Valvular Heart Disease Flashcards

1
Q

Valvular interstitial cells

A

-most abundant cells in heart valves, distributed throughout all layers, synthesize ECM and matrix matalloproteinases (MMPs)

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2
Q

Three types of valve pathology

A
  1. nodular calcification begins in interstitial cells: calcific aortic stenosis
  2. damage to collagen that weaken leaflets: mitral valve prolapse (MR)
  3. fibrotic thickening: key feature in rheumatic heart disease (MS)
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3
Q

Three types of valve disease

A
  1. stenosis: failure of valve to open completely, which impedes flow
  2. insufficiency (regurgitation or incompetence): primary-mitral valve prolapse, secondary-functional mitral regurgitation (normal leaflets, will improve w/ heart failure treatment/ischemia)
  3. combined stenosis & insufficiency
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4
Q

Valve issue seen in marfan sydrome

A

aortic regurgitaion

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5
Q

Acute and Chronic valve disease

A
  • acute: severe or lethal, no time to adapt to hemodynamic changes
  • chronic: better tolerated due to chamber adaptation
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6
Q

Result of mitral or aortic insufficiency

A
  • volume overload
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7
Q

Result of aortic stenosis

A
  • pressure overload

- cardiac hypertrophy

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8
Q

Calcific aortic stenosis

A
  • most common valvular abnormality
  • consequence of age “wear & tear”, hyperlipidemia, HTN, inflammation, atherosclerotic issues, deposition of hydroxyapatite
  • SATINS NOT HELPFUL
  • BICUSPID valves at increased risk, prone to endocarditis
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9
Q

Causes of valvular diseases

A
  • acquired

- genetic

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10
Q

Genetics of AV stenosis

A
  • 1%, possibly hereditary

- significant AS at age 50 (EARLIER THAN ACQUIRED)

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11
Q

Nonrheumatic AS feature

A
  • free edge is NOT effected
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12
Q

LaPlces’s Law and AS

A
  • in order to reduce stress of increased pressure ventricle wall must get thicker
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13
Q

Result of hypertrophic ventricle

A
  • myocardium tends to be ischemic due to diminished microcirculatory perfusion/demand-supply missmatch
  • ANGINA even in ABSENCE of CAD
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14
Q

Prognosis of AS (bicuspid/tricuspid)

A
  • bicuspid AS progresses faster

- treatment is surgical valve replacement

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15
Q

Mitral annular calcification & swinging calcified amorphous tumors (CATs)

A
  • calcific deposits develop in the FIBROUS ANNULUS
  • usually DOES NOT AFFECT valvular function but can lead to: regurgitation, stenosis, arrhythmias (by calcium deposits penetrating deep to impinge on AV conduction system)
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16
Q

Large risk with swinging CATs and mitral annular calcification

A
  • nodules provide site for thrombus formation
  • increased risk of embolic stroke
  • endocarditis
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17
Q

Acute rheumatic fever

A
  • inflammatory disease occurring 10 days to 6 wks after episode of GROUP A STREP PHARYNGITIS
  • acute rheumatic carditis is a common manifestation and may progress over time to rheumatic heart disease
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18
Q

Rheumatic heart disease

A
  • fibrotic valvular disease, involving mitral valve leading to MITRAL VALVE STENOSIS
  • result of RF acute rheumatic carditis progression
19
Q

Pathogenesis of RF

A
  • antigens to group A strep cross react with host proteins: antibodies against strep M proteins also recognize cardiac self-antigens
  • antibody binding can activate complement, cytokine production stimulated by T cells leads to macrophage activation (ASCHOFF BODIES)
20
Q

Clinical features of RF

A
  1. migratory polyArthritis of large joints
  2. panCarditis
  3. subcutaneous Nodules
  4. ERythema marginatum of the skin
  5. sydenham Chorea: involutary rapid, purposeless movements
21
Q

Diagnostic ‘Jones criteria’

