Muscoskeletal Flashcards
GOUT
Metabolic disease, in which an abnormal amount of urate deposits in the tissues and characterized by a recurring acute arthritis. Urate deposits occur when uric acid level is >6.8mg/dl. Hyperuricemia occurs with overproduction or under excretion of uric acid.
ETIOLOGY of Gout
Primary Gout- is common in Pacific islanders, men, over the age of 30. There is a hereditary component and genome research found linked risk of gout to several genes whose products regulate urate handling by the kidneys. In women, onset occurs after menopause.
Secondary Gout- may have hereditary component, but is related to acquired causes of hyperuricemia (medications, disease process such as myeloma, CKD, and hypothyroidism).
SIGNS AND SYMPTOMS of GOUT
Tophi found in the external ears, feet, hands, olecranon, and prepatellar bursae
Intense pain
Fever
Pruritus
LABORATORY AND DIAGNOSTIC FINDINGS of GOUT
Serial serum uric acid tests
Leukocytosis
Sodium urate crystals in joint fluid or material aspirated from a tophus
X-ray -negative early in disease process, later punched-out erosions with overhanging rim of bone (rat bite appearance) develop
DIFFERENTIAL DIAGNOSIS of GOUT
Cellulitis
Pyogenic arthritis
Rheumatoid arthritis
Sarcoidosis
Multiple myeloma
Hyperparathyroidism
TREATMENT of GOUT
Asymptomatic hyperuricemia should not be treated.
Medications should not be prescribed until arthritis, renal calculi, or tophi occur
ACUTE ATTACK
NSAIDs unless contraindicated (naproxen, indomethacin)
Colchicine-for acute gout, duration <36 hours
Corticosteroids-helpful in patients with contraindication to NSAIDs (methylprednisolone, prednisone)
Interleukin-1 inhibitors (anakinra, canakinumab, rilonacept)
CHRONIC MANAGEMENT
Diet (avoid alcohol particularly BEER, high purine food like organ meats)
Avoid hyperuricemic medications- thiazide and loop diuretics, ASA
Colchicine- to prevent attacks in patients who have mild hyperuricemia and when urate-lowering therapy has been started….DO NOT prescribe if patient has CKD
Xanthine oxidase inhibitors (allopurinol or febuxostat)
Uricosuria agents (pegloticase)
With rigorous medical compliance, allopurinol or febuxostat or pegloticase can shrink tophi and lead to their disappearance
Pseudo-gout occurs with calcium pyrosphosphate deposition in fibrocartilage and hyaline cartilage.
Pseudo-gout can be asymptomatic found incidentally on x-ray.
Prevalence increases with age.
Pseudo-gout is usually seen in patients over 60 years of age.
It is characterized by acute, recurrent, and rarely chronic arthritis of the large joints.
What food would you tell your gout patient to avoid? food high in uric acid -liver, kidney meat, mushrooms, asparagus, sardines
What medication would the NP NOT prescribe for CKD patient with gout and why? NSAIDS-cause worse , nephrotoxicity
Key points of GOut
Although increased purine intake and increased production can contribute to hyperuricemia, the most common cause of gout is decreased urate excretion secondary to kidney disorders or genetic variability in uric acid transporter efficiency.
Suspect gout in patients with sudden, unexplained acute monoarticular or oligoarticular arthritis, particularly if the great toe or midfoot is affected or there is a prior history of sudden, unexplained episodes of acute arthritis with spontaneous remission in 7 to 10 days.
Confirm the diagnosis by finding needle-shaped, strongly negatively birefringent urate crystals in joint fluid; or by dual-energy CT scans or ultrasound imaging.
Documentation of hyperuricemia is insufficient to confirm the diagnosis of gouty arthritis.
Treat acute flares of gout with oral colchicine, an NSAID, a corticosteroid, a combination of colchicine with an NSAID or a corticosteroid, or an interleukin-1 (IL-1) antagonist.
Decrease the risk of future flares by prescribing colchicine, an NSAID, and life-long use of drugs to decrease the serum urate level.
Give drugs that decrease serum urate levels if patients have tophi, > 2 flares of gout per year, urolithiasis, or multiple comorbidities that contraindicate the drugs used to relieve acute flares; individualize the use of urate-lowering ongoing therapy in other patients.
Decrease urate levels usually by prescribing allopurinol or febuxostat alone or in combination with a uricosuric drug.
GOUT
Acute , mono, articular, arthritis, often of the first MTP joint; reoccurrence is common.
Poly articular involvement more common in patients with long-standing disease.
Identification of your urate crystals in joint fluid or tophi is diagnostic.
Dramatic therapeutic response to NSAIDs
With conicity, urate deposits, in subcutaneous tissue, bone, Cartlidge, joints, and other tissues.
