Brainscape's Knowledge GenomeTM

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


See full index

PA MS > PAMS pharmacology: COX1 and COX2 inhibitors > Flashcards

PAMS pharmacology: COX1 and COX2 inhibitors Flashcards

1
Q

What are the actions of NSAIDs class of drugs ?

A

These are drugs with analgesic, anti-inflammatory, antipyretic, anti-platelet properties.

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

What is the principle mechanism by which NSAIDs act ?

A

They inhibit the Cyclooxygenase enzyme which is responsible for converting arachidonic acid to Prostaglandin H2 or PGH2.

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

what are the prostaglandin subforms to which PGH2 is converted by the tissue specific isomerases ?

A

PGD2, E2, F2, I2 ( prostacyclin), and TxA2.

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

What are the functions of PGD2?

A

Vasodilation and chemotaxis

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

What are the functions of PGE2 ?

A
  • Vasodilation
  • spinal neuronal sensitization to pain.
  • Fever induction
  • Inhibition of stomach acid secretion.
  • Increase uterine contraction and GFR.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the function of PGF2 ?

A

Induce uterine contraction

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

What is the function of PGI2 or prostacyclin?

A
  • Vasodilation
    Spinal neuronal pain sensitization.
  • Inhibit platelet aggregation and stomach acid secretion.
  • Increase GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the functions of thormboxane A2?

A

Increase vasoconstriction and platelet aggregation.

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

What is the difference between the physiological action of COX-1 and COX-2 enzymes ?

A

COX-1 mediates homeostatic functions. Whereas COX-2 is expressed in response to inflammation.

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

What are the pharmacological effects of COX-01 inhibitors ?

A
  • Increases stomach acid secretion and GFR by inhibiting PGE2 and PGI2
  • Reduces uterine contraction by inhibiting PGF2 and PGE2.
  • Increases platelet aggregation by inhibiting PGI2.
  • Decreases platelet aggregation by inhibiting TXA2.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the pharmacological effects of COX-02 inhibitors ?

A
  • Increases vasoconstriction by inhibiting PGD2, E2and I2.
  • increases vasodilation by inhibiting TXA2.
  • Desensitise spinal neurones to pain by inhibiting PGE2 and PGI2.
  • Inhibits fever by inhibiting PGE2.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are prostaglandins ?

A

They are also called eicosanoids or porstanoids they are molecules with a very short half-life. They are the main local mediators of inflammation and act on many cells to produce many effects.

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

What are the Gynaecological & Obstetric uses of prostanoids or Prostaglandin analogs ?

A

misoprostol ( stable PGE2 analog) can be used to induce labour and prevent post-partum haemorrhage.

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

What is the use of prostaglandin analogs in GI disease ?

A

Misoprostol a PGE2 analog can be used to prevent GI bleeding in patients taking NSAIDs

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

What is the cardiovascular use of Prostaglandin analog?

A

Iloprost; a stable PGI2 analogue can be used to inhibit platelet aggregation during dialysis.

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

What is the mechanism of NSAIDs induced anti-inflammatory effect ?

A

Reduction in prostaglandin production and reduced vasodilation reduces edema and inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the mechanism of NSAIDs induced anti-pyretic effects ?

A

Reduction in prostaglandin production resets the hypothalamic thermostat threshold to the normal range.

18
Q

What is the mechanism of NSAIDs induced analgesic effect ?

A

reduced prostaglandin production peripherally and its reduced effect on spinal pain centres induces analgesia.

19
Q

What is the mechanism of NSAIDs induced anti-platelet effect ?

A

Reduction in TXA2 causes anti-platelet effects.

20
Q

What is the manifestation of NSAIDS gastric side effects?

A

Gastric ulcers, nausea, bleeding.
*Increased risk in older age (>60)

*Increased risk if existing ulcer.

*Increased risk with higher dose and duration.
*Increased risk if concurrent drug use (anti-platelet/coagulant, glucocorticoid).

*Approx 10% of arthritis patients taking NSAIDs will be hospitalised for GI toxicity.

21
Q

What is the mechanism of NSAIDs induced GI side effects ?

A

The inhibition of PGE2 which is responsible for reducing gastric acid secretion and stimulation of bicarbonate and mucin secretion by the epithelial cells causes gastric acid hyper secretion and peptic ulcers.

