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PHA 332 > OSTEOPOROSIS THERAPEUTICS > Flashcards

OSTEOPOROSIS THERAPEUTICS Flashcards

1
Q

what is the bone composed of- basic?

A

outer layer of compact bone, the cortex and an inner spongy layer in which the bone is arrange in a loose mesh lattice of thin strands called bone trabeculae

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2
Q

what do the spaces between the trabeculae contain?

A

contain the bone marrow, which consists of fat and blood forming tissue

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3
Q

what is a bone?

A

Bone is a specialized type of connective tissue
•Composed of a dense connective tissue framework impregnated with calcium phosphate salts along with smaller amount of calcium carbonate and other minerals

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4
Q

what are the three different types of cells in bone?

A
  1. Osteoblasts
  2. Osteocytes
  3. Osteoclasts
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5
Q

what are bones of skeletons connected by? what are the 3 types?

A

Bones of skeleton are connected by joints

•There are three types of joints–Fibrous, Cartilaginous, Synovial

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6
Q

what are osteoblasts?

A
  • Active bone –forming cells that produce collagenase bone matrix
  • Secrete enzyme alkaline phosphatase – promotes deposition of calcium phosphate salts in the matrix to calcify the bone
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7
Q

what do osteocytes do?

A

As the bone matrix is formed and calcified the osteoblasts become incorporated within the bone and become transformed into relatively inactive mature bone cells called Osteocytes

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8
Q

what do osteoclasts do?

A

Multinucleated cells concerned with bone resorption

•Remove bone matrix by phagocytosis , dissolve the bone salts and release calcium and phosphate ions in circulation

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9
Q

how do osteoblasts and osteoclasts interact in bone remodelling?

A

(1) PTH,shear stress, TGF-β cause osteoblast precursors to express theosteoclast differentiation factor RANK-ligand (RANKL).(2)RANKL binds to RANK, a receptorexpressed on osteoclast precursors.(3)The RANKL–RANK binding interaction,together with macrophage colony-stimulating factor (M-CSF), causesosteoclast precursors to differentiateinto mature osteoclasts.(4)As mature osteoclasts resorb bone,matrix-bound factors such as TGF-β, IGF-1, other growth factors, and cytokines are released.
(5) These liberated factors stimulate osteoblast precursors to develop into mature osteoblasts, which begin to refill the resorption cavities excavated by the osteoclasts

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10
Q

what hormones influence bone formation and metabolism?

A
  • ParathyroidHormone-increase bone abs and formation
  • Calcitonin- increases calcium activity, reduces calcium ion concentration in body fluids
  • Oestrogen
  • Androgen- stimulates bone phosphate faster than the rate they expand
  • Growth hormone- osteoblast activity
  • Glucocorticoids- inhibit bone formation
  • Thyroid hormones
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11
Q

what local regulators influence bone remodelling?

A
  • Cytokines•IL-6•IL-1•Prostaglandins

* Growth factors•IGF-I•TGF-β

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12
Q

what vitamins and minerals influence bone formation and metabolism?

A
  • Calcium
  • Vitamin D
  • Copper
  • Magnesium
  • Potassium
  • Silicon
  • Zinc
  • Vitamin B6, B9, B12
  • Vitamin C
  • Vitamin E
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13
Q

what are metabolic bone diseases and how would they present?

A

osteoporosis- backpain, loss of height, fracture
pagets disease- deformity of long bones, pain in hips
osteomalacia- generalised bone pain, muscle weakness

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14
Q

what is osteoporosis?

A

Skeletal disorder characterized by the loss of bone mass and micro-architectural deterioration of the bone tissue with a subsequent increase in bone fragility and susceptibility to fractures

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15
Q

what are the causes of osteoporosis?

A

Can occur as the result of an endocrine disorder or malignancy–Most often associated with the aging process–Commonly postmenopausal women , men over 50years and in patients taking long term oral corticosteroids (glucocorticoids)

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16
Q

what influences bone mass?

A

physical activity, genetic, nutrition

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17
Q

how does menopause contribute to osteoporosis?

