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101 Cards in this Set
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What are the 4 parts to the pathophysiology of SLE?
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i)autoantibodies ii)complement activation iii)deposition of immune complexes iv)accompanying tissue destruction/vasculitis
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What are the 4 types of SLE?
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i)spontaneous SLE ii)discoid lupus(only skin) iii)drug induced lupus iv)ANA-negative lupus
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What are serology is found in ANA neg lupus (x2)? What are the symptoms? x3 What does it cause incr risk for?
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i)a)Ro+ (SS-A) b)ANA-neg. ii)a)arthritis b)cutaneous lupus c)raynaud's. iii)neonatal lupus in infants
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What are the clinical findings ass'd w/neonatal lupus? x3
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i)skin lesions ii)cardiac abnormalities (AV block, Transpo great vessels) iii)valvular and septal defects
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What are the symptoms of lupus?
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constitutional sxs and SOAPBRAIN MD: Serositis; Oral ulcers; Arthritis; Photosensitivity; Blood (hemolytic anemia, lymphopenia, thrombocytopenia); Renal: GN or nephrotic; ANA; Immuno d/o: Anti-Sm, Ro-La, DsDNA, APLS; Neuro; Malar rash; Discoid rash
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What are some cardiac and pulm features of SLE? x3 each.
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i)cardiac: a)pericarditis b)endocarditis c)myocarditis ii)pulm: a)pleuritis b)pleural effusion c)pneumonitis (may lead to fibrosis)
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What are 7 conditions where ANAs are elevated?
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i)SLE ii)RA iii)Scleroderma iv)Sjogrens v)MCTD vi)polymyositis and dermatomyositis vii)drug induced lupus
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What are the lab tests for Lupus? x9
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i)ANA ii)Anti-Sm iii)Anti-dsDNA iv)Anti ssDNA v)Anti-histone (drug induced) vi)VDRL+ vii)Lupus anticoag and APLS viii)Anti-Ro and La ix)complement levels are decreased
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What are Ro and La + in? x5
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i)complement deficiency (C2/C4) ii)Sjogren's iii)SLE iv)ANA neg lupus v)neonatal lupus
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How to treat Lupus? x5 What to monitor? x2
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i)a)NSAIDs for mild b)steroids: local/systemic for acute; systemic for severe c)cyclophosphamide for renal dz d)hydroxychloroquine for constituional, cutaneous, articular manifestations. ii)monitor renal dz; HTN
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What dz manifestations are not seen in drug induced lupus? x5 What are 3 agents causing it? What are lab findings in drug induced and what isn't present? x2
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i)a)CNS dz b)renal dz c)no butterfly rash d)alopecia e)ulcers ii)a)hydralazine b)procainamide c)INH iii)anti-histone Igs present but no anti-dsDNA or Anti-Sm Ab
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What is APLS? What are the findings x5? What are labs? x3 What is treat?
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i)hypercoag state that can be ass'd w/SLE or other collagen vasc dz. ii)a)livedo b)venous thrombus c)arterial thrombus d)abortions e)thrombocytopenia iii)a)lupus anticoag b)anticardiolipin Ig c)prolonged PTT/PT not corrected w/added normal plasma iv)long term anti-coag
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What is most common cause of death in Lupus? x2
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OI and renal failure
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What is the pathophys of scleroderma?
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Cytokines stimulate fibroblasts which deposit too much collagen. (quantity, not quality problem)
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What are clinical features of SS? x6
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i)Raynaud's: blanch->blue->red. ii)cutaneous fibrosis: tightened skin of face and extremities/sclerodactyly iii)GI involvement: eso immobility causes reflux and dysphagia, can lead to strictures iv)pulm: interstitial fibrosis w/w/o htn. v)cardiac: pericardial effusions; CHF, arrhythmias if myocardium involved. vi)renal: in diffuse dz
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What is most common cause of death?
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pulmonary involvement (interstitial fibrosis w/or w/o pulm HTN
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What serology is + for diffuse form vs limited form of SS? What test is common to both? What 2 tests can detect complications? What predicts prognosis? What dz do 20% have concurrently?
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i)a)diffuse: anti-topo I b)ltd: anticentromere. ii)elevated ANA iii)a)barium swallow for dysmotility b)PFT for fibrosis. iv)degree of skin involvement predicts prognosis (diffuse worse than ltd). v)20% have sjogrens
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What is treatment for SS? x4
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i)none ii)H2 block/PPI for GI iii)NSAIDs for muscle pain iv)Raynauds: no smoke or cold; use CCBs v)treat pulm/renal
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What is main diff b/w diffuse and ltd SS?
