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182 Cards in this Set
- Front
- Back
This disease is the most common form of arthritis. It occurs more frequently with aging but is not considered "normal"
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Osteoarthritis
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What is the pathology of osteoarthritis?
(gross) |
Irregularity of cartilidge, ulceration and loss of cart., bone-on-bone contact
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What is the pathology of OA?
(microscopic) |
fibrillation of cartilidge,
Not inflammatory!! |
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What is the pathology of OA?
(biochemically) |
decreased glycosaminoglycan, including less chondroitin sulfate, keratin sulfate, and hyaluronic acid.
increased MMP activity |
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OA is a disease of the _______ of the joints
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hyaline cartilidge
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What is the initiating event in OA?
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mechanical stress
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As OA progresses, crystals of ____________ are shed into the joint fluid.
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calcium phosphate
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What are the clinical features of OA?
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-pain and stiffness of joint
-morning stiffness, gelling -radicular symptoms in limbs due to impinging osteophytes |
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What is noted on Physical Exam with OA?
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Tenderness and bony enlargement of joints, especially at DIP and PIP joints.
-Crepitus, locking, varus deformity in knees |
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What are the Radiologic Features of OA?
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Assymetric joint space narrowing, subchondral bone sclerosis, s.c. bone cysts, osteophytes
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What are the Labs you would order when suspecting OA?
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WBC of synovial fluid (<200)
RF and esr to rule out other, more serious arthritides, however take results with caution |
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What is the treatment for OA?
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exercise, weight loss, heat, massage, OT, PT
Drugs: APAP, NSAIDS, capsaicin cream, chond. sulf./glucosamine, steroid inj, hyaluronic acid inj. Surgery |
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A metabolic disease characterized by hyperuricemia and has musculoskelatal consequences
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Gout
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What are risks for hyperuricemia?
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usually men over 40
alcohol, obesity, renal dysfunction |
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What are the causes of and what is the most common cause of hyperuricemia
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Overproduction of u.a. and underexcretion of u.a., or a combination. Underexcretion is the cause in 90% of pts.
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What happens when there is a high plasma concentration of urate?
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monosodium urate crystals tend to precipitate out of solution, especially in cooler, peripheral joints
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What joints are most affected by gout?
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ankles, toes, hands, soft tissue of ear.
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What is the clinical presentation of Acute Gout?
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Very abrupt, affects only one joint, usually overnight, extremely painful, resolves in days to weeks despite presence of crystals.
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What factors precipitate an acute gout attack?
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start of u.a. lowering tx.
start of diuretic surgury/trauma, illness, stroke, MI, alcohol binges |
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How do you diagnose gout?
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abrupt onset of mono or oligoarthitis of L.E.
Hyperuricemia aspiration of joint fluid shows needle shaped negatively birefringement crystals |
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What are the treatments for Acute Gout?
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NSAIDS: Indocin, Advil, naproxen (high doses) NO ASA
Colchicine:0.5mg/hr until relief or GI sx. Steroids if can't use either of above |
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What does colchicine do for gout?
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1. decreases neutrophil emigration into synovial space
2. blocks release of chemicals that are chemotactic for neutros and monocytes |
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What is the treatment for recurrent gout attacks? (and prophylaxis)
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lose weight, stop alcohol, avoid dehydration, avoid diuretics, keep serum u.a. below 5 mg/dl using probenicid or allopurinol
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What happens in pseudogout?
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similar to regular gout, however, instead of monosodium urate crystals, calcium pyrophosphate crystals are formed.
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What causes pseudogout?
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trauma, surgery, illness, aging
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What are the most common joints affected by pseudogout?
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knee and wrist joints are most affected.
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How to diagnose pseudogout?
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abrupt mono or oligoarthritis, but serum u.a. is not elavated, and c.p. crystals are found in joint fluid.(positively birefringent)
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How to treat pseudogout?
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NSAIDS, colchicine, intra-articular steroids
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What is the most typical skin lesion of psoriatic arthritis
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well demarcated pink to salmon plaques with loose silver/white scales, usually on scalp or extensor surfaces of elbows and knees
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What is the pathophys. of psoriasis?
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inc'd epidermal cell turnover --> acanthosis
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What else do you see in psoriasis besides lesions?
