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Analgesia & Opioids Flashcards

1
Q

Define opioid.

A

Any substance that mediates an analgesic effect through opioid receptors that can be blocked by naloxone

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2
Q

Give examples of natural opioids.

A

Morphine

Codeine

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3
Q

What are the four classes of synthetic opioids?

A

Phenylpiperidine
Diphenylpropylamine
Benzomorphan
Thebaine

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4
Q

Give examples of phenylpiperidine opioids.

A

Pethidine
Fentanyl
Alfentanyl

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5
Q

Give examples of diphenylpropylamine opioids.

A

Methadone

Dextropropoxyphene

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6
Q

Give examples of benzomorphan opioids.

A

Pentazocaine

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7
Q

Give examples of semi-synthetic opioids.

A

Diamorphine
Dihydrocodeine
Buprenorphine

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8
Q

Give an example of thebaine opioids.

A

Buprenorphine

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9
Q

What are the general undesired effects of opioids?

A

Modulation of GI, endocrine and autonomic function

Role in cognition

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10
Q

What are endogenous opioids derived from?

A

Precursor proteins via proteolytic cleavage of pro-opiomelanocortin

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11
Q

What are the two enkephalins?

A

Met

Leu

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12
Q

What are the two dynorphins?

A

A

B

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13
Q

What are the three endorphins?

A

A-neo
B-neo
Bh-neo

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14
Q

What are the two endomorphins?

A

1

2

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15
Q

What are the four subtypes of opioid receptor?

A

Meu (MOP)
Delta (DOP)
Kappa (KOP)
Nociceptin (NOP)

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16
Q

What are the IUPHAR standard nomenclatures for opioid receptors?

A

MOP 1-3
DOP 1,2
KOP 1a, 1b, 2a, 2b, 3

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17
Q

Describe the effects of MOP receptors.

A 
Analgesia
Depressions
Euphoria
Physical dependence
Respiratory depression
Sedation
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18
Q

Describe the effects of DOP receptors.

A

Analgesia
Inhibition of dopamine release
Modulation of MOP

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19
Q

Describe the effects of KOP receptors.

A

Analgesia
Diuresis
Dysphoria

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20
Q

Describe the mechanism of opioid receptors.

A

G-Protein Coupled receptors present on both pre and postsynaptic membrane
Inhibition of adenylate cyclase which reduces cAMP and neurotransmitter release by dissociated α substrate
Dampens down activity of pain nerves
Dissociated β and 𝜸 substrates alter ion movement
Activation of voltage-gated inward rectifying potassium channels
- Hyperpolarisation of cells
- Decreased responsiveness to depolarising stimuli
- Reduced neurotransmitter release
Inhibition of voltage gated (N type) calcium channels
Reduces neurotransmitter release

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21
Q

What are nociceptive fibres?

A

Free nerve endings present throughout the periphery

Respond to multiple types of stimuli

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22
Q

Describe the structure of C nociceptive fibres? What response are they responsible for?

A

Unmyelinated

Dull, diffuse, burning pain

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23
Q

Describe the structure of Aẟ nociceptive fibres? What response are they responsible for?

A

Myelinated

Sharp, localised pain

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24
Q

Describe the stimulation of nociceptors.

A

Release of neurotransmitters causing inflammation and exacerbation
Prostaglandins able to sensitise nociceptor to allow perception of pain

