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general path > Cardiac Valvular disase and vasculitis (CVIII) > Flashcards

Cardiac Valvular disase and vasculitis (CVIII) Flashcards

1
Q

what causes mitral valve stenosis

A

Acute Rheumatic fever (ARF)

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2
Q

what causes acquired stenosis

A

chronic recurrent rheumatic valvular disease

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3
Q

what is acquired stenosis

A

Failure of a valve to open completely

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4
Q

what kind of disase is Acute rheymatic fever

A

systemic diase usually in children

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5
Q

what does Acute Rheumatic fever usually follow

A

Group A beta-hemolytic streptococcal pharyngitis

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6
Q

what does Acute rheumatic fever lead to

A 
Myocarditis
Pericarditis
Arthralgia
Arthrisits
erythema marginatum (skin rash)
Subcutaneous nodules
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7
Q

what microscoppically characterizes the myocarditis vauses by Acute rheumatic fever

A

aschoff bodies

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8
Q

what are aschoff bodies

A

collection of mononuclear inflammatory cells and fibroblasts (grnulomatous inflammation)

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9
Q

what does Recurrent bouts of RF lead to

A

severe fibrosis and calcification of the mitral valve and other heart valves
- (stenosis)

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10
Q

why does RF lead to fibrosis and calcifiation of the mitral valve and other heart valves

A

production of antibodies against streptoccal bacteria

- cross reacts with antigens in the heart, joints, and others

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11
Q

what causes pericarditis in RF

A

Fibrinous

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12
Q

what causes endocarditis in RF

A

sterile vegetations

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13
Q

what is Regurgitation

A

Valves that fail to close completely allowing backflow of blood

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14
Q

what can cause Mitral valve regurgitation

A

IHD

Endocarditius

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15
Q

what is mitral valve prolapse

A

leaflets balloon into the left atrium during left ventricular contract

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16
Q

how common is mild prolapse of the valve

A

common at 5-10%

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17
Q

what level of prolapse is needed to cause Regurgitation

A

severe prolapse

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18
Q

what can be caused by severe regurgitation by prolapse

A

chest pain

Palpitation

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19
Q

what are some complications of a severe prolapse

A 
Endocarditis
Mitral regurgitation
Thoromboemboli
atrial fibrillation
Sudden death (rare) potential complication
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20
Q

what is seen in severe prolapse to the valve

A

vavle cusps are large
Microscoppically show fragmentation
loss of collagen
- myxomatous degeneration histolofy

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21
Q

what causes floppy mitral valve

A

Isolated abnormality

systemic conective tissue disease (marfan)

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22
Q

what causes aortic valve stenosis

A

Fibrosis and calcifiaction

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23
Q

what may lead to fibrosis and calcification of the aortic valve

A

chronic rheumatic valvular disease (also affects mitral valve)
old people

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24
Q

what may predisopse one to aortic valve stenosis

A

Bicuspid aortic valve

- tends to be calciiced and fibrosed at 40 year old

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25
Q

what can lead to aortic valve regurgitation

A

Valve cusp destruction (endocarditis)
myxomatous degeneration/ weakened vavlve cusps
dilation of aortic root

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26
Q

what causes aortic valve cusp distruction

A

infectious endocarditis

Rheynatic heat disaese

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27
Q

what causes dialtion of the aortic root

A

Media of the aorta degenerating

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28
Q

what are predisposing factors of infective endocarditis

A 
Intracardiac shunts
Valvular disease
Prosthetic valvues (10-20% of all IE cases)
IV drug abuse
immune suppression
diabetes mellitus
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29
Q

what causes ineffective Endocarditis

A 
Endocardial/endothelial injury (Blood flow)
fibrin thrombi (hypercoaguability)
organisms in the blood (sepsis)
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30
Q

what is infective endocarditis

A

bacterial infect of heart valve (also can be fungus)

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31
Q

Clinical manifestations of infective endocarditis

A 
Fever
heart murmur
fatigue
anemia
arthralgia
myalgia
splinter hemorrhages (nail bed)
roth spots (retinal hemorrhages, not specific to IE)
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32
Q

Complications of infective endocarditis

A

Rupture of chordae tendineae
spread of infetion to myocardium or aorta
thromboembolism with infarction
septic thrombi with metastatic abscesses
valvular dysfunction and CHF (regurgitation)

