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Med School > Arthritis > Flashcards

Arthritis Flashcards

1
Q

Oligoarthritis vs. Polyarthritis

A

Oligo - under 5 joints
Poly - 5+ joints

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2
Q

Typical Characteristics of RA

A
  • symmetrical
  • deformation (subluxation), damage, and erosion of joints
  • worse in the morning with prolonged stiffness (30m+)
  • involves any synovial joint (even neck) EXCEPT NOT DIPs
  • soft tissue swelling, ulnar deviation of fingers, swan neck, boutonniere, poor grip strength
  • more common (and often more severe) in indigenous
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3
Q

Typical Characteristics of Lupus (SLE)

A
  • symmetrical polyarthritis
  • Worse in the AM, prolonged morning stiffness (30m+)
  • does NOT involve the DIPs
  • does NOT result in erosions or sclerosis
  • Skin rash (butterfly rash), photosensitivity, alopecia, mouth ulcers, Raynaud’s, Sjorgen’s
  • 90% are female, genetic component
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4
Q

Typical Characteristics of Psoriatic Arthritis
- what are two subtypes of PsA?

A
  • asymmetric
  • oligoarthritis
  • worse in the AM, prolonged morning stiffness (30m+)
  • commonly involves the DIPs
  • both erosion and sclerosis present
  • psoriasis common on scalp, ears, extensor surfaces of elbows/knees, gluteal surface, onycholysis, nail pitting
  • sausage digits, dactylitis
  • more often skin precedes the joints
  • often assx with metabolic syndrome, CV, depression, pancreatic cancer, lymphoma
  • equally common in men and women
  • Psoriatic Spondylitis - ank spond in the presence of psoriasis
  • Arthritis Mutilans - rare, melting of joints
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5
Q

Sero (+) vs. (-) RA

A
  • either RA factor and/or CCP (+) or (-)
  • Sero (+) has a worse prognosis/ joint disease/ increased chance of extra-articular features
  • smokers are likely to have both CCP and RA (+)
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6
Q

Time Course of RA

A
  • Only 50% of patients are sero (+) in the beginning, but 85% of patients will be sero (+) after 1 year
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7
Q

What is RA factor?

A
  • IgM Ab against the Fc component of IgG (pentavalent and can form large complexes)
  • Non-specific and can be (+) in other conditions (i.e. 35% of lupus will be RA positive)
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8
Q

What is anti-Cyclic Citrullinated Peptide (anti-CCP or ACPA) ?

A
  • auto Abs that target peptides with cirtulline
  • often present early/ before RA factor
  • (+) in 60% of patients (not as sensitive) but highly specific
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9
Q

Pathophysiology of RA
- what is a pannus?

A
  • synovitis, synovial hypertrophy with pannus formation
  • pannus is many cell layers thick, neovascularization, macrophages and lymphocytes (invasive tumor in situ that erodes bone)
  • RA is a disease of subtraction (does not have sclerosis and osteophytes like OA does)
  • genetic (HLADR1), exogenous triggers such as virus, bacteria (p.gingivalis), smoking induced CCPs, molecular mimicry
  • macrophage presents Ag to TCR which requires co-stimulatory molecules (abatacept can block)
  • activated T cells release cytokines (TNFa, IL-6)
  • T cells tell B cells and plasma cells to make auto Abs (RA factor, which forms ICs and activates complement and chemotaxis by PMNs)
  • Adhesion molecules important for aggression and adhering of cells
  • Innate immunity also activated (TLRs and NB)
  • Osteoclasts activated which results in erosion of bone and cartilage, osteopenia of subchondral bone
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10
Q

Pharmacologic Treatment of RA
- Different classes of drugs used
- Mild vs active?

A
  • most important drugs early on are DMARDs
    • if mild –> plaquenil (hydroxychloroquine - will need eye exams), sometimes SZS and MTX
    • if very active –> combo of plaquenil, MTX, and SZS (and treat right away!!!)
      *DMARDs and biologics only drugs that prevent progression and damage
  • cortisone injections/ prednisone only used as a bridge while starting DMARDs (can cause osteoporosis and avascular necrosis)
  • NSAIDs often used
  • Biologics –> i.e. TNFa inhibitors (adalinumab), B lymphocyte inhibitors (Rituximab), co-stimulatory molecule inhibitors (abatacept), IL-6 inhibitor (toclizumab)
  • EXPENSIVE and not first line, have to fail DMARDs first

*non-pharm: exercise, diet (high protein), lower BMI, NO SMOKING, omega 3s

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11
Q

Extra-Articular Features of RA
- What is Sjorgen’s?

A
  • Sjorgen’s - keratoconjunctivitis sicca (dry eyes), dry mouth, parotid gland enlargement, cavities
  • rheumatoid nodules in lungs, heart, LNs, spleen, bone, skin, nerves
  • atlanto-axial subluxation (can lead to quadriplegia)
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12
Q

What should you always do before ordering ANA?

A
  • do a rheumatological ROS otherwise your ordering a sensitive but very non-specific test
  • ANA can be positive in both RA and lupus (but much more commonly + for lupus)
  • Do not order just for back pain or fatigue/rash/ hair loss
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13
Q

Examples of Sero (-) arthritis

A
  • Psoriatic arthritis (which i’m thinking is actually a subtype of…)
  • Ankylosing Spondylitis (and its 4 subtypes)
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14
Q

What should mono arthritis make you suspicious of?

A
  • infection
  • tap joint for synovial fluid
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15
Q

Synovial Fluid Analysis
- characteristics of OA/RA and infection/ Gout, lupus, and PsA
- numbering system

A

OA –> thick/viscous, clear, low WBC, mainly mononuclear cells

RA/infection –> watery, turbid, high WBC, mainly polynuclear cells

Gout/Lupus/PsA –> Similar to RA (gout specifically will have negatively birefringent crystals, yellow parallel and blue perpendicular)

0 - Normal, very low WBCs and mononuclear
1 - OA, viscous, clear, low WBCs (monos)
2 - Inflammatory, thin, watery, opaque, high WBCs (polys)
3 - Septic, (+) culture, very high WBCs (polys)
4 - Hemorrhagic, RBCs, no clotting

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16
Q

Typical Characteristics of Ankylosing Spondylitis (Spondyloarthritis)

A
  • Symmetric
  • Worse in the AM, prolonged morning stiffness (30m+)
  • Erosion, but no sclerosis
  • usually chronic LBP/ buttock pain in young patients (20-40), more common in men/ Haida natives
  • HLAB27 Genotype in 80%
  • lower limb oligoarthritis, sacroilitis
  • affects the axial spine with lesions often at the enthuses where ligaments and tendons insert, may be syndesmophytes (bone bridging)
  • can lead to MI/stroke/spine fractures
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17
Q

4 Types of Ankylosing Spondylitis (Spondyloarthropathies)

A
  1. Idiopathic (primary)
  2. Reactive arthritis (Reiter’s) - Triad of conjunctivitis, urethritis or dysentery, arthritis
  3. Psoriatic Spondylitis
  4. Spondylitis of IBD

*always ask about psoriasis, conjunctivitis, iritis, sx of IBD, sexual hx, diarrhea, dysentery, travel, etc.
*screen if one of these (including HLAB27 (+) and sx under 40/45 that have lasted at least 3 months)

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18
Q

What are features of inflammatory back pain? What should this make you suspicious of? Treatment?

A
  • 4 of: insidious onset, onset under 40 years lasting over 3 months, worse/nil with inactivity, better with exercise, pain at night that improves with getting up
  • prolonged AM stiffness, alternate butt pain, improved with NSAIDs
  • should be concerning for Spondyloarthropathies
  • postural exercises are best, also NSAIDs and TNF inhibitors
  • anti-TNF for axial
  • SSZ/MTX for peripheral
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19
Q

Common lab tests in rheumatology and when to order
- Which unique tests are only done once vs. retested?