22
Q

What are the strategies to avoid GI toxicity of NSAIDs?

A

*Reduce dose/duration of NSAID.

*Patient selection.

*Co-administer gastric protectant (misoprostol, PPI)
*Coxibs

23
Q

What is the effect of aspirin on COX activity ?

A

Aspirin irreversibly binds to the COX enzyme and it has a half life of 7 days, ergo, its anticoagulation effect can prolong for 7 days.

24
Q

What is the NSAIDs side effect on coagulation?

A

It inhibits the activity of thromoboxine A2. Therefore, it can cause bleeding by reducing platelet aggregation. The management is to stop the drug.

25
Q

What is the mechanism of cardiovascular adverse effects of NSAIDs ?

A

The cardiovascular adverse effects increases with age, pre-exciting conditions, dose and duration. All NSAIDs except Naproxin and low dose aspirin tend to increase BP by inhibiting the activity of PGI2 and TXA2 action on the vascular endothelial cells. Which may lead to cardiovascular necrosis, MI, and stroke.

26
Q

What should the ideal mode of administration of NSAIDS in a patient on aspirin ?

A

Aspirin should be given two hours prior to NSAIDs.

27
Q

What are the side effects of IV NSAIDs ?

A

*Renal Effects
*Liver effects
*Allergy
*CNS effects (headache, dizziness)
*Bronchospasm
*Skin reaction (rash or photosensitivity)
*Tinnitus and hearing loss (aspirin-specific).

28
Q

What are the benefits and side effects of COX2 inhibitors?

A

Reduced GI toxicity

Reduced bleeding effects

More compatible with aspirin

BUT still cardiovascular side effects

29
Q

What is the mechanism of action of aspirin ?

A

It irreversibly inhibits COX-1 and COX2 enzymes. Excessive consumption can cause salicylism.

30
Q

Why is aspirin is not recommended for children ?

A

Risk of Rey syndrome

31
Q

What is the main side effect of Aspirin ?

A

GI toxicity and increased bleeding time.

32
Q

What is the mechanism of action of ibuprofen?

A

It reversibly inhibits COX-1 and 2 enzymes. It can reduce the effect of aspirin, if you take them together. Therefore aspirin should be taken two hours before ibuprofen.

33
Q

What is Diclofenac ?

A

It is the most potent broad spectrum NSAIDs. It can inhibit COX enzymes, May inhibit lipooxygenease pathway, and may inhibit phospholipase A2 as well. The main side effect is GI toxicity secondary to longterm use.

34
Q

What is celecoxib ?

A

It is a selective COX two inhibitor. It has increased risk of CV side effects and decreased risk of GI side effects.

35
Q

What are semi selective NSAIDs ?

A

They have strong affinity for COX2 and weak affinity for COX1. Therefore, use with caution in patients with CV risk.

36
Q

What are some examples of semi selective NSAIDs?

A

Meloxicam, Diclofenac, Etodolac, Indomethacin, and Piroxicam.

37
Q

What are non-selective NSAIDs ?

A

They have decreased risk for CV events and increased risk for GI events. examples: Ibuprofen and Naproxen.

38
Q

What are irreversible non-selective inhibitors ?

A

It has cardio-protective effects at low dose and increased risk for GI bleeding.

39
Q

What is paracetamol and its mechanism of action ?

A

Its mechanism of action is still debated. It may selectively inhibit COX-3 and prevent hypothalamic prostaglandin synthesis. It may also scavenger the ROS required for COX. It is metabolised in the liver and has low therapeutic index. It has analgesic and anti-pyretic effects, but no anti-inflammatory effects.

40
Q

How to treat Paracetamol overdose?

A

The drug is basically converted to mercaptopuric acid by glutathione. In overdose (2 to 3 times the normal dose) the glutathione stores get depleted and the drug converts to protein adducts causing hepatotoxicity. The treatment is gastric lavage and N-acetylecystine.

41
Q

Why is Ibuprofen considered an NSAIDs of choice with Warfarin ?

A

All though it is highly plasma protein bound like warfarin. It does not displace warfarin. Therefore, it does not alter warfarin’s effectiveness.

42
Q
A

PA MS (44 decks)

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