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PR3154 MSK IC1,10-18 > IC18 Osteoporosis > Flashcards

IC18 Osteoporosis Flashcards

1
Q

What is osteoporosis? What is a possible patho?

A
  • Porous bone, weak and brittle bones
  • ↓bone mass:
    o Excess bone resorption
    o ↓bone formation

Patho:

  • When there is ↓vit D levels → ↓Ca plasma levels → ↑Parathyroid hormone (PTH) → ↓Renal excretion of Ca + ↑resorption of bones to release Ca into blood
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2
Q

What are the possible causes of OP? (8)
What are the 2 major pt groups at risk of OP?

A

Causes:

  1. Age (>65y/o)
  2. Menopause → ↓oestrogen, weakens bone
  3. Alcohol
    a. ↑RANKL → ↑osteoclast
    b. ↑oxidative stress → ↓osteoblast
  4. Smoking
  5. ↓serum Ca
  6. Physical inactivity
  7. Medication e.g. corticosteroids, cyclosporine, PPI, cancer therapy
    a. Long term use of Steroids
    i. Interfere with replacement and rebuilding process of bone
    ii. Affect all 3 bone cell types – osteoblast, osteocytes, osteoclasts
    iii. Induces ↓in osteoblast differentiation + ↑apoptosis of osteoblasts and osteocytes
  8. Secondary to other diseases

RF:

  1. Postmenopausal women
  2. Men >65y/o
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3
Q

What are the S&S of OP? When will one found out that they have OP?

A
  1. Asymptomatic
  2. Fragility fracture (low trauma e.g. fall) → spine(height loss), hip, wrist
  3. Pain and disability
  4. If spine: Stooped posture, back pain
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4
Q

How to diagnose OP?
What is the T-score that shows OP?
What are the % that show you are at high risk of fractures?

A

Diagnosis:

  1. History of fragility fracture
  2. Do OSTA (osteoporosis self-assessment tool for asians)
  3. If high (>20) / medium (0-20) risk, then do DXA scan
  4. DXA hip/spine
    a. T-score compares own BMD to young adult ref population BMD
    i. T-score >-1: normal
    ii. T-score -2.4 to -1: osteopenia
    iii. T-score <=-2.5: osteoporosis
    b. Z-score compared own BMD with expected BMD for patient’s age and sex
    i. Z-score <-2: coexisting problem
  5. Exclude secondary causes → do labs, Hx, PE
  6. FRAX scan
    a. Start anti-osteoporotic treatment if major osteoporotic fracture risk >20% / hip fracture risk >3%
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5
Q

*When to treat/give meds for OP?

A

When to treat:

  1. Fragility fracture
  2. T-score <=-2.5: osteoporosis
  3. T-score -1 to -2.4: osteopenia + FRAX score shows high risk of fracture
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6
Q

What are the goals of treatment for OP?

A

Goals of treatment

  1. Prevent future fracture
  2. ↑QOL
  3. ↓economic burden
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7
Q

What is the general hierarchy in the choice of pharmacologics for OP for the 2 distinct pt groups?
What is 1st line for OP

A

Pharmacotherapy

  1. Postmenopausal women
    a. (1st line) PO Alendronate / risedronate
    b. IV zoledronic acid / SC Denosumab
    c. Raloxifene
    d. Teriparatide (ex)
  2. Men >65y/o
  3. (1st line) PO Alendronate / risedronate
  4. IV zoledronic acid / SC Denosumab
  5. Teriparatide
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8
Q

What do you have to check before giving meds for OP?

A

Monitoring:

Before starting the above therapy and during (about every 3 months),
1. Check SCr, Ca &25(OH) vit D levels
a. 25(OH) vit D levels: >20-30ng/mL (normal)
b. If not enough, then give Ca and vit D supplements

BMD every 1-2 years since bone takes very slow

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9
Q

What is the normal 25(OH) vit D levels?

A

25(OH) vit D levels: >20-30ng/mL and <50-100ng/mL (normal)

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10
Q

What are the non-pharmacological management for OP?

A

Non-pharmacological management

  1. Ca
  2. Vit D
  3. Exercise e.g. weight bearing (30mins/day), muscle strengthening, balance (2-3x/wk) → walking, elastic band exercises, tai chi
    a. ↑BMD & mass
  4. Smoking cessation
  5. ↓alcohol intake
  6. ↓risk of falls → med review (↓meds that causes drowsiness/falls), Home environment modification/footwear/impaired vision
  7. Nutrition (lack of nutrition e.g. anorexia, will have weaken bones since ↓bone density / gastro-surgery)
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11
Q

What is the min. Ca intake?
When should you give Ca supplements?
What are the DDI of Ca?
How to manage the DDI?
What food contain Ca?

