Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

► Med - Pathology > Vasculitis > Flashcards

Vasculitis Flashcards

1
Q

What are the 2 pathogenic mechanism of vasculitis?

A
  • Immune‐Mediated Inflammation (more common)

* Direct invasion by infectious pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the characteristics of small and medium vessel vasculitis?

A

i. “inside-out” pathogenesis
ii. endothelial disruption
iii. neutrophils predominate
iv. fibrin deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the characteristics of large vessel vasculitis?

A

i. “outside-in” pathogenesis
ii. Adventitial antigen presenting cells
iii. T-helper/cell-mediated, macrophage infiltrate.
iv. NO fibrin deposition
v. Hypertrophy & stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the pathogenesis of small and medium vessel vasculitis?

A

Local or systemic inflammatory molecules trigger neutrophil & endothelial activation. Adhesion molecule upregulation with migration of the neutrophils into the
vessel walls which causes degranulation and damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pathogenesis of large vessel vasculitis?

A

Tissue dendritic cells in adventitia start to stimulate T helper (likely Th1) cells that circulate in from vasa vasorum by displaying antigen+ giving the second activation signal leading to inflammation and eventual disruption of the internal elastic lamina and intimal hypertrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 3 ways that vasculitis can cause occlusion?

A

a. Thrombosis
b. Stenosis
c. Aneurysm + rupture or dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which type of vasculitis is “leukocytoclastic”—neutrophil debris seen in?

A

Small Vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where are the most common places where small vessel vasculitis is seen?

A

Most common places: skin, lungs, kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which type of vasculitis is fibrinoid necrosis seen in?

A

Small and Medium Vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a complication of vasculitis in medium vessels?

A

Aneurysms as there is a muscular layer that can cause extreme weakening of the wall when it is broken down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which type of vasculitis is granuloma seen in?

A

Large Vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which type of vasculitis are giant cells seen in?

A

Large Vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which type of vasculitis is claudication seen in?

A

Large Vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is C-ANCA found and what is it associated with?

A

Cytoplasm. Usually associated with antibodies specific for proteinase-3. Very specific for an ANCA-associated vasculitis called granulomatous polyangiitis (i.e. Wegener’s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where is P-ANCA found and what is it associated with?

A

Perinuclear. Associated with antibodies specific for myeloperoxidase. In some GI conditions or with some drug hypersensitivity, can have P-ANCA on immunofluorescence, with negative MPO ELISA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the most common vasculitis?

A

Giant Cell Arteritis (GCA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What vessels does GCA affect?

A

Large. Involves aorta and major branches to the head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the pathogenesis of GCA?

A

T-cell mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the findings with GCA?

A
  1. Nodular thickening of the artery, intimal proliferation resulting in narrowing of the lumen
  2. Acute, chronic, granulomatous inflammation
  3. Giant cells may be present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the typical patient of GCA?

A

Involves adults usually after age 50, most are female and Caucasian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a lab finding for GCA?

A

Patients have elevated serum ESR and/or CRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are clinical findings for GCA?

A
  • Scalp tenderness
  • TA pulse abnormality
  • Ocular disturbance‐50%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the treatment for GCA?

A

Treatment is high dose corticosteroids (prednisone) with slow taper

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Takayasu’s Arteritis AKA?

A

Pulseless Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the findings with Takayasu’s Arteritis?

A
  • Thickening of arterial wall/intima, luminal narrowing
  • Granulomatous inflammation
  • Pulmonary Hypertension
  • Claudication/Weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the vessels that Takayasu’s Arteritis involves?

A

Large. Involves Aortic Arch and its branches.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Who is the typical patient of Takayasu’s Arteritis?

A

East Asian women under 50 years of age

28
Q

Why does the weakening of pulses occur with Takayasu’s Arteritis?

A

Weakening of pulses of upper extremities due to narrowing of lumen of vessels

29
Q

What are the 3 phases of Takayasu’s Arteritis?

A
  • Phase I: pre‐pulseless, inflammatory period characterized by nonspecific systemic complaints such as fever, arthralgias, and weight loss
  • Phase II: vessel inflammation dominated by vessel pain and tenderness.
  • Phase III: fibrotic stage, when bruits and ischemia dominate
30
Q

What types of vessels does Kawasaki Syndrome affect?

A

Medium. Coronary arteries frequently involved.

