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pharmacology 3 > metabolic bone disease > Flashcards

metabolic bone disease Flashcards

1
Q

T score of osteoporosis

A

T score of -2.5 or worse

-1 to -2.5 for osteopenia

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2
Q

second degree causes of osteoperosis

A 
increased PTH
glococorticoid use 
autoimmune 
hypogonadism 
calcium/vitamine D defciency 
renal disease 
aromatase inhibition (breast ca.)
androgen deprivation (prostate ca.)
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3
Q

diet and lifestyle appraoches

A 
adequate calcium and protein intake 
safe exposure to sunlight 
healthy weight and BMI 
cessation of smoking 
avoidance of alcohol
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4
Q

reducing risk of falls

A

falls risk assessments and initiate targeted fall-prevention programs in older adults

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5
Q

exercise

A

individuals over 50 years of age without osteoperosis should participate regularly in progressive resistance training and balance training exercise

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6
Q

patients who should not be recieving treatemtn

A

patients at low risk (10 year risk <10%)

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7
Q

recommendations for calcium

A

1300mg from diet and suppliment combined

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8
Q

recommendation for vit D

A

800-200 IU daily for age over 50

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9
Q

antiresorbtive drugs

A

aim to inhibit bone resorbtion by decreasing bone turnover or disrupting osteoclast formation and maturation

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10
Q

anabolic agents

A

aim to inverse the imbalance in bone remodelling by stimulating bone formation, therefore increasing BMD

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11
Q

3 antiresorptives

A
  • bisphosphates
  • denosumab
  • SERMs
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12
Q

3 anabolics

A

PTH (teriparatide)
PTHrP (abaloparatide)
sclerosin (romosozumab)

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13
Q

3 bisphosphonates

A

alendronate
risedronate
zoledronic acid

nitrogen containing R2 side chains

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14
Q

structure of bisphosphonates

A

structurally linked to inorgnic phyrophosphate, a naturally occuring compound consisting of two phosphate groups

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15
Q

bisphosphonates have a high affinity for

A

very high affinity for hydroxyapatite (inorganic phase of bone)

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16
Q

action of bisphosphonates

A

induce osteoclast apoptosis following resorption
inhibition of farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonic acid pathway
interferes with small GTP-binding proteins which play central roles in osteoclast function
collapse and death of osteoclast

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17
Q

use of bisphosphonates

A

prevention of vertebral fracture in women with ostepenia (>10 years postmenopause)
reduce vertebral and non-vertebral fractures in women and men >50yo at high risk
use for 5 years then reassess

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18
Q

administration of bisphosphonates

A

oral or IV

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19
Q

side effects of bisphosphonates

A 
oesophageal ulceration (oral)
musculoskeletal pain 
hypocalcaemia 
fever 
osteonecrosis of jaw
atypical femoral fracture (spontaneous)
adynamic bone disease
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20
Q

denosumab

A

inhibitor of rank ligand

is an IgG2 monoclonal antibody that suppresses bone resorption by mimicking the action of OPG in bone microenvironment

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21
Q

action of denosumab

A

anti-resoptive

denosumab ibinds to RANKL preventing its binding to RANK, reducing osteoclast development, survival and bone resorption

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22
Q

uses of denosumab

A

denosumab is recommended for the treatment of osteoperosis in post menopausal women and men at increased risk of minimal trauma fracture
considered alternative for bisphosphonates

23
Q

administration of denosumab

A

subcutaneously at a dise of 60mg once every six months

24
Q

side effects

A

denosumab used in the treatment of osteoperosis is generally well-tolerated

  • cellullitis (skin infections)
  • hypocalcaemia (chronic kidney disease)
  • osteonecrosis of jaw (ONJ)
  • atypical femoral fracture
  • multiple vertebral fractures upon discontinuation (rebound)
25
Q

denosumab vs. biphosphonates

A

unlike bisphosphonates, denosumab is not characterised by a long biological half life not is it incorporated into the bone
antiresorptive effect of denosumab caeses after suspension of treatment
concerns about a drug rebound ‘vertebral fractures following discontinuation’
re-evaluation of risk should be assessed after five years

26
Q

denosumab rebound

A

denosumab cessation should not be considered without alternative osteoporosis treatment

27
Q

patients discontinuing denosumab

A

should recieve follow-up treatment with bisphosphonate and be monitored closely

28
Q

1 selective estrogen receptor modulators (SERMs)

A

raloxifene

29
Q

structure of SERMs

A

synthetic non-steroidal agents

30
Q

action of SERMs

A

osterogen agonist and antagonist activities in defferent tissues as well as anti-fracture efficacy
oestrogen receptors are found on osteoclasts and osteobalsts and ostrogen depletion leads to bone loss
SERMs decrease osteoclast activity leading to educed bone resorption

