week 5 Flashcards
1
Q
rheumatoid arthritis
A
- chronic, systemic, inflammatory autoimmune disease of unknown etiology
- features: chronic, symmetric, erosive synovitis of peripheral joints
- can be associated with extra-articular manifestations
2
Q
RA fun facts
A
- RA affects 1% of adults
- > 70% of patients develop joint damage/erosions within 2 years of onset
- > 33% of patients are work disabled at 5 years
- > 50% of patients will be functional class III or IV within 10 years of disease onset
- if untreated, RA can result in joint destruction, deformity, disability, and premature death (3-7 years)
3
Q
RA is a chronic disease before the first symptoms
A
up to 40% of RA patients will have RF and/or anti-CCP antibodies in preclinical phase of desease
4
Q
RA etiology
A
- combination of unknown antigen(s) in genetically suscpetible host
- antigens: viruses (retroviruses, EBV, parvovirus), mycoplasma, heat shock proteins, cartilage antigens, citrullinated peptides
- genetic susceptibility: HLA-DR1, HLA-DR4
4
Q
RA etiology
A
- combination of unknown antigen(s) in genetically suscpetible host
- antigens: viruses (retroviruses, EBV, parvovirus), mycoplasma, heat shock proteins, cartilage antigens, citrullinated peptides
- genetic susceptibility: HLA-DR1, HLA-DR4
5
Q
RA pathophysiology
A
- synovial-based disease
- unknown antigen activates/injures synovial microvascular endothelial cells
- synovial inflammation and hypertrophy: CD4+ T cells, macrophages, B cells, plasma cells
- relase of inflammatory cytokines by synovial macrophages: IL-1, TNF alpha, IL-6, systemic symptoms
- cytokines induce fibroblasts and chondrocytes to produce PGE2, collagenase, and proteinases resulting in cartilage and bone destruction
6
Q
screening tool for inflammatory arthrtis (RA)
A
- significant discomfort with squeezing MCP and MTP joints
- presence of 3 or more swollen joints
- more than 1 hour of morning stiffness
7
Q
RA evaluation - history
A
- degree of joint pain
- duration of morning stiffness
- presence or absence of fatigue
- limitation of function: mobility, special hand functions, ADLs, work/recreation participation restrictions
- poor sleep patterns
- weight loss
8
Q
RA evaluation - physical exam
A
- joint count of actively inflamed joints
- mechanical joint problems: loss of motion, crepitus, instability, malalignment, deformity
9
Q
other RA symptoms
A
- scleritis: refer to ophthalmology ASAP
- nodules
- digital artery vasculitis
10
Q
RA poor prognostic indicators
A
- earlier age at onset
- female
- polyarticular synovitis (>13 joints)
- lab tests: high RF and/or anti-CCP, elevated ESR or CRP, HLA-DR4 (shared epitope)
- erosions or cartilage loss on x-ray (in < 1 year)
- poor functional status (Health Assessment Questionnaire - HAQ > 1 at 1 year disease)
- extra-articular manifestations: rheumatoid nodules, scleritis, ILD, pericarditis, vasculitis
11
Q
RA in cervical spine
A
- atalntoaxial (C1-C2) subluxation due to laxity/rupture of the transverse ligament or fracture or erosion of odontoid process
- anterior subluxation of atlas on axis is most common
- posterior subluxation of atlas on axis due to fracture/destruction of the odontoid peg (rare)
- vertical subluxation of odontoid in relation to the atlas (brainstem impingement)
- symptoms: asymptomatic, cervical/occipital pain, cord impingement
12
Q
RA in thoracic, lumbar, and sacral spine
A
- usually spared in RA
- compression fractures secondary to steroid therapy is a risk
13
Q
RA in shoulder
A
- GH joint and AC joints
- subacromial bursitis
- rotator cuff tendinitis/rupture
- bicipital tendinitis/rupture - Popeye’s sign
14
Q
RA in elbows
A
- radial-humeral: pronation, supination
- ulnar-humeral: flexion, extension
- flexion deformities and loss of lateral stability can develop
- entrapment of ulnar nerve or radial nerve (posterior interosseous) due to synovitis
- olecranon bursitis: RA, infection
- extensor surface of forearm: RA nodules
15
Q
RA in hand and wrist
A
- MCP/PIP/wrist synovitis (DIPs spared)
- ulnar drift at MCPs
- palmar subluxation of MCPs
- swan-neck and boutonniere deformities
- tenosynovitis: flexor tendons (carpal tunnel syndrome), extensor tendons (rupture)
16
Q
RA in hip
A
- about half of patients with RA have radiographic evidence of hip disease
- protrusio aceetabyli: about 5% of patients
- trochanteric, iliopsoas, and ischial bursitis
- avascular necrosis of femoral head (glucocorticoid therapy)
17
Q
RA in knees
A
- effusions and synovial thickening
- quadriceps atrophy, loss of full extension
- tricompartment loss of joint space on x-rays
- Baker’s/popliteal cyst
18
Q
initial treatment for RA
A
- NSAIDs: reduce joint pain and swelling, improve function (consider cost, GI tolerance, half-life, patient preference)
- multi-disciplinary care: rheumatology consultation, PT and OT, podiatry for the feets, orthopedics
- steroids/glucocorticoids?
