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Musculoskeletal > Vasculitis > Flashcards

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
Q

What is Takayasu’s arteritis?

A

Vasculitis of aortic arch and other major arteries

26
Q

Clinical features of Takayasu’s arteritis?

A

Hypertension, strokes, heart failure, absent peripheral pulse

27
Q

Management of Takayasu’s arteritis?

A

Corticosteroids

28
Q

What is polyarteritis nodosa?

A

Necrotising vasculitis affecting medium sized vessels, especially renal and visceral ones

It causes aneurysms and thrombosis in these vessels

29
Q

Who gets polyarteritis nodosa?

A

Middle age men

30
Q

What is the link between Hep B and polyarteritis nodosa?

A

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
Q

Clinical features of polyarteritis nodosa?

A

Fever
Malaise
Weight loss

Skin: rash and punched out ulcers

Renal, cardiac, GI and GU involvement

32
Q

Investigation of polyarteritis nodosa?

A

Blood:

  • raised ESR + CRP
  • raised WBC
  • anaemia

Angiography: of renal and mesenteric areas to look at blood flow

Renal biopsy

33
Q

Management of polyarteritis nodosa?

A

Control BP meticulously

Corticosteroids + immunosuppressants
If linked with Hep B, treat this

34
Q

There are 2 types of small vessel vasculitis. What are they?

A

ANCA positive

ANCA negative

35
Q

Name some small vessel vasculitides which are:

  • ANCA positive
  • ANCA negative?
A

ANCA +ve

  • GPA aka Wegener’s granulomatosis
  • Microscopic polyangiitis

ANCA -ve

  • Henoch Schonlein purpura
  • Goodpasture’s syndrome
36
Q

What is Granulomatosis with Polyangiitis (GPA) also known as?

A

Wegener’s granulomatosis

37
Q

What is GPA?

A

Necrotising, granulomatous vasculitis of small vessels all over the body:

  • arterioles
  • capillaries
  • post capillary venules
38
Q

Is GPA ANCA negative or positive?

A

ANCA positive

39
Q

Who gets GPA?

A

Any age, but peaks between 25-60

40
Q

Clinical features of GPA?

A

Affects vasculature of all organ systems

Saddle nose deformity
Eye proptosis (eye pushed outwards)
Many more
41
Q

Treatment of GPA?

A

Steroids
Biologics
DMARDs
Monitor for organ damage

42
Q

Investigations of GPA?

A

Blood:

  • raised ESR + CRP
  • anaemia

Urine:
- protein and haematuria

CXR: shows lung lesions

Musculoskeletal (15 decks)

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