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nail changes (discoloration, pitting)
Auspitz sign Koebner phenomenon |
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Multiple small bleeding points when scrape gently or lift scales
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Auspitz sign
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Psoriatic lesion at the sight of minor skin trauma
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Koebner phenomenon
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A seronegative spondyloarthropathy, may even be reactive arthritis
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Psoriatic Arthritis
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What are the clinical features of P.A.
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Oligoarthritis, arthritis mutilans (causes resorption and telescoping of distal phalanx.
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What is the extra-articular involvement of P.A.?
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psoriatic skin lesions, nail changes, dactylitis, enthesopathy
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What are the radiologic features of P.A.?
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marginal erosions of phalanges plus bone proliferation, "pencil in cup deformity", acroosteolysis, joint space loss, esp. interphalangeal
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What is the treatment for psoriasis and P.A.?
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Skin: topical steroids, coal tar preps, Vit. A&D derivatives, PUVA, Rheumatrex
Arthritis: NSAIDS, steroid inj., DMARDS Both: Enbrel (etanercept) |
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What is the arthritis that occurs after the triad of Gastroenteritis, Urethritis, and Conjunctivitis?
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Reiter's syndrome
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What are the sero-negative spondyloarthropathies?
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OA, Septic Arthritis, Lyme disease, Reactive Arthritis, Psoriatic Arthritis, Gout
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What is the time line for Reiter's syndrome?
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1)Gastroenteritis or V.D.
2)Nongonococcal urethritis w/ C. Trachomatis 3)Conjunctivitis 4)Articular manifestation (after others have subsided, 1-3 weeks after g.e. resolved. |
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What are the Articular Manifestations of Reiter's Syndrome?
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"sausage digits"
asymmetric oligoarthritis, Enthesopathy (heel most freq) Circinate balanitis kertodermal blennorrhagica |
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What lab studies/results can be done to Dx. Reiter's?
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increased esr and CRP
Synovial Fluid: turbid, high WBC, low viscosity, normal glucose |
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When to consider reactive arthritis?
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asym oligoarthritis in young person, extra-articular manifestations, h/o prior infection
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What is the treatment for Reiter's syndrome?
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NSAIDs, exercise, rarely steroids, DMARDs
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Inflammatory arthritis linked to bites by ixodes.
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Lyme disease
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Whate is the pathogen for Lyme disease?
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the spirochete Borrelia burgdorferi (and other Borrelia)
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What are the clinical features of Lyme disease?
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Occurs most often in summer and fall, Rash: erythema migrans, within 1 month of bite, anular, red, Fatigue, fever, h/a, arthralgias
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What are some complications of untreated lyme disease?
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Arthritis, headaches, nuchal rigidity, bilateral bell's palsy, cardiac symptoms
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What are the lab studies done for Lyme disease?
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Serum IgM response 3-4 weeks after bite, gradually replaced by IgG, both detected by ELISA
increase in WBC, esr, neutros in joint fluid, increased CSF protein |
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What is the treatment for Lyme disease?
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prevent with Tick repellants
-Abx: p.o. doxycycline, or amox, or iv Rocephin if cardiac/meningitis symptoms |
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What is the most feared possibility when someone presents with a red, hot, swollen, painful joint
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Septic Arthritis
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What occurs with a Bacterial Joint Infection (SA)?
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Hydrolytic enzymes irreversibly destroy cartilidge and may result in sepsis and death.
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How does bacteria gain access to the joint?
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Through the bloodstream, prosthetic joint, joint injection, joint penetrating injury, contiguous osteomyelitis.
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What is the most common bacteria to cause SA in teens and adults?
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Neisseria gonorrhea
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What Lab studies confirm SA?
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Blood culture + in 50%
Synovial Fluid dec. glucose, inc. protein and lactate, wbc > 10,000, with 90% neutros |
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What does normal synovial fluid look like?
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Clear and straw colored, very viscous due to H.A.
prot 2g/dl, gluc 10mg/dl less than serum value, wbc <200 |
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What is the Treatment for S.A.?
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Treat Early w/ abx. Therefore you may have to treat before confirmatory labs. most common is rocephin, or nafcillin + gentamicin, IV
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What is Paget's Disease?
