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MHD > Vasculitis > Flashcards

Vasculitis Flashcards

1
Q

How do immune processes leading to vasculitis progress in the large vessel?

A

outside-in

  1. Activation of naive t-cells by tissue resident DCs in adventitia
  2. oxidative damage
  3. Non-stenosing arteritis (window of opportunity)
  4. hypertrophy of intima and lumen occlusion. symptoms occur. scar is forming
  5. On top of chronic stenosis you can get a thrombosis and the intima gets thicker–>occlusion
  6. breakdown of internal elastic lamina–>aneurysm formation
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2
Q

How do immune processes leading to vasculitis progress in the small/medium vessel?

A

inside out

a. Immune complexes
b. Antineutrophil antibodies
c. direct endothelial adhesion
- primary neutrophil
- neutrophil goes in and degranulates and causes inflammation

small–> breaking open of the artery

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3
Q

What are common features of all vasculitides?

A
  1. fatigue
  2. fever
  3. muscle pain
  4. weight loss
  • *CRP
  • *Fibrinogen (sedimentation rate)
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4
Q

What is the pathophysiology of small vessels?

A
  1. Fibrinoid Necrosis
    - fibrin deposition –>breaking open the blood vessel
    - dead neutrophils fibrin deposition–>fibrin necrosis
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5
Q

What are typical findings in small vessel vasculitis?

A
  1. palpable purpura
  2. necrotizing glomerulonephritis
  3. pulmonary capillaritis and alveolar hemorrhage
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6
Q

What is the pathophysiology of medium vessels?

A
  1. focal lesions with fibrinoid necrosis
  2. segmental lesions
  3. aneurysms
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7
Q

What are typical clinical findings of medium vessel vasculitis?

A
  1. skin nodules
  2. livedo racemosa
  3. ulceration
  4. nerve infarcts
  5. abdominal pain
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8
Q

What is the pathophysiology of large vessels?

A
  1. cell mediated
    - not neutrophil or immune complex
  2. granulomas usually present
  3. Hyperplastic intima with stenosis
    - with neovascularization
  4. FIBRINOID NECROSIS UNUSUAL
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9
Q

What are typical clinical findings of large vessel vasculitis?

A
  1. ocular symptoms
  2. Claudication
  3. chest pain
  4. headache stroke
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10
Q

What type of study do you use to look at large and medium arteries?

A

Angiography or MRA

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11
Q

What type of study do you use to look at small and medium arteries?

A
  1. CT chest
  2. lung/kidney biopsy
  3. skin biopsy
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12
Q

C-ANCA

A

PR3

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13
Q

P-ANCA

A

MPO

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14
Q

What are 4 clinical diagnosis considerations?

A

1) vessel size
2) anca association
3) presence of granulomas
4) possible disease association

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15
Q

What vasculitides have granulomas?

A
  1. Giant cell arteritis
  2. takayasu arteritis
  3. wegener granulomatosis
  4. churg strauss
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16
Q

Giant Cell Arteritis
Epidemiology
Vessel

A

Epidemiology:
1. greater than 50, white, female

  1. a. Carotid
    i. External
    - especially temporal arteries
    ii. Internal
    - ophthalmic
    - not intracerebral

b. Upper aortic branches
i. vertebral arteries

NO STRoKES

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17
Q

What are the pathological features of GCA?

A
  1. patchy/segmental
  2. granulomatous inflammation
    - focused on the internal elastic membrane
  3. fragmentation of internal elastic membrane

chronic-may be smouldering even if clinically quiet

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18
Q

What are clinical features of GCA?

A
  1. headaches
  2. polymyalgia rheumatica
  3. scalp tenderness **
  4. TA (temporal artery) pulse abnormality **
  5. ocular disturbances
  6. visual loss
  7. extreme claudication
  8. cardiac or neurologic symptoms
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19
Q

How do you investigate for GCA?

A

temporal artery biopsy**

blood vessels imagin

20
Q

What is the treatment for GCA?

A

corticosteroids with slow taper

21
Q

What is the epidemiology and artery for pulseless disease (takayasu’s arteritis)?

A

50 or less
asian female

Aorta Great
Great vessels

STROKES
-favors bifurcation areas

22
Q

What are the pathologic features of takayasu’s?

A
  1. giant cells (more spread)
  2. transmural scarring more intense
  3. severe hyperplastic intima with neovascularization
    - severe luminal narrowing
23
Q

What are the three phases of takayasu’s arteritis?

