Orthopedic NP Review Course
CORRECT QUESTIONS &
ANSWERS(RATED A+)
Signs of inflammation - ANSWERswelling, warmth, erythema, loss of function,
tenderness
Articular inflammation - ANSWERAnatomic structure: synovium, cartilage, capsule
(whithin the joint)
Painful site: diffuse, deep
Pain on movement: Active/passive, all planes
Swelling: common
Noninflammatory joint disease features - ANSWERPain (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 - ANSWERInflammation (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 Monoarthitis Etiology - ANSWERTHE MOST CRITICAL DIAGNOSIS TO
CONSIDER: INFECTION!
Septic
Crystal deposition (gout, pseudogout)
Traumatic (fracture, internal derangement)
Other (hemarthrosis, osteonecrosis, presentation of polyarticular disorders)
Periarticular inflammation - ANSWERAnatomic 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 - ANSWERPain (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
Questions to ask: History helps in Differential Dx - ANSWERPain 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 - ANSWERThe 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, cytotoxics), 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 pruritis
and desquamation.
-GU: Renal colic with renal calculi formation in patients with hyperuricemia
Gout Dx - ANSWERUric 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 chemotatic 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 - ANSWERUsed 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 - ANSWERPeripheral 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 - ANSWERBeneficial 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 - ANSWERImmobilization 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 - ANSWERFrequent attacks >3/year, tophi development or urate
overproduction. Avoid use of meds that contribute to hyperuricemia: Thiazide and
loop diuretics, low-dose salicylates, niacin, cyclopsorine, 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 - ANSWERUsed for documented urate
overproduction. Goal is for serum urate concentartion 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
weekly 100mg/day until optimal urate levels achieved. Start lower doses with renally
impaired pts.
-Uricosuric drugs: Probeneicd or Sulfinpyrazone. Increased renal clearance of uric
acid by inhibiting tubular absorption. SE may prohibit use (GI and renal). Need
measurement of 24hr urine in anyone for whom Probenecid therapy is initiated.
CORRECT QUESTIONS &
ANSWERS(RATED A+)
Signs of inflammation - ANSWERswelling, warmth, erythema, loss of function,
tenderness
Articular inflammation - ANSWERAnatomic structure: synovium, cartilage, capsule
(whithin the joint)
Painful site: diffuse, deep
Pain on movement: Active/passive, all planes
Swelling: common
Noninflammatory joint disease features - ANSWERPain (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 - ANSWERInflammation (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 Monoarthitis Etiology - ANSWERTHE MOST CRITICAL DIAGNOSIS TO
CONSIDER: INFECTION!
Septic
Crystal deposition (gout, pseudogout)
Traumatic (fracture, internal derangement)
Other (hemarthrosis, osteonecrosis, presentation of polyarticular disorders)
Periarticular inflammation - ANSWERAnatomic 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 - ANSWERPain (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
Questions to ask: History helps in Differential Dx - ANSWERPain 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 - ANSWERThe 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, cytotoxics), 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 pruritis
and desquamation.
-GU: Renal colic with renal calculi formation in patients with hyperuricemia
Gout Dx - ANSWERUric 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 chemotatic 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 - ANSWERUsed 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 - ANSWERPeripheral 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 - ANSWERBeneficial 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 - ANSWERImmobilization 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 - ANSWERFrequent attacks >3/year, tophi development or urate
overproduction. Avoid use of meds that contribute to hyperuricemia: Thiazide and
loop diuretics, low-dose salicylates, niacin, cyclopsorine, 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 - ANSWERUsed for documented urate
overproduction. Goal is for serum urate concentartion 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
weekly 100mg/day until optimal urate levels achieved. Start lower doses with renally
impaired pts.
-Uricosuric drugs: Probeneicd or Sulfinpyrazone. Increased renal clearance of uric
acid by inhibiting tubular absorption. SE may prohibit use (GI and renal). Need
measurement of 24hr urine in anyone for whom Probenecid therapy is initiated.
