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brs (phase 1b) > (pharm) pharmacology of pain > Flashcards

(pharm) pharmacology of pain Flashcards

1
Q

which drugs are commonly prescribed for pain?

A

paracetamol

opioids (codeine, tramadol, morphine, fentanyl)

co-amoxiclav

lactulose

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2
Q

what is the primary mechanism of action of paracetamol?

A

1) activation of descending serotonergic pathways possibly via 5HT3 receptor activation

2) inhibits reuptake of endogenous endocannabinoids, which would increase activation of cannabinoid receptors.

3) mild inhibition of cyclooxygenase

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3
Q

what is the drug target for paracetamol?

A

1) 5HT3 receptors
2) cannabinoid reuptake proteins
3) cyclooxygenase

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4
Q

what are the main side effects of paracetamol?

A

relatively safe drug w few common side effects

(nausea + vomiting early features of poisoning)

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5
Q

what can paracetamol overdose cause?

A

liver damage and less frequently renal damage

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6
Q

which hepatological complication can occur due to excess paracetamolintake?

A

hepatic necrosis

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7
Q

how does hepatic necrosis present in patient who take paracetamol?

A

onset of right subcostal pain after 24 hours

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8
Q

what type drug is paracetamol classed as?

A

analgesic & anti-pyretic

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9
Q

is paracetamol an anti-inflammatory drug?

A

no!
paracetamol does not have anti-inflammatory properties

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10
Q

what are the groups of opioids available?

A

mild and strong opioids

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11
Q

name weak opioids

A

codeine, tramadol

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12
Q

name strong opioids

A

morphine, fentanyl, heroin

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13
Q

what is the mechanism of action of opioids?

A

1) activation of the opioid receptor at multiple sites in pain pathway = decreased perception or increased tolerance to pain

2) anti-tussive effect due to decreased activation of afferent nerves relaying cough stimulus from airways to brain

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14
Q

what is the drug target for opioids?

A

opioid receptor

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15
Q

what are the mild side effects of opioid usage?

A

nausea + vomiting (increased activity in the chemoreceptor trigger zone)

constipation (opioid receptors in the GIT can reduce gut motility)

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16
Q

why can opioid use lead to nausea & vomiting?

A

increased activity in the chemoreceptor trigger zone of the medulla oblongate

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17
Q

why can opioid use lead to constipation?

A

increased opioid receptor activation in the GI tract causes reduced gut motility

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18
Q

why is opioid overdose dangerous?

A

causes respiratory depression (direct & indirect inhibition of respiratory control centre)

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19
Q

what is co-codamol?

A

paracetamol + codeine

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20
Q

what is co-dydramol?

A

paracetamol + dyhydrocodeine

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21
Q

which two drugs make up co-amoxiclav?

A

amoxicillin

clavulanate

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22
Q

what is the mechanism of action of co-amoxiclav?

A

amoxicillin = binds to bacterial penicillin binding proteins (PBPs) to prevent transpeptidation, inhibiting the cross-linking process required for bacterial cell wall synthesis

clavulanate = beta lactamase inhibitor

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23
Q

what are the drug targets for co-amoxiclav?

A

amoxicillin targets the penicillin binding proteins (PBPs)

clavulanate targets beta lactamase

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24
Q

what is the function of penicillin-binding proteins?

A

membrane-associated proteins involved in the biosynthesis of peptidoglycan (PG), the main component of bacterial cell walls

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25
Q

what is transpeptidation?

A

the cross-linking process for bacterial cell wall synthesis

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26
Q

which bacterial process does amoxicillin inhibit?

A

transpeptidation = the process of cross linking that leads to bacterial cell wall synthesis

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27
Q

what is the mechanism of action of amoxicillin?

A

binds to bacterial penicillin binding proteins

= prevents transpeptidation (the cross linking process for bacterial cell wall synthesis)

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28
Q

what is the mechanism of action of clavulanate?

A

beta lactamase inhibitor that prevents bacterial beta lactamase from breaking down the beta lactam antibiotics (combatting resistance)

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29
Q

which enzyme is inhibited by clavulanate?

A

bacterial beta lactamase

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30
Q

what is the function of beta lactamase?

A

inactivate beta-lactam antibiotics, conferring resistance

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31
Q

name beta-lactam antibiotics and summarise their function

A

penicillin-derived antibiotics

cephalosporins

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32
Q

which property is conferred due to the presence of beta lactamase in bacteria?

A

(beta-lactam) antibiotic resistance

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33
Q

what are the side effects of amoxicillin?

A

well tolerated BUT most common side effects are nausea and diarrhoea

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34
Q

amoxicillin is a semi-synthetic antibiotic: what does this mean?

