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Clin Med Exam 3 > RA/OA/Polymalgia/Fibromyalgia > Flashcards

RA/OA/Polymalgia/Fibromyalgia Flashcards

1
Q

Most common inflammatory arthritis

A

RA

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2
Q

RA

A

autoimmune disease; chronic, systemic, inflammatory disorder that primarily involves SYNOVIAL JOINTS (cartilage erosion and inflammation of synovial membranes); extraarticular manifestations

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3
Q

Prevalence of RA

A

W>M

Peak age: 35-50 YO

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4
Q

Cause of RA

A

Genes (HLA) + enviorment

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5
Q

Sx of RA

A

SYMMETRICAL polyarthritis
Peripheral –> proximal
Axial skeleton usually spared (except cervical spine)
GRADUAL onset (difficult performing ADL’s)
Predominant Sx: pain, stiffness and swelling
MORNING STIFFNESS >1 HOUR
- better with movement

Constituional sx: myalgia, FATIGUE, low-grade fever, weight loss, poor sleep

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6
Q

Most common joints effected in RA

A

hands, wrists, and forefoot (others: elbows, shoulder, ankles, knee)

Joints: Wrists, MCP and PIP

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7
Q

Morning stiffness >1 hour

A

RA

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8
Q

Gets better with movement

A

RA

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9
Q

RA not found in these joints

A

DIP

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10
Q

PE for RA

A

joint inflammation; pain (TTP or movement of joint, squeeze tenderness of MCP and MTP)
Swelling: palpable synovial thickening (boggy), effusion (fluctuance)

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11
Q

Hands in RA

A

symmetrical inflammation of MCP and PIP
Flexor tendon tenosynovitis (decreased ROM, reduced grip strength, trigger finger)
Swan-neck and boutonniere deformities
Ulnar deviation

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12
Q

Ulnar deviation

A

RA

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13
Q

Swan-neck and boutonniere found in

A

RA

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14
Q

Trigger finger usually occurs with

A

RA

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15
Q

Other UE sx in RA

A

wrist: loss of extension, carpal tunnel syndrome*

Shoulder (late): frozen shoulder

Elbow: loss of extension, ulnar nerve compression, rheumatoid nodules

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16
Q

Most common site for rheumatoid nodules

A

Elbow

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17
Q

LE sx of RA

A

callus/hallus (bunion) on feet, hammer toes

Effusion & limited ROM (flexion) of knee; POPLITEAL CYST

Hips: longstanding disease
restriction of movement

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18
Q

Cervical spine in RA

A

Atlantoaxial joint instability (C1-C2); cervical subluxation

Sx: neck pain, stiffness, and radicular pain; can lead to cervical myelopathy

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19
Q

Can lead to cervical myelopathy

A

RA of cervical spine

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20
Q

Marker of disease severity of RA

A

extraarticular manifestations (increased morbidity and premature mortality; may antedate onset of polyarthritis)

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21
Q

Most likely to develop extrarticular disease from RA

A

Hx of smoking
Early onset of significant physical disability
Test (+) for RF

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22
Q

Extraarticular manifestations of RA

A 
Skin: nodules (advanced)
Eye: scleritis, uveitis, keratoconjunctivitis sicca (secondary Sjogren's syndrome)
Pulmonary: pleural effusion, pleuritis, interstitial lung disease
CV: CAD, myocarditis, pericarditis
MSK: osteopenia/osteoporosis
Heme: anemia of chronic disease
CNS: aseptic meningitis
Felty Syndrome (rare)
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23
Q

Felty syndrome

A

Triad of:
RA
Splenomegaly
Neutropenia

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24
Q

Secondary sjogren’s syndrome

A

RA extraarticular manifestation of eyes

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25
Q

Imagine for RA

A

Radiography*, MRI, U/S

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26
Q

Preferred initial imagine for RA & Findings

A

Radiography:

Findings: soft tissue swelling around joint, periarticular osteopenia, joint space narrowing, bony erosion, subluxation

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27
Q

MRI and U/S in RA

A

no established role in routine eval of RA; sensitive at detecting changes resulting from synovitis

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28
Q

What do you use to evaluate cervical spine in RA

A

MRI

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29
Q

Labs for RA

A

RF
Anti-cyclic citrullinated peptide antibodies (anti-CCP)
Antinuclear antibody (ANA)
CBC- anemia, thrombocytosis, mild leukocytosis
ESR/CRP- elevated
synovial fluid analysis (arthrocentesis)

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30
Q

First antibody associated with RA

A

RF (75-80% of patients); prognostic value

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31
Q

Anti-CCP anitbody

A

most specific for RA (in 60-70% of patients); correlate strongly with erosive disease

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32
Q

Antibodies for RA

A

ANA (not specific)
RF (moderate specificity)
ACCP (high specificity)

