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Flashcards in CV CPC 4 Deck (15):

Contrast primary and secondary cardio myopathies.

primary is dysfunction confined to the heart muscle, whereas secondary have myocardial involvement as a component of a systemic or multi organ disorder


List some of the gross morphological changes with dilated cardiomyopathy.

enlarged and/or heavy heart, flabby
mural thrombi are common
dilation of AV valve as a result of chamber dilation (functional regurgitation)


List some of the light microscopic changes with dilated cardiomyopathy.

histologic abnormalities are nonspecific to etiology normally
most muscle cells are hypertrophied with enlarged nuclei, some attenuated, stretched and irregular
interstitial and endocardial fibrosis of variable degree preset


Discuss role of genetic mutations in dilated cardio myopathy.

genetic (AD pattern is predominant): genes that encode cytoskeletal proteins i.e. dystrophin, a-actin, desmin, nuclear lamina proteins A and C or congenital anomalies in conduction


Discuss role of myocarditis and alcohol in dilated cardio myopathy.

triggered by viruses like coxsackie virus B and other enteroviruses

alcohol abuse is strongly associated with development of dilated cardiomyopathy, alcohol and its metabolites have direct toxic effect on the myocardium (also beriberi HD due to thiamine deficiency)

note chemotherapuetic agents like doxorubicin and daunorubicine can cause cardiomyopathy due to per oxidation of lipids as well as childbirth for unknown causes


Describe gross and microscopic changes characteristic of hypertrophic cardiomyopathy.

massive myocardial hypertrophy, usually without ventricular dilation with classic pattern of disproportionate thickening of the ventricular septum; ventricular shaped to banana like configuration; endocardial thickening or mural plaque formation in left ventricular outflow tract and thickening of mitral leaflet

extensive myocyte hypertrophy, haphazard disarray of bundles of myocytes, individual myocytes and contractile elements of sarcomeres within cells; interstitial replacement fibrosis


What is the cause(s) of hypertrophic cardiomyopathy?

mutations in any one of several genes that encode sarcomeric proteins (transmission usually AD)

ie. B-myosin heavy chain, cardiac TnT, a-trophomyosin and myosin binding protein C

prognosis correlates with type of mutation


Restrictive cardiomyopathy is a disorder characterized by a primary decrease in ____ ____, resulting in impaired ventricular filling during diastole.

ventricular compliance


List different causes of restrictive cardiomyopathy.

idiopathic or associated with radiation fibrosis, amyloidosis, sarcoidosis, meetastic tumors or deposition of metabolites that accumulate due to inborn errors of metabolism


Describe the gross and microscopic changes of restrictive cardiomyopathy.

normal sized ventricles, myocardium is firm and noncompliant, biatrial dilation is commonly observed

patchy or diffuse interstitial fibrosis, endomyocardial biopsy often reveals specific etiology


What is the cause of senile cardiac amyloidosis?

deposition of transthryetin, a normal serum protein synthesized in the liver that is responsible for transporting thyroxine and retinol-binding protein (better prognosis than systemic amylodosis)

mutation accelerating cardiac amylodosis more common in african americans


How can eosinophillic deposits of amyloid be distinguished from other hyaline deposits?

congo red stain which produces classic apple green birefringence when viewed under polarized light


List common causes of infectious myocarditis.

Coxsackieviruses A and B
Trypanosoma cruzi (Chagas disease)


List common non infections agents of myocarditis.

non infectious causes: hypersensitivity reaction to drugs (antibiotics, diuretics etc.) or associated with systemic disease of immune origin, such as rheumatic fever, systemic lupus erythmatous and polymyosistisis

also cardiac sarcoidosis and rejection of transplanted heart are also considered forms of myocarditis


What are gross and microscopic changes seen with myocarditis?

during active phase, heart may appear normal or dilated, some hypertrophy may be present , in advanced stages ventricular myocardium is flabby, often mottled with pale foci or minute hemorrhagic lesions ; mural thrombi may be present

active disease: interstitial inflammatory infiltrate associated with focal myocyte necrosis, diffuse mononuclear, predominantly lymphocytic infiltrate is most common (damage is focal or patchy) chronically inflammatory lesion either resolve or heal by progressive fibrosis