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35 Cards in this Set
- Front
- Back
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MI: Etiology and pathogenesis
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Atherosclerosis of coronary arteries (99% of AMIs)
75% stenosis of CA can produce symptoms of ischemia Transmural MIs usually have cracked plaque & occlusive thrombus |
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Ischemic heart disease epidemiology
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M:F::2-6:1
IMPORTANT: women do get CAD/IHD -Do NOT ignore obvious symptoms -Women have more variable presentations (fatigue, back pain, abdominal pain) |
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Ischemic heart disease distribution and patterns
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LAD → anteroseptal LV
LCX → lateral LV RCA → posteroseptal LV RV infarcts less common, usually extensions of large posterior LV infarcts |
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Duration, gross, and micro morphology of myocardial infarcts
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Early acute:
-6-24 hours -Gross: subtle, patchy pallor, slight hyperemia -Micro: thin wavy fibers, eosinophilia, few PMNs Acute: -1-6 days -Gross: obvious pale, yellow -Micro: necrotic myocytes, many PMNs Organizing: -1wk-3wks -Gross: red-brown edge around pale center -Micro: granulation tissue, acute and/or chronic inflammation Remote: -3 months or longer -Gross: firm, white scar, contracted, wall thinned -Micro: collagen, thinning of wall |
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Morphology of myocardial infarcts
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Transmural infarct
-Infarction of full thickness of ventricular wall -Caused by severe CAD w/ acute plaque disruption & occlusive thrombosis Subendocardial infarct -Limited to inner ⅓ to ½ of ventricular wall -Diminished perfusion |
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Transmural infarct pathogenesis
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90% due to CA stenosis & disrupted plaques
Significant plaques mainly in proximal CA Less common: vasospasm, Plt aggregation, emboli → MI w/o atherosclerosis Complete vessel occlusion may not cause MI if sufficient collateral blood flow Nearly all involve LV; 15% LV + RV; 1-3% RV alone Initial event: acute plaque disruption of partially stenosing atheroma Most vulnerable: soft lipid core w/ thin fibrous cap Thrombosis follows acute plaque disruption Time interval from myocardial ischemia → irreversible injury = 20 – 40 minutes In absence of SCD, thrombus may lyse or vasospasm may relax restoring blood flood & spare myocardium |
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Subendocardial infarct pathogenesis
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Diffuse CAD & global perfusion made transiently critical by:
-Increased demand -Vasospasm -Hypotension Disrupted plaque w/ overlying thrombus that lyses thus limiting extent of myocardial injury |
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Complications of myocardial infarcts
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May heal fully without complications
Complications (incidence, 5% of MIs) -Rupture (free wall, septum, papillary muscle) --acute stage -Mural thrombus (cause of systemic embolus) --acute and organizing stage -Congestive heart failure (CHF) --acute, organizing, and remote stage -LV aneurysm --organizing stage -Dysrhythmia or arrhythmia --early acute stage -Pericarditis (if transmural involvement) --organizing stage -Pulmonary thromboembolism (venous congestion → thrombosed leg vein) |
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Right sided heart failure
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Mainly due to LV failure
Pure RV failure due to intrinsic lung dz (cor pulmonale) or TV/PV dz Major manifestations: -Portal, systemic & dependent peripheral congestion & edema (feet, ankles, sacrum) and effusions (pleural and peritoneal [ascites]) -Hepatomegaly w/ CPC --With severe hypoxia → centrilobular necrosis --Subsequent central fibrosis → cardiac sclerosis -Congestive splenomegaly --Focal hemorrhages --Hemosiderin deposits -Renal congestion --ATN |
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Acute rheumatic fever
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Pancarditis in 40% (Acute Rheumatic Heart Disease)
-Endocarditis → murmurs of stenosis (rare) -Myocarditis → cardiac enlargement and failure, dilatation of ventricle and mitral ring → mitral insufficiency, & Aschoff bodies in myocardium |
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Rheumatic heart disease
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Predominantly left-sided valves (almost always mitral)
-Mitral > Aortic > Tricuspid > Pulmonic -Mitral alone 48%, Mitral + aortic 42% -R. sided valves only rarely; TR usually due to CHF MV morphology & sequelae -Thickening of valve leaflet, especially along lines of closure -Fusion of commissures -Thickening, shortening and fusion of chordae tendinae -Result is mitral stenosis, insufficiency, or both Changes in heart and lungs (depend on severity of valve disease) -Mitral stenosis - → left atrial hypertrophy and dilatation (AF, mural thrombi, systemic emboli) - → chronic passive congestion of lungs → pulmonary HTN → RVH -Mitral insufficiency → LV hypertrophy and dilatation, left atrial dilatation -Chronic L heart failure can cause Rt. heart failure, TR Aortic Valve Morphology and Sequelae -Valve --Thickening of valve cusp, especially along lines of closure --Fusion of commissures --Result is aortic stenosis, insufficiency or often both -Resultant changes in heart --Aortic stenosis--> LV hypertrophy --Aortic insufficiency--> LV hypertrophy and dilatation |
