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CPT > NSAIDs > Flashcards

NSAIDs Flashcards

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1
Q

Examples of prostanoids + their actions

A
  • Prostaglandins: vasodilators
  • Prostacyclin (PGI2): vasodilator | prevent platelet aggregation
  • Thromboxane: platelet granule > initiation of platelet aggregation | vasoconstrictor
  • PGE2: good for stomach > regulation of a stomach acid
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2
Q

How are prostanoids produced?

A

Produced locally on demand from arachnoid acid

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3
Q

Role of prostanoids in the GI system

A
  • PGE2: regulation of acid secretion in parietal cells
  • prostacyclin: maintenance of blood flow + mucosal repair
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4
Q

How do prostanoids signal?

A

Act locally via many GPCRs

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5
Q

What is a consequence of imbalance of prostanoids?

A

Hypertension
MI
Stroke

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6
Q

Why is the Mediterranean diet suggested to lower incidence of CVD?

A
  • diet is rich is fish oil
  • proposed to lead to conversion of thromboxane + PGI3 (better prostanoids)
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7
Q

What are the two functional isoforms of cyclooxygenase enzymes?

A

COX-1
COX-2

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8
Q

Compare the haemostatic function of COX-1 + COX-2

A

COX-1:
- GI protection
- platelet aggregation
- vascular resistance
.
COX-2:
- renal homeostasis
- tissue repair + healing
- uterine contractions
- inhibition of platelet aggregation

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9
Q

Compare the pathological functions of COX-1 + COX-2

A

COX-1:
- chronic inflammation
- chronic pain
- hypertension
.
COX-2:
- chronic inflammation
- chronic pain
- fever
- blood vessel permeability

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10
Q

Compare the active sites in COX-1 + COX-2

A

COX-2 has a larger + more flexible binding site

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11
Q

What is the common mode of action of NSAIDs?

A

Inhibition of COX
- decrease prostaglandin, prostacyclin + thromboxane synthesis
- compete with arachidonic acid for site of COX enzymes

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12
Q

What are three general actions of NSAIDs?

A

Analgesia
Anti-inflammatory
Antipyretic

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13
Q

How do NSAIDs work as analgesics?

A
  • COX inhibition
  • decreases PGE2 synthesis in dorsal horn
  • decrease neurotransmitter release > decrease excitability of neurone in pain relay pathway
  • inhibition reduces peripheral pain fibre sensitivity
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14
Q

How do NSAIDs work as anti inflammatories?

A
  • COX inhibition
  • reduce production of prostaglandins released at site of injury
  • reduces vasodilation + swelling
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15
Q

How do NSAIDs work as antipyretics?

A

Inhibition of hypothalamic COX-2 where cytokine induced prostaglandin synthesis is elevated > reduced temperature

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16
Q

Outline NSAID COX selectivity

A

COX1 selectivity
- aspirin
- ibuprofen
- naproxen
- diclofenac
- celecoxib
- etoricoxib
COX2 selectivity

17
Q

What are GI adverse drug reactions of NSAIDs?
What is this due to?

A
  • dyspepsia
  • nausea
  • peptic ulceration
  • bleeding + perforation
  • exacerbation of IBD
    .
  • decreased prostaglandins
  • reduction in mucosal blood flow > hypoxia
  • reduction in mucous + bicarb secretion > increased acid secretion
18
Q

What are important drug drug interactions of NSAIDs in relation to GI ARDs?

A
  • aspirin
  • Glucocortioid steroids
  • anticoagulants
    (PPI should be considered as additional drug)
19
Q

What are renal adverse drug reactions of NSAIDs?
What is this due to?

A
  • reversible decreases in renal blood flow + GFR
    .
  • reduction in prostaglandins
  • reduced vasodilation of afferent arteriole
  • reduced blood supply
20
Q

What are important drug drug interactions of NSAIDs in relation to renal ARDs?

A

ACEi
ARBs
Diuretics

21
Q

Examples of selective COX-2 inhibitors

A

Celecoxib
Etoricoxib

22
Q

Difference in selective COX2 inhibitors + non selective ADRs

A
  • less GI ADRs
  • renal ADRs similar
23
Q

Effect of thromboxane + prostacyclin on CVS

A

Thromboxane is generally bad
Prostacyclin is generally good

24
Q

How does NSAID use effect MI risk?

A
  • All NSAIDs (but baby aspirin) increase risk of MI
  • possibly due to decrease in prostacyclin
25
Q

What are considerations/possible contraindications of NSAIDs?

A
  • CVD
  • renal function
  • GI disease
  • DDIs
  • level of pain, pyrexia + inflammation
  • 3rd trimester of pregnancy
26
Q

What are indications for NSAID use?

A
  • inflammatory conditions
  • osteoarthritis
  • post op pain
  • Menorrhagia
  • low dose aspirin for platelet aggregation inhibition
  • topical use on cornea
27
Q

What is the mechanism of action of paracetamol?

A

COX-2 selective inhibition in CNS

28
Q

How can NSAIDs increase free plasma conc. of other drugs?

A

Competitively displaced other bound drugs > increase free drug conc.

29
Q

What builds up in paracetamol overdose?

A

NAPQI

30
Q

What is used to treat paracetamol overdose?
How does it work?

A

N-acteylcysteine
- replaces glutathione which is protective agaisnt NAPQI

31
Q

Difference in action of COX-1 + COX-2 inhibition in relation to platelet aggregation

A
  • COX-1inhibitors decrease thromboxane > decrease platelet aggregation
  • COX-2 selective inhibitor’s decrease PGI > unopposed aggregatory effects
32
Q

Why can NSAIDs exacerbated CKD?
Why do ACEi/ARB compound this?

A
  • NSAID use > reduction in prostaglandins > reduction in vasodilation > reduced GFR + renal blood flow
  • in CKD, there is a greater reliance on PG for vasodilation + renal perfusion
    .
  • ACEi/ARBs cause vasodilation > increase renal blood flow
33
Q

Describe how NSAIDs should be prescribed

A

Lowest effective dose for shortest time necessary

34
Q

Presentation + consequences of paracetamol overdose

A
  • asymptomatic at first
  • N+V + abdo pain in first 24 hours
  • maximal liver damage occurs at 3-4 days
35
Q

What NSAID is most selective for COX2?

A

Etoricoxib

36
Q

What are mechanisms by which NSAIDs can cause GI ADRs?

A
  • Decreased mucous secretion
  • Decreased bicarbonate secretion
  • Reduced mucosal blood flow
  • Inhibtion of PGE2 + PGI2 cause them

CPT (29 decks)

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