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episode of intense osteoclastic activity and hypervascularity, followed by intense abnormal osteoblastic activity
Repeated cycles results in excessive, abnormal, unstable bone. |
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Monostotic Paget's
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only one bone is involved in this Paget's disease
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polystotic Paget's
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more than one bone is affected in this Paget's. (most common)
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What is a pathognomic sign of Paget's disease?
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woven bone, in a mosaic pattern. It lacks the normal lamellar structure.
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What are the laboratory findings in Paget's disease?
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normal serum Ca and Ph, serum alk phos elavated during osteoblastic phase, urine Ca elevated during osteolytic, urine hydroxyproline elevated in active disease
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What are complications from Paget's disease? (hypervascularity)
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Inc'd Cardiac output
Possible CHF ischemic neuro events due to "steal phenomena" |
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What are complications from Paget's disease?
(Vertebral Crush fractures) |
back pain and radiculopathy
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What are complications from Paget's disease?
(Skull growth) |
narrowed cranial nerve foramina --> cranial nerve entrapment --> headache, visual disturbances, deafness
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What is the treatment for Paget's disease?
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Bisphosphonates, started when alk phos is high
eg: Aredia, actonel, Didronel, Fosamax |
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What is Polymyalgia Rheumatica?
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It is NOT autoimmune . . .
It IS dominated by myalgia of proximal muscle groups, but there is no permanent weakness or degeneration |
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Who is most commonly affected by polymyalgia rheumatica?
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white women over 50
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What are the most common clinical features of P.R.?
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slow onset, systemic fever, wt. loss, malaise
proximal muscle weakness: stairs, chairs, and pillows morning symptoms and gelling |
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What other, dangerous condition can develop with P.R.?
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Temporal Arteritis, which can lead to blindness
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What labs may indicate P.R.?
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increased esr (50-100 mm/hr)
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What is the treatment for P.R.?
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Without temporal arteritis, use low dose steroids, monitor esr every few weeks.
With Temporal arteritis, High dose steroids immediately |
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What characterizes scleroderma?
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fibrotic and degenerative skin changes
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What does CREST syndrome stand for and what disease is seen with it?
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Scleroderma
C-alcinosis R-aynaud's phenomenon E-sophogeal dysmotility S-clerodactyly T-elangectasias |
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What is the ab seen in limited scleroderma?
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Anti-centromere ab
(also sometimes ANA and RF) |
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What is diffuse scleroderma?
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Fibrotic and vascular changes affect not only hands, esophogus and face, but now intensify and cause problems in other systems.
AKA systemic sclerosis |
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What ab is seen in diffuse scleroderma?
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SCL-70 Ab
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What is treatment for scleroderma?
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No cure, steroids do not help, treat symptoms as they come.
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What is Sjogren's Syndrome?
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autoimmune inflammatory disorder characterized by salivary and lacrimal gland dysfunction
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Xerostomia
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drymouth
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Xerophthamia or keratoconjunctivitis sicca
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dry eyes
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What ab's are seen in Sjogren's syndrome?
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anti-SS-A (anti-Ro)
anti-SS-B (anti-La) |
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What tests are done to diagnose Sjogren's?
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Schirmer's Test, Rose Bengal, Whole Saliva Sialometry
definitive: Salivary Gland biopsy |
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What is the treatment for Sjogren's?
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avoid anticholinergics
use eye drops, saliva stimulants, lubricants, steroids, DMARDs |
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This is the prototype of autoimmune diseases and is characterized by productions of ab's to components of cell nucleus
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Systemic Lupus Erythematosus
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What signs/symptoms dominate SLE?
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Severe Fatigue, Arthralgias, some permutation of its many systemic effects, many of which are vasculitic
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What is the immunopathology of SLE?
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rampant production of auto-ab's to a variety of self ag's
Hyperglobulinemia, heightened immune responses |
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What ab tests can be done for lupus?
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Generic ANA, anti-dsDNA,
anti-sm |
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What are general clinical features of SLE?
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fever, weight loss, overwhelming fatigue
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What are the skin features of SLE?
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malar rash, erythema, photosensitivity, discoid lesions, alopecia, mucous membrane lesions, raynaud's phenomenon
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What are the musculoskelatal features of SLE?
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arthralgias, arthritis, myalgias, fibromyalgia
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What are the renal features of SLE?
