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95 Cards in this Set
- Front
- Back
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Articular cartilage composition (3)
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Chondrocytes
ECM - type II collagen w/ proteoglycans Avascular and aneural |
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Synovium composition (2 layers)
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Matrix layer - proteglycans, hyaluronan
Synovial cells - type A = macrophage like, type B = fibroblast like |
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Joint capsule features (2)
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Type I collagen
Innervated |
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How is hyaline cartilage nourished?
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Synovial capillary -> synovial fluid -> hyaline cartilage
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Synovial fluid composition (3)
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Plasma transudate
Hyaluronan - high viscosity Low cellular content |
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How are joints damaged in acute arthritis? (4)
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ROS released by neutrophils -> depolymerizes hyaluronan
Proteolytic enzymes Synovial fluid volume increases (swelling) Ishemia |
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Protein and glucose in inflamed joints
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Protein: normally protein diffusion is blocked, in disease unblocked -> more protein in joint
Glucose: normally glucose is actively transported into joint space, inflamed joint disrupts transport -> decr glucose |
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Common opioid CNS SE (7)
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Mood alterations
Miosis Seizures Respiratory depression N/V Cough suppression Sedation |
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Common opioid peripheral SE
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Constipation/Urinary retention
Peripheral vasodilation (pruritis, sweating |
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Morphine (2)
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Short duration of action - 1st line for pain
Excellent 1st pass metabolism Renal clearance |
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Codeine (2)
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Weak analgesic -> antitussive
CYP clearance |
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Oxycodone
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Short and long acting
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Methadone (activity, 2 uses, 1 SE)
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Similar activity to morphine but long acting
Use: chronic pain, opioid withdrawal maintenance QT prolongation |
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Meperidine
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Opioid agonist
Short duration of action Serotonin syndrome |
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Fentanyl
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Much more potent than morphine
Low bioavailability |
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Naloxone/Naltrexone (MOA, use)
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Competitive antagonist at opioid receptor
Use: reverse opioid effects |
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Buprenorphine
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Mixed opioid agonist/antagonist
Opioid withdrawal maintenance |
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Rheumatoid arthritis path
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Unknown Ag -> APC w/ HLA DR -> activates B and T cells
B cells make RF -> immune complexes T cells release IFNg and other cytokines to stimulate macrophages -> release TNF and IL-1-> synovial proliferation and pannus |
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Rheumatoid factor
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Ag against Fc of IgG
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Pathological features of RA (4, main infiltrating cell?)
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Villous hypertrophy
Vascular proliferation CD4+ T cells is major infiltrating cel in synovium Pannus release proteases -> erosions -> instability |
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RA pattern
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Symmetric
Polyarticular Inflammatory C1-C2 subluxation |
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Rheumatoid nodules
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Central fibrinoid necrosis surrounded by palisading fibroblasts
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Rheumatoid arthritis Rx
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Steroids/NSAIDs
DMARD: nonbiologic=methotrexate, biologic =etanercept, infliximab, adalimumab |
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Etanercept, infliximab, adalimumab
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Anti TNF Ab
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Lyme Disease 3 stages
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Early localized (days) - erythema migrans rash at bite site
Early disseminated (weeks) - flu-like, cardiac/neurologic Late (months to years) - lyme arthritis, encephalopathy/neuropathy |
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Lyme arthritis pattern (4)
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Mono/oligoarticular
Large joints (KNEE) Asymmetric Intermitten/recurrent |
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Lyme arthritis path
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B. Burgdorferi is latent
Arthritis occurs when T-cells activate against it Synovial lesion identical to RA |
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Seronegative spondyloarthropathies (5 features)
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Asymmetric inflammatory arthritis
Negative for RF HLA B27 Inflammation of sacroiliac/spine Enthesitis |
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Ankylosing spondylitis (epi, 3 clinical features)
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Men in 3rd decade
Morning stiffness improves w/ activity Fusion of spine Uveitis/iritis |
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Reactive arthritis (etiology, 2 pathogens, arthritic pattern)
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Follows urogenital or GI infection
Chlamyida, salmonella Oligoarthritis/enthesitis, 1-2 wks post infection |
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Inflammatory bowel disease associated arthritis
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Spondylytic form a/w B27, resembles AS
Peripheral arthritis form NOT a/w B27, resembles reactive arthritis |
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Sausage toes
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Psoriatic arthritis, anklyosing spondylitis
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2 causes of elevated uric acid
