Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology and Therapeutics 2 Y2 > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

How do NSAIDs work?

A

Inhibit prostanoid synthesis by inhibiting COX1 and 2 enzymes

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

Example of prostanoids? (2)

A

prostaglandin and thromboxane

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

What are all prostanoids derived from?

A

Arachidonic acid

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

What is the rate limiting step in prostanoid synthesis

A

COX

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

How’re different prostanoids produced

A

Different prostanoids are produced by different specific synthases downstream of the COX enzymes

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

How many known prostanoid receptors are there?

A

10 known receptors

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

How many known prostanoids are there

A

5

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

What receptors can PGE2 activate?

A

EP1, 3, 2 and 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which prostaglandin receptors increase Ca mobilisation?

A

EP1 and 3

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

Which prostaglandin receptors increase cAMP?

A

EP2 and 4

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

Which prostaglandin receptors downregulates cAMP?

A

EP3

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

What does PG receptor EP3 do?

A

Increase Ca mobilisation and downregulates cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does PG receptor EP4 do?

A

increase cAMP

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

What does PG receptor EP2 do?

A

increase cAMP

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

What does PG receptor EP1 do?

A

Increase Ca mobilisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Unwanted effects of PGE2? (6)

A
  • Increased pain perception
  • Increased body temp.
  • Acute inflammatory response
  • Immune responses
  • Tumorigenesis
  • Inhibition of apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do prostanoids lower the pain threshold? (receptors, location, other modulators, NT increased?)

A

 EP1 receptors
 EP4 receptors (in periphery and spine)
 Endocannabinoids (neuromodulators in the thalamus, spine ad periphery)
 Increasing beta-endorphin in the spine

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

What is stimulated by external irritants to produce PGE2

A

Keratinocytes

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

What are stimulated to give calcium release through EP3 receptors

A

Mast cells

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

PGE2 role in inflammation through EP3 receptors?

A

Keratinocytes are stimulated by external irritants to produce PGE2
EP3 receptors on mast cells are, in turn, stimulated to give calcium release and degranulation of histamine granules (histamine release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What PG is pyrogenic?

A

PGE2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does PGE2 cause a rise in body temp.?

A

PGE2 stimulates hypothalamic neurones initiating a rise in body temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Re. body temp, what do NSAIDs do?

A

NSAIDs reduce raised temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do PGE2 analogues do re. pain threshold?

A

Lower it by sensitising nociceptors in the periphery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Desirable actions of PGE2? (4)

A
  • Bronchodilation
  • Renal salt and water homeostasis
  • Gastroprotection
  • Vaso-regulation (dilation/constriction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Effect of NSAIDs on the respiratory system? Why?

A

Cause asthma attacks etc as COX products cause bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

COX inhibition favours what product that causes vasoconstriction?

A

Leukotrienes

28
Q

What group of people should never be put on NSAIDs

A

Asthmatics

29
Q

Regarding kidneys, what can NSAIDs induce?

A

Renal toxicity

30
Q

How do NSAIDs induce renal toxicity (3)

A
  • Constriction of afferent renal arteriole
  • Reduction in renal artery flow
  • Reduced GFR
31
Q

Which COX enzymes are involved in salt and water homeostasis?

A

Both COX1 and 2

32
Q

Role of PGE2 in gastric cytoprotection

A
  • Parietal cell normally produces HCl and secretes it into the stomach- therefore the stomach needs protection
  • This protection comes in the form of a mucus layer and bicarbonate secretion
  • PGE2 normally downregulates HCl secretion, and also stimulates mucus and bicarbonate secretion THESE ARE COX-1 DEPENDENT
33
Q

Which COX is involved in gastric cytoprotection

A

COX1

34
Q

Which isoforms of COX do most NSAIDs inhibit

A
  • Most NSAIDs reversibly inhibit both isoforms
35
Q

What family of drugs Selectively and reversibly inhibit COX-2

A

Coxib

36
Q

Example of a Coxib?