A
  • CBC
  • ESR, CRP (overly sensitive and non-specific)
  • Cr and urinalysis (follow especially if SLE/vasculitis)
  • CK as baseline in setting of muscle weakness/ statins
  • RA factor and CCP if likely inflammatory arthritis
  • ANA if likely lupus (very sensitive, poor PPV)
    - 1/640 is higher titre than 1/80

DON’T CHANGE OVER TIME
- if ANA is positive and suspicious –> ENA
- ENA is either SSA (Ro) or SSB (La) which can occur in lupus or Sjorgen’s
- this Ab crosses the placenta –> risk for congenital heart block (all fertile pts with lupus should do ENA)

FOLLOW
- if ANA is positive can also do DNA Ab (more specific, but only + in 50% of cases)
- can also order C3/4, which often decrease in lupus

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20
Q

Treatment of Lupus

A
  • plaquenil (hydroxychloroquine) for everyone –> helps skin/joints/hair/organs
  • prednisone, AZA, MTX, cyclosporine, tacrolimus, NSAIDs, cyclophosphamide (can cause early gonadal failure), biologics
  • SPF 50+, no smoking, immunization, bone protection, treat comorbidities
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21
Q

Artherosclerosis and Arthritis

A
  • both RA and lupus can increase mortality from atherosclerotic and endothelial cell damage in coronary vessels
  • risk increases with use of prednisone
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22
Q

Gout
- dx
- assx features
- increased risk
- tx

A
  • monosodium urate/ uric acid crystals
  • dx by microscope (yellow parallel, negatively birefringent crystals, blue perpendicular)
  • acute pain, red hot joint
  • often part of metabolic syndrome (BMI, DM, HTN, dyslipidemia), renal insufficiency
  • increased risk with diuretics (HCTZ) and low dose ASA as they interfere with uric acid excretion, also meat and beer
  • do NOT treat if asymptomatic hyperuricemia
  • NSAID (indocid) or Colchicine or Prednisone/Corticosteroid IV
  • do NOT start allopurinol right away as this will prolong acute attack via mobilization gout
  • only treat if 3+ attacks, and use colchicine/NSAID until uric acid is normal
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23
Q

Temporal/ Giant Cell Arteritis
- tx

A
  • CANNOT miss this –> blindness
  • new onset of headaches over 50, jaw claudication pain, scalp tenderness
  • assx with polymyalgia rheumatica
  • Tx - high dose prednisone, test ESR/CRP, temporal artery biopsy (but always treat first!!!)
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24
Q

Typical characteristics of OA

A
  • can be symmetric or asymmetric
  • no prolonged morning stiffness
  • worse in the PM
  • can involve DIPs
  • no erosion but yes sclerosis
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25
Q

Signs of RA on Xray?

A
  • generalized, concentric, uniform joint space loss
  • valgus deformity
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26
Q

Diagnosis of Spondyloarthritis?

A
  • XR (sometimes CT, MRI) of SI joints
  • sacroilitis on imaging AND at least 1 SpA feature OR
  • HLAB27 and at least 2 other SpA features
    *may take years for changes to develop, some may never develop
    *classification gold standard is a rheumatologists opinion
  • clinical sx –> STRONG - IBD, psoriasis, uveitis, peripheral arthritis
  • SPARCC Enthesitis Index –> look at 16 sites, score 0-16
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27
Q

Treatment of Spondyloarthropathies?

A
  • exercise and physiological (especially core strengthening), weight loss, education
  • NSAIDs, biologics (TNFis, IL-17Ais, JAKis), potentially surgery
  • NO: steroids, DMARDs
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28
Q

Psoriatic Arthritis Criteria

A

3 or more of:
- psoriasis (current or personal/family hx)
- nail signs
- (-) for RA factor
- dactylitis (current or personal/family hx)
- Xray evidence of new articular bone

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29
Q

Treatment of Psoriatic Arthritis
- non-pharm
- pharm - mild vs severe

A
  • exercise, assistive devices, relaxing, fatigue management, diet/weight, rarely surgery
  • mild –> NSAIDs, steroid injections (DMARDs if more than 3 months)
  • mod/severe –> DMARD (except plaquenil (and oral steroids) not recommended), biologics (must try 2 DMARDs)

*goal is to have max of one tender/swollen joint

30
Q

Pathophysiology of Lupus

A
  • autoimmune, auto Ab production against cell nuclei (may be stimulated by UV light)
  • formation of immune complexes, defective phagocytosis, increase innate and adaptive imunity
31
Q

