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Med School > Osteoporosis > Flashcards

Osteoporosis Flashcards

1
Q

Which component of bone comprises the majority of skeletal mass? Which component of bone has a higher turnover rate?

A
  • cortical bone (80% of bone mass)
  • trabecular bone has a higher turnover rate - markers are matrix proteins
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2
Q

When is peak bone mass achieved?
Describe the decline in bone mass.

A
  • Around 20 in white women, plateaus and then decreases around 40-50
  • Femoral neck is 18.5
  • Spine is 23
  • decreases 0.5-1% from peak, then 1-2% around menopause, then back to 0.5-1%
  • men have a more flat and slower rate of change
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3
Q

What are some factors causing bone loss? Medications?

A
  • cigarettes, alcohol, physical inactivity
  • prednisone (corticosteroids), glucocorticoids, anticonvulsants, anticoagulants, androgen deprivation (medroxyprogesterone)
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4
Q

What are three ways we assess bone quality?

A
  1. High-Res Peripheral Quantitative CT –> distal radius and tibia CT
  2. Trabecular Bone Scan –> pixels to estimate microarchitecture, images of trabecular bone in spine
  3. Bone Microindentation Testing –> 1mm probe to anterior tibia measures strength while cycling
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5
Q

What are outcome measurements of TBS?

A

1.35+ (normal)
1.2-1.35 (partially degraded)
under 1.2 (degraded)

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6
Q

Definition of Osteoporosis

A
  • low bone mass and micro architectural deterioration leading to bone fragility and susceptibility to fracture
  • low BMD is a result of low peak bone mass and increased bone loss
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7
Q

How do we assess bone quantity? Outcome scores?

A
  • Normal X-ray
  • Dual energy x-ray absorptiometry (DXA) –> special scanners

-1 or above (normal)
-1 to -2.5 (osteopenia)
- 2.5 and lower (osteoporosis)
- 2.5 and lower plus fracture (severe osteoporosis)

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8
Q

When should someone receive treatment for osteoporosis?

A
  • hip or vertebral fracture
  • 2+ falls in last year
  • T score under -2.5 after excluding secondary causes
  • low BMD between -1 to -2.5
  • 10 year probability of hip fracture over 3%
  • 10 year probability of any fracture over 20%

If someone is low risk –> lifestyle changes
If someone is mod/high risk –> medications

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9
Q

CAROC
- When would you increase someone to the next risk category?
- When would someone be automatically high risk? Moderate risk?

A
  • femoral neck T-score on y axis, age on the x axis (different graph for men vs women)
  • calculates 10 year absolute fracture risk (uses lowest T-score)
  • Increase to next category if –> prior fragility fracture over 40 or prolonged corticosteroid use
  • Med risk if lumbar/hip T score is under -2.5
  • High risk if prior hip or vertebral fracture or 1+ non-vertebral fragile fracture

*EASIER FOR RADIOLOGISTS, HOW 10Y FRACTURE RISK IS CURRENTLY REPORTED IN CANADA

low risk –> 10% (year fracture risk)
moderate –> 10-20%
high –> 20%

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10
Q

FRAX

A
  • estimates fracture risk, determine if patient needs treatment
  • takes into consideration age, sex, height, weight, previous fracture, family history, smoking, RA, glucocorticoids, alcohol
  • does not require a BMD but can include femoral neck T-score
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11
Q

Resporption vs formation time

A
  • resorption is fast (~3 weeks)
  • formation is slow (3-4 months) and mineralization can take years in cancellous bone
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12
Q

How do osteoclasts respond to calcitonin? What do clasts dissolve?

A
  • Calcitonin inhibits clasts –> their pseudopodia will retract. They dissolve type I collagen.
  • Calcitonin can be given to reduce risk of vertebral fractures in post-menopausal women.
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13
Q

What stimulates/ inhibits osteoblasts?

A

Stimulates –> testosterone and progesterone
Inhibits –> cortisol

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14
Q

What is periosteal apposition?

A
  • external cortical diameter increases but the cortical thickness decreases due to endosteal resorption
  • increases with age and exercise
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15
Q

What are some genetic conditions that can affect bone?

A
  • osteogenesis imperfecta
  • hypophosphatasia
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16
Q

What hormones decrease resorption and increase formation? (Overall formation of bone)

A
  • Estrogen in M/F and testosterone in M inhibit resorption
  • Progesterone in F and testosterone in M promote formation
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17
Q

What hormones increase resorption and inhibit formation? (Overall loss of bone)

A
  • Excess cortisol (stress), and an acute drop in estrogen and testosterone increases resorption (women on aromatase inhibitors for BC are at risk)
  • Excess cortisol (stress) inhibits formation
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18
Q

How does starting OCPs affect peak bone mass?

A
  • OCPs increase ethinyl estradiol, this suppresses modelling leading to a decrease in peak bone mass.
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19
Q

How is bone resorption affected by menstruation?

A

-Drop in estrogen during mid-cycle peak and rapid increase in progesterone (acute drop of estrogen promotes resorption) –> thus bone resorption is slightly increased and you are more at risk for fracture
- ovulatory disturbances can also cause a drop in progesterone (no formation to counter resorption)

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20
Q

Distribution of serum calcium? What factors can affect serum Ca?

A
  • 45% bound to albumin
  • 40% in free ionized active form
  • 15% bound to phosphate/citrate anions
  • serum Ca can be altered by hypoalbuminemia and pH
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21
Q

Where is the majority of calcium found in the body? What regulates calcium?

A
  • 99.9% in bone
  • regulated by diet, kidney (excretes 100-400mg/day), PTH, and calcitriol
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22
Q

Role of Calcitonin wrt Calcium? Where is it produced?

A
  • Calcitonin is made by the parafollicular cells of the thyroid
  • Decreases serum Ca, minor control of calcium
  • Protects the skeleton in pregnancy/lactation, helps restrict post-prandial hypercalcemia
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23
Q

Role of calcitriol (1,25-dihydroxy-vitamin D)? Where is it produced?

A
  • Increases absorption of dietary calcium and phosphorus (increases serum calcium)
  • Made by the kidney
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24
Q

Role of PTH wrt bone and kidney?

A
  • Kidney –> Calcium resorption, phosphate excretion, renal conversion of 25-OH Vitamin D to calcitriol
  • Bone –> increases resorption IF SUSTAINED, increases formation IF NORMAL EPISODIC RELEASE
    (increases serum calcium when given exogenously)
25
Q

Different causes of hypercalcemia? Signs of each?

A
  • Malignancy (decreased or normal PTH)
    • higher/more rapid increase in serum Ca, more sx
  • Primary hyperparathyroidism (increased PTH)
    • longstanding asymptomatic/mild, postmenopausal,
      normal physical exam, family history
26
Q

Symptoms of mild/longstanding/ acute hypercalcemia?

A

Mild –> constipation, fatigue, depression
Longstanding –> renal stones, polyuria/dipsia, osteoporosis, fractures, bone pain, anorexia, GI pain, depression
Acute –> stupor, coma, short QT

27
Q

Treatment of mild/ moderate/ severe hypercalcemia?

A

Mild (under 3) –> hydration, avoid lithium/ dietary/ thiazide diuretics

Moderate (3-3.5) –> see below

Severe (3.5+) –> IV saline, calcitonin, bisphosphontaes (Zolendronic Acid)

28
Q

Different causes of hypocalcemia?

A

If decreased PTH –> surgical, autoimmune, congenital, destruction or infiltration

If increased PTH –> vitamin D deficiency, sepsis, pancreatitis, CKD, hemorrhage, post-surgery

29
Q

Symptoms of acute vs chronic hypocalcemia?

A

Acute –> tetany, seizures, ventricular arrhythmia, long QT
Chronic –> dental, cataracts, Parkinsons

30
Q

Treatment of mild/chronic vs acute/severe hypocalcemia?

A

Mild/chronic –> oral calcium and vitamin D, treat cause
Severe/ acute –> rapid IV correction

31
Q

Why should you always check magnesium when hypocalcemic?

A
  • low Mg levels can decrease PTH
  • causes of low MG include malabsorption, diarrhea, alcoholism and malnutrition
32
Q

Sources of vitamin D? Recommend Vitamin D dose?

A
  • Sunlight
  • Cod liver oil, salmon, mushrooms, fortified milk, plant beverages, egg yolk
  • Higher incidence of vitamin D deficiency in darker skins
  • 600-1000 IUD (over 800 if 50+)
33
Q

Signs of vitamin D deficiency/ insufficiency? Associated comorbidities? Who is at risk for Vitamin D deficiency?

A

Deficiency –> rickets, osteomalacia, proximal myopathy
Insufficiency –> bone loss, falls, decreased BMD, fractures

  • cancer, RA, MS, T1DM, TB, glu, lung infections
  • at risk –> obese, malabsorption, institutionalized
34
Q

Recommended dietary calcium?

A

1000mg/day
1200mg/day if 70+ or a 50+ female

*do see increased BMD in female teens who ingested more calcium and milk
*giving too much results in renal stones, NOT linked to CV disease
*calcium or vitamin D are not sufficient treatment for osteoporosis

35
Q

What is sarcopenia? Myostatin?

A
  • decreased skeletal muscle and quality functioning with age –> decreased bone mass and more fractures
  • influenced by exercise, nutrition, immune/endocrine, genes
  • Myostatin results in poor muscle development, and thus we have developed an Ab against it
36
Q

What is a fragility fracture?

A
  • occurs spontaneously or from a minor trauma (fall from standing, sitting, supine, atypical movement, missed 1-3 steps)
  • FRAGILITY FRACTURE = OSTEOPOROSIS REGARDLESS OF BMD
37
Q

Risk factors for fracture?
Comorbidities?

A
  • 65+, fragility fracture, family history, 3+ months on glucocorticoids, malabsorption (Celiac’s, Crohn’s), primary hyperparathyroidism, hypogonadism, early menopause, RA, under 60kg, alcohol, smoking
  • COPD, T2DM, IBD, Celiac’s, RA
38
Q

What tests should you order when looking at osteoporosis?

