Step 1 - MSK 2

denniskwinn's version from 2015-04-25 16:11


Question Answer
OsteoarthritisMechanical-wear and tear of joints leads to destruction of articular cartilage, subchondral cysts, sclerosis, osteophytes (bone spurs), eburnation (polished, ivory-like appearance of bone), Heberden's nodes (DIP), and Bouchard's nodes (PIP).
Osteoarthritis Predisposing factors age (almost universal > 65y), obesity, joint deformity.
Osteoarthritis Classic presentation pain in weight-bearing joints after use (e.g., at the end of the day), improving with rest. in knees, cartilage loss begins on medial aspect ("bowlegged").Noninflammatory. No systemic symptoms.
Osteoarthritis common sitesFemoral head/knee, cervical, lumbar vertebrae, Hands(genetic)
Less common osteoarthritis sitesShoulder, elbow, feet (except bunions at first MTP)
Osteoarthritis secondary causes1. Legg-calve-Perthes disease 2. Osteochondritis dessicans 3. Obesity, trauma, neuropathic joint 4. Meniscus injuries, hemochromatosis
Osteoarthritis treatmentHeat, decrease weight bearing (cane), ROM exercises, NSAIDs, Acetaminophen, Viscosupplementation (Oral chondroitin, glucosamine)
Rheumatoid arthritisAutoimmune - Inflammatory disorder affecting Synovial joints, with pannus formation In Joints (MCP, PIP), subcutaneous rheumatoid nodules (fibrioid necrosis surrounded by palisading histiocytes), ulnar deviation, subluxation, Baker's cyst (behind the knee) . No DIP involvement. - Females> males. Type III hypersensitivity. 80% of RA patients have positive rheumatoid factor (anti-IgG antibody); anti-CCPP antibody is less sensitive but more specific. Strong association with HLA-DR4 - 30% ANA+, Normal/↑ C3, ↓ synovial C3
Rheumatoid arthritis classic presentationmorning stiffiless lasting> 30 minutes and improving with use, symmetric joint involvement, systemic symptoms (fever, fatigue, pleuritis, pericarditis, anemia of chronic disease)
Rheumatoid nodules↑ RF titers in extensor surfaces forearms, lungs
Rheumatoid arthritis treatmentPT w/joint movement (pool), NSAIDs early - disease modifying drugs: Methotrexate, cyclosporine, corticosteroids, TNF alpha blockers if others don’t work
Sjogren’s syndromeAutoimmune destruction of lacrimal and salivary glands. . classic triad: 1. Xerophthalmia (dry eyes, conjunctivitis, “sand in my eyes” 2. Xerostomia (dry mouth, dysphagia) 3. Arthritis. Parotid enlargement, ↑ risk of B-cell lymphoma, dental caries, autoantibodies to ribonucleoprotein antigen SS-A(Ro), SS-B(La), Confirm with lip biopsy to confirm destruction of glands - predominantly affects females between 40 and 60 y. 90% RF+,
Sicca syndromedry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis, no arthritis
Sjogren’s treatmentArtificial tears, Pilocarpine or cyclosporine drops, Cevimeline (for dry mouth)
Gout symptomsAsymmetnc joint distribution Joint is swollen, red, and painful. Classic manifestation is painful MTP of the big toe (podagra). Tophus formation (often on external ear, olecranon bursa, or Achilles tendon). Acute attack tends to occur after a large meal or alcohol consumption (alcohol metabolites compete for same excretion sites in kidney as uric acid, causing ↓ uric acid secretion and subsequent buildup In blood).
