rheum Flashcards
initial clin charac. of arthritis
-Acute duration (presenting within hours to
days) or chronic (persists for weeks or longer)
•Number of joints involved: monoarticular,
oligorarticular (2-4), or polyarticular (+5 joints)
-Symmetric or Asymmetric; Additive or
Migratory
•Accurate delineation of involved joints
•Inflammatory or Non-inflammatory
monoarthritis: bacterial inf. of joint space
1. acute
(+ fever, *rapid! dx quickly)
2. chronic
(both can be polyarthritis via hematogenous spread)
- staph aureus, GABHS, strep pneumo, G- orgs, gonococcal (prec. by migratory tenosynovitis or oligoarthritis assoc. w/ charac. skin lesions)
chronic:
lyme disease (other spirochetes), mycobacterial (TB), fungal, viral
monoarthritis: crystal-induced arthritis (painful!)
gout: monosodium urate crystals (hyperuricemia)in articular space–>rel. cytokines
pseudogout: calcium pyrophasphate dihydrate crystals (older, knee/wrist)
chronic:
calcium apatite crystals
other common causes of acute monoarthritis
trauma hemearthrosis -older-falls, athletes -coagulopathies, anticoags. -dx: arthrocentesis
chronic monoarticular pres. of oligoarthritis/polyarthritis
spondyloarthropathy (affect spine and joints) gout/pseudogout ulcerative arthritis rheumatoid arthritis (mostly poly) lupus, other syst. AI dis (mostly poly) foreign body pigment synovitis (tumor)
psoriatic infection
commonly unilateral
rheumatoid
symmetrical/bilateral
small jts in hands PIPs, MCPs, DIPs*rare
pas young women 20-30
migratory polyarthritis
rheumatic fever, post streptococcal, GC (can start as tenosynovitis)
osteoarthritis
around 50-70 yo (onset)
presents as unilateral painful hip, non-inflammatory,
common ddx of acute polyarthritis >5 joints
acute viral inf. (parvovirus, influenza, chiquengunya) (+ fever)
early disseminated lyme disease
Hep B,C
rheumatoid arthritis (symm. PIPs) (y. women)
SLE
uncommon ddx of acute polyarthritis
paraneoplastic polyarthritis
remitting seroneg. symm. polyarthritis w. pitting edema
acute sarcoidosis, (typ. w. erythema nodosum and hilar adenopathy)
adult: onset
still disease
secondary syphiilis
syst. AI diseases, vasculitides, whipple
psoriatic arthritis
ask pt if have psoriasis
skin disease (elbows, knees, scalp) *can hide
acute, oligoarticular, asymmetrical
SLE
AI, jt pain in young women, fever, malor rash (classic)
palpable purpura
hemorrhagic
think vasculitis: inflamm. BVs, polyarthralgia (no inflamm), typ. LE, ulcerated
henochschonlein purpura: kids, abd pn, nephritis, hematopesia?
GC infectious arthritis
pustule w/ arthritis
reactive arthritis
had infection, reacted w. arthritis
“can’t see, can’t pee, can’t climb a tree”
diarrhea, urethritis, salmonella, w/ inflammatory arthritis
think about septic joint w.
monoarticular arthritis
Still disease
kids: acute polyarticular onset JRA, splenomegaly, fever, rheumocytosis, rash
adults: 20-30s, FUO 6 wks, 102-104 fever, typ. rash, neg labs, hepsplenmeg, look for inf. dis.? ca?
inflammatory bowel–>arthritis
ulcerative colitis, Crohn's skin rash (erythema nodosum)
neodosum - sign of something else, can pres. w/ polyarthritis
sarcoidosis IBD (pres. w. polyarthralgia) OTC preg follow strep, meds med rxn Sjogren's
sarcoidosis
Loepren’s? syndrome
starts in lungs, get CXR acute: arthritis in ankles, rash whites diff than chronic dx. with CXR, bilat hilar adenopathy tx: steroids
paraneoplastic arthritis
remote effects of ca
HLA
(SmCC–>sec PTH, ACTH)
see clubbing, esp. w/ smoker–>CT/CXR
familial mediterranean fever
uncommon,
acute mono arthritis in knee/hip, acute abdominal
synovial fluid
made by synoviocytes
plasma infiltrate
lubricant/cushion
viscoelastic
arthrocentesis
sampling synovial fluid, looks turbent if abnormal (classed) clear is normal (or noninflamm: OA, trauma) Class I (WBC 2000 WBC: inflammatory gout, pseudogout, rheum, psoriatic, reactive, colitic, etc.
