Module 4.2 (Osteoporosis) Flashcards

1
Q

What is the definition of osteoporosis?

A

A disease characterised by low bone mass
and micro-architectural deterioration of
bone tissue leading to enhanced bone
fragility and consequent increased fracture
risk

A skeletal disorder characterised by
compromised bone strength predisposing to
an increased risk of fracture

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2
Q

What are the 4 types of osteoporosis?

A
  1. Most common – related to aging
  2. Secondary osteoporosis -> Potentially reversible
  3. Osteoporosis imperfecta
    - > Rare form possibly present from birth
  4. Idiopathic juvenile osteoarthritis -> Occurs in children aged 8 to 14 years
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3
Q

What is the difference between osteoblasts and osteoclasts?

A

Osteoblast: produce collagen and other matrix proteins

Osteoclast: resorb bone

Osteocytes: mature osteoblasts, line bone surface -> become embedded in bone matrix

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4
Q

How is osteoporosis diagnosed?

A

diagnosis is based on
>fracture after minimal trauma
>detection of low bone mineral density (BMD)

-> the lower the BMD -> the higher the fracture risk

A number of methods can be used to determine BMD.

Gold standard = dual x-ray absorptiometry (DXA) in a facility with high quality control.
>measurements of BMD done in the hip and spine.

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5
Q

Who should have a DXA scan?

A

Patients >50yrs with risk factors

Patients with a minimal trauma fracture

Suspected vertebral fracture

Patients >70 years

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6
Q

How does the T score indicate BMD results?

A

-1 or higher Normal BMD

Between -1 and -2.5 Osteopenia

-2.5 or lower Osteoporosis

The number of standard deviations a persons’ BMD, at any major skeletal site, deviates from the young adult mean for the same sex

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7
Q

How does the Z score indicate BMD results?

A

The number of standard deviations a person’s BMD is from the age and sex-matched mean BMD

>useful to assess patients <50 years (in addition to T-scores)

>useful to assess possible secondary osteoporosis

>low z-score (less than -2) indicates abnormal bone loss

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8
Q

What are clinical risk factors for osteoporosis?

A

Clinical risk factors include:

Constitutional factors (non-modifiable)

Diseases and drugs (modifiable)

Lifestyle and nutrition (modifiable)

Absolute risk can be calculated using internet-based calculators including:

Garvan assessment tool

FRAX assessment tool

IOF risk assessment tool (not numerical)

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9
Q

What are constitutional risk factors?

A

Female sex n

Post menopause/ early menopause n

Ageing n

Late menarche

Family history of osteoporosis n

Caucasian/Asian race n

Short stature n

Previous lowtrauma fracture

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10
Q

What are some disease risk factors?

A

Endocrine disorders

Mal-absorption syndromes

Chronic medical disorders

Low bodyweight and weight loss

RA & connective tissue disorders

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11
Q

What are some drugs that can cause bone loss?

A

Glucocorticoids

Excessive thyroid hormone

Antiepileptic drugs → especially those that are hepatic enzyme inducers

Glitazones

Long term heparin

Androgen deprivation therapy (prostate cancer)

Aromatase inhibitors (breast cancer)

Emerging evidence:

Long term high dose PPIs

SSRIs

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12
Q

What are some lifestyle and nutrition risks for osteoporosis?

A

Smoking

Excessive alcohol intake

Physical inactivity

Immobilisation

Low calcium intake

Vitamin D deficiency

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13
Q

True or False

>carbonated soft drinks may displace milk in the diet resulting in lower calcium intake

A

True → may lead to lower BMD indirectlyinnit cos not getting enough calcium

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14
Q

What are some factors that increase the risk of falls?

A

Chronic illness n

Balance, gait or mobility problems → parkinsons, stroke

Visual impairment n

Cognitive impairment → dementia

General deterioration associated with aging e.g. sarcopenia n

History of falls n Fear of falling n

Depression n

Blackouts/seizures n

Indoor and outdoor hazards n

Medications n

Physical inactivity n

Foot problems

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15
Q

What is the aim of the fracture risk assessment tool (FRAX)?