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Acquired aortic stenosis
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Almost always rheumatic
Fused commissures, thickening at lines of closure Almost always accompanied by mitral involvement More common in middle-age, females > males Onset of murmur in mid-adult life, usually |
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Degenerative aortic stenosis
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Hemodynamic injury, then dystrophic calcification
Calcium deep in sulci, on cusps (not on lines of closure and commissures) One of major causes of isolated aortic stenosis More common in elderly, and in males Onset of murmur late |
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Congenital aortic stenosis
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Three types:
-unicommissural (rare) -bicuspid (most common) -uneven tricuspid Ca++ deep in sulci, on cusps Causes isolated AS Frequency about 1%, no sex preference Often h/o a murmur since childhood, but significant stenosis only in adulthood |
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Diseases of aortic valve causing aortic insufficiency
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Cystic medial degeneration
Marfan Syndrome Dissecting aneurysm (medial degeneration or hypertension) Syphilitic aortitis Ankylosing spondylitis |
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Aortic insufficiency morphology
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Rheumatic - commissures fused
Syphilitic – AV commissures separated, ↑ Ao atherosclerosis due to aortitis Cystic medial degeneration - commissures separated Marfan's Syndrome - same as cystic medial degeneration (but distinctive body habitus and eye lesions) Bacterial endocarditis - destroys cusps, vegetations on valves High ventricular septal defect (VSD) with prolapse of cusp |
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Causes of endocarditis
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Non-infective (Non-microbial)
-Verrucous (acute rheumatic fever) -Atypical verrucous (Libman-Sacks) (SLE) -Non-bacterial thrombotic - NBTE (marantic) Infective (microbial) -Mainly bacterial or fungal (viral, rickettsial rare) -Destroys valve tissue (non-infective doesn't) -Thrombus w/ organisms deep within it |
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Subacute bacterial endocarditis
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Less virulent, often enteric organisms (Strep. viridans, most common)
Lengthy course - months if untreated Previously damaged valve (rheumatic, congenital defect, previous surgery) Symptoms: -Variable, insidious, often misdiagnosed -Low grade fever, malaise, fatigue, anemia, murmur(s) -Course: lengthy (months) Lab Diagnosis: series of positive blood cultures Treatment: IV bactericidal antibiotics for 4-6 weeks, necessary because organisms deep within vegetation |
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Acute bacterial endocarditis
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Symptoms:
Variable, insidious, often misdiagnosed Low grade fever, malaise, fatigue, anemia, murmur(s) Course: lengthy (months) Lab Diagnosis: series of positive blood cultures Treatment: IV bactericidal antibiotics for 4-6 weeks, necessary because organisms deep within vegetation Symptoms -Sudden onset, high fever, patient prostrated -Murmur(s) -Death due to heart failure, valve perforation, sepsis Lab diagnosis: same as for SBE Treatment: IV antibiotics, resect infected valve |
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Endocarditis in drug addicts
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Often Staph. aureus or fungal (from skin, contaminated drugs or cutting materials)
Right sided valve endocarditis more common in addicts than in non-addicts (but still the majority of cases in addicts are left sided) |
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Complications of infective endocarditis
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Intra-cardiac: perforation of cusp or leaflet, rupture of chordae tendineae, abscess, fistula, obstruction of valve or outflow tract, embolization to CA
Most common cause of death is CHF due to one of above Extra-cardiac: emboli to major organs (septic or bland), mycotic aneurysm formation, glomerulonephritis from immune complexes (not actually focal "embolic") Other toxic or allergic inflammation of vessel walls (petechiae and/or splinter hemorrhages, in skin, mucosa, conjunctiva, retina) |
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Non bacterial thrombotic endocarditis
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Marantic endocarditis
Small (1-5 mm), sterile fibrin & Plt thrombi loosely adherent to valves (lines of closure), mainly MV Due to systemic hypercoagulability May embolize systemically Often seen in CA patients 2nd to DIC |
