Osteoporosis Flashcards
Skeletal disease defined by compromised bone strength, increased risk of fracture
Osteoporosis
Increased bone resorption and decreased bone formation causes
Osteoporosis
These are the four phases of bone activity
Quiescent phase
Resorption phase
Formation phase
Quiescent phase after remodeling
Measures areal bone mineral density in gm/cm2, compares patient’s BMD to normative data
Duel-energy X-ray absorptiometry (DXA)
BMD score 0 to -1
normal
SERM medication, binds estrogen receptor
Raloxifene
Alendronate
Risendronate
Ibandronate
Zoledronic Acid
Bisphosphonates
BMD score of -2.5
osteoporosis
Hormones for osteoporosis
Calcitonin, Estrogen
Standard deviation difference between patient’s BMD and mean BMD of age-matched reference population
Z-score
Agonist, antagonist properties depending on target organ
Raloxifene
BMD score -1 to -2.5
low bone density for age (“osteopenia”)
Associated with estrogen use
breast cancer, cardiovascular
Raloxifene is an estrogen ______ in bone
agonist
- -> inhibits osteoclasts
- -> improves BMD
- -> decreases fracture risk
May be used for Paget’s disease of the bone
Calcitonin
Standard deviation difference between patient’s BMD and mean BMD of young adult
T-score
Anabolic osteoporosis medication
teriparatide
Raloxifene is an estrogen ________ in breast tissue
antagonist
–> reduces risk of breast cancer
disrupts protein prenylation –> cytoskeletal abnormalities in osteoclast –> detachment from bone –> reduced bone resorption
Bisphosphonates
Induces differentiation and maturation of osteoblast precursors, increases preexisting osteoblast function, reduces osteoblast apoptosis: increases BMD and decreases fractures
teriparatide
Risk factors for fracture
Prior fragility fracture,
parental history of hip fracture, glucocorticoid therapy, excess OH intake (>3/day), rheumatoid arthritis, cigarette smoking
Menopause, Advanced Age, Familial predisposition
Primary causes of bone loss
Side effects of Raloxifene
DVT, hot flashes
Possible secondary causes of bone loss:
Medications (excess glucocorticoids) Renal disease Vitamin D, calcium deficiency Hyperparathyroidism Idiopathic hypercalciuria (renal wasting) Hyperthyroidism Premature menopause/hypogonadism Multiple myeloma Cushing's syndrome Malabsorption (IBD, celiac) or malnutrition (anorexia) Smoking/excess OH Inflammatory diseases (RA)
Impair osteoclast function, decrease differentiation, increase apoptosis –> increase BMD, decrease fracture
Bisphosphonates
Non-pharm treatment for osteoporosis
Used for all patients
Calcium (12-1500/day)
Vitamin D (800/day)
Action of bisphosphonates
Inhibit farnesyl pyrophosphate synthase enzyme in mevalonate pathway (cholesterol biosynthetic pathway)
Who to treat for osteoporosis
T score less than -2.5
Low trauma fracture
T score of -1 to -2.5 if other risk
Side effects include: esophagitis, flu-like symptoms, bone/muscle pain, hypocalcemia, atypical subtrochanteric fractures, osteonecrosis
Bisphosphonates
Biologic receptor activator of nuclear factor kappa-B ligand
Denosumab
Increases BMD, decreases fractures
Denosumab
Side effects include hypocalcemia, infections, concerns about neoplastic effects/subtrochanteric fractures/ONJ
Denosumab
Use this for post-menopausal women, men over 50
T-score (compare to young population)
Used for children, premenopausal women, men under 50
Z-score (compare to peers)
Antiresorptive drugs
SERMs, Bisphosphonates, Biologic, Hormones
Antiresorptives work by
Inhibiting osteoclasts, reestablish balance between osteoclasts/osteoblasts, stop bone loss (do not gain bone density)
Neutral effect on cardiovascular system, endometrium
Raloxifene
Avoid these if patient has upper GI disease, Barret’s esophagus
Bisphosphonate oral drugs
May have some effect on acute pain control
Calcitonin
Where is the DXA scan measuring bone density?
hip, lumbar spine