A
  • evidence of preceding group A strep infection

- 2 major manifestations OR 1 major + 2 minor manifestations

22
Q

Antibodies of two enzymes detected in RF patients due to strep

A
  • steptolysin O

- DNase B

23
Q

Acute carditis symptoms with RF

A
  • pericardial friction rubs
  • tachycardia & Afib
  • functional mitral valve insufficiency due to cardiac dilation/CHF
  • 1% die of fulminant RF involvement of heart
24
Q

Recurrence of RF

A
  • increased vulnerability w/ subsequent pharyngeal infections
  • damage is cumulative
  • clinical manifestations appear years or decades after initial episode of RF and depend on valve involved
25
Q

Treatment for rheumatic heart disease

A
  • favor percutaneous balloon valvuloplasty > surgery

- MITRAL VALVE=REPAIR, AORTIC VALVE=REPLACE

26
Q

Different types of chronic rheumatic heart disease

A
  • vegetative valve disease*
  • RHD
  • infective endocarditis
  • nonbacterial thrombotic endocarditis
  • libman sacks endocarditis (in patients with SLE)
27
Q

Valves involved in chronic rheumatic heart disease

A
  • mitral valve alone: 40%
  • mitral & aortic: 40%
  • aortic alone: 20%
  • tricuspid: occasional
  • pulmonic valve: NEVER INVOLVED
28
Q

Characteristic feature of anterior MV leaflet on ultrasound

A
  • ‘hockey stick’ (diastole)
29
Q

Ventricle changes in chronic rheumatic heart disease

A
  • congestive changes in lungs may induce pulmonary vascular/parenchymal changes; over time, these can lead to RIGHT ventricle hypertrophy
  • left ventricle in unaffected by isolated mitral stenosis
30
Q

Side of MV more effected in rheumatic heart disease

A

ventricular side

31
Q

Appearance of MS in rheumatic heart disease

A
  • fish mouth
  • FREE EDGE IS EFFECED
  • candle stick appearance
32
Q

Major causes of mitral regurgitation

A
  • degenerative mitral disease (MVP): 65%

- ischemic mitral regurgitation: 27%

33
Q

Cause of mitral valve prolapse

A
  • myxomatous degeneration of mitral valve
34
Q

Mitral valve prolapse

A
  • one or both leaflets are floppy and prolapse into the left atrium during SYSTOLE
  • F:M=7:1 i.e. FEMALES MORE THAN MALES
  • most often incidental finding
35
Q

Histology of MVP

A
  • thickening of spongiosa layer w/ deposition of mucoid (myxomatous) material, called MYXOMATOUS DEGENERATION
  • attenuation of collagenous fibrosa layer
  • thrombi on atrial surface
  • calcifications at base of posterior MV leaflet
36
Q

Clinical features of MVP

A
  • usually anymptomatic, mid systolic click, murmur

- DIAGNOSIS IS CONFIRMED BY ECHO

37
Q

Treatment of MVP

A
  • most common cause for mitral valve surgery

- NATIVE valve repair over valve replacement

38
Q

Carcinoid syndrome

A
  • systemic disorder marked by flushing, diarrhea, dermatitis, & bronchoconstriction caused by bioactive serotonin released by carincoid tumors
39
Q

Result of serotonin release

A

fibrosis

40
Q

Carcinoid syndrome spread

A
  • 50% of patients w/ liver metastasis will develop carcinoid heart disease
41
Q

Parts of heart effected by carcinoid heart disease

A
  • endocardium, & valves of RIGHT heart

- left heart can occur in setting of PFO & ASD and direct right to left flow

42
Q

Plaque deposits in carcinoid heart disease similarities

A
  • similar to lesions occurring in patients taking FENFLURAMINE (appetite suppressant) or ERGOT ALKALOIDS (migraines)
  • agents also affect serotonin release
43
Q

Clinical manifestation of carcinoid heart disease

A
  • exam: elevated JVP, palpable RV impulse, murmurs of tricuspid & pulmonary valve regurgitation
44
Q

Tri-layered structure of cardiac valves

A
  • fibrosa: dense collagenous outflow surface, connected to supporting structures
  • spongiosa: central core loose CT, proteoglycan rich
  • ventricularis/atrialis(depending on chamber it faces): elastin rich layer on inflow surface