A

derivatives of natural antibiotics with slightly different but advantageous characteristics

35
Q

which types of bacteria are targeted by amoxicillin?

A

broad-spectrum antibiotic against many gram-positive and gram-negative microorganisms

36
Q

many individuals have penicillin hypersensitivity

how does this manifest most commonly?

A

anaphylactic reaction (e.g. rash)

37
Q

what is lactulose?

A

non-absorbable disaccharide

38
Q

what is the mechanism of action of lactulose?

A

1) reaches the large bowel unchanged

= water retention via osmosis + makes it easier to pass stool

2) sugar metabolised by colonic bacteria which adds to the laxative effect

39
Q

which condition is lactulose most commonly used to treat?

A

constipation

40
Q

what does colonic metabolism of lactulose cause?

A

adds to the laxative effect of lactulose

41
Q

what is the drug target for lactulose?

A

no specific drug target

42
Q

what are the side effects of lactulose?

A

abdominal pain, diarrhoea, flatulence, nausea

43
Q

how long does lactulose take to act?

A

begins working within 8-12 hours but may take up to 2 days to improve constipation

44
Q

why is lactulose administration important prior to opioid therapy?

A

opioids can activate the opioid receptors in the GI tract which can reduce gut motility and cause constipation

lactulose counters this by increasing water content in the GI tract, causing a laxative effect

45
Q

what is the main way that patients manage dehydration?

A

oral rehydration

46
Q

what is the WHO pain ladder?

A

describes pain in terms of intensity and recommends analgesics to be prescribed at each stage

47
Q

describe the WHO pain ladder

A

1) mild pain = nonopioid +/- adjuvant therapy

2) mild-moderate pain = weak opioid +/ nonopioid +/- adjuvant therapy

3) moderate-severe pain = strong opioid +/- nonopioid +/- adjuvant therapy

48
Q

what are the main therapeutic objectives for a patient diagnosed w gastroenteritis?

A

1) oral rehydration = as they are likely losing lots of fluid due to vomiting and diarrhoea, that needs to be replaced

2) analgesic = to reduce possible pain associated w gastroenteritis

49
Q

how is gastroenteritis normally managed?

A

normally managed at home w the following steps:
1) analgesic
2) oral rehydration
3) take approx 2 days (48 hours) off work
4) practice healthy hygiene to avoid cross-contamination

50
Q

explain how pain pathways work

A

1) transduction = painful stimulus kick starts the process (nociceptor sensory afferents activated)

2) transmission = up the spinal cord to the higher brain centres

3) perception

4) modulation = depending on the severity of the stimulus, the level of inhibition descending from the brain varies

51
Q

what is the function of anandamide?

A

activates downstream descending pain pathways
= has an analgesic effect

52
Q

what is anandamide commonly converted into?

A

commonly metabolised into arachidonic acid

53
Q

which two specific enzymes are essential in the production of prostaglandins?

A

1) cyclooxygenase (COX)
2) peroxidase

54
Q

where in the prostaglandin production pathway do NSAIDs act?

A

act to inhibit cyclooxygenase activity

55
Q

where in the prostaglandin production pathway does paracetamol act?

A

act to inhibit peroxidase activity

56
Q

differentiate between the therapeutic effect achieved between NSAIDs and paracetamol

A

NSAIDs = anti-inflammatory, analgesic, anti-pyretic

paracetamol = analgesic, anti-pyretic

57
Q

differentiate between the mechanism of action between NSAIDs and paracetamol

A

NSAIDs = inhibit the action of the cyclooxygenase enzyme

paracetamol = inhibit the action of the peroxidase enzyme

58
Q

how do NSAIDs achieve their analgesic effect?

A

1) inhibit COX enzyme, inhibit prostaglandin production, reduced activation of nociceptive neurones, reduced stimulation of pain sensation

2) inhibit COX enzyme, increased accumulation of arachidonic acid, increased subsequent accumulation of anandamide, increased anandamide = more activation of descending pain pathways

59
Q

what characteristic of NSAIDs does paracetamol lack?

A

while NSAIDs are anti-inflammatory medicines, paracetamol is not

(both, however, are analgesics and anti-pyretics)

60
Q

how does paracetamol achieve its analgesic effect?

A

inhibits peroxidase enzyme

1) inhibition of prostaglandin production so reduced nociceptive neurone activation

2) accumulation of anandamide and increased subsequent activation of descending pain pathways

61
Q

what is the function of nociceptive neurones?

A

transmit action potentials that stimulate pain sensation and trigger the withdrawal reflex

62
Q

describe the most common presentation of acute appendicitis

A
  • pain in the right iliac fossa
  • fever
  • in the RIF = guarding, rebound tenderness, extremely tender
  • pyrexia, hypotension, tachycardia
63
Q

what is the most common management plan for a patient with acute appendicitis?

