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Neurology > Neuropharmacology > Flashcards

Neuropharmacology Flashcards

1
Q

2 ascending pathways and functions of each?

A

spsinothalamic tract
- info from A delta fibres
- deals with first fast pain
- fibres cross over immediately in spinal cord level
- gives info about location and intensity of pain
spinoreticulothalamic tract
- deals more with emotive aspect of pain
- A delta, A beta and C fibres
- noxious and innoculous information
- from spinal cord to brain stem reticular formation
- relayed indirectly to cerebral cortex

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2
Q

what needs to be stimulated for pain to be perceived?

A

for pain to be perceived, neurons in lamina 1 and 5 need to be stimulated

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3
Q

analgesics may reduced nociception and pain via what 5 methods?

A
  1. acting at site of injury (blocking sensitisation of primary afferent terminal by blocking synthesis of prostaglandins)
  2. suppress nerve conduction by blocking/inactivating voltage activated Na channels
  3. suppressing synaptic transmission of nociceptive signals in the dorsal horn of the signal cord
  4. activating (or potentiating) descending inhibitory controls
  5. targeting ion channels upregulated in nerve damage
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4
Q

how do NSAIDs work?

A

acting at site of injury (blocking sensitisation of primary afferent terminal by blocking synthesis of prostaglandins)

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5
Q

how do local anaesthetics work?

A

suppress nerve conduction by blocking/inactivating voltage activated Na channels (e.g local anaesthetics - lidocaine)

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6
Q

how do opioids and some antidepressants work?

A

suppressing synaptic transmission of nociceptive signals in the dorsal horn of the signal cord (e.g opioids and anti-depressants)

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7
Q

how else may opioids and some tricyclic antidepressants work?

A

activating (or potentiating) descending inhibitory controls

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8
Q

how do anti-epileptics such as GABA pentinoids work?

A

targeting ion channels upregulated in nerve damage

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9
Q

describe the steps in the anaelgesic ladder?

A
  1. NSAIDs and/or paracetamol
  2. weak opioid (codeine, tramadol, dextropropoxyphene)
  3. strong opioid (morphine, oxycodone, hydromorphone, heroin, fentanyl)
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10
Q

what combinations of analgesics may be used in moderate - severe pain?

A

1+2
1+3
(cant combine 2 and 3 as they work on same receptors/have same action so would be illogical)

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11
Q

opiates vs opioids?

A 
opiates = substances extracted from opium or of similar structure to those in opium
opioids = any agent (including endogenous peptides which already exist in the body known as endorphins/enkephalins) that act upon opioid receptors
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12
Q

supraspinal anti-nociception is mediated by what?

A

descending pathways from the brainstem

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13
Q

brain stem involved with pain regulation receives input from where?

A

brain regions involved with pain perception and emotion

  • cortex
  • amygdala
  • thalamus
  • hypothalamus
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14
Q

what 3 regions of the brain stem are involved with pain regulation?

A

periaqueductal grey (PAG) matter (midbrain)
locus ceruleus (LC) (pons)
nucleus raphe magnus (NRM) (medulla)
neurones from here give rise to efferent pathways which project to the spinal cord to modify afferent input

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15
Q

how can PAG be used in analgesia?

A

excitation of PAG neurones by electrical stimulation produces profound analgesia
can also be excited by endogenous opioids or morphine and related compounds

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16
Q

how does PAG cause analgesia?

A

activated PAG neurones project to NRM and excite serotonergic and enkephalinergic neurones projecting to the dorsal horn causing suppression of noceiceptive transmission
(morphine can also excite NRM neurones)
PAG neurones also excite LC neurones projecting to dorsal horn and inhibit nociception

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17
Q

diagram

A

//

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18
Q

opioid action is mediated by what type of receptors?

A

GPCRs

all of which signal to Gi/Go

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19
Q

what are the 3 actions of opioids acting on GPCRs signalling to Gi/Go?

A

inhibition of voltage activated Ca2+ channels (suppresses neurotransmitter release from 1st order neurone)
opening of K+ channels (suppresses excitation of 2nd order neurones)
inhibition of adenylate cyclase
all mediated by BY subunit of Gi/o GPCR

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20
Q

classifications of opioid receptor?

A 
u = action of most analgesic action of opioids
delta = contributes to analgesia but can cause convulsions
K = contributes to analgesia at spinal and peripheral level, can cause sedation, dysphoria and hallucinations
21
Q

in addition to the addictive potential of opioids, how can they affect respiration?

A

apnoea

can trigger bronchospasm in asthmatics

22
Q

how do opioids cause resp depression?

A

blunting of medullary resp centre to CO2

23
Q

effect of opioids on cardio system?

A 
orthostatic hypotension
(reduced sympathetic tone and bradycardia)
24
Q

how can opioids affect the GI system?

A 
nausea
vomiting
constipation
increased intrabiliary pressure
(decreased motility, action of CTZ)
25
Q

CNS effects of opioids?