31
Q

raloxfene use

A

a treatment opton for postmenopausal wmen with osteoperosis where vertebral fractures are considered to be the major osteoperosis rsk and where other agents are porly tolerated
may be particularly useful in younger postmenopausal women at risk of vertebral fracture and who have a prior or family history of breast cancer

32
Q

administration of raloxifene

A

oral at a dose of 60mg per day

33
Q

side effects of raloxifene

A

oestrogen replacement
- increased risk of invasive breast cancer
- increased coronary heart disease
- increased risks of thromboembolic events and cerebrovascular accident
raloxifene
- may increase hot flushes
- increased thromboembolic events (2.5x) but not heart disease or overall risk of stroke
- has little to no effect on endometrium and may not predispose to uterine cancer

34
Q

teriparatide

A

part of parathyroid hormone
anabolic
binds to PTH type 1 receptor, a g-protein coupled receptor, expressed on osteoblasts
increased new bone formation by osteoblasts
increased the osteoblasts survival by reducing apoptosis and inducing recruitment and formation of new osteoblasts

35
Q

use of teriparatide

A

increases lumbar spine and femorral neck BMD
decreases vertebral and non-vertebral fractures in postmenopausal osteoperosis with prior fracture
recommended for postmenopausal women and men over 50 years of age with osteoperosis wh have sustained a sebsequent fracture while on anti-resorbtive therapy

36
Q

PBS qualification for teriparatide

A

a BMD score of <3 or less
had two or more fractures due to minimal trauma
experiencced at least one symptomatic new fracture after at lleats 12 months continuous therapy with an antiresorptive agent

37
Q

administration of teriparatide

A

subcutanous 20 micro gram daily (intermittant stimulation) for 18 months (switch to antiresorbtive)

38
Q

teriparatide side effects

A 
dizziness
leg cramps 
nausea
headache 
transient hypercalcaemia 
mild increases in uric acid without the development of acute gout 
increased risk of osteogenic sarcoma
39
Q

teriparatide is not recommended for patients with

A

paget disease, prior skeletal irridation, bony metastases or prior skeletal malignancies, and for those with metabolic bone disease (other than osteoperosis) or pre-existing hypercaalcaemia

40
Q

cessation of teriparatide

A

BMD decreases within 12 hours after cessation, required sequential treatment with antiresobtive drug

41
Q

abaloparatide

A

is a synthetic human parathyroid hormone related peptide

42
Q

action of abaloparatide

A

anabolic
like teriparatide, acts as an agonist at the PTH1 receptor
this results in activation of the cAMP signalling pathway is osteoblasts
increase bone formation by osteoblasts
anabolic profile similar to teriparatide but has reduced bone resorption by an unknown mechanism

43
Q

uses of abaloparatide

A

for osteoporosis patients at very high fracture risk or do not respond to other osteoporosis drugs

44
Q

administration of abaloparatide

A

once-daily 80 micrograms subcutaneous injection

18 months then switch to antiresorbtive

45
Q

side effects of abaloparatide

A

similar to teriparatide but show dose dependant increased risk of osteosarcoma in rates
same cessation effecs

46
Q

issues with anti-resorbtives

A

administered late - patients are already osteopenic/osteoporotic
poor compliance
undesirable effects
- atypical subchanteric femoral fractures
- osteonecross of the jaw

47
Q

issues with anabolics

A
  • few approved
  • administeres late - patinets are. already osteoporotic, sustained a fracture
  • expensive
  • invasive injection
  • fracture efficacy limites
  • antiresoorptive required after cycle
  • osteosarcoma and cardiovascular risks
48
Q

anti-sclerosin

A

new therapy
sclerosin inhibits canonical Wnt signalling pathways
Wnt signally pathway in osteoblasts is responisble for stimulating bone formation in response to mechanical loading by stimulating osteoblast proliferation
sclerosin in synthesized by osteocytes when bone is inloaded, inhibiting bone formation

49
Q

1 anti-sclerostin

A

romosozumab

50
Q

structure of romosozumab

A

a humanised monoclonal antibody against sclerostin

51
Q

action of romosozumab

A

anabolic - potent
inhibitss sclerostin
stimulates canonical WNT signalling in osteoblasts
increased bone formation and reduced fracture risk

52
Q

use of romosozumab

A

for the treatment of osteoporosis in postmenopausal women at high risk for fracture

53
Q

administration of romosozumab

A

210mg subcutaneous injection once monthly for 12 months

54
Q

side effects of romoszumab

A

increased cardiovascular/stroke risk?

pharmacology 3 (8 decks)

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