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Overproduction - 10%, HGPRT/Lesch-Nyhan, PRPP over activity --> gout onset in early 20s
Underexcretion - renal failure, lead, drugs |
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Gout risk factors (3)
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Hyperuricemia is necessary but not sufficient
Low dose aspirin Weight gain |
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4 stages of gout
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Asymptomatic hyperuricemia - don't treat
Acute gout - podagra, tendonitis Intercritical gout - time b/w 1st and second attacks: less than a year in 2/3, more than a year in 1/3--> treat AFTER SECOND ATTACK Chronic tophaceous gout - preventable |
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Gout Dx
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Polarized light: parallel = Yellow = allopurinol = gout
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Gout Rx
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Colchicine - acute gout
Probenecid - chronic gout, inhibits reabsorption of uric acid in PCT Allopurinol = chronic gout, inhibits xanthine oxidase -> decreases conversion of xanthine (from purines) to uric acid |
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Calcium pyrophosphate dihydrate (CPPD) deposition disease (epi, pattern, rx)
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Pseudogout is 20% of CPPD cases
Women > 70 Wrist, hand, knee, elbow Rx - colchicine, NSAIDs |
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Main 4 characteristics of fibromyalgia
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Diffuse pain, stiffness, fatigue, CNS fibro-fog
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Main "path" of fibromyalgia
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Decreased "noxious threshold"
Augmented pain processing |
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RA Rx (3)
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Methotrexate - most effective non-biologic
Low dose steroids - may be better for osteoporosis TNFa inhibitors (best in combo w/ methotrexate) |
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What disease might TNFa inhibitors help? (4)
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RA
Ankylosing spondylitis Psoriasis/psoriatic arthritis Crohn's |
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SLE possible path
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Defective apoptosis -> survival/activation of autoreactive T and B cells then infection leads to enough cell death/debris to overhwlem the defective clearance
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SLE abnormalities (3)
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B cell hyperactivation -> autoAb
Increased CD4 and failure of Treg to suppress Immune complex formation w/ complement consumption |
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SLE auto Ab (2)
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ANA - 99% sensitivity but low specificity (15% of normals have ANA)
anti-dsDNA - highly specific for SLE -> marker for disease activity |
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SLE arthritis pattern
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Migratory and nonerosive (unlike RA)
Hands, elbows, feet, knees |
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Lupus nephritis (path and progression)
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Immune complex deposits in glomerular capillary wall in subendothelium w/ mesangial proliferation -> focal -> diffuse (gets worse as complexes deposit not just in mesangium but in capillaries)
Clinical: htn, peripheral edema, weight gain, rbc casts |
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Lupus nephritis Rx
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Cyclophosphamide
Mycophenolate |
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SLE management (4 classes)
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NSAIDs - minor manifestation
Antimalarials (hydroxychloroquine, chloroquine) Corticosteroids Immunosuppresives (mtx, cyclophosh) - severe systemic disease |
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Aspirin (activity (4), moa, se (4))
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Analgesic, anti-pyretic, anti-inflammatory, anti-platelet
Irreversible COX (1 more than 2) inhibition -> platelet aggregation, have to regrow platelets (1wk) GI bleeding, nephro, hypersensitivity, Reye's (avoid in < 12 y.o. esp w/ varicella |
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COX-1 vs COX-2 actions
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COX-1: Cytoprotective prostaglandings protect gastric mucosa and aid in platelet aggregation
COX-2: Inflammatory prostaglandins recruit inflammatory cells, sensitize skin pain receptors, regulate hypothalamic temp control |
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NSAIDs (activity (3), moa, se (4))
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Analgesic, anti-inflammatory, anti-pyretic
Inhibit COX-1 and 2 equally, but is competitive so antiplatelet effect is only as long as NSAID is in body GI disturbance (take w/ food), bleeding, nephro, dont use in pregnancy |
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NSAID vs Aspirin platelet aggregation inhibition
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Aspirin binds irreversibly so inhibits platelet aggregation until platelet regrowth (1 wk)
NSAIDs are reversible, so platelets are inhibited only as long as NSAID is in body (few days) |
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How to minimize risk of GI ulcers for pt's taking NSAIDs? (2)
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Misoprostol - Prostaglandin E1 analog given w/ NSAID to
Proton pump inhibitors |
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Celecoxib (moa, how does it cause major adverse event?)
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COX-2 specific inhibitor
Increased risk for cardiovascular thrombotic events by decreasing PGI2 (platelet inhibitor) and increasing TXA2 (platelet agonist) |
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Acetominophen (activity, se)
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Analgesic, antipyretic
Hepatotoxic w/ alcohol, liver disease, drugs |
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N-acetylcysteine (what is it, use)
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Precursor of glutathione
Antidote for acetominophen overdose Metabolizes toxic intermediate |
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Corticosteroids moa (2)
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Suppress arachidonic acid
Impair release of cytokines |
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Corticosteroids se (5 + 3 chronic)
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Glucose intolerance
Electrolyte disturbances Weight gain GI ulcers (due to PG inhibition) Chronic: immunosuppresion, cataracts, osteoporosis Mood |
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Osteoarthritis presentation (4, which joints?)
