Valvular Diseases - Cochran Flashcards

1
Q

Describe the structure & function of normal cardiac valves.

A

Lined by endothelium and divided into leaflets. If AV valve, connected to ventricle via chordae tendineae & papillaries.

Function to allow unidirectional flow of blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What can cause valvular insufficiency?

A

Functional regurgitation (disruption of supporting structure, eg aortic dilation)

Structural disease affecting the valve cusps.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which are more frequent: Stenoses of insufficiencies?

A

Stenoses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the most common congenital valvular abnormality? What does this predispose to?

A

Bicuspid aortic valve, which is more prone to calcification.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Calcific Aortic Stenosis

Describe the pathophysiology.

Who does it generally affect?

A

“Wear & Tear” resulting in fibrosis and eventual calcification.

Wear & tear results in fibrosing and eventual calcification of the valves.

Occurs in normal valves in very late life (8th-9th decades), as well as in abnormal valves in the 5th-6th decades.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the signifiance of a Notch mutation in valvular heart disease?

A

Notch is involved in signaling during heart valve development; mutation predisposes to heart pathologies including CAS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Calcific Aortic Stenosis

Describe its morphology.

A

Calcific Aortic Stenosis

Calcified masses in cusps, rarely involving the cuspal edges.

No fusion of commissures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mitral Annular Calcification

Describe the pathogenesis.

Who does it affect?

What are its complications?

A

Mitral Annular Calcification

Wear & tear degeneration resulting in calcification on the base of the valve (fibrous ring).

Usually women >60, especially with myxomatous valves or increased LV pressure.

Doesn’t affect function, but forms sites for thrombi/infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mitral Degeneration

Describe the pathogenesis.

Who does it affect?

What are its complications?

A

Mitral Degeneration

Myxoid changes weaken the mitral valve, causing it to prolapse back into the left atrium during systole.

Young women, and those with connective tissue disorders (Marfan, Ehler-Danlos).

Usually asymptomatic. Sometimes IE, regurgitation, formation of thrombi and arrhythmia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the auscultatory finding of mitral prolapse, and why does it occur?

A

Holosystolic “blowing” murmur. During systole, left ventricular contraction causes the valve to prolapase into the Left atrium, creating a “blowout” sound akin to a parachute inflating.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What valve is most typically affected chronic rheumatic fever?

What is the trigger for ARF?

A

Usually mitral valve, but may also involve the aortic.

Preceding group A Strep pharyngitis infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acute Rheumatic Fever

Describe the 3 components of its pericarditis.

A

Acute Rheumatic Fever

“Bread & Butter” pericarditis.

Myocarditis with Aschoff bodies (eosinophilic foci with lymphocytes, plasma cells, & anitschkow cells).

Endocarditis with formation of MacCallum plaques (irregular fibrous thickening), fibrinoid necrosis & verrucae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

A patient presents with aortic stenosis. How could you distinguish calcific stenosis from that caused by rheumatic fever based on the heart findings alone?

A

Aortic stenosis due to rheumatic fever would be accompanied by mitral stenosis.

Involvement of the cusp edges.

Fusion of the commissures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the findings seen in chronic rheumatic heart disease.

A

Valve leaflet thickening

Commissure fusion (“Fishmouth” or “Buttonhole” deformities)

Thickening of chordae tendineae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Rheumatic Heart Disease

Describe the pathogenesis.

A

Rheumatic Heart Disease

GAS pharyngitis generates antibody response against M protein, which is then directed against an unknown heart antigen. (Type II HSR)

(some genetic predisposition to this molecular mimicry response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Rheumatic Heart Disease

Describe the criteria used to diagnose this disease.

A

Rheumatic Heart Disease

JONES criteria (major manifestations; Joint pain, heart involvement, Nodules, Erythema marginatum, Sydenham chorea)

Minor criteria: Fever, elevated ESR/ARPs.

Positive ASO or Anti-DNAse B titers.

17
Q

Rheumatic Heart Disease

When does chronic rheumatic disease develop, relative to an acute GAS infection?

What role do recurrent infections play?

A

Rheumatic Heart Disease

Can take years or decades to develop.

Recurrent infections & relapses increase the risk of developing chronic disease.