A
  1. Ca intake (>50y/o: 1000mg/day)
    a. ADR: nephrolithiasis, constipation
    b. Give supplementation if dietary Ca intake is <700mg/day
    c. DDI:
    i. ↓Ca absorption: PPI, fibre
    ii. ↓ following drug’s absorption (Gaviscon have Ca): Fe, tetracyclines, fluoroquinolones, bisphosphonates, thyroid
    d. Management: space Ca & bisphosphonates 2 hrs apart → e.g. bisphosphonate taken 1/2hr before breakfast, then eat breakfast, then take Ca
    e. Food: milk, yoghurt orange juice
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12
Q

What is the amt of Vit D that should be given if it is below normal range?
What are the DDI with vit D?

A

Normal range: >20-30ng/mL

  1. Vit D intake (50-70y/o: 600IU/day; >70y/o: 800IU/day)
    a. Give 800IU/day cholecalciferol when vit D insufficient
    b. DDI: anticonvulsants (PHY< CBZ, VA), rifampicin, cholestyramine, orlistat (fats), aluminum-containing products
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13
Q

What is the dose and dosing interval of all your bisphosphonate?
What is the total duration?

A

Admin.:

  • For PO (cheapest):
    Alendronate: 70mg once weekly
    Risedronate: 35mg once weekly
    Risedronate: once monthly
  • For IV: 5mg once yearly as 30min infusion, if Ca/vit D def take Ca+ vit D before infusion

Duration:

  • 5years for PO
  • 3years for IV
    If high fracture risk (T-score<-3), then 10years PO, 6years IV
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14
Q

What is the MOA and place in therapy of bisphosphonates?

A
  • slow bone loss by ↑osteoclast cell death

Place in therapy:

  • PO are 1st line (mild-sev)
    → convenient, cheap, effective, acceptable ADR
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15
Q

What are the ADRs of bisphosphonates?

A

Common:
PO:
1) Nausea
2) abdominal pain
3) Diarrhea
4) Heartburn like sx
5) Sev bone, joint, muscle pain

IV:
6) Flu-like sx
7) Hypocalcemia
8) Fever, malaise, headache, musculoskeletal aches
9) Ocular effects

Rare:
9) Atypical femur fracture (prolong use)
- Stop bisphosphonates
10) Osteonecrosis of jaw/ear
RF: tooth extraction, cancer, radiotherapy, poor oral hygiene, other drugs e.g. steroids, denosumab
Advise: smoking cessation, good oral hygiene, avoid dental procedures

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16
Q

What are some counselling points when taking bisphosphonates?

A

For PO:
1) take at least 30mins before breakfast in the morning
2) A glass of plain water
3) Sit up and do NOT lie down for 30mins (to prevent acid reflux & irritation)

17
Q

*What are the CI of bisphosphonates? (5)

A

CI:
1) Hypocalcemia
2) esophagus abnormalities / reflux for PO (can delay emptying)
3) Sev renal impairment
CrCL: <35mL/min (IV)
CrCL: <30mL/min (PO)
Since kidneys are impt in regulating blood Ca levels
4) Preg & Lact
5) inability to stand / sit upright >30mins
6) aspiration risk (inability to swallow well)

Precaution:

  • Active upper GIT disease
  • RF for developing osteonecrosis
18
Q

What is the patho of Denosumab?
How to administer it?

A

SC Denosumab

  • human mab against RANKL (RANK Ligand)
  • prevents development of osteoclasts
  • similar efficacy as bisphosphonates

Admin.:

  • SC once q6months
  • co-administer 1000mg Ca + >400IU vit D daily (due to intense ↓osteoclast resorption, thus sign. ↓plasma [Ca])
19
Q

What are the ADRs of denosumab?
What are the special precautions & CI?

A

1) Muscle, back, bone, joint pain
2) N&V
3) C&D
4) slight tiredness
5) Hypocalcemia
6) ↑cholesterol

Rare (the mabs):
6) Osteonecrosis of jaw
7) Atypical femur fracture

Do NOT discontinue as may ↑risk of spinal column fractures

Special Precaution:

  • Sev renal impairment CrCL<10mL/min

CI:
1) Hypocalcemia
2) Preg

20
Q

Which drug causes ONJ & atypical femoral fracture?

A

bisphosphonates, denosumab, romosozumab,

21
Q

Which drug can be used when CrCL<30mL/min?

