CVM Valve Pathology stoopidest
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stoopidest on April 12, 2011
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59 terms
Terms | Definitions |
|---|---|
major causes of valvular pathology | congenital defectbacterial infectious endocarditis nonbacterial thrombotic endocarditis metabolically mediated endocarditis aging and attendant degeneration |
isolated valvular disease | disease affecting a single valve |
combined valvular disease | disease affecting multiple valves |
valvular stenosis | inability of valve to open fully leads to reduced forward flow through valve |
valvular insufficiency | inability of valve to close fullyallows for backward flow through valve |
functional regurgitation | incompetence in a valve caused by structural problems in the heart rather than any inherent defect in the valvee.g. may involve dilation of the ventricle which alter the chordae tendenae preventing them from effectively pulling the valve closed |
most common acquired valvular disease | aortic stenosis |
dystrophic calcification | deposition of calcium phosphate crystals found in normal concentrations on to an abnormal structure |
metastatic calcification | deposition of calcium phosphate crystals found in abnormally high concentrations on to normal structures |
calcific aortic stenosis [CAS] | deposition of calcium on an abnormal aortic valve; this process occurs at normal physiologic calcium concentrations, ie is usually dystrophic |
potential effects of calcific aortic stenosis [CAS] | LVH -> ischemia -> MI or LV failure, congestion calcium deposits on valve leaflets prevent the valve from opening fully as a result, the LV may experience pressure overload, it may hypertrophy resulting in increased O2 demand with the attendant risk of ischemia and MI CAS may also contribute to LV failure, congestion, and then RV failure |
CAS murmur | high-pitched systolic murmur with crescendo-decrescendo patternheard at right sternal border at 2-3 ICS; may radiate to the apex becomes longer with handgrip [b/c left-sided] |
the most common congenital heart malformation | bicuspid aortic valvethis valve is usually asymptomatic, but may predispose to CAS, endocarditis and may be a/w other aortic anomalies |
mitral annular calcification [MAC] | deposition of calcium on the annular ring, a support structure, of the mitral valveoften asx, but may contribute to regurgitation, stenosis, arrhythima or even sudden death nodules may embolize with r/o stroke; nodules are also potential sites of infection |
conditions a/w mitral annular calcification | the following may contribute to or be caused by MAC: hypertension aortic stenosis hypertrophic cardiomyopathy |
mitral valve prolapse [MVP] | insufficiency of mitral valve due to weak valve leaflets which may prolapse back into the left atriumvalve leaflets may be floppy, loose, thick, rubbery most common in younger women; often asx a/w congenital connective tissue defects; often seen in Marfan's Syndrome [fibrillin-1 defect] |
secondary valve changes a/w MVP | thickening or fibrosing of valve leafletsthickening of LV endocardium thickening of LA in response to prolapsing leaflets LA thrombi calcification |
complications relating to MVP | infectious endocarditisinsufficiency with r/o cordae tendenae rupture embolization arrhyhmias |
MVP murmur | mid-to-late systolic murmur, often preceded by a clickmurmur is not precipitated by exertion valsalva moves the murmur closer to S1 inspiration moves the murmur closer to S2 |
course of rheumatic fever | 1. strep A pharyngitis2. rheumatic fever [6-10 wks later] 3. pancarditis, arthritis 4. chronic rheumatic heart disease with mitral valve stenosis |
Aschoff bodies | foci of lymphocytes and Anitschkow cells found in any layer of cardiac tissue in pancarditis of acute rheumatic fever |
Anitschkow cells | large, round or ovoid marcophages with owl-eye multinucleation, caterpillar-like chromatin, and abundant cytoplasm these cells are found in Aschoff bodies in acute rheumatic pancarditis |
common clinical findings a/w rheumatic fever | 1. polyarthritis2. pancarditis, including mitral valve inflammation and vegetations 3. subcutaneous nodules 4. erythema marginata 5. Sydenham chorea |
clinical findings a/w acute rheumatic pancarditis | 1. murmurs2. weak heart sounds 3. pericardial friction rub 4. tachycardia 5. arrhythmias |
cardiac structures commonly affected by rheumatic heart disease | mitral valve [in all cases]: - leaflet thickening - commisural fusion - thickening of tendinous cords LA: - dilation - thrombi with r/o embolization aortic valve [25% of cases] - stenosis also: pulmonary congestion may develop leading to RVH and failure |
typical effect of valvular stenosis on the heart | pressure overload -> concentric hypertrophyturbulent jets of blood flow may also cause thrombi on the endocardium |
typical effect of valvular insufficiency on the heart | volume overload -> series hypertrophy, i.e. dilation |
most frequent causes of aortic valve stenosis | calcification of normal valve or of congenitally bicuspid valve |
most frequent cause of aortic valve insufficiency | dilation of ascending aorta, esp in hypertension and aging |
most frequent cause of mitral stenosis | rheumatic heart disease |
most frequent cause of mitral insufficiency | mitral valve prolapse |
conditions contributing to acquired aortic stenosis | chronic conditions including: - HPT - hyperlipidemia - inflammation these factors also play a role in atherosclerosis |
