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Rheumatology > E: Polymyalgia Rheumatic + Giant Cell Arteritis > Flashcards

E: Polymyalgia Rheumatic + Giant Cell Arteritis Flashcards

1
Q

What is polymyalgia rheumatic

A

Autoimmune, Inflammatory, Rheumatic Disease

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2
Q

What age does PMR tend to occur and what is the peak incidence

A

Occurs in >50y

Peak incidence is 70-80y

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3
Q

In which gender is PMR more common

A

Female (3:1)

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4
Q

What is the aetiology of PMR

A

Combination of genetic and environmental factors:

  • Genetic: HLA DR4
  • Environmental: parvovirus B19 and adenovirus infection
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5
Q

What genetic factor predisposes to PMR

A

HLA DR4

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6
Q

What condition if PMR associated with

A

Giant Cell Arteritis

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7
Q

What % of patients with PMR will have GCA

A

10-20%

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8
Q

What are the musculoskeletal symptoms of PMR

A
  • Bilateral shoulder, pelvic girdle and neck pain. (May start in one side - and progress to be bilateral in weeks)
  • Morning stiffness >45m
  • Nocturnal pain
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9
Q

What are the systemic symptoms of PMR

A
  • Lethargy
  • Low grade fever
  • Malaise
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10
Q

What are the two investigations for PMR

A
  1. ESR

2. Creatinine kinase

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11
Q

How will ESR present in PMR

A

> 50

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12
Q

How will Creatinine Kinase present in PMR and why is this important

A

It will be NORMAL - this is important to differentiate PMR from other inflammatory rheumatic disorders

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13
Q

What drug is given to manage PMR

A

Prednisolone

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14
Q

What dose of prednisolone is initially given in PMR and how long is this continued

A

15mg/day. This is continued until symptoms resolve

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15
Q

Explain dose tapering of prednisolone

A
  • 15mg/d. until symptoms resolve
  • 12.5mg/d for 3W
  • 10mg/d for 4-6W
  • then reduce by 1mg every 4-8W until dose is stopped
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16
Q

What should anyone on prednisolone be given

A

Blue steroid card

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17
Q

What are 5 complications of PMR

A
  • GCA
  • Fibromyalgia
  • Dermatomyositis
  • Polymyositis
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18
Q

What is giant cell arteritis

A

vasculitis affecting medium to large sized vessels

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19
Q

which gender is GCA more common

A

female

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20
Q

which age is GCA typically seen in

A

> 50y.

Peak incidence of 70-80y

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21
Q

which heritage is giant cell arteritis commonly seen in

A

Northern European Descent

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22
Q

what is the aetiology of giant cell arteritis

A

Thought to be a combination of genetic and environmental factors.
Genetic = due to HLADR4
Environmental = infection with parvovirus B19 or adenovirus

23
Q

what % of patients with GCA will have polymyalgia rheumatic

A

50%

24
Q

how will GCA present clinically

A
  • dull, throbbing, pulsating headache over temples
  • tenderness over temporal artery to palpate (combing hair)
  • jaw claudication
  • fever
  • malaise
  • lethargy
25
Q

why is the headache a pulsating, dull throbbing over the temples

A

due to GCA affecting temporal artery

26
Q

why do patients have jaw claudication

A

due to GCA affecting facial artery

27
Q

what eye symptoms will patients eventually present with in GCA

A

First present with a scintillating scotoma which will then progress to amaurosis fugax

28
Q

what is amaurosis fugax

A

painless sudden loss of vision in one eye

29
Q

what causes amaurosis fugax in GCA

A

anterior ischaemic optic neuropathy due to affecting the ophthalmic artery

30
Q

what other symptoms may patients with GCA have

A

symptoms of PMR (50%)

- bilateral shoulder, pelvic, neck pain

31
Q

Explain pathophysiology of GCA

A
  • activation of dendritic cells in adventitia of blood vessels recruits monocytes
  • monocytes differentiate to macrophages and produce cytokines (IL6)
  • macrophages produce MMP which destroy blood vessels
  • PDGF and VEGF from macrophages causes proliferation of blood vessel intima that reduces blood flow and leads to ischaemia
32
Q

what should be done before investigating in GCA and why

A

management. As individuals with GCA can go blind within 48h

33
Q

What 3 tests may be ordered in GCA

A
  1. ESR
  2. FBC
  3. Temporal artery biopsy
34
Q

what will ESR show in GCA

A

Isolated raised ESR. (CRP may also be raised but disproportionately to CRP)

35
Q

what will FBC show in GCA

A

normocytic normochromic anaemia

36
Q

what is gold-standard investigation for GCA

A

temporal artery biopsy

37
Q

which patients should receive a temporal artery biopsy

A

All patients

38
Q

why may a temporal artery biopsy return normal

A

due to skip lesions

39
Q

if temporal artery biopsy is negative, but you suspect GCA what should be done

A

treat as GCA

40
Q

what will be seen on temporal artery biopsy

A

granulomatous inflammation of tunica intima

41
Q

what criteria is used to identify GCA

A

American college of rheumatology

42
Q

what is a mneumonic to remember american college of rheumatology criteria for GCA

A

H.A.T.E.H

43
Q

what does the american college of rheumatology state must be present to identify GCA

A 
Headaches 
Age >50y 
Temporal artery dysfunction
ESR >50
Histological evidence on temporal artery biopsy
44
Q

what is first-line management for giant cell arteritis

A

Oral prednisolone

45
Q

if people have visual symptoms of GCA what dose of prednisolone should be given

A

60mg

46
Q

if people with GCA do not have visual symptoms, what dose of prednisolone should be given

A

40-60mg

47
Q

if individuals do not respond to prednisolone in 48h what should be done

A

Seek advice - consider alternative diagnosis

48
Q

over what time frame is the dose of prednisolone tapered

A

1-2y. Whilst during this time recurrence may occur

49
Q

if someone with GCA has visual disturbances what is done

A

same-day referral to ophthalmology

50
Q

in addition to prednisolone what other medication is given

A

aspirin

51
Q

what dose of aspirin is given in GCA

A

75mg

52
Q

what must be given with aspirin

A

omeprazole 20mg

53
Q

what are 3 complications of GCA

A
  • cerebral ischaemia
  • aortic aneurysm
  • permanent visual loss
54
Q

what % of individuals with GCA will develop permanent visual loss

A

20-30%

Rheumatology (10 decks)

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