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33
Q

length of acute and subacute endocarditis

A

Acute is short,

subacute is longer

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34
Q

what causes acute and subacute endocarditis

A

Acute is a virulent organisms (Staphylococcus auresus)

subacute is low virulences(strptococcus viridans)

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35
Q

vegetatation of acute and subacute endocarditis

A

Acute is large friable vegetation

Subacute is small

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36
Q

vale shape before acute and subacute endocarditis

A

Acute was previously normla

subacute was previously abnormal

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37
Q

tissue distruction of acute and subacute endocarditis

A

Acute has prominent tissue destruction

subactue is less tissue destruction

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38
Q

what is the most important factor that may cause infective endocarditis

A

prosthetic valve

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39
Q

why does hypercoaguability tend to lead to infective endocarditis

A

bacteria like to eat what is made from hypercoaguability

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40
Q

what are some side causes of Infective endocardium

A

mess with papillary trends

occlusion via bacteria

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41
Q

what are the causes of vasculities

A 
Infection
Immunologic mechanisms
Radiation
Trauma
Caustic susbstance
Unknown
42
Q

what is vasculitis

A

Infection of the vessel wall

43
Q

what vasculitis is for large vessel

A 
Giant cell (temporal) arteritis
Takayasu arteritis
44
Q

what vasculitis is for medium vessel

A 
Polyarteritis nodosa (Classic)
Kawasaki syndrome
45
Q

what vasculitis is for small vessels

A

Microscopic polyarteritis

Granulomatosis with polyangiitis (wegener granulomatosis

46
Q

what could lead to an immune complex forming in immune mediated vasculitis

A

Reaction to drugs or viruses

47
Q

what can lead to immune-mediated pathogenesis

A

Immune complexes
Antineutrophilic cytoplasmic antibodies
Anti-endothelial cell antibodies
Cell-mediated immune mechanisms

48
Q

what is ANCA associated wtith in immune mediate vasculitis

A

Microscopic polyangiitis

Wegener granulomatosis

49
Q

what are the types of antineutrophilic cytoplasmic antibodies that lead to immune-mediated vasculitis

A

Anti-myeloperoxidase

Anti-proteinase-3

50
Q

what does anti-myloperoxidase ANCA lead to

A

perinuclear localization (microscopic polyarteritis)

51
Q

what does Anti-proteinase-3 lead to

A

diffuse cytoplasmic distribution (wegener’s granulomatosis)

52
Q

what causes Giant cell (temporal arteritis

A

Unknown

(t-cell mediated maybe)

53
Q

what are the clinical signs of giant cell arteritis

A 
Fever
weight loss
headache
visual problems (blindness
claudiction of jaw (weak jaw )
pain and tenderness over temporal artery
polymyalgia rheumatica
54
Q

who tends to get griant cell (temporal arteritis

A

over age of 50

55
Q

pathology of Giant Cell (remporal) arteries

A
  • Granulomatous inflammation with giant cells
  • fibrosis
  • eventualy causes narrowing of vessel lumen with decreased blood flow to affected tissues
56
Q

what causes problems in giant cell (temporal) arteries

A

elastic lamina breaks down so stuff gets inside vessel and blocks things

57
Q

what causes Takayasu Arteritis

A

Unknown, similar to temporal arteritis

58
Q

who tends to get takayasu arteritis

A

Younger people

more femailes

59
Q

what are the clinical signs of takayasu arteritis

A

Weak arm pulses (pulseless disease)
visual disturbances
Neurologic manifestations

60
Q

Patholgoy of takayasu arteritis

A

Involves aortic arch and branches
Intimal fibrosis
Granulomatous inflammation withfibrosis