Lupus Criteria

A

At least 4 of (must be 1 clinical, 1 immune) and ANA > 1:80:
- Clinical –> acute or chronic cutaneous, oral/nasal ulcers, pericarditis, non-scarring alopecia, arthritis, serositis, proteinuria, neurologic, hemolytic anemia, leukopenia, thrombocytopenia

  • Immune –> ANA, anti-DNA, anti-smith, antiphospholipid Abs, low C3/C4/CH50, direct Coombs test
  • is a clinical diagnosis
32
Q

Signs and Symptoms of Lupus by system

A
  • Mucocutaneous - malar/annular/ discoid rash, nasolabial sparing, photosensitivity, buccal/palate/tongue/nose ulcers, non-scarring alopecia
  • MSK - worse in AM, stiffness for more than 30m+, improves with activity and NSAIDs, joint swelling
  • Renal - lupus nephritis, biopsy if rising serum Cr, proteinuria over 500mg, active sediment w RBC casts
  • CV - peri/endo/myocarditis, vasculitis, thromboembolisms, Raynaud’s (pallor –> cyanosis –> erythroderma)
  • Pulmonary - pleuritis, pleural effusions, ILD, pneumonitis, pull HTN, shrinking lung syndrome
  • Neuropsych - stroke, seziures, headaches, neuropathy, psychosis, depression, transverse myelitis, mood change
  • GI/hepatic - common adverse med reactions
  • Hematologic - anemia, leukopenia, thrombocytopenia
  • Other
  • antiphospholipid Ab syndrome (hypercoaguable state leading to VTE, pregnancy losses, pre-eclampsia, stroke, MI, will have lupus anticoagulant Ab and anticardiolipin Ab)
  • shingles, atherosclerosis, avascular necrosis, osteoporosis, cataracts, bladder/cervical cancer, premature gonadal failure
33
Q

Different derm types of lupus

A
  • subacute cutaneous (80% SSA/SSB +, very photosensitive)
  • discoid (red raised with keratitis scaling, follicular plugging, erythema, atrophy, scarring, telangiectasias)
  • bullous/ mucosal/ maculopapular/ photosensitive/ etc.
34
Q

Different classifications of Lupus nephritis

A
  • III - focal –> hema/proteinuria, nephrotic, under 50% glomeruli
  • IV - diffuse –> most severe, same as III but over 50% glomeruli, HTN, low complement
  • V - membranous –> hema/proteinuria, nephrotic, may present with no other signs
35
Q

Tests for Lupus

A
  • CBC, Cr, AST/ALT, TSH, CK, Ca/SPEP, CRP, urinalysis, ACR, HEP/HIV
  • specific –> ANA, ENA, C3/4 (will be low), dsDNA (will be high), RA factor, anti-CCP, ANCA, anti-phospholipid Abs
36
Q

Drug Induced Lupus

A
  • equal in men and women
  • sx will stop once drug stopped
  • fever, rash, arthritis, serositis, my/arthralgias
  • rarely: nephritis, CNS, heme
  • C3/4 and dsDNA will be normal but may be ANA+ and anti-histone+
  • causes: isoniazid, diltiazem, anti-TNF, procainamide, chlorpromazine, hydralazine, minocycline
37
Q

Neonatal Lupus
- tx

A
  • transplacental passage on anti-SSA/SSB Abs
  • congenital heart block (any degree), bradycardia, hydrops
  • rash present at or near birth, photosensitivity, scalp and periorbital area, should resolve by 6-8 weeks
  • do a fetal echo, treat with dexamethasone
38
Q

Fibromyalgia
- tx

A
  • achey pain all over, non-articular but at least 11/18 painful/tender joints in all quadrants
  • benign, normal labs, no inflammation - believed to be a increase in centralized pain response, soft tissue disorder
  • usually sleep and mood disorders, anxiety
  • more common in women
  • education and reassurance, aerobic exercise, CBT, psychotherapy
  • nighttime tricyclics (ami/noritryptiline), NSAIDs, tramadol (?), melatonin, pregabalin/gabapentin, duloxetine
39
Q

Polymyalgia Rheumatica

A
  • inflammation, muscle pain, stiffness/ aching in shoulder/ pelvic girdle
  • 50-55 y, increased ESR/CRP
  • responds in 72h to low dose prednisone
  • only test for CRP/ESR

*can be assx with giant cell/temporal arteritis

40
Q

Plaquenil (Hydroxychloroquine)

A
  • an anti-malarial
  • often used if mild RA or lupus is suspected
  • oral
  • S/E - rash, diarrhea, annual eye exam for depositions
41
Q

Sulfasalazine

A
  • sulfa and ASA together
  • oral, daily
  • may be used along with MTX and plaquenil
  • useful if PsA/SpA/IBD arthritis
  • cannot give if sulpha allergy, have to follow blood work
42
Q

Methotrexate

A
  • often used alone in moderate/ severe RA
  • oral/IM/SC once a week
  • highly teratogenic (even in males), have to watch liver enzymes, always put patients on folic acid
  • cannot take sulfa ABX, limit EtOH, may cause pneumonitis
43
Q

Leflunomide (Arava)
- S/E

A
  • very teratogenic
  • GI upset, diarrhea, need to follow liver enzymes
  • in system for 2 years so need cholestyramine washout
44
Q

Tests before taking biologics, when not to use

A
  • Hep B/C/HIV/TB
  • CXR for TB (treat 1st if positive)
  • hold before elective surgery and during infections/ bad colds
45
Q

Articular vs non-articular pain

A

Articular - throughout ROM, in all planes of movement, swelling in joint

Non-articular - only with certain movement, may be unrelated to joint movement, swelling is not in the joint but may be around

46
Q

Inflammatory vs non-inflammatory pain

A

Inflammatory - worse with rest, better with movement, AM stiffness for more than 30 minutes

Non-inflammatory - worse with movement, no pain/ improvement with rest, AM stiffness under 30 minutes

47
Q

Sensitivity
Specificity
PPV
NPV

A

Sensitivity - ability to identify those with disease
Specificity - ability to identify those without disease
PPV - proportion of + results that are actually +
- true positives/ everyone with the disease
NPV - proportion of - results that are actually -
- true negatives/ everyone without the disease

*PPV increases with increased prevalence
*PPV = true positives/ all positive results

48
Q

Auto Ab Testing

A
  • take patients serum and expose to target Ag, variable region will bind to Ag (thus leaving fixed portion exposed)
  • 2nd Ab targeted to Fc of Ab with enzyme/fluorescent tag
  • most common are ELISA, IIF, MPBI
49
Q

Inflammatory Markers

A
  • CRP - acute phase reactant, non-specific opsonin for bacteria
  • ESR (erythrocyte sedimentation rate) - measures rate of fall of erythrocytes (mm of clear plasma in tube after 1 hour). Moderate increase indicates inflammation/ anemia/ infection/ pregnancy/ aging, high increase indicates severe infection
50
Q

ANA

A
  • anti-nuclear Ab
  • auto Ab that targets nuclear Ags
  • test if SLE suspected (very sensitive, poor specificity)
51
Q

anti-dsDNA Ab

A
  • auto Ab that target dsDNA
  • supports SLE, may correlate with disease activity and flares but not diagnostic
52
Q

ENA

A
  • extractable nuclear Ag Ab
  • auto Ab that targets Ags present in nucleus (i.e. smith Ag, SSA/SSB Ag, histone Ag)
  • helps classify CT disorders
53
Q

Confirmatory Tests for SLE

A
  • anti-dsDNA Ab (specific, cannot exclude if -)
  • anti-smith Ab (specific, cannot exclude if -)
  • SSA (Ro) Ab (neonatal lupus - rash and heart block)
54
Q

Small Vessel Vasculitis

A
  • disease targeting small vessels, NOT infection
  • i.e. granulomatosis with polyangitis (GPA)
  • associated with anti-neutrophil cytoplasmic Ab (ANCA) - test if glomerulonephritis, pulmonary hemorrhage, chronic sinusitis
55
Q

What comprises a motor unit?
Structure of a muscle?

A
  • motor neuron, NMJ, muscle fibers randomly scattered in a limited area of muscle
  • all fibers in a single unit are the same type (fast vs slow)
  • muscle –> fascicle –> fiber –> myofibril –> thick/thin filaments –> actin/ myosin
56
Q

What happens at the NMJ?

