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PA MS > MSPA: Analgesics, Pain Medication & Local Anesthetics > Flashcards

MSPA: Analgesics, Pain Medication & Local Anesthetics Flashcards

1
Q

Sharp and localised pain from mechanical or thermal stimuli are mediated by which caliber fibers ?

A

Small mildly myelinated A delta fibers.

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2
Q

Dull, slow, diffuse or throbbing pain is mediated by what caliber fibers ?

A

The unmylinated C fibers.

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3
Q

Mechanical non-noxius stimuli are processed by what caliber fibers ?

A

Heavily myelinated A-beta fibers.

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4
Q

What are the four major process involved in pain physiology ?

A

transduction, transmission, perception and modulation.

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5
Q

What is the anatomy of Spinothalmic tract ?

A

*https://youtu.be/-VYvEAudEgA
*https://youtu.be/oas7yemSG5g.

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6
Q

what is the difference between opioid and opiates ?

A

Opiates refer to natural opioids such as heroin, morphine and codeine. Opioids refer to all natural, semisynthetic, and synthetic opioids.

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7
Q

What are the 3 major class of opioid receptors ?

A

*μ – m1, m2, m3
*κ - κ1, κ2, κ3
*δ - δ1, δ2

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8
Q

What is the signaling mechanism of opioid receptors ?

A

These are GPCRs consists of seven transmembrane spanning proteins that are couple to intracellular G proteins. opioid agonists inhibit the conversion of adenylyl cyclase to cAMP leading to reduced activation of PKA system. This results in opening of V-gated K channels which reduces neuronal excitability and inhibition of V-gated Ca2+ channels which inhibits neurotransmitter release.

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9
Q

What are the major effects associated with main types of opioid receptors ?

A
  • Induction of analgesia through supraspinal, spinal and peripheral mdoulation.
  • respiratory depression through Mu and delta receptor activation.
  • Physical dependence tthrough Mu and to some extent Kapaa receptor activity.
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10
Q

What is the mechanism of supraspinal analgesia ?

A

Stage 01: A sub-tract of the Anterior spino-thalamic tract known as spino- mesenciphalic tract stimulates Enkephalin- releasing neurons(ERNs) at the PAG.

Stage 02: The ERNs project to activate serotonergic neurons(SN) at the dorsal Raphe nucleus (DRN).

Stage 03: The SNs projects to the Enkephalin and dynorphin releasing interneurons at the substantia gelatinosa.

Stage 04: The Enkephalin and dynorphin releasing INs activate Mu and Kappa receptors of C and delta fibers carrying pain input from peripheral nociceptors.

Stage 05: The activation of Mu and Kappa receptors inhibit release of substance P at first order synapses in the Dorsal column of the spinal cord. This results in inhibition of the peripheral pain signal transmission through the spino-thalamic and trigeminal-thalamic tracts to the VPL and VPM of the thalamus.

All these steps lead to supraspinal analgesia.

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11
Q

what is the mechanism of spinal analgesia ?

A

Activation of opioid receptors in substantia gelatinosa causes opening of voltage gated K+ in post synaptic neurones leading to hyperpolarization of these neurones. It also inhibits the activation of Ca2+ channels leading to inhibition of pre-synaptic neurotransmitter release.

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12
Q

Mechanism of Peripheral analgesia ?

A

Through local anaesthetic effect and COX pathways inhibitions as in NSAIDs.

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13
Q

What is the action of μ-opioid receptors in pre-synaptic terminals ?

A

In the presynaptic terminal, μ-opioid receptor activation decreases Ca2+ influx in response to an incoming action potential
↓ neurotransmitter release

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14
Q

What is the action of μ-opioid receptors in post-synaptic terminals ?

A

Postsynaptic μ-opioid receptor activation increases K+ conductance and thereby decreases the postsynaptic response to excitatory neurotransmission
↓AP generation

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15
Q

What is Morphine ?

A

It is the gold standard, most valuable opioid for severe pain. It is a m, k and d receptor agonist.

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16
Q

What are the effects of Morphine?

A
  • Analgesic: Marked elevation in pain threshold without loss of consciousness (m and k receptors).
  • Euphoria: pleasant, ‘floating’ sensation with freedom from anxiety(m receptors).
    *dysphoria in some subjects (k receptors)
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17
Q

What are the modes and factors to consider in Morphine administration ?

A

*It can be administered through several routes.
*Usual starting dose 5 -10mg every 4 h – no ceiling dose.
*Sustained release oral preparations to increase duration of action (usually 12 h).
*Management of breakthrough pain (usually 1/6th of standard dose).
* Can be used for Patient-controlled IV analgesia.

18
Q

What is the half life and bioavailability of Morphine ?

A

Bio-avilability approx. 25% and modest 1/2 life of 3 to 4 hours.

19
Q

What are the side effects of Morphine?

A

*Sedation
*Respiratory depression: inhibits brain stem regulatory centre,
*Nausea, vomiting: due toChemoreceptor trigger zone.
*Constipation: increased GIT muscle tone, decreased propulsive movements, reduced sensory stimuli for defecation reflex.
*Miosis: due to μ and κ receptor mediated stimulation of Edinger-Westphal nuclei.
* Hyperalgesia: paradoxical nociceptive sensation suggesting loss of efficacy.
*Depression of cough reflex
*Histamine release

20
Q

What is the effect of Morphine on Biliary tract ?

