Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

z md1 locomotor and exercise block > pharmacology for bone disorders and inflammation > Flashcards

pharmacology for bone disorders and inflammation Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

bisphosphates
selective oestrogen receptor moedulators
RANK Ligand inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is an example of a drug that is a bisphosphonate

A

alendronate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are bisphosphonates

A

resistant analogues of pyrophosphate (analogue of the bone matrix)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

action of bisphosphonates

A
  • inhibit the recruitment of osteoclasts

- promote apoptosis of osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

explain the administration of bisphosphonates

A

administered weekly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the disadvantage of taking bisphosphonates

A
  • oesophagitis risk
  • oesophageal cancer risk
  • atypical fracture risk
  • osteonecrosis of the jaw risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how is oestrogen administered for bone disorders

A

administered with a progestagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

side effects of taking oestrogen for bone disorders

A

increased risk of cardiovascular disease and breast cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

selective oestrogen receptor modulators (SERM’s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is an example of a drug that is a SERM

A

Raloxifene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is Denosumab

A

a RANK ligand inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

action of Denosumab

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

GI disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are 2 drugs called that are oral calcium drugs

A

calcium gluconate

calcium lactate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

when is Vitamin D drug treatment used

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)

A
  • Vit D2 –> converted to D3 in liver

- calcitriol (biologically active)

22
Q

what are the two types of calcitonin medications

A 
natural calcitonin (porcine) 
synthetic calcitonin (salcatonin)
23
Q

how do you administer calcitonin to a patient

A

given by SC or IM injection or nasal spray

24
Q

anti inflammatory medications target what

A

eicosanoids

25
Q

how are glucocorticoids anti-inflammatory

A

they inhibit AA release and metabolism –> suppressing the formation of pro-inflammatory prostaglandins and leukotrienes

26
Q

how are NSAIDs anti-inflammatory

A

inhibit COX 1 and 2 –> suppresses the formation of pro-inflammatory prostaglandins

27
Q

how are CysLT1 receptor antagonists anti inflammatory

A

they block LTC4 and LTD4 actions

28
Q

what is the difference between COX1 and COX2

A

COX1 - constitutively expressed in most cells

COX2 - expressed in inducible inflammatory cells

29
Q

what cells express COX2

A

macrophages
fibroblasts
SM
endothelium

30
Q

what are the effects of cannabinoid 1 and 2 receptors

A 
appetite stimulation
anti-nauseant
analgesia
sedation
psychoactivity
ANTI-INFLAMMATORY
31
Q

where is the distribution of CB1 and CB2 receptors

A

CB1 - CNS

CB2 - in the periphery

32
Q

what are two drugs that are used that mimic the actions of prostaglandins

A

epoprostenol PGI2 analgoue

misoprostol PGE1 analogue

33
Q

what is the action of epoprostenol PGI2 analogue

A

vasodilates the pulmonary vasculature - used in pulmonary hypertension

34
Q

what is the use of misprostol PGE1 analogue

A

as an adjuvant to mifepristone as abortifacient

35
Q

what are the effects and indications of NSAIDs

A
  • anti-inflammatory - acute and chronic inflammatory conditions
  • analgesic - headache, menstrual pain…
  • anti-pyretic
  • (anti-aggregatory)
36
Q

why is aspirin contraindicated in gout

A

because aspirin and uric acid crystals use the same anion transporter in the kidney

37
Q

what are the adverse effects of NSAIDs

A
  • gastrointestinal ucers
  • increased bleeding time
  • renal effects
  • pulmonary effects
38
Q

why do NSAIDs cause gastrointestinal side effects

A

because it inhibits mucosal synthesis of PGI2 and PGE2 which are protective in the stomach

39
Q

what are the roles of PGE2 in the stomach

A
  • increases mucus secretion
  • reduces gastric acid secretion
  • promotes blood flow
  • promotes angiogenesis
40
Q

why do NSAIDs cause an increased bleeding time

A

because they decrease TXA2 synthesis –> impaired platelet aggregation

41
Q

how can NSAIDs cause renal effects

A
  • because they cause a decreased prostacyclin synthesis –> decreased dilatation of renal artery
  • may decrease PGE2 –> decreased natriuresis –> increased blood pressure
42
Q

NSAIDs may cause renal failure in which kind of patients

A
  • hypovolaemic patients
  • patients with underlying renal disease
  • patients with heart failure
43
Q

how can NSAIDs cause pulmonary effects

A

can push the arachadonic acid pathway down the leukotriene route –> aspirin sensitive asthma

44
Q

what are the 2 effects of aspirin

A
  • irreversible acetylation of COX –> PGI2/TXA2 ratio increased
  • acetylated COX synthesis aspirin triggered lipoxins (ATLs)
45
Q

what is the action of aspiring triggered lipoxins

A

pro resolution mediatory –> turns off the infiltration of the tissue by neurtrophils

46
Q

why is paracetamol special

A

it is analgesic and antipyretic… but NOT anti-inflammatory

47
Q

what is celecoxib

A

a selective COX2 inhibitor

48
Q

why was celecoxib made

A

because COX2 selective means:

  • less GI adverse effects
  • less anti-platelet effect
49
Q

3 principle mechanisms of glucocorticoids

A

direct transactivation
direct transrepression
tethered transrepression

z md1 locomotor and exercise block (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions