Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

.Pathology 2 > Valvular Diseases > Flashcards

Valvular Diseases Flashcards

1
Q

describe the gross and histological morphology in systemic hypertensive heart disease

A
  • gross:
    • concentric hypertrophy of LV
    • 400-600 g
    • long-standing cases → right ventricular hypertrophy and dilation
  • histo:
    • enlarged myocytes with large hyperchromatic rectangular “box-car” shaped nuclei
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe clinical features of systemic hypertensive heart disease

A
  • clinical features:
    • early stages = asymptomatic
    • angina pectoris
    • signs and symptoms of LHF with progression
    • cerebrovascular accidents (stroke) or renal failure as a consequence of HTN
    • sudden cardiac death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe acute cor pulmonale

A
  • acute cor pulmonale
    • pulmonary embolism causing sudden increase in burden on the right heart
    • RV is dilated but no hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe causes of chronic cor pulmonale

A
  • chronic cor pulmonale
    • COPD = most common cause
    • others: IPF, CF, marked obesity
  • morphology:
    • RV hypertrophy and often RA hypertrophy +/- dilatation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

name the etiology of mitral stenosis

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

name the etiology of aortic stenosis

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

name the etiology of mitral regurgitation

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

name the etiology of aortic regurgitation

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

describe signs and symptoms of mitral stenosis vs. mitral regurgitation

A
  • mitral stenosis
    • dyspnea (pulm. edema), fatigue, hemoptysis
    • signs: late low pitched diastolic murmur and crepitations in lungs
  • mitral regurgitation (MR)
    • dyspnea (pulm. edema), palpitation, fatigue
    • signs: pansystolic murmur radiating to axilaa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe signs and symptoms of aortic stenosis vs. aortic regurgitation

A
  • aortic stenosis:
    • angina, syncope, CHF
    • signs: ejection systolic murmur loudest at base and radiates to the neck after S1
  • aortic regurgitation
    • volume overload LHF
    • signs: bounding pulses, early diastolic murmur, displaced apex beat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe the pathogenesis of rheumatic fever

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

describe how rheumatic fever affects the myocardium

A
  • myocarditis:
    • paravascular Aschoff bodies:
      • central zone of eosinophilic matrix infiltrated by T-cells, plasma cells and activated macrophages within the CT of the heart
    • Anitschkow cells: wavy ribbon-like chromatin (caterpillar cells)
    • giant cells can be seen in all 3 layers of the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe how rheumatic fever can affect the endocardium and pericardium

A
  • endocardium:
    • edematous and thickened valves with foci of fibrinoid necrosis
    • multiple tiny 1-2 mm wart-like vegetations along the lines of closure of mitral valve; no effect on cardiac fxn
  • pericardium:
    • fibrinous pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe how rheumatic fever affects the mitral valve

A
  • chronic mitral valvulitis: most frequent
    • conspicuous irregular fibrous thickening (neovascularized) and calcification of the leaflets, often with fusion of the commissures and shortening of the chordae tendinae; fixed narrow opening (fish mouth, buttonhole)
    • mitral stenosis and regurgitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe how rheumatic fever affects the aortic valve

A
  • chronic aortic valvulitis:
    • cusps are thickened, firm and adherent to each other
    • valve orifice is reduced to rigid, triangular channel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

describe clinical features of chronic rheumatic carditis

A
  • valvulitis (M>A>T>P) murmurs
  • cardiac hypertrophy and dilation
  • CHF
  • arrhythmias
  • infective endocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe the diagnosis of RF

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe calcific aortic stenosis

A
  • morphology:
    • degenerative calcific stenosis (dystrophic calcification)
    • leaflets are rigid and deformed by irregular calcified masses
    • the calcium deposits lie behind the valve cusps and extend into the sinus of Vasalva → coronary ischemia
    • marked LVH
20
Q
A
21
Q

describe clinical features of calcific aortic stenosis

A
  • due to aortic stenosis:
    • angina pectoris: increased requirement of hypertrophied myocardium
    • syncope: poor perfusion of the brain
    • death usually occurs due to CHF or arrhythmias
22
Q

there is an intrinsic defect of ____ in mitral valve prolapse

A

there is an intrinsic defect of connective tissue synthesis and remodeling in mitral valve prolapse

