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YEAR 3 NEURO > PHARMACOLOGY - Analgesic drugs > Flashcards

PHARMACOLOGY - Analgesic drugs Flashcards

1
Q

how do NSAIDs reduce pain

A

decrease nociceptor sensitisation by blocking synthesis of prostaglandins

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2
Q

how does lidocaine reduce pain

A

suppresses nerve conduction by blocking VG Na channels

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3
Q

outline the WHO analgesic ladder

A

Step 1 (mild to moderate pain) – Non-opioid (paracetamol or NSAID) +/- an adjuvant (low dose tricyclic antidepressant/ anticonvulsant/ muscle relaxant/ other NSAIDs)

Step 2 (moderate to severe pain) – Weak opioid (codeine/ tramadol) +/- a non-opioid +/- an adjuvant

Step 3 (Severe pain) – Strong opioid (morphine/ fentanyl/ diamorphine) +/- a non-opioid +/- an adjuvant

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4
Q

give 5 examples of NSAIDs

A 
aspirin
diclofenac
ibuprofen
indomethacin
naproxen
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5
Q

what is meant by supra-spinal antinociception

A

regulation of pain by descending pathways - brain regions involved in pain perception and emotion project to specific brainstem nuclei

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6
Q

what are some areas of the brain involved in pain perception and emotion

A

cortex
amygdala
thalamus
hypothalamus

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7
Q

neurones of the brainstem nuclei give rise to efferent pathways that project to spinal cord to modify afferent input. Name 3 important brainstem regions:

A

periaqueductal grey - midbrain
locus ceruleus - pons
nucleus raphe magnus - medula

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8
Q

excitation of ____ causes profound analgesia

A

PAG

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9
Q

what 2 things cause excitation of the PAG

A

electrical stimulation

opioids - endogenous (enkephalins) or morphine

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10
Q

activated PAG neurones projecting to the ___ excites _____ and _____ neurones projecting to the dorsal horn resulting in

A

NRM
serotonergic and enkephalinergic neurones
suppression of nociceptive transmission

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11
Q

____ also excites the NRM

A

morphine

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12
Q

opioid action is mediated by what receptors

A

GPCR (Gi/o)

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13
Q

GPCORs signal Gi/o to produce… (3)

A

inhibition of opening of VGCaCs
opening of K channels
inhibition of adenylate cyclase

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14
Q

what is the effect of inhibition of opening of VGCaCs

A

pre-synaptic effect - suppresses excitatory neurotransmitter release from nociceptor terminals
(Gi/o BY subunit)

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15
Q

what is the effect of opening of K channels

A

post synaptic effect - suppresses the excitation of projection neurones
(Gi/o BY subunit)

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16
Q

what is the effect of inhibition of adenylate cyclase

A

long term effect

Gi/o a subunit

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17
Q

what are the 3 types of opioid receptor

A

u
d
k

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18
Q

which receptor contributes to most of the analgesic effects of opioids

A

u

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19
Q

which receptor can have proconvulsant effects if activated

A

d

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20
Q

which receptor can cause sedation, dysphoria and hallucinations if activated

A

k

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21
Q

what are the main side effects of opioids

A

apnoea
orthostatic hypotension
GI
CNS

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22
Q

what are the CNS side effects of opioids

A

confusion, euphoria, dysphoria, hallucinations, dizziness, myoclonus, hyperalgesia

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23
Q

what are the GI side effects of opioids

A

N,V, constipation, increased intrabiliary pressure

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24
Q

why can opioids cause apnoea

A

blunting of medullary respiratory centre to CO2

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25
Q

why can opioids cause bronchospasm in asthmatics

A

morphine but not all opioids can cause degranulation of mast cells

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26
Q

why can opioids cause orthostatic hypotension

A

reduced sympathetic tone and bradycardia via action on medulla

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27
Q

why can opioids cause GI side effects

A

action on chemoreceptor trigger zone

action on enteric neurones - increased smooth muscle tone and decreased motility

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28
Q

where is morphine metabolised and excreted

A

metabolised - liver

excreted - kidney

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29
Q

how can morphine be delivered

A

acute severe pain - IV IM SC or oral

chronic pain - oral (oramorph)

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30
Q

is diamorphine or morphine more lipophilic

A

diamorphine

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31
Q

diamorphine has a ____ onset of action when given IV

A

rapid

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32
Q

name a weaker opioid than morphine or diamorphine used for mild/moderate pain

A

codeine

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33
Q

how is codeine given

A

oral

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34
Q

what is codeine metabolised by demethylation to in the liver

A

morphine

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35
Q

what metabolised codeine to morphine

A

CYP2D6 and CYP3A4

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36
Q

name 2 semi-synthetic derivatives of codeine with higher potency

A

oxycodone

hydrocodone

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37
Q

name an opioid 75-100 fold stronger than morphine

A

fentanyl

38
Q

how can fentanyl be delivered

A

IV

transdermal (and buccal)

39
Q

when is IV fentanyl used

A

analgesia in maintenance anaesthesia

40
Q

when is transdermal fentanyl used

A

chronic pain states

41
Q

how does analgesia occur with use of opioids

A

agonists of u-opioid receptor - prolonged activation of receptor

42
Q

pethidine has a ____ onset of action and is used in ___ pain for example ____

A

rapid
acute
labour

43
Q

Pethidine should not be used in conjunction with ____ as can cause convulsions

A

MAO inhibitors

44
Q

name a partial agonist of opioid receptor that is used in chronic pain due to its slow onset but long duration of action

