Osteoporosis Flashcards

1
Q

What are the clinical manifestations of osteoporosis?

A

No clinical manifestations until a fracture

Common sites of fracture:

  • Vertebral compression #
  • Hip # (neck of femur, intertronchanteric)
  • Distal Radius Fracture (e.g. Colle’s #)
  • Humoral Head #
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2
Q

How is osteoporosis diagnosed?

A

Fragility fracture, ANY FRACTURE that occurs from standing height or less, without major trauma e.g. vehicle accident OR

T-score ≤ -2.5 standard deviations (SD) at any site based upon bone mineral density (BMD) measurement by dual-energy x-ray absorptiometry (DEXA)

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3
Q

How do you interpret the T scores on DEXA scans?

A

Compares pt’s results to a healthy 20YO person matched for race and sex

Used to determine Osteoporosis & Osteopenia for post-menopausal women and men >50YO

  • Osteoporosis ≤-2.5
  • Osteopenia = -1 ~ -2.4
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4
Q

How do you interpret the Z scores on DEXA scans?

A

Compares pt’s results to those of an age-matched population that also is matched for race and sex – aka compared to peers w same age, race and sex

Used to determine Osteoporosis only for pre-menopausal women and men <50YO

Osteoporosis ≤-2.0 (for pre-menopausal women and younger men)

Z score is not used to determine osteopenia! Hence if a younger male / pre-menopausal woman has NO osteoporosis (Z score <2.0), they are also considered to have NO osteopenia

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5
Q

What are the primary causes of osteoporosis?

A

Post-menopausal

  • Increased bone resorption due to withdrawal of estrogen which restricts osteoclastic activity
  • Accelerated rate of bone loss

Senile (aka old age): Gradual slowdown in osteoblastic activity

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6
Q

What are secondary causes of osteoporosis ?

A

Endocrine causes

  • Hyperthyroidism
  • Cushing’s Syndrome: Important to ask for Exogenous Steroid use / TCM
  • Hyperparathyroidism
  • Hypogonadism (eg: Klinefelter’s)
  • CKD: Secondary & Tertiary hyperPTH; Low Vitamin D

GI Causes

  • Liver Disease: due to low Vitamin D
  • Nutritional deficiencies (chronic alcoholism, malabsorptive disorder, IBD, malnutrition, Coeliac disease)

Drug causes

  • SSRI, Antiepileptics
  • Exogenous Steroid use / TCM

Rheumatological causes eg; Rheumatoid Arthritis

ID cause eg: HIV

Others e.g. Multiple myeloma – causes lytic lesions

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7
Q

What is the history to take in a patient with osteoporosis?

A

Risk Factors for osteoporosis

  • CKD, CLD, Endocrine conditions
  • Prolonged steroid use
  • FHx of Osteoporosis / Osteoporotic Fractures
  • PMHx of fractures
  • Early menopause / Surgical Menopause
  • Smoking

FRAX (Fracture Risk Assessment Tool)

  • advanced age
  • previous fracture
  • glucocorticoid therapy
  • low body weight
  • current cigarette smoking
  • excess alcohol consumption
  • rheumatoid arthritis
  • 2’ osteoporosis (e.g. hypogonadism or premature menopause, malabsorption, chronic liver disease, IBD)
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8
Q

What are the investigations required for osteoporosis?

A

Laboratory

  • FBC: any inflammation, chronic illnesses
  • Renal Panel, LFTs (including albumin, AST)
  • Ca/Mg/Po4: Hormonal patho & CKD can lead to derangements
  • 25[OH]D: to pick up Vit-D Deficiency

Imaging

  • XR – if # (Visualise trabeculae, identify pathological fractures)
  • DEXA for BMD
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9
Q

Why do we need to correct calcium for albumin?

A

When measuring 🡪 we measure the TOTAL Ca i.e. both Bound and Unbound

When albumin ↓ 🡪 Ca bound to Albumin ↓ but unbound Ca remains unchanged

Since ionised unbound Ca is what exerts effects, pt has falsely low measured ions

Treatment in this case should not be Ca infusion!
Corrected Ca = Measured Ca * 0.02 (40-albumin)

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10
Q

What are additional assessents to evaluate for etiology of osteoporosis?

A

Serum TSH, fT4: Assess for hyperthyroidism

Serum PTH: Think HyperPTH when HyperCa, Hypercalciuria, Stones, Osteopenia

Serum and Urine Protein Electrophoresis

  • Assess for multiple myeloma/cancer; Suspect when hypercalcemia, weight loss, anemia, proteinuria
  • CRAB = HyperCa, Renal Impairment, Anaemia, Bony Lesions

24hr Urinary Cortisol / LD-DST / Late night salivary cortisol: Cushing’s Syndrome;

24-hour urine for calcium and creatinine

  • Assess adequate Ca intake in GI disease e.g. IBD/Surgery
  • Necessary if kidney stones present, to look for idiopathic hypercalciuria (FHH)

Serum Testosterone & SHBG – Assess hypogonadism in men

FSH, LH, E2 – to assess hypogonadism for women

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11
Q

What is the non pharmacological management of osteoporosis?

A

Calcium

  • Requirement is 1200mg daily in postmenopausal; 1000mg daily in premenopausal/men
  • If inadequate intake, can take calcium supplements (500 to 1000mg/day but aim to give ≤50% of requirement via pills, ≥50% from diet because Ca pills increases CV risk by causing calcification in vessels

Smoking and Alcohol Cessation

Exercise
- Appropriate exercise 30 minutes 3 times a week
- Effect on BMD is small, but may reduce # via ↓ fall risk/
↑ muscle strength
resistance exercise, weight bearing exercises (e.g. running, weight lifting)

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12
Q

What are the indications of pharmacological therapy in patients with osteoporosis?

