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Pharm OTL > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What are the opposing effects of thromboxane A2 and PGI2/prostacyclin?

A

TXA2: plt aggregation, and vasoconstriction

PGI2: inhibition of plt aggregation, and vasodilation

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2
Q

Name four NSAIDs

A 
Aspirin
Ibuprofen
Naproxen
Diclofenac
Celecoxib
Perecoxib
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3
Q

What is the MoA of NSAIDs on COX enzymes?

A

Inhibition of the COX enzymes by competing with arachidonic acid for the hydrophobic site of COX.

Causes reduced formation of prostaglandins, prostacyclins and thromboxane A2.

Aspirin is an irriversible COX-1 inhibitor (slight COX-2 action).

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4
Q

What are the two mechanisms of the analgesic effects of NSAIDs?

A

Reduced PGE2 synthesis in the dorsal horn leads to reduced excitability of pain pathways. Full effect after several days of dosing.

Also acts at the site of inflammation and pain by reducing the synthesis of prostaglandins to reduce activation of the nociceptors.

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5
Q

What is the mechanism of the anti-inflammatory effects of NSAIDs?

A

Reduced production of prostaglandins - mainly PGE2 and PGD2.
Reduces vasoD and leakiness of BVs.

Full effect after several weeks e.g. for RA

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6
Q

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

A

Inhibition of COX-2 in the hypothalamus.

Stops cytokine-induced prostaglandin synthesis here.

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7
Q

What is the mechanism of the anti-platelet effects of NSAIDs?

A

Inhibiton of COX-1 which reduces thromboxane A2 synthesis

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8
Q

Name a COX-2 selective NSAID

A

Celecoxib*
Etoricoxib
Parecoxib

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9
Q

How can the half-life of NSAIDs differ from theraputic duration?

A

NSAIDs accumulate at side of inflam, e.g. synovial fluid, so can have a theraputic action exceeding their half-lives

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10
Q

How do half-lives vary between NSAIDs?

A

Can be short: 1-5hrs

Or long: 10-60hrs

Can have modified release preparations to change half-life

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11
Q

NSAIDs are highly protein bound with a small Vd. What is an implication of this?

A

Can displace other drugs e.g. methotrexate, anticonvulsants, warfarin

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12
Q

Most NSAIDs are weak acids. What effect does this have on absorption?

A

Can be absorbed from the stomach

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13
Q

What is the mechanism of GI side effects?

A

Reduced prostacycling and PGE2 synthesis in the stomach leads to:

  • Reduced mucus and bicarb secretion.
  • Reduced mucosal blood flow.

NSAIDs are acidic, and can reduce the hydrophobicity of the mucus layer, allowing acid to cause damage.

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14
Q

State two GI side effects of NSAIDs

A 
Dyspepsia
Nausea
Peptic ulceration
Bleeding
Perforation
Exacerbation of IBD
Local irritation and bleeding from rectal administration

Fewer ADRs in COX-2 selective

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15
Q

State a renal side effect of NSAIDs

A

More likely in CKD, CHF, cirrhosis with ascites, blood flow compromise

  • Hypertension and oedema (due to salt and water retention bc of ↓GFR)
  • Hyperkalaemia due to renin release
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16
Q

State two CSV side effects of NSAIDs

A
  • Hypertension (due to salt and water retention)
  • Vasoconstriction due to reduced antagonism of ADH by prostaglandins
  • Reduced efficacy of anti-hypertensives
  • Increased risk of MI (increased risk with time bc of the imbalance between prostacyclin and TXA2 esp in COX-2 selectives) (ex low dose aspirin)
17
Q

What are the guidelines surrounding prescribing NSAIDs to patients at risk of stroke or heart attack?

A

Don’t, except for a single dose

18
Q

State two drug-drug interactions of NSAIDs

A
  • Reduced efficacy of antihypertensives

- Highly protein-bound so can effect Sulphonylureas, Methotrexate, Warfarin

19
Q

Why can’t NSAIDs be used by pregnant women, especially in the third trimester?

A
  • Delay labour
  • Increase blood loss during birth
  • Premature closure of the ductus arteriosus
20
Q

Why shouldn’t NSAIDs be used in children under 12?

A

Can lead to Raye’s syndrome - rapidly progressing encephalopathy

21
Q

State 5 uses of NSAIDs

A
  • Headaches and other pains
  • Inflammatory condition e.g. RA, OA
  • Postoperative pain
  • Topical use on the cornea
  • Menorrhagia (reduced blood loss)
  • Low dose aspirin for reduced plt aggregation
  • Close ductus arteriosus
22
Q

How should a single dose of ibuprofen be taken by a pt on low dose aspirin?

A

Competition for COX-1, can cause reduced CVS protection

Either:

  • 8hrs before daily aspirin tablet
  • 30mins after daily aspirin tablet (aspirin irreversibly inhibits COX-1 on plts .·. doesn’t matter about ibuprofen after that)
23
Q

State the two effects of paracetamol

A

Analgesic

Antipyretic

24
Q

State the symptoms of paracetamol overdose in the first 24hrs, 24-48hrs, and 3-4 days

A

First 24hrs: N+V, abdo pain

24-48hrs: RUQ pain

3-4 days: Maximal liver damage

25
Q

What is the antidote for paracetamol overdose?

A

Acetylcysteine

Pharm OTL (18 decks)

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