Giant cell arteritis

Question 1

what is it?

Answer 1

the most common form of systemic vasculitis in adults

Question 2

pathogenesis

Answer 2

histopathologically - transmural inflammation of intima, media, adventitia or affected arteries - patchy infiltration - lymphocytes, macrophages, multinucleated giant cells vessel wall thickening - arterial luminal narrowing - distal ischaemia

Question 3

who gets it?

Answer 3

no known cause mainly over 50s

Question 4

how does it present?

Answer 4

visual disturbances - 50% patients headache jaw claudication scalp tenderness (e.g. with hair combing)temporal artery may be thickened, prominent, tender to touch constitutional manifestations: fatigue, malaise, fever new onset headache in >50y with elevated CRP, PV/ESR - always consider GCA

Question 5

what are the visual disturbances associated with GCA?

Answer 5

unilateral visual blurring vision loss (most significant morbidity)often painless occasionally diplopia alternatively - partial field defect may progress to complete blindness over days permanent visual impairment in 20%

Question 6

what type of headache is associated with GCA?

Answer 6

continuous temporal/occipital areasfocal tenderness on direct palpation

Question 7

what is the jaw claudication associated with GCA?

Answer 7

fatigue/discomfort of muscles during chewing/speaking most pathognomonic of temporal arteritis ischaemia of the maxillary artery

Question 8

how is it diagnosed?

Answer 8

raised inflammatory markers temporal artery biopsy - most definitive ASAP- if +ve 100% specificity - low sensitivity 15-40% (patchy involvement)- mononuclear infiltration/ granulomatous inflammation (multinucleated giant cells)

Question 9

how is it managed?

Answer 9

corticosteroids - prednisolone 40mg if no visual impairment, 60mg if visual symptoms - start as soon as diagnosis is suspected - not be delayed for the biopsy prednisolone gradually tapered over 2 years - majority will resolve