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Cardiovascular System > Valvular Heart Disease Pathology and Clinical > Flashcards

Valvular Heart Disease Pathology and Clinical Flashcards

1
Q

What is the purpose of cardiac valves?

What are the different types of valves in the heart?

A

To maintain unidirectional flow of blood

There are

SEMILUNAR valves (aortic and pulmonary) and

ATRIOVENTRICULAR valves (mitral and tricuspid)

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2
Q

what are the two main categories of valvular heart disease? How do they usually occur?

A

Stenosis (failure of a valve to open completely):

  1. chronic process affecting a valve cusp

and

Insufficiency (failure to close completely):

  1. Functional regurgitation of valvular incompetence due to disruption of supporting structures
  2. Intrinsic disease of valve cusps
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3
Q

What are the major valvular diseases discussed?

A

Congenital: Bicuspid aortic valve (most common)

Acquired:

Aortic stenosis: senile calcific aortic stenosis

Aortic insufficiency: Dilation of ascending aorta related to HTN and aging

Mitral stenosis: Rheumatic heart disease

Mitral insufficiency: Myxomatous degeneration

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4
Q

What are different examples of calcific valvular diseases?

What is it?

A

Calcific aortic stenosis and Mitral annular calcification

Dystrophic calcification- damage causing wear and tear complicated by deposits of calcium phosphate?

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5
Q

Calcific Aortic Stenosis (AS)

When does it occur?

What are the clinical effects?

What is the treatment?

A

Calcific Aortic Stenosis (AS)

5th/6th decades-biscuspid, unicuspid valves (assoc w/ Notch gene)

8th/9th decades- normal valves (“senile”)

Clinical effects:

LV: increased pressure causes hypertrophy

Angina, ischemia, CHF

Syncope

Death for 50% within 2 years

Treatment: valve replacement

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6
Q

Mitral Annular Calcification

What is it?

Who gets it?

Why is it bad?

A

Mitral Annular Calcification

Degenerative calcific deposits on fibrous ring, at base of valve

Occurs in women older than 60 yo, increased in pt. with myxomatous valves or elevated LV pressure.

Usually does not affect fxn but calcifications are sites for thrombi/infection

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7
Q

Myxomatous Degeneration of Mitral Valve (prolapse)

What is it?

In who does it occur?

What are the complications?

How does it happen and Assoc w/ what?

Clinical features?

A

Myxomatous Degeneration of Mitral Valve (prolapse)

One or both leaflets enlarged, hooded, redundant, floppy (myxoid). Prolapse or balloon back into left atrium during systole

Occurs in Young women

Usually no serious complications but can have regurgitation. Infective endocarditis, mitral insufficiency, thrombi on atrial surfaces leading to stroke or other systemic infarcts due to emboli, arrythmias leading to sudden death.

Unknown pathogenesis but probably developmental anomaly of connective tissue. Associated with Marfan syndrome (fibrillin gene mutation) and other hereditary disorders.

Clinically presents with mid systolic click on auscultation when asymptomatic or late systolic/holosystolic mumur when regurgitation happens

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8
Q

Acute Rheumatic Fever

When does it occur?

Most important complication?

How does it present?

A

Acute Rheumatic Fever

Follows episode of Group A Beta-hemolytic Streptococcal (pyogenes) pharyngitis

Most important complication is the progression to chronic valvular dysfunction (mitral stenosis)

Presents as widely disseminated inflammatory lesions in many sites:

Pancarditis (all three layers)

Bread and butter pericarditis

Myocarditis w/ Aschoff bodies

Endocardium and left sided valves w/ fibrinoid necrosis and verrucae

Subendothelial (MacCallum) plaques: irregular fibrous thickening of endocardium)

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9
Q

What are Aschoff Bodies?

A

Classic lesion of Acute Rheumatic Fever

Foci of swollen eosinophilic collagen surrounded by T lymphocytes, plasma cells, and plump macrophages- Anitschkow cells (caterpillar cells)

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10
Q

What happens in Chronic rheumatic heart disease?