A

SC denosumab & (SC Romosozumab but special precaution)

PO Bisphosphonates <30mL/min
IV Bisphosphonates <35mL/min
SC Denosumab <15mL/min (special precaution)
Raloxifene <30mL/min
SC Romosozumab <30mL/min (special precaution)
SC Teriparatide <30mL/min

22
Q

Who is oestrogen mainly indicated for?

A

Indicated only for:

  • bone health in younger women
  • women w menopausal sx that needs treatment
  • premenopausal w ↓BMD/ postmenopausal
23
Q

What is the MOA of raloxifene?

A
  • selective estrogen receptor modulator (mix agonist & antagonist)
  • (agonist aspect) mimics effects of estrogen on bone density
  • (antagonism aspect) ↓risk of breast cancer, CV ADR
24
Q

What are the ADRs & CI of raloxifene?

A

ADR:
1) VTE & stroke
2) Hot flashes

CI:

  • Sev renal impairment CrCL<30mL/min
25
Q

What is the MOA of calcitonin?

A

Calcitonin
IV, SC, IM, Nasal spray

  • peptide hormone secreted by parafollicular cells in thyroid glands
  • inhibits osteoclastic bone resorption
  • ↓plasma Ca
26
Q

What are the ADRs of calcitonin?

A

1) Red streaks on skin
2) injection site reaction
3) warmth
4) redness on face, neck, arms, chest

27
Q

What are the CI of calcitonin?

A

CI:
1) hypersensitivity
2) Hypocalcemia

28
Q

Which OP drugs causes hypocalcemia?

A

bisphosphonates
denosumab
calcitonin
romosozumab

29
Q

Which OP med causes hypercalcemia?

A

Teriparatide

30
Q

What are the anti-resorptive drugs?

A
  1. Bisphosphonates
  2. SC denosumab
  3. Raloxifene
  4. Calcitonin
31
Q

What are the anabolic agents?

A

SC romosozumab
SC Teriparatide

32
Q

What is the MOA, indication, place in therapy and administration of SC romosozumab?
What is the duration of treatment?

A

SC Romosozumab
MOA

  • humanized mouse mab against sclerostin
  • inhibits sclerostin inhibition of canonical Wnt signaling pathway that regulated bone growth
  • ↑ bone formation + ↓ bone resorption

Indicated only for:

  • high risk of fractures
  • failed/intolerant to other osteoporotic therapy

Place in therapy:

  • still new so not commonly used

Admin.:

  • SC once monthly for 12 mths as this period is sufficient to ↑BMD
33
Q

What are the ADRs of romosozumab?
What are the CI and precautions?

A

1) MI
2) CV death
3) Stroke
4) Transient hypocalcemia
5) hypersensitivity reaction

Rare (the mabs):
6) Osteonecrosis of jaw
7) Atypical femur fracture

CI:
1) Hypersensitivity
2) Uncorrected hypocalcemia
3) History of MI/stroke

Special Precaution:

  • Sev renal impairment CrCL<30mL/min
34
Q

What are the MOA and administration of SC teriparatide?

A

SC Teriparatide

MOA

  • parathyroid hormone similar
  • ↑bone formation
  • ↑bone strength

Admin.:

  • SC daily
  • Max 24 months (2yrs) due to risk of Osteosarcoma shown in animal studies
35
Q

What is the ADR for teriparatide?
What are the CI of teriparatide?

A

ADRs:
1) Calciphylaxis
2) worsening of cutaneous calcification
3) transient orthostatic hypotension
4) Hypercalcemia

CI:
1) Hypersensitivity
2) hypercalcemia
3) skeletal malignancies
4) Paget’s disease (cause weakened bones & deformities), bone radiation, hyperparathyroidism
5) severe renal impairment CrCL<30mL/min
6) Pregnancy

36
Q

What are RANKL and sclerostin?

A
  • RANK Ligand – stimulates pre-osteoclast to be converted into osteoclast → ↑osteoclast
  • Sclerostin – repress differentiation of osteoblast → ↓bone growth
37
Q

What is the reason that some drugs causes atypical fractures?

A

Diff. bones have diff. patterns of osteoclasts and osteoblasts activity, for bones under extreme pressure where balance is important in the maintaining the structural integrity of the bone e.g. jaw bone → if take meds e.g. bisphosphonates which ↓osteoclast, this changes mechanical properties → ↑risk of atypical fractures (jaw, ear, femur)

38
Q

When do you continue beyond 5 years for bisphosphonates?

A

Bisphosphonate treatment is generally 5 years

  1. Only continue if high risk for fractures (>20%),
  2. previous vertebrae fracture
  • But usually when go beyond 5yrs, there is not much improvement

PR3154 MSK IC1,10-18 (8 decks)

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