A
  • decreased oestrogen
    increased IL1,6 tnf levels
    increased expression of RANK,RANKL
    increased osteoclast activity
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18
Q

how does aging influence osteoporosis?

A

decreased replicative activity of osteoprogenitor cells
decreased synthetic activity of osteoblasts
decreased biological activity of matrix-bound growth factors
reduced physical activity

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19
Q

what causes osteoporosis?

A

increased production of cytokines
longer lifespan of osteoclasts- dec apotosis
shorter lifespan of osteoblasts - inc apoptosis
shorter lifespan of osteocytes
leads to bone fracture

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20
Q

what are the risk factors associated with osteoporosis?

A
  • Personal characteristics–Aging female, small bone structure, postmenopausal, family history
  • Lifestyle–Sedentary, vitamin D deficiency, low calcium intake, high-protein diet, excessive alcohol and caffeine intake, smoking
  • Drug related
  • Disease related
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21
Q

what are risk factors causing reduction in bone mass?

A 
Glucocorticoid treatment
Cushing's  syndrome
Hyperthyroidism
Hyperparathyroidism
Gluten sensitive enteropathy
Inflammatory bowel disease
22
Q

what medicines are associated with risk factors of osteoporosis?

A 
Oral glucocorticoids (steroids)
–TZDs –pioglitazone–PPIs
–Cancer treatments (radiation, chemo)
–Thyroxine
–Antiepileptic medications
 –phenytoin, CMZ
–Gonadal hormone suppression -medroxyprog
–Immunosuppressive agents
23
Q

when should an assessment of fracture risk be done?

A

In all women aged 65 years and over and all men aged 75 yearsand over
•In women aged under 65 years and men aged under 75 years inthe presence of risk factors, for example:

24
Q

what are the risk factors you would assess someone u65 for fracture risk ?

A

previous fragility fracture–current use or frequent recent use of oral or systemic glucocorticoids–history of falls–family history of hip fracture–other causes of secondary osteoporosis–low body mass index (BMI) (less than 18.5 kg/m2)–smoking–alcohol intake of more than 14 units per week for women and more than 21 units per week for men.

25
Q

what are indicators of low bone mineral density?

A 
low body mass index below 18.5 kg/m2–
ankylosing spondylitis
–Crohn’s disease
–conditions resulting in prolonged immobility
–untreated premature menopause.
26
Q

when do you assess fracture risk for someone u50?

A

unless they have major risk factors(forexample, current or frequent recent use of oral or systemic glucocorticoids, untreated premature menopause or previous fragility fracture), because they are unlikely to be at high risk.

27
Q

how do you diagnose osteoprosis?

A

Bone mineral density (BMD) assessment•Z score (compared to the excepted BMD forpatient’s age and sex)
•T score (compared to young adults of the same sex)Dual-energy x-ray absorptiometry (DEXA) of the spineand hip

28
Q

what do the T scores indicate?

A
  • T score between -1.0 and -2.5 defines osteopenia

* T score of less or less than -2.5 defines osteoporosis

29
Q

how do you treat osteoporosis?

A

Important factors in preventing osteoporosis
•Regular exercise
•Adequate calcium intake
•Oral bisphosphonates for prevention of postmenopausal osteoporosis

Important in the maintenance of bone mass
•Weight-bearing exercises such as walking, jogging ,rowing, and weight lifting

30
Q

what does the treatment of osteoporosis depend on?

A
  • BMD values less than -2.5
  • BMD value less than -1.5 in corticosteroid –induced osteoporosis
  • Treatment in patients with vertebral fracture irrespective of BMD, unless resulted from significant trauma
31
Q

how do bisphosphonates work? give an example

A

•Inhibitors of bone resorption and increase BMD by altering osteoclast activation and function.
alendronate, etidronate, risedronate
1- incorporate into ATP anlogues that accumulate within the osteoclasts and promote their apoptosis
2-Prevent bone resorption by interfering with the cell surface proteins on the osteoclast membrane by prenylation, thereby preventing osteoclast attachment to bone

32
Q

when are oral bisphosphonates recommended?

A

e person is eligible for risk assessment as defined in NICE’s guideline on osteoporosis
–the 10-year probability of osteoporotic fragility fracture is at least 1%.