23
Q

describe the morphology of mitral valve prolapse

A
  • morphology:
    • soft pulled up rubbery mitral valve cusps
      • ballooning of the valve leaflets into the LA during systole (mid-systolic click)
    • the chordae tenindae, which are often elongated and fragile, may rupture in severe cases
    • the mitral annulus may be dilated (regurgitation)
24
Q
A
26
Q

describe clinical features of mitral valve prolapse

A
  • most patients are asymptomatic
  • palpitations
  • fatigue or atypical chest pain
  • midsystolic click – abrupt tension on leaflets and chordae when valve tries to close
  • severe complications in about 3% of cases:
    • mitral regurgitation and CHF
    • IE
    • ventricular arrhythmias (may lead to SCD)
    • thromboemboli stroke
  • rarely syndrome characterized by scoliosis and high arched palate
27
Q

describe acute endocarditis

A
  • acute endocarditis
    • typically, infection of previously normal valve
    • destructive and fulminant
    • caused by highly virulent organisms
    • mortality is high despite antibiotics and/or surgery
28
Q

describe subacute endocarditis

A
  • subacute endocarditis
    • infxn of previously abnormal valve (deformed valves)
    • less destruction
    • caused by low virulent organisms
    • most patients recover with appropriate therapy
29
Q

name the causative organisms in native valve IE

A
30
Q

name the causative organisms involved in prosthetic valve IE

A
31
Q

describe the pathogenesis of IE

A
32
Q

name predispoing factors for infective endocarditis

A
  • preexisting cardiac abnormality:
    • rheumatic valvular disease
    • mitral valve prolapse
    • congenital defects
    • degenerative calcific aortic stenosis
  • prosthetic heart valves
  • IVDU = tricuspid valve
  • transiet bacteremia:
    • dental procedures, urinary catheterization, endoscopy
33
Q

describe the complications and host consequences caused by persistent bacteremia (as a consequence of vegetation)

A
34
Q

describe the complications and host consequences caused by tissue destruction (as a consequence of vegetation)

A
35
Q

describe the complications and host consequences caused by fragmentation (as a consequence of vegetation)

A
36
Q

describe the complications and host consequences caused by release of bacterial antigen (as a consequence of vegetation)

A
40
Q

____ are the classic hallmark of IE and are prone to ___ that can lead to _____

explain this

A

vegetations are the classic hallmark of IE and are prone to embolization → septic infarcts, abscesses, mycotic aneurysms

  • friable, bulky, potentially destructive lesions
  • contain fibrin, inflammatory cells, bacteria
42
Q
A
46
Q

describe general features associated with IE

A
  • fever
  • clubbing of fingers
  • splinter hemorrhages under nail beds
  • Osler nodes: tender (painful) subcutaneous nodules
  • Janeway lesions: nontender (not painful) maculae on palms and soles
  • Roth spots: retinal hemorrhages with clear center
  • systemic embolization → stroke, distal organ infarcts
47
Q

name clinical features associated with acute bacterial endocarditis

A
  • acute bacterial endocarditis
    • high grade fever with chills
    • new cardiac murmur
    • features of septicemia
  • subacute bacterial endocarditis
    • low grade fever; malaise
    • changing cardiac murmurs
    • weight loss
    • splenomegaly
48
Q

describe the diagnosis and treatment of IE

A
  • diagnosis
    • Duke criteria
    • repeated blood cultures for both aerobic and anaerobic organisms
    • echocardiography
  • treatment
    • difficult infxn to eradicate because of the avascular nature of the valves
    • antibacterial therapy (IV, long term)
49
Q

describe nonbacterial thrombotic endocarditis (NBTE)

A
  • characterized by the presence of sterile thrombi on the leaflets of previously normal valves
  • encountered in debilitated patients e.g. cancer (hence the name marantic (from marasmus) endocarditis)
  • usually asymptomatic
50
Q

describe the pathogenesis and complications of NBTE

A
  • pathogenesis:
    • associated with endothelial abnormalities, hypercoagulable states, adenocarcinomas
  • complications:
    • embolization and IE
52
Q

describe Libman-Sacks endocarditis

A
  • characterized by presence of sterile vegetations on the cardiac valves in patients of SLE (LSE in SLE)
  • deposition of immune complexes
53
Q

describe complications of mechanical prosthetic valves

A
  • complications:
    • thrombo-embolism
    • life anticoagulation → hemorrhage
    • IE
    • RBC destruction (hemolysis)
    • inadequate healing → paravalvular leak
54
Q

describe complications of tissue valves (bioprostheses)

A
  • no anticoagulation needed
  • complications
    • less durable: matrix deterioation, rigidity, calcification → stenosis, can perforate
    • IE
    • inadequate healing → paravalvular leak

.Pathology 2 (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions