Osteoporosis Flashcards

1
Q

What are two cardinal changes of osteoporosis?

A

Low BMD

Micro-architectural disruption– “bone quality”

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2
Q

What are the rates of osteoporosis in women? In men?

Are certain racial groups more susceptible?

A

1 in 2 women
1 in 5 men

More common in caucasian/asian ancestry

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3
Q

Which fractures are most common? How do they present?

A

Vertebral fractures– 2/3 are asymptomatic

Chronic pain, deformity and increase in morbidity and mortality can result

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4
Q

Which fracture is most concerning? What are mortality rates during first year?

A

Hip fractures are most serious

Mortality rates during first year:
30% in men
17% in women

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5
Q

What are the two main causes of low bone density?

A

Low peak bone mass “Modeling”

Excess bone loss later in life “remodeling” (i.e due to loss of estrogen in postmenopausal women)

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6
Q

What are primary causes of osteoporosis? Secondary causes? (list)

A

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

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7
Q

Diagnosis of osteoporosis: DXA scan

What sites are used? What measurements are used, and for which populations?

A

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.

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8
Q

What are parameters for normal, low bone mass and osteoporosis on DXA scan?

A

Normal: T>-1
Low bone mass (osteopenia): T between -1 and -2.5
Osteoporosis: T

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9
Q

What is severe/established osteoporosis?

A

Patients with T

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10
Q

Interpretation of T-score in DXA scan– which areas do you use? Which value do you use– total or lowest observed?

A

Femoral neck and lumbar spine

Use lowest observed T-score

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11
Q

Who should be screened for osteoporosis?

Difference for clinical risk factors?

A

No clinical risk factor: Women>65, men>70

Risk factors: Younger postmenopausal women, men between 50 and 69

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12
Q

A decrease in one SD in BMD is associated with what increase in fracture risk?

A

The fracture risk doubles with every SD decrease in BMD

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13
Q

What are risk factors for osteoporosis that are considered in fracture risk assessment tool (FRAX)? (8)

A

Age, low BMI, previous facture, family history of hip fracture, current smoking, alcohol, glucocorticoids, secondary cause of osteoporosis (i.e RA)

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14
Q

What probabilities does FRAX give? Which values are high enough to warrant treatment?

A

FRAX measures risk for osteoporotic fracture and for hip fracture

Treat puts with
>20% for all osteoporotic fracture
>3% for hip fracture

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15
Q

In general what is criteria for treatment?

A

Postmenopausal women, men>50

T-score 20% osteoporotic fracture, >3% hip fracture

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16
Q

What is the mnemonic for non-pharmacological osteoporosis treatment?

A

CDEFGs

Calcium, vitamin D, exercise, prevent falls, good nutrition, smoking cessation

17
Q

What pharmacological treatments are available for osteoporosis?

A

BCDE & T
Bisphosphonates, calcitonin, denosumab, estrogen/SERM

Teriparatide (rPTH)

18
Q

How do BCDE pharmacological treatments for osteoporosis work?
AKA what is its MOA

A

Prevent RANKL binding to RANK.

This prevents differentiation to osteoclasts– no bone resorption

19
Q

What is first line therapy for osteoporosis?

A

Bisphosphonates

20
Q

What is effect of bisphophonates on osteoclasts?

A

Inhibits osteoclast activity

Promotes osteoclast death

21
Q

What are the AE for bisphosphonat?
Short term (3)
Long-term (2)

A

Short term: GI (difficulty swallowing, inflammation of esophagus, gastric ulcers), increase in creatinine, flu-like illness

Long term: Atypical femur fracture, osteonecrosis of jaw

22
Q

What is denosumab? What is its MOA

A

A human monoclonal antibody that inhibits RANKL (like OPG)

23
Q

Why is denosumab good for patients with renal problems?

A

It is NOT renally excreted

24
Q

What are AE of denosumab? (3)

A

Hypocalcemia, infections, skin rxns

25
Q

When do you prescribe tripartite/forteo?

A

Moderate-severe osteoporosis as a second line therapy

26
Q

What is MOA of teriparatide?

A

Increase osteoblast activity

27
Q

What is problem with teriparatide? How do you fix this?

A

Also stimulates RANKL–>Increased osteoclast differentiation and increased bone resorption

Also prescribe denosumab or bisphosphonates

28
Q

What are AE for teriparatide? (

A

Nausea, headaches, leg cramps, hypercalcemia, orthostatic hypotension, palpitations
Osteosarcoma
CI: paget’s disease, hypercalcemia, history of osteosarcoma

29
Q

What is calcitonin? What is MOA?

A

Third line therapy for osteoporosis

Works by inhibiting osteoclast activity

30
Q

What are AE for calcitonin? (5)

What are CI? (2)

A

Nausea, vomiting, injection site rxn, flushing, rhinitis

CI: hypertensive or hypocalcemic

31
Q

Why use estrogen or raloxifen?

A

Prevention/treatment of osteoporosis

32
Q

What are AE of estrogen/raloxifen? (5)

A

Headache, hot flashes, flushing, leg cramps, VTE

33
Q

What are CI for estrogen/raloxifen? (2)

A

history of VTE, women of childbearing age