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33
Q

Arthrocentesis of RA

A

dx or exclusion of: gout, pseudogout, infection

Synovial fluid analysis: usually reveals an inflammatory effusion

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34
Q

Who should be tested for RA

A
  • have at least 1 joint with definite clinical synovitis

- synovitis not better explained by another disease

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35
Q

Dx of RA

A

meet 6/10 on ACR/EULAR chart (joint involvement, serology, acute-phase reactants, duration of symptoms)

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36
Q

Seronegative RA

A

lack RF and ACCP anitbodies

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37
Q

Dx of seronegative RA

A

based on findings otherwise characteristic of RA if appropriate exclusions have been met

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38
Q

Tx for RA

A 
early recognition and dx
refer to rheumatology
DMARD's* 
target-to-treat strategy
antiinflammatory agents as adjunct therapy
prevention of joint injury
maintain muscle strength, joint alignment, joint mobility
Preserve ADL
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39
Q

Non parm treatment for RA

A

rest, exercise, PT/OT
nutritional and dietary counseling
SMOKING CESSATION
psychosocial intervention

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40
Q

Pharm tx for RA

A

DMARD’s + NSAID or glucocorticoid

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41
Q

DMARDs

A

slow/halt disease progression, preserving joint function (start early)

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42
Q

Pretreatment evaluation for DMARDs

A

Baseline serology: CBC, serum creatinine, LFTs, ESR/CRP, Hep B or C

Opthamologic screening (for hydroxychloroquine use)

TB test

Vaccines

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43
Q

Risk of DMARDs

A

infection, malignancy

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44
Q

Nonbiologic DMARD

A

Methotrexate (MTX)*, hydroxychloroquine, sulfasalazine, leflunomide

45
Q

Biologic DMARD

A

TNF-inhibitors*, IL-1, IL-6 antagonists
T-cell inhibitor
monoclonal antibody
JAK inhbitor

46
Q

TNF inhibitors

A

etanercept
infliximab
Adalimumab

47
Q

Most common joint disorder

A

OA

48
Q

Leading cause of chronic disability in OLDER ADULTS

A

OA

49
Q

Prevalence of OA

A

W>M older than 55

50
Q

Primary sx of OA

A

joint pain and functional impairement

51
Q

Joints involved in OA

A

knees, hips, hands (DIP, PIP, 1st CMC), spine (cervical and lumbar), feet (1st MTP joint)

52
Q

Difference in locations of OA and RA

A

RA- MCP, PIP, wrists, cervical spine

OA- DIP, PIP, 1st CMC, knees, hips, cerivcal & lumbar spine, feet (1st MTP)

53
Q

Pathogenesis of RA

A

cartilage erosion and synovial inflammation

54
Q

Pathogenesis of OA

A

involves ALL joint tissues: cartilage, bone, ligaments and synoviium

Progressive loss and destruction of cartilage, overtime joint space narrows

Bone changes: bone sclerosis, subchondral cysts, osteophytes (spurs)

Synovitis

Soft tissue: ligaments, joint capsule, menisci (knee), muscles and nerves

55
Q

Factors contributing to OA

A 
aging
joint injury (postraumatic OA)
obesity
genetics (FHx)
Anatomic factors (joint shape, aligment)
female
56
Q

Sx of OA

A

Joint pain: worse with use, relieved by rest, worse in afternoon/early evening

Stiffness: worse after effort, evening stiffness, morning stiffnes <30 min

57
Q

Morning stiffnes >1 hr

A

RA

58
Q

Morning stiffness <30 min

A

OA

59
Q

Worse with exercise

A

OA

60
Q

Evening stiffness

A

OA

61
Q

Better with activity

A

RA

62
Q

Usage related pain

A

OA

63
Q

PE for OA

A 
TTP
reduced ROM
bony enlargement/swelling
joint deformity
joint instability
64
Q

OA hands

A

Heberden’s and bouchard’s nodes, first CMC joint (squared off)

65
Q

Squared off CMC

A

OA

66
Q

Node on PIP

A

Bouchard’s

67
Q

Node on DIP

A

Heberden’s

68
Q

OA knees

A

bilateral, swelling/effusion, joint line tenderness, crepitus, limitation of ROM

69
Q

Hips OA

A

frequently unilateral
restricted internal ROM
pain around hip/groin
may have referred pain to knee (distal)

70
Q

OA radiological findings

A

joint space narrowing, OSTEOPHYTE, sclerosis, cysts

71
Q

Lab findings for OA

A 
No specific test:
Synovial fluid analysis (r/o other diseases)
CBC (no leukocytosis)
Negative RF &amp; anti-CCP antibodies
Normal ESR and CRP
72
Q