higher white count
Class II +
more turbent-septic if pustular (or crystals), higher WBC
septic joint
v. turbent, > 80,000 WBC
dirty yellow
red-sanguinous or
seroussanguinous
coag., trauma, blood disorders (hemophilia)
WBC: 200-2000
may get PCR if suspect
lyme, TB
cytology
rarely unless suspect malignancy
normal synovial fluid does NOT
clot
no clotting factors can get into synovial fluid unless inflammation
synovium
“egg-like”
major comps of syn. fluid analyses
fluid clarity and color
det. cell count
exam. for crystals
obtain Cx
joint aspiration and injection (if not septic)
Perform Aspiration when septic arthritis is suspected
because synovial fluid cell count, Gram stain, and culture
are necessary to establish or exclude joint space infection
• Analysis diagnostic in crystalline arthritis
• Synovial fluid white cell count most reliable means of
distinguishing inflammatory from other forms of arthritis
• Injections with glucocorticoids are swiftest way to provide
relief to patients with inflamed joints
eburnation
loss of cartilage, deteriorates
-PIPs, DIPs, almost never MCPs (exc. 1st MCP), hips, knees, lumbar, cervical spine
can form osteophytes–
->can cause reticulopathy, pinched nerve, sciatica, radiculopathy
osteoarthritis
-A degenerative disorder with minimal articular
inflammation
•No systemic symptoms, no fevers, rashes
•Pain relieved by rest; brief morning stiffness (60 w. rheum)
•X-ray findings: narrowed joint space (loss of cartilage), sclerotic (lose cushion): looks whiter
(bone on bone, abn. stress) osteophytes, increased density subchondral
bone, bone cysts
osteoarthritis continued
• Absence of prominent constitutional symptoms
• Examination notable for increased bony prominence at
the joint margins, crepitus or a grating sensation upon
joint manipulation, and tenderness over the joint line
of the symptomatic joint
• Diagnosis supported by radiographic features of joint
space narrowing and spur (or osteophyte) formation
s/s osteoarthritis
- Joint pain that increases with activity
- Morning stiffness that is relatively brief and self limited
- Crepitus(a grating sensation with motion)
- Bony enlargement at the joint margin
- Tenderness to palpation over the joint
- Non-inflammatory synovial fluid (
risk factors osteoarthritis-primary
age female obesity high bone mass occupations req. physical labor fam hx
risk factors osteoarthritis-secondary
joint sx crystal arthritis (chondocalcinosis, gout) inflam. arthritis (RA, septic) acromegaly hemochromatosis hyperchromatosis hyperPTH hypermobility (Ehlers-Danlos) trauma, stress Pagets
lumbar canal stenosis can cause pseudoclaudication
pressure on nerve roots, not vascular problem
2 helpful labs in RA
many presentation, labs are supportive
ID crytalloid joint
Positive Cx
*need to be able to interpret, do not “shot-gun” labs
rheumatoid factor
IgM, IgG
order lab, but cons: lots of other disease cause + (list)
bac. endo, sarcoidosis, Sjogrens, TB, pulm. fibrosis, leprosy, silicosis, polymyositis, dermatomyositis, syphilis, asbestosis, scleroderma, Hep C,B, Ca, ANCA-assoc. vasculitis, polyarteritisnodosa, viral*, primary biliary cirrhosis, parasite
parvovirus
polyarthralgias, can pres. w. + RF
+ RF: always screen for
Hep C
ANAs
anti-nuclear Abs, ab in pt serum binds to hum epi cell (Ag)–>secondary Ab–>immunofluorescence
“ana patterns”
rim pattern: anti-DNA (SLE)
homogenous: non-spec.