A
  • Ca, CBC, creatinine, ALP, TSH, Spep (multiple myeloma), 25(OH) Vit D
39
Q

Which osteoporosis drugs are antiresorptives? How do they work?

A
  • bisphosphonates
  • denosumab
  • raloxifene
  • HRT (estrogen)
  • target clasts, decrease remodelling
40
Q

Which osteoporosis drugs are anabolics? How do they work?

A
  • teriparatide
  • romosozumab
  • target blasts, increase remodelling
41
Q

How do bisphosphonates work? Side effects?

A
  • inhibit clasts at the bone surface
  • i.e. alen/risen/zole/etidronate
  • can be either oral or IV
  • GI (need to take on an empty stomach following 2h fast, no food for 30-60m), hypocalcemia (IV), flu-like sx
  • Osteonecrosis of the jaw
  • Esophageal cancer
  • Potentially atypical femoral fracture if prolonged use
42
Q

How does denosumab work? Side effects?

A
  • binds RANK-L which prevents binding to RANK, thus inhibiting clast formation/function/survival
  • more potent than bisphosphonates
  • given subcutaneously every 6 months, expensive
  • eczema, cellulitis, flatulence, hypocalcemia, ONJ and atypical fractures of femur
  • if discontinued, can lead to decreased BMD and increased fractures
43
Q

How does teriparatide work? Side effects? Main indication? Contraindications?

A
  • PTH analog given INTERMITTENTLY –> increases ca reabsorption, increases blasts (because given intermittently), increases vitamin D
  • injection, expensive
  • dizziness, orthostatic hypotension, leg cramps, mild hypercalcemia
  • mainly indicated for glucocorticoid osteoporosis
  • cannot use for hip fractures
  • hypercalcemia, major renal impairment, hyperparathyroidism, Paget’s, radiation, malignancies, pregnancy, nursing, youth with open epiphyses
44
Q

How does romosozumab work? Side effects? Main indication?

A
  • inhibits sclerostin released from osteocytes
  • injection, expensive
  • MI, stroke, CV death (avoid if any of these in last year)
  • main indication is normal osteoporosis
45
Q

How does raloxifene work?

A
  • selective estrogen receptor modulators
  • 1st line for vertebral fractures
  • decreases risk of breast cancer in ER+ women
46
Q

When would you give HRT?

A
  • only give if significant symptoms of menopause and NO history of CHD/ stroke
  • increases risk for CHD/ stroke/ VTE/ breast cancer
47
Q

How do you monitor treatment effectiveness? Should you stop treatment for people at high risk for fracture?

A
  • look at BMD - DXA every 1-3 years for new or moderate risk
  • if someone is at high risk do not stop therapy, benefits outweigh any risks
48
Q

Which drugs (especially in poly pharmacy) increase the risk of falls?

A
  • antihypertensives
  • anticholinergics
  • pain medications (i.e. morphine)
49
Q

What is likely cause of fall if:
- preceded by LOC?
- preceded by dizziness?

A

LOC –> seizure, stokes-dams attack, get an ECG and cardiac workup
Dizziness –> change of posture –> orthostatic
–> spinning –> being positional vertigo
–> unsteady –> dizziness of legs, check gait
–> decreased vision/ hearing/ near –> astronaut

50
Q

Which order of drugs may be beneficial in severe osteoporosis?

A
  • anabolics followed by antiresorptives
  • build up more bone and earlier fracture prevention
51
Q

Osteoporosis in Men

A
  • same risk factors as women
  • higher rates of fracture related mortality
    #1 primary, #2 glucocorticoids, #3 hypogonadism, #4 excessive alcohol intake, #5 anticonvulsants
52
Q

BMD in different ethnicities

A
  • blacks have increased BMD, and Mexicans compared to whites
53
Q

Effect of androgens on bone? Should we test it often? How?

A
  • helps periosteal bone formation, larger peak bone mass in men
  • if deficient –> less bone formation/ vertebral width/ femoral neck width (i.e. could happen with androgen deprivation therapy)
  • No data showing replacement leads to less fractures
  • 8am bioavailable testosterone
54
Q

Which is the only drug not recommended for male osteoporosis?

A

Calcitonin, which is only prescribed for Paget’s

55
Q

What drug is the only treatment for male and female hormone inhibition?

A

Denosumab

56
Q

Glucocorticoid effect on bone

A
  • stimulate clasts by increasing PTH, and inhibit blasts and cytes
  • get a FRAX within 6 months if over 40 and on GCs
  • Most common secondary cause of OP! See initial rapid loss w early fractures, trabecular bone affected first, fractures occur at higher BMD than normal
57
Q

What to do following GC discontinuation? Which drugs can you not use for GC osteoporosis?

A
  • can discontinue bisphosphonate/ transition denosumab to BP, etc. as long as fracture risk is low
  • Romosozumab and calcitonin
58
Q

Which drugs should never get a drug holiday?
What to do once stopping a BP?

A
  • HRT, raloxifene, denosumab
  • reassess BMD after 1-3 years based on which drug

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