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25
Describe the ascending pain pathway.
Nociceptor is stimulated Action potential travels along axon to cell body in dorsal ganglion First order afferent- peripheral to dorsal ganglion Action potential potentiated along to dorsal horn Signal transferred up to next nerve- second order afferent Action potential travels to the thalamus Signal transferred to next nerve which terminates in somatosensory cortex- third order afferent
26
Describe the descending pain pathway.
Somatosensory cortex connects with brain regions which co-ordinate response The amygdala, anterior cingulate cortex, insular cortex and hypothalamus send projections to the periaqueductal grey PAG sends signals to rostroventral medulla RVM sends signals to dorsal horn, where nerve interacts with ascending pathway Descending pathway may synapse onto the nociceptor AND/OR cell body in the spinal cord to dampen activity
27
How do opioids act on the pain pathway?
At the spinal cord, opioids are able to interact and dampen down the ascending transmission to reduce pain stimulation Acts as negative feedback
28
List the neurotransmitters involved in the ascending pain pathway.
Glutamate Substance P CGRP (calcitonin gene-related peptide) Nitric oxide
29
List the neurotransmitters involved in the descending pain pathway.
``` Endogenous opioids 5-HT Noradrenaline Endo-cannabinoids Glycine GABA ```
30
Describe the role of MOP receptors in pain.
Involved in motor and sensory processing, integration and perception of pain Located pre-synaptically on primary afferent neurones in the dorsal horn Inhibit glutamate release and therefore transmission of nociceptive stimuli
31
Describe the role of DOP receptors in pain.
Located pre-synaptically on primary afferent neurones in the dorsal horn and secondary afferent neurones in the brain Inhibit neurotransmitter release and therefore transmission of nociceptive stimuli
32
Give examples of opioid analgesics that are full agonists.
Morphine, diamorphine, fentanyl, pethidine, dyhydrocodeine, codeine, hydrocodone, levorphanol, methadone, oxycodone
33
Give examples of opioid analgesics that are mixed agonist-antagonists.
Pentazocine weak agonist at KOP and weak antagonist at MOP
34
Give examples of opioid analgesics that are mixed partial agonist-antagonists.
Buprenorphine partial agonist at MOP, weak antagonist at KOP
35
Describe the additional properties of the opioid meptazinol.
MOP receptor agonist and muscarinic agonist
36
Describe the additional properties of the opioid tramadol.
MOP receptor agonist | Blocks neuronal serotonin and noradrenaline uptake
37
Describe the additional properties of the opioid methadone.
MOP receptor agonist Blocks neuronal serotonin and noradrenaline uptake Antagonist at NMDA receptors
38
What are opioids most effect against?
Chronic visceral pain | Peripheral noxious stimuli consistently activating
39
Give examples of strong opioids.
``` Morphine Pethidine Fentanyl Alfentanil Remifentanil ```
40
Give examples of intermediate opioids.
Buprenorphine | Pentazocaine
41
Give examples of weak opioids.
Codeine
42
Describe the pharmacokinetics of opioids.
Opioids are weak bases (pKa 6.5-8.7) Opioids are highly ionised in the stomach, therefore poorly absorbed Highly absorbed in the small intestine Undergo extensive first pass metabolism in the intestinal wall and liver, resulting in low oral bioavailability High lipid solubility facilitates opioid transport into biophase or site of action, therefore a more rapid onset of action Most are extensively distributed in the body, volumes of distribution exceed total body water Small IV doses of short acting opioids produce short duration of action because plasma concentration remains above threshold for therapeutic action for only a brief period as drug rapidly redistributes from CNS to other tissues
43
Describe the metabolism of opioids.
Mainly occurs in the liver Main mechanism is conjugation with glucuronide Entero-hepatic recirculation can occur Morphine-6-glucuronide has greater analgesic effect than morphine itself Diamorphine and codeine both have active metabolites
44
Describe the mechanism by which opioids cause N+V.
Opioids stimulate chemoreceptor trigger zone Tends to be short lived Worse in ambulatory patients In equi-analgesia, codeine is worse than morphine for vomiting Blocked by dopamine antagonists Apomorphine is a dopamine receptor agonist with a similar structure to morphine
45
Describe the mechanism by which opioids cause convulsions.
