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Z MD1 locomotor and exercise block > pharmacology for bone disorders and inflammation > Flashcards

pharmacology for bone disorders and inflammation Flashcards

(49 cards)

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1
Q

what two major types of drugs are used in bone disorders

A 
antiresorptive agents (anti-osteoclast)
bone anabolic agents (pro-osteoblasts and osteocyt
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2
Q

what are the drugs used that are anti-resorptive agents for bone disorders

A

bisphosphates
selective oestrogen receptor moedulators
RANK Ligand inhibitors

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3
Q

what are the drugs used that are bone anabolic agents for bone disorders

A

parathyroid hormone
oral calcium
oral vitamin D analogues
calcitonin

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4
Q

what is an example of a drug that is a bisphosphonate

A

alendronate

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5
Q

what are bisphosphonates

A

resistant analogues of pyrophosphate (analogue of the bone matrix)

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6
Q

action of bisphosphonates

A
  • inhibit the recruitment of osteoclasts

- promote apoptosis of osteoclasts

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7
Q

explain the administration of bisphosphonates

A

administered weekly

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8
Q

what is the disadvantage of taking bisphosphonates

A
  • oesophagitis risk
  • oesophageal cancer risk
  • atypical fracture risk
  • osteonecrosis of the jaw risk
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9
Q

how is oestrogen administered for bone disorders

A

administered with a progestagen

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10
Q

side effects of taking oestrogen for bone disorders

A

increased risk of cardiovascular disease and breast cancer

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11
Q

what do we use now instead of giving oestrogen for treating bone disorders

A

selective oestrogen receptor modulators (SERM’s)

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12
Q

what is an example of a drug that is a SERM

A

Raloxifene

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13
Q

what is the action of Raloxifene

A
  • agonist at oestrogen receptors in bone and cardiovascular tissue
  • antagonist at oestrogen receptors in mammary tissue and uterus
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14
Q

what is Denosumab

A

a RANK ligand inhibitor

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15
Q

action of Denosumab

A

binds to RANKL and inhibits RANKL activity –> reducing osteoclastic activity

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16
Q

what is the advantage of Denosumab over other drugs for bone disorders

A

it has been shown to increase bone density in post menopausal women

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17
Q

explain the paradoxical behaviour of PTH

A
  • Acutely: promotes osteoblast development and activity –> favours bone anabolism
  • Continuous/high exposure: promotes osteoclast activity –> promotes bone catabolism
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18
Q

what are the side effects of taking oral calcium for bone disorders

A

GI disturbances

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19
Q

what are 2 drugs called that are oral calcium drugs

A

calcium gluconate

calcium lactate

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20
Q

when is Vitamin D drug treatment used

Study These Flashcards
A
  • deficiency states (rickets and osteomalacia)
  • endocrine dysfunction (hypoparathyroidism)
  • chronic renal disease (where calcitriol cannot be generated in kidney)
21
Q

how do you give Vitamin D to a patient (other than sunlight)

Study These Flashcards
A
  • Vit D2 –> converted to D3 in liver

- calcitriol (biologically active)

22
Q

what are the two types of calcitonin medications

Study These Flashcards
A 
natural calcitonin (porcine) 
synthetic calcitonin (salcatonin)
23
Q

how do you administer calcitonin to a patient

Study These Flashcards
A

given by SC or IM injection or nasal spray

24
Q

anti inflammatory medications target what

25
how are glucocorticoids anti-inflammatory
they inhibit AA release and metabolism --> suppressing the formation of pro-inflammatory prostaglandins and leukotrienes
26
how are NSAIDs anti-inflammatory
inhibit COX 1 and 2 --> suppresses the formation of pro-inflammatory prostaglandins
27
how are CysLT1 receptor antagonists anti inflammatory
they block LTC4 and LTD4 actions
28
what is the difference between COX1 and COX2
COX1 - constitutively expressed in most cells | COX2 - expressed in inducible inflammatory cells
29
what cells express COX2
macrophages fibroblasts SM endothelium
30
what are the effects of cannabinoid 1 and 2 receptors
``` appetite stimulation anti-nauseant analgesia sedation psychoactivity ANTI-INFLAMMATORY ```
31
where is the distribution of CB1 and CB2 receptors
CB1 - CNS | CB2 - in the periphery
32
what are two drugs that are used that mimic the actions of prostaglandins
epoprostenol PGI2 analgoue | misoprostol PGE1 analogue
33
what is the action of epoprostenol PGI2 analogue
vasodilates the pulmonary vasculature - used in pulmonary hypertension
34
what is the use of misprostol PGE1 analogue
as an adjuvant to mifepristone as abortifacient
35
what are the effects and indications of NSAIDs
- anti-inflammatory - acute and chronic inflammatory conditions - analgesic - headache, menstrual pain... - anti-pyretic - (anti-aggregatory)
36
why is aspirin contraindicated in gout
because aspirin and uric acid crystals use the same anion transporter in the kidney
37
what are the adverse effects of NSAIDs
- gastrointestinal ucers - increased bleeding time - renal effects - pulmonary effects
38
why do NSAIDs cause gastrointestinal side effects
because it inhibits mucosal synthesis of PGI2 and PGE2 which are protective in the stomach
39
what are the roles of PGE2 in the stomach
- increases mucus secretion - reduces gastric acid secretion - promotes blood flow - promotes angiogenesis
40
why do NSAIDs cause an increased bleeding time
because they decrease TXA2 synthesis --> impaired platelet aggregation
41
how can NSAIDs cause renal effects
- because they cause a decreased prostacyclin synthesis --> decreased dilatation of renal artery - may decrease PGE2 --> decreased natriuresis --> increased blood pressure
42
NSAIDs may cause renal failure in which kind of patients
- hypovolaemic patients - patients with underlying renal disease - patients with heart failure
43
how can NSAIDs cause pulmonary effects
can push the arachadonic acid pathway down the leukotriene route --> aspirin sensitive asthma
44
what are the 2 effects of aspirin
- irreversible acetylation of COX --> PGI2/TXA2 ratio increased - acetylated COX synthesis aspirin triggered lipoxins (ATLs)
45
what is the action of aspiring triggered lipoxins
pro resolution mediatory --> turns off the infiltration of the tissue by neurtrophils
46
why is paracetamol special
it is analgesic and antipyretic... but NOT anti-inflammatory
47
what is celecoxib
a selective COX2 inhibitor
48
why was celecoxib made
because COX2 selective means: - less GI adverse effects - less anti-platelet effect
49
3 principle mechanisms of glucocorticoids
direct transactivation direct transrepression tethered transrepression

Z MD1 locomotor and exercise block (13 decks)

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