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NSB Lectures > Analgesics and sedative drugs > Flashcards

Analgesics and sedative drugs Flashcards

1
Q

What different tools can be used to assess pain?

A

McGill Pain Questionnaire
Brief pain inventory (body map)
Memorial Pain Assessment Card (faces and numbers)

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2
Q

What is used to guide the treatment of pain?

A

WHO analgesic ladder.

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3
Q

According to the WHO analgesic ladder, what types of analgesia would you give someone for mild, moderate and severe pain?

A

Mild - NSAIDS + Paracetamol
Moderate - Codeine, Dihydrocodeine, Tramadol
Severe - Morphine, Diamorphine, Fentanyl

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4
Q

What is an adjuvant medication in pain management?

A

A medication that is commonly used for something else, but is also used for pain e.g. antidepressants in chronic pain.

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5
Q

What type of medication is preferred for patients with primary chronic pain?

A

Anti-depressants.

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6
Q

What is breakthrough pain?

A

Where patients experience a peak or rise in pain in the middle of their analgesia when the analgesic affect should still be present.

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7
Q

Do NSAIDs affect the PNS or CNS?

A

Both, but mainly PNS.

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8
Q

What is the MOA for NSAIDs?

A

Ibuprofen + Naproxen: Competitive inhibitors of COX (reversible action).
Aspirin: Irreversible inhibitor of COX.
Both reduce the production of prostaglandins (as COX is needed for the conversion of arachidonic acid into prostaglandins).
Prostaglandins increase Na+/Ca2+ influx into nociceptors, making them more sensitive to thermal, mechanical or chemical stimuli. Thus blocking production of prostaglandins, makes them less sensitive.

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9
Q

Which type of COX can be induced by inflammatory stimuli?

A

COX 2 - Aids in pain, inflammation + fever.

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10
Q

Which physiological functions does COX 1 have?

A

Protects gastric mucosa (PGE2)
Renal homeostasis (PGE2/PGI2) - effects on Na+ + fluid retention.

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11
Q

Why is there a risk of gastric ulcers or renal problems with NSAIDs?

A

NSAIDS block COX1+2 - blocking COX2 reduces inflammation + pain, but blocking COX1 will result in less production of PGE2, and therefore it’s protection of the gastric mucosa.
COX1+2 also both help with renal homeostasis, and blocking these may result in renal problems.

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12
Q

Which drugs can selectively block COX2?

A

COXIBs: Selective Cox-2 inhibitors.

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13
Q

Does paracetamol affect the PNS or CNS?

A

Mainly the CNS - but no one really knows how.

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14
Q

What is paracetamol thought to inhibit?

A

COX 1/2/3(if there is a COX3)
Also thought to affect the endocannabinoid and serotoninergic systems.

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15
Q

How does paracetamol get metabolised?

A

Through the liver - which is why is can cause hepatic necrosis and liver failure in an overdose.

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16
Q

How is paracetamol different from NSAIDs?

A

Paracetamol doesn’t injure the gastric mucosa, is well tolerated in peptic ulcer disease + has no effect on platelets.

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17
Q

What is the primary drug class for the acute management of moderate to severe pain?

A

Opioids.

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18
Q

Which opioids are naturally occuring?

A

Morphine, codeine.

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19
Q

Which opioid is semi-synthetic?

A

Diamorphine.

20
Q

Which opioid is fully synthetic?

A

Fentanyl - also the most potent.

21
Q

Opioid receptors (Miu, Delta + Gamma) are all coupled to which second messenger protein?

A

Gai

22
Q

Which opioid receptor is responsible for most of the analgesic + some unwanted effects?

A

Miu

23
Q

What is the MOA of opioids?

A

Activates Gai - Inhibits AC –> Reduces cAMP (affecting phosphorylation) –> Voltage gated Ca2+ channels inhibited (so reduces NT release) + K+ channels activated (causing hyper-polarisation of the cell membrane).

24
Q

What is a ceiling dose?

A

When a dose of medication is increased past a certain amount, but the therapeutic effect no longer increases with it.

25
Q

How is codeine (a weak opioid) metabolised?

A

Gets metabolised in the liver to morphine by cytochrome CYP2D6.

26
Q

10% of caucasians lack the active enzyme to metabolise which drug?

A

Codeine.

27
Q

Which opioid receptor does codeine bind to?

A

Miu, but most of its affect comes from being metabolised to morphine.

28
Q

What is the dosage of strong opioids dependent on?

A

Previous medications
Age
General condition
Liver and kidney function

29
Q

What is morphine metabolised to?

A

Active metabolites (meaning it’s an active form of the drug)

30
Q

How is morphine excreted?

A

Through kidneys

31
Q

Does morphine have a ceiling effect?

A

No - increasing the dose will increase the therapeutic effect.

32
Q

What are some common adverse affects of opioids and how are these managed?

A

Constipation - laxatives
N+V - anti-emetics
Resp. depression (rare) - Naloxone

33
Q

Which medication can relieve agitation in opioid toxicity?

A

Haloperidol

34
Q

What management can be given in opioid toxicity?

A

Reduce dose
Hydrate patient
Low dose Haloperidol (for agitation)
Naloxone (Opioid antagonist - if resp. depression)

35
Q

What is the MOA for Ketamine?

A

Antagonist NMDA receptor.
Classed as a dissociative anaesthetic (Psychedelic)

36
Q

What is the goal of sedation, and is it always purposefully induced?

A

To produce a state of calm or sleep.
No - can be a an adverse effect also.

37
Q

Which A2 agonist can be used for analgesia?

A

Clonidine (Primarily an anti-hypertensive but also used in chronic pain)

38
Q

Which anti-convulsant can be used for analgesia?

A

Gabapentin (In particular for nerve pain)

39
Q

Which pharmacological hypnotic sedative used in intensive care, acts on GABA?

A

Propofol

40
Q

Which A2 agonist is used in intensive care for sedation?

A

Dexmedetomidine

41
Q

Diazepam, Midazolam + Lorazepam all have a sedative effect. What drug class are they?

A

Benzodiazepines.

42
Q

Which Z drug has a sedative effect?

A

Zopiclone

43
Q

What is the MOA of benzodiazepines + Z-drugs?

A

Facilitate the binding of GABA (GABA is the main inhibitory NT) to GABAA receptor.
Benzos + Z drugs bind to GABAA receptor, but to a different binding site than GABA.
They positively modulate GABA to GABAA receptor, and facilitate the responsiveness and opening of the GABAA receptor channel.
When opened, Cl- goes inside cell, cell becomes hyper-polarised + less excitable.

44
Q

What are the common side effects of Z-drugs?

A

Dry mouth + a metalic taste

45
Q

For sleep management, are long-acting or short-acting benzodiazepines preferred?

A

Short acting (midazolam) or Z drugs.
Long-acting would be lorazepam.

46
Q

Are opioids generally agonists or antagonists?

A

Agonists. Codeine + morphine are both agonists.
There are mixed agonist-antagonists also available.

47
Q

What is the drug class of Zopiclone?

A

Non-benzodiazepine hypnotic (Z-drug)

NSB Lectures (48 decks)

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