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Anaesthesia > Pharmacology of analgesics > Flashcards

Pharmacology of analgesics Flashcards

0
Q

How can pain be modulated?

A

down-regulation causes temporary suppression of pain transmission e.g. adrenaline will block pain to allow the fight or flight response.
Up-regulation enhances pain transmission and ensures protection of injured tissue.

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1
Q

What is the neural mechanism of pain?

A

Unmyelinated slow C fibres and myelinated fast Ad fibres transmit to the nociceptive bodies in the DRG. The pain fibres terminate in the superficial dorsal horn of the spinal chord where they asced via the spinothalamic tract to the thalamus.

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2
Q

What is the Gate control theory?

A

Nociceptive information is modulated in the substantia gelatinosa of the dorsal horn, inhibitory neurones can be stimulated by either descending inhibitory neurones or non-nociceptive afferent input.

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3
Q

Where are the descending inhibitory neurones?

A

In the periaqueductal area of the midbrain which terminate in the substantia gelatinosa. Both of these contain opioid receptors.

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4
Q

What do hyperallgesia, Allodynia and “wind up” mean?

A

Increased amount of pain associated with a non-noxious stimulus.
Pain provoked by a non-noxious stimulus (burn and feather)
increase of synaptic potential with each stimulus (chronic pain)

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5
Q

What are the pharmacodynamics of analgesics?

A

They act at the site of injury, they alter nerve conduction, they modify transmission in the dorsal horn and affect the central component and the emotional aspects of pain.

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6
Q

What are the functions of: Substance P+glutamate, Bradykinnin and 5-HT and histamine?

A

most important mediator of pain
most potent inducer of pain
transporters of pain

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7
Q

What do nociceptors respond to?

A

Chemical, mechanical and thermal stimuli.

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8
Q

What are the six groups of analgesic?

A

Opioids, NSAIDS, Local anaesthetics, NDMA antagonists, Alpha-2 agonists and other analgesics.

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9
Q

What is the structure of morphine?

A

Phenanthrene derivative with 2 planar rings and 2 aliphatic rings.

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10
Q

What are the three series of synthetic derivatives of morphine?

A

Phenylpiperidine series- pethidine and fentanyl
Methadone series- Methadone
Semisynthetic thebaine derivatives- etorphine and buprenorphine

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11
Q

What are the characteristics of morphine metabolism?

A

It undergoes the first pass effect, its half life is 3-6hrs, it is conjugated in the liver and morphine-6-glucuronide is an active analgesic. It is absorbed via mucous membranes. Need to be careful with doses if the spp cannot conjugate in the liver.

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12
Q

What are the characteristics of morphine elimination?

A

Morphine glucuronides are eliminated in the urine. Some of the glucuronides are hydrolysed in the gut but morphine is reabsorbed by enterohepatic circulation.

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13
Q

What are the side effects of morphine?

A

Occur if the animal is not in pain.
Sedation, respiratory depression, negative chronotropy (except pethidine which inc. HR), emesis, dysphoria, histamine release if pethidine is given IV- give it IM.

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14
Q

What are the opioid receptors and what do they do?

A

GPCRs, inhibit andenylate cyclase which decreases levels of cAMP. This promotes opening of K channels and inhibits opening of voltage gated Ca channels.

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15
Q

What do the individual opioid receptors do?

A

The delta receptor is for supraspinal and spinal analgesia.
The kappa receptor is spinal analgesia.
The mu receptor is for supraspinal and spinal analgesia and has the most analgesic effect- e.g. full or partial mu agonist.
(Non selective opioid receptor- dysphoria)

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16
Q

What are the pharmacodynamics of opioids?

A

Reduced neuronal excitability (inc. K= hyperpolarisation)
Reduced neurotransmitter release (inhibited Ca entry)
Principle site of action is the spinal chord. Inhibition of transmission of nociceptive impulses and inhibition of substance P.

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17
Q

What are the pharmacological effects of opioids?

A

Analgesia
Sedation
Cough suppression, suppression of the resp. centre, pupillary constriction (mu and kappa in the occulomotor nucleus), reduced GI motility (HORSES!!) , Histamine release- bronchoconstriction and hypotension.

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18
Q

What are four example of full mu agonists?

A

Morphine, Pethidine, fentanyl and methadone. All schedule two controlled drugs.

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19
Q

What are the characteristics of fentanyl and what is the new form of the drug?

A

Rapid onset, duration 15-20mins, (rescue analgesia). It is now available in a transdermal solution put on like a spot on. This will last for 4 days so it is good for post op, it can only be administered by a vet and can be absorbed through skin.

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20
Q

What are 2 examples of partial mu agonists?

A

Buprenorphine- moderate pain and can be used for partial reversal of a full mu agonist.
Butorphanol- Synthetic, for mild pain, potent anti tussive (relieves coughing) mixed partial agonist for K and d so lasts longer.

21
Q

What is an example of a neuroleptananalgesia drug?

A

Hypnorm= fentanyl+fluanisone

22
Q

What is the definition of a local anaesthetic?

A

An agent that reversibly interferes with the action potential generation and conduction of a noxius impulse. They do not affect resting membrane potential.

23
Q

What is the chemical structure of a local anaesthetic?

A

Lipid soluble hydrophobic aromatic ring and basic hydrophillic amid group, the two groups are linked by either an amide e.g. Lidocaine and bupivicaine or an ester group e.g. procaine and cocaine.

24
Q

What are the differences between amide and ester links?

A

ester links are easily broken by tissue esterases so are less stable in solution. Amide links will last longer in storage and are heat stable. Their metabolism can cause formation of para-aminobenzoates which cause allergic reactions.

25
Q

What is stereoisomerism?