What is the major effect?

A

Organization of inflammation and fibrosis leads to>

Thickened valve leaflets

Fusion of commissures (fishmouth or buttonhole deformities)

Fusion/thickening of chordae tendinae

Major effect is mitral stenosis, leads to left atrial dilatation (someitmes thrombus formation). REDUCED CARDIAC OUTPUT b/c mechanical obstruction prevents filling of LV

Pulmonary congestion, eventual right ventricular hypertrophy, and right sided heart failure.

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11
Q

To what extent are the different valves affected by chronic rheumatic heart disease?

A

Mitral valve alone (65-70%)

Mitral and aortic (25%)

Tricuspid less often

Pulmonary rare

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12
Q

What is the pathogenesis behind Rheumatic heart disease?

What is the diagnosis for this?

A

Hypersensitivity reaction induced by group A streptococci

Antibodies against M protein cross react w glycoprotein antigens in heart, joints, and other tissues.

Diagnosis through Jones criteria:

Preceding Group A strep infection

2 major manifestations or 1 major and 2 minor

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13
Q

For diagnosis of Rheumatic heart disease, (2 major or 1 major 2 minor) and preceding Group A strep infection

What are the major manifestations?

and

What are the minor manifestations

A

Migratory polyarthritis (large joints)

Carditis- pericardial friction rub, weak heart sounds, tachycardia, arrhythmia

Subcutaneous nodules -rare (extensor surfaces of joints)

Erythema marginatum of skin- rare (trunk)

Sydenham chorea (involuntary purposeless, rapid movements)

Minor: non specific signs and symptoms of:

fever

arthralgia

elevated acute-phase reactants

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14
Q

What is a specific biomarker clinical feature of acute rheumatic fever in regards to gropu a beta hemolytic strep?

A

ASO titers and antibodies to DNAase B

(anti-Streptolysin O) and DNAase are protein produced by group a strep

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15
Q

Prognosis for acute rf?

Prognisis for chronic?

A

Acute: good for primary attack. increased vulnerability to reactivation

Chronic: Years or decades after initial episode. Valvulitis. Surgical repair of valves improves outlook

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16
Q

What are the two basic clinical forms of infective endocarditis?

A

Acute: Highly virulent organism, normal valve, 50% mortality

Necrotizing ulcerative invasive infection requiring surgery

Subacute: Low virulence, deformed valve

Less destructive lesions, respond to antibiotics

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17
Q

What are the factors for getting infective endocarditis?

A

Cardiovascular abnormalities (RHD, myxomatous mitral valve, calcific valvular stenosis, artificial valves)

Host factors (Neutropenia, immunodeficiency, malignancy, diabetes, alcoholics, and IV drug users)

18
Q

Common causative agents of infective endocarditis

A

Strep viridans for 50-60% of cases of infected deformed valves

Staph aureus is 10-20% of overall infective endocarditis (most common in IVDA)

19
Q

What are the major and minor clinical criteria of bacterial endocardiits?

A

Major:

Positive blood cultures

ECG findings

New valvular regurgitation

Minor:

Predisposing heart lesion or IVDA

fever

Uncommon finding sfrom septic emboli

20
Q

Complications of bacterial endocarditis?

Treatment?

A

Valvular insufficiency or stenosis and possible heart failure

Myocardial abscesses and possible perforation

Embolic complications from vegations break off

Glomerulonephritis

Treatment: IV antibiotics, valve replacement if necessary, prophylactic antibiotics after valve damage

21
Q

What are examples of non infective vegetations and describe them.

A

Nonbacterial thrombotic endocarditis

Depositions of small masses of fibrin, platelets, and other blood products on leaflets occuring in debilitated patients. Can results in emboli and infarcts.

Caused by hypercoagulable states, assoc w mucin producting adenocarcinomas.

