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Musculoskeletal > Vasculitis > Flashcards

Vasculitis Flashcards

1
Q

What is the most common form of systemic vasculitis in adults?

A

giant cell arteritis

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2
Q

what histologically is seen in giant cell arteritis?

A

transmural inflammation (involving intima, media and adventita) as well as patchy granulomatous infiltration of lymphocytes, macrophages and multinucleated giant cells

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3
Q

why can giant cell arteritis cause distal ischaemia?

A

the artery wall becomes thickened due to the inflammation. This causes luminal narrowing.

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4
Q

what should you always consider in a patient over 50 y/o with a new onset headache and raised CRP/PV/ESR?

A

giant cell arteritis

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5
Q

what artery is commonly affected in giant cell arteritis?

A

temporal artery

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6
Q

what is the most serious consequence of giant cell arteritis in the temporal artery?

A

permanent visual impairement

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7
Q

describe the headache commonly seen in patients with temporal arteritis?

A

continuous and located in the temporal or occipital areas

focal tenderness on direct palpation

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8
Q

why can patient with temporal arteritis experience jaw claudication?

A

ischamia of the maxillary artery

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9
Q

what is jaw claudication?

A

jaw fatigue or discomfort during chewing or prolonged speaking

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10
Q

what is the most definitive test for suspected giant cell arteritis?

A

temporal artery biopsy

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11
Q

compare specificity to sensitivity in terms of a temporal artery biopsy for GCA?

A

high specificity

low sensitivity

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12
Q

why does temporal artery biopsy have a low sensitivity for GCA?

A

because there is patchy involvement- some segments of temporal artery might be normal

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13
Q

what is the treatment for temporal arteritis with visual symptoms?

A

60mg prednisolone tapered over 2 years

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14
Q

what is the treatment for temoral arteritis without visual symptoms?

A

40mg prednisolone tapered over 2 years

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15
Q

when should treatment with steroids be started for a patient with suspected temporal arteritis?

A

as soon as diagnosis is suspected

don’t wait for biopsy results

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16
Q

what is large vessel vasculitis?

A

primary vasculitis that causes chronic granulomatous inflammation predominantly of the aorta and its branches

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17
Q

what are the 2 major categories of large vessel vasculitis?

A

Takayasu arteritis

Giant cell arteritis

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18
Q

who tends to get takayasu?

A

young women

mainly in east asian countries

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19
Q

what are the clinical signs of large vessel vasculitis?

A

reduced pulses

bruits

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20
Q

what is the mainstay treatment of large vessel vasculitis?

A

40-60mg prednisolone
tapering doses

steroid sparing agents eg methotrexate and azathioprine may be used

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21
Q

what are the 2 main classes of small vessel vasculitis?

A

ANCA-associated

Non-ANCA- associated

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22
Q

within ANCA-associated small vessel vasculitis, what is the further subdivision?

A

granulomas - GPA or EGPA

no granulomas- MPA

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23
Q

What are the main differences between EGPA and GPA?

A

EGPA- eosinophilia, late onset asthma, cANCA

GPA- common ENT symptoms, pANCA

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24
Q

what is the most important complication of microscopic polyangitis?

A

glomerulonephritis

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25
Q

what is the management of ANCA-associated vasculitis?

A

IV steroids

cyclophosphamide

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26
Q

what is Henoch-Schonlein purpura?

A

an acute IgA mediated disorder which commonly affects children after a history of a upper respiratory tract infection

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27
Q

what is the treatment of Henoch schonein purpura?

A

self-limiting

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28
Q

what is vasculitis?

A

inflammation of blood vessels, often with ischamia, necrosis and organ inflammation

29
Q

why can vasculitis lead to blood clot formation?

A

lumen becomes narrower and irregular which promotes blood clots formting

30
Q

what are the 2 main classes of medium vessel vaculitis-?

A

polyarteritis nodosa

kawasaki disease

31
Q

what are both takayasu arteritis and giant cell arteritis characterised by?

A

granulomatous infiltration of the walls of large vessels

32
Q

why are granulomas generally formed in the body?

A

to wall off a ‘threat’ from the body

one that can’t be expelled

33
Q

what type of cells from a granuloma merge together to form giant cells?

A

macrophages

giant cell arteritis

34
Q

what are the main clinical findings of large vessel vasculitis?