A

When a drug is in two forms that are mirror images of each other, the drug will have to fit exactly into the receptor so the enantomers can be isolated or available in 50:50 solutions.

26
Q

What is an example of a local anaesthetic that exhibits stereoisomerism?

A

Bupivicaine has an asymmetric carbon atom. Levobupivicaine which is the L -ve isomer and dextrobupivicaine D + isomer.
Dextrobupivicaine is more cardiotoxic- there are preparations of just levobupivicaine.

27
Q

How are local anaesthetics absorbed?

A

They can be injected, inhaled, creams and gels.

They are administered around the nerve that requires the block.

28
Q

How do pH and pKa affect absorption?

A

They are weak bases that can be ionised or non-ionised. The pKa is the pH at which the non-ionised and ionised forms are equal. So at tissue pH of 7.4 all local anaesthetics will be ionised. Infected tissue has an even lower pH so this is poor absorption, the closer the pH of the tissue is to the pKa of the drug the better it is absorbed.

29
Q

How can local anaesthetics be administered?

A

local infiltration, splash blocks, specific nerve blocks, IVRA, extradural and topical application.

30
Q

What does EMLA stand for and what is it?

A

Eutectic Mixture of Local Anaesthetic.

it is an oil based cream that is used topically on the skin to facilitate venepuncture, apply 30-60min before.

31
Q

What do local anaesthetics do to the vascular system and what influences their distribution?

A

They cause vasodilation, vasoconstrictors (adrenaline) are added to reduce systemic absorption. Distribution is affected by the degree of PPB. e.g. lidocaine is 65% PPB whereas bupivicaine is 95% PPB so bupivicaine has a longer duration.

32
Q

How do sites of injection vary in systemic absorption?

A

Intercostal, Epidural, Brachial plexus, Subcutaneous.
Highest systemic conc. Lower systemic conc.
Higher concs=cardiotoxicity.

33
Q

How are local anaesthetics metabolised?

A

The ester linkages are broken down by tissue esterases.

Amides are metabolised by hepatic amidases then excreted by kidneys.

34
Q

What are the pharmacodynamics of local anaesthetics?

A

They block transmission of APs by binding to v-gated Na channels-prevent depol. The Na channel is either open, closed or resting. LA penetrates the sheath via open channels, they bind more readily to inactive Na channels so active fibres are more readily blocked.

35
Q

How does the charge of the local anaesthetic affect its interaction with Na channels?

A

An ionic charge is needed to penetrate the Na channel but a non-ionised molecule is needed to penetrate the nerve sheath.
So a block is more effective in an alkaline environment.

36
Q

How do nerve fibres differ in their interaction with Local anaesthetics?

A

They vary in their sensitivity- small fibres are blocked more readily than larger ones, myelinated fibres are blocked better than non-myelinated ones and Ad fibres are blocked before C fibres.

37
Q

What are the adverse effects of local anaesthetics?

A

CNS- tremors, convulsions and respiratory depression.
CV effects- reduced myocardial contractility, vasodilation, bupivicaine is cardiotoxic.
Other- reduces epithelial repair, inadvertent IV admin, tissue irritation, allergic reactions.

38
Q

What is Lidocaine?

A

It is an amide linked local anaesthetic, adrenaline prolongs duration of activity, it can be used as an anti-arrythmic, infusion lowers MAC.

39
Q

What is bupivicaine?

A

It is an amide linked long acting local anaesthetic. It is used for extradural anaesthesia, it causes cardio toxicity so is not suitable for IVRA.

40
Q

What is Mepivicaine?

A

It is an amide-linked local anaesthetic. It is equivalent potency to lidocaine, less vasodilation than lidocaine, less irritant to to tissues, expensive and non penetrative.

41
Q

What is Proxymetacaine?

A

It is an amide linked local anaesthetic that s used for conjunctival sac anaesthesia but is toxic to the corneal epithelium, it has a rapid onset and short duration.

42
Q

What is Procaine?

A

It is an ester linked local anaesthetic, it has a short duration and causes VASOCONSTRICTION, it has para-aminobenzoates= allergic reactions. It is added to penicillin to reduce pain on injection. It is the only local anaesthetic licensed in cattle.

43
Q

What are the characteristics of NMDA receptors?

A

N-methyl-D-aspartate receptors are found in the CNS. They are ligand receptors for excitatory amino acids (EAA)- glutamate and aspartate. Binding of EAA modulates pain transmission and enhances pain perception.

44
Q

What do NMDA antagonists do?

A

They block EAA receptors which reduces CNS activity. At low doses= analgesia and at high doses= anaesthesia.

45
Q

What is Ketamine?

A

It is an NMDA antagonist that is derived from cyclohexane. It is used for chemical restraint and anaesthesia. It gives very good visceral and somatic analgesia and can be given as a bolus or constant rate infusion.

46
Q

What is Tramadol?

A

It is an unlicensed atypical synthetic opioid. It reduces nociceptive transmission by binding at mu receptors, it inhibits re uptake of seratonin and NA= good for chronic pain.

47
Q

What is Gabapentin?

A

It is an unlicensed anti-epileptic drug for humans. It stabilises nerve activity and is used as an analgesic for neuropathic pain (wind up).

48
Q

How is nitrous oxide used as a local anaesthetic?

A

Mixed with air- entonox.

It is an adjunct to gaseous anaesthesia and it good as it promotes anaesthetic sparing. It is linked to foetal problems.

49
Q

What is important about the PPB capacity of local anaesthetics and specific patients?

A

If the patient has low plasma protein there will be more free drug. This can be a problem in pregnant animals as the free drug can cross the placenta and get ion trapped due to the acidic environment of the foetus.

Anaesthesia (5 decks)

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