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pathology starting with vasculitis > Vasculitis > Flashcards

Vasculitis Flashcards

1
Q

What is Type 3 immune mechanism?

A

Immune complex deposition formed locally or deposited in areas of increased vascular permeability

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2
Q

What happens to complement and neutrophils in type 3?

A

Fixation of complement and infiltration of neutrophils

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3
Q

In severe cases what does type 3 cause?

A

Fibrinoid necrosis

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4
Q

Examples of type 3?

A

SLE
Serum sickness
Cryoglobulinemia
Chronic viruses

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5
Q

Cytoplasmic ANCA indicative of what?

A

Wegener’s granulomatosis

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6
Q

Perinuclear ANCA indicative of what?

A

Micro PAN

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7
Q

Are ANCA’s intrinsic part of pathogenesis or correlated phenomenon?

A

Unclear

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8
Q

What do ANCA’s serve as?

A

Diagnostic clinical marker

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9
Q

Granulomas associated with what?

A

Type 2 or 3 processes

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10
Q

Type 4 mechanisms present as?

A

Herpes and measles with no vasculitis

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11
Q

What infiltrate is there in type 2?

A

Leukocytes with direct cytotoxicity of endothelium

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12
Q

Type 3 infiltrates?

A

Immune complex deposition, complement fixation, and neutrophils

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13
Q

Type 4 infiltrate?

A

Monocytic infiltrate

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14
Q

What is associated with collections of eosinophils?

A

Allergic angiitis/Churg-Strauss syndrome

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15
Q

What are leukoclastic lesions?

A

Fragmentation of neutrophils

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16
Q

Where are granulomas in vascular wall?

A

Within vessel wall or directly adjacent to wall

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17
Q

What is fibrinoid necrosis?

A

Necrosis of cells within the vessel wall + accumulation of fibrin

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18
Q

Fibrinoid necrosis accompanies what?

A

Immune complex deposition and infiltration of leukocytes as in polyarteritis nodosa

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19
Q

How does hyalin accumulate?

A

Secondary to endothelial injury
Leakage of fibrin and synthesis of ECM
Long standing benign hypertension

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20
Q

What does hyper plastic lesions cause?

A

Activation of endothelial cells and proliferation of smooth muscle

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21
Q

Where are hyper plastic lesions seen?

A

Malignant hypertension, due to cytokines as in scleroderma

22
Q

Chronic or repetitive damage to endothelium forms what?

A

Hyperplastic lesions

23
Q

Polyarteritis Nodosa (Classic) presents where?

A

Small and medium arteries

24
Q

PAN spares what organ?

A

Lungs

25
Q

What do lesions of PAN look like?

A

Sharply segmental, branching points and bifurcations

26
Q

In PAN what type of dilation occurs?

A

Segmental aneurysmal dilation, palpable nodule in skin

27
Q

What causes the vessel wall weakening in PAN?

A

Inflammatory involvement

28
Q

In PAN, renal involvement causes many deaths, how does this happen?

A

Due to renal arterioles, not glomerulonephritis

29
Q

What do you see in acute phase of lesions?

A

Transmural infiltrates inflammatory cells and fibrinoid necrosis

30
Q

Chronic phase of lesions?

A

Fibrous thickening of bessel wall/mononuclear infiltrate

31
Q

Symptoms of PAN?

A

Melena (black tarry stools indicative of blood in feces)

Peripheral neuritis

32
Q

Where does microscopic PAN occur?

A

Post capillary venules

33
Q

What disorders are involved with Microscopic PAN?

A

Necrotizing glomerulonephritis (90%) and pulmonary capillary involvement.

34
Q

In microscopic PAN what does cutaneous lesions manifest as?

A

Palpable purpura

35
Q

What differs between microscopic PAN and normal PAN>

A

Lesions tend to be of the same age in microscopic

36
Q

Characteristic of microscopic PAN?

A

Few or no immune deposits

37
Q

P or C ANCA?

A

P (80%)

38
Q

Giant cell arteritis occurs in who?

A

Older individuals

39
Q

Where does Giant Cell Arteritis occur?

A

Temporal, vertebral, ophthalmic arteries. Rarely aortic arch

40
Q

Symptoms of Giant Cell Arteritis?

A

Blindness, tenderness over involved arteries

41
Q

What does Giant Cell Arteritis respond too?

A

Corticosteroids

42
Q

Takayasu’s Arteritis occurs in who?

A

Women younger than 40

43
Q

What does Takayasu’s Arteritis involve?

A

Origins of great arteries arising from aortic arch

44
Q

Takayasu has what affect on the mediastinum?

A

Widening

45
Q

How will Takayasu present?

A

Lower blood pressure and diminished or asymmetric pulses in upper extremities

46
Q

Classical triad of Wegener’s Granulomatosis

A

Acute necrotizing granulomas
Granulomatous vasculitis
Renal disease with social/necrotizing glomerulonephritis

47
Q

Wegener’s Granulomatosis associated with what?

A

Associated with epistaxis and hemoptysis and ulcerative lesions of nose, palate, pharynx

48
Q

Good marker of disease activity in Wegener’s?

A

c-ANCA present in 90%

49
Q

How quickly will Wegener’s kill you?

A

1 year

50
Q

Kawasaki disease in who?

A

Young children

51
Q

What type of lymph node syndrome is Kawasaki?

A

Mucocutaneous

pathology starting with vasculitis (7 decks)

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