A
  1. pre-pulseless, inflammation period. patients under 20 usually present in this phase
  2. vessel inflammation dominated by vessel pain and tenderness
  3. fibrotic stage, when bruits and ischemia predominate
    - arterial bypass or angioplasty for things like heart failure and htn often needed*
24
Q

What are the clinical features of takayasu’s?

A
  1. abnormal pulses
  2. claudication/weakness
  3. pulmonary hypertension
  4. carotidynia
25
Q

What is fundamental to diagnosis of takayasu’s?

A

Blood vessel imaging**
Echocardiography

  • non specific lab tests
  • ESR can be normal in 50%
26
Q

What is the epidemiology of kawasaki’s?

A

children

27
Q

What are the pathological features of kawaskis?

A

self limiting

-anti-endothelial/smooth muscle cell antibodies

28
Q

What is window of opportunity to treat in kawasaki?

A

Stage 1: 0-2 weeks after fever
-perivasculitis of microvessels

Other stages
Stage 2: 2-4 weeks
-progression to medium vessel vasculitis
-thrombosis and aneurysms

Stage 3:
reduction in inflammation

Stage 4: scar with weakened wall and intimal thickening

29
Q

What are clinical features of kawasaki’s?

A

fever rash bilateral conjunctivitis, strawberry tongue, extremity changes, cervical lymphadenopathy, MI

30
Q

What do you do to treat kawasaki’s?

A

IVIG
High dose aspirin
within 1st 10 days of fever
incidence of coronary aneurysm 25–>3-5%

31
Q

What is the epidemiology of PAN?

A

medium vessel
uncommon, all ages

associated-
autoimmune
heme malignancies
viruses- HEP B 30% *****

32
Q

What vessels are affected by PAN?

A

medium to small MUSCULAR arteries

  • renal
  • coronary
  • hepatic
33
Q

What are the pathologic features of PAN?

A
  1. focal *
  2. segmental *
  3. transmural destruction *
  4. coexisting stages of activity*
  5. fibrinoid necrosis
  6. pleomorphic cellular infiltrate
  7. thrombosis
  8. aneurysms
34
Q

What are clinical features of PAN?

A
  1. organ infarcts *
  2. abdominal injury
  3. renal injury/ hypertension
  4. cutaneous lesions
  5. arthralgia/arthritis
  6. acute peripheral neuropathy
    - pain/paresthesia
    - motor deficits hours later
    - mononeuritis multiplex
35
Q

Does PAN need treatment? What is the treatment?

A

rapidly progressive and fatal if not treated
Treatment
-corticosteroids
-HBV associated-plasma exchange, antiviral treatment
-cyclophosphamide chemotherapy if severe

36
Q

Out of GPA (granulomatosis with polyangiitis-Wegners) , MPA (microscopic polyangiitis) and CS (churg-strauss) which are associated with granulomas?

A

Granulomatosis with polyangiitis

Churg strauss

37
Q

What clinical feature of granulomatosis with polyangiitis?

A
  • Destructive upper airway disease
  • pulmonary nodules/cavities/infiltrates
  • Necrotizing crescentic glomerulonephritis
  1. destructive sinusitis
  2. subglottis stenosis
  3. gingival hyperplasia
  4. orbital pseudotumor
  5. necrotizing scleritis

C-ANCA/PR3

38
Q

What clinical feature of microscopic polyangiitis?

A

Alveolar hemorrhage
-Necrotizing crescentic glomerulonephritis
P-ANCA/MPO

39
Q

What clinical feature of churg strauss?

A

Nasal polyps/allergic rhitnitis
Asthma, allergy, eosinophilia
-Necrotizing crescentic glomerulonephritis
-cardiomyopathy due to eosinophilic cardiac infiltrate
P-ANCA/MPO

40
Q

What do you see in the urine of these three small vessel things?

A

proteinuria

RBC casts +/-

41
Q

What is epidemiology of HSP?

A

most frequently children
-can occur in adults

small vessels
-arterioles, capillary, or venules

42
Q

What are the pathologic features of HSP?

A

immune complex deposition

IgA and C3

43
Q

What are the clinical features of HSP?

A

palpable purpura
arthritis
abdominal pain
renal impairment

44
Q

Buerger?

A

smoking disease
medium and small arteries
gangrene of extremities
corkscrew collaterals

45
Q

Which diseases can be treated with steroids?

A
  1. GCA
  2. Takayasu’s
  3. HSP

MHD (81 decks)

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