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Pharamacology, theraputics and prescribing > Anaethetics & analgesics > Flashcards

Anaethetics & analgesics Flashcards

1
Q

Name 3 volatile/ inhaled general anaesthetics

A

Nitrous oxide, isoflurane, sevoflurane, Xe, chloroform, halothane, diethyl- ether, fluroxene

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2
Q

Name 2 IV general anaesthetics

A

Propofol, Barbiturates, ketamine

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3
Q

Name 3 local anaesthetics

A

Lidocaine, procaine, buprivacaine, roprivacaine

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4
Q

What class of drug is fentanyl?

A

An opiate

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5
Q

What do pancuronium and suxamethonium chloride do?

A

they both block neuromuscular junctions to cause paralysis

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6
Q

Describe the process of putting someone under a general anaesthetic for surgery

A

Premedication to make them drowsy (midazolam)-> induction with anaesthetic (IV or inhaled-> muscle paralysis for intubation (pancuronium)-> intraoperative opiate (morphine)-> reversal or paralysis-> provision for post operative nausea and vomiting + opiate for pain

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7
Q

Describe the gruedels signs/ stages of anaesthetic

A

1- normal
2- breathing erratic, eye movements increase, muscle tone increases
3- eye movements slow down to a stop, muscles start to relax and breathing become more regular and shallow
4- pt is completely flacid, no eye movements, breathing is very shallow and erratic so require incubation
This process can take mins for volatile agents or seconds for IV

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8
Q

What is the minimum alveolar concentration?

A

The alveolar concentration at which 50% of the pts fail to move due to surgical stimulus

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9
Q

Give 4 factors affecting minimum alveolar concentration and state how they affect it

A
  • Age (high in infants and lower in elderly)
  • hyperthermia (increased) and hypothermia (decreased)
  • pregnancy (increased)
  • alcoholism (increased)
  • central stimulants (increased)
  • other anaesthetics and sedatives (decreased)
  • opioids (decreased)
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10
Q

What effect does nitrous oxide have on MAC and what is the significance of this?

A

It decreases MAC so you can give lower doses of anaesthetics and so reduce ADRs and side effects

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11
Q

What is the effect on induction of a drug with a low blood: gas partition?

A

this means it dissolved into blood more easily so the pt will be induced faster

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12
Q

What is the effect on induction of a drug with a lower oil: gas partition?

A

lower value= better dissolution into fat= larger Vd= longer induction and recover + longer half life + lower potency

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13
Q

How do anaesthetics such as sevoflurane work?

A

Bind to GABAa receptors, increase Cl- conductance and so inhibiting the reticular formation and cortical activity. The hippocampus is the first to be inhibited, leading to the amnesia. The dorsal and ventral horns of the spinal cord are also inhibited/ affected leading to analgesia and paralysis.

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14
Q

How do NO2, Xe and ketamine work as anaesthetics?

A

They inhibit NMDA receptors, reducing glutamate levels, so inhibiting reticular formation, cortex, hippocampus, dorsal and ventral horns etc.

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15
Q

What molecular feature of local anaesthetics influences length of action?

A

Ester link= short acting

Amide link= longer acting

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16
Q

What effect does increasing lipid solubility have on potency of local anaesthetics?

A

more lipid soluble= higher potency

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17
Q

How are regional anaesthetics done?

A

Use a local anaesthetic or opioid but inject it into a large nerve/ nerves eg femoral, sciatic, epidural space, etc

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18
Q

Give 3 side effects of general anaesthetic?

A
  • N+ V
  • Hypotension
  • cognitive dysfunction (esp in old)
  • chest infections (more due to intubation)
  • myalgia, sore throat, headaches
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19
Q

Give 2 ADRs of local anaesthetic

A
  • can be cardiotoxic if spread is systemic and high enough conc reaches heart
  • anaphylaxis
  • swelling
  • confusion, headaches, dizziness
  • GI upset
20
Q

Name 3 NSAIDs

A

Ibuprofen, naproxen, diclofenac, celecoxib

21
Q

What are the 3 main theraputic effects of NSAIDs

A
  • anti inflammatoy
  • analgesia
  • antipyretic
22
Q

Describe the process of prostaglandin synthesis

A
  • cell membrane phospholipids cleaved to arachidonic acid by phospholipase A2
  • COX1/2 convert arachidonic acid to prostaglandin G
  • G–> H by COX1/2
  • prostaglandin H converted to E, which is most important mediator of inflammation
23
Q

Describe the difference between COX 1 and COX2

A 
COX1= constiutively expressed in range of tissues- gastric mucosa, myocardium, renal parenchyma, this is to ensure good local blood flow, smaller active site, so only smaller drugs like aspirin can inhibit it 
COX2= expression induced by mediators such as bradykinin
24
Q

Describe the effect of prostaglandin E stimulating the EP1 GPCR (q)?