nucleolar: scleroderma, sjogrens
speckle: SLE, sjogrens, MCTD
others: ELISA
*can get false neg., highly sensitive, low specificity
-DNA is more specific (+ is helpful) but maj. of + SLE pts will have - DNA (not v. sense)
“CREST” acronym
anti-centromere pattern (local slceroderma) Calcinosis Esophageal dysmotility Sclerodactyly Telangectasia w. centromere staining pattern
drug induced lupus
ANA +, DNA -, anti-histone +
i.e. hydrolyzine for heart failure/HTN
RA
AI, inflamm. of synovium, infilt leukocytes
highly destructive, cytokines/ILs produced, unknown cause
periosticular ostepenia: bone loss, cartilage destroyed, narrow/closed joints
*tx as fast as you can!
can alter not cure process
meds in RA
anti-TNFs: infliximab, etanercept, adalimumab, certolizumab, golimumab
anti-IL-1s: anakinra
anti-IL-6s: tocilizumab
RA
young women, 20-30s Chronic symmetric polyarthritis
•Symptoms start in PIP, MCP, and MTP joints
•Serum rheumatoid factor, antibodies to anti-
CCP(specific), or both in 70%
•Radiographic changes include juxtaarticular
erosions and joint space narrowing (early on normal)
RA manifest.
Gender: Female (3:1 ratio)
• Age: Late childbearing years in women (60s-80s in
men)
• Insidious onset
• Symmetric distribution in small joints (MCP, PIP, and
MTP joints)
• **Spares DIP joints
• Joint stiffness worse in morning, pain, swelling
• Fatigue, weight loss, occasional low grade fevers
RA Lab tests
anemia, elevated ESR or CRP or both, elevated platelets,
thrombocytosis, positive rheumatoid factor in 60-80%
DMARDS: RA tx
hydroxychloroquin sulfasalazine *methotrexate* (anti-folate)-most common, anchor drug lefunomide azathioprine
steroids: RA tx
methylprednisolone:
sev. organ-threatening disease flare: RA, SLE, syst. vasculitis
prednisone:
giant cell arteritis, inflamm. myopathy, polymyalgiarheumatica, RA flare or bridge tx for SLE flare
*long-term high dose: many SEs
biologic drugs if DMARD unsucc: RA tx
infliximab etanercept adalimumab golilmumab certolizaumab rituximab abatacept tocilizumab
SEs: fever, bad cough–>call! sig. risk of bac/fungal inf
$$
highly effective
usually added when not responding to methotrexate
earlier the better, but don’t give out readily
suggested monitoring guide for RA drug tx (RA)
(may include CBC, BUN, Cr, LFTs, UA, eye exam, BP, bone dens, glucose, fasting lipids, Hep B,C, albumin) NSAIDs glucorts hydroxychloroquine methotrexate sulfasalazine leflunomide azathioprine mycophenolatemofetil cyclophosphamide biol. tx (immun. stat, PPD/Quant)
other conditions can look like RA
arthritis with... radiographic erosions \+ rheumatoid factor nodules MCP and wrist joints (hemochromatosis, Ca phos deposition)
pts. w/ lupus, RA
at risk for dev. secondary sjogren’s
primary sjogren’s
dry eyes, dry mouth see chart *more serious than primary interstitial lung disease, kidneys, brain AI-->lymphoma* women in 20-30s can be manifest. of RA
SLE
• Predilection for females of childbearing age
• Multi-system disease, often with a relapsing-remitting course
• Photosensitive rash, polyarthritis, serositis, and fatigue
• Renal disease and central nervous system involvement
are important causes of morbidity
-CNS: psychosis, hallucinations, seizures, depression, dementia
• Presence of antinuclear antibodies
• Certain autoantibodies(anti-dsDNAand anti-SM) have
a greater specificity for diagnosis of SLE, but lack
sensitivity
• Hypocomplementemiamay occur during flares
clin manifest of SLE
see chart
“great masquerader”
i.e. rash, lymphad, polyarthritis, pericarditis, endocarditis, pleurisy, pneumonia, peritonitis, hep, pancreatitis, glomnephritis, leukopenia, anemia, etc.