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glomerulonephritis, nephrotic syndrome, renal failure
proteinuria, hematuria, pyuria, urinary casts, azotemia |
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What are the neuropsychiatric features of SLE?
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CNS problems, cranial and peripheral neuropathies, headaches, seizures, chorea, cva's, organic brain syndrome
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What are the serous membrane features of SLE?
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pleurisy, pericarditis
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What are the GI features of SLE?
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abd. pain, nausea, vomitting, anorexia, peritonitis, pancreatitis, IBD, mesenteric vasculitis
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What are the Cardiac features of SLE?
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pericarditis, myocarditis, endocarditis, coronary vasculitis, atherosclerosis
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What are the Vascular features of SLE?
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acute necrotizing vasculitis
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What are the reticuloendothelial features of SLE?
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splenomegaly, lymphadenopathy
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What are the hematologic features of SLE?
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increased esr, cytopenia
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What is the clinical course for SLE?
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usually relapsing/remitting, some can go down hill to death within months, 70% survival rate after 10 years.
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What is the treatment for SLE?
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avoid sun, NSAID's and steriods, DMARDS
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What is the Systemic Inflammatory disease that is dominated by joint destruction?
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Rheumatoid Arthritis (RA)
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What is it that develops in joints in RA?
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progressive synovitis
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What are the commonly affected joints in RA?
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MCP, PIP, carpal bones and wrist, knees and MTP joints
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What is the pathology in RA?
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Early: injury to the synovial microvasculature, accompanied by hyperplasia of Type A and B synoviocytes, synovial congestion and edema, fibrin leakage, early T cell emigration into synovial joints, hypertrophic synovium, which grows over joints and develops a pannus, which destroys cartilage.
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What is a pannus?
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The hypertrophic synovium which grows medially and progressively covers one or both articular cartilage surfarces. As it grows, it invades and destroys the cartilage and subchondral bone.
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What are Rheumatoid Factors?
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They are antibodies to the Fc portion of the IgG in the serum and synovial fluid.
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Is RF specific to RA?
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No, it is also seen in some normal people, and it is not seen in all people with RA. However, it is associated with severe RA and extra-articular manifestations are usually only seen in RF positive patients.
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What is essential for the Dx of RA?
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doc. of inflammatory synovitis (synovial fluid leukocytes) and typical erosions on X-Ray
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What are the laboratory features of RA?
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-RF in 80%
-increased esr and CRP -anemia of chronic disease |
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What are the clinical manifestions of RA?
(general) |
synovial hypertrophy and pannus may cause peripheral nerve entrapment in selected joints.
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Is morning stiffness seen in RA?
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Morning stiffness is generally greater than 2 hours
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What are the cervical features of RA?
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neck stiffness throughout ROM
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What are the upper extremity manifestations of RA?
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loss of ROM in shoulder, ulnar nerve entrapment, MCP and PIP joint involvement, nodules on finger tendons, "swan neck", boutonniere, opera glass hands, carpal tunnel syndrome, Guyons canal syndrome
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What are the lower extremity manifestations of RA?
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Hip pain, Baker's cyst at knee, tarsal tunnel syndrome, MTP subluxations.
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What are the skin manifestations of RA?
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Rheumatoid nodules in skin, bursae, tendons, and pressure points
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What is the ocular manifestation of RA?
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Keratoconjunctivitis sicca (dry eyes)
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What are the respiratory manifestations of RA?
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Interstitial fibrosis, pleurisy/pleural effusion
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What are the cardiac manifestions of RA?
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pericardial effusion, restrictive pericarditis, with signs of R heart failure
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What is the Treatment of RA?
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NSAID's, corticosteroids (both injected into joints and short-term p.o.),
and DMARD's. |
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What is the difference between polymyositis and dermatomyositis?
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PM is an inflammatory disease of muscle, and DM is PM with dermatologic manifestations as well.
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What are the four main clinical features of PM and DM? (and one more for DM alone)
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1. proximal muscle weakness
2. inc'd muscle enzymes 3. electromyographic evidence 4. Biopsy evidence of muscle inflammation 5. (DM only) skin rash |
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What is the onset of PM and DM?
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slow onset over 3-6 months without a precipitating event
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What is the proximal muscle weakness seen in PM and DM?
