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MSK 2 > Rheum D/O 1 > Flashcards

Rheum D/O 1 Flashcards

1
Q

giant cell arteritis affects which vessels (general)

A

large and medium vessels

MC extra cranial branches of arteries originating at aortic arch

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2
Q

GCA large artery affected (3) (originate at aortic arch)

A
  1. Brachiocephalic
  2. L Common Carotid
  3. L Subclavian A
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3
Q

pathophys of GCA

A

leukocyte invasion and immune mediated reaction (CD T4) to elastin causing patchy, concentric intimal proliferation

Thrombosis and vessel occlusion due to immune damage that leads to fibrous, scarring, and stenosis (decreased vasodilation and vasoconstriction)

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4
Q

GCA most commonly affects which SPECIFIC arteries ? why?

A
  1. superficial temoral
  2. occipital
  3. ophthalmic
  4. posterior ciliary arteries

highest elastin content

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5
Q

etiology of GCA

A

unknown

believed to have viral trigger

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6
Q

epidemiology of GCA

A

individuals age 50+ , mean age 75 (rare before 50)

genetic predisposition (Scandinavian ancestry)

MC in women

DM reduced risk, smoking, arteriosclerosis increased risk

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7
Q

presentation of GCA (5)

A
  1. systemic symptoms
  2. new HA (temporal)
  3. jaw claudication
  4. visual changes
  5. PMR

GRADUAL onset

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8
Q

systemic symptoms of GCA

A

fever
fatigue
weight loss

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9
Q

pathognomonic for GCA

A

jaw claudication

severe pain or fatigue after chewing or prolonged speaking

caused by masseter ischemia

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10
Q

GCA on PE

A

chronically ill

painful, nodular thickening of temporal arteries, superficial erythema and decreased pulses

carotid tenderness, carotid bruits

abnormal visual exam

PMR symptoms (limited ROM)

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11
Q

most feared complication of vision loss

A

permanent vision loss

MC occurs before starting tx therefore start STEROIDS RIGHT AWAY

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12
Q

lab findings of GCA

A 
reactive thrombocytosis 
elevated ESR (>100) and CRP
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13
Q

diagnostic procedure of choice GCA

A

temporal artery biopsy (100% specific but low sensitivity due to patchy)

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14
Q

imaging in GCA

A

aortic arch and cerebral angiography

evaluates for aneurysm formation (typically aneurysms are asymptomatic)

must also r/o stroke with MRI

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15
Q

tx of GCA

A

prednisone (40-60 mg daily or high dose)

low dose ASA (ischemic, thrombotic events)

PPI (GI ulceration)

bisphosphonates, vitamin D, Ca (bone loss from steroid)

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16
Q

prednisone dosing GCA

A

40-60 mg/day for suspected/confirmed GCA - vision loss

high dose parental steroid for visual changes

continued 2-4 weeks and tapered gradually over 9-12 MONTHS

17
Q

monitoring in GCA management

A

ESR and CRP monikered over recover while tapering

recurrence of symptoms or new symptoms = flare

evaluation for new aneurysm or dissection (UE ischemia, claudication)

18
Q

steroid refractory GCA tx

A

MTX or Tocilizumab (Actemra) IL-6

19
Q

PMR epi

A

affects older individuals (50+), median 72, rare <40

caucasians, northern latitudes, F:M 2:!1

20
Q

PMR affects what?

A

disease of the joints (synovitis, bursitis, tenosynovitis around joints)

21
Q

which joints particularly affected by PMR

A

shoulder and hip MC

also knees, metacarpal phalangeal joints, wrists

22
Q

pathophys PMR

A

systemic inflammation and activation of immune cytokines

possibly due to a viral activation

23
Q

pt presentation of PMR

A

acute or chronic onset of proximal myalgia of hip and shoulder girdles

MORNING STIFFNESS

typically progress to bilateral

describe great difficulty rising from chair or lifting arm above shoulder due to pain

24
Q

PMR associated illnesses

A

GCA

pts are at risk for GCA development and should seek medical attention if they develop symptoms

25
Q

PE of PMR

A

systemic symptoms (50%+) - LOW fever, weight loss, depression, malaise

appear ill and fatigued

NO muscle atrophy but pain with movement

26
Q

PMR work up

A
  1. ESR/CRP (ESR > 40)
  2. CBC (thrombocytopenia)
  3. CK normal
  4. Autoantibody testing ALL NORMAL

normal radiographs

27
Q

how is PMR diagnosed

A

clinically

right population (>50) + absence of abnormal fingings + rapid relief with steroid initiation

28
Q

tx of PMR

A

corticosteroids in low dose (15mg/day)

symptoms should improve dramatically after 48-72 hrs (if not, consider alternative diagnosis)

biologics are ineffective

29
Q

steroid taper in PMR

A

SLOW taper

typically steroid dependent for 3+ years

30
Q

PMR prognosis

A

relapse occurs in 25% of pts, MC due to rapid tapering

MSK 2 (10 decks)

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