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PA3201 final > Vascular Patho > Flashcards

Vascular Patho Flashcards

1
Q

when will you hear murmur, friction rub, indistinct sounds

A

murmur- turbulence of blood flow thru stenotic or incompetent valves

Friction rub- Pericarditis

Indistinct sounds- Pericardial effusion

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2
Q

When will you see raised jugular venous pressure

A

increased central venous pressure due to right or congestive cardiac failure

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3
Q

When will u get edem

A

if due to vascular disease, attributable to raised venous pressure exceeding plasma oncotic pressure

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4
Q

when will you have raised troponin or creatine phosphokinase

A

due to myocardial infarction

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5
Q

mechanisms of vasculitis

A

Disordered immunity or direct injury induced by infectious agents

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6
Q

what will most pts with vasculitis have in their blood

A

increased lvls of circulating immune complexes and the complement concentrations may be lw
autoantibodies are present in some pts

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7
Q

tx for vasculidis

A

Anti inflammatory and cytotoxic drugs may induce clinical remissions in 75% of pts

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8
Q

Important complication of vasculiditis

A

Thrombosis of the inflamed vessel segments resulting in ischemia or infarction of affected organ

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9
Q

What is polyarteritis nodosa

A

Systemic vasculitus (except ling) in young adults (M>F)

symptoms varied and depend on system
low grade fever
weight loss
malaise

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10
Q

lab findings in polyarteritis nodosa

A

Hepatitis B antigen- pos in 30% of cases

Perinuclear antineutrophil cytoplasmic autoantibodies (P-ANCA)

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11
Q

what is churg strauss syndrome and main pathology of it

A

variant of PAN: rare syndrome that affects small to medium sized arteries, associated w bronchial asthma

Pathology- granulomas and eosinophilia

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12
Q

What is weaner granulomatosis, aetiology

A

rare multisystem autoimmune disease
M>F 40-60s

hallmark feature include necrotizing granulomatous inflammation and immune vasculitis in small and med sized blood vessels

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13
Q

clinical pathology and pres of wegener granulomatosis

A
  • necrotizing vasculitis w granulomas
  • classically involves the nose, sinuses, lungs, kidney

Signs- saddle nose deformity (mc signs)

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14
Q

Lab findings in wagerers granulomatosis

A

Cytoplasmic antineutraphil cytoplasic antibodies (C-ANCA)

–antibodies against proteinase 3

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15
Q

temporal arteritis epidemiology and what marker is it associated w

A

mc form of vasculitis
elderly F>M
Associated w HLA DR4

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16
Q

Why does GCA not cause widespread vasculisis

A

Because intracranial arteries lack an internal elastic laminaa

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17
Q

What arteries does GCA usually target

A

Common, external and internal carotid artery (extracranially)

post ciliary and ophthalmic (intracranially)

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18
Q

Clinical features of GCA

A
  • throbing HA
  • Tender, firm temporal aa
  • amaurosis fugal- non perm loss of vision in one eye due to temporary lack of blood flow to retina
  • facial pain
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19
Q

Pathology of temporal arteritis

A

Segmental granulomatous vasculitis

–multinucleated giant cells and fragmentation of int elastic lamina

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20
Q

What is takayasu arteritis, epidemiology

A

Asian women <50

inflammatory disease of large and medium sized arteries with predilection for aorta and branches

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21
Q

What is pathology of takayasu arterities

A
  • Granulomatous vasculitis w extensive intimal fibrosis
  • irrecular fibrosis thickening of wall of aortic arch
  • loss of pulse in upper ex*
22
Q

What is buerger disease highly correlated to

A

tabaco use

23
Q

features of buerger disease

A
  • Absence or minimal presence of atheromas
  • segmental vascular inflammation
  • vasooccusiove phenominem

Younge males <40

24
Q

pathology of buerger disease

A
  • Recurrent neutrophilic vasculitis w micro abscesses
  • segmental thrombosis leading to vascular insufficiency and vascular occlusion
  • Organized thrombus and fibrosis are found in blood vessels in end stage
25
Q

kawasaki disease age

A

< 5years old

26
Q

pathology of kawasaki disease

A

Segmental necrotizing vasculitis
70% affected in coronary artery
-large, medium sized and small arteries