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-also see tenderness, myalgia, arthralgia
-large muscles of neck limb and trunk (stairs, chairs, pillows), dysphonia |
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What are the serum muscle enzymes seen in PM and DM?
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increased CPK-MM, aldolase, ALT, AST, LDH
also inc'd esr, positive hemoglobinuria, though really myoglobinuria (rhabdomyolysis) |
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What electrical evidence is seen in PM and DM?
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the electromyogram will show abn. which indicate muscle disease.
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What will the muscle biopsy show in PM and DM?
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muscle fibers in various stages of vacuolization and necrosis, destroyed fibers replaced by fibrous connective tissue and fat.
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What is the immunopathology of PM and DM?
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cytotoxic T cells and macros surround non-necrotic muscle fibers
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What ANA is specific for PM and DM?
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anti-JO-1 abs
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In Dermatomyositis, what may precede the muscle weakness by up to a year?
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skin rash
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What is Gottron's sign?
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erythematous or violaceous atropohic macules and plaques overlying the dorsal IP joints and sparing IP spaces.
-may also occur on elbows, patellae, or medial malleoli (pathognomic for DM) |
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What is a heliotrope rash?
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-seen in DM
-violaceous eruption of both eyelids and periorbital skin, with periorbital edema |
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What is a Shawl Sign?
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-seen in DM
-poikilodermatous macules in a shawl distribution, over shoulders, arms, and upper back. (pigmented and atrophic changes in skin) |
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What is a V Sign
|
-seen in DM
-same as shawl sign, but over forehead, face, anterior neck and upper chest. |
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What is Mechanics Hands?
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-seen in DM
-darkened lines on the lateral and palmar aspects of fingers, hands appear fissured, scaly, and hyperpigmented |
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What are periungual telanectasias?
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dilated vessels of skin surrounding fingernails.
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What are the treatments for PM and DM?
|
steroids like predinisone or methylprednisone, dc'd when cpk is nl
DMARD's methotrexate or azathioprine if no improvement on steroids. |
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Fibromyalgia Syndrome
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-soft tissue rheumatism
-no organic pathology -real pain at muscle and tendon insertions -disordered, non-refreshing sleep |
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What are the clinical features of Fibromyalgia?
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widespread pain, concentrated on muscles and tendons of axial area, also arms and legs
-extreme fatigue -morning stiffness |
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What are associated sx. with Fibromyalgia?
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tension headaches, IBS, sicca syndrome, urinary frequency and urgency, sensation of swollen hands without objective swelling
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What is the epidemiology of Fibromyalgia?
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typical middle age onset, mostly women.
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What is the pathophys. of Fibromyalgia?
|
-unknown, but maybe CNS related
-inc'd substance P, decreased blood flow to thalamus and caudate nucleus, nonrestorative sleep -may be precipitated by illness or trauma |
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How to Diagnose Fibromyalgia?
|
No diagnostic labs, test 18 trigger points
-a diagnosis of exclusion |
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What is the treatment for fibromyalgia?
|
-steroids do not work,NSAID's not much help
-exercise, muscle relaxants, tricyclic antidepressants(elavil), SSRI's (prozac) |
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What is Osteoporosis?
|
Most common metabolic bone disease, causes pathalogic fractures due to dec'd bone mass.
|
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What bones are usually affected with Osteoporosis?
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Vertebrae, pelvis, femur, distal radius
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What are the signs and symptoms of Osteoporosis?
|
osteopenia on x-ray, pathologic fractures, back pain due to crush fractures, bone fragments impinging on spinal cord or dorsal root (radiculopathy)
|
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What is localized Osteoporosis?
|
only affects one bone, typically due to disuse
|
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What is Primary Osteoporosis?
|
Postmenopausal OP, senile OP
-most frequently affects white women |
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What is Secondary Osteoporosis?
|
OP due to various causes:
-eg: hyperparathyroidism, cushing's syndrome, multiple myeloma, malnutrition, malabsorption, Vit. C or D def., alcohol, long term steroids, immobilation long term |
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Where is bone loss most dramatic?
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The parts of the skeleton containing abundant trabiculae
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When does bone mass peak?
|
It increases steadily throughout childhood and peaks in young adulthood. Bone mass in later life depends on childhood factors such as nutrition and exercise.
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Is bone loss age-related?
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Yes, osteoblastic activity begins to decrease around age 20.