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i)visceral involvement significant in diffuse whereas in ltd occurs late. ii)ltd only has cutaneous sxs of head and neck and extremities but spares trunk. iii)diffuse is more rapidly onset iv)diff Igs (centromere in ltd; topoiso in diffuse). CREST in limited form wherease more pulm fibrosis, heart, GI in diffuse
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What is Sjogrens caused by? What is primary Sjogren's? What is secondary? What do pts have incr risk of getting? What is most common cause of death?
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i)lymphocytes infiltrate and destroy lacrimal and salivary glands. ii)primary: dry eyes and dry mouth only iii)2/2: 1/1 + CT dz (RA, SS, SLE, polymyositis). iv)NHL v)malignancy is most common cause
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What are the extraglandular manifestations of sjogren's? x3
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i)arthritis ii)interstitial nephritis iii)vasculitis
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What are pts w/Ro Igs at incr risk of having?
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baby w/congen heart block (neonatal SLE)
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What are the Igs ass'd w/Sjogren?
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i)Ro and La ii)ANA iii)sometimes RF
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What is tx for Sjogren's? For 2/2?
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i)pilocarpine: incr secretions ii)eye drops iii)NSAIDs/steroids for joints iv)therapy for CT dz
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What is Ig for MCTD? What are clinical findings?
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i)Anti-U1 RNP Igs ii)overlap syndrome for SLE, RA, SS, polymyositis. Can have pulm dz, raynaud, eso dysfcn, etc
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Where does RA affect of the joint? what does this cause? Who is it more common in w vs m? what is etiology?
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i)inflammation of synovium of joints. ii)causes damage to cartilage and bone iii)women iv)caused by infection w/genetic predispo
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What is the symmetry of RA? Which joints most common? x3 What are the 3 hand deformities? What are 3 things that can rule it out?
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i)bilateral ii)PIP, MCP, wrists; knees, ankles... iii)a)Ulnar deviation of MCP b)Boutonniere deformity of PIP: PIP flexed; DIP hyperextended. c)Swan-neck contractures: MCP flexed; PIP hyperextended; DIP flexed. iv)a)not symmetric b)DIP involved c)morning stiffness absent/no constitutional sxs
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What is life threatening complication of RA? If pt w/RA and needs sx, what should be done? Why?
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i)Instability of cervical spine (C1-2 subluxation) ii)spine radiograph b/c neurologic injury possible during intubation
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What pulm, heart, skin, ocular and mucosal abnormalities can occur in RA?
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i)pulm: pleural effusions(low glucose); interstitial fibrosis ii)heart: pericaritis, pericardial effusions, conduction abnormalities(because nodule). iii)skin: rheumatoid nodules over extensor surfaces; also can occur in visceral structures (lungs, pleura, pericard) iv)Sjogren xerostomia v)ocular: epi or scleritis
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What is Felty's syndrome?
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variant of RA: anemia, splenomegaly, RA; also thrombocytopenia, lymphadenopathy; high titers of RF w/extraarticular dz
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What heme abnormalities can occur in RA?
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i)anemia of chronic dz and thrombocytosis ii)vasculitis than can become PAN or other vasculitides
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What dz's w/ANA? x4
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i)SLE ii)polymyositis iii)scleroderma iv)Sjogren's
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What is ESR seen in? x4 Wat is the use of it? x2
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i)a)infection (acute or chronic) b)malig c)rheumatologic dz ii)a)dx or r/o inflam process and monitor course of inflamm process
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What is CRP elevated in? x3 What is it used for? If >15, what does it mean?
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i)a)inflamm states and infection b)misc conditions: MI, vasculitis, trauma, malig, panc ii)For infection: more sens and sp than ESR iii)>15=bacterial infection probably present
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What are 4 poor prognostic indicators in RA?
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i)High RF titers ii)subQ nodules (ass'd w/high RF) iii)erosive arthritis iv)autoIgs to RF
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How to DX RA x2 modalities?
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i)Labs: a)RF b)elevated ESR, CRP ii)XRay: narrowed joint space, bony erosions at margins of joint
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What is used for symptomatic tx in RA? x2
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i)NSAID: best for pain ii)steroids: if nsaid no good; low dose long term may be Dz modifying (decr radiographic progression)
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What are the general principles for dz modifying drugs in rA?
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reduce morbidity and mortality by limiting complications, slow px of dz, preserve jt fcn. Initiate early and gradully taper NSAID and steroids once kick in.