A

Increased pain sensation by increased neuronal sensitivity to bradykinin, inhibiting K+ channels and increasing sensitivity of Na+ channels of the C fibres (carry pain sensation). Also increases intracellular Ca2+ for faster synaptic transmission.

25
Q

Describe the effect of prostaglandin E stimulating the EP2 GPCR (s)?

A
  • Vasodilation
  • also on secondary sensory neurones in dorsal horn–> increased sensitivity and discharge rate by inhibiting glycinergic inhibition (decrease glycine receptor binding affinity)
26
Q

Describe the effect of prostaglandin E stimulating the EP3 GPCR (i)?

A

Involved in pyrexia- Il-1 from macrophages causes COX2 production in hypothalamus, PG3 produced acts on EP3 to raise core body temp, mechanism is complex and dw too much about

27
Q

What is allodynia?

A

the idea that neurones become sensitised so stimuli which wouldnt normally stimulate pain, do. Can also get spontaneous pain associated- IE no stimuli but still feels painful

28
Q

What is hyperalgesia?

A

Painful stimuli become more painful than normal

29
Q

What is the half life of typical NSAID?

A

<6hrs

30
Q

Describe the binding of NSAIDs to proteins?

A

90-99% bound to plasma proteins- therefor interacts w/ other protein bound drugs

31
Q

Give 3 GI ADRs of NSAIDs

A
  • stomach pain
  • Nausea
  • heart burn
  • Gastric bleeding
  • gastric ulceration
32
Q

Which pts taking NSAIDS are more likely to experience ADRs?

A

elderly, heart failure, renal failure, liver failure, those taking other drugs

33
Q

How can GI ADRs of NSAIDs be offset?

A

by giving a PPI or misoprostol (steroid) as well.

34
Q

Give 3 non GI ADRs of NSAIDs?

A
  • Renal blood flow compromise–> drop in GFR–> H20 retention
  • increased bleeding time (bruise and haemorrhage)
  • skin rash
  • stevens johnson syndrome (severe rash)
  • induce bronchial asthma in asthmatics
  • reyes syndrome (rare by serious brain/ liver injury seen in paediatrics w/ viral infections + aspirin)
35
Q

Since most ADRs of NSAIDs come about by inhibition of COX1, why are COX2 selective inhibitors not used?

A

They showed significant cardiovascular ADRs with long term use

36
Q

Why are NSAIDs and opiates often used together?

A

Gives good pain relief while reducing opiate dose, and so reduce opiate side effects

37
Q

Give 3 important highly protein bound drugs which interact with NSAIDs?

A

methotrexate, penicillins, sulphonylureas, warfarin

38
Q

How does aspirin work?

A

Hydrolysed in plasma to salicylate, which is active and has half life of 4 hrs. This inhibits COX enzymes irreversibly by acetylation. This reduced prostaglandin release (NSAID) and thomboxane A2 production (anti- platelet)

39
Q

How does paracetamol work?

A
  • some COX activity
  • Not really known
  • thought to be involved with TRP channels in the CNS
40
Q

Give 2 weak and 2 strong opiates?

A

weak: codine, tramadol, low dose morphine
strong: fentanyl, morphine, buprenorphine

41
Q

Name the 3 endogenous opiates

A

endorphines, enkephalins, dynorphins

42
Q

Name the 3 opiate receptors and what response theycause

A

Mu (u) receptors= euphoria// delta receptors= dysphoria// Kappa receptors= sedation

43
Q

Describe the mechanism of action of opiates

A

Bind to Gi opiate receptors at synapses, this inhibits AC so decreases cAMP, so less influx of Ca2+ so less neurotransmitter release and so reduced transmission of nociceptive impulses. They also act on the efferent neurone at the synapse to cause increased K+ release

44
Q

Give 3 ADRs of opiates

A
  • constipation
  • reduced consciousness
  • N+ V
  • confusion
  • constricted pupils
  • dependancy
  • respiratory depression
  • tolerance
45
Q

Give one drug which can reverse the effects of opiates

A

Naloxone

46
Q

How should opiates be prescribed?

A

Need to write numbers (2) out as words (two)

47
Q

How should regular morphine doses be decided after PRN use?

A

Total dose PRN in last 24hrs, split into two doses.

Eg if 6x 5mg in last 24 hrs, prescribe 2x 15mg

Pharamacology, theraputics and prescribing (15 decks)

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