• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/36

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

36 Cards in this Set

  • Front
  • Back
What are 3 forms of aortic stenosis?
1. degenerative calcification of normal tricuspid aortic valve
2. degenerative calcification of a bicuspid aortic valve
3. aortic stenosis due to chronic rheumatic aortic valvulitis
How does dystrophic calcification of the aortic valve lead to stenosis?

How does the effect compare between tricuspid and bicuspid aortic valves?
Wear and tear on valves --> calcified nodules on outflow surface of valves, fused commissure--> more difficult for valves to open --> stenosis, concentric LV hypertrophy

Bicuspid accumulate damage and calcium sooner
Clinical features of aortic stenosis?
angina, syncope, CHF
What is myxomatous mitral valve?
Ballooning of mitral leaflets, chordae tendinae elongated, fibrosa thin
Clinical features of myxomatous mitral valve?
Mid-systolic click

Can have chest pain, palpitations, dyspnea, regurgitation

can develop regurgitation, infective endocarditis, sudden death due to ventricular arrhythmia
What happens in acute rheumatic fever?
antibodies against M proteins of Group A strep cross-react with glycoproteins in the body
What are the clinical manifestations of acute rheumatic fever?
migratory polyarthritis
carditis
What are the Jones criteria for diagnosing acute rheumatic fever?
1. carditis
2. migratory polyarthritis
3. subcutaneous nodules
4. erythema marginatum
5. Sydenham chorea (involuntary movements)

must have at least 2
What are Aschoff bodies?

Anitschow cells?
Aschoff bides = central zone of degenerating, hypereosinophilic material infiltrated by T lymphocytes and large macrophages (Anitschkow cells)
What happens in chronic rheumatic fever?
Scarring of valves (mitral, aortic)
What is the morphology of chronic rheumatic valvulities?
thick leaflets, chordae tendinae are short and thick

Left atrial dilation from stenosis of mitral valve
Fusion of all commissures in aortic valve
What is infective endocarditis?
infection of the cardiac valves, usually bacterial
What are 2 traditional forms of infective endocarditis?
acute - rapid, highly virulent
subacute - insidious, infects previous abnormal valve, low virulence
How does infective endocarditis come about?
Abnormal valve produces jet streams --> platelet-fibrin deposits form on valves --> become infected by bacteria
What are the clinical features of infective endocarditis?
acute: fever, chills weakness

Subacute: fever may be absent, non-specific

Both can have murmur, petechiae hemorrhages
What are 3 complications of infective endocarditis?
Glomerulonephritis, septicemia, emboization
What are 3 agents of infective endocarditis?
1. Viridans Strep - infects previously damaged valves
2. S. aureus - infects normal valves
3. HACEK group
What is marantic endocarditis (non-bacterial)?
Sterile vegetations (fibrin, platelets) on valves organize into strands called Lambl excrescences

Occurs in hypercoagulable states
What is the difference between a primary and a secondary cardiomyopathy?
Primary - disease confined to heart
Secondary - multi-organ disorder
What is the morphology of dilated cardiomyopathy?
Dilation of all four chambers from eccentric hypertrophy of the myocardium
What are the causes of dilated cardiomyopathy?
viral (Coxasackie B or enterovirus)
alcohol
genetic (lamins A and C, B-myosin heavy chain, dystrophin, a-cardiac actin mutations)
peripartum state (pregnancy-induced hypertension, volume overload, cardiac defect)
What are the clinical features of dilated cardiomyopathy?
CHF (dilation of LV), mitral insufficiency, abnormal cardiac rhythms, emboli
What is the morphology of hypertrophic cardiomyopathy?
Myocardial hypertrophy without dilation; thick interventricular septum;

Myofiber disarray, fibrosis, sclerosis of blood vessels
What is the pathogenesis of hypertrophic cardiomyopathy?
mutations in sarcomeric proteins (dominant) --> B-myosin heavy cahin, myosin-binding protein C, troponin T
What are the clinical features of hypertrophic cardiomyopathy?
Impaired diastolic filling --> reduced CO, increase in pulm pressure --> dyspnea

Systolic ejection murmur if outflow obstruction

Ischemia
What are the complications of hypertrophic cardiomyopathy?
arrhythmias, CHF, sudden death
What is the morphology of restrictive cardiomyopathy?

Pathogenesis?
Ventricles mostly normal (may be enlarged), chambers not dilated

Infiltrative process of myocardium --> reduced ventricular compliance --> impaired diastolic filling
What are the causes of restrictive cardiomyopathy?
idiopathic, amyloidosis, hemochromatosis, sarcoidosis, radiation fibrosis, inborn error of metabolism
What are 2 variants of restrictive cardiomyopathy?
1. Endomyocardial fibrosis - fibrosis of endocardium and subendocardium --> reduced compliance

2. Loeffler endomyocarditis - dense endocardial fibrosis + peripheral eosinophilia
What is arrhythmogenic right ventricular carddiomyopathy?
dilation of RV associated with thinning of the wall and fibrosis --> right heart failure or sudden cardiac death
What is myocarditis?

3 variants?
Inflammation of heart causing damage to myocardium

Lymphocyte, hypersensitivity (eosinophils), Giant cell (macrophages and giant cells)
What are the clinical features of myocarditis?
asymptomatic

fatigue, dyspnea, palpitations, pain, fever

sudden CHF, arrhythmias
What is preicarditis?

3 types?
Inflammatory infiltrate is in the pericardial sac

fibrinous (fibrin)
fibrinopurulent (bacteria)
fibrinohemorrhagic (malignancy)
acute pericarditis?

chronic?

constrictive?
acute = fibrinous and fibrinopurulent, can resolve completely

chronic = pericarditis with scarring

constrictive = fibrosis in pericarditis so extensive as to impair diastole
clinical findings of pericarditis?
atypical chest pain (not exertion related)
tamponade (fill sac with fluid --> compress LV, inhibit diasolic filling)
What are 3 types of pericardial effusions and their cuases?
Serous: CHF, hypoalbuminemia
Serosanguinous: trauma, malignancy, ruptured MI
Chylous: lymphatic obstruction