61
Q

what does takayasu arteritis do to the aortic arch

A

thickening of the walls reduces flow to branches

62
Q

what causes polyarteritis nodosa

A

Unknown

63
Q

hep b and polyarteritis nodosa

A

30% had hep B surface antigen in serum

mow 8% due to immunization

64
Q

Clinical signs of polyarteritis nodosa

A 
Fever
weight loss
hematuria
renal failure
hypertension
abdominal pain
melenena
65
Q

is it easy to diagnose polyarteritis nodosa

A

no, multiple parts of the body invovled

66
Q

Pathology of polyarteritis nodosa

A

haphazard and segmental involvement of medium and small muscular arties

67
Q

acute leasions from polyareitis nodosa shows what

A

fibrinoid necrosis, thrombosis, neutrophils, and aneuysms

68
Q

what happens with healing of Polyarteritis nodosa

A

predominance of macrophages and plasma cells

progressive fibrous scarring

69
Q

where is polyarteritis nodosa found

A 
Kidney 
heart
liver
Gi tract
 = most common to least common
70
Q

how does polyarteritis nodosa show itself in the kidney

A

Blood in urine from blockage of kidney vessels

71
Q

what is the key sign of polyarteritis nodosa

A

Renal failure

72
Q

other name for Kawasaki disease

A

Mcocutaneous lymph node syndrome

73
Q

what may cause kawasaki disease

A

anti-endothelial antibody triggered by viral infection

74
Q

who tends to get kawasaki disase

A

Infants and young children

75
Q

clinical signs of kawasaki disaese

A

Fever
mucous membrane erythema (eyes/mouth)
skin rash
cervical lymphadenopathy

76
Q

does kawasaki disease spread easily

A

no, self limiting

77
Q

pathology of kawasaki disesaes

A

Coronary artery vasculitis

78
Q

how does one treat kawasaki disease

A

Immunosuppressants

79
Q

what causes microscopic polyangiitis

A

Antigen-antibody complexes

80
Q

what are the clinical signs of micrscopic polyangiitis

A 
Fever
rash
joint swelling
pleural effusion
pulmonary infiltrates
myocarditis
GI bleeding
renal failure
PResence of circulating anti-neutrophilic cytoplasmic antibodies (MPO-ANCA)
81
Q

what would micrscopic polyangiitis preciptate

A

Drugs
microoganisms
Foreign proteins
tumorproteins

82
Q

what vessels does micrscopic polyangiitis involved

A

arterioles
capilaries
Venules

83
Q

microscopic Polyangiitis pathology

A

Fribrinoid
necrosis
neutrophils (leukocytoclasic vasculitis

84
Q

what is leukocytoclastic vasculitis

A

eating of th eblood vessels by tons of white blood cells

- blood vessels dissappear

85
Q

what is granulomatosis with polyangiitis

A

wegener granulomatosis

86
Q

what causes granulomatosis with polyangiitis

A

Abnormal expression of proteinase 3 on endo cell surface

Followed by ANCA binding and neutrophil activation

87
Q

what does binding of ANCA to proteinase 3 on the endo cell surface lead to

A

damage to endothelium and vessel

88
Q

what are the clinical signs of granulomatosis with polyangiitis

A

presence of anti-neurophilic cytoplasmic antibodies direct aginast proteinase 3

89
Q

what does granulomatosis with polyangiitis involve

A

Sinuses
lungs
kidneys
- cavities in the body

90
Q

what does granulomatosis with polyangiitis lead to

A

Necrotizing granulomas w

vasculitis with fibrinoid necrosis

91
Q

how can granulomatosis with polyangiitis affect the gingiva

A

strawberry gingivitus due to high inflammation

92
Q

what causes Thromboangiits obliterans (buerger disease

A

Endothelial injury from substance in Cigs

93
Q

clinical signs of thromboangiitis obliterans

A 
Cig smoking
less than 35 years old
pain in extremities
ischemic ulcers
gangrene
94
Q

Pathology of throboangiitis obliterans

A

Vasculitis with thrombosis

95
Q

what does Thromboangiitis obliterans affect

A

Small arties

96
Q

what is an intimal tear in dissecting aortic hematoma

A

Split between mid and outer 1/3 of the media

97
Q

what can happen to the mdia of a dissecting aorta hematoma

A

Normal or have degeneration

98
Q

what complications can dissection aortic hematoma lead to

A

rupture - hemorrhage

Brnach obstruction

99
Q

what are the predisposing conditiosn for dissection aortic hematoma

A

Hypertension

connective tissue disorders (marfan)

100
Q

what is type A dissection

A

cending aorta in isolation (type I) and as as part of a more extenisve disection (type II)

101
Q

what is type B disection

A

after the take off of the great vessels

102
Q

what causes more problems, type A or type B dissection

A

Type A

general path (16 decks)

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