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171 Cards in this Set
- Front
- Back
alloantibodies |
=isoantibodies antibodies produced by one individual that react with antigens from another individual of the same species |
|
central tolerance mechanism |
negative selection of T-cells occurs in the thymus when T-cells that react with self antigens are deleted
B-cells in the bone marrow that react with self antigen either undergo receptor editing or apoptosis |
|
AIRE protein |
stimulates the expression of peripheral antigens within the thymus so that T-cells develop tolerance |
|
peripheral tolerance 3 mechanisms |
T regulatory cells activation induced cell death anergy |
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T regulatory cells |
self reactive T-cells that suppress antigen presenting cells presenting self antigen via IL-2R and FoxP3 |
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activation induced cell death |
either via the mitochondrial/Bcl2 pathway or Fas death receptor pathway |
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anergy |
2 signals are required for full activation of lymphocytes: antigen couple to self MHC costimulatory CD28 on the T-cell and B7 on the APC
-absence of the second signal or an inhibitory T-cell costimulatory molecule CTLA4--> anergy |
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autoimmune thrombocytopenic purpura: type, antigen, mechanism, manifestations |
type: II antigen: platelet membrane proteins mechanism: opsonization and phagocytosis of platelets manifestations: bleeding |
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pemphigus vulgaris: type, antigen, mechanism, manifestations |
type: II antigen: intercellular junction proteins mechanism: Ab activation of proteases--> destruction of the intercellular adhesions manifestation: skin vesicles |
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ANCA vasculitis: type, antigen, mechanism, manifestations |
type: II antigen: neutrophil granule proteins mechanism: neutrophil degranulation--> inflammation manifestations: vasculitis |
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goodpasture syndrome: type, antigen, mechanism, manifestations |
type: II antigen: non-collagenous basement membrane proteins mechanism: complement/Fc receptor mediated inflammation manifestations: nephritis, lung hemorrhage |
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insulin-resistant diabetes: type, antigen, mechanism, manifestations |
type: II antigen: insulin receptor mechanism: inhibition of insulin binding manifestations: hyperglycemia, ketoacidosis
|
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pernicious anemia: type, antigen, mechanism, manifestations |
type: II antigen: intrinsic factor of gastric parietal cells mechanism: decreased absorption of B12 manifestations: abnormal erythropoiesis/anemia |
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systemic lupus erythematosus: type, antigen, manifestations |
type: III antigen: nuclear antigens manifestations: nephritis, skin lesions, arthritis, others
|
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poststreptococcal glumerulonephritis: type, antigen, manifestations |
type: III antigen: streptococcal wall antigens manifestations: nephritis |
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polyarteritis nodosa: type, antigen, manifestations |
type: III antigen: sometimes Hep B antigens manifestations: systemic vasculitis
|
|
reactive arthritis: type, antigen, manifestations |
type:III antigen: bacterial antigens manifestations: acute arthritis |
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serum sickness: type, antigen, manifestations |
type: III antigen: foreign proteins manifestations: arthritis, vasculitis, nephritis |
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type I diabetes: type, antigen, manifestations |
type: IV antigen: pancreatic beta cells manifestations: loss of insulin production |
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multiple sclerosis: type, antigen, manifestations |
type: IV antigen: CNS myelin proteins manifestations: demyelination of CNS w/ perivascular inflammation paralysis and ocular lesions |
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crohn's disease: type, antigen, manifestations |
type: IV antigen: possibly commensal bacteria manifestations: chronic inflammation and intestinal obstruction |
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Guillain Barre: type, antigen, manifestations |
type: IV antigen: peripheral nerve myelin manifestations: neuritis, paralysis |
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immune privileged sites |
-testes, brain, eye have hidden antigens -trauma may expose them-->autoimmune rxn |
|
clinical features of Rheumatoid arthritis |
