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Pharmacology Drugs > Analgesics > Flashcards

Analgesics Flashcards

1
Q

Give some examples of NSAIDs.

A
  • Aspirin
  • Ibuprofen
  • Naproxen
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2
Q

What is the mechanism of action of NSAIDs?

A

Competitive inhibition of COX-1 and COX-2.

Main Effect is via inhibition of COX-2

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3
Q

What are the effects of NSAIDs?

A

Analgesia
Anti-inflammatory
Antipyretics

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4
Q

What is the action of Aspirin?

A
  • Irreversibly inhibits COX enzymes by acetylation

- Converted to salicylate.

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5
Q

Describe the pharmacokinetics of Aspirin?

A
  • Lower doses show first order kinetics

- Higher doses show zero order kinetics

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6
Q

What are the specific uses of Aspirin?

A
  • Cardioprotective functions

- Prophylactic for GI/Breast cancers

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7
Q

What are side effects of NSAIDs?

A
  • Long term use in elderly has iatrogenic morbidity and mortality
  • Renal ADR occur in compromised individual with hypovolaemia or HRH
  • Stomach/GI tract ADRs. Includes varying degrees stomach pain, nausea, heartburn, gastric bleeding, ulceration.
  • Vascular such as increased bleeding time and increased bruising haemorrhage
  • Hypersensitivity
  • Reyes syndrome which is a rare serious brain/liver injury
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8
Q

What causes Renal ADRs in compromised individuals as a result of NSAIDs?

A
  • PGE2 and PGI2 maintain renal blood flow. if reduced by NSAIDs then GFR decreases which can lead to further risk of renal compromise
  • Na+/K+/Cl- and H2O retention follow with increased likelihood of hypertension
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9
Q

What causes Stomach/GI tract ADRs as a result of NSAIDs?

A
  • COX-1 PGE2 stimulates cytoprotective mucus secretion throughout GI, reduce acid secretion and promote mucosal blood flow
  • Can be offset with PPIs or Misoprotolol
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10
Q

What are the features of Hypersensitivity as a result of NSAIDs?

A
  • Skin rashes that are usually mild

- Bronchial asthma so care in asthmatics

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11
Q

Describe the pharmacodynamic of NSAIDS

A
  • Mainly heavily bound to plasma protein (90-99%)
  • In combination with low dose opiates extend therapeutic range for treating pain. Act by different mechanism to extend range
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12
Q

Which drugs can be affected by NSAIDs?

A

Can displace the drug into plasma

  • Suphonylurea (hypoglycaemia)
  • Warfarin (increased bleeding)
  • Methotrexate (wide ranging serious ADRs)
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13
Q

What are some examples of non-narcotics?

A

Paracetamol

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14
Q

What is the mechanism of action of non-narcotics (paracetamol)?

A

Unknown mechanism but thought to be:

  • Weak COX-1/COX-2
  • Primarily acts in the CNS on the TRP channels
  • Activation of serotogernic pathway
  • Prostagladin inhibition
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15
Q

What are the uses of paracetamol?

A

Analgesia

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16
Q

How is paracetamol metabolised?

A
  • Normally mainly use phase 2 conjugation to break down. Some Phase 1 oxidation occurs (10%) which forms NAPQI which is very reactive and toxic.
  • At normal dose, NAPQI is detoxified by phase 2 conjugation with Glutathione. Conjugation is linear but limited by glutathione availability
17
Q

What happens at high doses of paracetamol?

A
  • At high doses, phase 2 metabolism is saturated. Leads to increased phase 1 production of NAPQI.
  • Phase 2 conjugation of NAPQI with glutathione is rate limited and saturated.
  • Unconjugated NAPQI is highly reactive and bind with cell macromolecules/mitochondria.
  • This can lead to hepatic cell death. Can also lead to renal failure in paediatric and elderly patient primarily
18
Q

Describe the pharmacokinetics of Paracetamol

A
  • High dose, PKs become zero order
  • Phase 2 metabolism saturated so phase 1 increases so more NAPQI.
  • Conjugation of NAPQI with glutathione is rate limited. GLuthathione is also rapidly depleted.
19
Q

How is paracetamol overdose treated?

A
  • Treatment must be given as soon as possible.
  • Delayed hepatoxic effect peak 72-96 hours post ingestion
  • 0-4 hours, activated charcoal orally reduce uptake by 50-90%
  • 0-36 hours, start with acetylcysteine. Methionine given by mouth if N- Acetylcysteine cannot be given promptly
20
Q

What are some example of Narcotics?

A
  • Oral codeine (metabolised to morphine)
  • Oral tramadol
  • Morphine
  • Diamorphine
  • Fentanyl patch
  • Oxycodone
21
Q

What is the mechanism of action of narcotics?

A
  • Bind to opiate receptor
  • Inhibits adenyl cyclase
  • Decreases cAMP
  • Cause decreased influx of Ca2+
  • Reduced neurotransmitter release
  • Reduced transmission of nociceptive impulses
22
Q

What are the uses of narcotics?

A

Good agent for moderate to severe pain such as cancer pain, chronic pain and post-operative pain

-Used in Acute, Chronic, and Non analgesias

23
Q

What are the side effects of narcotics?

A
  • Constipation
  • Reduced conscious levels
  • Respiratory depression
  • Nausea and vomiting
  • Confusion
  • Constricted pupils
24
Q

What can be given to reverse the effects of opiates if needed?

A

Naloxone is an opiate antagonist that can be given in toxicity to reverse opiate overdose

25
Q

What is the interaction when combination NSAIDS are used?

A
  • Combination NSAIDs can affect PK/PD due to competition for plasma protein binding sites and therefore cause ADRs.
  • NSAIDs + low dose aspirin compete for COX-1 binding sites which may interfere with cardio-protective action of aspirin
26
Q

Which acute clinical cases require Narcotics?

A

-Acute: trauma, burns, perioperative, MI

27
Q

Which Chronic Clinical Cases require Narcotics?

A

-Chronic: refractory pain, malignancy

28
Q

Which non-analgesic situations use narcotics?

A

-Non analgesis: cough suppression, manage diarrhoea, breathlessness

Pharmacology Drugs (22 decks)

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