A

To identify people at risk of developing osteoporosis

>Model integrates clinical risk factors and BMD at femoral neck

>Helps clinicians decide if preventative measures are necessary

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16
Q

What is the aim of the Garvan Assessment tool?

A

To calculate bone fracture risk

>for use by GPs and other health professonals

>the calculator estimates both the 5 and 10 year risk of fracture based on

  • age
  • gender
  • number of fractures
  • number of falls
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17
Q

What is a major impact of osteoporosis?

A

A major feature of osteoporosis is fractures that occur following little or no trauma = minimal trauma fractures

Most common fractures in people with osteoporosis:

>weight bearing bones e.g spine, pelvis and hips

>bones that take the stress in falls e.g. wrists, forearm and upper arm

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18
Q

What is the impact of fractures?

A

Pain

Functional limitations and disability

Social isolation

Quality of life and mental health

Loss of independence

Mortality

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19
Q

What is some information about hip and pelvic fractures?

A

Associated with high levels of morbidity and mortality

In 2012-1698 deaths in Australia associated with hip/pelvic fracture

63% of deaths were in patients >85 years and associated with falls

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20
Q

Info about wrist and foerarm fractures?

A

Associated with sudden force when person catches themselves in a fall n

Colles’ fracture n

Scaphoid fracture

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21
Q

Info about vertebral fractures?

A
  • Most common type of spinal fracture in people with osteoporosis is called a wedge or compression fracture
  • Usually occurs in the lower end of the thoracic region or the upper end of the lumbar region
  • In this type of fracture, one or more of the vertebrae collapses forming a wedge shape
  • A number of spinal compression fractures è characteristic bent forward hunched posture and loss of height (kyphosis)
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22
Q

Stats about

A) Hip fractures

B) Vertebral fractures

C) Wrist fractures

A

A)

90% occur in above 50 years old

80% occur in women

>most devastating result of osteoporosis → patient admitted to hospital → disability + mortality → most occur after a fall

B)

¼ result from falls

C)

Most in women, 50% older than 65 years old.

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23
Q

What are some clinical risk factors that can be modified for osteoporosis?

A

Can take action to improve bone health at every stage of life

Modify clinical risk factors where possible

>stop smoking

>maintain an adequate food intake and ideal bodyweight

>ensure adequate calcium intake and Vit D concentration

>Reduce alcohol intake (≤ 2 standard drinks/day)

>Increase appropriate weight-bearing physical activity

>Consider whether osetrogen/progestin therapy is appropriate

>Be aware of increased risk for patients taking glucocorticoids

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24
Q

What diet for osteoporosis?

A

Adequate intake of foods containing calcium

E.g. dairy products, green leafy vegetables, fish with edible bones, tofu, chickpeas, almonds, dried figs and

>try to include 3 serves of dairy per day

  • glass of milk (250mL)
  • tub of yoghurt (200g)
  • slice of cheese (40g)
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25
Q

Importance of calcium in osteoporosis?

A

Calcium is essential for building and maintaining bone

Calcium gives bones strength

Almost 99% of the body’s calcium is found in bones n

A small amount of calcium is in the blood and is essential for healthy functioning of the heart, muscles, blood and nerves n

Dairy food is the main source of calcium

Less than 50% of Aust. adults get their recommended intake of calcium

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26
Q

What is the recommended intake of calcium?

A

The BEST way to get calcium is from the diet

Osteoporosis Australia suggests 3-5 servings of calcium rich food per day

Calcium requirements depend on age an sex

Menopause is a time of moe rapid bone loss for women

Older adults absorb calcium less effectively

Other factors can influence calcium resorption

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27
Q

When to give calcium supplements?

A

If a person’s diet does not meet their daily calcium requirement a calcium supplement can be considered*

Need to consider the elemental calcium content of supplements

Considerations in counselling:

>effects on the absorption of other drugs

>differences in calcium salts (with or without food)

>common side effects e.g. bloating and constipation

>take supplement in the vening and dont take more than 500mg at a time of CaCarbonate

>calcium citrate better absorbed

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28
Q

Calcium supplements for prevention of osteoporosis?