-small joint pain, swelling, and morning stiffness -pain lasts >1hr, improves w/ movement, worse w/ inactivity -fatigue/weight loss -rheumatoid nodules -pleuritis/pericarditis -sjogren's syndrome -interstitial lung disease -Eye inflammation -other rare complications (vasculitis, splenomegaly/leukopenia, amyloidosis) |
|
lab tests for rheumatoid arthritis |
-rheumatoid factor: sensitive but not specific -Anticitrullinated protein Ab's: 60-75% of RA patients-->specific not sensitive -high ESR and CRP -anemia -high ferritin -mildly low albumin |
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rheumatoid arthritis imaging studies |
-soft tissue swelling on X-ray -late RA may have marginal erosions, and joint space narrowing -MRI/ultrasound show synovitis |
|
complications of rheumatoid arthritis |
-progressive disease in 10% of cases -permanent joint damage especially in seropositive cases: ulnar deviation, subluxation, atlanto-axial instability -increased mortality |
|
treatment of Rheumatoid arthritis |
DMARDS: eg. methotrexate Biologics: anti-TNF eg. infliximab Corticosteroids: rapid control NSAIDS: non-disease modifying for pain relief |
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Juvenile Idiopathic Arthritis: systemic onset
(Still's disease) |
-fever 1-2 times/day -salmon colored, evanescent rash -polyarthritis in ~50% of cases -pericarditis in 30% of cases -macrophage activation syndrome: leukopenia, anemia, ALT/AST, very high ferritin -treat w/ IL-1 blocker |
|
Juvenile Idiopathic Arthritis: oligoarticular |
-most common form of JIA -onset before 5 yrs -arthritis in 1-4 joints -uveitis -ANA+ in 40-80% --> higher risk of uveitis -treat w/ NSAIDS, steroids, methotrexate |
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Juvenile Idiopathic Arthritis: polyarticular |
can be RF +/- RF- affects mostly larger joints RF+ affects smaller joints, starts after 12 yrs, may persist into adulthood -treat w/ DMARDS, biologics
|
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Juvenile Idiopathic Arthritis general features |
-high rate of uveitis -likely to resolve before adulthood -dysfunction rather than pain -micrognathia -accelerated bone growth |
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sjogren's syndrome: 'sicca' or glandular features |
-dry eyes -dry mouth -dry nose/upper airway -dry skin/vagina |
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extraglandular features of sjogren's |
-arthralgias/arthritis -raynaud's -interstitial nephritis -liver involvement -neuropathy -vasculitis -LYMPHOMA |
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diagnosis of sjogren's |
-SSA (Ro), SSB (La) Ab's -schirmer test for tears -eye stains -saliva measurements -salivary gland biopsy |
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sjogren's treatment |
-symptomatic management w/ lubricants, cholinergic agents etc -mild extraglandular: hydroxychloroquine, low dose steroids -severe extraglandular: high dose steroids, DMARDS, biologics |
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genetic component of lupus |
-HLA loci and possibly complement -high monozygotic concordance -20x relative risk in close relatives |
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epidemiology of lupus |
-1/2000 prevalence -8:1 female: male -more common in african americans |
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clinical features of Lupus |
-photosensitivity -malar rash -discoid rash -oral ulcers -arthritis -serositis -renal involvement -neurologic: psyochosis -hemolysis/cytopenia -immunologic rise in specific Ab's |
|
ANA for lupus |
-used as a screening test (sensitive not specific) -high titer >160:1 is common in lupus and other autoimmune disorders -low + titers are common in healthy ppl |
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Lupus specific antibody tests |
dsDNA- pathogenic--> nephritis
Smith- may predispose to GI involvement |
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limited systemic sclerosis 'CREST syndrome' |
-skin involvement distal to elbows and knees -raynaud's phenomenom -pulmonary hypertension -pulmonary fibrosis -anti-centromere antibodies+ -dilated capillary loops in the nailfolds |
|
diffuse systemic sclerosis |
-total skin involvement -raynaud's phenomenon -sometimes anti-topoisomerase antibodies+ -capillary dilation and destruction in nailfolds -early organ involvement |
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internal organ involvement in systemic sclerosis |
-esophageal and GI dysmotility -GERD -pulmonary HTN and fibrosis -renovascular HTN and progressive renal insufficiency -myositis/arthritis |
|
pathogenesis of systemic sclerosis |
-autoantibodies and dysregulated lymphocytes -vascular abnormalities -fibrosis via myofibroblasts |
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examples of localized vs systemic autoimmune diseases |
