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Clin Med- P > RA > Flashcards

RA Flashcards

1
Q

RA is a _________ ________ disease characterized by what type of arthritis and synovitis?

A

systemic autoimmune disease;

chronic inflammatory arthritis and erosive symmetric synovitis

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2
Q

extraarticular manifestations are __________ and may involve what?

A

common; may involve almost any organ system

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3
Q

how many joints affected by RA?

A

common to have polyarticular involvement

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4
Q

affects __% of the population. what is the male to female ratio?

A

1%; female to male 3:1

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5
Q

what decades of life is RA most common? but can start as early as?

A

3rd-5th; infancy

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6
Q

__-__% concordance among identical twins

A

30-50%

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7
Q

RF includes what three antibodies?

A

IgM, IgG, IgA (IgA is rare tho)

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8
Q

how do RF antibodies cause RA symptoms?

A

the antibodies form immune complexes due to their ability to bind to the Fc region of IgG; complexes then stimulate complement activation and inflammation (including in the synovial fluid) causing RA symptoms

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9
Q

what three places are RA antibodies found?

A

blood, synovial fluid and synovial membrane

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10
Q

what is the sensitivity and specificity for RF?

A

65% sensitive

87% specificity

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11
Q

Can RA occur without positive RF?

A

yes, in about 30% of cases

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12
Q

probability that a patient has RA _______ in proportion to the titer of RF

A

increases

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13
Q

what test is more specific for RA than RF?

A

anti-cyclic citrulline antibodies(anti-CCP)- 90-95%

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14
Q

what are the two Anti-CCP antibodies? how do they relate to RA?

A

IgM and IgG: they bind to a protein called filaggrin that is produced in inflamed joints, these proteins attract the antibodies (primarily in RA patients)

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15
Q

what is one cytokine that contributes to immune response/inflammation that RA drugs can target?

A

tumor necrosis factor alpha

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16
Q

what is the hallmark of RA in affected joints?

A

proliferative synovial pannus

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17
Q

what is a pannus?

A

destructive inflammatory vascular granulation tissue that extends from synovium to bone not covered by cartilage

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18
Q

pannus progressively destroys what?

A

bone and cartilage (creates erosions)

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19
Q

what test can distinguish between pannus and cartilage?

A

MRI

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20
Q

when does pannus show up in someone with RA?

A

early, even before many symptoms

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21
Q

signs and symptoms of RA? (6)

A

synovitis, warmth, soft tissue swelling, effusion, tenderness, decreased ROM

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22
Q

what four things might you also see in an RA joint?

A

subchondral cyst formation (cyst coming off bone in the joint- more common in OA)
juxta-articular osteopenia, joint space narrowing, ankylosis (stiffening or fusion of a joint- occasional)

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23
Q

how do you diagnose RA?

A

depends on constellation of signs/symptoms that are supported by labs and radiology (no 100% specific lab tests)

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24
Q

what is often the key to RA diagnosis?

A

involvement of the small joints of hand and feet

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25
Q

ARA diagnostic criteria (7)

A

must meet 4 of the 7, present for at least 6 weeks

1) . morning stiffness lasting at least 1 hour
2) . at least 3 joint areas simultaneously swelling
3) . swelling in wrist, MCP, or PIP
4) . symmetric involvement of same joint areas
5) . subcutaneous nodules observed by physician
6) . demonstration of positive RF
7) . radiographic changes typical of RA (erosions, bony decalcification)

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26
Q

what’s the usefulness of US in RA disease?

A

can be used to see pannus and seeing tenosynovitis can be an early predictor of RA development

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27
Q

typical RA distribution?

A

shoulders, wrists, knuckles and middle joints of fingers, ankles, middle joints of toes, balls of feet

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28
Q

what does a bone scan tell us?

A

shows us where there is high metabolic activity

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29
Q

what happens at the hand joints when you have RA

A

fusiform swelling and tenderness at MCP and PIP

- ulnar deviation at these joints too

30
Q

what is fusiform swelling?

A

smooth elliptical shape

31
Q

what two deformities of the fingers can form in RA? describe them both

A

boutonniere: PIP flexion and DIP extension

swan neck: PIP hyperextension and DIP flexion

32
Q

what is enthesitis?

A

inflammation on the joint where tendons/ligaments insert

33
Q

where can RA nodules occur?

A

can be outside or inside the body, even in the eye

34
Q

what can happen to the bones of the wrist?

A

they can erode, usually ulnar styloid is first to be affected
-radial deviation of wrist

35
Q

what happens to extensor tendons at the wrist?

A

synovial proliferation with rupture of extensor tendons (hard to extend fingers actively)

36
Q

what can happen in the hip with RA?

