Orthopedic NP Review Course Questions & Answers 2024/2025

Orthopedic NP Review Course Questions & Answers 2024/2025 Signs of inflammation - ANSWER-swelling, warmth, erythema, loss of function, tenderness Articular inflammation - ANSWER-Anatomic structure: synovium, cartilage, capsule (within the joint) Painful site: diffuse, deep Pain on movement: Active/passive, all planes Swelling: common Periarticular inflammation - ANSWER-Anatomic structure: Tendon, bursa, ligament, muscle, bone (outside the joint) Painful site: focal "point" Pain on movement: Active, in a few planes Swelling: uncommon Inflammatory joint diseases features - ANSWER-Pain (when?): Yes (AM) Swelling: soft tissue Erythema: sometimes Warmth: sometimes AM stiffness: prominent Systemic features: Sometimes Increased ESR, CRP: Frequent Synovial fluid WBC: >2000 Ex: Septic, RA, SLE, Gout Noninflammatory joint disease features - ANSWER-Pain (when?): Yes (PM) Swelling: bony Erythema: absent Warmth: absent AM stiffness: minor (<30') Systemic features: absent Increased ESR, CRP: uncommon Synovial fluid WBC: <2000 Ex: OA, AVN Acute Monoarthritis - ANSWER-Inflammation (swelling, tenderness, warmth) in one joint Occasionally polyarticular diseases can present with monoarticular onset: RA, JRA, Reactive and enteropathic arthritis, Sarcoid arthritis, viral arthritis, psoriatic arthritis Acute Monoarthritic Etiology - ANSWER-THE MOST CRITICAL DIAGNOSIS TO CONSIDER: INFECTION! Septic Crystal deposition (gout, pseudogout) Traumatic (fracture, internal derangement) Other (hemarthrosis, osteonecrosis, presentation of polyarticular disorders) Questions to ask: History helps in Differential Dx - ANSWER-Pain come suddenly, minutes? - fracture Over several hours or 1-2 days? - infectious, crystals, inflammatory arthropathy. History of IV drug abuse or a recent infection? - septic joint. Previous similar attacks? - crystals or inflammatory arthritis. Prolonged courses of steroids? - infection or osteonecrosis of the bone. Indications for arthrocentesis - ANSWER-The single most useful diagnostic study in initial evaluation of monoarthritis: SYNOVIAL FLUID ANALYSIS -Suspicion of infection -Suspicion of crystal-induced arthritis -Suspicion of hemarthrosis -Differentiating inflammatory from noninflammatory arthritis Tests to perform on synovial fluid - ANSWER--Low threshold for doing Gram stain and cultures. -Total leukocyte count/differential: inflammatory vs. non-inflammatory. -Polarized microscopy to look for crystals Synovial fluid analysis - ANSWER--Less viscous seen with inflammation -Cloudy - infection, WBC, Crystals -Reddish = blood -Glucose - significantly lower w/infection and inflammation -Protein increased with infection -LDH - increased with infection, RA, gout -Uric acid = gout Septic Joint - ANSWER--Most articular infections - a single joint -15-20% cases polyarticular -Most common sites: knee, hip, shoulder -20% patients afebrile -Joint pain is moderate to severe -Joints visibly swollen, warm, often red -Comorbidities: RA, DM, SLE, cancer, etc Septic Joint - Nongonococcal - ANSWER--80-90% monoarticular -Most develop from hematogenous spread -Most common: Gram positive aerobes (80%); majority with Staph aureus (60%); gram negative 18% Septic Joint: Gonococcal - ANSWER--Most common cause of septic arthritis -Often preceded by disseminated gonococcemia -Sexually active individual, 5-7 days h/o fever, chills, skin lesions, migratory arthralgias and tenosynovitis -> persistent monoarthritis -Women often menstruating or pregnant -Genitourinary disease often asymptomatic Gout - ANSWER--Caused by monosodium urate crystals -Most common type of inflammatory monoarthritis -Typically: first MTP joint, ankle, midfoot, knee -Pain very severe; cannot stand bed sheet -May be with fever and mimic infection -The cutaneous erythema may extend beyond the joint and resemble bacterial cellulitis Risk factors for gout - ANSWER--Primary gout: obesity, HLD, DM, HTN, atherosclerosis -Secondary gout: alcoholism, drug therapy (diuretics, cytotoxic), myeloproliferative disorders, chronic renal failure Gout presenting s/s - ANSWER--Systemic: fever rare but may occur, chills and malaise -MS: Acute onset of monoarticular joint