localized: hashimoto thyroiditis, autoimmune atrophic gastritis, autoimmune hemolytic anemia
systemic: SLE, sjogren's, systemic sclerosis, RA |
|
4 ANA immunofluorescence patterns |
-homogenous: non-specific -speckled: non-specific, includes Ro, La, smith + others -nucleolar: systemic sclerosis -centromere: CREST syndrome |
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sjogren's pathology |
-lymphocytic (mostly CD4+) infiltrate of lacrimal and salivary glands-->fibrosis -may also progress to involve synovia, lungs, peripheral nerves |
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systemic sclerosis pathology |
-extensive fibrosis -sclerotic atrophy of the skin -GI fibrosis w/ villi loss and barretts esophagus -renovascular fibrosis-->HTN-->kidney failure -pulmonary fibrosis and HTN -pericarditis, myocardial fibrosis |
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rheumatoid arthritis pathology |
CD4+ cells, plasma cells, macrophages in synovium--> hyperplasia, edema, fibrin deposition, increased vascularity--> pannus formation--> joint deformity and fusion |
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rheumatoid factor |
-forms immune complexes -underlies most extra-articular manifestations -not always present or specific |
|
Hydroxychloroquine mechanism and use |
-normally an anti-malarial -accumulates in lysosome often of B-cells -used for Lupus or RA in combination w/ other drugs |
|
side effects of hydroxychloroquine |
-accumulation in retina causing damage that requires monitoring |
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sulfasalazine mechanism and uses |
-NFkB signal inhibition -causes T-cell apoptosis -used in combo for RA and spondyloarthropathies |
|
sulfasalazine side effects |
hemolytic anemia in G-6-PD deficiency |
|
methotrexate mechanism and uses |
-fist line therapy alone or in combo for rheumatoid disease -folate analog that inhibits thymidine synthase and blocks purine synthesis -antineoplastic at high doses
|
|
methotrexate side effects |
-mucositis -liver damage -teratogen/abortifacient -renal clearance via OATP |
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azathioprine mechanism and use |
-prodrug that inhibits purine synthesis--> B and T cell death -used in SLE, vasculitis, myositis |
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azathioprine side effects |
-bone marrow suppression -infection -malignancy -metabolized by TPMT |
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leflunomide mechanism and use |
-prodrug with long half life due to enterohepatic circulation -blocks de novo pyrimidine synthesis -used for arthritis and vasculitis |
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leflunomide side effects |
-diarrhea -high ALT/AST
|
|
cyclophosphamide mechanism and use |
-prodrug activated by CYP -DNA alkylating agent -suppresses T-cells -used in combo for vasculitis -used in chemotherapy |
|
cyclophosphamide side effects |
-bone marrow suppression -infertility -alopecia |
|
Infliximab mechanism and use
|
-chimeric Ab against TNFa
- used for arthritis, ankylosing spondylitis |
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Side effects of infliximab
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-infusion rxn
-infections esp. TB -worsens heart failure -development of Ab-->tolerance |
|
Abatacept mechanism and use
|
-fusion protein: IgG and CTLA-4
-binds B7 and blocks CD28 -used in RA |
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Side effects of abatacept
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-Infusion rxn
-infection -immunization antagonism |
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Rituximab mechanism and use
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-chimeric Ab that binds CD20 on B cells |
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Signs of vasculitis
|
-prolonged constitutional illness |
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Wegener's granulomatous
(GPA) |
-C-ANCA/PR-3 positive |
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Churg Strauss syndrome |
-3 main features: eosinophilia, extra vascular granulomas, necrotizing vasculitis
-usually begins w/ severe asthma and upper airways symptoms-->high eosinophilia and lung infiltrates-->vasculitic phase often w/o glomerulonephritis |
|
takayasu's arteritis |
-large vessel involvement (1' aortic branches) -females <40yrs mostly -arterial stenosis--> fatigue, weak pulses |
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giant cell arteritis |
-most common vasculitis -mostly affects temporal artery--> jaw claudication, headache, vision loss -occurs mostly in the elderly -abnormal artery on biopsy -often comes w/ polymyalgia rheumatica |
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polymyalgia rheumatica |
-severe arthralgia, stiffness and weakness -often in the hips and shoulders -worse in the morning -must occur after 50 y/o -must be monitored for giant cell arteritis
|
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kawasaki's disease |
-exclusively pediatric vasculitis -affects primarily the coronaries-->aneurysms |
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pathogenesis of osteoarthritis |
repeated stress on the avascular articular cartilage--> release of chemo/cyto-kines that stimulate chondrocytes to grow and secrete matrix degrading enzymes--> focal cartilage loss, osteophyte formation, synovial inflammation, cyst formation in the sclerotic subchondral bone |
|
clinical features of osteoarthritis |
-pain w/ usage of joint relieved w/ rest -insidious onset -short morning stiffness -joint instability -late stage disease may cause pain at night/rest -on exam: joint line tenderness, effusions, bony enlargements, laxity of the knees |
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therapy fo osteoarhtritis |
-acetaminophen is first -NSAIDs next -intraarticular steroids -alternative supplements: hyaluronic acid, glucosamine -muscle strengthening to stabilize joint -assistive devices -weight loss may help -eventually total joint replacement |
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pathogenesis of septic arthritis |
-hematogenous seeding of joints -often by gram + bacteria -synovial tissue has no basement membrane to prevent bacterial access
|
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diagnosis of septic arthritis |
-acute onset monoarthritis often in the knee -fever, high WBCs, other extraarticular signs of infections -synovial fluid opaque, WBCs above 50k and PMNs over 90% -culture fluid |
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complications and treatment of septic arthritis |
-osteomyelitis, joint destruction, ankylosis -treat w/ frequent drainage and IV antibiotics |
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disseminated gonococcal infection |
-causes either migratory arthritis and tenosynovitis or monoarthritis -may also pustular rash -difficult to culture from joint but may be present in other places -rapid response to antibiotics |
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parvovirus B19 infection |
-children likely to have slapped cheek rash -adults likely to get polyarticular arthritis similair to RA -diagnose via IgM -often resolves spontaneously -treat w/ NSAIDs |
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Hep C arthritis |
-occurs in 20% of cases -half of cases have +RF -prone to develop cryoglobulinemic vasculitis -antiviral therapy |
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Hep B arthritis |
-acute onset -symmetric small joint polyarthritis/tenosynovitis -associated w/ fever, urticaria/maculopapular rash -early finding in hep B -predisposed to polyarteritis nodose |
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rubella arthritis |
-migratory polyarthritis in 30% of cases -can also occur w/ vaccination -may precede rash -NSAIDs
|
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tuberculous arthritis |
-chronic monoarthritis of large joint -AFB not always + -multi-drug combo effective |
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fungal arthritis |
-usually chronic monoarthritis -balstomycosis cause an acute septic joint -consider immune status and geographic location |
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acute rheumatic fever |
-cross reactive Abs against strep -Jones criteria: Joints, cardiO, Nodules, Erythema marginatum, Sydenhams chorea -migratory polyarthritis -aschoff bodies in the heart -treat w/ penicillin, NSAIDs, possibly prednisone |
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lyme disease |
-borrelia burgdoferi transmitted by ixodes scapularis nymph -early symptoms: erythema migrans, migratory polyarthralgias -disseminated symptoms: meningitis, neuropathy, heart block etc -persistant: encephalitis, inflammatory monoarthritis -diagnosed by elisa and western blot -treat w/ doxycycline |
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gout pathogenesis |
-urate concentration in the serum>6.8 -monosodium urate crystals form and deposit in the joints -mostly underexcretion not over production/intake -risks include hypertension, obesity, CVD, renal insufficiency, alcohol/BEER, high fructose corn syrup, red meat, fish, family history |
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Gout presentation |
-episodic joint pain, swelling, redness -usually starts as monoarticular in big toe -affects medium and and small joints |
|
gout diagnosis |
joint aspiration will show high leukocyte count 50-100K and negatively birefringent monosodium urate crystals -serum uric acid is not helpful in acute attacks -tophi may be seen in advanced cases -eventually kidney stones may develop |
|
probenecid |
