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YEAR 3 NEURO > PHARMACOLOGY - Analgesic drugs > Flashcards

PHARMACOLOGY - Analgesic drugs Flashcards

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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
why can opioids cause bronchospasm in asthmatics
morphine but not all opioids can cause degranulation of mast cells
26
why can opioids cause orthostatic hypotension
reduced sympathetic tone and bradycardia via action on medulla
27
why can opioids cause GI side effects
action on chemoreceptor trigger zone | action on enteric neurones - increased smooth muscle tone and decreased motility
28
where is morphine metabolised and excreted
metabolised - liver | excreted - kidney
29
how can morphine be delivered
acute severe pain - IV IM SC or oral | chronic pain - oral (oramorph)
30
is diamorphine or morphine more lipophilic
diamorphine
31
diamorphine has a ____ onset of action when given IV
rapid
32
name a weaker opioid than morphine or diamorphine used for mild/moderate pain
codeine
33
how is codeine given
oral
34
what is codeine metabolised by demethylation to in the liver
morphine
35
what metabolised codeine to morphine
CYP2D6 and CYP3A4
36
name 2 semi-synthetic derivatives of codeine with higher potency
oxycodone | hydrocodone
37
name an opioid 75-100 fold stronger than morphine
fentanyl
38
how can fentanyl be delivered
IV | transdermal (and buccal)
39
when is IV fentanyl used
analgesia in maintenance anaesthesia
40
when is transdermal fentanyl used
chronic pain states
41
how does analgesia occur with use of opioids
agonists of u-opioid receptor - prolonged activation of receptor
42
pethidine has a ____ onset of action and is used in ___ pain for example ____
rapid acute labour
43
Pethidine should not be used in conjunction with ____ as can cause convulsions
MAO inhibitors
44
name a partial agonist of opioid receptor that is used in chronic pain due to its slow onset but long duration of action
Buprenorphine
45
how can Buprenorphine be given
injection or sublingual
46
____ is a weak u-receptor agonist given orally and should be avoided in epilepsy
tramadol
47
what is the most likely reason for tramadol's analgesic effect
potentiation of the descending serotonergic (NRM) and adrenergic (LC) systems
48
methadone is a ____ oral u agonist with a ____ duration of action
``` weak long (plasma half life > 24 hours) ```
49
what other sites does methadone work on
K channels NMDA glutamate receptors some 5-HT receptors
50
give 2 scenarios where methadone is useful
withdrawal from heroin | chronic cancer pain
51
are agents with a short or long half life more addictive
short
52
what is used to reverse opioid toxicity
naloxone
53
what is the mechanism of action of naloxone
competitive antagonist of u-receptor (and to a lesser extent k and d)
54
why must you monitor the effects of naloxone
short half life - with strong opioid agonists with a long half life opioid toxicity may recur
55
how is naloxone given
IV | IM or SC if IV not possible
56
naloxone can trigger what in opioid addicts
withdrawal
57
why might naloxone be given to a new born
for opioid toxicity
58
what happens in opioid toxicity
respiratory depression | neurological depression
59
name a drug similar to naloxone with oral availability and much longer half life
naltrexone
60
what gives NSAIDs their analgesic, anti-inflammatory and anti-pyretic actions
inhibiting the synthesis of prostaglandins by cyclo-oxygenase (COX) enzymes 1 and 2
61
what do COX 1 and COX 2 do
convert arachadonic acid to endoperoxides
62
what converts endoperoxides to prostaglandins
prostaglandin isomerase
63
what converts phospholipids to arachadonic acid
phospholipase A2
64
aspirin, diclofenac, ibuprofen, naproxen, indomethacin are all selective/non-selective
non-selective
65
etoricoxib / celecoxib / lumiracoxib are all selective / non selective
selectie COX 2 inhibitors
66
therapeutic benefit of NSAIDs largely derived from inhibition of COX-_ as it is induced locally at sites of inflammation
2
67
what limits the use of cox 2 selective NSAIDs
they are prothrombotic
68
what can occur with long term use of non-selective NSAIDs
GI damage
69
why can GI damage occur with long term use of non-selective NSAIDs
PGE2 produced by COX-1 protects against the acid/pepsin environment
70
what can occur as a result of cox-2 inhibition
nephrotoxicity - it is expressed by kidney
71
NSAIDs act peripherally and centrally to (3)
- 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
what kind of pain doesnt respond to opioids (unless high dose) or NSAIDs
neuropathic
73
give 4 examples of neuropathic pain
trigeminal neuralgia diabetic neuropathy post-herpetic neuralgia (shingles) phantom limb pain
74
what are some drugs that may be used in the treatment of neuropathic pain
gabapentin and pregabalin TCAs carbamazepine
75
how do gabapentin and pregabalin (antiepileptics) treat neuropathic pain
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
what is neuropathic pain
pain caused by damage or disease affecting the somatosensory nervous system
77
gabapentin is used in ---
migraine prophylaxis
78
pregabalin is used in ---
painful diabetic neuropathy
79
give 3 examples of TCAs
amitriptyline nortriptyline desipramine
80
how do TCAs work
act centrally to reduce uptake of NA
81
how does carbamazepine work
blocks subtypes of VGNaCs that are upregulated in damaged nerve cells
82
what is the first line treatment of trigeminal neuralgia to control pain and reduce frequency of attacks
carbamazepine
83
what is nociceptive pain
pain from injury relayed through a normal nervous system
84
what is allodynia
pain from a stimulus that is not normally painful
85
what is hyperalgesia
more pain than expected from a stimulus e.g. pin prick
86
what is peripheral sensitisation
reduction in the threshold of peripheral afferent nociceptors after injury
87
what is central sensitisation
increased excitability of spinal neurones / rewiring in the spinal cord / changes in the brain after injury
88
if someone doesnt have SCN9A voltage gated calcium channel subtype what will be wrong with them
inability to feel pain
89
if someone has an abnormal SCN9A voltage gated calcium channel subtype what will be wrong with them
paroxysmal extreme pain disorder
90
how does topical capsaicin work
depletion in substance P - peptide that amplifies cellular processes
91
how does topical levomenthol work
activator of transient receptor potential melastatin-8

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