A

Recommendation is to get calcium from diet n Where not possible – supplement dose = 500-600mg/day

Controversy over calcium supplementation and cardiovascular risk → Studies reported calcium supplements increased risk of MI by about 25% and stroke by 15-20%

Confusion and repositioning on advice about supplements

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29
Q

Excercise osteoporosis?

A

Weight bearing & resistance exercise → Important for improving bone density and helping to prevent osteoporosis

benefits of exercise

exercise maintains/improves

  • muscle strength
  • muscle mass
  • flexibility
  • motility
  • balance
  • ease of movement

THEREFORE reduced frequency and severity of falls

Effect of exercise on fracture risk → unclear

Caution - recommending exercise in patients with asymptomatic vertebral fractures

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30
Q

What type of exercise?

A

Important in all stages of life

Must be regular → at least 3x per week

Should progress over time → increase the challenge

routines should be varied

performed in short intensive bursts

exercise must be tailored to the patient

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31
Q

Consider what exercise you would recommend for a patient (female aged 63 years) diagnosed with osteoporosis who has had a previous fracture?

A

Patient with diagnosed osteoporosis

>combination of weight bearing exercise with supervised progressive resistance training and challenging balance and mobility exercises at least 3x per week

>avoid forward flexion and twisting of the spine as they can increase risk of spinal fractures

>moderate to high impact activities are only recommended for people with osteoporosis who do not have a previous fracture

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32
Q

Vitamin D osteoporosis? How is vitamin D absorbed into the skin?

A

Regulates calcium homeostasis & bone metabolism

For most Australians the main source of Vitamin D is from exposure to sunlight.

Vit D produced when skin is exposed to UVB light from the sun

The amount of sun exposure required to produce adequate levels of Vit D is relatively low

Sun exposure times required vary based on:

>season

>location in Australia

>skin type

>area of skin exposed

Many australians do not have adequate vit D

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33
Q

Sun exposure recommendations?

A
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34
Q

Is sunscreen use associated with lower Vit D levels?

A

Sunscreen prevents sunburn by blocking UVB light. Theoretically that means sunscreen use lowers vitamin D levels. But as a practical matter, very few people put on enough sunscreen to block all UVB light, or they use sunscreen irregularly, so sunscreen’s effects on Vitamin D might not be that important. An Australian study thats often cited showed no difference in vitamin D between adults randomly assigned to use sunscreen one summer and those assigned a placebo cream.

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35
Q

Who are patients at low risk of low Vit D?

A

There is evidence that almost 1/3rd of Australians are Vit D deficient

Consider patient groups at risk

>Institutionalised or housebound

>Lack of UVB exposure due to lifestyle

  • Chronic illness/hospitalisation
  • Complex disability
  • Covering clothing worn
  • Southerly latitude

Have dark skin

Certain medical conditions or medications

36
Q

If people can’t get enough Vit D from appropriate sun exposure and diet then supplementation doses recommended are?

A

<70years – at least 600 IU Vit D per day

≥70years – at least 800 IU Vit D per day

1000 – 2000 IU per day may be required for sun avoiders or those people at high risk of deficiency

>few AE related to vit D supplementation.

>small risk of hypercalcaemia when combined with calcium

37
Q

General Principles of Treating Osteoporosis?

A
  1. Restore mobility & institute measures to prevent falls
  2. Exclude and treat underlying diseases
  3. Establish severity of osteoporosis by bone densiometry
  4. Stratify fracture risk and choose appropriate therapy
  5. Modify underlying risk factors
  6. Exercise – professional guidance – to maximise benefit and minimise harm (exercise physiologist, physiotherapist)
38
Q

How to prevent falls through exercise?

A

Physiotherapists can assist with a falls prevention program and advise on programs run in the community

>Supervised Resistance Training to strengthen muscles (this can also give confidence and reduce the fear of falling).

>Balance exercises, for example, heel-to-toe walking, Tai Chi, standing on one leg.

39
Q

Medical Review to avoid falls?

A

Doctor to review any conditions or medicines that may be causing poor balance or dizziness.

Doctor may recommend a visit to an optometrist to correct vision and/or a podiatrist for proper footwear

40
Q

How to avoid falls around the home?

