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- Large Granular Lymphocytes (LGL)
- Cogan’s syndrome
- Neonates
- Synovial fluid
- Fungal
- Poncet’s disease
- Hyperuricemia
- Podagra
- Diagnosis
- Allopurinol
- Presentation
- Associated metabolic conditions
- Work-up
- Pseudogout (Type A) (25% of CPPD)
Palindromic RAwaxing and waning course / usually resolves within 24-48 hrs / joint involvement atypical compared to classic RA Felty’s syndrome neutropenia, splenomegaly, leg ulcers, polyarticular arthritis (RA~) or SLE More: nodules (75%), weight loss (70%), Sjögren’s (55%), LAD (35%), leg ulcers (25%), pleuritis (20%), skin pigmentation (15%), neuropathy (15%), episcleritis (10%) caused by autoantibodies and cytokine/T cell suppression of granulocytopoesis / more common in elderly patients with RA (especially if untreated) / may also have vasculitis etc.
Usually polyclonal, 20% have RA (the rest are considered neoplastic) / usually associated with Felty’s / course is variable Juvenile Rheumatoid Arthritis (JRA) (Still’s disease) children under 16 Presentation: fever, rash (transient, macular), hepatosplenomegaly, serositis Findings: RF and nodules usually absent (only in older, more severe cases) Complications: pericarditis, myocarditis, pulmonary fibrosis, glomerulonephritis, growth retardation, iridocyclitis (anterior uveitis – main systemic symptom in up to 25% of girls with mono/pauciarticular RA, insidious yet may lead to blindness), 40% incidence of myopia / 70% recover, 10% with severe deformities
Presents with fever, transient rash, joint inflammation / notable for persistent plaques and linear pigmentation Labs: over 2/3 will have elevated AST/ALT (2-5x) and AST/GGT / (-) RF, ANA / often extremely elevated ferritin Cogan’s syndrome Still’s + hearing loss / Treatment: high-dose steroids and pulse Cytoxan Infectious Arthritis Infectious Monoarthritis Neonates: group B strep, H. influenza Children: S.aureus (45%), Strep A (25%), GNR (20%), Gonococcus (5%), Tb (1%) Adults: Neisseria (50%), S. aureus (35%), Strep A (10%), GNR (5%), Tb (1%) Other causes: Pseudomonas (IV drugs, wounds), Klebsiella/E. Coli (IV users, GU infections), lyme disease, Salmonella in sickle cell patients, syphilis (2nd stage and Charcot’s joints) / HACEK organisms Pathology: usually hematogenous spread / polymicrobial from surgical implantation or elderly with peripheral vascular disease / usually monostotic (except newborns and sickle cell pts) Neonates: metaphyses, epiphyses Children: usually metaphyseal only as growth plate prevents spread into joint Adults: growth plate closed, vessels reunite, bacteria can go everywhere Clinical symptoms: early: fever, skin, arthralgias / knee is hot, tender (pain on active AND passive movement; joint movement that is NOT limited by passive motion suggests soft-tissue problem, e.g. bursitis)) Gonococcal: hand and feet lesions (erythematous, +/- pustular) Non-gonococcal: another focus / debilitating illness / other? / pre-existing joint abnormality Synovial fluid from joint aspiration or arthrocentesis of knee [video] WBC is a helpful value: < 200 is normal ( < 25% WBC) 200-2000 is non-inflammatory ( < 25% WBC; PMNs) 2000-100,000 is inflammatory ( > 50% WBC) > 80,000 is purulent/septic ( > 75% WBC) Fungal: 10-40 WBC, 70% neutrophils Syphilis: 10-40 WBC in 2nd glucose: 25% less than fasting blood glucose indicates infection culture and gram stain (60-80% sensitive) wet prep (not always used, many false negatives by non-expert labs) synovial biopsy (may be needed to diagnose Tb or hemochromatosis) XR shows pale bone necrosis (sequestrum) / surrounding deposition of new bone (involucrum) Treatment: empiric antibiotics / joint drainage Tuberculous arthritis (see TB) Usually knees / most common is chronic granulomatous monoarthritis / 1% of Tb / 10% of extrapulmonary Tb / onset is months/years / systemic symptoms only in ½ / Synovial fluid: 20 WBC 50% neutrophils, culture positive in 80%, gram stain