Valvular Heart Disease Flashcards

1
Q

stenosis

A

failure of a valve to open completely, obstructing forward blood flow.
- results from severe fibrosis or calcification and distortion of the valvular leaflet anatomy - slow to develop

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2
Q

insufficiency

A

failure of a valve to close completely thereby allowing reverse flow of blood. either intrinsic disease of the valve cusps or damage to associated structures and by slow or rapid

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3
Q

pure disease

A

if only stenosis or insufficient is present

if both -> mixed lesion

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4
Q

consequences of valvular lesions

A

varies for slight and physiologically unimportant to severe requiring surgical intervention
- depends on the rate of development of the lesion

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5
Q

secondary changes

A

lungs and liver are most affected - congestion of pulmonary htn

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6
Q

etiology : mitral stenosis

A

post inflammatory scarring ( rheumatic heart disease )

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7
Q

etiology : aortic stenosis

A

calcification of anatomically normal and congentially bicuspid aortic valve ( degenerative calcific AS)

  • senile calcific aortic stenosis*
  • post inflammatory scarring ( rheumatic heart disease)
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8
Q

etiology of aortic regurg

A
-aortic dilation *
 intrinsic valvular disease -> rheumatic 
- infective endocarditis 
-syphilitic aortitis 
-ankylosing spondylitis 
-rheumatic arthritis 
-marfan syndrome
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9
Q

etiology : mitral regurg

A

abnormal leaflets and commissures

  • mitral valve prolapse * (myxomatous degeneration)
  • post inflammatory scarring
  • infective endocarditis
  • fen-phen-induced valvular fibrosis

abnormal tensor apparatus

  • rupture papillary muscle
  • papillary muscle dysfunction
  • rupture of chordae tendineae

abnormal left ventricular cavity or annulus

  • LV enlargement ( myocarditis , dilated cardiomyopathy)
  • calcification of mitral ring
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10
Q

critical stenosis

A

2/3 reduction of valve area or a pressure gradient of at least 50 mm HG

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11
Q

pathology of mitral valve prolapse

A
  • too much valve tissue with billowing up of tissues between chordal attachments
  • leaflets are thickened , soft grey white gelatinous appearing and have atrial smooth muscle
  • chordae are elongated and attenuated or thinned
  • soo much spongiosa -> floppy valve
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12
Q

mitral valve etiology

A

unknown: underlying connective tissue problem

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13
Q

mitral annular calcification

A

see stony hard calcified nodules behind the leaflets

  • nodules give site for thrombin to form-> embolized -> stroke
  • infective endocarditis
  • women over 60 and ladies with a myxomatous mitral valve or elevated left ventricular pressure
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14
Q

clinical features: rheumatic heart disease

A

major criteria:

  • carditis
  • migratory polyarthritis
  • chorea
  • subcutaneous nodules
  • erythema marginatum

minor criteria:

  • arthralgia
  • fever
  • elevated acute phase reactants
  • EKG changes ( increased P-R interval)

evidence of prior streptococcal infection

    • throat culture or rapid strep Ag test
  • elevated or rising strep antibody titer

2 majors or one major and 2 minor and ecidnce of prior strep infection

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15
Q

epidemiology of RHD

A

1-3% of strep infection lead to RF

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16
Q

Pathogenesis of RF

A
  • heightened immunologic reactivity to step Ags with resultant ABs and possible cytotoxic T cells that cross-react with cardiac antigens. this group A carbohydrate moiety shares antigenic similarity with a glycoprotein found in cardiac calces the M antigen may cross react with myocardial Antigens.
  • possible toxic effect of a toxin secreted by strep ( anti streptolysin O)
  • possible genetic predisposition
17
Q

pathology of RF

A

pancarditis may occur ( endocardial to pericardial inflammation)

  1. endocarditis - valvulitis with verrucae ( small vegetations along line of closure of mitral valve leaflet)
  2. myocarditis - aschoff bodies -> pathognomonic
    - inflammatory focus of lymphocytes, plasma cells and plump modified histiocytes (anitschkow macrophages) surround an area of central fibrinoid necrosis
  3. pericarditis - a bread and butter -( mozzarella) fibrinous pericarditis is present - friction rub
18
Q

chronic rheumatic heart disease

A

65-70% mitral
mitral and aortic - 25%
- diffuse fibrosis , commissural fusion, calcification, post-inflamm neovascularization
-mitral valve thickening, shortening and fusion of the chordae tendinae -> fish mouth
-COMMISSURAL FUSION
- complications: stenosis or insufficiency and increased incidence of infective endocarditis

19
Q

carcinoid heart disease

A

cardiac manifestation of the systemic syndrome cause by carcinoid tumors

  • tumor made of neuroendocrine cells and secretes vasoactive amines
  • amine are broken down in liver and lung- > if they arent broken down-> you get carcinoid syndrome
  • results in a thickening of heart valve - > amines form plaques that thickens the endocardium - made of smooth muscle cells within a matrix
  • limited to the heart because they get deactivated in the lung
20
Q

valve replacement

A

60% of substitute valve recipients get a serious prosthesis related problem within 10 yrs post-op

21
Q

mechanical heart valves

A
  • made of something other than tissue ( metal, plastic)
  • prone to thromboembolic complications - local obstruction by thrombus, patient requires long term anticoagulation
  • lasts a long time but the anti-coag is a problem if people fall or want to be in contact sports
22
Q

tissue valves

A

bioprostheses consisting of chemically treated animal tissue mounted on a prosthetic frame

  • tissue valves are flexible and function somewhat like natural semilunar valves
  • structural deterioration is a major failure mode of bioprostheses, with calcification and/or tearing causing secondary regurgitation
  • will probably need a replacement in 10-20 yrs
23
Q

complications of valve replacement

A
  • infective endocarditis
  • hemolysis
  • inadequate or exuberant healing - paravalvular leak or overgrowth of fibrous tissue