A 
confusion
euphoria
dysphoria
hallucinations
dizziness
myoclonus
hyperalgesia (with excessive use)
26
Q

opioid analgesia occurs mainly through what action?

A

prolonged activation of u opioid receptors

27
Q

how is morphine metabolised?

A

in the liver at 3 and 6 positions by glucuronidation yielding M3G (inactive) and M6G (retains analgesic activity and is excreted by the kidney)

28
Q

how is morphine delivered?

A

acute severe pain = IV (in incremental doses), IM or SC and oral
chronic pain = oral (immediate - oramorph or sustained release over 12-24 hrs - MST continus)

29
Q

describe the action of diamorphine (heroin)

A

more lipophilic than morphine
rapid onset of action when administered IV (crosses blood brain barrier and enters CNS very quickly)
can be used for severe post-op pain

30
Q

how is codeine used? what alternatives can be used?

A 
naturally occurring weaker opioid
given orally (not IV) for mild-mod pain
has additional anti-diarrhoeal and antitussive activity that may be useful (or bad - constipation)
its semi-synthetic derivatives with higher potency include oxycodone and hydrocodone
31
Q

how is codeine metabolised?

A

in the liver by demethylation(in small amounts) to morphine by CYP2D6 and CYP3A4

32
Q

how is fentanyl given and why?

A

75-100 times more potent than morphine
given IV to provide analgesia in maintenance anaesthesia (given during surgery to reduce amount of general anaesthetic needed)
suitable for transdermal and buccal delivery (as lipophilic) in chronic pain states but not in acute pain

33
Q

describe the use of pethidine (merperidine in USA)

A

used in acute pain, particularly labour pain
rapid onset of action when given IV, IM or SC but short duration of action so not good for chronic pain
shouldn’t be used in conjunction with MAO inhibitors (causes excitement, convulsions etc)
norpethidine is a neurotoxic metabolite (causes seizures)

34
Q

describe the use of bupreophine?

A

partial agonist
can be given via injection or sublingually in chronic pain with patient controlled injection systems
has slow onset but long duration of action

35
Q

describe action of tramadol? when should it be avoided?

A

weak u-receptor agonist
exerts significant analgesic action by potentiation of the descending serotonergic (from NRM) and adrenergic (from LC) systems
given orally
avoid in epilepsy

36
Q

how does methadone work?

A 
weak u-receptor agonist of the phenylheptylamine class
additional actions at other CNS sites including K channels, NMDA glutamate receptors and some 5-HT receptors
37
Q

describe use of etorphine (immobilon)

A

used in vet medicine, not human
1000X more potent than morphine
can down an elephant/rhino in one dart
action can be reversed by diprenorphine (revivon)

38
Q

name 3 analgesics with antagonistic action

A

naloxone
naltrexone
alvimopan, methylnaltrexone

39
Q

how is naloxone used?

A

used to reverse opioid toxicity
given incrementally IV (IM or SC if IV not available)
can be given to newborn with opioid toxicity from mother
short half life

40
Q

how do NSAIDs work generally?

A

diminish nociceptor sensitization by inhibiting synthesis and accumulation of prostaglandins by COX enzymes COX1 and COX2

41
Q

describe the pathway of prostaglandin production

A

phospholipids > (phospholipase A2) > arachidonic acid > (COX1 and COX2) > endoperoxides > (prostaglandin isomerase) > prostaglandins
- prostaglandins cause hyperalgesia, allodynia, pain etc

42
Q

3 specific actions of NSAIDs?

A

suppress the decrease in activation threshold of peripheral nociceptor terminals caused by prostaglandins
decrease recruitment of leukocytes that produce inflammatory mediators
suppress production of pain producing prostaglandins in dorsal horn (if they cross BBB)

43
Q

how do NSAIDs cause stomach ulcers?

A

PGE2 produced by COX1 protects against acid/pepsin environment in stomach

44
Q

COX 1 vs COX2?

A

COX1 always active

COX2 = induced locally at sites on inflammation when needed

45
Q

neuropathic is usually insensitive to what analgesics? what can be used instead?

A 
NSAIDs and opioids
instead can use
- gabapentin and pregabalin (antiepileptics)
- tricyclic antidepressants
- carbamazepine
46
Q

how do gabapentin and pregabalin work?

A

reduce the cell surface expression of subunit a2d of some voltage gated Ca2+ channels which are upregulated in damaged nerves
this causes a decrease in neurotransmitter release from central terminals of nociceptive neurones

47
Q

how do tricyclic antidepressants relieve pain?

A

act centrally by decreasing reuptake of noradrenaline
some also decrease reuptake of 5-HT
(SSRIs don’t gave analgesic action)

48
Q

how does carbamazepine relieve pain?

A

blocks subtypes of voltage activated Na+ channel that are upregulated in damaged nerve cells
first line in trigeminal neuralgia

49
Q

describe the use of methadone?

A

given orally
long duration of action
can be used in chronic cancer pain
assists in opioid withdrawal

Neurology (53 decks)

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