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How would you differentiate an inflammatory arthritis from a degenerative arthritis?
- 1. Pain at rest, relieved by motion
- 2. morning stiffness > 1 hr
- 3. warmth, erythema, swelling
- 4. extra-artic manifestations
- 1. pain with motion, relieved by rest
- 2. morning stiff < 0.5 hr
- 3. joint instability, locking, buckling
- 4. bony enlargement
How would you distinguish articular from peri-articular pain
- periarticular: active ROM is limited/painful
- articular: passive AND active ROM is limited/painful
How would you differentiate acute from chronic articular pain. What are some examples of each?
- acute (< 6 weeks): trauma, septic joint, crystal (gout and psuedogout)
- chronic (> 6 weeks): OA, RA, Ankylosing Spondylitis
Three most commonly affected joints in RA?
PIP, MCP, wrist pain
What are the 4 patterns of joint involvement?
- Symmetrical vs asymmetrical
- Small vs Large
- Mono vs oligo vs poly
- axial vs peripheral
What two joints are NEVER involved in RA alone
- joints of the lower back
Which NSAID do you never use in gout?
ASA - weak acid which decreases the excretion of uric acid
Top three etiologies in monoarthritis
How would you differentiate gonococcal from non-gonococcal infectious arthritis?
gonococcal: migratory arthritis, tenosynovitis, skin manifestations (petechiae, purpura), young adults
non-gonococcal: monoarticular, recent joint surgery, old people
When you have a monoarthritis come in with a joint effusion, what to you NEED to do??
Have the joint aspirated/drained
What joint is most commonly affected in gout? Why?
first MTP (matatarsalphalyngeal). Constant microtrauma from walking, lower temperature decreases the solubility of uric acid
What do the crystals look like in gout and pseudogout?
gout - negatively birefringent, strongly birefringent, needles
pseudogout - positively birefringent, weakly birefringent, rhomboid or rods
If you have a normal serum urea, does this rule out gout? If you have hyperuricemia does that mean you have gout?
NOOOOOO to both
Six precipitating factors in gout
- overindulgence in purine-rich foods
4 drugs that precipitate gout
- ASA (low dose only)/Alcohol
- Thiazide diuretics
How do you treat acute gout?
- corticosteroids (injected)
Don't start allopurinol until attack is under control!! Keep them on it if they are already on it.
When should you give gout phophylaxis? What drug would you use?
- -3+ attacks/year
- -uric acid nephrolithiasis
- -uric acid nephropathy
How would you treat pseudogout?
- 1. aspirate/drain joint
- 2. treat like acute gout: NSAIDS, colchicine, intra-articular steroids
What are Bouchard's and Heberden's nodes?
- Bouchard's: osteophytes in PIP
- Heberden's: Osteophytes in the DIP
What are the 4 things you see on an x ray with someone with OA?
- Subchondral sclerosis
- subchondral cysts
- osteophyte formation
- loss of joint space
three most commonly affected joints in OA
knee, base of thumb, DIP
DDx for acute polyarthritis
- -Infections: septic arthritis, viral (parvovirus, EBV, etc)
- -Crystalline: gout, pseudogout
- -Drug or hypersensitivity
DDx for chronic polyarthritis (>4 joints involved)
- Autoimmune: RA, spondyloarthropathies, psoriatic arthritis, CTD
- Crystalline: chronic gout
What do positive IgG and IgM antibodies signify?
- IgM in recent/acute infection
- IgG in past infection
What are the three C's to test for in joint aspiration?
- Cell count (WBC's)
What cervical spine problem are you worried about in RA?
atlanto-axial subluxation, especially in older people.
Extra-articular manifestations of RA
- -Rheum. nodules
- -Ocular: episcleritis, keratoconjunctival sicca
- -Pulm: nodules, pleural effusions, ILD
- -Cardio: valvular, pericarditis
- -vasculitis: results in spots of necrosis
What lab tests should you order if you are suspicious of RA? What should you note about the antibodies?
- -RF and/or Anti-CCP: 70-80 of people with RA are seropositive, but the rest are not. Therefor cannot rule out
- -Synovial fluid to check for inflammation
How would you treat RA?
- -Methotrexate: need to use contraception in both M/F. Can cause hepatic and pulm probs
- -hydrochloroquine: borrowed malaria drug, can cause retinopathy, annual eye exam. Can use in pregnancy
- -TNF-alpha inhibitors like Infliximab
If you see and HIV patient come in with a red spot, what are you worried he will develop. What does that look like
- Psoriatic arthritis
- A number of different patterns, can look like a lot of stuff. telescoping digits, pencil-in-cup joints. A Hx of psoriasis is the key!
How do you treat psoriatic arthritis?
- Basically the same as RA, but also treat skin probs:
- -TNF-alpha blockers
What are the 4 seronegative arthritises?
- Anyklosing spondylitis
- Reactive arthritis
- Psoriatic arthritis
- enterohepatic arthritis
What is the classic presentation (1) and clinical features of ankylosing spodylitis (5)? Populations
- Presentation: chronic lower back pain, lasting more than an hour in the morning that improves with exercise
- Clinical manifestations
- -achille's tendon swelling
- -calcaneal spurs
- -swelling of toes (dactylitis)
- -IgA nephropathy
- Populations: first nations/inuit
How do you treat AS?
Same as RA, except use TNF blockers before using DMARDS. This is because DMARDS are more effective in peripheral joint problems
What is the classic triad for Reactive Arthritis? What usually causes this? What other two features do you see?
- triad: urethritis, conjunctavitis, arthritis
- Usually follows a GI infection or an STD
- Other features: Penis lesions (circinate balanitis); skin lesion on bottom of feet (ketatoderma)
What are the diagnostic criteria for RA (7)?
- Need 4 of the following:
- ->1 hr morning stiffness for 6+ weeks
- -swelling of wrists, MCP, PIPs for 6+ wks
- -swelling of 3+ joints for 6+ wks
- -symmetric joint swelling for 6+ wks
- -x-ray shows joint erosions
- -+ve RF or Anti-CCP
- -elevated ESR or CRP
In which disease is the HLA-B27 gene present in over 90% of patients?
What do you see in Takayasu's arteritis
Large vessel involvement. unequal pulses, usually found in the aorta and its branches.
What are the 6 important signs that should make you think of GCA?
- 1) new onset headache in a 50+ year old patient
- 2) JAW CLAUDICATION
- 2) Tender/pulseless temporal headaches
- 3) elevated ESR
- 4) abnormal artery biopsy
- 5) patient has polymyalgia rheumatica
What should you do if suspect GCA? Why?
Start them on high dose prednisone IMMEDIATELY (don't wait for biopsy).
You are concerned about ophthalmic artery involvement causing blindness.
What is GCA?
large/medium vessel vasculitis with granulomatous involvement of the aorta and it's branches (tunica intima)
What would you see with someone with polymyalgia rheumatica? How would you treat?
- Aching/stiffness in the shoulder/hip girdles
- almost always 50+ years old
Treat with low dose prednisone and they come in dancing the next day!
What disease is polyarteritis nodosa (PAN) commonly associated with?
Hep B. Always do a Hep B test when you suspect PAN.
What are two S&S you commonly see in PAN? What do you almost NEVER see in PAN?
- 1) Mononeuritis (motor/sensory, e.g. foot drop)
- 2) Microaneurysms of abdominal arteries
- 3) involvement of skin, GI, kidneys, nerves. NOT the lungs!!
What S&S make you think of GPA (Wegener's)?
- URT symptoms (ENT especially), think of this in a chronic rhinitis that isn't getting better despite treatment.
- positive ANCA
- Renal involvement
- There can also be LRT involvement
How do you differentiate GPA (wegeners) from microscopic polyangitis (2)?
- No URT involvement
- No granuloma
These features ARE present in GPA
What is the Churg-Strauss (EGPA) Triad?
- 1) allergic rhinitis and asthma
- 2) eosinophilic infiltration (looks like pneumonia)
- 3) systemic vasculitis
How would you treat any of the primary small vessel vasculitides (GPA, Micro polyangitis, EGPA)?
- high dose corticosteroids
- induction therapy: cyclophosphamide
- maintenance: azathioprine
What does cocaine vasculitis look like? how do you treat?
- 1) necrotizing, facial involvement
- 2) drug cessation before any other therapy
What is the cardinal sign for immune-complex vasculitis? what is the most common cause?
- palpable purpura
- drug hypersensitivity
If you have a pulmonary-renal syndrome, what should you consider?
- ANCA-associated vasculitis
List some of the adverse effects in systemic vasculitis treatment
- corticosteroid AE's
- Cytotoxic therapies: cyclophosphamide causes cancer, low fertility
- Immunomodulating therapies: methotrexate, azathioprine, etc
- Biologics: Rituximab
With regards to translucency, color, viscosity, WBC count, PMN%, and culture, what would you expect to see in a normal , non-inflamm, inflamm, and septic joint aspirate?
- Normal: Transparent, clear, <0.2x10^9, <25%, negative
- Non-inflamm: transparent, clear, 0.2-2, <25%, negative
- Inflamm: trans to opaque, yellow to opaque, 2-10, 50, negative
- Septic: Opaque, yellow to green, >100, 75%+, positive
What lab results would you see in an acute phase response?
increased complements, platelets ferritin, haptoglobin
What should you think of when you see a normal WBC count?
- 1) no inflammatory process or,
- 2) they have a disease that normally decreases their WBC count and now they are in the "normal" range with an inflammation. E.g. SLE
What are the normal upper limits for ESR and CRP?
- ESR: M: age/2; F: (age+10)/2
- CRP: <7
How many people with RA have +ve RF?
Prevalence of +ve RF in gen. pop.? prevalence of RA?
therefore only 20% of people with +ve RF actually have RA
Why is the RF test important in people with RA?
seropositive RA is generally more aggressive and there are more extra-articular manifestations
How is Anti-CCP and RF similar/different in RA testing?
- similar sensitivities
- However Anti-CCP is WAYYYY more specific
When would you order an ANA? What will you do with a positive/negative result?
- When they suspect a CTD
- negative: generally can rule out a CTD
- positive: still a huge differential, order an expanded AB profile.
What is the relationship with ANA and SLE? If someone has a positive ANA what is their likelihood of having SLE?
- 99% sens.
- very low specificity
- ANA prevalence: 5%
- SLE prev: 0.1%
1 in 50 chance of having lupus
Not a good general population screening tool!
What are 2 antibodies that are specific for SLE? What if you see a positive SSB/La or SSA/Ro?
- Anti-SM (Smith)
SSA/SSB: Can either be SLE or sjorgrins syndrome
What are three clinical situations where you should order specific antibodies even if there is a negative ANA?
Suspect CTD in pregnant woman: SSA can cross placenta and cause neonatal lupus (heart block)
Anti-phospholid (recurrent abortions, A/V thromboembolism): check for anti-cardiolipin and anti-beta glycoprotein
idiopathic inflamm myopathies: order anti-Jo
What two conditions should you be thinking with a positive ANCA
GPA (wegener's) and Microscopic polyangitis (MPA)
What advice would you give a patient with OA (integrative med)
- 1) weight loss (eat breakfast, low GI, etc)
- 2) Exercise (muscles support joint, strength and aerobic)
- 3) Vit D (necessary for articular cartilage turnover)
- 4) SAMe (may help, expensive)
- 5) Antiinflammatory herbs (e.g. ginger)
- 6) Acupuncture
What is the integrative therapy for RA?
- 1) antiinflammatory diet (tea, ginger, more omega 3)
- 2) fish oil (EP acid is an antinflamm.)
- 3) fasting followed by diet
- 4) mind-body medicine (lower stress, journalling)
- 5) multivit, vit D
What is the integrative therapy for gout?
- 1) stay away from dietary triggers (seafood, red meat, fructose, beer/liquor)
- 2) Lose weight (low GI foods)
- 3) eat low fat dairy, drink coffee
- 4) increase vit C
What is it important to do in patients with gout that want advice?
screen them for renal problems (90% of gout is underexcretion)
What CTD does widespread cytopenias make you think of?
What CTD's often have renal involvement?
SLE, scleroderma, Sjogren's
When you see decreased C3, C4 complement, what CTD should you be thinking?
What should you be thinking if you get positive results for any of the following:
- ANA: non-specific
- Anti-ds-DNA/Anti-Smith: SLE
- SSA/SSB: Sjogren's or SLE
- Anti-Scl-70/anti-centromere: Scleroderma
- Anti-Jo: Inflammatory myositis
What are two things that can precipitate an SLE flare up?
Describe the immunopathology in SLE
- -B cell hyperreactivity causes excessive auto-AB production
- -Causes immune complex formation (therefor decreasing complement levels)
- -causes immunological-mediate tissue injury
What are the diagnostic criteria for SLE (11)?
- Need 4 of 11 to diagnose (MD SOAP BRAIN)
- -Malar rash
- -discoid rash
- -serositis (pleuritis or pericarditis)
- -oral/nasopharyngeal ulcers
- -ANA positive
- -Blood (cytopenias, hematological disorders)
- -Immunological disorders
- -Neurological (Seizures/psychosis)
Name 4 drugs that cause drug-induced lupus. What AB are we testing for here?
Test for anti-histone AB
What would you use to treat SLE?
- SMOKING CESSATION!!
- NSAIDs: arthritis and serositis
- Corticosteroids: internal organ, topical, joints
- -Hydroxychloroquine: maintenance therapy
- Cytotoxic drugs:
- -cyclophosphamide for sever cases
What are three common clinical manifestations of Antiphospholipid Antibody Syndrome (3)?
- Thromboembolotic Events
- Spontaneous abortions
What is the Sjogren's Triad?
- Dry eyes
- dry mouth (xerostomia -> dysphagia)
- Arthritis (small joint and asymmetrical)
What are two specialized tests for Sjogren's (what is a positive result)
Schirmer's dry eye test: fiter paper in eye for 5 mins (<5mm is a positive result)
Rose-Bengal stain for dry eyes (looks purple where the cornea has been worn away)
What is involved in limited scleroderma (CREST Syndrome)? How is it different from diffuse?
- Calcinosis: calcium on skin
- Esophageal dysfunction
- Sclerodactyly: tightening of skin on digits
- Telangiectasia: superficial dilated BVs
Much better prognosis than diffuse! More visceral involvement in diffuse.
Why is age important when someone comes in with Raynaud's?
Primary (better prog) first presents in teens or 20's
If it presents in 30's or 40's more likely to be associated with some other condition
What are the clinical features of scleroderma
- Skin: skin tightening, pruritis, ulceration, calcium deposits
- MSK: arthralgias, tendon sheath fibrosis, myopathy
- Pulm: interstitial fibrosis, pulm HTN
- Cardio: pericardial probs, card. myopathies, abnormal ECG
- GI: hypomotility (eso and intestines), GERD, telangiectasis in lining
- Renal: HTN, high creatinin, proteinuria, renal crisis
What is a sclerodermal renal crisis and why is it important?
a high renin state, causes hemolytic anemia. This is a medical emergency!!
How do you treat Scleroderma?
Treat each of the systems. ACEi for renal probs, CCB's for Raynaud's, PPi for GERD, etc.
Which muscles are NOT involved in inflammatory myositis?
- Not distal (hands and feet)
- Not eyes (use to differentiate from MG and E-L syndrome)
- Not facial
What are the 5 diagnostic criteria for Polymyositis and Dermatomysitis?
- Diagnose if 4+ are present
- 1) proximal symmetrical muscle weakness
- 2) Elevated CK (and aldolase)
- 3) typical EMG findings (fibrillations, high freq discharges, low amp motor unit discharge)
- 4) Muscle biopsy (segmental fibre necrosis, basilar regeneration)
- 5) Typical rash of dermatomyositis (gottron's papules are redness over MCPs and PIPs)
How do you differentiate Polymyositis from dermatomyositis?
Poly: lung fibrosis and ILD, esophageal dysfunction, CD8 cells in musc. biopsy
Dermato: shawl sign, gottron's papules, mechanic's hands, rash on eyelids, CD4 and b-lymphocytes in musc. biopsy
How is inclusion body myositis different from PM/DM?
More distal muscle weakness which can be asymmetric. Doesn't respond well to treatment.
How do you treat the myositises?
- 1) HIGH dose corticosteroids
- 2) If this fails try DMARDS (methotrexate, azathioprine)
- 3) IVIg
- 4) hydrochloroquine for cutaneous lesions of DM
How would you differentiate Inflammatory myopathy, polymyalgia rheumatica, and fibromyalgia
inf. myo: Hx of weakness, PE shows proximal musc. weakness, Labs show elevated CK and ESR
Poly Rheum: Hx of proximal stiffness and pain, PE shows normal muscle strength, Labs show normal CK and elevated ESR
Fibromyalgia: Hx of diffuse pain, fatigue, sleep disturbance; PE shows paired tender points, normal muscle strength; Labs are normal.
What are the 6 Abs tested in an extractable nuclear antigen's test (ENA)?
- SSA (anti-ro)
- SSB (anti-la)
What are the risks of cyclophosphamide use?
they can make you sterile. Long term, they can cause cancer.
What is the classic triphasic change in Reynaud's
Fingers turn white (low blood flow), blue (deoxygenated blood), and red (overcompensation when vessels open again)
In terms of Bone Mineral Density, differentiate normal, from low bone mass (osteopenia), from osteoporosis
- normal: 0-1 Steddev's from the mean BMD
- osteopenia: 1-2.5 Stddev's
- Osteoporosis: 2.5+ stddevs
How many people in the USA have osteoporosis? In a woman 50+ years old, what is the risk of an osteoporotic fracture?
10 million; 40%
What are the main RF's for osteoporosis?
- 1) advanced age (start losing bone after 20's)
- 2) Female sex
- 3) low body weight
- 4) Late menarche/early menopause
- 5) previous fracture
- 6) smoking
- 7) mother broke lots of bones
When would you do a multifactorial fall risk assessment
- Ask these questions (asses if they answer yes to any):
- 1) 2+ fall in past year
- 2) presents with an acute fall
- 3) Difficulty with walk or balance
If no -> have they fallen in the past 6 months -> if yes test their Timed up and Go (TUG; <10 s is normal) -> if they fail go to risk assessment
What risk factors would you look at for fall risk?
- 1) Hx of falls
- 2) Meds
- 3) Gait and mobility
- 4) Visual acuity
- 5) other neuro probs
- 6) Muscle strength
- 7) Cardio OK? (postural HTN? arrhythmias?)
- 8) feet and footwear
- 9) Environmental hazards
What would you do for PE for someone you thought was at fall risk?
- 1) lying and standing BP&HR (>20 sBP or >10dBP; do they go back to baseline in 3-5 minutes?)
- 2. look for vertebral fractures (osteoporosis): wall-to-occiput distance (should be < 5cm); rib-pelvic gap should be less than 2 fingers
- 3. Vision and hearing
- 4. feet and footwear
- 5. TUG
- 6. sit to stand
What multifactorial interventions would you take for someone at risk for falls
- 1) minimize med (especially psychoactive)
- 2) exercise program (tailored to patient)
- 3) treat poor vision
- 4) manage postural HTN
- 5) manage heart rate and rhythm probs
- 6) Vit D
- 7) manage foot and footwear probs
- 8) modify home environment
- 9) provide education
What first line drug would you use to inhibit osteoclast activity? Firstline drug for OP.
Kawasaki disease symptoms
- CRASH and BURN
- Strawberry tongue
- Hands and feet are red, swollen, and flaky
- BURN (fever for 5+ days)
What lifestyle modifications can people with OP make?
- increase Ca and Vit D intake
- 3x30 min weight bearing exercises/week
- cessation of smoking and coffee
- stop osteoporosis-inducing meds
Read juvinile arthritis and make flash cards (did not do this for 8 systems)