CPR 7.14 Pathology of Cardiomyopathies and Endocarditis Flashcards
Describe DCM
Ventricular chamber enlargement with impaired Systolic contractile function.
Describe the gross and microscopic pathologic findings of DCM
- Gross Pathology: Cardiomegaly, 4 chamber dilatation, Mural thrombi. p. 8
- Microscopic Pathology: Non-specific. 75% of cases have myocytes hypertrophy and interstitial fibrosis. P. 9
What are some common etiologies and contributing factors for DCM?
Idiopathic. Contributing factors include genetics, ETOH toxicity, post-viral myocarditis, and peripartum cardiomyopathy
Define Hypertrophic CM
marked ventricular hypertrophy leading to reduced compliance and diastolic relaxation→ Impaired filling during Diastole
Describe the gross and microscopic pathologic findings of HCM
- Gross Pathology: Disproportionate thickening of ventricular septum vs. left ventricle free wall 3:1, Compressed banana shaped left ventricular cavity, Endocardial mural plaque (from contact b/t anterior mitral leaflet and septum). P.15-16
- Microscopic Pathology: Massive myocytes hypertrophy, Haphazard myofiber disarray, Interstitial fibrosis. P. 17.
What is the most common etiology for HCM?
Genetic (all). >50% autosomal dominant related to disorder of sarcomeric proteins.
Define Restrictive CM
abnormally stiffened myocardium (due to fibrosis or infiltrative process) with impaired Disatolic relaxation
Describe the gross and microscopic pathologic findings for primary idiopathic RCM
(2) Gross Pathology: Dilated atria. Normal cardiac size but firm myocardium.
(3) Microscopic Pathology: myocytes hypertrophy and patchy/diffuse interstitial fibrosis. P. 21
Endocardial fibroelastosis, Endomyocardial fibrosis, Loeffler endocarditis, and myocardial deposition are all examples of what?
Secondary Restrictive Cardiomyopathy
Describe the findings and gross pathology of endocardial fibroelastosis. (RCM)
(1) Endocardial fibroelastosis: focal/diffuse fibroelastic thickening of left ventricle.
i Gross pathology: Left ventricle>Right ventricle. Associated with CHD.
Describe the findings and etiology of endomyocardial fibrosis. (RCM)
endocardial and subendocardial fibrosis with plaques.
i Etiology: Nutrition deficieicy or helminth induced inflammation. Africa and tropical areas. Most common form wordwide
Describe the findings and prognosis associated with Loeffler endocarditis (RCM)
(3) Loeffler endocarditis: endocardial fibrosis with eosinophils with mural thrombus. Rapidly fatal.
Describe how deposition of materials into the myocardium can result in amyloidosis as well as the gross and micro pathologic findings.
i Amyloid-insoluble proteins forming beta-pleated sheets.
• Gross: Waxy. P. 26
• Micro: pale pink between myocardial fibers. P. 27. Congo red stain causes amyloid to stain apple green with polarized light. P. 28
Cardiogtoxic drugs, catecholamines, and hyper/hypothyroidism are all examples of what?
Secondary cardiomyopathy.
Describe the most common viral and non-viral etiologies for myocarditis.
(a) Most often Viral. Coxsacki A&B virus or other enteroviruses.
(b) Non-viral: Trypanosoma cruzi (parasite), Borellia burgdorferi (bacteria).
Describe the gross and microscopic pathologic findings associated with myocarditis.
- Gross Pathology: Dilated CM, flabby ventricular myocardium, patchy diffuse hemorrhaging mottling, mural thrombi.
- Microscopic Pathology: myocyte necrosis or degeneration, focal lesions, isolated myofiber necrosis with interstitial edema and mononuclear cell infiltrate with viral infections. P. 39
(a) Giant cell p. 40
(b) Chaga’s p. 43
What area some non-infectious causes of myocarditis?
immune mediated (rheumatic fever, lupus, drug allergies/toxins), Idiopathic (sarcoidosis, giant cell myocarditis, Fiedler myocarditis).
Define endocarditis and the general pathogenesis
- Definition: microbial infection of the heart valaves or mural endocardim leading to formation of vegetations cmposed of thrombotic debris and organisms.
- Pathogenesis: bactermia colonize in cardiac tissue.
Describe the pathologic findings, at risk population, and common infectious microbe for acute IE
vegetations cause erosion of leaflet and abscess cavities. Common in IV drug users. Most often causd by Staph aureus (coag positive)
Describe the pathologic findings and common microbe for IE
smaller vegetations that rately erode or cavitate. P. 56. Caused by streptococcus viridans. (30-40% of all IE).
Infective endocarditis of prosthetic valves usually present with what pathologic finding?
ring abscess
Patient’s who develop IE in a native valve were most likely infected with what organism?
Streptococcus viridans.
A patient who develops IE in a prosthetic valve was most likely infected with what organism? Coagulase state?
S. epidermidis. Coagulase negative.
Could also be Staph. aureus (coagulase positive)
IE in ulcerative pt with colitis or colorectal cancer was most likely caused by what organism?
Streptococcus bovis
Where are the vegetations of non-infective endocarditis typically found?
What do they look like?
- Loosely adhered to valve leaflets along closure lines.
- Bland, faint pink microscopically p. 59
What is a common form of Non-infectious endocarditis seen in SLE patients? Describe the hallmarks of this disease
Libman-Sacks endocarditis
-Mitral and Tricuspid disease disease with valve necrosis and degeneration. p. 62-63
What is the most common etiology of rheumatic heart disease?
-Post GAS pharyngeal infection (could also be from skin infection)
Describe the 2 most common cardiac lesions seen in the pancarditis of RHD
(1) Pericarditis “bread and butter” exudate. Myocarditis. And Endocarditis: MacCallum patch (thickening in left atrium); small warty vegetations along cusp closure . P. 66
(2) Aschoff nodules: swollen conglomeration of cells in interstitium of myocardium.. P. 68. Caterpillar cell p. 70.
What is a common valvular complication of RHD?
Mitral stenosis
What laboratory diagnostic tests can be used in prevention and confirmation of rheumatic fever/RHD?
: Pharyngeal culture for Group A Strep usually negative by te time illness begins. Serum titers for AB’s to DnaseB and streptlysin O will be welevated in patients with ARF
