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Neurology > Physiology Analgesia and Analgesic Drugs > Flashcards

Physiology Analgesia and Analgesic Drugs Flashcards

1
Q

what are the different mechanisms for analgesics reducing nociception

A

acting at site of injury (decrease nociceptor sensitisation in inflammation by blocking synthesis of prostaglandins)

suppressing nerve conduction (blocking/ inactivating v-activated sodium channels) (local anaesthetics)

suppressing synaptic transmission of nociceptive signals in dorsal horn (opioids and some antidepressants)

activating descending inhibitory controls (opioids and tricyclin ADs)

targeting ion channels upregulated in nerve damage (gabas)

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2
Q

what is the who analgesic ladder

A

NSAID (aspirin, diclofenac, ibruprofen, naproxen) and/or paracetamol

weak opioid (codeine, tramadol, dextropropoxyphene)

strong opioid (morphine, oxycodone, hydromorphone, heroim, fentanyl)

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3
Q

whats the difference between opiates and opioids

A

Opiates – substances extracted from opium, or of similar structure to those in opium
Opioids – any agent (including endogenous peptides, known collectively as endorphins/enkephalins) that act upon opioid receptors

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4
Q

does paracetamol have anti inflammatory effects

A

no

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5
Q

what mediates supraspinal anti-nociception

A

descending pathways from the brainstem:
-brain regions involved in pain perception (cortex, thalamus, hypothalamus) project to specific brainstem nuclei
-neurones of brainstem nuclei give rise to efferent pathways that project to spinal cord to moderate afferent input
(the gate theory)

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6
Q

what areas of brain stem are important in supraspinal nociception

A

the periaqueductal grey (midbrain)
locus ceruleus (pons)
nucleus raphe magnus (medulla)

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7
Q

what activates PAG

A 
electrical stimulation
endogenous opioids (enkephalins) 
morphine/ related compounds (excite it by inhibiting inhibitory GABA interneurones)
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8
Q

what does PAG activation cause

A

profound analgesia

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9
Q

how doe PAG neurones work

A

activated PAG neurones project to the nucleus raphe magnus and excite serotonergic and enkephalinergic neurones
+ also project to dorsal horn causes suppressed nociceptive transmission

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10
Q

what do locus coeruleus noradrenergic neurones do

A

project to the dorsal horn and inhibit nocicpetive transmission

excited by PAG neurones

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11
Q

opioids also activate NRM neurones, what do these release

A

5-HT and enkephalins

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12
Q

how do opioids suprpress pain

A

activate descending pathways which suppresses pain:

-excites PAG and NRM by disinhibition

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13
Q

what are the resp adverse effects of opioids

A

apnoea:

-blunts medullary resp centre to CO2

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14
Q

what are the cardio adverse effects of opioids

A

orthostatic hypotension:

  • reduced sympathetic tone and bradycardia
  • histamine evoke vasodilation
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15
Q

what are the GI adverse effects of opioids

A

nausea
vomiting
constipation
increased intrabiliary pressure

  • acts on chemoreceptor trigger zone
  • increased smooth muscle tone
  • decreased motility
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16
Q

what are the CNS adverse effects of opioids

A

confusion, euphoria, dysphoria, hallucinations, dizziness, myoclonus, hyperalgesia (with excessive use)

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17
Q

what are the agonist types of opioids and how do they work

A 
morphine
diamorphoine 
codeine 
fentanyl 
pethidine 
buprenophine
tramadol 
methdone

prolonged activation of μ-opioid receptors

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18
Q

how is morphine metabolised

A

metabolised in the liver

excreted by the kidney

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19
Q

how can morphine be administered

A

IV, IM, SC or orally

epidural, intrathecal

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20
Q

what is oral morphine good for

A

immediate breakout pain

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21
Q

what is morphine not good at

A

reducing neuropathic pain

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22
Q

what is diamorphine used for

A

rapid onset- used in severe post op pain

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23
Q

what is codeine used for

A

mild/ moderate pain

24
Q

how is codeine metabolised

A

in liver (metabolised into morphine)

25
Q

how is codeine administered

A

orally (not IV)