positive in 1/3 / Pott’s (spine) / scrofula (TB of neck) Poncet’s disease reactive arthritis from Tb / bilateral, no organisms found in joints Lyme arthritis (see Lyme Disease) large joints, weeks to months duration, periods of remission, permanent deformities in 10% Viral Arthritis (from systemic infection) Parvovirus B19, rubella, HBV, HCV Gout usually not before 30 yrs / many are asymptomatic / asymptomatic intervals get shorter over time (severe cases can mimic RA) Pathology: tophi may occur in joints, ligaments, tendons, soft tissue, earlobes, palms, soles, kidney (uric acid > 8 causes gout, > 20 causes renal damage (due to very rapid cell turnover) Hyperuricemia (10%) ( > 750 mg/dl) ?HGPRT deficiency Increased turnover: myeloproliferative disorders, hemolytic anemias, lymphoproliferative malignancy, psoriasis, glycogen storage diseases Impaired renal excretion of uric acid (90%) ( < 700 mg/dl) polygenic inheritance hypovolemia (adrenal insufficiency, diabetes insipidus) Toxins: heavy alcohol use / lead toxicity / ASA interferes with tubular secretion / organic acids compete for secretion (ketones, LA) Other drugs: thiazide, radiocontrast agents, allopurinol/probenecid (if given during attack)
more at night, last hours to weeks, 1st attack usually only in one joint / Podagra (90%) – 1st MTP (great toe) III – intercritical gout most patients have next attack within 1-2 years IV – chronic tophaceous gout erosion of underlying bone from chronic inflammation Precipitation: dietary excess, alcohol, acute medical illness, surgical procedures, joint trauma Renal complications: urate crystals in medullary interstitium (pyelonephritis, obstruction) / 20% of chronic gout die of renal failure (typical to have mild albuminuria, not glomerulonephritis) Diagnosis: needle-shaped urate crystals in synovial fluid - yellow, parallel to polarizing light Note: don’t rule out infection just because you see crystals as infection frequently coexists with hyperuricemia Treatment: Acute attack: colchicine (0.6 mg bid or until diarrhea, unless renal impairment) NSAIDs (indocin and tolectin thought to work best) steroids (prednisone 40 mg qd x 2-3d with rapid taper) Prevention: low purine diet / weight loss / avoid alcohol / colchicine (low dose daily) Probenecid: frequent attacks / stones / tophi / do not use with renal insufficiency Allopurinol: diminishes uric acid production (do not start during acute attack) Pseudogout (CPPD) far less common than gout elderly man/woman (over 85) / calcium pyrophosphate dihydrate in synovial membranes et al / usually asymptomatic rhomboid crystals / familial form chr 8q and chr 5p Labs: mildly elevated ESR / chondrocalcinosis (+ / -) / CPPD crystals - coffin-shaped, weakly (+) positive birefringence (blue when parallel) Presentation: warmth, erythema, tenderness, swelling, may have fever, leukocytosis / self-limited to several days / usually knee (50% of acute attacks) / pseudopodagra is almost impossible Radiography: calcific deposits (chondrocalcinosis present in 26% of asymptomatic adults > 60 yrs) / hook-like osteophytes/subchondral cysts (similar to OA) Associated metabolic conditions: Hyperparathyroidism (primary or secondary) Hemochromatosis (perform basic Fe studies), maybe Wilson’s, A1AT Hypothyroidism Gout Hypomagnesemia (mild hypomagnesemia potentiates PTH action) Hypophosphatemia Amyloidosis Neuropathic joints, aging, trauma/surgery Note: urate gout and rheumatoid arthritis have a strong negative association (10x)
correction of underlying metabolic problem does not always stop progression Pseudogout (Type A) (25% of CPPD) Almost never causes podagra / males / asymptomatic between attacks / usually have radiographic evidence (such as chondrocalcinosis seen in AP pelvis, PA wrists) 20% with hyperuricemia, 5% with urate gout HC associated shows 2nd/3rd MCP enlargement and/or attacks of pseudogout Download 3.95 Mb. Share with your friends:
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