drug induced lupus
- Chlorpromazine
- Hydralazine** (vasculitis)
- Isoniazid
- Methyldopa
- Minocycline
- Procainamide
- quinidine
lupus nephritis
+proteinuria +hematuria
use steroids, tx early to prevent scarring of kidneys (glomeruli) from lupus, want to prevent
–>renal failure, need transplant
spinal tap in Lupus
look for neuropsychiatric syndromes (ddx from MS)
(elev. WBC: pleocytosis)
can be MS, many others
SLE tx
mild: NSAIDs, hydoxychloroquine
mod: corticosteroids, mycophenolate, azathoprine, cyclosporine
severe: IV pulse corticosteroids, cyclophaosphamide, mycophenolate, azathoprine
raynaud’s
vasospactic
red–>white–>blue
s/s of another disease
think AI illness, thoracic outlet, carpal tunnel (vasc. occlusive disorders)
pregnancy
causes lupus flares
• The inherently hypercoagable state assoc. with pregnancy can be heightened in pts with the antiphosphoplipid syndrome, with risks for mom and fetus: @ risk for thrombosis, inf/hem. complications
• The diagnosis of anti-phospholipid syndrome is a strong contraindication
to pregnancy
rheumatoid arthritis attacks the
synovium
questions to ask
onset? how many joints? symm/asymm? additive or migratory? inflamm/noninflamm?
swollen painful big toe
gout
acute,(pedagra), typ. 1 jt
asymmetric, oligoarthritix
psoriatic arthritis
rheumatoid arthritis
symmetrical
migratory polyarthritis
rheumatic fever
post-strep reactive arthritis
GC arthritis (GC in blood–>tenosynovitis (wrist, migrates to knees, hips)
most common non-inflammatory arthritis
typically manifests where?
mono/oligo/polyarthritis??
osteoarthritis hands, DIP, PIP >50 yo monoarthritis (painful knee/hip) \+/- mild inflammation
ddx chronic noninflamm. monoarthritis
*osteo internal derangements (torn meniscus) chondromalacia patellae osteonecrosis (trauma, steroids, etOH) neuropathic (DM, charcot) arthropathy sarcoidosis amylodiosis
ddx acute inflamm. oligoarthritis: infectious
dissem. GC infection non-GC septic arthritis (typ. mono) bac endocarditis (prev. rheumatic fever, valv. disease) (may have rash) *IR to bacteria* viral
ddx acute inflamm. oligoarthritis: post-inf
reactive arthritis
rheumatic fever (post-strep)
psoriatic arthritis (ext. surface knees, elbow, scalp, CAN HIDE, pts often don’t know)
IBD
ddx acute inflamm. arthritis: spondyloarthropathy
ankylosingspondylitis
anti-Ro/SSA
anti-La/SSB
assoc. w. Sjogrens, SLE, neonatal lubus, cong. heart block
antiphospholipid
arterial, venous thrombosis
pregnancy morbidity
hypercoag, strokes
B2-GP
organ sp. AI dis. w/ +ANA test
AI hepatitis (looks like SLE)
Thyroid disease (Grave’s/Hashimoto’s)
Idiop. pulm. HTN
primary biliary cirrhosis
non-AI conditions w/ +ANA test
viral inf (HIV, Hep B,C, EBV) bac inf (bac endocard) MTB blood Ca (AML) age >65 healthy (up to 10% pop) drugs (anti-TNFs)
SLE labs
typically +ANA, not DNA (+w. lupus nephritis)
low complement levels
rheumatic dis. in pregnancy
most report IMPROVEMENT in jt pain and swelling during prey.
- pts w. mod-high disease activity do better than low disease (CI!)
- returns to prior state after giving birth
moms w/ anti-Sjogren Abs
screen for SS-Ab
can cross placenta and binds heart tissue–>heart block
fetal echo: look for bradycardia, need to be paced when born
-born w/ SLE: fever, rash goes away, heart block can be permanent