A

contraction of biliary sphincter muscle, increased pressure in bile duct and gall bladder, colic, caution: gallstones.

21
Q

What is the Neuroendocrine effect of Morphine ?

A

Inhibit hormones in Hypothalamic Pituitary Adrenal (HPA) axis, lower testosterone, menstruation irregularities.

22
Q

What are the limitations in the clinical use of Morphine?

A

*Gradual loss in effectiveness due to desensitisation of opioid receptors.
*Cessation of chronic therapy due to dependency.
* Withdrawal syndrome- Which presents as hypertension, agitation, diarrhoea, pupil dilation.

23
Q

What is Fentanyl ?

A

It is an extremely potent Highly lipid soluble synthetic opioid. administered either Parental or transdermal routes due to poor oral absorption. It has a rapid onset and offset of effects. It can cause Respiratory depression.

24
Q

What is sufentanil ?

A

It is a fentanyl variant ~ 1000 times more potent than morphine.

25
Q

What is Methadone?

A

It is a Mu receptor agonist and an NMDA receptor antagonist which has Similar potency to morphine. It has >24hr 1/2 life and is administered orally. It is used for the Treatment of opioid addiction, cough suppression, palliative care.

26
Q

What is codeine?

A

It is a Weak opioid agonists with higher affinity for Kappa than Mu receptors. It is a pro-drug with ~ 10% converted to Morphine. It is used as mild analgesic, anti-Tussive and anti- diarrhoeal

27
Q

What is the effect of Genetic polymorphism in the CYP2D6 gene on Codeine metabolism ?

A

This is seen in 10% of Caucasian population and can variably affect the conversion of pro-drug codeine to morphine.

28
Q

What is tramadol ?

A

It is a Weak μ agonist metabolised to O-desmethyltramadol and inhibits uptake of 5-HT and NA. The side effects are respiratory depression, Increased risk of seizures, serotonin syndrome and physical dependence.

29
Q

What is Buprenorphine
?

A

It is an Opioid partial agonists because it has agonistic action on Mu receptors and antagonistic action on kappa and delta receptors. It can display full antagonism when used with a full agonist. It causes less euphoria, less sedation, milder withdrawal symptoms.

30
Q

What are the indications for Buprenorphine
?

A

*It can be given sublingually with naloxone for the Tx of opioid addiction.
* It can be given transdermal/sublingual for moderate pain in non-opioid tolerant individuals.

31
Q

What is Naloxone ?

A

It has more affinity to μ than k receptor and is a competitive antagonists with a very rapid onset of action. It is used to rapidly reverse opioid overdose.

32
Q

What is the indication for Naloxone ?

A
  • It can be given to reverse opioid actions e.g. alleviate respiratory depression in acute opioid overdose. However, repeated dosing maybe needed as it has a short half life (1-2 hours) compared to morphine.
  • It can be given with Oxicontin to reduce constipation.
33
Q

What is the contraindication for aspirin in > 16 year olds ?

A

Kawasaki disease.

34
Q

What are the pharmacological treatments for neuropathic pain ?

A

TCA – inhibit NA reuptake, independent of AD activity
Gabapentin and pregablin – bind to Ca2+ channel inhibiting neurotransmitter release
Lidocaine – topically or IV, analgesic activity unclear
Other drugs – ketamine, cannabinoids, botulinium

35
Q

What is cocaine ?

A

It is a Weak bases with a pKa of 8-9, partially ionised at physiological pH which makes it capable of penetrating the nerve sheath and axon membrane. The cocaine subtypes with the Ester bonds are rapidly inactivated in plasma and tissues by non specific esterases (shorter half life). whereas, the ones with Amide bonds are more stable with longer half life’s (metabolised in the liver).

36
Q

what are the examples of Cocaines with ester bonds ?

A

Benzocaine, Chloroprocaine, Cocaine, Proparacine, Procaine and Tetracaine.

37
Q

what are the examples of Cocaines with amide bonds ?

A

Articaine, Bupivacaine, Lidocaine, Levobupivacaine, Ropivacine.

38
Q

What is the key to identify whether a cocaine is ester or amide by looking at its name ?

A

The presence of ‘I’ before caine.

39
Q

What is the mechanism of action of Cocaine ?

A

It acts by Blocking the initiation and propagation of APs by preventing voltage dependent increase in Na+ conductance. It has more affinity for small than large fibers and can cause vasodilation, ergo, Addition of vasoconstrictor diminishes local blood flow - slows absorption - prolonged effect.

40
Q

Why is lidocaine used as surface anaesthetic?

A

Because it is a lipid soluble amide bond cocaine and can be absorbed from the mucous membrane and subcutaneous fat. It has a short half life of 1-2 hrs.

41
Q

What are the side effects of cocaine derivative local anasthetics?

A

Accidental administration into the blood vessels can cause: *Agitation, confusion, tremor progressing to convulsions and respiratory depression.
* myocardial depression, conduction block and vasodilation.
* allergic dermatitis and acute anaphylactic reactions (rare), mainly ester bond.

PA MS (44 decks)

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