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What is 1st line in RA and what are 3 s/e?; what is alternate 1st lines (x2) and what do you need to do?
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i)MTX: a)GI upset; oral ulcers; BM suppression ii)a)hydroxychloroquine: eye exams b/c can get retinopathy iii)sulfasalazine
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Does sx modify dz in RA? What is last line therapy?
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i)synovectomy: decr jt pain and swell but no prevention of xray progression ii)jt replacement
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Who mostly gets gout? When are men affected and when women?
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i)men ii)>30; iii)women post menopause
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What is pathogenesis of gout? x2 What are examples of each type of pathogenesis?
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i)incr uric acid production: a)HGPRT def (Lesch) b)PPRT overactivity c)incr cell turnover: cancer chemo; chronic hemolysis; hematologic malignancies. ii)a)renal dz b)NSAIDs, diuretics, acidosis
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What is pathophysiology of inflammation in gout?
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i)Uric acid crystals collect in synovial fluid and IgGs coat it->PMNs phagocytize and release inflammatory mediators and proteolytic enzymes
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What is acute gouty arthritis?
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one jt of lower extremeity attacked, where there is sudden onset of pain (pt awoken at night). Get erythema, swelling, tenderness and warmth, and as it resolves, get desquamation of overlying skin
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What is intercritical gout?
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asx period after initial attack (probably another w/in 2 years tho); and as incr attacks, becomes polyarticular and worse
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What is chronic tophaceous gout?
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Aggregations of urate crystals get surrounded by giant cells (inflammation), which is usually after several attacks. Tophi deform and destroy hard and soft tissues, which leads to destruction of cartilage and bone, so get 2/2 degen and then arthritis.
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How to dx gout? x2
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i)synovial fluid w/neg birefrigent and needle shaped. ii)x-ray: punched out erosions w/overhanging rim of cortical bone
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How to avoid 2/2 causes of hyperuricemia? x3
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i)meds increasing uric acid levels (thiazides and loop diuretics). ii)decr EtOH intake iii)decr dietary purine intake
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What are 5 precipitants of acute gouty attack?
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i)decr in temp ii)dehydration iii)stress iv)excessive EtOH intake v)starvation
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What is worst thing on ddx w/gout? What do you do to r/o?
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i)septic arthritis ii)gram stain and culture of synovial fluid.
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What are 2 complications of gout?
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i)nephrolithiasis ii)degenerative arthritis
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How to treat acute gout? x4
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i)bed rest** ii)NSAIDs: tx of choice iii)colchicine: if unresponsive to NSAID or if can't take them. Get N/V/Cramps/D. C/o in renal insufficiency iv)steroids: oral if no response to above 2 drugs; joint injections if only one jt involved.
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What drugs should you avoid in gout? x2
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i)ASA: makes gout worse ii)acetaminophen (no anti-inflamm)
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When do you initiate ppx therapy in gout? why? What should you give w/the prophylactic drugs? What are the 2 ppx drugs and which pathogenesis do they cure/
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i)after 2 attacks: risk benefit w/harsh drugs ii)Give NSAID or colchisine to prevent acute attack, then d/c. iii)probenecid: peeps that don't excrete gout, but need normal kidney function iv)allopurinol: over producers, but don't give w/acute gout!
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What is pseudogout? What does deposition increase w/? x2 What are 3 dz's that incr crystal deposition?
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i)Ca-PP crystals in jt cause inflammation ii)a)age b)OA iii)a)hemochromatosis b)HPTH c)hypothyroidism.
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Which jts are affected in pseudogout? x2 Is it mono or polyarticular?
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i)knees and wrists ii)mono usually, can be poly.
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How to DX pseudogout definitively? What is another way to dx?
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i)jt aspiration w/pos birefrigent rhomboid crystals ii)xray: chondrocalcinosis.
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What types of nodes are seen in OA and where are they?
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i)Bouchard: PIP ii)Heberden (less common): DIP
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What is diff b/w poly and dermatomyositis? Who do they occur in?
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poly=w/o skin manifestations; dermato=w/skin manifestations. ii)women
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What is inclusion body myositis? x4
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oddball: i)men ii)distal muscles iii)no autoIgs iv)low elevated CK
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What causes the pathologic changes in muscle for poly vs dermatomyositis?
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i)dermato: humoral immune mech ii)poly and inclusion body: cell mediated process
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What is the diagnostic criteria of polymyositis?