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Pain with use
Morning stiffness < 30 min ** (RA > 30 min) Swelling (DIP and PIP nodes Crepitus Weight bearing joints (think of hands/wrists as weight bearing) |
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Osteoarthritis radiographic findings (3)
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Joint space narrowing - eroded cartilage
Osteophytes - bone spurs Whitening - bony sclerosis |
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Osteoarthritis path
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Hyaline cartilage:
Collagen degradation Proteoglycan loss Edema Hyperplastic chondrocytes (w/ catabolic properties) Trabecular bone has lower mechanical competence |
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Osteoarthritis and inflammation
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Most OA pts have TNF and IL-1 in joints
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Osteoarthritis Rx
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Exercise/weight loss
Orthotics Pharm: NSAIDs, COX-2 inhibitors, Joint aspiration/injection w/ hyaluronate or corticosteroids Surgery (very effective) |
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Scleroderma phenotypes and classification
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Localized: morphea and linear
Generalized/Systemic: limited and diffuse |
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Localized scleroderma (2 types)
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Morphea - small discrete spots or patches of skin thickening
Liner - linear pattern of thickening (often on scalp) |
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Generalized scleroderma 3 path processes
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Tissue fibrosis
Inflammation/Autoimmunity Vascular damage |
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Generalized scleroderma: limited vs diffuse (localization, antibodies)
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Diffuse: Anti-scl70
Proximal to elbows and knees More likely to rapidly develop ILD, cardiac, renal problems Limited: anti-centromere and distal to elbows and knees |
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Scleroderma hallmark features
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Calcinosis
Raynaud's Esophageal dysmotility Sclerodactyly Telangiectasia |
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Scleroderma path
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Skin thickening caused by fibrosis of dermis w/ excessive collagen fibers
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Scleroderma key vascular path
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Intimal thickening
In fingers -> raynaud's In kidney -> ischemic activation of RAA In heart -> ischemic heart disease In lung -> pulmonary HTN |
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Giant Cell (Temporal) Arteritis (epi, 2 key symptoms, 2 labs)
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Old
Jaw claudication, headaches, loss of vision Elevated ESR and CRP Rx - high dose steroids |
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Takayasu Arteritis (epi, 2 clinical)
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Young female
Large vessels of aorta are occluded -> arm claudication -> decreased pulse CN abnormalities |
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Kawasaki disease (epi, 5 clinical)
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Children
Fever, conjunctivitis, strawberry tongue, coronary aneurysms |
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Wegener's Granulomatosis (clinical triad, marker, CXR)
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Focal necrotizing vasculitis, necrotizing granulomas in LUNG and UPPER AIRWAY, necrotizing glomerulonephritis
c-ANCA CXR large nodular densities |
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Churg-Strauss (2 clinical, 1 marker)
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Granulomatous vasculitis w/ eosinophilia
Asthma, sinusitis pANCA |
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Microscopic polyangitis (clinical, marker)
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Like Polyarteritis but involving LUNG
pANCA |
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Henoch-Schonlein purpura (epi, when does it happen? 2 markers, some clinical)
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Children
Follows URI IgA immune complexes Leukocytoclastic vasculitis Purpura, arthralgia, GI hemorrhage, abd pain |
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Polyarteritis Nodosa (age, 4 clinical, 1 a/w)
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Adults
Non blanching purpura Footdrop Normal urinalysis b/c involves arteries to kidney not glomeruli NOT lung Hep B |
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cANCA (disease, target)
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Wegener's
Cytoplasmic -> proteinase 3 |
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pANCA (disease, target)
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Churg Strauss
Microscopic PAN Perinuclear -> myeloperoxidase |
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Hypersensitivity vasculitis (3)
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Henoch-Schonlein
Cryoglobulinemic vasculitis 2/2 malignancy, lupus |
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LCV, IgA
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Henoch Schonlein Purpura
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Young female, pulseless
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Takayasu
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Strawberry tongue, fever, coronaries (rx?)
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Kawasaki's
Rx - IVIG + ASA ASAP |
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Juvenile Idiopathic Arthritis definition (3)
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Onset < 16 y.o
Persistent arthritis > 6 wks No labs to diagnose |
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JIA genetic associations
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HLA B27 - males w/ oligoarticular, enthesitis
HLA DR4 - polyarticular disease, older children BASICALLY SAME ASSOCIATIONS AS RA AND SA |
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Juvenile Idiopathic Arthritis definition (3)
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Onset < 16 y.o
Persistent arthritis > 6 wks No labs to diagnose |
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JIA: oligoarticular subtype (epi, ana?, rf?, leads to 2)
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40-60% of JIA
ANA in most RF- -> iridocyclitis (uveitis) and growth disturbances |
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JIA genetic associations
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HLA B27 - males w/ oligoarticular, enthesitis
HLA DR4 - polyarticular disease, older children BASICALLY SAME ASSOCIATIONS AS RA AND SA |
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JIA: polyarticular disease (two types)
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RF- or RF+
RF+ corresponds to RA in adults |
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JIA: systemic onset (Still's disease) (definition) (RF, ANA)
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Arthritis w/ or preceded by fever of at least 2 wks (rash, organomegaly)
RF - ANA - Macrophage activation -> death |
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JIA: oligoarticular subtype (epi, ana?, rf?, leads to 2)
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40-60% of JIA
ANA in most RF- -> iridocyclitis (uveitis) and growth disturbances |
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JIA: polyarticular disease (two types)
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RF- or RF+
RF+ corresponds to RA in adults |
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JIA: systemic onset (Still's disease) (definition) (RF, ANA)
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Arthritis w/ or preceded by fever of at least 2 wks (rash, organomegaly)
RF - ANA - Macrophage activation -> death |
