Osteoporosis Flashcards
What are two cardinal changes of osteoporosis?
Low BMD
Micro-architectural disruption– “bone quality”
What are the rates of osteoporosis in women? In men?
Are certain racial groups more susceptible?
1 in 2 women
1 in 5 men
More common in caucasian/asian ancestry
Which fractures are most common? How do they present?
Vertebral fractures– 2/3 are asymptomatic
Chronic pain, deformity and increase in morbidity and mortality can result
Which fracture is most concerning? What are mortality rates during first year?
Hip fractures are most serious
Mortality rates during first year:
30% in men
17% in women
What are the two main causes of low bone density?
Low peak bone mass “Modeling”
Excess bone loss later in life “remodeling” (i.e due to loss of estrogen in postmenopausal women)
What are primary causes of osteoporosis? Secondary causes? (list)
No known cause in postmenopausal women/aging men
Secondary osteoporosis causes include glucocorticoids or genetic diseases, lifestyle factors, endocrine disorders, GI disorders, hematological disorders, other medications, rheumatological disorders
Diagnosis of osteoporosis: DXA scan
What sites are used? What measurements are used, and for which populations?
Total hip, femoral neck, lumbar spine, forearm (if hyperparathyroidism, hip replacement pts)
T-score used for diagnosis– compares to normal young adult control
Z-score used to predict propensity for developing osteoporsis–compares to age/race/gender-matched controls.
What are parameters for normal, low bone mass and osteoporosis on DXA scan?
Normal: T>-1
Low bone mass (osteopenia): T between -1 and -2.5
Osteoporosis: T
What is severe/established osteoporosis?
Patients with T
Interpretation of T-score in DXA scan– which areas do you use? Which value do you use– total or lowest observed?
Femoral neck and lumbar spine
Use lowest observed T-score
Who should be screened for osteoporosis?
Difference for clinical risk factors?
No clinical risk factor: Women>65, men>70
Risk factors: Younger postmenopausal women, men between 50 and 69
A decrease in one SD in BMD is associated with what increase in fracture risk?
The fracture risk doubles with every SD decrease in BMD
What are risk factors for osteoporosis that are considered in fracture risk assessment tool (FRAX)? (8)
Age, low BMI, previous facture, family history of hip fracture, current smoking, alcohol, glucocorticoids, secondary cause of osteoporosis (i.e RA)
What probabilities does FRAX give? Which values are high enough to warrant treatment?
FRAX measures risk for osteoporotic fracture and for hip fracture
Treat puts with
>20% for all osteoporotic fracture
>3% for hip fracture
In general what is criteria for treatment?
Postmenopausal women, men>50
T-score 20% osteoporotic fracture, >3% hip fracture
What is the mnemonic for non-pharmacological osteoporosis treatment?
CDEFGs
Calcium, vitamin D, exercise, prevent falls, good nutrition, smoking cessation
What pharmacological treatments are available for osteoporosis?
BCDE & T
Bisphosphonates, calcitonin, denosumab, estrogen/SERM
Teriparatide (rPTH)
How do BCDE pharmacological treatments for osteoporosis work?
AKA what is its MOA
Prevent RANKL binding to RANK.
This prevents differentiation to osteoclasts– no bone resorption
What is first line therapy for osteoporosis?
Bisphosphonates
What is effect of bisphophonates on osteoclasts?
Inhibits osteoclast activity
Promotes osteoclast death
What are the AE for bisphosphonat?
Short term (3)
Long-term (2)
Short term: GI (difficulty swallowing, inflammation of esophagus, gastric ulcers), increase in creatinine, flu-like illness
Long term: Atypical femur fracture, osteonecrosis of jaw
What is denosumab? What is its MOA
A human monoclonal antibody that inhibits RANKL (like OPG)
Why is denosumab good for patients with renal problems?
It is NOT renally excreted
What are AE of denosumab? (3)
Hypocalcemia, infections, skin rxns
When do you prescribe tripartite/forteo?
Moderate-severe osteoporosis as a second line therapy
What is MOA of teriparatide?
Increase osteoblast activity
What is problem with teriparatide? How do you fix this?
Also stimulates RANKL–>Increased osteoclast differentiation and increased bone resorption
Also prescribe denosumab or bisphosphonates
What are AE for teriparatide? (
Nausea, headaches, leg cramps, hypercalcemia, orthostatic hypotension, palpitations
Osteosarcoma
CI: paget’s disease, hypercalcemia, history of osteosarcoma
What is calcitonin? What is MOA?
Third line therapy for osteoporosis
Works by inhibiting osteoclast activity
What are AE for calcitonin? (5)
What are CI? (2)
Nausea, vomiting, injection site rxn, flushing, rhinitis
CI: hypertensive or hypocalcemic
Why use estrogen or raloxifen?
Prevention/treatment of osteoporosis
What are AE of estrogen/raloxifen? (5)
Headache, hot flashes, flushing, leg cramps, VTE
What are CI for estrogen/raloxifen? (2)
history of VTE, women of childbearing age