-increases renal clearance of uric acid by blocking proximal tubular reabsorption -may increase risk of kidney stones -ineffective with kidney disease -blocks OATP-->drug interactions |
|
allopurinol |
-inhibits xanthine oxidase -should be used in combo with colchicine -acute lowering of uric acid may precipitate gout flair -goal to decrease uric acid <6.0 -may cause hypersensitivity can be severe -may have significant interactions w/ drugs affecting purine synthesis |
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rasburicase |
-uric acid degrader -not commonly used except in pediatric patients with tumor lysis syndrome |
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colchicine |
-suppresses inflammatory response to crystals -used in acute attack and prophylactically -commonly causes diarrhea and other GI effects |
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Pseudogout |
-calcium pyrophosphate dihydrate crystal deposition disease -presents similarly to gout but may also be associated with osteoarhtritis -often seen in wrists, knees, shoulders and hips -short rhomboid, positively birefringent crystals -risk w/ increasing age -anti-inflammatory therapy, no specific treatment |
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pattern of osteoarthritis |
heberden (DIP), bouchard (PIP) wrist (CMC) bunions Hips knees neck lumbar spine |
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pattern of rheumatoid arhritis |
symmetric PIP/MCP wrist (CMC) elbow shoulder knee less often the neck |
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pattern of Ankylosing spondylitis |
affects the lumbar spine and sometimes the neck as well |
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pattern of psoriatic arhritis |
DIP neck lumbar spine |
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pattern of reactive arthritis |
usually in the ankles and lumbar spine can affect the knee |
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pattern of gout |
toes (esp. big toe) ankles knees |
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pattern of tendonitis |
common at the shoulder elbow knee ankle |
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pattern of bursitis |
elbows shoulders hips knees |
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common causes of acute monoarthritis |
septic joint gout pseudogout fracture hemarthosis |
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common causes of chronic monoarthritis |
mechanical trauma psoriatic arthritis rheumatoid arthritis TB neuropathic pain |
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common causes of distal symmetric joint pain |
rheumatoid arhtritis lupus psoriatic arthritis gout/pseudogout |
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common causes of DIP pain |
heberden osteoarthritis psoriatic arthritis gout |
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common causes of oligoarthritis (<4 joints) |
psoriatic arthritis reactive arthritis lyme gout pseudogout rheumatoid arthritis |
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common causes of spondylitis/sacroiliitis |
ankylosing spondylitis reactive arthritis psoriatic arthritis IBS JIA |
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common causes of enthesopathy |
reactive arthritis ankylosing spondylitis psoriatic arthritis IBS |
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common causes of arthritis + rash |
lupus vasculitic urticaria dermatomyositis psoriatic arthritis reactive arthritis sarcoidosis |
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common causes of polyarthralgia (>4 joints) |
fibromyalgia hypothyroidism viremia osteomalacia |
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Normal synovial fluid analysis |
viscous, clear WBC: 0-150 %PMN: 0-50 no crystals culture negative |
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Class I synovial fluid |
clear, very viscous WBC: 0-2k %PMN: 0-50 no crystals culture negative |
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Class II synovial fluid |
turbid, less viscous WBC: 2k-50k %PMN: 50-80 no crystals culture negative |
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Class II-III synovial fluid |
turbid, less viscous WBC: 2k-100k %PMN: 50-90 MSU or CPPD culture negative |
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Class III synovial fluid |
opaque, not viscous WBC: >50k %PMN: >90 no crystals culture positive |
|
mechanism of acetaminophen |
-low potency COX inhibitor -may have greater effect in CNS vs periphery |
|
use of acetaminophen |
-mild-moderate pain -non inflammatory -combo with narcotics -preferred analgesic/antipyretic in children -initial treatment for osteoarhtritis |
|
side effects of acetaminophen |
-safer than most NSAIDs -hepatic centrilobular necrosis occurs w/ overdose: caused by minor metabolite which depletes glutathione but can be treated with N-acetylcysteine -analgesic nephropathy w/ chronic high dose uage |