A

hip is affected later than most joints but can be axial migration of femoral head with acetabular protrusion

37
Q

what can you see on the ankles and feet for RA?

A 
Hallux valgus (toe points laterally like a bunion
**angulation due to loss of joint integrity
collapse of arches, MTP joint synovitis, pain in balls of feet,
38
Q

what are some extra articular manifestations? (6)

A

fever, anorexia, weight loss, fatigue, muscular weakness, increased CVD risk

39
Q

what skin disease also increases your risk for CVD?

A

psoriasis

40
Q

what did a study find out about ACS (acute coronary syndrome) risk factors?

A

clinical markers of inflammatory activity, disease activity and net days of sick leave/disability pension during the first year after RA onset are ACS risk factors

41
Q

what are rheumatoid nodules?

A 
granulomatous lesions (rubbery) that develop around small blood vessels
**most common extra articular manifestation of RA
42
Q

where do nodules usually occur?

A

subcutaneous areas exposed to pressure (elbows, knuckles of hand)

43
Q

treatment of nodules?

A

no specific therapy to treat but usually surgery

44
Q

when is there usually organ involvement in RA? (3)

A

when there’s severe RA, high titers of RF and Anti-CCP, and nodule formation

45
Q

what two things can RA do to lungs?

A

pleurisy with effusions and nodules in the parenchyma

46
Q

what three things can RA do to heart?

A

nodule formation, myocarditis, valvular fibrosis

** rarely symptomatic

47
Q

what two things can RA do to the blood/blood vessels?

A

anemia and vasculitis

48
Q

what is the hallmark of early RA?

A

vasculitis

49
Q

what are some GI complications due to RA?

A

pretty rare for RA to affect GI except when using NSAIDS

50
Q

what is best seen on XRAY?

A

bony erosions: cyst-like radiolucencies best seen at joint margins
(not helpful in early RA though*)

51
Q

what can be seen on MRI for RA?

A

distinguishes synovial pannus from cartilage and picks up many other detailed features of joints

52
Q

what two things can US help with for RA?

A

can pick up early soft tissue changes and predict disease severity

53
Q

what anemia is RA associated with?

A

normocytic

54
Q

what four lab tests are normally elevated in RA?

A

ESR, CRP, WBC (leukocytosis), and ANA (antinuclear antibody- not always high)

55
Q

can RF results change over time?

A

yes, usually absent in 1st year but eventually positive in 80%

56
Q

what two things are important about anti-ccp?

A

1) may be elevated before symptoms in patient who will develop RA later on
2) . CCP-positivity predicts worse disease

57
Q

what antibodies are found on labs for RA?

A

anti ss-DNA antibodies

58
Q

what does synovial fluid analysis show?

A

WBC range from 2,000-50,000 (mostly neutrophils- 50 to 80%), glucose is usually normal (unless chronic and severely inflamed)

59
Q

what does a WBC count over 50,000 in synovial fluid suggest?

A

infection- think more septic arthritis

60
Q

what are the four progressions of RA?

A

1) . spontaneous remission (10-20% of patients)
2) . remitting: recurrent flares but patient returns to normal during flares
3) . remitting progressive: no complete return to normal between flares
4) . progression- on-going synovitis and progressive pain, swelling and joint damage (MOST COMMON)

61
Q

what are three non pharmacologic therapies of RA?

A

1). joint progression
2). exercise
3). nutrition- vitamin D helps prevent and may improve symptoms
(also notes that no climate or diet alters the course of RA)*

62
Q

what type of drugs are usually used as first treatment?

A

NSAIDS (symptomatic relief)

63
Q

what drugs are used for RA flares? what’s another use for them?

A

steroids for flares AND bridge to DMARDs

64
Q

what are mainstream RA drugs? how do we use these?

A

DMARDs
1 or more should be used early in dz course: methotrexate FIRST, most patients require 2nd add on (TNF a inhibitor)
** maybe plaquenil or sulfasalazine as non biologic add on

65
Q

how does methotrexate treat RA? what do we supplement this with?

A

inhibits cell division; folate

66
Q

3 main TNF a inhibitors we use for RA

A

Adalimumab (Humira), Infliximab, Etanercept

67
Q

methotrexate combined with what TNF inhibitor resulted in 49% remission of early and aggressive RA after 2 yrs of treatment?

A

adalimumab

68
Q

how does leflunomide help RA?

A

decrease production of pyrimidines, inhibiting T and B cell function

69
Q

how does rituximab help RA?

A

depletes B cells

70
Q

who do you not want to start on methotrexate?

A

someone who has cancer or an active infection

71
Q

what are some surgical benefits for RA?

A

control pain, repair ligaments/tendons, remove inflamed synovial tissue, restore function

Clin Med- P (124 decks)

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