18
Q

Infectious Endocarditis

Distinguish between acute and subacute infections.

A

Infectious Endocarditis

Acute endocarditis involves highly virulent organisms affecting a normal valve. Infection is necrotizing & ulcerative, requiring surgery and resulting in high mortality.

Subacute preferentiallya ffects deformed valves, is less destructive and may be managed by antibiotics alone.

19
Q

Infective Endocarditis

Who is predisposed to IE?

What organisms are generally responsible?

A

Infective Endocarditis

Those with cardiovascular abnormalities, or with immunosuppression (eg diabetics, alcoholics, cancer patients). IV drug users.

Strep viridans > Staph Aureus* > commensals (eg staph epidermidis)

*SA highest in IVDUs.

20
Q

Infective Endocarditis

What valves are most commonly affected? Why is this different in IVDUs?

Describe the lesion.

A

Infective Endocarditis

Usually mitral and aortic. IVDUs contract endocarditis from venous inoculation, so tricuspid valve is involved.

May range from mild fibrosis & granulation tissue reaction, to formation of bulky, friable vegetations at the bases of valves. May erode the myocardium.

21
Q

Infective Endocarditis

What should be present on histology?

A

Infective Endocarditis

Abundant neutrophils, dense regions of bacteria corresponding with the vegetations.

22
Q

Infectious Endocarditis

Describe the criteria used in the diagnosis of this disease.

A

Infectious Endocarditis

Duke criteria: Major (positive culture, echo findings, & valvular insufficiency), Minor (predisposing lesion or IVDU, fever, & septic emboli)

23
Q

Recall the names given to of septic embolization to the following sites:

Nail bed

Palms & soles

Digits

Retina

A

Nail bed: Splinter hemorrhages

Palms & soles: Janeway lesions

Digits: Osler nodes

Retina: Roth spots

24
Q

Infectious Endocarditis

What are its complications?

How is it treated?

A

Infectious Endocarditis

Valvular stenosis/insufficiency, myocardial abscess/perforation, septic emboli, glomerulonephritis.

IV antibiotics and possibly valve replacement.

25
Q

Nonbacterial Thrombotic Endocarditis

What are the valve findings?

Describe its pathogenesis & etiology.

A

Nonbacterial Thrombotic Endocarditis

Deposition of fibrin, platelets, & other blood products (thromboses!). May result in emboli & infarcts. Small, noninflammatory & nondestructive lesions lining the cusp edges.

Results from hypercoagulable states. Associated with mucin producing adenocarcinomas & endocardial trauma.

26
Q

Libman-Sacks Endocarditis

What is it associated with?

Describe its morphology.

A

Libman-Sacks Endocarditis

Systemic Lupus Erythematosus (Anti-PL antibodies present).

Forms intensely inflamed verrucae on valve leaflets & endocardium. Targets mitral, tricuspid valves.

27
Q

Carcinoid Syndrome

Describe its etiology & pathogenesis.

What impact can this have on the heart?

A

Carcinoid Syndrome

A result of carcinoid tumors in tissues such as lung and GI, which produce vasoactive products resulting in flushing, nausea, vomiting, etc.

50% of carcinoid syndrome results in carcinoid heart disease: “plaque-like fibrosis of right-heart endocardium & valves” probably due to endothelial damage.

28
Q

Carcinoid Heart Disease

Why is the right heart preferentially affected?

Where do the carcinoid tumors have to be located?

When can the left heart be affected?

A

Carcinoid Heart Disease

Many of the vasoactive agents are inactivated by MAO, which is highly concentrated in the lungs.

GI with metastasis to liver, or anywhere that dumps to non-portal venous system.

In primary lung carcinoids, or tumors that secrete extremely high levels of vasoactive produces.

29
Q

Carcinoid Heart Disease

Describe the changes found in the heart.

A

Carcinoid Heart Changes

Thickening of the endocardium. Expansion of smooth muscle cells & collagen. May result in tricuspid insufficiency or pulmonic stenosis.

30
Q

What problems are associated with both mechanical and biological heart prosthesis?

What problems are distinct to either?

A

Both are more prone to infectious endocarditis.

Mechanical prosthesis are a possible substrate for thromboembolus formation.

Cow & Pig valves are prone to deterioration; half need replacement by 15 years.