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Stage 3 - Case 3 (Musculoskeletal) > Lecture 4 & 5: Pathophysiology and Pharmaceutical care of Osteoporosis > Flashcards

Lecture 4 & 5: Pathophysiology and Pharmaceutical care of Osteoporosis Flashcards

1
Q

What are some risk factors to osteoporosis?

A
  • Non-modifiable: Previous fracture, Family history, early menopause, women, age
  • Modifiable: Low BMI, Smoking, Alcohol
  • Coexisting Disease: Diabetes, Inflammatory (RA), malabsorption, CKD
  • Drug Therapy: Long-term antidepressants, Antiepileptics, PPI, Oral corticosteroids
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2
Q

What is osteopenia?

A
  • Low bone mineral density - weaker than normal
  • Not enough for osteoporosis
    • 30-40yrs
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3
Q

What is the effect of excerise on bone?

A
  • Athletes have higher BMD
  • Hip fractures associated with lower activity levels between 15-45
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4
Q

What are some of the hormones involved with bone growth and maintenance?

A
  • Calcitriol (active form of vitD)
  • Growth hormone
  • Thyroxine
  • Sex hormones (oestrogen/androgen)
  • Parathyroid hormone
  • Calcitonin
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5
Q

What are the functions of Growth hormone, Thyroxine and sex hormone and where are each produced?

A
  • Stimulates osteoblast activity and more bone synthesis
  • GH: Pituitary gland
  • Thyroxine: Thyroid Gland
  • Sex hormones: ovaries and testes
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6
Q

What are the different parts of the body that deal with Calcium?

A
  • Bones: Calcium is stored
  • Digestive tract: Calcium absorbed
  • Kidneys: Calcium excreted
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7
Q

What is the function of the Parathyroid hormone and where is it produced?

A
  • Parathyroid gland
  • Increases intestinal absorption of calcium
  • Reduces excretion
  • Stimulates Osteoclast activity: Resorption and
  • Increases Ca2+ conc
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8
Q

What is the function of the Calcitonin hormone and where is it produced?

A
  • Thyroid gland
  • Inhibits osteoclast activity
  • Promotes CA2+ loss in kidneys
  • Causes Ca2+ to deposit in the bones
  • Increases longevity of osteoblasts
  • Decreases Ca2+ conc
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9
Q

How does vitamin D help calcium absorption?

A
  • 7-dehydrocholestrol-UV>Vit D3-liver enzyme> calcidiol - kidney> calcitriol.
  • Stimulates enterocytes to increase calbindin -D proteins which increase calcium absorption and facilitate transport to basolateral membrane -> blood
  • Stimulates PTH release
  • Excessive calcitriol -> to less active
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10
Q

What is osteomalacia and its treatment?

A
  • Softening of bones, insufficient ca2+ and vit D or long-term anticonvulsant (phenytoin/carbamazebine) - induce CYP450) causes Vit D -> Inactive metabolites
  • Abnormal bone formation cause of inadequate mineralisation but has normal resorption and formation
  • Weak and flexible
  • Treatment: high doses of Vit D
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11
Q

What is osteoporosis?

A
  • Severe bone loss which affects normal function
  • Bone reabsorption outpaces bone deposit - trabecular bone more susceptible (vertebrae, hip, wrist)
  • Compromised bone strength -> risk of fracture
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12
Q

How is osteoporosis developed?

A
  • Osteoclast recruitment is increased
  • Osteoclast-osteoblast coupling is interrupted
  • Factors recruiting osteoclasts may not adequately recruit osteoblasts
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13
Q

What are the types of osteoporosis?

A
  • Postmenopausal osteoporosis (type 1)
  • Type 2: age related
  • Secondary osteoporosis
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14
Q

How does postmenopausal osteoporosis work?

A
  • Hormone dysregulation accelerates osteoporosis
  • Oestrogens and androgens maintain bone mass
  • Oestrogen defieciency causes increased proliferation and activation of osteoclasts and their increased survival
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15
Q

What are the causes of secondary osteoporosis?

A
  • Endocrine disorders: Hyperthyroidism/ parathyroidism
  • Medications: Glucocorticoids, Anticoagulants, Gonadotropin-releasing hormone agonists, antiepilptic, diuretics
  • Disorders of calcium balance, malabsorption
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16
Q

How do longterm glucocorticoids cause secondary osteoporosis?

A
  • Reduced calcium absorption (by impairing vit D) and more elimination
  • Leads to PTH release which causes bone resorption - secondary hyperparathyroidism)
  • Inhibitory effect on sex hormones
  • Direct inhibition of osteoblast function -> could be reversed when therapy = stopped
17
Q

How do anticoagulants cause secondary osteoporosis?