A

1) NBM, but IV fluids for hydration
2) IV antibiotics
3) analgesics
4) perhaps surgery (laparoscopy)

64
Q

why are IV antibiotics given for acute appendicitis?

A

1) an obstructed appendix can lead to bacterial overgrowth

2) increased risk of post-surgical infection

65
Q

why is paracetamol ineffective in an inflammatory setting?

A

paracetamol inhibits the peroxidase enzyme (to in turn, inhibit prostaglandin production)

when peroxide levels are high in inflammation, peroxide will outcompete paracetamol in a way that it cannot inhibit peroxidase

(can give higher doses of paracetamol BUT overdose of paracetamol is dangerous as it can lead to renal/liver damage)

66
Q

what are the three depressant effects that morphine has at a cellular level?

A

1) inhibits adenylate cyclase so less ATP is converted into cAMP so reduced cellular activity = depressant effect

2) reduced Ca2+ influx into the cells = reduced vesicular neurotransmitter exocytosis = reduced post-synaptic neurone activation = depressant effect

3) increased K+ efflux = hyperpolarisation (so neurone cannot depolarise again) = depressant effect

67
Q

within the pain pathway, what are the possible opioid sites of action?

A

1) opioid receptors on the sensory afferent neurones = inhibit sensation of pain stimulus

2) opioid receptors on the spinal cord = depressant effect on the spinothalamic neurones

3) opioid receptors on the descending pathway = depressant on the already inhibitory pathway leads to disinhibition

68
Q

something about descending pathway disinhibition due to opioid activation ??

A

waff

69
Q

what must occur in order for any drugs to produce an effect in the brain?

A

they must be able to access the brain tissue

70
Q

what is the main route for drug permeation into the brain?

A

passive diffusion

(requires a level of lipid solubility)

71
Q

what is the major determinant of passive diffusion?

A

lipid solubility

72
Q

what determines if the opioid is able to bind to the opioid receptor?

A

the chemical structure of the drug

(determines the ability to bind to the receptor)

73
Q

what are the classical signs of opioid overdose?

A
  • lips/nails are blue
  • constricted pupils
  • skin feels cold and clammy
  • slow breathing
74
Q

what normally happens to the pupils in an unconscious state?

A

when you lose consciousness, you lose the brain stimulus that keeps the pupils in a constricted state
= pupils dilate

75
Q

what happens to the pupils in an unconscious patient w opioid overdose?

A

normally the stimulus for pupillary constriction is lost when a patient is unconscious HOWEVER

if opioid overdose, increased activation of opioid receptors that stimulates the pupils to remain CONSTRICTED (even when unconscious)

76
Q

why must you be cautious when administering opioids to a patient w renal failure?

A

need to ensure the drug is effectively being excreted by the renal system
= so it does not build-up to dangerous levels in the blood
= prevents the over-enhancement of the depressant effect

(could otherwise lead to depression of the cardiorespiratory system)

77
Q

what is the function of agonists?

A

bind to AND activate receptor

78
Q

what is the function of antagonists?

A

only bind to the receptor

(thereby blocking it)

79
Q

differentiate between the function of agonists and that of antagonists

A

agonists = bind to + activate (target affinity & efficacy)

antagonists = bind to only (target affinity only)

80
Q

explain, biochemically, why naloxone is administered to manage the opioid overdose

A

(morphine = agonist
naloxone = antagonist)

in opioid overdose = opioid receptors are occupied by morphine

naloxone is a competitive antagonist and far more naloxone is available than morphine
= so naloxone will outcompete morphine and will instead occupy more opioid receptors, displacing morphine
= reverses the effects of the opioid (morphine) overdose

81
Q

what is the relationship between codeine and morphine?

A

codeine is a pro-drug for morphine

and depending on the liver enzyme used, it can be metabolised ‘fast’ into norcodeine OR metabolised ‘slow’ into morphine

82
Q

why is lactulose often taken alongside morphine?

A

a side effect of morphine is constipation

= lactulose helps to combat constipation by stimulation more fluid retention within the bowels, allowing for easier passage of stool

83
Q

what happens when oral codeine is ingested?

A

1) codeine taken orally
2) transported to the liver where it is metabolised by liver enzymes
3) approx 90% is metabolised quickly into inactive norcodeine while the remaining 10% is metabolised slowly into active codeine

84
Q

how is codeine processed by the liver?

A

approx 90% is metabolised quickly into inactive norcodeine while the remaining 10% is metabolised slowly into active codeine

brs (phase 1b) (71 decks)

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