|
side effects of NSAIDs |
-inhibition of platelets -increased risk of MI -GI bleed/ulcer -can cause increased Na/H20 retention -aspirin intolerance syndrome -delays labor |
|
back pain in pregnancy |
-most severe @ 36 wks -due to relaxin-->sacroiliac hypermobility if in 1st trimester -due to hyperlordosis in 3rd trimester -nocturnal back pain may be caused by IVC compression |
|
herniated discs |
- most commonly at L4-5 or L5-S1 -pain is worse when sitting and can be: referred: sclerotomal/aching radicular: dermatomal/burning/sharp |
|
cauda equina syndrome |
-urinary retention -loss of rectal tone -saddle anesthesia w/ bilateral leg pain -caused by large central herniated disc compressing sacral roots |
|
vertebral fracture |
-sudden severe back pain w/ any movement -tenderness over affected level -usually secondary to osteoporosis |
|
septic spondylitis/sacroiliitis |
-progressive pain even w/o movement -assc w/ fever, chills, infections source -tenderness over affected level -staph is common cause w/ IVDU, DM, age risk factors |
|
muscle spasm |
-commonly a secondary phenomenon -can't fully extend -relief w/ lying down |
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causes of acute lower back pain |
muscle spasm compression fracture infection herniated disk |
|
causes of chronic lower back pain |
spondylosis spinal stenosis spondyoarthritis tumor fibromyalgia |
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lumbar spondylosis |
-pain worse with activity/end of day -lower back or lateral hip -relieved w/ lying down -pressure on the facet joint--> osteoarthritis that can lead to spondylolisthesis, scoliosis, spinal stenosis |
|
spinal stenosis |
-caused by a combo of degenerative disk disease and joint disease -pain is relieved w/ sitting or bending forward -neurogenic claudication |
|
spondyloarthritis |
-associated w/ seronegative spondyloarthritis eg. ankylosing spondylitis, psoriatic arthritis etc -also seen in JIA -pain is worse in the morning for >1hr -relieved with exercise -starts in sacroiliac and ascends |
|
visceral lower back pain |
GI: w/ bowel movements, colitis, ieitis, tumors GU: menstrual, kidney, prostate, uterus, ovaries Aortic aneurysm |
|
sacroiliac pain |
-pain in back, buttock, thigh -worse w/ walking and esp. stairs -positive FABER test |
|
imaging for lower back pain |
-low yield of unexpected findings -MRI has a high false positive rate -MRI is best but done after plain films -CT gives good bone resolution |
|
epidemiology of ankylosing spondylitis |
-typically occurs in younger men -similar prevalence to RA (~1%) -high association w/ HLA B27 |
|
clinical features of ankylosing spondylitis |
-inflammatory back pain mostly w/ osteoproliferation -peripheral arthritis: mono or oligo often in lower limbs -enthesitis -anterior uveitis -restriction of chest motion |
|
exam features of ankylosing spondylitis |
-pain and stiffness -measure tragus to wall - modified schober (lumbar flexion test) -cervical rotation - chest expansion -intermalleolar distance |
|
treatment of ankylosing spondylitis |
-physical therapy - NSAIDs -anti TNF-a |
|
psoriatic arthritis |
-psoriasis usually comes first but not always -small joints like RA -asymmetric oligoarticular -affects DIP joints -telescoping digits/pencil in cup deformity -nail pitting -enthesitis -axial disease -dactylitis (sausage finger) -treat w/ methotrexate and anti-TNF-a |
|
reactive arthritis |
-aseptic arthritis 4wks after a GU or GI infection -organisms include: chlamydia, shigella, salmonella, yersinia, campylobacter, c. diff. -conjunctivitis -urethritis -nail changes, stomatitis, nail changes, balanitis, keratoderma blenorrhagicum -treat w/ NSAIDs then sulfasalazine -possibly use antibiotics in chronic case w/ chlamydia cause |
|
IBD related spondyloarthropathies |
-asymmetric oligoarthritis in lower extremities -can be acute/remitting or chronic/frequent -may see erythema nodosum or pyoderma gangrenosum -treat w/ NSAIDs, steroids, sulfasalazine and anti-TNF-a (not etanercept) |
|
De Quervain's tenosynovitis |
-tendons get trapped in the extensor retinaculum -caused by repetitive activity using the thumb and radial wrist -pain over the radial styloid -worse when make a fist w/ thumb inside and ulnar deviate (finkelstein test) -splint, steroids, NSAIDs, PT |
|
Carpel Tunnel syndrome |
-compression of the median nerve in the wrist -causes paresthesia and numbness of 1st-3rd digits and radial side of the 4th -On physical exam: symptoms w/ 1 of 90 degree flexion (Phalens) or extension and tapping (Tinels), thenar atrophy may also be seen -stepwise treatment: splint, steroids, surgery
|
|
trigger finger |
-locking of the digit in flexion -thickened flexor tendon 'pops' past hypertrophied A1 pulley -corticosteroids or surgery |