Sterile nondestructive noninflammatory small 1-5 mm.

Libman-Sacks endocarditis-a primary antiphospholipid syndrome

Systemic lupus erythematosus.

Mitral and tricuspid valves involved.

Antiphospholipid antibodies present.

Either or both sides of leaflets may also be on endocardium. Presents as 1-4 mm verrucae w/ fibrinous material may have intense inflammation

22
Q

What is carcinoid syndrome?

How does it present?

What happens in the heart?

What is the exact cause?

A

Caused by carcinoid tumors that produce serotonin kallikrein bradykinin histamine prostaglandins and tachykinins.

Presents as flushing, cramps, nausea, vomiting, diarrhea

(serotonin and bradykinin inactivated by MAO in pulmonary vasculature AND also inactivated by passage through functioning liver.

Half of patients get plaque like fibrosis of right heart endocardium and valves. Usually on right not left b/c of inactivation of mediators by MAO in lung.

Exact cause unknown. Related to endothelial injury caused by vasoactive agents.

23
Q

What are complications of artificial valves?

A

Mechanical prosthesis:

Thromboembolic complications

Infective endocarditis

Bioprosthesis:

Structural deterioration (half need replacement by 15 yrs)

Infective endocarditis

24
Q

For Aortic Stenosis, what are the two major etiologies?

For one of the etiologies, age plays a factor. How so?

A

Calcific degeneration

<65= bicuspid valve

>65= tricuspid valve

<30=congenitally abnormal valve

Rheumatic

almost always involves mitral valve as well

25
Q

What happens with severe aortic valve stenosis in regards to pressures

A

Left ventricle increases dramatically in pressure whereas the aortic decreses. Left atrial pressure also increases

On a graph of LVP by LVV you get a right and upward shift

26
Q

How do you diagnose aortic stenosis?

A

Physical exam- Sustained LV impulse w/ little to no displacement. Weakened and late carotid impulse. Absent A2 or paradoxically split A2, murmur is systolic crescendo decrescendo (later peaking/worse stenosis). Heard at the base of the heart or the right upper sternal border radiating to the carotid arteries.

CXR- Little cardiac enlargement due to LVH. Post stenotic dilation of the ascending aorta. Calcification of the aortic valve.

EKG- Shows left ventricular hypetrophy

Echocardiogram-Shown decreased valve area

Cardiac catheterization- Peak to peak between LV and Aortic pressures.

27
Q

Prognosis for Aortic stenosis?

A

Key point is when symptoms begin to develop

Angina (5 yr mean survival)

Syncope (3 yr mean survival)

CHF (2 yr mean survival)

28
Q

Treatment for aortic stenosis?

What is a classic presntation of aortic stenosis on physical exam?

A

Valve replacement for when severe aortic stenosis WITH SYMPTOMS occurs.

Systolic crescendo decrescendo murmur at the right upper sternal border radiating to the carotids

29
Q

What are causes of aortic regurgitaiton?

A

Abnormalities of the valve leaflets

  • Congenital
  • Endocarditis
  • Rheumatic

Dilation of the aortic root

  • Aortic aneurysm
  • Aortic dissection
  • Annuloaortic ectasia
  • Syphilis
30
Q

What is aortic regurgitation?

What is it acutely?

What is it chronically?

A

Part of the blood the LV ejects into the aorta during systole returns to teh LV in diastole across an incompetent valve.

Resulting in VOLUME OVERLOAD of the left ventricle

Acute: Left ventricle normal size with low compliance. Diastolic pressure rises quickly. This backs up to the left atrium and into pulmonary vasculature. Results in pulmonary congestion and or edema (surgical emergency)

Chronic: Left ventricle undergoes compensatory adaptation in response to regurgitation. There is volume overload and some pressure overload of teh left ventricle. Ventricle dilates over time. Left ventricle compliance increases. Reduced pressure to the left atrium and pulmonary vasculature

31
Q

Patient complaints w/ aortic regurgitaiton?