- disease modifying drugs (DMARDs) - start within 2-3 months of diagnosis
19
Q
RA drug treatment options
A
- NSAIDs: symptomatic relief, improved function, no change in disease progression
- low-dose steroids (Prednisone): may substitute for NSAID, used as bridge therapy, osteoporosis risk if long term
- intra-articular steroids: useful for flares
20
Q
RA disease modifying drugs (DMARDs)
A
- immunosuppressive drugs: impact T or B cells
- methotrexate (MTX): most effective single DMARD, may be used in combination with other meds
- hydroxychloroquine
- biologic therapies
- TNF inhibitors
21
Q
RA and health maintenance
A
- osteoporosis: DEXA scans
- cardiovascular disease: assess risk/modify
- smoking cessation
- infection risk (particularly pulmonary infections): yearly flue shot, pneuomococcal vaccine, shingles vaccine
22
Q
important lessons RA
A
- inflammation can be suppressed in early RA
- when inflammation is suppressed, patients benefit
- more medical therapy is not necessarily more toxic
- long term benefits from early diagnosis and medical therapy
23
Q
fibromyalgia (FMS)
A
- chronic, non-inflammatory, non-autoimmune diffuse central pain-processing syndrome
- cardinal manifestations: widespread pain, diffuse tenderness on physical exam, fatigue, depression, general somatic hyperawareness, cognitive problems (fibro fog), poor sleep
- not a primary disorder of muscle or connective tissue
24
demographics of FMS
* disorder or young and middle-aged women (consider alternative diagnosis in men and people > 55 yo)
* about 2-5% of US women
* heterogenous disorder for severity: patients with mild disease are rarely seen at tertiary centers
* secondary FMS
25
etiology/pathogenesis of FMS
* "pathogenesis of fibro is medicalization of misery" - some jerkwad
* unknown, but evidence argues for central pain processing disorders
* supported by: CSF (substance P and inflam cytokines), genetic, fMRI studies
26
fMRI evidence for FMS
* associated with lower pain threshold
* innocuous pressure stimulation to healthy control evoked significantly less pain
27
evaluation in FMS
* complete and thoughtful history and physical
* not everyone that hurts has FMS
* common themes: pain everywhere/head to toe, fatigue, not good sleep, depression, physical exam and labs should be normal
28
FMS medical treatment
* not just meds!! -- exercise/PT and CBT, sleep, fatigue
* start low, go slow
* avoid opioids
* NSAIDs don't work
* change only one medication at a time
* target central neurologic mechanisms
29
exercise in FMS
* aerobic training superior to resistance training for pain benefit in women with FMS
* moderate intensity resistance training improves functional status, pain, tenderness, and muscle strenght
* exercise may improve depressive symptoms
* flexibility training may help for pain and functional status but less than aerobic and resistance training
* supervised group exercise can enhance adherence
* exercise needs to be tailored to the patient's starting fitness level and symptom severity
* aquatic therapy (warm water): moderate evidence for improving wellness, symptoms, and fitness
30
FMS conclusions
* FMS is a real illness with objective evidence of augmented central pain processing
* appropriate treatments address the neurological pathophysiology
* non-pharmacological therapy is key
* FMS diagnosis alleviates stress about mysterious, underlying conditions
* patients can't get better if they are constantly trying to prove they really are sick
