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CPR II Exam 1 > Vascular Pathology II > Flashcards

Vascular Pathology II Flashcards

1
Q

what are the three types of arteriosclerosis?

A
  1. arteriolosclerosis 2. atherosclerosis 3. Monckeberg medial sclerosis
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2
Q

what is monckeberg medial sclerosis?

A

age related degenerative calcific change where calcium deposits are found within the media of the artery; very little clinical significance

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3
Q

what is the inheritance pattern in most genetic cases of atherosclerosis?

A

multifactorial inheritance

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4
Q

what effect does estrogen have on atherosclerosis?

A

a protective effect

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5
Q

what is key to the drive of pathogenesis of atherosclerosis?

A

the endothelium becomes activated

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6
Q

what occurs during smooth muscle recruitment due to endothelial activation?

A

smooth muscle cells migrate from the media of the vessel to the intima and synthesize extracellular matrix. end result: intimal thickening

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7
Q

what 3 factors cause smooth muscle proliferation and extracellular matrix deposition?

A

PDGF, fibroblast growth factor, an TGF-alpha

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8
Q

what is the difference between a saccular aneurysm and a fusiform aneurysm?

A

saccular bulges out on one side and fusiform is on both sides

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9
Q

what is the difference between a true and false aneurysm?

A

a true aneurysm has an intact thinned muscular wall; false aneurysm has a defect through the wall

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10
Q

what is cystic medial degeneration and what can it lead to?

A

the process where the normal elastin of the media is disrupted and replaced with areas of amorphous ground substance. It can cause aneurysm and dissection

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11
Q

when might you see cystic medial degeneration?

A

Marfan syndrome, Ehlers Danlos syndrome, and systemic hypertension

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12
Q

what mutation leads to marfan syndrome?

A

FBN1 fibrillin gene

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13
Q

what occurs in marfan syndrome?

A

defective synthesis in fibrillin leads to its inability to bind TGF-beta. the increased TGF-beta activity causes weakening of the elastic tissue, predisposing to aortic aneurysm and aortic dissection

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14
Q

what mutation leads to Ehlers Danlos syndrome?

A

mutation in collagen

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15
Q

which form of Ehlers danlos syndrome predisposes the patient to arterial rupture of large arteries?

A

the vascular form, which is caused by a mutation in collagen 3

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16
Q

what is the most important risk factor for AAA?

A

atherosclerosis

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17
Q

where is the typical location for an AAA?

A

below the renal arteries, above the aortic bifurcation

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18
Q

5-10% of aortic aneurysms are of inflammatory type with abundant lymphoplasmacytic inflammation. A subset of these are caused by IgG4 related disease. What does this mean?

A

it is a chronic inflammatory disease= numerous lymphocytes and IgG4 secreting plasma cells associated with prominent fibrosis

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19
Q

what is the clinical relevance of IgG4 disease and AAA?

A

it responds well to steroids

20
Q

what is the most important risk factor for thoracic aortic aneurysm?

A

hypertension

21
Q

besides HTN, what are the other causes of thoracic aortic aneurysm?

A

untreated syphillis, connective tissue diseases, and vasculitis

22
Q

when does tertiary syphilis present?

A

after a latency period of 5 years or more after the initial infection

23
Q

what cardiovascular effects can syphilis cause?

A

obliterative endarteritis of vasa vasorum–> thoracic aneurysm; aortitis; aortic regurgitation

24
Q

aortic dissection has a classic clinical triad of what?

A

1) abrupt onset of thoracic pain with a sharp, tearing or ripping character 2) variation of pulse (absence of proximal extremity or carotid pulse) and a greater than 20 point blood pressure difference between arms 3) mediastinal widening on chest x-ray as blood expands the vessel

25
Q

what are the two main causes of aortic dissection?

A

hypertension and connective tissue disorders

26
Q

what does biopsy of the temporal artery show in a patient with GCA?

A

intimal thickening and granulomatous inflammation with fragmentation of internal elastic lamina

27
Q

what are the signs and symptoms of takayasu arteritis?

A

nonspecific, but ocular disturbances and weakened pulses in the upper extremity are often present

28
Q

what is the classic presentation of polyarteritis nodosa (PAN)?

A

rapidly accelerating HTN, abdominal pain and bloody stools, myalgias, peripheral neuritis

29
Q

what does histology show in a patient with PAN?

A

necrotizing (fibrinoid necrosis) with mixed segmental inflammation

30
Q

how do you treat PAN?

A

immunosuppression

31
Q

what is kawasaki disease caused by?

A

activated T cells which are thought to be provoked by viral infectious illnesses

32
Q

what is churg-strauss syndrome associated with?

A

asthma, hypereosinophilia, lung infiltrates

33
Q

what is the pathogenesis of GPA (Wegener’s granulomatosis)?

A

T cell hypersensitivity reaction thought to be mediated by inhaled environmental or microbial material

34
Q

what do the lung biopsies show in a patient with wegener granulomatosis?

A

cavitary necrotizing granulomatous inflammation

35
Q

what do kidney biopsies show in a patient with wegener’s granulomatosis?

A

focal necrotizing and crescentric glomerulonephritis

36
Q

what is the prognosis of GPA (wegener’s granulomatosis)?

A

left untreated, GPA is rapidly fatal

37
Q

how do you treat wegener’s granulomatosis?

A

steroids, cyclophosphamide and TNF-antagonists

38
Q

which vasculitides affect the aorta?

A

GCA and takayasu

39
Q

what vasculitides has neutrophils present?

A

behcet’s disease

40
Q

what vasculitides has eosinophils present?

A

churg-strauss syndrome

41
Q

which vasculitis must have a granuloma present?

A

wegener’s granulomatosis

42
Q

what is the serum ANCA for wegener?

A

pr-3 ANCA

43
Q

what is the serum ANCA for churg strauss syndrome?

A

MPO ANCA

44
Q

what is the serum ANCA for microscopic polyangiitis?

A

MPO ANCA

45
Q

what are two types of coronary intervention?

A

balloon angioplasty and endovascular stenting

46
Q

what is the solution to restenosis following balloon angioplasty and endovascular stenting?

A

drug eluting stent

47
Q

which vein graft has the longer patency?

A

internal mammary artery

CPR II Exam 1 (13 decks)

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