A

Occupational therapist can conduct a home audit and suggest important changes to the home environment (and may recommend walking aids if needed).

Use a ‘home checklist’:

>Install handrails on steps and in bathrooms (beside toilet, shower, baths).

>Non-slip strips on stairs and non-slip mats in bathroom.

>Ensure rooms are well lit.

>Ensure edges of rugs and mats are flat or remove altogether

>Secure electrical cords and remove loose cords from walkways.

>Ensure regularly used items in kitchen are within easy reach.

>Maintain outside paths.

41
Q

Nutrition to avoid falls?

A

Improving nutrition can assist muscle strength. This includes adequate calcium and vitamin D levels.

42
Q

Pharmacotherapy in osteoporosis?

A

Vit D & Calcium

Oral biphosphonates

Intravenous bisphosphonates

Denosumab

HRT/Raloxifene

Teriparatide

43
Q

What needs to be done before starting therapies for osteoporosis?

A

Need to ensure all patients have adequate Vitamin D and Calcium concentrations

>Need to avoid hypocalcaemia that can occur with treatment

>Ensure total daily calcium intake of 1300mg

>calcium should not be sole therapy → can improve BMD but not necessarily fracture rates except in select populations

>Maintain serum 25-hydroxyvitamin D (25-(OH)D) concentration of ≥75nmol/L

BUT people with a serum 25(OD)D concentration from 50 to 75 nmol/L are not deficient. A supplement is not warranted.

44
Q

What indicates mild,moderate and severe deficiency for vitamin D levels at the end of winter

A

Mild deficiency 30-49 nmol/L

Moderate deficiency 12.5-29 nmol/L

Severe deficiency <12.5 nmol/L

45
Q

What are the two causes of vitamin D?

A

Vitamin D Deficiency with normal Parathyroid Function

For primary hyperparathyroidism → low vitamin D is protective

46
Q

How to treat vit d deficiency:

A) mild

B) moderate to severe

C) when to measure levels?

A

A)

first line → lifestyle (increased skin exposure)

Vit D3 (colecaciferol)

>25 to 50mcg (1000-2000IU) daily OR

>175 to 350mcg (700-14000 IU) weekly

B)

Vit D3 (colecalciferol)

75 to 125mcg daily (3000-5000IU) for at least 6-12 weeks then decrease to 25mcg to 50mcg (1000-2000IU) daily

megadoses (monthly) not routinely recommended

  • measure 25-OH Vit D levels after 6 months (mild), 3 months (mod/severe). Most patients need ongoing treatment at the lower dose of cholecalciferol (1000IU daily)
47
Q

What is calcitriol? What is it indicated for?

A

Active form of Vit D (1,25-(OH)2 D3)

Useful in kidney impairment leading to reduced hydroxylation of Vit D3

Indicated for

Hypocalcaemia, hypoparathyroidism, hypophosphateaemic rickets, Vitamin D-resistant rickets, renal osteodystrophy, chronic renal dialysis, established osteoporosis, prevention of corticosteroid induced osteoporosis

>rarely used for osteoporosis

48
Q

What is there a risk of with calcitriol?

A

Risk of hypercalcaemia an hypercalcuria – requires regular monitoring of serum calcium levels during dose optimisation

monitoring; baseline; twice a week for first week; at 2-4 weeks; then every 2-3 months or more

49
Q

What are examples of oral biphosphonates? How do they work and what are they indicated for?

A

Alendronate, risedronate, zoledronic acid

>Bisphosphonates decrease bone resorption by inhibiting osteoclasts → slow bone loss, improved BMD and reduce fracture rates

>Demonstrated to reduce vertebral, non-vertebral and hip fractures

Indicated for:

>prevention and treatment of osteoporosis → including post-menopausal and corticosteroid induced

>other indications include Paget’s disease and malignancies

50
Q

Compare oral biphosphonates

A

Drugs shown to have similar efficacy in clinical trials

Alendronate (Fosamax®) 70mg orally once WEEKLY n

Risedronate 35mg (Actonel®)orally once WEEKLY OR 150mg once MONTHLY n

Zoledronic acid (Aclasta®) 5mg IV over 15 minutes once a YEAR

Oral formulations → dosing requirements important to effectiveness

Zoledronic acid

>Hypocalcaemia especially when risk factors present

>influenxza like symptoms (take paracetamol before infusion and after)

51
Q

Duration of therapy?