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all four means definite, 3 is probable.i)symmetric prox muscle weakness ii)elevated CK iii)EMG findings of myopathy iv)biopsy evidence of myositis
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Besides prox muscle weakness, what else can be seen in muscle? x2
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i)dysphagia ii)myalgia
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What are features unique to dermatomyositis? x5
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i)heliotrope rash (butterfly) ii)Gottron's papules: papular, erythematous, scaly lesions over knuckles. iii)V sign: rash on face, chest iv)shawl sign: rash on shoulders, upper back, elbows. v)periungual erythema w/telangiectasias
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What are 3 ass'd findings in both poly and dermato?
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i)arthralgias ii)interstitial lung dz (rare) iii)CHF and conduction defects (rare)
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What ass'd findings are seen only in dermato? x2
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i)vasculitis of GIT, kidney, lung, eyes. ii)incr incidence of malignancy in older adults: if dermato dx'd, uncover malignancy bc if cure that, will make dermato go away.
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How to DX polymyositis? x3
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i)labs: a)CK elevated, b)anti-synthetase Igs (anti-Jo 1) (fever, cracked hands, raynauds, ILD, arthritis). c)anti-signal recog particle: worst px. ii)EMG: abnormal in 90%. iii)muscle bx: dermato=perivascular and perimysial; polymyositis an inclusion body myositis=endomysial.
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What is tx of polymyositis? x3
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1st: steroids, then taper 2nd: immunosuppressives if don't respond to steroids (MTX, cyclo) ii)Phys therapy
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What is inclusion body myositis features? What muscles are involved and symmetric? How to DX? What else is diff from polymositis?
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i)men; insidious onset of slowly progressive prox and distal weakness ii)quads, forearm flexors that is assymetric; dysphagia and facial weakness possible. iii)lose DTRs (neuro probs not in polymyo) iv)DX: slight elevation of CK
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How long does polymyalgia rheumatica last for? What are clinical features x3? what is tx?
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i)self limited in 1-2 yrs (diff from RA). ii)a)constitutional sxs b)hip and shoulder stiffness that is b/l; morning stiffness c)jt swelling in knees, wrists, hands possible. iii)Elevated ESR. iv)treat w/steroids to suppress inflammation till dz resolves
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Who is affected in fibromyalgia? What is key to dx? What is the course?
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i)women ii)chronic nonprogressive course that waxes and wanes. iii)multiple trigger points that are symmetric, esp occiput, neck, shoulder, ribs.
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What are clinical features of fibromyalgia? x3
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i)stiffness, body aches, fatigue aggravated by weather changes, stress, sleep deprivation ii)sleep patterns fucked and unrefreshing iii)depression and anxiety common
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What is dx criteria for fibromyalgia? x2 How to treat x3?
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i)tender points at 11/18 places ii)widespread pain including axial pain for 3 mths. iii)a)stay active and productive b)SSRI and TCAs, no narcotics c)CBT, exercise, psych eval
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What are the 5 seronegative sponyloarthopathies?
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i)Ankylosing spondy ii)Reiter's iii)psoriatic iv)arthropathy of IBD v)undiff
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What is undiff spondyloarthropathy?
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migrating polyarthritis (like Reiter's but no urethritis or uveitis)
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What do all the seroneg spondy's have in common? x7
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i)negative RF ii)strong ass'n w/HLA-B27 iii)oligoarthritis (symmetrical) iv)enthesitis (inflamm at sites of insertion of fascia, ligament, tendon) v)inflamm arthritis (axial and sacroiliac jts) vi)extra-articular features (eyes, skin, GU) vii)familial predispo
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What makes ankylosing spondy better and worse?
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improve w/exercise and hot shower; worsen w/rest or inactivity
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How to DX anklyosing spondy? x2 What is relation w/B27
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i)imaging: film, MRI or CT showing sacroilitis: sclerotic changes in sacroiliac area that eventually forms bamboo spine. ii)incr ESR in up to 75% of pts iii)B27 not required
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What is tx for Ankylosing spondy? x4
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i)NSAID for sympto relief ii)PT iii)SX for severe spinal deformity iv)strictly immobilize if neck or back pain and have trauma until image it
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What is Reactive arthritis pattern of arthritis? Wen does it occur? What are the organisms? x4
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i)assymetric oligoarthritis of lower extremities that progresses sequentially from one jt to another, preceded by infectious process that is remote from site of arthritis (1-4 wks prior), usually after enteric or urogenital infections. ii)shigella, campy, chlam, salmon, NOT gonococcal urethritis
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How to DX reactive arthritis? What is TX? x2
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i)synovial fluid analysis (r/o infection or crystals) ii)a)NSAIDs are 1st line b)immunosuppressive: sulfasalazine, azathioprine. NO ABX!
