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STEP Pathology > deck_5069718 > Flashcards

deck_5069718 Flashcards

1
Q

What is the composition of valves?

A

collagen, GAGs, and elastin

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2
Q

What is valvular stenosis?

A

failure of a valve to open completely, impairing blood outflow

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3
Q

Is valvular stenosis typically an acute or chronic event?

A

chronic

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4
Q

Causes of valvular stenosis?

A

calcification (very common) or valve scarring (common in chronic rheumatic disease)

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5
Q

What are some things that can cause degenerative valve disease and affect the ECM?

A

-calcification, which can be cuspal (typically in the aortic valve) or annular (in the mitral valve)-decreased numbers of valve fibroblasts and myofibroblasts-alterations in the ECM-changes in the production of matrix metalloproteinases or their inhibitors

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6
Q

T or F. Valves with congenital anomalies are more prone to injury

A

T. For example, bicuspid aortic valves are more susceptible to aortic stenosis due to calcification

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7
Q

Where are the calcifications present in calcific aortic valve disease (CAVD)?

A

more on the leaflets than the edges so you don’t usually see fusion of the cusps (helps differentiate from rheumatic heart disease)

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8
Q

Outline the development of CAVD.

A

-proinflammatory monocytes are recruited via activated endothelial cells-macrophages accumulate and release pro-osteogenic cytokines-cytokines stimulate the differentiation of myofibroblasts and osteoblast-like cells resulting in generation of calcified matrix vesicles or apoptotic bodies followed by formation of micro- and macro calcifications

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9
Q

What is myxomatous degeneration of the mitral valve?

A

one or both mitral leaflets are floppy and prolapse (balloon back into the left atrium during systole)

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10
Q

What are the main causes of valvular prolapse?

A

most primary cases have unknown cause, typically benign course, but some increase risk of endocarditis Marfan syndrome a common cause/risk factor (fibrillin-1 mutations)

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11
Q

What causes rheumatic heart disease?

A

immune mediated-antibodies to bug are cross reactive (common cause is GAS B-hemolytic) causing inflammation in all area of the heart that leads to valve scarring and mitral stenosis

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12
Q

What happens in RHD?

A

Antibodies against GAS M proteins bind myocardium and valves and activate complement and Fc receptor bearing cells, including macrophages and CD4 T cells that promote cytokine-mediated inflammation

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13
Q

T or F. Cultures are often negative for GAS at the time of symptom onset

A

T, but serum titers of one or more streptococcal antigen (SLS or DNAase) are elevated

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14
Q

What valves are most commonly affected by RHD?

A

aortic and mitral

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15
Q

IV drug use typically affects what valve?

A

tricuspid (staph aureus mediated usually)

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16
Q

What are some features of rheumatic heart disease?

A
  • pancarditis (pericardium, myocardium, and valve involvement)
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17
Q

How does RHD affect valves?

A

-fibrinoid necrosis-fibrin along line of closure (as opposed to CAVD)- not on the leaflets- causing fusion

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18
Q

What are some of the results of recurrent RHD?

A

chronically lead to scar formation on the valvesvalve cusps becomes thickened and retracted and fuse chordae tendineae become thick and fuseneo-vascularization

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19
Q

The most important functional consequence of RHD is what?

A

valvular stenosis and regurgitation (insufficiency)

20
Q

How is acute rheumatic fever diagnosed?

A

Jones criteria:1) serological evidence of previous strep infection2) carditis3) migratory polyarthitis of large joints4) arrhythmia marginatium skin rashes 5) Sydenham chorea

21
Q

What is Sydenham chorea?

A

neurologic disorder characterized by involuntary purposeless, rapid movements (aka St. Vitus dance)50% recover after 2-6 months

22
Q

What other problems can RHD cause?

A

-murmurs-cardiac hypertrophy and dilation-CHF-infectious endocarditis due to scarred valves-a fib and mural thrombi

23
Q

What is infective endocarditis?