A

Bisphosphonates are retained in the skeleton after treatment withdrawal

-beneficial effects persist for several years (alendronate, zoledronic acid)

  • beneficial effects persist for several years (alendronate, zoledronic acid)
  • low risk patients stop therapy

>5 years oral biphosphonates

>3 years IV

  • patients at high risk of minimal trauma fracture

>10 years oral therapy

>6 years IV

>Evidence is lacking >10 years

52
Q

Who are patients at high risk of minimal trauma fracture

A

≥ 75 years n

Previous hip or vertebral fracture

Minimal trauma fracture post commencement of treatment

Hip T-score ≥ - 2.5

53
Q

What are the adverse effects of biphosphonates? When is it contraindicated?

A

Use of bisphosphonates limited in renal impairment due to adverse effects

Significant upper GI adverse effects include:

Common: (>1%) nausea, vomiting, diarrhoea n

Infrequent (0.1-1%): oesophagitis, oesophageal erosions and ulcers, gastritis, duodenitis

Rare (<0.1%) but serious adverse effects include:

Heart failure

Renal impairment

Osteonecrosis of the jaw (ONJ)

Contraindicated:

When eGFR < 35mL/min/1.73m2 n Patient experiencing dysphagia, achalasia

54
Q

What is osteonecrosis of the jaw? What causes it?

A

ONJ manifests as exposed bone involving the maxillofacial structures which begin to necrotise due to lack of blood supply

>Mainly occurs in patients receiving IV bisphosphonates for multiple myeloma or metastatic breast cancer

>Anti-resorptive drugs (bisphosphonates & denosumab) have been associated with ONJ

Other risk factors for ONJ include: dental extractions, dental implants, pre-exisiting oral disease, ill fitting dentures, glucocorticoids and smoking

55
Q

More details of ONJ pls

A

The jaw bone becomes exposed and begins to “starve” from lack of blood

Most cases occur after dental extraction

ONJ is associated with cancer treatments (including radiation), infection, steroid use, or antiresorptive medications used for osteoporosis.

56
Q

When can atypical fracture of femur occur?

A

Atypical subtrochanteric or diaphyseal femoral fractures are rare.

Risk is low but ↑ with long duration antiresorptive therapy

Benefits generally outweigh risks

Risk declines when therapy is stopped

Risk = 113 new cases occur for every 100 000 patients taking the drug for 1 year AFTER 8 to 10 years of therapy

57
Q

Counselling for bisphosphonates

A

“Take in the morning with a full glass of plain water at least 30 minutes before food or drink. Remain upright during this time and until after you eat. Swallow whole; do not chew or suck on the tablet.

“Do not take antacids, calcium, iron or mineral supplements within 30 minutes of alendronate as they may interfere with its absorption.”

“Stop tablets and see your doctor immediately if you have pain on swallowing, or new or worsening heartburn.

58
Q

How to minimise risk of ONJ?

A

Consider a full dental assessment and complete any dental procedures before commencing treatment n

Any necessary dental treatment should be completed before or shortly after starting antiresorptive therapy (eg within 6 months) n

“Always tell your dentist you are taking this medication.” n

Advise patients to maintain good oral hygiene, have regular dental health reviews, and to seek early management of any oral or dental concerns.

>alarm symptoms requiring immediate referral

-“If you develop severe pain in your bones, joints or muscles, pain on swallowing, chest pain or new or worsening heartburn, seek immediate medical attention.”

59
Q

How does denosumab work?

A

Human monoclonal antibody that prevents activation of RANK receptors resulting in decreased formation and activity of osteoclasts and thus reducing bone resorption

>Increases BMD at lumbar spine and hip, reduces vertebral, non-vertebral and hip fractures

60
Q

What are the indications of denosumab?