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Which joints are affected in psoriatic arthritis? What is initial tx?
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i)upper ext ii)NSAIDs, may need same drugs as RA
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What happens in vasculitic syndromes? x2 when do you entertain dx of vasculitis?
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i)inflamm of vessels w/vascular necrosis. ii)pt w/systemic illness not explained by another process (or has ischemia involving one or more systems)
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What are the large vessel vasculitides? medium? x5 Small? x2
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i)Temporal and Takayasu's ii)Wegener's, Churg strauss, PAN, MPA, Kawasaki's iii)HSP, hypersensitivity vasculitis
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What other arteries can be involved w/temporal arteritis? What is it ass'd w/incr risk of? x2
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i)aorta or carotids ii)a)aortic dissection b)aortic aneurysm
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What are keys to diagnosing temporal arteritis? x5
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i)age >50 ii)new h/a iii)tender/palpable temporal artery iv)high ESR v)jaw claudication vi)amaurosis fugax
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How to DX giant cell arteritis?
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i)BX. but, single neg bx doesn't r/o
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How to treat temporal arteritis?
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Give steroids as soon as suspected, don't wait for bx. If visual loss, admit and give IV steroids. May need steroids for 2 years. ii)follow up ESRs to monitor effectiveness
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What is Takayasu's vessel involvement? How to DX? What triad do you think of for Takayasu's?
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i)aortic arch and its major branches: get narrowed vessels. ii)arteriogram iii)a)decr/absent peripheral pulse b)discrepancies of BP (arm vs leg) c)arterial bruits.
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What are complications of takayasu's x4. What is prognostic indicator?
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i)limb ischemia ii)aortic aneurysm iii)AR iv)2ndary HTN to renal artery stenosis iv)presence or absence of these sxs.
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How to treat Takayasu's? x3
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i)steroids ii)treat HTN iii)sx or angioplasty may need for stenosed vessels
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What organ systems does Churg strauss hit 6? What is triad (+1 sometimes)?
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i)pulm, renal, skin, neuro, GI, cardiac. ii)constitutional findings; resp tract findings (asthma and dyspnea); skin lesions (subQ lesions, palp purpura).
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How to dx CS-syndrome? How to treat?
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i)bx of lung or skin (have eosinophils). P-Anca ii)steroids, but poor px
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What are the features of wegners?x5
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i)upper resp sxs (sinusitis); purulent or bloody nasal d/c ii)pulm sxs (cough, hemoptysis, dyspnea) iii)GN iv)eye dz (conjunc, scleritis) v)constituional findings
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How to DX Weg's? what confirms dx?
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i)cxr w/nodules or infiltrates ii)labs: incr ESR; anemia; hematuria; pos c-ANCA, possible thrombocytopenia iii)open lung bx
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What to TX wegs with? How is px?
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i)steroids + cyclophos ii)poor px; consider renal xplant if ESRD
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What is diff b/w PAN and weg? what systems does PAN hit x2. What are its assn's? x3 What is the WBC type that is responsible?
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i)no pulm involvement in PAN. ii)a)nervous system and GI tract iii)a)Hep B, HIV, drug rxns iv)PMN invade all layers and fibrinoid necrosis+intimal proliferation leads to reduced luminal area. v)PMN
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What are findings in PAN? x5
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i)constitutional ii)myalgias and arthralgias iii)ab pain (bowel angina) iv)HTN v)livedo
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How to DX PAN? x3 How to TX?
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i)BX of involved tissue or mesenteric angio ii)ESR elevated and PANCA present iii)test for fecal occult blood iv)start steroids, can use cyclophos
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What are stimuli in hypersensitivity vasculitis x3? What is predom involved and what other sx? How to DX? How to TX?
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i)a)drug(pcn, sulfa) b)infection c)other ii)skin: palpable purpura, macules, vesicles iii)constituional sxs iv)BX of tissue for DX v)steroids and w/d cause
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What is Behcet's syndrome's organ systems? x5 How to DX? How to TX?
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i)a)recurrent oral and genital ulcers b)arthritis c)eyes: uveitis, optic neuritis, iritis, conjunctivitis d)CNS: meningoencephalitis, intracranial HTN e)fever and wt loss. ii)DX by BX iii)Tx w/steroids
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