Vasculitis Flashcards

1
Q

What is vasculitis?

A

Inflammation of blood vessels

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2
Q

What happens to the blood vessels in vasculitis?

A

Necrosis

Destruction of vessel walls leading to perforation and haemorrhage into tissues

Endothelial injury leading to thrombosis and ischaemia of tissue

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3
Q

What cells are involved in the inflammatory process?

A

Vessel wall infiltration by:

  • neutrophils
  • mononuclear cells
  • giant cells
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4
Q

What would you see under a microscope looking at a biopsy of a vessel affected by vasculitis?

A

Neutrophils
Mononuclear cells

Fibrinoid necrosis

Leukocytoclasis

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5
Q

What is fibrinoid necrosis?

A

Necrosis of tissue in which there is accumulation of amorphous, basic, proteinaceous material in the tissue matrix with a staining pattern reminiscent of fibrin.

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6
Q

What is leukocytoclasis?

A

The damage cause by nuclear debris from infiltrating neutrophils

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7
Q

What are some vasculitides that affect large arteries?

A

Giant cell arteritis

Takyasu’s arteritis

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8
Q

What are some vasculitides that affect medium arteries?

A

Polyarteritis nodosa

Kawasaki disease

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9
Q

What are some vasculitides that affect small arteries?

A

Wegener’s granulomatosis

Churg Strauss

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10
Q

What are some vasculitides that affect small vessels?

A

Henoch Schonlein purpura

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11
Q

What are some secondary causes of vasculitis?

A

Infection
Drugs
Malignancy

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12
Q

What is ANCA?

A

Anti-neutrophil cytoplasmic antibodies

Specific for the antigens found in cytoplasmic granules of neutrophils and monocytes

Attack the body’s own cells = autoimmune

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13
Q

What conditions must you exclude when considering a diagnosis of vasculitis?

A

Sepsis
Malignancy
Cholesterol Emboli

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14
Q

What are some other names for giant cell arteritis?

A

Temporal arteritis

Cranial arteritis

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15
Q

What is GC arteritis?

A

Granulomatous thickening of the inner portions of large vessels:

  • aorta
  • extra-cranial branches of carotid

This causes inflammation of the vessels and pain

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16
Q

What are the branches of the extra-cranial artery that can be affected in GC arteritis?

A

Ophthalmic artery

Temporal artery

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17
Q

Who gets GC arteritis?

A

Almost all patients are over 50
Incidence increases with age

Twice as common in women as in men

18
Q

Clinical features of GC arteritis?

A

Headache

Temporal + scalp tenderness (brushing hair is painful)

Jaw claudication

Amaurosis fugax
Sudden, painless blindness in 1 eye

Non-specific malaise

Polymyalgia rheumatica

Temporal arteries: tender, palpable, reduced pulsation

19
Q

What is amaurosis fugax?

A

Transient visual loss

Looks like a curtain coming down in front of the eyes
It often occurs a few times before full blindness occurs

20
Q

What is polymyalgia rheumatica?

A

Pain in many joints, especially shoulder, neck, hips

21
Q

What would you see examining the temporal artery of someone with GC arteritis?

A

Palpable
Tender
Reduced pulsation

22
Q

Investigation of GC arteritis?

A

Temporal artery biopsy: you will see evidence of inflammation

Bloods: raised ESR and CRP

Look at their optic disc:

  • pale
  • swollen
  • flame shaped haemorrhages at margin
23
Q

Treatment of GC arteritis?

A

Start corticosteroids immediately! to prevent blindness

Continue steroids but gradually reduce them over time

Consider non-steroids: methotrexate

Prophylaxis for steroid induced osteoporosis

24
Q

Time is of the essence in GC arteritis, why?

A

Because it can lead to permanent bilateral blindness if not treated quickly enough

25
What is Takayasu's arteritis?
Vasculitis of aortic arch and other major arteries
26
Clinical features of Takayasu's arteritis?
Hypertension, strokes, heart failure, absent peripheral pulse
27
Management of Takayasu's arteritis?
Corticosteroids
28
What is polyarteritis nodosa?
Necrotising vasculitis affecting medium sized vessels, especially renal and visceral ones It causes aneurysms and thrombosis in these vessels
29
Who gets polyarteritis nodosa?
Middle age men
30
What is the link between Hep B and polyarteritis nodosa?
Presence of Hep B antigens in the blood is linked with polyarteritis nodosa. It is thought that the immune complexes (antigen-antibody) are deposited in places they shouldn't be causing an inflammatory response
31
Clinical features of polyarteritis nodosa?
Fever Malaise Weight loss Skin: rash and punched out ulcers Renal, cardiac, GI and GU involvement
32
Investigation of polyarteritis nodosa?
Blood: - raised ESR + CRP - raised WBC - anaemia Angiography: of renal and mesenteric areas to look at blood flow Renal biopsy
33
Management of polyarteritis nodosa?
Control BP meticulously Corticosteroids + immunosuppressants If linked with Hep B, treat this
34
There are 2 types of small vessel vasculitis. What are they?
ANCA positive | ANCA negative
35
Name some small vessel vasculitides which are: - ANCA positive - ANCA negative?
ANCA +ve - GPA aka Wegener's granulomatosis - Microscopic polyangiitis ANCA -ve - Henoch Schonlein purpura - Goodpasture's syndrome
36
What is Granulomatosis with Polyangiitis (GPA) also known as?
Wegener's granulomatosis
37
What is GPA?
Necrotising, granulomatous vasculitis of small vessels all over the body: - arterioles - capillaries - post capillary venules
38
Is GPA ANCA negative or positive?
ANCA positive
39
Who gets GPA?
Any age, but peaks between 25-60
40
Clinical features of GPA?
Affects vasculature of all organ systems ``` Saddle nose deformity Eye proptosis (eye pushed outwards) Many more ```
41
Treatment of GPA?
Steroids Biologics DMARDs Monitor for organ damage
42
Investigations of GPA?
Blood: - raised ESR + CRP - anaemia Urine: - protein and haematuria CXR: shows lung lesions