31
Q

What is the most common cause of acquired heart disease in children?

A

Kawasaki Syndrome

32
Q

What is the main patient population for Kawasaki Syndrome?

A

Children under the age of 5 - more prevalent in Japan

33
Q

What is the pathogenesis of Kawasaki Syndrome?

A

Anti‐endothelial/anti‐smooth muscle cell antibodies

34
Q

What are some of the findings of Kawasaki Syndrome?

A 
• Fever
• Fibrinoid necrosis
• Destruction of internal elastic lamina
– No granulomas
• Aneurysmal rupture or acute thrombosis
35
Q

What is the window of opportunity to treat Kawasaki Syndrome?

A

0-2 weeks after fever

36
Q

What is the treatment for Kawasaki Syndrome?

A

• High dose Aspirin - one of the few cases to treat a child with aspirin

37
Q

What is Polyarteritis Nodosa (PAN) often associated with?

A

Hepatitis B and C

38
Q

What vessels does PAN affect?

A

Medium to small muscular arteries
• Renal arteries
• Coronary arteries
• Hepatic arteries

39
Q

What does PAN often spare?

A

Lungs

40
Q

What are some of the clinical findings with PAN?

A
  • Organ infarcts
  • Abdominal pain
  • Renal injury/Hypertension
  • Cutaneous lesions
  • Arthralgia/Arthritis
  • Acute peripheral neuropathy
41
Q

What are some of the lab findings of PAN?

A
  • ANCA negative

* Hypocomplementemia

42
Q

What is the progression of PAN?

A

Rapidly progressive & fatal if not treated

43
Q

What types of vasculitis are ANCA associated?

A

Granulomatosis with Polyangiitis (GPA)
Microscopic Polyangiitis (MPA)
Churg‐Strauss (CS)

44
Q

What vessels do ANCA associated vasculitis affect?

A

Small vessels:
• Glomerular capillaries
• Pulmonary capillaries

But can also affect medium sized vessels

45
Q

What are the findings with granulomatosis with polyangiitis?

A

– Leukocytoclastic fibrinoid necrosis

– Granulomas in lung or upper respiratory tract

46
Q

What are the findings with microscopic polyangiitis?

A

– Leukocytoclastic fibrinoid necrosis

– NO Granulomas

47
Q

What are the findings with Churg Strauss?

A

– Leukocytoclastic fibrinoid necrosis
– Granulomas
– Peripheral & tissue eosinophilia

48
Q

What will be absent in ANCA mediated vasculitis?

A

Immune complexes - “pauci-immune”

49
Q

What does saddle nose indicate?

A

GPA

50
Q

What does eosinophilic cardiac infiltration indicate?

A

CS

51
Q

What does pulmonary hemorrhage indicate as a possible vasculitis?

A

MPA

52
Q

What is the incidence of GPA by gender?

A

More in males than females

53
Q

What type of ANCA is GPA associated with?

A

c-ANCA

54
Q

What type of ANCA is CS associated with?

A

p-ANCA

55
Q

What type of ANCA is MPA associated with?

A

p-ANCA

56
Q

What vasculitis are nasal polyps associated with?

A

CS

57
Q

What vessels does Henoch-Schonlein Purpura involve?

A

Small - arterioles, capillaries, venules

58
Q

What is the pathogenesis of Henoch-Schonlein Purpura?

A

Infection or drug, or other environmental exposure causes IgA immune complexes to form & deposit in vessel walls, instigates complement cascade

59
Q

What is the typical HSP patient?

A

Children - but CAN occur in adults

60
Q

What is the triad of HSP symptoms?

A

Triad usually is arthritis, abdominal pain & palpable purpura

61
Q

What are the lab findings with HSP?

A
  • Immune complex deposition
  • H&E shows neutrophils
  • Immunofluorescence shows IgA & C3
62
Q

What is the typical patient of thrombiangiitis obliterans?

A

Seen in SMOKERS younger than 40

63
Q

What vessels does thrombiangiitis obliterans affect?

A

Inflammation of medium & small arteries

64
Q

What can thromboangiitis obliterans result in?

A

Gangrenous extremities

65
Q

What does imaging show about the vessel affected by thromboangiitis obliterans?

A

“Corkscrew” collaterals on imaging

► Med - Pathology (203 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions