osteo, fractures, & gout Flashcards
T scores
-1 or greater → normal → normal bone mineral density
between -1 and -2.5 → low bone mass → osteopenia
less than or equal -2.5 → “porous bone” → osteoporosis
less than or equal -2.5 with a hx of a fragility fx → severe osteoporosis
how do we measure bone mineral density
DEXA scan
results reported with T-score
osteoporosis risk factors
aging female caucasian & asian hx fracture as an adult family hx low body weight (<127 lbs) smoking alcohol corticosteroids & immune suppressive drugs
other risk factors for osteoporosis
thin and small frame lack of weight bearing exercises lack of Ca and vit d eating disorders, gastric bypass surgery lack of estrogen/testosterone excess caffeine
FRAX
prediction tool for assessing individual risk of fx
used to provide treatment guidelines
can use dexa scan or other methods
3 common fxs caused by osteoporosis
hip
wrist
vertebrae: compression fx
50% of all women greater than 50 years old will have a fx in one of these in their lifetime
hip fracture complications
death after a fall (d/t complications r/t immobility)
lifetime risk: 18% women, 6% men
women experience 3/4 of all hip fxs
mortality rate 12-37%
osteoporotic hip fxs are specifically linked to an ↑ risk of mortality
clinical presentation of hip fx
sudden onset of hip pain before or after fall inability to walk severe groin pain tenderness affected leg is externally rotated affected extremity is shortened typically no bruising
complications of hip fx
infection: UTI’s, PNA
venous thromboembolism
osteoporosis primary prevention
calcium (1200-2000mg daily post-menopausal)
vit d (800-1000IU daily)
exercise at least 30 min/3x week
osteoporosis treatment
promote bone formation
decrease bone resorption
bisphosphonates
1st line treatment for prevention and treatment of osteoporosis
alendronate
moa
binds permanently to surfaces of bones
inhibits osteoclasts
↓ fxs by 50% for men & women
bishphosphonate
bisphosphonate
SE
GI most common: N/D, discomfort
risk of esophageal ulceration: don’t lie down after taking
bisphosphonate
alendronate
nursing implications
- take with water
- don’t lie down for 30 min after taking
- no food, drink, calcium or vitamins for 2 hrs (only 1% bioavailable
- drug holiday - after 5 years take a break to ↓ risk of jaw necrosis & esophageal cancer
raloxifene
selective estrogen receptor modulator (SERMs)
raloxifene
moa
mimics estrogen
inhibits bone resorption (not as well as bisphosphonates)
it is NOT hormone replacement therapy
only used in post-menopausal women to prevent & treat osteoporosis
SERMs
SE and nursing implications
hot flashes, leg cramps
important to take adequate calcium & vit d
d/c at least 72 hrs before and during prolonged immobilization
no tobacco or alcohol
teratogenic
black box - stroke
calcitonin-salmon
class & moa
hormone: bone resorption inhibitor (parathyroid agent)
inhibits bone removal by osteoclasts
not a 1st line drug, not used long-term
calcitonin-salmon
uses & effects
routes
treatment only
↓spinal fxs by 30% only (have to take 5 yrs to see benefit)
slows down bone loss
increases spinal bone density
may have an analgesic effect in pt that have acute, painful vertebral fxs
SQ, IM, nasal - can cause nasal irritation
causes of fractures
traumatic
fatigue - bone subjected to repeated, prolonged stress
pathologic - weakened bone, may break spontaneously, highest risk pop. is the elderly
describing a fracture
- name of bone
- location on bone
- orientation of fx
- alignment of fx (displaced v aligned)
- condition of overlying tissue (closed v. open)
fracture orientation
- transverse (90 degree to length of bone)
- spiral
- longitudinal (along length)
- oblique (diagonal)
- comminuted (> 1 fx line & more than 2 fragments)
- impacted (jumping from heights, crushing)
- greenstick (bends, doesn’t completely break, common in children)
- stress
- avulsion (fx of patella)
clinical manifestations of fractures
P.E.D.