A

Patients with osteoporosis (fragility fracture or T score ≤ -2.5)

High risk patients with osteopenia (T score b/n -1 to -2.5);

However: All pt must have normal Ca and 25-VitD levels prior to starting therapy, and they should receive supplemental elemental calcium and vitamin D

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13
Q

What is the initial therapy to begin in patients with osteoporosis?

A

Oral Bisphosphonates e.g. Alendronate: Every week

  • Inhibits osteoclasts; leading to indirect increase in BMD
  • Oral, take on empty stomach, with full glass of water; take first thing in the morning, sit upright for 30min (causes GI irritation if supine)
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14
Q

What are the side effects of oral bisphosphonates?

A

Hypocalcaemia

GI side effects – Diarrhoea, nausea, GERD (esophagitis)

Osteonecrosis of jaw (<1%, after tooth extraction/ infection usually)

Atypical Femoral Fracture (AFF) – on prolonged IV bisphosphonate use (>3 years)

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15
Q

What is osteonecrosis of the jaw?

A

Usually occur after dental procedure while on meds!. Hence, we refer dentition to remove these teeth first BEFORE starting meds

Bisphosphonates (and denosumab) prevent bone healing 🡪 causing prolonged exposure of mandible 🡪 increased risk of infection 🡪 osteonecrosis

Hence for patients, we often ask them to get rid of bad teeth before starting on medications that increases risk of ONJ

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16
Q

What are the C/Is to oral bisphosphonates?

A

CKD: eGFR <35 (mechanism is unknown, but risks causing AKI/ AoCKD)

Oesophageal Disorders e.g. achalasia (can cause oesophagitis)

Bariatric Surgery (can cause anastamotic ulcers)

BGIT

17
Q
What is the second line therapy of osteoporosis? 
What is the 
- MOA
- route of administration
- indication?
A

Denosumab (inhibits osteoclasts hence SE are similar to Bisphosphonates)

MoA

  • Monoclonal Ab that serves as RANKL Inhibitor
  • RANKL is produced by osteoblasts and stimulates osteoclastogenesis by acting on RANK on osteoclasts.

Administration: Subcutaneous injection, every 6 months

Use – Patients that are not adherent to oral bisphosphonates, avoid IV bisphosphonates, impaired renal function 😊

18
Q

What are the side effects of denosumab?

A

Similar side effects as bisphosphonates because they are both inhibitors of osteoclasts

  • Hypocalcaemia
  • Osteonecrosis of jaw (<1%, after tooth extraction /infection usually)
  • Infusion related reaction
  • Atypical Femoral Fracture (AFF) – on prolonged IV bisphosphonate use (>3 years)

However, Denosumab is given SC 🡪 hence no GI side effects

19
Q

How do you manage severe osteoporosis (T-score of -3.5 or below even in the absence of fractures or T-score of -2.5 or below plus a fragility fracture)? How is it administered?

A

Teriparatide (a PTH analogue!): PTH analogue that induce osteoblastic bone formation by daily administration

Non-Continuous, daily SC PTH administration (in the case of Teriparatide)

  • Short ½ life of PTH 🡪 causes daily pulsatile fluctuations 🡪 will stimulate osteoblasts instead
  • Since it DIRECTLY builds bone – it is the most powerful medication out of all of the above! 🡪 but is V expensive, only given as last resort!

Administration – Subcutaneous injection daily, for maximum duration of 2 years

20
Q

What are the side effects of Teriparatide (a PTH analogue!)

A

Hypercalcemia (due to PTH effects), GI side effects

However, cannot be given >2Y 🡪 excessive bone building may cause osteosarcoma (bone CA)

21
Q

What is the C/I of Teriparatide (a PTH analogue!)?

A
  • HyperCa (will worsen hyperCa)
  • Hx of ANY form of CA, treated or untreated (Teriparatide encourages bone mets)
  • Pt refused trtmt or BMD
  • CKD: eGFR < 30
  • Life expectancy <1y due to terminal illness
  • Pt is bedbound -> trtmt is for reducing risk of recurrent #s, while bedbound pts have v low risk of #
22
Q

How do you monitor osteoporososi?

A

DXA (Spine and Hip): Follow up in 1 to 2 years. Less frequent monitoring thereafter if condition is stable

If decrease in BMD,

  • Ascertain compliance and other factors e.g. new medical conditions
  • If change in BMD <5%, continue same therapy and repeat BMD 2 years later
  • If change in BMD ≥5%, switch to IV bisphosphonates /🡪 Teriparatide/ 🡪 Denosumab
23
Q

What are the indications for screening of osteoporosis? Screening every 2-5 years

A

All women >65 years

All men >70YO

Adults who have a fracture after age 50

Postmenopausal women <65YO w/ OSTA > 20

  • OSTA = Osteoporosis self-assessment tool for Asians (OSTA)
  • OSTA = Age – BW (kg); high risk if >20

Postmenopausal women <65YO w/ OSTA 0-20 w/ other RF:

  • Early menopause POI (i.e. <40YO)
  • Prolonged steroid use (≥ 5 mg prednisolone/day or equivalent for ≥ 3 months)
  • Family history of fragility fracture