clinical features of aortic stenosis | NB: once symptoms appear, prognosis is not good; asymptomatic CAS is commonly fine narrowing of valve orifice -> ventricular pressure build-up and high pressure gradient b/w the chambers - LVH from pressure overload - ischemia of hypertrophic tissue - angina progression can lead to systolic dysfunction and CHF |
infectious endocarditis [IE] | a serious infection characterized by colonization or invasion of the heart valves or the mural endocardium by a microbe, usually bacterial |
acute infectious endocarditis | infection of normal valve by highly virulent microbe producing necrotizing, ulcerating, destructive lesionsdifficult to cure and often fatal |
most common causes of IE | mitral valve prolapsedegenerative calcific valvular stenosis bicuspid aortic valve artificial (prosthetic) valves unrepaired and repaired congenital defects history of IE |
most common bacterial pathogen causing IE | strep viridansNB: s. viridans is normal oral flora |
HACEK organism | haemophilusactinobacilus cardiobacterium eikenella kingella NB: the organisms are oral commensals and can cause IE |
percentage of IE cases attributed to s. aureus | 10-20%s. aureus is a common epidermal flora and is the most common cause of IE in IVDA |
clinical features of IE | fever, chills, weakness, lassitudenew murmurs, esp in left-sided IE, from IE-derived valvular anomalies/defects Janeway lesions, Osler nodes, retinal hemorrhages |
most common sites of IE infection | mitral and aortic valvestricuspid IE may be seen in IVDA |
morphological hallmark of IE | vegetations: accumulations on the valves; these consist of: - bacteria - thrombotic elements - fibrin - inflammatory cells vegetations may be single or multiple and may appear on one or more valves vegetations present the r/o of embolization -. abscesses and septic infarcts |
characteristics of normal pericardial fluid | 30-50 mL in volume of thin, clear, straw-colored fluid |
key factor in determining effect of pericardial effusion on heart function | rate of fluid accumulation: - slow effusion allows the pericardium to dilate so it can accommodate large amounts of fluid, up to 500 mL - rapid effusion into non-dilated pericardium can constrict the atria, venae cava or ventricles interfering with normal heart function and may lead to tamponade; 200-300 mL can have this effect |
cause of pericarditis | primary pericarditis is rare and usually viral in originsecondary pericarditis is the more common form, is usually acute, and is caused by: - various cardiac disease - metastasis - thoracic or systemic infections - surgery |
types of pericarditis | - serous- fibrinous/serofibrous - purulent - hemorrhagic - caseous |
causes of serous pericarditis | noninfectious inflammatory processes, e.g.: - RF - SLE - sclerodoma - uricemia - tumors infectons in adjacent structures may also cause serous pericarditis w/o actually infecting the pericardium NB: unlikely to organize |
causes of fibrinous/serofibrinous pericarditis | NB: this is the most common form of pericarditisfluid is a serous exudate w/fibrinous components causes may include: - acute MI - Dressler syndrome [post-MI] - RF - SLE - chest radiation - uremia - trauma - surgery |
most common clinical sign of fibrinous pericarditis | pericardial friction rub pain signs of CHF |
causes of purulent pericarditis | microbe infection deriving from: - direct extension from neighboring infections [e.g empyema of the pleural cavity, lobar pneumonia, mediastinal infections, or extension of a ring abscess through the myocardium or aortic root] - seeding from the blood - lymphatic extension - direct introduction during cardiotomy |
microscopic features of purulent pericarditis | red, granular serosal surface covered w/exudatesigns of inflammation are present full resolution is rare and usually leads to scarring, organization, and ultimately constrictive pericarditis |
morphology of fibrinous pericarditis | dry serosal surface with fine granular rougheningmay become organized |
morphology of serofibrinous pericarditis | yellow-brown, cloudy, turbid fluid w/immune cells and RBCs resulting from a more intesne inflammatory responseserofibrinous pericarditis may become organized |
clinical features of purulent pericarditis | spiking fever, chillspericardial friction rub pain signs of CHF |
causes of hemorrhagic pericarditis | - usually metastasis of malignant tumors [neoplastic cells are often found in the exudate]- baxterial infection - bleeding diathesis - TB |
subtypes of chronic/healed pericarditis | soldier's plaqueadhesive pericarditis adhesive mediastinopericarditis constrictive pericarditis |
constrictive pericarditis | fibrous scarring of the pericardium which encases the heart and prevents dilation or hypertrophy- inability to dilate becomes problematic in exertion when increased CO is required NB: mimics restrictive cardiomyopathy |
adhesive pericarditis | fibrotic fusion of the layers of the pericardium following pericarditisusually has no effect on heart function |
adhesive mediastinopericarditis | obliteration of the pericardial sac following pericarditis and resulting in the fusion of the parietal layer to mediastinal structuresmay severely inhibit cardiac fxn as the heart has pull on the now attached structures when it contracts |
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