High doses excite hippocampal pyramidal neurones Inhibition of GABA release Blocked by opioid antagonists Pethidine is metabolised to norpethidine which is a proconvulsant, blocked by anti-convulsant not opioid antagonist
46
Describe the mechanism by which opioids cause respiratory effects.
Action at medullary respiratory centre by µ2 µ1- receptor selective less depression i.e. meptazinol Decreased respiratory rate and response to increased pCO2 Decreased FEV1
47
Describe the mechanism by which opioids cause GI effects.
Increased tone in propulsive muscle Decreased contractions in propulsive muscle Contracts GIT sphincters, increased pain in biliary colic Leads to decreased water movement into lumen, likely to result in constipation
48
Describe the mechanism by which opioids cause endocrine effects.
Suppression of hypothalamic-pituitary-adrenal axis leading to decline in plasma cortisol Increased prolactin release Reduction in LH release leading to testosterone and oestrogen deficiencies
49
Describe the mechanism by which opioids cause ocular effects.
Mediated via MOP and KOP on the Edinger-Westphal nucleus of the occulomotor nerve (3rd cranial nerve) Increased parasympathetic outflow to iris sphincter and ciliary body Accommodation for near vision affected Pinpoint pupils can be a sign of overdose
50
Describe the mechanism by which opioids cause itching.
Basic nature of morphine greater than histamine Displaces histamine from histamine-heparin complex in mast cells Causes urticaria, itching, bronchospasm, hypotension More pronounced on face, nose and torso
51
What is naloxone?
Opioid antagonist Competitive at all three receptors Used to treat respiratory depression in neonates and opioid overdose
52
Define pyresis.
Thermostat raised by hypothalamus Heat production and loss is in balance Feel cold
53
Define hyperthermia.
Thermostat not altered Heat production > heat loss Feel hot
54
Describe the mechanism of a fever.
Occurs due to release of cytokines in response to tissue injury or infection Cause release of prostaglandins and increased synthesis PGE2 raises thermostat in hypothalamic thermoregulatory centre via binding to E-prostanoid receptors (3 and 4) Core temperature is sensed as too low, hence feeling cold Increased heat gain/conservation, despite body temperature not actually matching what the brain thinks
55
Describe the production of prostaglandins.
Inflammatory stimulus causes phospholipase to mediate conversion of membrane phospholipids to arachidonic acid COX then converts this to PGs
56
What is the role of the COX-1 enzyme?
Constitutive Present in many tissues Functions to maintain physiological levels of PGs
57
What is the role of the COX-2 enzyme?
Induced during inflammation Synthesised in response to inflammatory stimulus Rapidly produced by macrophages, endothelial cells, synoviocytes, chondrocytes In CNS (hypothalamus), microvascular endothelial cells are the most important in producing COX-2
58
What is the role of the COX-3 enzyme?
Constitutive Splice variant of COX-1 Present in the spinal cord and brain
59
Describe the action of antipyretics.
Prostaglandin production reduced, thermostat returned to normal Aspirin and ibuprofen inhibit COX-1 and COX-2 Paracetamol inhibits COX-3 and (weakly) COX-2 Celebrex is a selective COX-2 inhibitor Action of aspirin is irreversible Ibuprofen is a reversible, competitive inhibitor Paracetamol is reversible and non-competitive
60
Describes the mechanisms of analgesia of paracetamol.
Paracetamol inhibits COX-3 and (weakly) COX-2 AM404 is similar in structure to anandamide, acts as a cannabinoid (CB1) receptor agonist producing analgesic effect at level of spinal cord and brain Also activates TRPV1 channels causing analgesia through desensitisation of channels after initial activation Also a free radical scavenger, reactive oxygen free radicals produced by neutrophils and macrophages in response to inflammation
61
What are the physiological and pathophysiological roles of COX-1?
GI protection Platelet aggregation Blood flow regulation Inflammation, chronic pain, increased blood pressure
62
What are the physiological and pathophysiological roles of COX-2?
``` Renal and CNS function Tissue repair and healing Reproduction Uterine contraction Pancreas Blood vessel dilation Inhibition of platelet aggregation Inflammation Fever Blood vessel permeability Chronic pain ```
63
Describe the side effects of aspirin and NSAIDs.
Increased HCl in GIT Bronchoconstriction, promotion of AA to leukotriene production Change in platelet behaviour, bleeding risk Hyperventilation, respiratory alkalosis Increased lactic acid and keto-acid production

Pharm Y3S2 (29 decks)

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