Gout epiMen> women, >30y,
Gout causessecondary causes more common: underexcretion of uric acid (90%) = alcoholism, lead poisoning, diets rich in red meats, seafood, beer, Over production of uric acid (10%): Psoriasis, treating leukemia. Primary gout from inborn metabolism error (HGPRT deficiency in Lesch Nyhan)
Gout findingsJoint is hot, red and swollen, fever, tachycardia, serum acid>7mg/dl (men) or 6 (women). Crystals are negatively birefringent = yellow in parallel light, Common in MTP and foot extensor tensynovitis
Gout treatment Diet modification, Colchicine, NSAIDs, (indomethacin), probenacid (for under excretors), Allopurinol (for overproducers)
PseudogoutCaused by deposition of calcium pyrophophate crystals within the joint space. Forms basophilic, rhomboid crystal that are weakly positive ly birefringent. Usually affects large joints (classically the knee). > 50 years old; both sexes affected equally. - Crystals are yellow in perpindicular light, blue in parallel light
Pseudogout treatmentColchicine prophylaxis, Acute tx w/ aspiration and steroid injection
Septic arthritisS.aureus (most common non gonococcal), Strep, N. Gono are common. Gono presents as monoarticular, migratory arthritis with asymmetrical pattern - swollen red painful joint. Synovitis, tenosynovitis, dermatitis
Septic arthritis treatmentNaficillin for S. Aureus, Ceftriaxone for gono
Chronic infectious arthritisTB, lyme disease ( happens in late disease), Pasteruella multocida (from dog or cat bite)
Seronegative spondyloarthropathiesArthritis without rheumatoid fac tor (no anti-lgG antibody). Strong assocIation wIth HLA B27. Occur more often In males, sometimes caused by IBD
Ankylosing spondylitisChronic inflammatory disease of spine and sacroiliac joints → ankylosis (stiff spine due to fusion of joints), uveitis, and aortic regurgitation - bamboo spine
Ankylosing spondylitis treatmentNSAIDS, Methotrexate,cyclosporine, corticosteroids , TNF alpha inhibitors (very effective in slowings progression of disease)
Reactive arthritis (reiters)Classic triad: 1. Conjunctivitis and anterior uveitis 2. Urethritis (due to chlamydia) 3. Arthritis (Achilles tendon periosteitis) - Can’t see, pee or climb a tree
Psoriatic arthritisJoint pain and stiffness associated with psoriasis. Asymmetric and patchy involvement. Dactylitis (sausage fingers), pencil in cup deformity on x-ray - seen in fewer than 1/3 of patients with psoriasis, extensive nail pitting.
SLE symptomsfever, fatigue, weight loss, non bacterial verrucous endocarditis, hilar adenopathy, and Raynaud's phenomenon, Wire-loop lesions in kIdney with immune complex deposition (usually nephritic syndrome); death from renal failure and infections. False positives on syphilis tests (RPR/VDRL) due to antiphospholipid, antibodies, which cross-react with cardiolipin used in tests
Lab tests for SLE1. Antinuclear antibodies - sensitive but not specific for SLE 2. Antibodies to dsDNA (anti-dsdna) very specific, poor prognosis 3. Anti-smith antibodies - very specific, but not prognostic 4. Antihistoe antibodies - drug induced lupus
Most common cause of death in SLEinfection due to immunosuppression
SOAP BRAIN MDSerositis, Oral ulcers, Arthritis, Photosensitivity, Blood (all low), Renal, ANA, Immunologic, NEurologic, Malar, Discoid
Positive ANA diseasesSLE, Sjogren's (and sicca ). scleroderma, polymyositis, dermatomyositis, rheumatoid arthritis, juvenile arthritis, mlxed connectIve tissue disease.
SarcoidosisCharacterized by immune-mediated , widespread noncaseating granulomas and elcvatcd serum ACE levels. Common in black femal es. Associated with restri ctive lung disease, bilateral hilar lymphadenopathy, ely th ema nodosum, Bell's palsy, epithelial granulomas containing microscopic Schaumann and asteroid bodies, uveoparotitis, and hypercalcemia (due to elevated conversion of vitamin D to its active form in epithelioid macrophages)
Sarcoidosis treatment75-90% spontaneous remission in 2 yrs. TNF inhibitors, hydroxychloroquine if skin involve
Sarcoidosis mnenomicGRAIN - Gammaglobulinemia (polyclonal) Rheumatoid arthritis, ACE increase, Interstitial fibrosis, Noncaseating granulomas
Polymyalgia rheumatica symptomsPain and stiffness in shoulders and hips, often with fever, malaise, and weight loss. Does not cause muscular weakness. Occurs in patients> 50 year of age; associated with temporal (giant cell) arteritis
Polymyalgia rheumatica findings↑ESR, normal CK
Polymyalgia rheumatica treatmentPrednisone
PolymyositisProgressive symmetric proximal muscle weakness caused by CD8+ T-cell induced inury to myofibers. Most often involves shoulders. Muscle biopsy with evidence of inflammation is diagnostic
Dermatomyositissimilar to polymyositis, but also involves malar rash (similar to SLE) Heliotrope rash “shawl and face” rash, Gottron’s papules (knuckles, PIP), mechanics hands, ↑ risk of malignancy,
Dermato/polymyositis findings↑CK, ↑ aldolase and positive ANA, anti-Jo,
Polymyositis treatmentSteroids
Myasthenia gravisMost common NMJ disordcr. Autoantlbodies to postsynaptlc AChR cause ptosis, diplopia, and general weakness. Associated with thymoma. Symptoms worsen with muscle use. Reversal of symptoms occurs With AChE Inhibitors
Lambert-Eaton syndromeAutoantibodies to presynaptic Ca2+ channel results in ↓ ACh release leading to proximal muscle weakness. Associated with paraneoplastic diseases (small cell lung cancer) - symptoms improve with muscle use, no reversal of symptoms with AChE inhibitors alone
Mixed connective tissue diseaseRaynaud's phenomenon, Fatigue, Arthralgias, Myalgias, and Esophageal hypomotility. Antibodies to U1RNP. Responds to steroids.
