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BRS YR2 > Pharmacology of Pain > Flashcards

Pharmacology of Pain Flashcards

1
Q

What is the primary mechanism of action of Paracetamol?

A

unclear

  • activation of descending serotonergic pathways via 5HT3 receptor activation
  • inhibits reuptake of endogenous endocannabinoid receptors
  • mild inhibition of COX
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2
Q

What is the drug target of paracetamol?

A

unclear

- 5HT3 receptors/cannabinoid reuptake proteins/COX

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3
Q

What are the main side effects of paracetamol?

A 
signs of poisoning:
- nausea
- vomiting
- right subcostal pain (hepatic necrosis)
OVERDOSE
- liver damage 
- renal damage
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4
Q

How would you describe the properties of paracetamol?

A
  • analgesic

- anti-pyretic

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5
Q

What are some examples of weak opioids?

A
  • codeine

- tramadol

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6
Q

What are some examples of strong opioids?

A
  • morphine

- fentanyl (heroin)

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7
Q

What are is the primary mechanism of opioids?

A
  • depressant effect on cellular activity
  • activation of opioid receptors leads to decreased perception or increased tolerance of pain
  • anti-tussive effect due to decreased activation of afferent nerves relaying cough stimulus from the airways to the brain
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8
Q

What are is the drug target of opioids?

A

opioid receptors

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9
Q

What are the main side effects of opioids?

A

mild:
- nausea
- vomiting
(increased activity in chemoreceptor trigger zone)
- constipation
(opioid receptor in the GIT can reduce gut motility)

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10
Q

What are the signs of a opioid overdose?

A

respiratory depression

caused by both direct and indirect inhibition of respiratory control centre

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11
Q

What the primary mechanism of Co-amoxiclav?

A

Amoxi-
- binds to bacterial penicillin binding proteins.
- prevents transpeptidation (the crosslinking process for bacterial cell wall synthesis)
-Clav
- beta lactamase inhibitor
(bacterial enzyme that degrades beta lactam antibiotics and therefore confers resistance.

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12
Q

What is the drug target of Co-Amxoclav?

A

Amoxicillin:
penicillin binding proteins
Clavulanate:
beta lactamase

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13
Q

What does projectile vomiting suggest?

A

norovirus

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14
Q

What are the main side effects of Co-Amoxiclav?

A

generally well tolerated

  • nausea
  • diarrhoea
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15
Q

What is the recommended management of gastroenteritis?

A
  • oral rehydration

- analgesis

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16
Q

What bacteria does Amoxicillin act on?

A

semisynthetic broad spectrum ABx, against gram positive and negative microorganisms

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17
Q

what needs to be given when administering home management plans?

A

safety netting, if not improved in xxx, go to hospital

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18
Q

How do hypersensitivities to penicillin present?

A
  • rash

- can lead to anaphylactic reactions

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19
Q

*What is the primary mechanism of Lactulose?

A
  • non-absorbable disaccharide
  • reaches the large bowel unchanged
  • water retention via osmosis and an easier to pass stool
  • can be metabolised by colonic bacteria
  • the colonic metabolism of sugars has an additional laxative effect.
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20
Q

Describe a pain pathway?

A
  • sensory neurone
  • synapses with a spinothalamic neurone in the spine (to the hypothalamus)
  • return of an inhibitory response (modulation), to prevent pain stimulus relay
  • inhibitory effect dependent on the size of the pain/extent of the trauma
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21
Q

What is the drug target of lactulose?

A

no drug target

22
Q

What are the main side effects of Lactulose?

A
  • abdominal pain
  • diarrhoea
  • flatulence
  • nausea
23
Q

How long does it take for Lactulose to have a clinical effect?

A
  • works in 8-12 hours

- may take up to 2 days to improve constipation

24
Q

When is lactulose prescribed?

A

prescribed prior to commencement of opioid therapy to improve symptoms associated with constipation

25
Q

What is released from inflammatory tissue?

A
  • peroxides
26
Q

Why is paracetamol not an anti-inflammatory?

A
  • inhibits the action of peroxidase activity
27
Q

What is the impact of cannabis on pain?

A

enhances anandomides, causing an increased inhibitory effect from the hypothalamus

28
Q

How do NSAIDS/paracetamol cause a central analgesic effect?

A

paracetamol - arachadonic acid buildup

- preventing the metabolism anandomide is broken down into arachodonic acid (similar to negative feedback)

29
Q

What is the management plan for acute appendicitis?

A
  • analgesia
  • NBM, IV fluids (crystalloids)
  • IV ABx
30
Q

What is the effect of morphine on a cellular level?

A
  • binds to the opioid receptor (G-protein coupled)
  • inhibition of ATP to cAMP conversion, causing reduced cellular activity
  • reduced calcium influx, less exocytosis (less neurotransmitter release)
  • increased K+ efflux, hyperpolarising the cell
  • the neurone is hyperpolarised and therefore cannot depolarise
31
Q

Where do opioids act on the pain pathway?

A
  • loss of peripheral opioid receptors around the sensory nerves
  • spinal cord, decreased action of the spinothalamic innervation due to depressive effect
  • neurone modulation (inhibitory effect on pain),, GABA inhibition is inhibited by the opioids. Therefore the descending pathway is now active, by removing the inhibitory factor (GABA)
32
Q

what happens on to the pain pathway when not in pain?

A

inhibition of the modulation of the descending inhibitory perception of pain by GABA

33
Q

What are the properties of effective drugs that are able to permeate the blood brain barrier?

A
  • lipid based

- able to actually bind to the receptor when reached

34
Q

What is the optimal oil-water partition coefficient to pass the blood brain barrier?

A

1.5-2.7

35
Q

What is opioid receptor binding dependent on?

A
  • hydroxyl group at position 3

- tertiary nitrogen

36
Q

What happens in the conversion of a phase 1 to a phase 2 metabolite?

A

active metabolite with a side chain to reduce reactivity to ease clearance

37
Q

What is a phase 1 metabolite?

A

highly reactive metabolite

38
Q

What is a phase 2 metabolite?

A

reactive metabolite + side chain to provide stability

39
Q

What happens to codeine and heroin in order to act on the brain?

A

once in the brain, converted into the morphine

40
Q

What is thought to be the most effective opioid?

A

heroin (due to lipid solubility)

41
Q

What is used to treat an opioid overdose?

A

naloxone (IV or nasal spray)

42
Q

What are the properties of agonists?

A
  • affinity

- efficacy

43
Q

What are the properties of antagonists?

A

only affinity

44
Q

What are the structural differences between morphine (agonist) and naloxone (antagonist)

A
  • tertiary H (short side chain allows for efficacy)

- side chain >2 carbons means that there is no efficacy

45
Q

What can codeine be metabolised into?

A

inactive: norcodeine
active: morphine

46
Q

How long does it take for naloxone to come into effect?

A

instantaneous

47
Q

How does opioid overdose cause respiratory depression?

A
  • cardio-respiratory control centre
  • multiple opioid receptor
  • opioids bind to the opioid receptors causing a depressive effect
  • only seems to happen at high doses due to resistance
48
Q

What causes pupil constriction in opioid overdose?

A
  • opioids cause pupil constriction directly

- diagnostic

49
Q

What is responsible for the metabolism of codeine into morphine?

A

cytochrome P450 enzymes in the liver

  • CYP3A4, fast codeine to norcodeine
  • CYP2A6, slow codeine to morphine
50
Q

What is the effect of taking codeine orally (why is it considered weak)

A

due to the difference in the metabolism into the different metabolites

  • codeine to norcodeine (90%) cause fast
  • codeine to morphine (10%) cause slow
51
Q

How do you calculate the dosage of codeine for opioid pain management?

A
  • total codeine/day
  • conversion factor for morphine to codeine
  • morphine/conversion factor = codeine/day

BRS YR2 (70 decks)

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