A

microbial invasion of heart valves or mural endocardium resulting in bulky, friable vegetations composed or necrotic debris, thrombi, and organisms

24
Q

T or F. Infectious endocarditis is DESTRUCTIVE to the valve

A

T, the bacteria will eat through it

25
Q

What are the risk factors for infectious endocarditis?

A

-pre-exisitng structural heart disease (RHD, ventricular aneurysm, sub-aortic stenosis etc.)-degenerative valve disease-cardiac interventions (prosthetic valve, pacemaker, defibrillator)-congenital heart disease

26
Q

What is the number one bacteria responsible for infective endocarditis?

A

50-80% Strep viridans-some s. aureus and epi (common with valve replacement)HACEK organisms (difficult to culture)

27
Q

What are some clinical manifestations of infective endocarditis?

A

-B symptoms-development of new murmur or change in old one-Osler node (on digits)-Janeway lesions (on palms)-Roth spots in the eye-neuro and renal involvement Oslers and Janeways are small thrombi

28
Q

Complications of infective endocarditis?

A

-cardiac failure (volume overload due to regurgitant lesions, infarcts)-systemic infarcts (emboli)-systemic abscess (infected emboli)-aneurysms (infected emboli)-renal failure (immune mediated glomerulo-nephritis)

29
Q

What are the HACEK organisms associated with infective endocarditis? 1-2% of cases

A

Haemophilus parainfluenzaActinobacillus actinomycetemcomitans Cardiobacterium hominisEikenella speciesKingella species

30
Q

What two factors are need for establishment of endocardial infection?

A

endothelial denudation over valve cusp with platt depositions (thrombus)-episode of bacteremia

31
Q

Infective endocarditis progression on a prosthetic valve

A

Endocarditis on a prosthetic valve usually begins in the valve ring and may protrude into the valve orifice causing obstruction and regurg. Over time, vegetation decreases in size and organizes as a fibrous nodule which may calcify

32
Q

Nonifected vegetations of the heart is aka?

A

marantic endocarditis

33
Q

What is marantic endocarditis?

A

mainly fibrin and platelet deposit on cardiac valves that is non-destructive

34
Q

When is marantic endocarditis common?

A

patients in hyper coagulable states and those with mucinous adenocarcinomas (mass in pancreas a common example)!!

35
Q

What is a common complication of mar antic endocarditis?

A

can give rise to emboli that can cause infarcts in the brain, heart, etc.

36
Q

What is Libman-sacks endocarditis?

A

small to medium-sized inflammatory vegetations that can be attached on either side of valve leaflets; heal with scarring seen on BOTH sides of the valve

37
Q

When is Libman-sacks endocarditis common?

A

Patients with SLE or anti-phospholipid antibody syndrome

38
Q

What is carcinoid heart disease?

A

results from bioactive compounds such as serotonin released by carcinoid (aka low grade neuro-endocrine) tumors

39
Q

What does the release of bioactive compounds such as serotonin from carcinoid tumors result in?

A

-flushing-diarrhea-dermatitis-bronchoconstriction -cardiac impact

40
Q

When do symptoms and carcinoid heart disease occur?

A

The tumor has to grow large enough to metastasize to the liver and disrupt the liver’s ability to break down the tumors bioactive compounds to cause symptoms

41
Q

Where are carcinoid tumors common?

A

GI tract

42
Q

What do carcinoid tumors do to the heart?

A

give it a distinctive, glistening white intimal plaque-like thickening on the endocardial surfaces of the cardiac chambers and valve leaflets due to abundant acid mucopolysaccharides

43
Q

What are the two types of prosthetic valves currently used?

A

-mechanical-bioprosthetic

44
Q

Describe mechanical valves.

A

made of pyrolytic carbon, durable and long longer but can cause significant red cell hemolysis require chronic anticoagulation

45
Q

Describe bioprosthetic valves.

A

glutaraldehyde-fixed porcine or bovine tissues, or cryo-preserved human valves- less durable and will eventually fail due to matrix deterioration do not require chronic anticoagulation

STEP Pathology (80 decks)

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