non-opioids and adjuvants Flashcards

1
Q

where do non-steroidal anti-inflammatory drugs (NSAIDs) work

A

on blocking the COX2 sites to stop the production of prostaglandins which decreased activation threshold

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2
Q

what do COX1 help to produces/ cause

A
  • homeostasis
  • prostaglandins
  • prostacyclin
  • thromboxane A2
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3
Q

what does COX2 help to produce/ cause

A

inflammatory prostaglandins

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4
Q

what does 5-lipoxygenase help to produce/ cause

A

inflammatory leukotrienes

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5
Q

what is involved in the inflammatory pathway after arachidonic acid

A
  • COX1
  • COX2
  • 5-LOX
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6
Q

what are examples of NSAIDS

A
  • aspirin
  • ibuprofen
  • diclofenac
  • naproxen
  • piroxicam
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7
Q

what adverse affects can NSAIDS cause

A
  • GI disturbance
  • Skin reactions
  • bronchospasm
  • reversible renal insufficiency
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8
Q

what are the adverse affects of paracetamol

A
  • liver failure
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9
Q

what are examples of anti-depressents

A
  • tricyclic antidepressants eg amitriptyline
  • serotonin-norepinephrine reuptake inhibitors eg duloxetine
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10
Q

what is the mechanism of action of antidrepessents

A
  1. inhibit 5-HT reuptake
  2. enhances descending inhibition of neuropathic pain
  3. increase on 5-HT and dopamine reinforce the inhibitory effect of NA in an auxiliary manner
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11
Q

what are adverse effects of antidepressents

A
  • mouth dryness
  • constipation
  • weight gain
  • nausea
  • dizziness and drowsiness
  • erectile dysfunction
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12
Q

what are the 2 different types of anticonvulsants

A
  1. voltage gated Na+ channel blockers
  2. voltage gated Ca2+ channel modulators
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13
Q

how do voltage gated Na2+ channel blocker AEDs work

A
  • blocks the voltage gated Na+ channels
  • stops depolarisation
  • action potential cannot be created
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14
Q

how do voltage gated Ca2+ channel modulator AEDs work

A
  • blocked the alpha1delta subunit of voltage gated Ca2+ channel
  • reduces Ca influx
  • synaptic vesicles can’t be released
  • reduces release of nociceptive neurotransmitters
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15
Q

what are the adverse effects of anticonvulsants (AEDs)

A
  • drowsiness
  • hyponatremia
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16
Q

what is the mechanism of action of ketamine

A
  • blocks NMDA receptors
  • reduces wind-up in dorsal horn
17
Q

what are the effects of ketamine

A
  • dissociative anaesthesia
  • increased ICP
18
Q

how does ketamine create an effect

A
  • stimulate central sympathetic outflow
  • stimulates the heart with increased BP and CO
19
Q

what are the adverse effects of ketamine

A
  • hallucinations
  • delirium
  • uncontrolled movements
20
Q

what are the contraindications of ketamine

A
  • head trauma
  • increased ICP
21
Q

what does magnesium sulfate do

A
  • bronchodilation
  • anti-seizure
  • membrane stabilising activity
  • reduces pain postopritavely
22
Q

how does magnesium sulfate work

A
  • antagonises calcium release
  • inhibits catecholamine release
  • antagonises NMDA receptors
  • anti-inflammatory - reducing IL6 & TNFa why contribute to its analgesia
23
Q

what does lidocaine do

A
  • local anaesthetic
  • sodium channel blocking
  • regional anaesthesia
  • intra and post op analgesia
24
Q

what is nefopam used for

25
how does nefopam work
- serotonin, norepinephrine, dopamine reuptake inhibitor - sodium and calcium channels inhibiting glutamatergic transmission
26
how does nitrous oxide work
- inhibits ligand gated ion channels - NMDA receptor antagonism - potentiation of GABA receptor activation
27
how does nitrous oxide produce analgesia
- release of endogenous opioid peptides - target PAG
28
what are the adverse effects of nitrous oxide
- diffusion hypoxia - postop nausea and vomiting - anaemia and neuropathy - recreational use
29
what are the contraindications of nitrous oxide
- decompression sickness - head injuries - impaired consciousness - suspected bowel obstruction - recent middle ear surgery - pneumothroax
30
what is methoxyflurane used for
analgesia acting on brain and spinal cord
31
what does methoxyflurane work on
- GABA receptors - potssium channels - glutamate receptors - glycine receptors - reducing in synapses and condition in neurones
32
how is methoxyflurane administered
inhalation giving 30mins analgesia
33
what are contraindications to methoxyflurance
- malignant hyperthermia - allergies to anaesthetic vapours - impaired consciousness - significant head injury - cardiovascular instability - renal impairment - ventilatory compromise
34
what is the 1st mechanism of action of NSAIDS
- acts as a OGG2 substrate and heme reducing agent - inhibits POX, converting its heme group to an inactive state
35
how does POX become active or inactive
- POX (Fe (IV), active -> POX (Fe(III), inactive) - POX (inactive) -> hydroperoxides -> POX (active) - hydroperoxides shifts to the right making inactive active
36
what is the 2nd mechanism of action of NSAIDs
- conjugated in the brain with arachidonoyl - inhibiting uptake of anandamide - now more present in synaptic celts - acts as an agonist by TRPV1 - inhibits COX2 - causes analgesia and euphoria
37
what is the 3rd mechanism of action of NSAIDs
activates the descending serotonergic pathways