Osteoporosis Definition: A skeletal disorder characterized by decreased bone osteoid that reduces bone integrity
ETIOLOGY
Hormone deficiency (estrogen-women) (androgen-men)
Hormone excess (thyrotoxicosis, hyperparathyroidism, Cushing syndrome, Corticosteroid use)
Alcoholism
Inflammatory bowel disease
Immobilization and microgravity
Tobacco use
Genetic disorders (Marfan syndrome, Osteogenesis imperfect, Hypophosphatasia, Homocystinuria, Aromatose deficiency, Collagen disease processes, Ehlers-Danlos syndrome)
Long-term medication use (heparin, aromatase inhibitors, SSRIs, Vitamin A, Vitamin D
Osteoporosis
SIGNS AND SYMPTOMS
Usually asymptomatic until fractures diagnosed,
Backache-depending on severity of fracture or collapse of vertebrae
LABORATORY AND DIAGNOSTIC FINDINGS
Serum calcium, phosphate and PTH are normal
Alkaline phosphatase may be normal or slightly elevated (ie after fracture)
Vitamin D is decreased
Assess serum determining of 25-hydroxyvitain D if low bone density
Assess for thyrotoxicosis and hypogonadism
Assess for celiac disease with serum tissue transglutaminase antibody determinants
DEXA (dual energy x-ray absorptiometry) determine bone density of lumbar spine, hip, and distal radius
T score is the simple manner of reporting DEXA
> -1.0: Normal
-1.0 to -2.5: Osteopenia
<-2.5: Osteoporosis
< -2.5 with fracture: severe Osteoporosis
People with T score -1.0 to -1.5 need DEXA every 5 years
People with T score -1.5 to -2.0 need DEXA every 3-5 years
People with T score <-2.0 need DEXA every 1-2 years
Osteoporosis
DIFFERENTIAL DIAGNOSIS
Osteomalacia
Myeloma
Metastatic bone disease
TREATMENT
Diet: adequate in protein, total calories, calcium, vitamin D
Reduce/discontinue use of corticosteroids
Smoking cessation
Reduce/stop alcohol consumption
Increase exercise
Fall prevention: adequate home lighting, handrails on stairs, handhold in bathrooms, use of can or walker, PT/OT
Discontinue medications causing dizziness, orthostasis, or hypotension
Pharmacologic treatment indicated for T score below -2.5 & for all patient with fragility fractures
Prophylactic medication treatment for T score -2.0 and -2.5
Vitamin D and calcium: recommend vitamin D intake of 600-800 units/day, 1000mg/day of calcium for all adults and 1200mg/day for postmenopausal women
Bisphosphates for patients with pathological spine fracture or low impact hip fracture and those with osteoporosis (DEXA T score of -2.5 or less)
Fosamax, Binosto, Actonel, Boniva
If cannot tolerate oral bisphosphonates IV bisphosphonates are indicated: Aredia, Zometa, Reclast
Denosumab-(monoclonal antibody ) increases bone mineral density by inhibiting the proliferation and maturation of pre osteoblasts into mature osteoclast bone-resorbing cells
Forteo, parathar-stimulate production of new collagenous bone matrix. When administered in 20mcg/day SC for 2 years, it was found to improve bone density particularly in distal radius
Consult orthopedic or neurosurgery- for vertebroplasty or kyphoplasty if patient has vertebral compression fracture and have failed conservative pain management
Sex hormones- can prevent osteoporosis but not effective therapy for diagnosis of osteoporosis
Selective estrogen receptor modulators (SERMs)- can prevent but not treat established diagnosis of osteoporosis.
Raloxifene
Bazedoxifene
Calcitonin- less effective but helps reduce pain of acute compression fractures, ineffective for chronic pain
SIDE EFFECTS OF BISPHOSPHONATES
Fever, chills, flushing, musculoskeletal pain, nausea, vomiting, diarrhea, fatigue, dyspnea, edema, headache, dizziness, ocular inflammation
IV bisphosphonates have caused seizure
Symptoms are usually transient, lasting a few days but resolving
If have a severe acute response they can receive corticosteroids and ondansetron before any other IV infusion
COMPLICATION OF BISPHOSPHONATES
Osteonecrosis of the jaw: particularly after tooth removal
Atypical low-impact “chalkstick” fractures of the femoral shaft
21 foods that may help with osteoporosis, blueberries, oranges, broccoli, cabbage, feta cheese, fish oil, apples, bananas, kiwis, spinach, watercress, salmon, pumpkin seeds, grapes, strawberries, kale, sardines, sunflower, seeds, papayas, walnuts, spurulina
OSTEOMYELITIS
Osteomyelitis is an infection of bone.
It is often difficult to diagnosis. Over 50% of cases are due to Staph Aureus.
Osteomyelitis can be the result of direct exposure from open fracture, the result of surgery, contiguous focus of infection, open wounds, or hematogenous spread.
The long bones and vertebrae are the most common sites of infection.
Complication: Epidural abscess. Abscess should be considered if fever, severe back/neck pain, radiculapothy, or signs of spinal cord compression (incontinence, weakness, pathologic extremity reflexes).
Osteomyelitis
SIGNS AND SYMPTOMS
Fever
Chills
Pain
Sensory loss
Motor loss
Malaise
Anorexia
Night sweats
Draining sinus tracts