27
Q

major risk of kawasaki disease

A

Coronary artery anuerysims occurring in up to 25% of untreated cases

28
Q

what can secondary raynaud phenom be due to

A

Scleroderma (CREST)
SLE
Buerger disease
Atherosclerosis

29
Q

what is varicose veins ue to

A

Dilated torturous veins caused by increased intraluminal pressure

30
Q

What are esophgeal varicies

A

abnormal dilated veins of the esophagus

31
Q

how do esophageal varies occur

A

Redirection of flow thru left gastric vein secondary to portal hypertension or portal venous occlusion

32
Q

What are arteriovenous fistulas

A

Abnormal, typically small, direct connections between arteries and veins that bypass the intervening capillaries (developmental defect or result from rupture of an arterial aneurysm into adjacent vein)

33
Q

What is fibromuscular dysplasia

A

Focal irregular thickening of walls of medium and large muscular arteries

-may develop vascular aneurysms

34
Q

What is arteriosclerosis and 3 main types

A
  • sclerosis of the arteries
  • monchemberg medial calcification
  • arteriolosclerosis
  • atherosclerosis
35
Q

What is moncheberg medial calcification

A

condition that leads to stiffening of the elastic layer of the arterial wall (media of muscular aa), does not block lumen though

36
Q

two step processes of arteriosclerosis

A
  1. endothelial injur

2. tissue response of the vascular wall to the injurious agents

37
Q

atherogenesis in arteriosclerosis

A

intraintimal macrophages release LDL oxidizing enzymes

-Oxidized LDL is engulfed by macrophages and SMC creating foam cells

38
Q

pathogenesis of atherosclerosis

A

Fatty streak- intimal accumulation of foam cells
Atheroma- intimal accumulation of foam cells and extracellular lipid
Fibroatheroma- atheroma with development of fibrous cap

39
Q

atherosclerosis favourite sites

A

Elastic and medium site muscular arteries

most severity at ostia

40
Q

What consititues systemic hypertension

A

-elevated BP leading to end organ damage

  • -sustained DP>90mmHg
  • -Systolic pressure >140mmHg
41
Q

etiology of systemic hypertension

A

Primary- 95%

Secondary- 5%

42
Q

What is malignant hypertension and what is it associate dw

A

most often occurs in pts with long standing uncontrolled hypertension
–associated w diastolic pressure above 120mmHg

43
Q

What is the dif between true and false aneurysms

A

True- involve all 3 layers (intimal, media, adventitia)

False/psuedo- collection of blood or hematoma which has leaked out of the artery but then is confined by surrounding tissue

44
Q

What is syphilic aneurysms

A

Tertiary stage of inf with treponema palladium

45
Q

What is Dohle-Heller syndrome

A

Aortitis secondary to suphylis
predominantly younger males
Will see De Mussets sign (rhythmic nodding of the head syncrouns w heart beat)

46
Q

Where are micro aneurysms mc seen

A

Biliary or microaneurysms 300micron diameter

lenticulostriate vessels of basal ganglia

47
Q

What can happen with a mycotic aneurysm

A

Septic emboli (mycotic aneurysm) from heart can occlude the vasa vasorum of the vessel or vessel lumen leading to vascular wall inf

48
Q

What is a hemangioma

A

common benign vascular timor

‘port wine stains’ large flat vascular ectasia

49
Q

What is kaposi sarcoma + 4 types

A

Low grade spindle cell malignant timor that are derived from endothelial cells

  • epidemic of aids related
  • immunocompromised
  • classic or sporadic
  • endemic (african)
50
Q

lesions in kaposi sarcoma

A

Cutaneous lesions may occur at any location but typically are concentrated on the lower extremities and the head and neck regions
-lesions may have macular, papular, nodular or plaque like appearence

51
Q

What is an angiosaecoma

A

Uncommon malignant neoplasm characterized by rapidly proliferating, extensively infiltrating anapaestic cells derived from blood vessels and lining irregular blood filled spaces

PA3201 final (20 decks)

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