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MSK 2 > RA > Flashcards

RA Flashcards

1
Q

RF for RA

A
  1. Genetics
  2. infectious agent
  3. Sex hormones
  4. Smoking
  5. Parental Hx of substance abuse
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2
Q

infectious agents that cause RA

A

EBC
mycoplasma
Rubella

innate susceptibility but infxn causes it to switch on

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3
Q

sex hormones and RA

A

more common in women

subsides during pregnancy

less common in women taking OC

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4
Q

RA patho (general)

A

trigger sets off an autoimmune reaction in a genetically susceptible person

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5
Q

RA patho (8) (long)

A
  1. inflammation in synovial membrane and synovial space
  2. destructive enzyme activation
  3. reactive oxygen species form
  4. synoviocyte cells proliferate extensively, cross synovial membrane and get into cartilage
  5. synovium relates MMP that destroys cartilage and stimulate osteoclastic bone reabsorption
  6. pro inflammatory cytokines released cause systemic symptoms
  7. osteoclast activation = osteoporosis
  8. articular surface damage causing destruction of the bones
  9. fibrous adhesions = permanent joint deformities
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6
Q

cells that cause RA inflammation

A

CD4/T cells
monocytes
neutrophils
fibroblasts

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7
Q

enzyme destruction to which joint

A

cartilage
tendons
ligaments
bone

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8
Q

PDGF

A

angiogenesis into the joint

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9
Q

pro inflammatory cytokines RA

A

TNF alpha
IL-6

produce systemic symptoms

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10
Q

systemic symptoms caused by cytokines

A

weight loss
organ inflammation
fever

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11
Q

pathogenies of RA

A
  1. activation of pro inflammatory cytokines causing joint swelling, stiffness, destruction
  2. pannus acts like locally invasive bone tumor
  3. cytokines cause systemic inflammation symptoms and worsened comorbidities
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12
Q

Epidemiology of RA

A

F > M

MC in Native American, least common in Caribbean Black

35-50 years

Family hx

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13
Q

hallmark feature of RA

A

persistent symmetric poly arthritis that affects small joints of hands, wrists, ankles and feet

insidious onset

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14
Q

RA joints on PE

A

swelling, tenderness, warmth and decreased ROM

atrophy of interosseous muscles

worse in AM

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15
Q

lab eval of RA (6)

A
  1. ESR/CRP
  2. CBC (ACD, thrombocytosis)
  3. RF (non diagnostic)
  4. Anti-CCP
  5. Anti MCV
  6. ANA
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16
Q

RF

A

IgM against IgG

60-80% of pts with RA over course of dz but NOT specific for RA

NEITHER necessary nor specific

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17
Q

seropositive RA

A

presence of RF in serum

increased likelihood of severe erosive arthritis, rheumatoid nodules, extra-articular dz

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18
Q

ACPA abs include

A

anti-CCP abs

AntiMCV

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19
Q

anti-CCP Abs

A

MOST specific biomarker for RA but found in other dz

indicates higher likelihood of erosive arthritis and worse prognosis

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20
Q

ANA in RA

A

if NEGATIVE can help distinguish RA from SLE

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21
Q

joint aspiration

A

inflammatory fluid (>10k WBC)

  • crystals, - culture
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22
Q

imaging study of choice

A

Plain fim XR

bone erosion and uniform joint space narrowing

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23
Q

RA on plain film

A

osteopenia
symmetric narrowing of joint spaces
erosions
bony crowding due to loss of cartilage

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24
Q

first 4 criteria for RA diagnosis (1987)

A
  1. Morning stiffness lasting at least 1 hr
  2. soft tissue swelling or fluid in 3 joint spaces
  3. at lease one area swollen in wrist, MCP, PIP
  4. symmetric arthritis
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25
Q

joints MC involved in RA

A
  1. MCP
  2. wrist
  3. PIP

also knee, MTP, joint, ankle. C spine, hip/elbow/temporomandibular joint

26
Q

4 criteria for RA in 2010

A
  1. joint involvement
  2. serology test results
  3. actue phase reactant test results
  4. duration of symptoms
27
Q

why is early diagnosis of RA essential?