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What are complications of osteoporosis?
|
vertebral fx -- radiculopathy
other fx -- immobilization --more bone loss, pneumonia, DVT, PE |
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What are the Lab findings in Osteoporosis?
|
in primary OP, serum tests are all normal
-DEXA scan shows decreased bone density, osteopenia seen on XRAYs |
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How can one try to prevent osteoporosis?
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Stay active, weight-bearing exercise, drink milk, eat yogurt (at least 2 gms of Ca/day)
|
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What are the treatments for Osteoporosis?
|
HRT-has risks, but works well for post/peri-menopause
EVISTA-hormone, but has less risks, not as much help Bisphosphonates - very popular, inhibits osteoclasts Miacalcin-Nasal spray, also has analgesic effect |
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A chronic granulomatous disease
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Sarcoidosis
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Granuloma
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a distinct type of localized, nodular chronic inflammation
|
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What is the first thing that happens at a site of chronic inflammation on its way to becoming a granuloma?
|
-macros arrive and become "angry"
-they morph into squamous cells that form a tightly stacked and packed center of the granuloma |
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What is the second thing that happens during granuloma formation?
|
Lymphos arrive and squirt cytokines on the macros, keeping them angry.
-Some macros fuse will 20 other ones and form a mulitnucleated Giant cell, which compose part of the center of the granuloma |
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What is the third thing that happens during granuloma formation?
|
the lymphos form the collar of the granuloma, attracting monocytes, more macros, and fibroblasts, all forming the collar. The fibroblasts wall off the center with an organized scar layer.
|
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Non-caseating granuloma
|
The type of granuloma formed in sarcoidosis
--does not have the white, cheesy consistency of caseating granuloma (Tb) |
|
Where are the granuloma's in sarcoidosis widely distributed?
|
lungs, lymph nodes, and liver
|
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Who is generally affected with Sarcoidosis?
|
20-40 y/o, african americans and northern european whites
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In sarcoidosis, there is generally depressed ________ immunity and hightened _______ immunity.
|
Cellular -lymphopenia
Humoral - autoantibody production (25% RF or ANA +) |
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What are the constitutional clinial features of Sarcoidosis?
|
fever, weight loss, malaise
|
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What are the skin clinical features of Sarcoidosis?
|
Erythema nodosum - acute, good prognosis
Lupus pernio - chronic, poor prognosis |
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What are the lymph clinical features of Sarcoidosis?
|
peripheral lymphadenopathy, nontender,
cervical, and often axillary, epitrochlear and inguinal nodes |
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What are the pulmonary clinical features of Sarcoidosis?
|
interstitial disease, hemoptysis, bilateral hilar and mediastinal lymphadenopathy
|
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What are the musculoskeletal clinical features of Sarcoidosis?
|
myalgia, arthritis
|
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What are the hepatic clinical features of Sarcoidosis?
|
mild increase in ALT and AST associated with hepatic granulomas.
|
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What tests help to diagnose Sarcoidosis?
|
transbronchial lung biopsy
ACE levels (double NL) hypercalcemia, hypercalciuria, Kveim-Siltzbach test |
|
Kveim-Siltzbach test
|
heat treated suspension of sarcoidosis is injected intradermally. Biopsy 4-6 weeks later shows granulomatous reaction in 75% of those with Sarcoid
|
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What is the treatment for Sarcoidosis?
|
No tx for asx. hilar adenopathy, colchicine for arthritis, steroids p.o. for hypercalcemia or severe sarcoid of other organs. (Risk of osteoporosis)
DMARD's can be used in chronic disease |
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What is the prognosis of sarcoidosis?
|
most remit and do well, some develop pulmonary disability, even less progress to death.
|
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The antibodies tested for in SLE
|
generic ANA's
anti-dsDNA anti-Sm |
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The antibodies tested for in Systemic Sclerosis (diffuse scleroderma)
|
generic ANA's
-SCL-70 ab |
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The antibodies tested for in limited scleroderma
|
generic ANA's
Anticentromere ab (limited, only got to centromere) |
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The antibodies tested for in Sjogren's syndrome
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SS-A (anti-Ro)
SS-B (anti-La) |
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The antibodies tested for in polymyositis
|
Jo-1 ab
(po - - > jo) |