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MC II > week 5 > Flashcards

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
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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)
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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

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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
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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
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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
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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
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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
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8
Q

RA evaluation - physical exam

A
  • joint count of actively inflamed joints
  • mechanical joint problems: loss of motion, crepitus, instability, malalignment, deformity
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9
Q

other RA symptoms

A
  • scleritis: refer to ophthalmology ASAP
  • nodules
  • digital artery vasculitis
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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
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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
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12
Q

RA in thoracic, lumbar, and sacral spine

A
  • usually spared in RA
  • compression fractures secondary to steroid therapy is a risk
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13
Q

RA in shoulder

A
  • GH joint and AC joints
  • subacromial bursitis
  • rotator cuff tendinitis/rupture
  • bicipital tendinitis/rupture - Popeye’s sign
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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
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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
Q

demographics of FMS

A
  • 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
Q

etiology/pathogenesis of FMS

A
  • “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
Q

fMRI evidence for FMS

A
  • associated with lower pain threshold
  • innocuous pressure stimulation to healthy control evoked significantly less pain
27
Q

evaluation in FMS

A
  • 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
Q

FMS medical treatment

A
  • 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
Q

exercise in FMS

A
  • 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
Q

FMS conclusions

A
  • 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

MC II (7 decks)

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