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Pharmacology > General and Local Anaesthesia > Flashcards

General and Local Anaesthesia Flashcards

1
Q

What is the general structure of a local aesthetic?

A

aromatic ring (allows it to be lipid soluble and cross the membrane)
linker group (amide or ester)
amine group (acts as a base can accept H+)

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2
Q

what is linkage is metabolised quicker ester or amide?
give an example of a local anaesthetic which has each of these

A

ester metabolised faster than amide (e.g. procaine and cocaine have short duration)
lidocaine has an amide linkage (medium duration)

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3
Q

how do local anaesthetics enter the cell?

A

diffuse in their uncharged form

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4
Q

how do local anaesthetics act inside the cell?

A

can become ionised, blocking sodium channels of the neuron
prevents action potentials from firing
use dependant (only block the channel when its open)

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5
Q

How does inflammation reduce the efficacy of local anaesthetics?

A

inflammation, decrease PH, increases the ionisation state of drug in extracellular space, means it cant cross the membrane as much and act on the channels

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6
Q

how are local anaesthetics differentially sensitive?

A

target those with smaller axons particularly those that detect nociception
they have much less affinity for motor neurons

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7
Q

how is topical local anaesthetics applied?

A
  • Washing over surface e.g. throat lozenge, rubbing cream on gums
  • Not very effective due to skin thickness
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8
Q

how is infiltration
local anaesthetics applied?

A
  • More effective - anesthetic injected into tissues e.g. site of injury / surgical wound
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9
Q

how is nerve block
local anaesthetics applied?

A
  • Injected near a nerve that supplies a specific region of the body
  • Has a wide spread effect due to the thousands of axons on nerves
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10
Q

how is epidural
local anaesthetics applied?

A
  • Injected into the epidural space just outside the spinal cord
  • Large wide ranging effect from there
    Commonly used in childbirth
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11
Q

how is spinal cord
local anaesthetics applied?

A
  • Inject into the cerebral spinal fluid
    Large widespread numbing due to all the nerves that pass through that region
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12
Q

what are the non specific side effects of local anaesthetics?

A

hypersensitivity, allergic reactions, can be due to solvent drug is dissolved in

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13
Q

what are the specific side effects of local anaesthetics?

A

binding in wrong places, and tissues
can lead to tremors, excessive vasodilation, hence a drop in blood pressure

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14
Q

what type of drug is commonly applied with
local anaesthetics ?

A

vasoconstrictors e.g. adrenaline applied in conjunction with lidocaine

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15
Q

what is the definition of a local anaesthetic?

A

reversibly block nerve conduction when applied to a restricted area of the body without the loss of consciousness

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16
Q

what factors make a good local anaesthetic?

A
  • They are reversible
    • Specifically block nociception neurons
    • Effective for time of procedure (estimate from linkage)
      Low toxicity
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17
Q

what are the 3 mains aims of a General anaesthetic (GA)?

A

analgesic
muscle relaxation
loss of consciousness

18
Q

what is the lipid theory of how GA work?

A

due to their lipid solubility, they integrate themselves into the cell membrane
this increases fluidity, expansion and interferes with action potentials

19
Q

what is the required conc of GA and membrane expansion for them to work?

A

0.05mM for any agent and the volume of lipid need to be expanded by 0.4%

20
Q

what is the structure of GA?

A

small unreactive molecules that have no chemical class

21
Q

what is the protein theory?

A

membrane needs to be more fluid for the drugs to interact with proteins such as ion channels, allows them to get through

22
Q

what evidence supports the protein theory?

A

longer chains = more potent as they make the membrane more fluid for drugs to get through
however there is a cut off phenomenon where at a certain length increasing the chain further actually stops the anaesthetic working this suggest that size and therefore protein binding may be important
Also protein binding has been seen to mimic the same effects that lipid solubility has

23
Q

what is evidence for the lipid theory?

A
  • Experiments with tadpoles revealed that the conc of anaesthesia needed to stop them moving was inversely proportional to its lipid : water coefficient
24
Q

Give examples of channels GA act on

A

GABA receptors, they increase the inhibition produced by these, they also interfere with
K+ channels causing hyperpolarisation
It also inhibits excitatory ligand gate ion channels e.g. NDMA receptors, Ach nicotinic receptor and 5-HT3
It also acts on inhibitory ligand- gated channel such as glycine

25
Q

list the 4 stages of anaesthesia

A
  • Analgesia- drowsiness reflexes intact, still conscious
    • Delirium / induction phase - excitement, incoherent speech, loss of consciousness, unresponsive to non-painful stimuli
      dangerous side effects such as muscle rigidity, spasmodic movements as well as cardiac arrythmias vomiting and choking
      surgical anaesthesia- unresponsive to painful stimuli, breath regularly, abolition of reflexes, muscle relaxation, synchronised EEG
      medullary paralysis- respiration and circulation cease, EEG wanes, death occurs
26
Q

how is the potency of inhalation anaesthetics measured?

A

Minimum alveoli conc required (MAC)
% of inspired air v/v
To produce immobility in 50% of patients

27
Q

how is MAC and lipid solubility related?

A

lipid solubility inversely proportional to MAC

28
Q

what patient variables affect potency of GA?

A

sex, height and weight are all variables that affect the drugs potency

29
Q

what 2 main factors effect the induction rate of GA?

A

drug properties
physiological factors

30
Q

why are faster acting GA safer?

A

bypass dangerous induction phase faster
more control over depth of anaesthesia

31
Q

what is the blood : gas partition coefficient?

A

proportion of drug dissolved in blood compared to proportion in gas form

32
Q

what does a high blood: gas coefficient mean for induction?

A

makes it slower

33
Q

Why is the tissue : blood partition coefficient much higher than 1 for GA in adipose tissue?
why is this important

A

lipid soluble drugs greatly favour, lipid enviroment
hence those with more adipose tissue need higher doses of anaesthesia due to distrutbion of it

34
Q

how is the tissue : blood partition coefficient of adipose tissues counteracted naturally by the body

A

poor vascularity

35
Q

what is the tissue : blood partition coefficient of the brain for GA?

A

1

36
Q

how are most anaesthetics eliminated?

A

by exhalation, metabolism has a minimal effect

37
Q

what GA is metabolised by the liver?

A

methoxyflurane which comes with a risk of liver toxicity

38
Q

when are IV GA used?

A

fast acting over a short period, can be used to intially induce induction at the start of surgery to overcome the dangerous phase

39
Q

What is the mechanism of IV GA?

A
  • They work by increasing the potentiation (increasing effect when NT’s bind) of the GABA a receptor e.g.
    THIOPENTAL (barbiturate)
    inhibit excitatory receptors e.g. antagonists on the NDMA receptor - ketamine is an example, it is a dissociative anaesthetic that lasts 10-20 mins , it causes sensory loss, dissociation and paralysis’s surgical anaesthesia but no loss of consciousness
40
Q

what medications are given before GA?

A

Benzodiazepines - (sedation, anxiolysis, amnesia) e.g. lorazepam
reduce anxiety

41
Q

what other drugs are given in conjunction with GA?

A
  • Opioids e.g. morphine and fentanyl for pain relief
    • Antimuscarinics (to facilitate intubation and ventilation) e.g. Atropine relaxes smooth muscle in throat = put tube down it
    • Muscle relaxants may be applied e.g. neuromuscular blockers such as gallamine, this allows the relaxation of deep abdominal tracheal muscles without the need for very high conc of anaesthesia
    • May also give anti-emetic drugs to prevent nausea e.g. metoclopramide

Pharmacology (7 decks)

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