A

Buprenorphine

45
Q

how can Buprenorphine be given

A

injection or sublingual

46
Q

____ is a weak u-receptor agonist given orally and should be avoided in epilepsy

A

tramadol

47
Q

what is the most likely reason for tramadol’s analgesic effect

A

potentiation of the descending serotonergic (NRM) and adrenergic (LC) systems

48
Q

methadone is a ____ oral u agonist with a ____ duration of action

A 
weak
long (plasma half life > 24 hours)
49
Q

what other sites does methadone work on

A

K channels
NMDA glutamate receptors
some 5-HT receptors

50
Q

give 2 scenarios where methadone is useful

A

withdrawal from heroin

chronic cancer pain

51
Q

are agents with a short or long half life more addictive

A

short

52
Q

what is used to reverse opioid toxicity

A

naloxone

53
Q

what is the mechanism of action of naloxone

A

competitive antagonist of u-receptor (and to a lesser extent k and d)

54
Q

why must you monitor the effects of naloxone

A

short half life - with strong opioid agonists with a long half life opioid toxicity may recur

55
Q

how is naloxone given

A

IV

IM or SC if IV not possible

56
Q

naloxone can trigger what in opioid addicts

A

withdrawal

57
Q

why might naloxone be given to a new born

A

for opioid toxicity

58
Q

what happens in opioid toxicity

A

respiratory depression

neurological depression

59
Q

name a drug similar to naloxone with oral availability and much longer half life

A

naltrexone

60
Q

what gives NSAIDs their analgesic, anti-inflammatory and anti-pyretic actions

A

inhibiting the synthesis of prostaglandins by cyclo-oxygenase (COX) enzymes 1 and 2

61
Q

what do COX 1 and COX 2 do

A

convert arachadonic acid to endoperoxides

62
Q

what converts endoperoxides to prostaglandins

A

prostaglandin isomerase

63
Q

what converts phospholipids to arachadonic acid

A

phospholipase A2

64
Q

aspirin, diclofenac, ibuprofen, naproxen, indomethacin are all selective/non-selective

A

non-selective

65
Q

etoricoxib / celecoxib / lumiracoxib are all selective / non selective

A

selectie COX 2 inhibitors

66
Q

therapeutic benefit of NSAIDs largely derived from inhibition of COX-_ as it is induced locally at sites of inflammation

A

2

67
Q

what limits the use of cox 2 selective NSAIDs

A

they are prothrombotic

68
Q

what can occur with long term use of non-selective NSAIDs

A

GI damage

69
Q

why can GI damage occur with long term use of non-selective NSAIDs

A

PGE2 produced by COX-1 protects against the acid/pepsin environment

70
Q

what can occur as a result of cox-2 inhibition

A

nephrotoxicity - it is expressed by kidney

71
Q

NSAIDs act peripherally and centrally to (3)

A
  • suppress the decrease in activation threshold of peripheral terminals of nociceptors that is caused by prostaglandins
  • decrease recruitment of leukocytes that produce inflammatory mediators
  • if they cross BBB - suppress the production of pain producing prostaglandins in the dorsal horn of the spinal cord that reduce the action of inhibitory glycine
72
Q

what kind of pain doesnt respond to opioids (unless high dose) or NSAIDs

A

neuropathic

73
Q

give 4 examples of neuropathic pain

A

trigeminal neuralgia
diabetic neuropathy
post-herpetic neuralgia (shingles)
phantom limb pain

74
Q

what are some drugs that may be used in the treatment of neuropathic pain

A

gabapentin and pregabalin
TCAs
carbamazepine

75
Q

how do gabapentin and pregabalin (antiepileptics) treat neuropathic pain

A

reduce the cell surface expression of the a2d subunit of some VGCaCs which are upregulated in damaged sensory neurones - decreases neurotransmitters such as glutamate and substance P

76
Q

what is neuropathic pain

A

pain caused by damage or disease affecting the somatosensory nervous system

77
Q

gabapentin is used in —

A

migraine prophylaxis

78
Q

pregabalin is used in —

A

painful diabetic neuropathy

79
Q

give 3 examples of TCAs

A

amitriptyline
nortriptyline
desipramine

80
Q

how do TCAs work

A

act centrally to reduce uptake of NA

81
Q

how does carbamazepine work

A

blocks subtypes of VGNaCs that are upregulated in damaged nerve cells

82
Q

what is the first line treatment of trigeminal neuralgia to control pain and reduce frequency of attacks

A

carbamazepine

83
Q

what is nociceptive pain

A

pain from injury relayed through a normal nervous system

84
Q

what is allodynia

A

pain from a stimulus that is not normally painful

85
Q

what is hyperalgesia

A

more pain than expected from a stimulus e.g. pin prick

86
Q

what is peripheral sensitisation

A

reduction in the threshold of peripheral afferent nociceptors after injury

87
Q

what is central sensitisation

A

increased excitability of spinal neurones / rewiring in the spinal cord / changes in the brain
after injury

88
Q

if someone doesnt have SCN9A voltage gated calcium channel subtype what will be wrong with them

A

inability to feel pain

89
Q

if someone has an abnormal SCN9A voltage gated calcium channel subtype what will be wrong with them

A

paroxysmal extreme pain disorder

90
Q

how does topical capsaicin work

A

depletion in substance P - peptide that amplifies cellular processes

91
Q

how does topical levomenthol work

A

activator of transient receptor potential melastatin-8

YEAR 3 NEURO (12 decks)

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