A

high risk of permanent joint deformities

decreased ability to do ADLs

28
Q

extra articular disease of RA (who gets it, MC_

A

fatigue, myalgia, malaise

mc in pts with seropositive RF

29
Q

rheumatoid nodules (MC site)

A

extensors surfaces and areas of mechanical trauma

olecranon, ulna. back of heel, occiput

30
Q

ocular manifestations of RA

A

dry eyes/MM

Uveitis
Episcleritis
Nodular scleritis (red eye, painful with movement)

31
Q

list of RA organ systems affected:

A
  1. anemia (microcytic)
  2. infections
  3. GI issues (stomach and intestinal upset)
  4. osteoporosis
  5. pulmonary dz
  6. lymphoma
32
Q

pulmonary disease and RA

A

increased risk of intersistial lung dz,pleuritis, pleural effusion, rheumatoid pulm nodules

33
Q

Cardiac Dz in RA

A

CAD not attributable to typical risk factors

MI, pericardial effusion, myocardial dysfunction

34
Q

MSK dz in RA

A

synovial cysts
tendon rupture
nerve entrapment
tenosynovitis

35
Q

cervical spine dz in RA

A

subluxation of C1 and C2

36
Q

boutonniere deformity

A

contracture of PIP joint and hyperextension of DIP joint

37
Q

swan neck deformity

A

hyperextension of PIP joint and flexion contracture of DIP

38
Q

tx goals of RA

A

control pain
preserve joint fxn
prevent joint deformity

early referral + therapy

39
Q

NSAIDs in RA

A

pain management and improve daily fxn

do NOT inhibit disease progression/disability and NOT as sufficient as mono therapy

risk of GIB/GI ulcer, renal dysfunction, HF exacerbation

40
Q

w/u prior to RA tx

A

CBC, Chem Panel, ESR/CRP

LFTs, viral hepatitis panel, TB screen

41
Q

pharm tx of RA (list) (

A
  1. Glucocorticoids
  2. non biologic DMARDs
  3. Biologic DMARDs
42
Q

glucocorticoids use in RA

A
  1. acute exacerbation
  2. starting DMARD
  3. unable to take DMARD
43
Q

long term SE of glucocorticoids

A

weight gain
HTN
osteoporosis
hyperglycemia

44
Q

when do you start DMARD?

A

EARLY (<6 mo) of tx is standard

45
Q

vaccinations and DMARDs

A 
pneumococcal 
hep A, hep B
influenza vax
HPV
herpes zoster
46
Q

pts started on DMARDs MUST be tested for”

A

TB
viral hep
endemic fungal infections

47
Q

initial DMARD of choice

A

Methotrexate

therapy should be adjusted after 6 mo if incomplete response

48
Q

biologic prescribing rules

A

all are equally efficacious

more effective than non biologics

should only give one at a time

49
Q

Biologic CIs

A

Chronic viral hep B and C
malignancy in last 5 yrs
CHF AHA class III or IV
fungal infection/tb

50
Q

biologic DMARDs and vaccines

A

cant receive live virus vaccine (MMR, yellow fever, intranasal, herpes zoster, varicella)

give all killed viruses

HZE live should be given before starting DMARD or Biologics

51
Q

monitoring while taking DMARDS biologics

A

CBC, liver, renal panel, and viral hep panel at baseline and q 4 months

52
Q

HF and TNF agents

A

CI in pts with NYHA class II or IV

ESP infliximab

53
Q

RA prognosis

A

disabled in 10 years

typically die 10-15 years before (2.5x mortality)

54
Q

MC cause of premature death

A

CAD

not associated with traditional risk factors

secondary to chronic inflammation

55
Q

factors indicating poor RA prognosis

A

RF seropositivity
>30 joints involved
Extra-articular manifestation

56
Q

Felty’s syndrome MC in

A

RF positive,
long duration of RA (>10 yrs),
extra articular manifestations

57
Q

Felty’s syndrome patho

A

splenic sequestration and destruction of granulocytes

58
Q

Felty’s syndrome triad

A

RA
Splenomegaly
neutropenia

59
Q

tx of Felty’s syndrome

A

IV abx (Neuopgen)
usual RA tx
Steroids (limited efficacy)

60
Q

Triple therapy

A

Max MTX dose
Sulfasalazine
Hydroxychloroquine

if this fails go to biologic

MSK 2 (10 decks)

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