A

Celecoxib

37
Q

Celecoxib is an example of what drugs

A

COX2 selective inhibitor

38
Q
  • NSAIDs can have serious unwanted cardiovascular effects such as: (3)
A

Vasoconstriction
Salt and water retention
Reduced effectiveness of anti-hypertensives
Bronchoconstriction

39
Q

Which COX inhibition poses a higher risk of CVD

A

COX2

40
Q

Which COX inhibition poses a higher risk of GI bleed

A

COX1

41
Q

COX1 inhibition poses a higher risk of what

A

GI Bleeds

42
Q

COX2 inhibition poses a higher risk of what

A

CVD

43
Q

Dosage of NSAID for analgesic effect

A

Low

44
Q

Dosage of NSAID for anti-inflammatory effect

A

High

45
Q

Which carries less side effects, analgesic or anti-inflammatory uses of NSAIDs and why

A

Analgesic use (as its mainly only occasional)

 Anti-inflammatory use (sustained):

  • Higher doses
  • Relatively high risk of side effects
46
Q

STRATEGIES OTHER THAN COX-2 SELECTIVE NSAIDs FOR LIMITING GI SIDE EFFECTS: (5)

A
  1. Topical application – reducing dose and reducing amount in systemic circulation
  2. Minimise NSAID use in patients with history of GI ulceration
  3. Treat H pylori if present
  4. If NSAID essential, administer with omeprazole or other PPI (proton pump inhibitors to reduce acid production and provide a gastroprotective effect)
  5. Minimise NSAID use in patients with other risk factors and reduce risk factors where possible:
    Alcohol consumption
    Anti-coagulant or glucocorticoid steroid use
47
Q

Aspirin is selective for?

A

COX1

48
Q

Aspirin effects? (4)

A
  • Has anti-inflammatory, analgesic and anti-pyretic actions

- Reduces platelet aggregation in low doses

49
Q

How does aspirin interact with COX

A
  • Binds IRREVERSIBLY to COX enzymes – to overcome it you must synthesise new enzymes
50
Q

Which prostaglandin is anti-inflammatory/platelet aggregation

A
  • PGI2 (prostacyclin from endothelial cells)
51
Q

Aspirin effects on platelet aggregation (think TXA2 and PGI2)

A
  • Aspirin inhibits thromboxane production because that requires COX-1
  • PGI2 can use both COX-1 and COX-2 so it is only partially inhibited
  • OVERALL: Endothelial cell recovers and continues to produce prostacyclin, but the platelet has no nucleus so it can’t do this- you get no re-synthesis of COX-1 The overall effect of this is reduced platelet aggregation
52
Q

why can’t platelets resynthesise COX1 after aspirin irreversibly binds to it

A

Platelet has no nucleus

53
Q

Difference between effect on platelet aggregation of High dose of aspirin vs low dose

A

High dose of aspirin has no action on platelet aggregation because you also block endothelial cell re-synthesis of COX

54
Q

Aspirin side effects (4):

A
  • Gastric irritation and ulceration
  • Bronchospasm in sensitive asthmatics
  • Prolonged bleeding times
  • Nephrotoxicity
55
Q

Why is paracetamol technically not an NSAID

A
  • Does NOT have anti-inflammatory effect
56
Q

Effects of paracetamol? (2+1 thing it doesn’t do)

A
  • A good analgesic for mild-to-moderate pain
  • Has anti-pyretic action
  • Does NOT have anti-inflammatory effect Therefore TECHNICALLY it’s not an NSAID
57
Q

What do we theorise aspirin interacts with?

A
  • Via cannabinoid receptors (?)
  • Interactions with endogenous opioids (?)
  • Interaction with 5HT (serotonin) and adenosine receptors (?)
58
Q

What metabolises aspirin

A

CYP450

59
Q

What is the metabolite of aspirin involved in overdose

A

NAPQI

60
Q

What converts the toxic metabolite of aspirin NAPQI into an inactive form

A

Glutathione

61
Q

How does paracetamol OD work?

A
  • NAPQI is the metabolite involved in overdose
  • Glutathione usually converts this into an inactive form
     If glutathione is depleted (O.D.), NAPQI oxidises thiol groups of key hepatic enzymes and causes cell death
62
Q

What group is the antidote for paracetamol poisoning?

A

-SH

63
Q

What is given for paracacetamol poisoning

A

Acetylcysteine

64
Q

What is acetylcysteine used for

A

Paracetamol OD

65
Q

Why is methionine no longer added to paracetamol to prevent overdose

A

issa expensive drug

66
Q

What used to be added to paracetamol to prevent OD

A

Methionine

67
Q

Legislation of paracetamol? pack size and pack number

A

No more than 2 packs per transaction

Illegal to sell more than 100 paracetamol in one transaction

Pharmacology and Therapeutics 2 Y2 (24 decks)

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