DIffuse sclerodermawldespread skin involvement, rapid progression, early visceral involvement. assocIated with anti-ScI-70 antibody (anti-DNA topoisomerase I antibody). Excessive fibrosis and collagen deposition throughout the body. Commonly sclerosis of skin, manifesting as puffy and taut skin with absence of wrinkles. Also sclerosis of renal, pulmonary, cardiovascular. and GI systems. 75% female. Raynauds is most common initial symptom.
CREST syndromeCalcinosis, Raynaud's phenomenon. Esophageal dysmotility, Sclerodactyly, and Telangiectasia. Limited skin involvement, often confined to fingers and face. More benign clinical course. Associated with antiCentromere antibody (C for CREST)
CREST treatmentPenicillamine, recombinant human relaxin
LipomaSoft, well-encapsulated fat tumor. Belllgn. Simple excision IS usually curatIve.
LiposarcomaMalignant fat tumor that can be quite large. Will recur unless adequately excised.
RhabdomyomaBenign tumor derived from striated muscle (skeletal or cardiac). Rhabdomyoma of the heart occurs in tuberous sclerosis.
RhabdomyosarcomaMost common soft tissue tumor of childhood. lVlalignant. Arises from skeletal muscle, most often in head/neck.
MaculeFlat discoloration < 1cm - s.a. Tinea versicolor
PatchMacule > 1 cm
PapuleElevated skin lesion < 1cm s.a Acne vulgaris
PlaquePapule > 1cm s.a Psoriasis
VesicleSmall fluid containing blister s.a. Chicken pox
Whealtransient vesicle (hives)
Bullalarge fluid-containing blister (bullous pemphigoid)
KeloidIrregular, raised lesion, resulting from scar tissue hypertrophy (follows trauma to skin ) t. Pertenue (yaws)
Pustuleblister containing pus
Crustdried exudates from a vesicle, bulla or pustule - impetigo
Hyperkeratosisincreased thickness of stratum corneum (psoriasis)
ParakeratosisHyperkeratosis w/retentiong of nuclei in stratum corneum (psoriasis)
AcantholysisSeparation of epidermal cells
Acanthosisepidermal hyperplasia (increased spinosum)
Dermatitisinflammation of the skin
VerrucaeWarts. Soft, tan-colored, cauliflower-like lesions. Epidermal hyperplasia, hyperkeratosis, koilocytosis. Verruca vu lgaris on hands; condyloma acuminatum on genitals (caused by HPV).
Verrucae treatmentcryo, salicylic acid, imiquimed (induces cytokines)
Nevocellular nevusCommon mole (benign)
UrticariaHives, intenstly pruritic wheals that form after mast cell degranulation
Ephelisfreckle, normal number of melanocytes - increased melanin pigment
Atopic dermatitis (eczema)Pruritic eruption, commonly on skin flexures. Often associated with other atopic diseases (ashtma, allergic rhinitis)
Allergic contact dermatitisType IV hypersensitivity reaction that follow exposure to allergen. Lesions occur at site of contact
Psoriasispapules and plaques with silvery scaling, especially on knees and elbows - Acanthosis with parakeratotic scaling (nuclei still on stratum corneum) ↑ stratum spinosum, ↓ stratum granulosum. Auspitz sign (bleeding spots when scales are scraped off). Can be associated with nail pitting and psoriatic arthritis.
Seborrheic keratosisFlat, greasy, pigmented squamous epithelial proliferation with keratin-filled cysts (hom cysts). Looks "pasted on." Lesions occur on head, trunk, and extremities. Common benign neoplasm of older persons. Sign of Lescr-Trelat-sudden appearance of multiple seborrheic keratoses indicating an underlying malignanc\ (e.g., C I, lymphoid)
AlbinismNormal melanocyte number with ↓ activity of tyrosinase - can also be caused by failure of neural crest cell migration during development.
VitiligoIrregular areas of complete depigmentation - caused by ↓ in melanocytes
MelasmaHyperpigmentation associated with pregnancy (mask of pregnancy) or OCP use
Melasma treatmenttopical hydroquinone (bleaching agent)
Impetigovery superficial infection - usually from S.aureus or S.pyogenes - highly contagious - honey crusting (usually begins on face
Impetigo treatmentMucopirocin + systemic (diclox)