A

Treatment of postmenopausal osteoporosis

To increase BMD in men with

>osteopenia and receiving androgen deprivation therapy for non-metastatic prostate cancer

>osteoporosis

effective in patients with kidney disease → no dose adjustment required

Dose: 60mg SC once every 6 months

61
Q

Precautions with denosumab

A

Vitamin D deficiency should be corrected before initiating therapy

Monitor plasma calcium concentrations in patients with increased risk of hypocalcaemia (e.g. dialysis patients)

Maintain good oral hygiene (ONJ risk)

Latex sensitivity - needle cover of the pre-filled syringe

>(Prolia® brand) contains latex

Temperature

Storage in fridge (2-8°C) n

Inject room temperature (25°C)

62
Q

Referral for denosumab?

A

If jaw or dental problems occur

If signs or symptoms of cellulitis

If new or unusual hip, thigh or groin pain occurs

63
Q

Concerns with long term treatment of denosumab?

A

Long-term effects of suppressing bone turnover by denosumab are unclear

The cumulative effect on bone of taking denosumab after a bisphosphonate is unknown

RANKL is expressed on immune cells - concern about the effect of denosumab on the immune system.

Effects don’t persist after stopping therapy with denosumab

Increased incidence of multiple spontaneous vertebral fractures when denosumab is stopped or a dose is delayed for more than 4 weeks

If denosumab is stopped, a replacement drug (typically a bisphosphonate) must be started to prevent rapid bone loss and vertebral fracture

64
Q

Denosumab and severe hypocalcaemia?

A

Health professionals are reminded to closely monitor patients being treated with denosumab for signs of severe hypocalcaemia, which in some cases can be fatal. Preexisting hypocalcaemia must be corrected before initiating therapy with denosumab.

65
Q

Denosumab and QT prolongation?

A

has something to do with it, check it out later

66
Q

HRT/MHT indications?

A

Relief of menopausal symptoms

Prevention of postmenopausal osteoporosis when there is a high risk of fractures and alternative treatment is inappropriate

67
Q

When does benefits of MHT on bone health outweigh risks

A

started <60 years of age or within 10 years of menopause and in women with a hysterectomy

68
Q

When is reduction in fracture risk lost after stopping HRT

A

A few years after, therefore short term use for menopausal symptoms unlikely to have a significant effect on fracture risk after age 70 when risk is greatest

>vaginal oestrogens do not appear to offer any protection against osteoporosis

69
Q

What is raloxifene? What are the indications and how does it reduce postmenopausal bone loss?

A

A selective oestrogen receptor modulator (SERM)

Indications

Prevention and treatment of postmenopausal osteoporosis

Primary prevention of invasive breast cancer in high risk postmenopausal women

Reduces postmenopausal bone loss

Reduces risk of vertebral fractures but not non-vertebral fractures n

Oestrogen agonist effects on bone mass and lipids n

Antagonistic effects at other oestrogen receptive tissues (e.g. breast and endometrium)

70
Q

Considerations with raloxifene?

A

Increased risk of hot flushes

Increased risk of VTE or stroke

Decreased risk of breast cancer

Decreased total and LDL cholesterol levels

  • Not indicated for pre-menopausal women → may cause ovarian stimulation
  • Discontinue in the event of a condition or illness leading to prolonged immobilisation → 3 days before
  • Move about during prolonged travel
  • Does not cause endometrial proliferation → unexplained uterine bleeding should be investigated
  • Oestrogen induced hypertriglyceridaemia may be exacerbated and should be monitored
71
Q

What is teriparatide? How does it work? What are the indications?

A

Synthetic form of the active fragment of human parathyroid hormone (PTH)

Promotes bone formation and increases BMD

>The only treatment that increases bone formation

2nd line treatment → initiated by a specialist only

Indications (in patients at high risk of fractures)

postmenopausal osteoporosis

primary osteoporosis in men

corticosteroid induced osteoporosis

72
Q

Dose of teriparatide?

A

Dose: 20mcg via SC injection daily for a maximum of 24 months

>Decreased incidence of vertebral facture by 65% in postmenopausal women with osteoporosis

-Overall incidence of non-vertebral fractures reduced but not incidence of hip fractures

>Ensure adequate intake of calcium and Vit D

>When measuring calcium concentrations take blood just before a teriparatide injection as it may cause hypercalcaemia lasting some hours

73
Q

teriparatide restrictions?