Physical signs?

A

Complaints of

  • dyspnea on exertion
  • fatigue
  • Decrased exercise tolerance
  • chest pain

Physical signs:

Hyperdynamic pulses, head bobibng, water hammer pulse.

Widened pulse pressure (diastolic bp less than half of systolic bp)

Decrescendo diastolic murmur–increases w increased SVR, heard best at end expiration w patient leaning forward

Austin Flint murmur a diastolic rumble

32
Q

What shows on Chest x ray for aortic regurgitation

A

Enlarged left ventricular silhouette (chronic)

Acute less likely to show this but more to show pulmonary vascular congestion.

33
Q

How do you treat aortic regurgitation?

A

For acute: surgical emergency w/ immediate surgical replacement

For chronic:

If asymptomatic and normal LVEF (>50%): periodic followup with echocardiography and consider afterload reduction w calcium channel blocker or ACE inhibitior if patient has HTN

If asymptomatic and low LVEF (<50%): Refer for surgery for valve replacement

If symptomatic and normal LVEF: Refer to surgery for valve replacement

34
Q

What are the etiologies for mitral regurgitation?

A

Organic (primary):

Myxomatous disease /MVP (degenerative)

Rheumatic valve disease

Endocarditis

Congenital (cleft leaflet)

Functional (secondary):

Ischemic CM

Dilated CM

Hypertrophic CM

35
Q

What are the signs of acute mitral regurgitation?

A

Normal LA size and compliance

High left atrial pressure

High pulmonary venous pressure

Pulmonary congestion and edema

See prominent V waves on catheterization

Acute mitral regurgitation is considered medical emergency

36
Q

Signs of chronic mitral regurgitation?

A

Increased left atrial size and compliance

More normal left atrial and pulmonary venous pressures

Lower forward cardiac output

See increased left ventricular size

Eventual systolic dysfunction over time

* hear a holosystolic murmur at the apex of the heart upon auscultation

37
Q

MAnagement of acute mitral regurg

Management of chronical mitral regurg

A

acute: stabilize the patient w/ diuretics and vasodilators and also depending on the cause, consider emergent surgery for management

Chronic: if asymptomatic continue to monitor. If symptomatic and severe mitral regurgitation see about repair or replacement of the valve (repair preferred)

IF there is severe left ventricular dysfucntion often little can be done

38
Q

For the papillary muscles, what portions supply chordae to what parts of the leaflets

What are the blood supplies

A

2 main papillary muscles w several heads

Anterolateral portion provides chordae to the anteroalteral half of both mitral leaflets

Posteromedial portion provides chordae to the posteromedial half of both mitral leaflets

Posteromedial portion blood supply from right coronary artery.

Anterolateral portion blood supply dual supply

39
Q

What etiology causes mitral stenosis?

A

Mostly rheumatic fever

rare causes: congenital stenosis/calcification of the mitral annulus/endocarditis with large vegetattions obstructing valve orifice

40
Q

What is the normal valve area?

What is seen w/ mitral stenosis?

A

3-4 cmsquared in normal

in Mitral stenosis, MVA<2cmsquared

41
Q

symptoms of mitral stenosis

A

Dyspnea and reduced exercise capacity

In milder, no symptoms at rest only w exertion or increase dhr activities

in more severe, shortness of breath occurs at rest, patients develop symptoms of heart failure w orthopnea, paroxysmal nocturnal dyspnea.

Also signs of rightsided heart failure w jugular venous distension. hepatomegaly ascites, edema

Rare symptoms: hoarseness and hemoptysis

42
Q

treatment for mitral stenosis

A

Duretics if vascular congestion

beta blcoekrs calcium channel blockers digoxin if atrial fibrilliation

chronic anticoagulation if atrial fibrilliaton present

IF medical not working or if significant pulmonary hypertension then Balloon valvulplasty or valve replacement

Cardiovascular System (35 decks)

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