Paid
Edema
Deformity
delayed healing
- delayed union
bone pain & tenderness ↑ 3 months - 1 yr after fx
risk factors - smoking, malnutrition - malunion
improper alignment - maybe began wt bearing too soon - nonunion
no healing 4-6 months post-fx
causes: poor blood supply, repetitive stress
compartment syndrome
increased pressure within limited anatomic space
manifestations: extreme pain, often very rapid onset, assess 5 P’s (paresthesia, paralysis, pulselessness, pain, pallor)
fat embolism
fat molecule in lung following long bone fx, major trauma
typically occurs 24-48 hrs after injury
triad of manifestations:
hypoxemia
altered LOC
petechiae - often last sx
no treatment - provide supportive care
osteomyelitis
acute or chronic pyogenic (pus producing) infection of the bone
Staph aureus usual cause
Peds- long bones
adults - vertebrae, hips
risk factors for osteomyelitis
recent trauma diabetes - ↓ immune response hemodialysis IV drug use splenectomy PVD
DM & PVD → ↑ risk for chronic osteomyelitis
2 routes of contamination that cause osteomyelitis
direct - open wound, gunshot, puncture, etc.
hematogenous (direct) - from bloodstream (most common)
usually occurs in long bones
children < 16 y.o. at highest risk
clinical manifestations of osteomyelitis
Local local tenderness, warmth, redness wound drainage restricted movement spontaneous fx
Systemic
spiking fevers
positive blood cultures
↑ WBCs
Tx of osteomyelitis
Broad spectrum
nafcillin
cefazolin
vanco
bacteria specific once C&S comes back
often IV therapy 4-6 weeks then transfer to PO
sources of purine
alcohol - specifically beer
organ meat (liver)
red meat
seafood, shellfish, sardines, scallops
waste product of purine metabolism
uric acid
gout predisposing factors
male genetics diet obesity diuretic therapy and kidney insufficiency
gouty arthritis patho
elevated uric acid levels → uric acid accumulates in body fluids → formation of uric crystals → deposition in or around joints → inflammation → gouty arthritis
often big toe affected
gouty arthritis manifestations
Pain
- intense
- great toe
- early morning → peaks 24-48 hrs → 5-10 days for flare up to resolve
Inflammation
- edema
- tenderness
- redness
Fever
Malaise
Complications of gout
urate kidney stones
pharmacotherapy for gout
ACUTE
- NSAIDS
- steroids - only if pt can’t tolerate NSAIDs or is not responding to them
- colchicine - acute and prophylactic
PROPHYLACTIC
- allopurinol
- colchicine
- probenecid
allopurinol
inhibits production of uric acid (xanthine oxidase inhibitor which ↓ uric acid synthesis)
prophylactic only
AE: rash, typically well tolerated
nursing implications with allopurinol
if gi upset, take with food or milk
monitor serum/urine uric acid
monitor serum glucose (may cause hypoglycemia)
monitor PT/INR of pts on warfarin
improve 2-6 weeks
colchicine
anti-inflammatory, anti-gout
mostly unknown, inhibits leukocyte infiltration (disrupts cell division)
gout flares & prophylaxis
colchicine
SE & nursing implications
GI effects → stop drug immediately (1st sign of toxicity)
PO
contra: renal disease
Teach pt to avoid: they all inhibit breakdown of drug
- ETOH
- grapefruit
- B12 vitamins
substrate of CYP450 system
check for other drugs that could interact
probenecid
uricosuric agent
inhibits reabsorption of uric acid in the kidneys, promoting excretion
treats hyperuricemia with gout
used alone or in combo with allopurinol when not effective alone
probenecid
SE & nursing implications
GI upset - take with food, drink plenty of fluids
dizziness, HA
kidney/liver impairment - report hematuria, changes in urine output, wt gain/urine retention, jaundice, clay color stools
lots of drug interactions