|
olecranon bursitis |
4 causes: infection, trauma, gout, arthritis -distinguished for joint swelling by extension/supination/pronation without pain |
|
lateral epicondylitis |
-'tennis elbow' -pain over extensor tendons reproduced w/ wrist/finger extension, or supination against resistance -rest, splint/brace, PT*, analgesics, steroids, botox |
|
differential diagnosis of shoulder pain (6) |
rotator cuff tendonitis* acromioclavicular arthritis adhesive capsulitis referred from C-spine glenohumeral arthritis bicipital tendonitis |
|
rotator cuff tendonitis |
-associated w/ repetitive overhead motion -supraspinatous: pain w/ resisted abduction+internal rotation (empty can, bra strap)* -infraspinatous: pain w/ resisted external rotation -subscapularis: pain w/ resisted internal rotation
-severe tears may allow deltoid to pull humeral head upwards-->glenohumeral osteoarthritis
|
|
subacromial bursitis |
-often occurs w/ rotator cuff injury -full passive range of motion and no crepitus -treat w/ aspiration and steroid injection |
|
adhesive capsulitis |
-pain and tenderness lateral to coracoid -limited active and passive range of motion in all directions -may be caused by DM or imobility -treat w/ PT, NSAIDs, steroid |
|
bicipital tendonitis |
-tenderness over bicipital groove -pain on supination against resistance -surgery in athletes and younger patients |
|
radicular neck pain |
-test range of neck motion -extension+ipsilateral rotation+downward pressure on head should reproduce pain (spurling's maneuver) |
|
trochanteric bursitis |
-lateral thigh pain and tenderness -worse w/ climbing stairs or standing up (abduction and external rotation) -associated w/ leg length discrepancy, IT band tightness, gluteal weakness, back arthritis |
|
pes anserine bursitis |
-tendonitis at the attachment just medial and distal to the tibial tuberosity |
|
plantar fasciitis |
-tightening/fibrosis of plantar aponeurosis -usually caused by microtrauma -rest, NSAIDs, shoe inserts, stretching, possible steroids |
|
Dermatomyositis presentation |
-progressive proximal muscle weakness -symmetric and may-->dysphagia, hoarseness -Gottron's sign: rash over IP, MCP or elbows -heliotrope rash on eyelids -shawl or V sign on chest/back w/ UV exposure -mechanics hands (associated w/ ILD) -calcinosis (juvenile form) |
|
complications of dermatomyositis |
-associated w/ increased risk for malignancies -interstitial lung disease associated with anti-synthetase Ab's (Jo-1) |
|
diagnosis of dermatomyositis |
-elevated CK and aldolase -abnormal EMG: increased membrane irritability w/ fibrillations, discharges, low amplitude -Ab's: ANA, anti-tRNA synthetase, anti-signal recognition peptide, anti-M2 -biopsy: perifascicular inflammation (CD4+) often w/ perivascular involvement |
|
polymyositis |
-progressive proximal muscle weakness -symmetric and may-->dysphagia, hoarseness -mechanics hands (associated w/ ILD) -elevated CK and aldolase -abnormal EMG: increased membrane irritability w/ fibrillations, discharges, low amplitude -Ab's: ANA, anti-tRNA synthetase, anti-signal recognition peptide, -biopsy: CD8+ infiltrate into the muscle fibers |
|
Inclusion body myositis |
-occurs mostly in older men -progressive weakness/atrophy often seen in hand flexors and quads -low elevation of muscle enzymes -abnormal EMG -treatment resistant -rimmed vacuoles w/ mild inflammation seen on biopsy |
|
mimics of inflammatory muscle disease |
-Drug induced myopathy: steroids (normal enzymes&EMG), colchicine, hydroxychloroquine, AZT, cocaine, statins and others -Viral -Hypothyroidism |
|
properties of amyloid |
-non-branching fibrils ~7.5 nm wide -beta pleated sheet conformation -stains w/ congo red-->apple green birefringence -insoluble |
|
components of amyloid |
-proteoglycans -P component -protein fibrils: either... AL= Ig light chains (mostly lambda) AA= serum amyloid associated protein made in liver w/ chronic inflammation AF/TTR=transthyretin, carrier protein for thyroxine |
|
organs affect by amyloidosis |
Kidney: proteinuria-->nephrotic syndrome spleen: enlargement either 'sago' (white pulp) or lardaceous (diffuse) liver:enlargement, deposits in space of dis heart: restrictive cardiomyopathy bone marrow: may have high plasma cells tongue swelling |
|
diagnosis of amyloid |
-abdominal fat pad aspirate -gingival/rectal biopsy -visceral organ biopsy -serum/urine electrophoresis -bone marrow biopsy |
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clinical presentation of AL amyloidosis |
-caused by plasma cell dyscrasia or multiple myeloma -fatigue, weight loss -multiple organ involvement: kidney, heart, GI, tongue, liver, spleen+ others
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treatment of AL amyloidosis
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-melphalan or other chemotherapeutics -autologous stem cell transplant |