A

Teriparatide cannot be given to people who:

>Are age under 25 years,

>Have known or suspected Paget’s disease of bone or certain other metabolic bone disorders,

>Have previously had radiotherapy involving bone

Contraindications to use:

>Pre-existing hypercalcaemia, malignancy, renal disease, primary hyperparathyroidism

Lifetime exposure limited to 24 months; informed consent is required.

74
Q

PBS authority restrictions for teriparatide?

A

Must have T score ≤ -3 n

≥ 2 minimal trauma fractures (at least one fracture occurring after 12 months of antiresorptive therapy) e.g. biphosphonate and denosumab

Subsidy only currently for 18 months

75
Q

Teriparatide considerations

A

Previous and concomitant treatment with anti-resorptive drugs may influence the response to teriparatide

>n Increase in BMD is lower when previously treated with alendronate (NOT seen with risedronate)

>Concomitant treatment with bisphosphonates not recommended

>Concomitant denosumab does not impair the response to teriparatide

>Following a course of teriparatide patients should receive antiresorptive therapy to increase BMD further and maintain anti-fracture effect

76
Q

What is corticosteroid induced osteoporosis?

A

Underlying mechanism is multifactorial

↓osteoblast function ↓intestinal calcium absorption

Hypercalciuria n

Gonadal suppression

77
Q

How to use corticosteroids if required?

A

Use lowest effective dose for the shortest possible time

Use inhaled or topical therapies rather than oral therapy where possible

78
Q

What to do if starting on corticosteroids?

A

BMD measurements:

Before starting long-term glucocorticoid therapy n

Doses equivalent to > 5mg per day prednis(ol)one - measure BMD annually for first few years

>minimise other risk factors for osteoporosis

79
Q

What to do for corticosteroid induced osteoporosis?

A

Optimise calcium & vit D; manage risk factors

Prophylactic bisphosphonate therapy considered in patients with:

>T-score < -1.5

>Will receive ≥7.5mg oral prednis(ol)one daily (or equivalent) for at least 3 months

  • Clinical judgement required to assess fracture risk and duration of treatment
  • Prophylaxis may only be required while using steroids if other risks are low
  • Bisphosphonates (alendronate, risedronate and zoledronic acid) are first-line in preventing & treating glucocorticoid induced osteoporosis

post-menopausal women = estrogen therapy

80
Q

What to do for post menopausal women with osteoporosis?

A

Assess harms, benefits and patient preference

Preferred drugs are bisphosphonates & denosumab

Initiating HR in a woman >60 years for sole purpose of reducing osteoporotic fractures is NOT recommended

Combination of oestrogen and any other osteoporotic drug should generally be avoided

Consider VTE risk

81
Q

What to do for a premenopausal women with osteoporosis?

A

Osteoporosis uncommon therefore an alert for secondary causes

Treat secondary causes

Optimise calcium and Vit D

82
Q

Men and osteoporosis

A

Osteoporosis due to secondary cause in ~60% of cases

Modify risk factors e.g. hypogonadism, smoking, glucocorticoid use, antiepileptic drugs, excessive alcohol intake & Vit D deficiency

Limited data on treating osteoporosis in men

Evidence available for alendronate, risedronate and zoledronic acid

83
Q

How to decide whether to treat patient or not with moderate fracture risk?

A

Discussion of benefits (e.g. fracture risk reduction) and risks (e.g. adverse events) of treatment

Assessment/understanding of patient preferences and health priorities

Based on 10 year risk of assessment using a validated tool

Osteopenic patients usually don’t require pharmacotherapy.

Optimising calcium, Vit D, exercise and leading a “bone friendly lifestyle are key to improving bone health

84
Q

What is the impact of fractures?

A

Pain

Functional limitations and disability

Social isolation

Quality of life and mental health

Loss of independence

Mortality

85
Q

What is the difference between osteoblasts and osteoclasts?

A

Osteoblast: produce collagen and other matrix proteins

Osteoclast: resorb bone

Osteocytes: mature osteoblasts, line bone surface -> become embedded in bone matrix