A
  • bruit (usually carotid)
  • blood pressure difference of extremities
  • vessel tenderness (usually unilateral)
  • hypertension
35
Q

what clinical sign may indicate temporal arteritis?

A

prominent temporal arteries

reduced pulsation

36
Q

who tends to get kawasaki disease?

A

children under 5

37
Q

aneurysms to what arteries are a significant risk in kawaski disease?

A

coronary arteries

38
Q

when do you choose to give treatment in kawaski disease?

A

when coronary arteries are affected

if they aren’t affected this condition will subside without treatment

39
Q

where in the blood does polyarteritis nodosa tend to affect?

A

birfucations

40
Q

what can result from the necrotising inflammatory lesions caused by polyarteritis nodosa?

A

microaneurysm and aneurysm formation

41
Q

what viral disease is polyarteritis nodosa associated with?

A

hepatitis B

42
Q

what is the new name of Wegner’s granulomatosis?

A

granulomatosis with polyangiitis (GPA)

43
Q

what is the new name of Churg-Strauss syndrome?

A

Eosinophilic granulomatosis with polyangitiis (EGPA)

44
Q

what respiratory disease to patients with eosinophilc granulomatosis with polyangitiis frequently get?

A

late-onset asthma

45
Q

what is a ‘saddle nose’?

A

collapse of nasal cartilage

46
Q

what causes a saddle nose?

A

collapse of nasal cartilage caused by cartilage ischaemia

ENT features such as this present in GPA

47
Q

what are the main 2 cutaneous features of small vessel vasculitis?

A 
ulcers
palpable purpura (ie raised purpura)
48
Q

why must you always do a urinalysis in a patient with suspected small vessel vasculitis?

A

glomerulonephritis can occur

this is asymptomatic until late stage so you actively try to catch it early

49
Q

what is mononeuritis multiplex?

A

impairment of blood supply to nerves (usually long nerves eg perineal or radial)

50
Q

what is the clinical feature when a patient with mononeuritis multiplex of the common perineal nerve can’t extend their ankle?

A

drop foot

51
Q

what are ANCAs?

A

anti-neutrophil cytoplasmic antibodies:

autoantibodies against antigens in the cytoplasm of neutrophil granulocytes

52
Q

what type of ANCAs do ANCA-associated small vessel vasculitis have?

A

GPA and EGPA- cANCA

MPA- pANCA

53
Q

what is localised ANCA-associated vasculitis?

A

upper/lower resp tract disease

no other systemic involvement or constitutional symptoms

54
Q

what is early systemic ANCA-associated vasculitis?

A

any involvement without organ or life threatening involvement

55
Q

what is generalised ANCA-associated vasculitis?

A

renal or other organ threatening involvement

56
Q

what is systemic ANCA-associated vaculitis?

A

renal or other vital organ failure

57
Q

what is refractory ANCA-associated vasculitis?

A

progressive disease unreponsive to steroids + cyclophosphamide

58
Q

what is the treatment of localised ANCA-associated vasculitis?

A

methotrexate + steroids

59
Q

what is the treatment of early systemic ANCA- associated vasculitis?

A

methotrexate + steroids

60
Q

what is the treament of generalised ANCA- associated vasculitis?

A

cyclophosphamide + steroids

rituximab + steroids alternative

61
Q

what is the treatment of systemic ANCA- associated vasculitis?

A

cyclophosphamide + steroids

rituximab + steroids alternative

62
Q

what is the treatment of refractory ANCA-associated vasculitis?

A

IV immunoglobulins

rituximab

63
Q

what is Henoch-Schonlein Purpura?

A

a non-ANCA associated small vessel vasculitis

acute IgA mediated disorder

64
Q

who tends to get Henoch-Schonlein Purpura?

A

children 2- 11

but rarely infants

65
Q

what usually precedes Henoch-Schonlein Purpura?

A

an upper respiratory infection, pharyngeal infection, GI infection
(a few weeks before)

66
Q

what is the most common organism involved in the infection preceding Henoch-Schonlein Purpura?

A

Group A Strep

67
Q

what is the treatment of Henoch-Schonlein Purpura?

A

usually self limiting

if evidence of gut or renal involvement- hospital admittance with supportive therapy

68
Q

what is the difference between purpura and telangiectasia?

A

purpura doesn’t blanche

telangiectasia does

Musculoskeletal (16 decks)

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