Exam 2; Cardiovascular III Flashcards

1
Q

This is failure of a valve to open completely, obstructing forward flow and sometimes is caused by rheumatic fever and typically is always stenotic

A

mitral valve stenosis

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2
Q

Acute rheumatic fever is a systemic disease usually in children which follows which bacteria

A

Group A beta hemolytic; streptococcal pharyngitis

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3
Q

What are the clinical features of rheumatic fever

A
myocarditis
pericarditis
arthritis
erythema marginatum
subcutaenous nodules
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4
Q

What is characteristic of the pericarditis caused by rheumatic fever

A

fibrosis

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5
Q

What is characteristic of the endocarditis caused by rheumatic fever

A

sterile vegetations

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6
Q

What is characteristic of the myocarditis caused by rheumatic fever

A

Aschoff bodies; collections of mononuclear inflammatory cells and fibroblasts (granulomatous infection)

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7
Q

What is the longer term complication after recurrent bouts of acute rheumatic fever

A

chronic valvular disease with mitral valve stenosis (severe fibrosis and calcification)

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8
Q

How does rheumatic fever cause mitral valve stenosis

A

due to the production of antibodies against the streptococcal bacteria which cross react with various antigens in the heart, joints, and other sites

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9
Q

This is the insufficiency of a valve that fails to close completely, allowing back flow of blood

A

regurgitation

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10
Q

This is a condition in which the leaflets ballon into the left atrium during left ventricular contraction (systole)

A

mitral valve prolapse

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11
Q

What occurs regarding floppy mitral valve (severe prolapse)

A

the valve cuss are large and microscopically show fragmentation, separation, and loss of collagen (myxomatous); may be isolated or part of Marfan’s Syndrome

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12
Q

What are three complications of mitral valve regurgitation; develops in about 3% of affected patients

A
endocarditis
thromboemboli
sudden death (rare)
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13
Q

What are three causes of aortic valve stenosis

A

chronic rheumatic valvular disease
degenerative
congenital bicuspid valve

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14
Q

What is the onset of degenerative aortic valve stenosis compared to congenital bicuspid valve

A

degenerative is associated with advanced age (70s or 80s)

congenital bicuspid valvue is a much younger initial onset (40-50 years)

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15
Q

What three things can cause aortic valve regurgitation

A

valve cusp destruction (endocarditis)
weakened cusp valves (Marfans/myxomatous)
dilation of the aortic root

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16
Q

What usually causes infective endocarditis

A

bacterial infection in a heart valve, although it can also be caused by fungi or other infections

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17
Q

What are six predisposing factors of IE

A
intracardiac shunts
valvular disease
prosthetic valves (10-20% of all cases)
IV drug abuse
immune suppression
diabetes
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18
Q

What are the three factors that have been identified as having importance in the pathogenesis of IE

A

endocardial or endothelial injury dur to abnormalities in blood flow
fibrin thrombi
organisms in the blood

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19
Q

What are the clinical manifestations of infective endocarditis

A
fever
fatigue
anemia
myalgia/arthralgia
roth spots (retinal hemorrhages) and splinter hemorrhages (nail bed)**
heart murmur
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20
Q

What is the difference in duration between acute endocarditis and subacute endocarditis

A

acute - short

subacute - longer

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21
Q

What is the difference in the organism between acute endocarditis and subacute endocarditis**

A

acute - virulent organism (Staph. aureus)

subacute - low virulence organism (Strep. viridians)

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22
Q

What is the difference in the vegetations between acute endocarditis and subacute endocarditis

A

acute - large

subacute - small

23
Q

What is the difference in tissue destruction between acute endocarditis and subacute endocarditis

A

acute - prominent tissue destruction

subacute - less tissue destruction

24
Q

What is the difference in valve between acute endocarditis and subacute endocarditis

A

acute - previously normal

subacute - previously abnormal valve

25
Q

What are five complications of infective endocarditis

A
valvular regurgitation/valvular dysfunction/CHF
rupture of the chord tendineae
contiguous spread of infection
thromboembolism with infarction
septic emboli with metastatic abscesses
26
Q

What are the top two causes of vasculitis (inflammation of the BVs)