pain. First MTP most common. Usually affected in 90% of patients with gout. Other joints include knees, foot and ankle. Less common in upper extremities (Postulated that decreased solubility of MSU at lower temps of peripheral structures such as toe and ear) -Skin: warmth, erythema and tenseness of skin overlaying joint. May have pruritic and desquamation. -GU: Renal colic with renal calculi formation in patients with hyperuricemia Gout Dx - ANSWER-Uric Acid (limited value as majority of hyperuricemic pts will never develop gout; levels may be normal during acute attack) CBC (mild leukocytosis in acute attacks, but may be higher than 25,000/mm) ESR (mild elevation or may be 2-3 x normal) 24 hr urine uric acid (only useful in pts being considered for uricosuric therapy or if cause of marked hyperuricemia needs investigation) Trial of colchicine (Positive response may occur in other types of arthritis to include pseudogout Gout treatment goals - ANSWER--Gout can be treated without complications -Therapeutic goals include: terminating attacks; providing control of pain and inflammation; preventing future attacks; preventing complications such as renal stones, tophi, and destructive arthropathy Acute gout attack treatment - ANSWER--NSAIDS most commonly used, all work the same, Indocin most commonly used, remember to use with caution with CAD, GI bleed, RF -Indocin 50 mg PO BID-TID for 2-3 days and then taper -Ibuprofen 400mg PO q4-6hr max 3.2g/day -Ketorolac 60 mg IM or 30mg IV x1 dose in pts <65 (30mg IM or 15mg IV in single dose in pts >65 yo, or w pts who are renally impaired -Continue meds until pain and inflammation have resolved for 48 hr Colchicine for acute gout - ANSWER--Inhibits microtubule aggregation which disrupts chemotaxis and phagocytosis -Inhibits crystal-induced production of chemotactic factors -Administered orally in hourly doses of 0.5 to 0.6 mg until pain and inflammation have resolved or until GI side effects (diarrhea) prevent further use. Max dose 6mg/24hr -2mg IV then 0.5mg q6hr until cumulative dose of 4mg over 24hr Corticosteroids for acute gout - ANSWER-Used for pts who cannot tolerate NSAIDs, or failed NSAID/colchicine therapy. Daily doses of prednisone 40-60 mg a day for 3-5 days then taper 1-2 weeks. Improvement seen in 12-24 hr. ACTH (Adrenocorticotropic hormone) for acute gout - ANSWER-Peripheral anti-inflammatory effects and induction of adrenal glucocorticoid release. 40-80 IU IM followed by second dose if necessary Intra-articular injection with steroids for acute gout - ANSWER-Beneficial in pt with 1-2 large joints affected. Good option for elderly pt with renal or PUD (peptic ulcer disease) or other illness. Triamcinolone 10-40mg or Dexamethasone 2-10mg alone or in combination with Lidocaine Non-Pharm Tx for acute gout - ANSWER-Immobilization of joint. Ice packs. Abstinence of ETOH (consumption can increase serum urate levels by increasing uric acid production. When used in excess it can be converted to lactic acid which inhibits uric acid excretion in the kidney). Dietary modification (low carb, increase protein and unsaturated fats, decrease in dietary purine-meat and seafood. Dairy and vegetables do not seem to affect uric acid - bing cherries and vitamin C) Gout prophylaxis - ANSWER-Frequent attacks >3/year, tophi development or urate overproduction. Avoid use of meds that contribute to hyperuricemia: Thiazide and loop diuretics, low-dose salicylates, niacin, cyclosporine, ethambutol (Losartan promotes urate diuresis and may even normalize urate levels. This action does not extend to other members of the ARB class. Useful in elderly with HTN + gout). Colchine 0.6 mg daily-BID. Use alone or in combination with urate lowering drugs. Prophylaxis w/o urate lowering drugs may allow tophi to develop. Gout prophylaxis: Urate lowering drugs - ANSWER-Used for documented urate overproduction. Goal is for serum urate concentration to 6mg/dL or less. Start of therapy can precipitate acute attack; therefore, may need to use colchicine as long as six months. -Xanthine oxidase inhibitors: Allopurinol. Blocks conversion of xanthine to uric acid. Works for underexrectors and overproducers. Start typically 300mg/day and titrate