolic dysfxn)
- alchol, doxorubicin, sarcodosis, hemochromatosis, anemia B. compliance issue (diastolic) - Friedreich ataxia, storage disease, diabetic mother C. compliance issue (diastolic) - amyloidosis, radiation-induced fibrosis |
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Dilated cardiomyopathy
A. morphology B. arrhythmogenic right ventricular cardiomyopathy |
A. enlarged and flabby
- mural thrombi, mitral regurg results for m LV dilation B. inherited dz of cardiac muscle that case RV failure and rhythm disturbances - RV thinned with extensive fatty infiltration/fibrosis |
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Hypertrophic cardiomyopathy
A. features B. etiology C. vs dilated |
A. myocardial hypertrophy + intermittent ventricular outflow obstruction
B. mutations in genes encoding sarcomeric proteins C. thick-walled, hypercontracting vs flabby, hypocontracting - HCM = mut of sarcomere proteins vs DCM = abl of cytoskeletal proteins |
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Hypertrophic cardiomyopathy
A. morphology |
- asymmetric septal hypertrophy: thickening of ventricular septum compared to free wall
- endocardial thickening in LV ouflow tract - thickening of anterior mitral leaflet b/c contact of leaflet with septum during ventricular systole - myofiber disarray |
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Hypertrophic cardiomyopathy
A. sx B. consequences |
- impaired diastosis = reduced stroke volume
- secondary incr in pulmonary venous pressure = exertional dyspena - harsh systolic ejection murmur b/c ventricular outflow obstruction as anterior mitral leaflet moves toward septum B. atrial fibrillation, mural thrombosis, arrhythmias |
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Restrictive cardiomyopathy
A. morphology B. endomyocardial fibrosis C. Loeffler endomyocarditis D. endocardial fibroelastosis |
A. myocardium firm, noncompliant
- biatrail dilation B. fibrosis of ventricular end/subendocardium that extends form apex to tricuspid/mitral valves C. eosinophilic infiltrates release toxic products initate endomyocardial necrosis --> thrombus D. 1st 2 yrs of life = fibroelastic thickening invlving mural LV endocardium |
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Myocarditis
A. etiology B. sx |
A. viral infxn most common: coxsackieviruses
- protozoa: trypanosoma cruzi (Chagas) - bacteria: C diphtheriae, Borrelia burgdorferi (Lyme) - noninfectious: hypersensitivity rxn, rheumatic fever, SLE, polymyositis - fatigue, dyspnea, palpitations, discomfort, fever |
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Myocaridtis
A. morphology B. hypersensitivity myocarditis morphology C. morphology of giant cell myocarditis D. morphology of chagas dz |
A. advanced: ventricular myocardium flabby + mottled
- inflam infiltrate (lymphs) with focal myocyte necrosis B. lymph (prodom eosinophils) infiltrate C. inflam infiltrate with multinucleate giant cells = poor prognosis D. parasitization of scattered myofibers accompained by neutrophilic inflam - |
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Myocardial disease: catecholamines causes
A. morphology B. etiology C. pathogenesis |
A. myocaridal necrosis with contraction bands, assoc with sparse mononuclear inflam infilatrate
B. pheochromocytoma - autonomic sitmulation (stress, intracranial lesions) - vasopressor agents (dopamine) C. catechoalmines toxic to myocytes via Ca overload |
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Myocaridal disease: amyloidosis
A. pathogenesis B. types C. consequences |
A. insoluble extracellualr fibrillar deposits = beta-sheets
B. systemic amyloidosis - senile cardiac amyloidosis: transthyretin depositis = protein syn by liver for transporting thyroxine & retinol C. restrictive cardiomyopathy, arrhythmias |
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Amyloidosis
A. morphology |
- eosinophilic deposits of amyloid seen in Congo red
- amyloid deposits form rings around cardiac myocytes - amyloid can occlude vessels = small vessel dz |
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Myocardial dz: iron overload
A. etiology B. area of affect C. morphology |
A. hemochromatosis, hemosiderosis
B. in ventricles > atria; myocardium > conduction system C. rust-brown color = abudnant perinuclear siderosomes (Fe-containing lysosomes) - dilated cardiomyopathy |
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Mocardial dz: hyperthyroidism, hypo
A. moprhology in hypo |
A. heart flabby, enlarged, dilated
- myofiber swelling with interstital mucopolysaccharide edema fluid |
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Myocardial causes (Misc)
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- catecholamines
- amyloidosis - iron overload - hyper/hypothyroidism |
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Pericardial Dz
A. pericardial effusion/hemopericardium B. pericarditis (name them) |
A. rapidly developing = atrial compression --> cardiac tamponade
B. serous pericarditis - fibrinous and serofibrinous pericardits - purulent or suppurative pericarditis - hemorrhagic pericarditis - caseous pericardits |
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Serous Pericardits
A. etiology |
- noninfectious inflammatory dz
- rheumatic fever - SLE, scleroderma - uremia, tumor |
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Fibrinous/Serofibrinous pericarditis
A. etiology B. fibrinous morphology C. serofibrinous morphology |
A. MI, postinfarction (Dressler) syndrome, uremia, RF, SLE
B. surface is dry. loud pericardial friction rub most striking C. more inflammatory = fluid of leukoctes and red cells |
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Purulent pericarditis
A. etiology B. pathophysio |
A. microbes
B. extension, seeding from blood, lymphati cextension, direct intro from cardiotomy |
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Hemorrhagic Pericarditis
A. etiology Caseous Pericarditis B. etiology |
A. spread of malignant neoplasm
B. tuberculous in origng |
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Chronic Pericarditis
A. adhesive mediastinopericarditis B. constrictive pericarditis |
A. pericardial sac gone --> adhere to external = great strain
B. heart encase din dense fibrous scar = limit diastolic expansion and cardiac output |
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Tumors
A. order of freq |
1. myxoma (benign)
2 firboma 3. liposma: fat cells 4. papillary fibroelastomas: on vlaves, hairlike projections 5. rhabdomyomas: 6. angiosarcoma 1st five benign |
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Myxoma
A. etiology B. location C. clinical manifestations D. assoc |
A. clonal abnl of chromosomes 12 and 17
B. left sided, fossa ovalis in atrial septum C. ball-valve obstruction D. familial syndrome = Carney complex (AD) = skin myxomas, endocrine overactivity |
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Rhabdomyoma
A. epidemio + location B. assoc w/ C. morphology |
A. infants/children, ventricular
B. tuberous sclerosis C. spider cells = myocytes with cytoplasm reduced to thin webs extended to cell membranes |
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Noncardiac neoplasms
A. ways to metastases to heart |
- retrograde lymphatic extension (carcinomas)
- hematogenous seeding (tumors) - direct contigous extension (lung, breast, esophagus) - venous extension (kideny, liver tumors) |
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Caridac Transplantation
A. complications |
- allograft rejection: only endomyocardial biopsy = reliable of x acute rejection before substantial myocardial damage
- diffuse stenosing intimal proliferation of coronary + denervated heart = not know ischemic chest pain = silent MI |