26
Q

what are the extra effects of codeine

A

anti diarrhoeal (constipation) and antitussive

27
Q

what is fentanyl

A

agonist opioid

more potent that morphine

28
Q

what for and how is fentanyl used

A

maintenance anaesthesia

IV (in acute), transdermal (in chronic pain states)

29
Q

what for and how is pethidine used

A

acute pain (labour)
IV, IM, SC
not suitable for chronic pain
should not be given with MAO inhibitors

30
Q

what for and how is buprenophine used

A

chronic pain
patient controlled injection systems
long duration
can be given via injection or sublingually

31
Q

how is tramadol given

A

orally

avoid in epilepsy can cause seizures

32
Q

what for and how is methadone given

A

orally
has long duration of action so used in opioid withdrawal
used in chronic cancer pain

33
Q

what are the antagonist opioids and how do they work

A

naloxone
naltrexone
alvimopan
methylnaltrexone

competitive antagonist at μ-opioid receptors

34
Q

what are antagonist opioids used for

A

to reverse opioid toxicity associated with strong opioid overdose

35
Q

how are antagonist opioid given

A

incrementally IV. IM and SC routes are alternatives if IV is not practical

36
Q

why is the half life of naloxone important

A

short half-life – very important since opioid toxicity can recur to ‘strong opioid’ agonists with a longer duration of action. Clinically, you must monitor the effect of naloxone very carefully, titrating the individual dose, and frequency, to that required to reverse opioid toxicity and do not leave the patient unattended

37
Q

what is the advantage of naltrexone

A

oral availability and a much longer half-life

38
Q

what is the advantage of alvimopan and methylnaltrexone

A

do not enter CNS, reduce G.I. effects of surgical and chronic opioid agonist use

39
Q

how do NSAIDs work

A

diminish nociceptor sensitisation by inhibiting the synthesis and accumulation of prostaglandins (cause hyperalgesia, allodynia and pain) by COX enzymes 1 and 2

suppress the decrease in the activation threshold of the peripheral terminals of nociceptors that is caused by prostaglandins
decrease recruitment of leukocytes that produce inflammatory mediators
if they cross the BBB, suppress the production of pain-producing prostaglandins in the dorsal horn of the spinal cord (that, for example, reduce the action of the inhibitory neurotransmitter, glycine)

40
Q

what are all the effects of NSAIDs

A

analgesic
antipyretic
anti inflammatory

41
Q

what are the non specific NSAIDs

A 
aspirin
ibruprofen 
naproxen 
diclofenac 
indometacin
42
Q

what are the specific COX 2 NSAIDs

A

ones ending in ib
etoricoxib
celecoxib
lumiracoxib

43
Q

when are COX enzymes active

A

COX-1 is constitutively active, COX-2 is induced locally at sites of inflammation by various cytokines

44
Q

does paracetamol act peripherally or centrally

A

only centrally

45
Q

what can long term administration of non selective NSAIDs cause

A

GI damage

(PGE2 produced by cox-1 protects against acid/ pepsin environment(

46
Q

what can paracetamol damage

A

kidney- cox 2 inhibition here can compromise renal hemodynamics

47
Q

what is the downside of selective cox 2 NSAIDs

A

are prothrombotic

48
Q

does neuropathic pain respond to NSAIDs

A

no

49
Q

what is used to treat neuropathic pain

A

gabapentin and pregabalin (antiepieptics)
amitriptyline, nortyptiline and desipramine (tricyclic antidepressants)
carbamazepine

50
Q

how do gabapentin and pregabalin work

A

DO NOT WORK VIA GABAERGIC SYSTEMIC

reduce the expresison of V activated Ca2+ channels which are upregulated in damaged sensory neurones

this causes a decrease in neurotransmitters (glutamate and substance P) from central terminal of nociceptive neurones

51
Q

what is gabapentin used in

A

migraine prophylaxis

52
Q

what is pregabalin used in

A

diabetic neuropathy

53
Q

how do tricyclic antidepressants work

A

work centrally

decrease the reuptake of noradrenaline

54
Q

how does carbamazepine work

A

blocks subtypes of v activates Na+ channels that are upregulated in damaged nerve cells

55
Q

what is the first line Tx to control pain intensity and frequency of attacks in trigeminal neuralgia

A

carbamazepine

Neurology (35 decks)

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