A
  • Ap arrives at axon terminal –> voltage gated Ca channels open –> Ca binds Ach vesicles and trigger snare protein complex formation and fusion with pre-synaptic membrane –> Ach released into cleft and bind to AchRs on post-synaptic membrane –> influx of Na along t-tubules of muscle fiber –> depolarized muscle cell allows influx of Ca and cross-coupling/ contraction
57
Q

Type I vs II Muscle Fibers

A

I –> slow, more mitochondria, endurance, oxidative metabolism

II–> fast, glycolytic pathway, fatigues easily, subtypes (A,B,C)

58
Q

Myopathic changes on biopsy

A
  • fibre size variation, internalized nuclei, rimmed vacuoles, ring fibres, abnormal staining, round, ragged-red

*want to order from a muscle that is 4/4-

59
Q

Muscle Power Grading

A

0 - no contraction
1- flicker of contraction
2 - full ROM no gravity
3 - full ROM against gravity
4- - minimal resistance
4 - some resistance
4+ - definite but slight weakness
5 - normal power

60
Q

Positive and Negative symptoms suggesting a muscle disorder

A

Positive - cramps, contractures, hypertrophy, myalgia, myoglobinuria, stiffness

Negative (most common and predominant) - weak, fatigue, exercise intolerance, atrophy

*prominent pain is not common in most muscle disorders

61
Q

Examples of:
- proximal muscle weakness
- distal symptoms
- craniobulbar symptoms

A
  • brushing teeth/ hair, lifting overhead, getting in our of chair or car
  • foot drop, opening jars, zippers
  • dysarthria, dysphagia, ptosis, diplopia
62
Q

Common Patterns of Weakness

A

Limb-Girdle - most common/treatable and least-specific, shoulders and hips
- inflamm/immune myopathies, dystrophies
- proximal muscle weakness +/- neck flexors and extensors, orthopnea

Distal Arm-Leg - uncommon, must rule out neuropathy

Distal Forearm Proximal Leg - usually asymmetric
- inclusion body myositis, amyloid, few hereditary forms

63
Q

Dermatomyositis

A
  • immune mediated myopathy
  • rash on back of hands and heliotrope rash on face/nail changes
  • may also see interstitial lung disease (pulmonary fibrosis)
  • CK is often high
64
Q

NMJ Disorders
- common example and treatment

A
  • often improve with rest
  • clinically and electrically testable (NCS/EMG)
  • i.e myasthenia gravis - autoimmune, post-synaptic
  • fatigue, diplopia, ptosis, fatiguable dysarthria/chewing/swallowing/weakness
  • treat with Acetycholinesterase inhibitors (pyridostigmine) and immunosupressants
65
Q

Pseudogout

A
  • calcium pyrophosphate dihydrate
  • chondrocalcinosis on xray, positively birefringent crystals
  • can cause severe inflammatory OA in atypical joints
66
Q

Scleroderma

A
  • fibrosis of skin/lungs/kidney, CREST localized cutaneous variant…
  • Calcinosis in skin
  • Raynauds
  • Esophageal dysfunction (reflux)
  • Sclerodactyly (thickening and tightening of fingers)
  • Telangiectasis
67
Q

Statins can cause…

A

polyarthralgia and myalgia, can increase CK

68
Q

Uveitis

A
  • sight-threatening intraocular inflammatory disease
  • umbrella term for many disease
  • can be anterior (painful), intermediate (vitritus), posterior (blind spots), panuveitis, extraocular (pemphigoid, keratitis, etc.)
69
Q

Examples of life threatening vs non life-threatening eye conditions

A
  • Non- Life threatening - dry eyes, blepharirits, viral conjunctivitis, allergic, subconjunctival hemorrhage
  • Life threatening - infection, inflammation (uveitis, vasculitis, scleritis, keratitis), trauma, masquerades (neoplasms, acute angle closure glaucoma)
70
Q

Relations Between eye disease and rheumatoid arthopathies and tx

A

Scleritis - RA, SLE, gout, ANCA vasculitis
Retinal vasculitis - SLE, ANCA vasculitis, antiphospholipid
Uveitis - IBD, HLAB27, PsA, Reiter’s

tx - local steroids, NSAIDs, prednisone, immunosuppression

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