A
infection
immunologic mechanism (usually associated with other problems)
27
Q

What is the etiology of giant cell (temporal) arteritis

A

unknown, but may be T cell mediated

28
Q

What are the clinical features of giant cell (temporal) arteritis

A
rare before the age of 50
fever
weight loss
headache
visual disturbances
pain and tenderness over the temporal artery
caudication of the jaw (weakness when chewing due to decreased blood supply)
polymyalgia rheumatica
29
Q

What is the pathology of giant cell (temporal) arteritis

A

granulomatous inflammation

intimal proliferation/fibrosis - narrowing of the lumen decreasing blood flow

30
Q

What is the etiology of Takayasu Arteritis

A

unknown

31
Q

What are the clinical manifestations of Takayasu Arteritis

A

thickening of the wall reduces blood flow in the major branches - reducing pulse
usually affects < 40 females
neurologic manifestations

32
Q

What is the pathology of Takayasu arteritis

A

granulomatous inflammation with fibrosis affecting the aortic arch and arch branches

33
Q

What is the etiology of polyarteritis nodsa

A

unknown in most cases, thought there was a link to HepB

34
Q

What are the clinical manifestations of polyarteritis nodsa

A
It's acute-relapsing chronic; confusing due to multiple organ systems involved
RENAL FAILURE
fever
weight loss
hematuria
hypertension
abdominal pain
melena (blood in stool)
35
Q

What is the pathology of polyarteritis nodsa

A

haphazard and segmental involvement of med/small muscular arteries
fibrinoid necrosis, thrombosis, neutrophils, aneurysms
with healing there is a lot of macrophages and PNMs

36
Q

What are the usual sites of involvement involving polyarteritis nodsa

A

kidney (85)
heart (75)
liver (65)
GI tract (50)

37
Q

What is the etiology of Kawasaki disease

A

suspected that a viral infection causes hypersensitivity reaction; anti-endothelial antibodies
“mucocutaneous lymph node syndrome”
medium vessels

38
Q

What are the clinical manifestations of Kawasaki disease

A
typical in infants in young children
skin rash
mucous membrane lesions
servical lymphadenopathy
usually self limiting but 1-2% due with coronary artery vasculitis
39
Q

What is the etiology of microscopic polyangiitis

A

antigen-antibody complexes

40
Q

What are the clinical manifestations of microscopic polyangiitis

A
skin rash
joint swelling
pleural efffusion
pulmonary infiltrates
myocarditis
GI bleeding
renal failure
41
Q

What may microscopic polyangiitis be precipitated by

A

drugs
microorganisms
foreign proteins or tumor proteins

42
Q

There is a presence of this regarding microscopic polyangiitis

A

circulating anti-neutrophilic cytoplasmic antibodies (MPO-ANCA)

43
Q

What is the pathology of microscopic polyangiitis

A

involves arterioles, capillaries, venules (microvasculature)
fibrinoid necrosis
karyorrhexis of neutrophils (leukocytoclastic vascilitis)

44
Q

What is the etiology of Wegener granulomatosis

A

abnormal expression of proteinase 3 on endothelial cell surface followed by ANCA (anti-neurtophilic cytoplasmic antibodies) binding and neutrophil activation resulting in damage to the endothelium and vessel

45
Q

What are the clinical manifestations of Wegener granulomatosis

A

sinusitis
pneumonitis
renal failure
glomerulonephritis

46
Q

What is the pathology of Wegener granulomatosis

A

necrotizing granulomas with vasculitis

47
Q

Which systems does Wegener granulomatosis affect

A

kidnes

upper and lower respiratory tract

48
Q

What is the etiology of thromboangiitis obliterates (Buerger)

A

endothelial injury from substance in cigarette smoke

49
Q

What are the clinical manifestations of thromboangiitis obliterates (Buerger)

A

pain of the extremities
ischemic ulcers
gangrene

50
Q

What is the pathology of thromboangiitis obliterates (Buerger)

A

segmental acute and chronic vasculitis mainly in the extremities with thrombosis

51
Q

This is a longitudinal tear of the aortic media which begins in the ascending aorta and extends variable distance proximal (toward the heart) and distal to the descending aorta

A

dissecting aortic hematoma

52
Q

What are the complications of a dissecting aortic hematoma

A

severe hemorrhage from rupture

organ ischemia due to luminal compression by the expanding hematoma

53
Q

What are the predisposing factors of a dissecting aortic hematoma

A

hypertension

inherited connective tissue disorders (Marfan’s)