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Libman sacks endocarditis
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Non-infective
Valvulitis occurring in SLE & anti-phospholipid syndrome MV & TV most commonly affected Microscopic: fibrinoid necrosis Fibrinous vegetations on either side of valve Valve deformations may occur |
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Carcinoid heart disease
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One feature of carcinoid syndrome
Elaboration by argentaffinomas of bioactive products including serotonin, bradykinin, histamine, PG, etc. Mainly right-sided valvular lesions |
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Mitral valve prolapse: epidemiology, clinical features, complications, morphology
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Epidemiology
-Frequency: estimated 7% have some abnormality -Sex: F:M:: 6:4 -Age: 20 - 40 Clinical features: -may be asymptomatic -mid-systolic click; atypical CP, dyspnea, fatigue, pysch. manifestations Complications: -Mitral (or other) prolapse, insufficiency -Secondary infective endocarditis -Some patients have sudden cardiac death (uncommon) Morphology -Stretched, redundant valves, usually mitral, sometimes also tricuspid and semilunar valves |
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HTCVD: Diagnostic criteria, morphology
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Diagnostic criteria:
-Concentric LVH -H/O or extra-cardiac evidence of HTN -Absence of other lesion that can cause LVH (e.g., AS or coarctation of aorta) Morphology -Concentric LVH --LV usually > 2 cm in thickness -Cardiomegaly --Heart weight: > 500 gm -Myocytes & nuclei enlarged -Long term: diffuse interstitial fibrosis, focal myocytic degeneration, LV chamber dilation & thinning |
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HTCVD: clinical features
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CHF is COD in ⅓ of HTN patients
HTCVD ↑ risk of SCD Remainder die of renal dz, CVA or unrelated causes Rx: may in time → regression of myocyte hypertrophy and ↓ heart size |
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Cor pulmonale: overview, morphology
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Right-sided counterpart of systemic HTCVD
RVH or dilation is 2nd to pulmonary HTN by disorders affecting lung structure or fxn Must EXCLUDE: RVH 2nd CHD or LV dz Morphology -RVH: often > 1 cm RV thickness -Dilation may or may not be present -RV dilation may → TV regurgitation -Pulmonary arteriolar wall thickening -PA atherosclerosis -LV & LA: normal |
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Cor pulmonale: clinical features
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Chronic cor pulmonale is common 2nd widespread COPD
May cause cardiac decompensation Cardiac Sx may be masked by underlying lung dz |
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Myocarditis: morphology
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Soft myocardium w/ 4 chamber dilation; patchy hemorrhagic mottling
Mural thrombi may form Myocardial inflammatory infiltrate w/ associated myocyte necrosis or degeneration Lesions: often focal |
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Hypertrophic cardiomyopathy
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Familial in 50% (AD, variable penetrance)
Obstructive or non-obstructive Thickening of septum narrows LV outflow tract Microscopic: myofiber disarray Clinical: impaired ventricular compliance, pump failure, systolic murmur, dysrhythmias sudden death |
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Dilated or congestive cardiomyopathy
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Pathogenesis
-alcohol, peri-partum, sarcoid, autoimmune, myocarditis, and chemotherapy (adriamycin) -can be autosomal dominant, autosomal recessive, or X-linked -idiopathic - may be sequela of viral myocarditis (most common) Morphology -Cardiomegaly (up to 900 gm) -Wall thickness may not reflect degree of hypertrophy -Mural thrombi may form -Valves & CA usual for age -Microscopic changes: subtle → myocytic hypertrophy & interstitial fibrosis -Endocardial thickening may be present |
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Restrictive cardiomyopathy
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Amyloidosis
-Infiltrates myocardium, characteristic Congo Red staining -Can mimic ischemic heart disease in symptoms (failure, EKG changes) -Can have amyloid limited to heart and vessels |
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Obliterative cardiomyopathy
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Endomyocardial fibrosis (EMF)
-Occurs typically in children/young adults in Africa -Subendocardial fibrosis → ↓ ventricular chamber volume Fibroblastic endocarditis (Loeffler's) -Endomyocardial fibrosis -Mural thrombi -Peripheral eosinophilia -Eosinophilic infiltration of multiple organs -Rapidly fatal Endocardial fibrosis -Usually in children < 2 yrs. -Primary or secondary |
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Arrhythmogenic cardiomyopathy
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RV adipose or fibro-adipose replacement - autosomal dominant
RV aneurysms - autosomal recessive LV dilation – myocarditis Serious dysrhythmias, sudden death |