Biggest way to distinguish between OA and RA

A

look at locations and LAB WORK IS REALLY DIFFERENT (ESR/CRP, RF, ACCP, Leukocytosis)

73
Q

Dx of OA

A

CLINICAL: without imagine/lab investigations

Criteria: presence of s/sx, at-risk age group

74
Q

Nonpharm tx for OA

A

exercise, weight loss, PT/OT, assisted devices if needed

75
Q

Pharm therapy for OA

A 
pain and inflammation:
NSAIDs (Topical, PO)
Topical Capsaicin
Duloxetine
Intraarticular glucocorticoids
Tramadol/tylenol
* use opiods sparingly if at all
76
Q

Surgical tx for OA

A

reserved for those who failed less invasive modes of therapy

77
Q

3 overarching tx for OA

A
  1. Lose weight
  2. Anti-inflammatory
  3. Surgery if resistant to other tx
78
Q

Hard and bony joints

A

OA

79
Q

soft, warm and tender joints

A

RA

80
Q

Extrarticular manifestations

A

RA only (not OA)

81
Q

Autoimmune disease

A

RA

82
Q

Degenerative disease

A

OA

83
Q

Polymyalgia rheumatica (PMR)

A

chronic, inflammatory rheumatic condition

84
Q

Sx of PMR

A

proximal aching and stiffness (shoulder, pelvic girdle, neck); worse in morning >1 hr/ gel phenomenon (stiffness with inactivity)
BILATERAL
recent, discrete change in sx

Systemic: malaise, fatigue, low-grade fever

85
Q

Prevalence of PMR

A

> 50 YO
peak: 70-80 YO
F>M; northern european

86
Q

PMR cause

A

Genetic (HLA) + environmental (virus);

Association with giant cell (temporal) arteritis (GCA) (50%)

87
Q

Sx of PMR due to

A

nonerosive synovitis and tenosynovitis

88
Q

PE for PMR

A

limited ROM (abduction of shoulders), normal strength (subjective weakness), synovitis

89
Q

Labs for PMR

A

ESR/CRP: elevated (ESR >50)
normocytic anemia
negative ANA, RF, ACCP
CK normal

90
Q

RA similar to PMR in labs BUT

A

negative ANA, RF, ACCP

91
Q

imaging for PMR

A

MRI and U/S (burisitis, synovitis)

92
Q

Dx of PMR

A

no criteria:
>50 YO
proximal and symmetrical w/ morning stiffness (shoulder, neck, pelvic girdle)
Elevated ESR/CRP
Rapid resolution with low-dose glucocorticoids*

93
Q

Improves rapidly with glucocoticoid

A

PMR

94
Q

Tx for PMR

A

GLUCOCORTICOID (10-20mg/day)

Limited use of MTX (select patients)

95
Q

Fibromyalgia (FM)

A

widespread musculoskeletal pain and tenderness; often accompanied by fatigue, psych symptoms and multiple somatic symptoms; etiology unknown

96
Q

Prevalence of FM

A

W>N

Increased: age 20-50

97
Q

FM cooccurs with

A

RA and SLE

98
Q

Pathophys of FM

A

central pain processing (central sensitive due to altered pain processing); strong genetic predisposition

99
Q

Sx of FM

A

widespread MSK pain (>3 mo)
FATIGUE and POOR SLEEP
Cognitive distrubance (fog)
psych distrubance (depression/anxiety)

Additonal:
H/A, pelvic pain, IBS, IC (painful bladder), OSA, RLS (restless leg syndrome), parathesia, balance issues, sensitive to light, noice, odor, cold

100
Q

PE of FM

A 
TTP in characteristic locations :
under SCM
near 2nd costochondral junction
lateral epicondyle 
greater trochanter
medial fat bad of knee
insertion of suboccipital muscle
traps
supraspinatus
buttock
101
Q

Dx of FM

A

hx and PE
absence of other systemic condition accounting for pain
Coexist with other disorders

102
Q

Criteria of FM

A

widesprain pain >7
Sx >3 mo
no other disorder

103
Q

Tx of FM

A

Nonpharm: exercise, PT, CBT

Pharm: tricycline antidepressants (amitriptyline OR cyclobenzaprine)

Serotonin and NE reuptake inhibitors (SNRIs)- Duloxetine and Milnacipran

Anticonvulsants: pregabalin, gabapentin

104
Q

Labs for FM

A

unremarkable

105
Q

Anticonvulsants for FM

A

Pregabalin

Gabapentin

106
Q

SNRIs for FM

A

Duloxetine

Milnacipran

107
Q

Tricyclic antidepressant

A

Amitryptyline

Cyclobernzoaprine

108
Q

Duloxetine use

A

OA or FM

Clin Med Exam 3 (7 decks)

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