33
Q

when are IV bisphosphonates recommended?

A

–the person is eligible for risk assessment as defined inNICE’s guideline on osteoporosis
–the 10-year probability of osteoporotic fragility fracture is at least 10%
OR–the 10-year probability of osteoporotic fragilityfracture is at least 1% and the person has difficultytaking oral bisphosphonates(alendronic acid,ibandronic acid or risedronate sodium)or these drugs are contraindicated or not tolerated.

34
Q

how should oral bisphosphonates be taken?

A

taken on an empty stomach with plain water only and no food, beverage or other medicines for 30 min
- NOT lie down for at least 30 min after taking
GIT disturbances are commonly seen

35
Q

when may adjustments have to be made with oral bisphosphonates?

A

Dose adjustments may be needed in renal impairment(e.g. alendronic acid should be avoided if eGFR<35ml/min/1.73m2).
•Certain bisphosphonates should be used with caution in hepatic impairment (e.g. zoledronic acid in severe hepatic impairment)

36
Q

give examples of clinical applications of bisphosphonates

A
  • prophylaxis of glucocorticoid osteoporosis
    hypercalcaemia of malignancy
    pagets disease
    bone metastases
37
Q

what are the side effects of bisphosphonates?

A
  • Oesophageal irritation
  • Flu-like syndrome
  • GI disturbances
  • Headache
  • Musculoskeletal pain
38
Q

what interacts with bisphosphonates?

A
  • Reduced absorption of bisphosphonates with
  • Antacids
  • Calcium salts
  • Iron supplements
39
Q

what is a first line option bisphosphonate?

A

•Oral bisphosphonates are first-line options.
•Intravenous zoledronic acid or teriparatide are alternatives in patients intolerant of oral
bisphosphonates or in whom they are contra-indicated.
•Dose: Intravenous Zoledronic Acid5mg once peryear

40
Q

what is SERM?

A

SERM (raloxifene) has selective agonist or antagonist activities on tissues responsive to oestrogen.

41
Q

how does SERM work?

A
  • Stimulates osteoblasts and inhibits osteoclasts
  • Acts - agonist on bone and partially on cholesterol metabolism (decrease in total and LDL-cholesterol)•Acts - antagonist hypothalamus, or in the uterine or breast tissues.
42
Q

how does teripartide work?

A

A recombinant fragment of human parathyroid hormone
•Stimulates new formation of bone and increases structural integrity and bone strength.
•By increasing the number of osteoblasts and by activating those osteoblasts already in bone
•Reduces osteoblast apoptosis

43
Q

what are the side effects of teripartide?

A
  • Nausea
  • Oesophageal reflux
  • Hypotension
  • Dyspnoea
  • Depression
  • Dizziness
44
Q

when is teripartide recommended?

A

alternative treatment option for the secondary prevention of osteoporotic fragility fractures in postmenopausal women:
•Unable to take alendronate and risedronate, or have a contraindication to or are intolerant of alendronate and risedronate,
•Unsatisfactory response to treatment with alendronate or risedronate and who are 65 years or older and have a T-score of –4.0 SD or below, or a T-score of –3.5 SD or below plus more than two fractures, or who are aged55–64 years and have a T-score of –4.0 SD or below plus more than two fractures

45
Q

how long should you use teripartide for?

A

Maximum duration of treatment is 24 months only and a course should never be repeated

46
Q

what are disorders involving softening of the bones?

A

osteomalacia

rickets

47
Q

what is osteomalacia?

A

–A generalized bone condition in which inadequate mineralization of bone results from a calcium or phosphate deficiency, or both

48
Q

what is rickets?

A

A disorder of vitamin D deficiency, inadequate calcium absorption, and impaired mineralization of bone in children

49
Q

what is paget disease?

A

A progressive skeletal disorder that involves excessive bone destruction and repair

50
Q

what are the manifestations of paget disease?

A

increasing structural changes of the long bones, spine, pelvis, and cranium

51
Q

what are the drugs used to treat paget disease?

A

Bisphosphonates

•Calcitonin

PHA 332 (42 decks)

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