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Neurology - professional - batt > Analgesic Drugs > Flashcards

Analgesic Drugs Flashcards

1
Q

What is the difference between an opiate and an opioid?

A

an opiate is a substance extracted from opium or similar in structure whereas opioids are any agent which acts upon the opioid receptors

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2
Q

How do NSAIDs work?

A

decrease nociceptor sensitization in inflammation

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3
Q

What is segmental ant-nociception?

A

gate control theory

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4
Q

What is supraspinal anti-nociception?

A

descending pathways from brainstem

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5
Q

What areas of hte brain are involved in pain perception and emotion?

A

cortex, amygdala, thalamus and hypothalamus

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6
Q

What areas of hte brainstem are invovled in supraspinal anti-nocicpetion?

A

periaqueductal grey and nucleus raphe magnus; locus coeruleus

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7
Q

What happens in response to electrical stimulation in the PAG?

A

profound analgesia

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8
Q

How do opioids work on the PAG?

A

cause excitation by disinhibition

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9
Q

Where do axons from the nucleus raphe magnus and locus coeruleus project via?

A

dorsolateral funiculus

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10
Q

What neurotransmitters does the nucelus raphe magnus use?

A

5-HT and enkephalins

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11
Q

What neurotransmitter does the locus coeruleus use?

A

noradrenaline

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12
Q

What type of receptor are opioid receptors?

A

GPCR which couple to Gi/o

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13
Q

What is the effect of activation of the opioid receptors?

A

inhibition of opening of Ca channels presynptically and opens K channels postsnyaptically

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14
Q

How does inhibition of Ca channels by opioids contribute to analgesia?

A

suppresses excitatry neurotransmitter release from nociceptor terminals

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15
Q

How does opening of K channels by opioids contribute to analgesia?

A

suppresses excitation of projection neurons

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16
Q

What are the types of opioid receptor?

A

mu; delta; kappa and ORL

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17
Q

What type of opioid receptor is responsible for most of the analgesic action of opioids?

A

mu receptors

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18
Q

What problem does mu receptor activation cause?

A

respiratory depresssion; constipation; euphoria; sedation and dependece

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19
Q

What is the problem with activation of delta receptors?

A

proconvulsant

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20
Q

Where does kappa contribute to analgesia?

A

spinal and peripheral levels

21
Q

What is kappa receptor activation associated with?

A

sedation; dysphoria and hallucinations

22
Q

What happens with ORL1 activation?

A

anti-opioid effect

23
Q

What is fentanyl used for?

A

providing analegsia in maintenance anaesthesia

24
Q

Why is buprenorphine useful in chronic pain?

A

long duration of action

25
Q

What should pethidine not be used with?

A

MAO inhibitors as cause convulsions and hyperthermia

26
Q

Who should tramadol be avoided in?

A

epileptics

27
Q

What type of agents are more likely to be abused?

A

short half-life are more addictive

28
Q

How does tramadol work?

A

weak um agonist; potentiates descending serotonergic and adrenergic systems

29
Q

How does methadone work?

A

weak m agonist; works at potassium channels; NMDA receptors and some 5-HT receptors

30
Q

What is naloxone?

A

competitive antagonist at um receptors (a little at kappa and delta)

31
Q

What is the use of naloxone?

A

reverse opioid toxicity

32
Q

Why is the short half life of naloxone important?

A

opioid toxicity can recur to strong opioid agonists with a longer duration of action

33
Q

What enzyme converts phospholipis to arachiodonic acid?

A

phospholipase A2

34
Q

What enzyme converts arachiodonic acid to endoperoxides?

A

COX 1 and COX 2

35
Q

What are the 3 products of endoperoxides?

A

prostaglandins; thromboxane A and prostacyclin (PGI2)

36
Q

What is the function of prostaglandins?

A

hyperalgesia by sensitising nocieptive neurons

37
Q

What is the function of thromboxane-A2?

A

platelet aggregation and vasoconstriction

38
Q

What is the function of prostacyclin?

A

platelet disaggregation and vasodilation

39
Q

Name some COX2 selective inhibitors?

A

etoricoxib; celecoxib and lumiracoxib (COXIBs)

40
Q

When is COX2 induced?

A

during inflammation

41
Q

What causes GI toxicity in COX inhibition?

A

COX-1 inhibition

42
Q

When do cells generate prostaglandins?

A

in reponse to mechanical, thermal or chemical injury

43
Q

Why do NSAIDs have limited analgesic efficacy?

A

mulitple signalling pathways not involving arachidonic acid metabolism also cause nociceptor sensitisation

44
Q

Why does long-term administration of non-selective NSAIDs produce GI damage?

A

prostaglandins produced by COX-1 protect against the acid/pepsin environment

45
Q

What is the problem with selective COX-2 inhibitors?

A

prothrombotic

46
Q

What can cause neuropathic pain?

A

trigeminal neuralgia; diabetic neuropathy; post-herpetic neuralgia; phantom limb pain

47
Q

What drugs are effective in neuropathic pain?

A

gabapentin and pregabalin; TCAs; carbamzepine

48
Q

How do gabapentin and pregabalin work?

A

reduce cell surface expression of some voltage-gated Ca channels which are upregulatedi n damaged sensory neurones which reduces neurotransmitters from central terminals

49
Q

How does carbamazepine work?

A

blocks subtypes of voltage-activated Na channels that are upregulated in damaged nerve cells

Neurology - professional - batt (40 decks)

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