A
  • Long term heparin: causes reversible osteoporosis
  • Incraesed osteoclast and decreased osteoblast activity
  • Increases collagenase activity: breaks down collagen (connective tissue in bone)
  • Decrease in active Vit D by reduced activity of kidney enzyme
  • Warfarin: antagonistic effect on Vit K - key in syntheiss of bone matrix proteins (inadequate mineralisation)
18
Q

What are some important points Gonadotropin-releasing hormone agonists on osteoporosis?

A
  • e.g. leuprolide, goserlin
  • Use limited to 6 months
  • If more longer: a bone protective agent as low-dose oestrogen, progesterone or bisphosphonates
19
Q

How do antiepleptic drugs and diuretics cause secondary osteoporosis?

A
  • Induces CYP450 which converts vit D-> inactive metabolites
  • Decrease serum calcium. Block Na+/K+ transporter in ascending limb - loss of electrochemical gradient
20
Q

How is osteoporosis diagnosed?

A
  • Bone mineral density - measured at lumbar spine and hip - xray - repeated evry 2-5yrs
  • DXA scan
  • T score: number of SDs from peak bone mass of 30yr old of same sex and Z score: number of SDs from average bone mass of same age and sex
  • T score between -1 & -2.5 = osteopenia, -2.5 less = osteoporosis, -2.5 + fracture = established osteoporosis
21
Q

What is the main complication of osteoporosis?

A
  • Fragility fracture
  • Usually remains undiagnosed until a fracture
22
Q

How do you calculate fracture risk in patient?

A
  • Consider assessment in Women 65 older and men 75 older or younger w/ risk factors
  • Q fracture (faces) and FRAX score: assesses 10 yr probability of fracture (red, yellow, green graph)
23
Q

What are the non-pharmacological strategies for treating osteoporosis?

A
  • Lifestyle modification: stop alcohol, smoking, increase Ca in diet
  • Regular excerise
  • Avoid drugs that cause osteoporosis
24
Q

What are the pharmacological treatment strategies of osteoporosis?

A
  • Bisphosphonates
  • Calcium
  • Vit D
  • Oestrogen
  • Oestrogen receptor modulators (SERM)
25
Q

How do Bisphosphonates work and some examples?

A
  • First line prevention of osteoporotic fractures
  • Reduce bone resorption by inhibiting osteoclast removing calcium from bone
  • Bind to hydroxypatite on bone mineral surface
  • Taken up by osteoclast and induces apoptosis
  • Alendronic acid, risedronate
26
Q

What is the absorption and elimination like for bisphosphonates and what are their adverse side effects?

A
  • Poorly absorbed from intestine and low bioavailability
  • Excreted primarily by kidneys - not recommended in impaired renal function
  • Oesophagitis, gastritis, petic ulcer, fever aches, osteonecrosis of jaw (teeth death) and external auditory canal (ear pain, discharge)
27
Q

What are some counselling tips for bisphosphonates?

A
  • Dont crush
  • Once weekly
  • Sit upright and take with lots of water
  • On empty stomach
  • Not at night and keep upright for 30mins
28
Q

What are some drug interactions with calcium administration and some adverse effects?

A
  • Iron therapy impairs absorption
  • Tetracyclines causes intestinal chelation of Ca
  • Nausea, Constipation, Abdominal distension, Kidney stones
29
Q

What is Denosumab and how does it work?

A
  • 2nd line and fully human monoclonal antibody to RANK Ligand (which activates osteoclasts)
  • Reduces osteoclast development and increases BMD.
  • RANK L is secreted by osteobalasts and bind to RANK on pre-osteoclast. This activation converts pre-osteoclast to osteoclast - Denosumab inhibits
30
Q

What are some counsellling and side effects of Denosumab?

A
  • SC injection given every 6 months
  • Ensure Ca2+ and Vit D are adequate before starting
  • Rebound effect
  • Similar side effects to bisphosphonates
31
Q

How do selective oestrogen receptor modulators (SERM) work and name an example?

A
  • Partial agonists of oestrogen receptors
  • Induce osteoblast activity
  • Used for postmenopausal osteoporosis
  • PE/DVT risk
32
Q

How do Parathyroid Hormone analogues (Teriparatide) work and what are some adverse effects?

A
  • Mimics endogenous PTH hormone
  • Ensure Ca2+ and Vit D are adequate before starting
  • For serious osteoporosis in men and postmenopausal women
  • Injected daily SC
  • Adverse Effects: Postural hypertension, hypercalcaemia

Stage 3 - Case 3 (Musculoskeletal) (4 decks)

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