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L2 pharmacology > General anaesthetics > Flashcards

General anaesthetics Flashcards

1
Q

What substances were used as early general anaesthetics? (3)

A
  • Nitrous oxide
  • Ether
  • Chloroform
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2
Q

What are the 2 main categories of general anaesthetics?

A
  • Chemical
  • Physical
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3
Q

What are the 2 forms of chemical general anaesthetics?

A
  • Inhalational
  • Intravenous
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4
Q

Why are volatile liquid general anaesthetics no longer used? (3)

A
  • Ether and chloroform
  • Highly flammable/explosive
  • Hard to control dose
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5
Q

What are physical general anaesthetics? (2)

A
  • Low atmospheric pressure
  • Hypothermia
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6
Q

What kind of general anaesthetic is nitrous oxide?

A

Inhalational (chemical)

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7
Q

What are examples of intravenous general anaesthetics? (2)

A
  • Barbiturates e.g. thiopental
  • Steroids e.g. alphaxalone
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8
Q

What is the lipid theory of general anaesthetics? (3)

A
  • Direct correlation between lipid solubility of drug and its effectiveness as anaesthesia
  • Theory that drugs insert into lipids of plasma membrane and increase its fluidity
  • More lipid soluble = less of the drug needed to cause unresponsiveness
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9
Q

What is the Meyer-Overton rule? (2)

A
  • The anaesthetic effect of a drug is proportional to the molar concentration of the drug in the lipid membranes
  • Anaesthesia results from membrane disruption
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10
Q

What are the issues with the lipid theory? (3)

A
  • Doesn’t explain the anaesthetic effect of temperature (lipids lose fluidity when cold)
  • Doesn’t explain saturation effect (indicates limited number of receptors)
  • Doesn’t explain evidence that anaesthetics alter GABAa receptor affinity for agonists
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11
Q

Which proteins are targets for general anaesthetics? (3)

A
  • GABAa receptors
  • Two Pore Domain K+ channels
  • NMDA receptors
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12
Q

How are GABAa receptors involved in anaesthesia?

A

Increase inhibitory neurotransmission in the CNS

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13
Q

How do volatile general anaesthetics interact with GABAa receptors?

A

Bind to the interface between the alpha and beta subunits of GABAa

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14
Q

How do intravenous general anaesthetics interact with GABAa receptors?

A

Bind to the beta subunit of GABAa

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15
Q

How do volatile general anaesthetics interact with Two Pore Domain K+ channels? (3)

A
  • Activate the channels
  • Membrane potential is more hyperpolarised (more negative)
  • Harder for neurons to fire action potentials
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16
Q

What are NMDA receptors?

A

Ionotropic glutamate receptors

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17
Q

Which protein does ketamine and nitrous oxide act on?

A

Blocks NMDA receptors

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18
Q

Which general anaesthetics target GABAa receptors? (2)

A
  • Volatile
  • Intravenous
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19
Q

Which general anaesthetics activate Two Pore Domain K+ channels?

A

Volatile

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20
Q

Which general anaesthetics block NMDA receptors? (2)

A
  • Nitrous oxide
  • Ketamine
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21
Q

Where are protein binding sites for general anaesthetics located?

A

Plasma membrane

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22
Q

What do general anaesthetics regulate? (2)

A
  • Ion channels
  • Synaptic transmission
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23
Q

How do general anaesthetics interfere with synaptic transmission? (2)

A
  • Inhibit action potentials in neurons
  • Interfere with exocytosis of neurotransmitter vesicles
24
Q

What does inhibition of the reticular formation cause?

A

Unconsciousness

25
Q

What does inhibition of the hippocampus cause?

A

Short term amnesia

26
Q

What does inhibition of the thalamic sensory relay nuclei of the cortex cause?

A

Analgesia

27
Q

What are the 4 stages of anaesthesia?

A

Stage 1 - Analgesia
Stage 2 - Excitement
Stage 3 - Surgical anaesthesia
Stage 4 - Medullary paralysis

28
Q

What stage of anaesthesia does nitrous oxide achieve?

A

Stage 1 - analgesia

29
Q

What happens during the excitement stage of anaesthesia?

A

Exaggerated reflexes (kick/gag)

30
Q

What happens during the surgical stage of anaesthesia? (4)

A
  • Unconscious
  • Unresponsive to painful stimuli
  • Loss of reflexes
  • Short term amnesia
31
Q

What happens during the medullary paralysis stage of anaesthesia? (2)

A
  • Loss of cardiovascular reflexes and respiratory paralysis
  • Death
32
Q

Which stages of anaesthesia need to be avoided?

A

Stages 2 and 4

33
Q

What drugs are examples of intravenous anaesthetics? (3)

A
  • Propofol
  • Thiopental (barbiturate)
  • Etomidate
34
Q

What are the advantages of propofol? (2)

A
  • Highly lipid soluble so rapid induction
  • Fast recovery time due to rapid metabolism
35
Q

What are the disadvantages of thiopental? (4)

A
  • Painful at site of injection
  • Complex pharmacokinetics
  • Hangover due to accumulation in body fat
  • Not much of an increase required to move from stage 3 to stage 4 = dangerous so not widely used anymore
36
Q

Which type of general anaesthetic is best for induction of anaesthesia?

A

Intravenous

37
Q

Why are intravenous anaesthetics ideal for induction of anaesthesia? (2)

A
  • Easy to administer
  • Rapid induction because enter the brain easily
38
Q

Which intravenous anaesthetic doesn’t cause cardiovascular depression?

A

Etomidate

39
Q

What are the disadvantages of intravenous anaesthetics? (2)

A
  • Respiratory depression
  • Cardiovascular depression
40
Q

What kind of anaesthetic is ketamine?

A

Dissociative anaesthetic

41
Q

What useful anaesthetic effects does ketamine cause? (3)

A
  • Sensory loss
  • Powerful analgesia
  • Amnesia
42
Q

Why is ketamine unsuitable as an anaesthetic for long surgeries?

A

No complete loss of consciousness

43
Q

What is an advantage of ketamine?

A

No respiratory depression

44
Q

What are the side effects of ketamine? (3)

A
  • Hallucinations
  • Involuntary movements
  • Increased intracranial pressure
45
Q

When is ketamine used as an anaesthetic? (2)

A
  • Paediatrics
  • Veterinary
46
Q

Which type of general anaesthetic is best for maintenance of anaesthesia?

A

Inhalational

47
Q

What drugs are examples of inhalational anaesthetics? (4)

A
  • Nitrous oxide
  • Isoflurane
  • Desflurane
  • Sevoflurane
48
Q

Why are inhalational anaesthetics ideal for maintenance of anaesthesia? (2)

A
  • Very easy to control their concentrations in the CNS by controlling conc of inhaled air and ventilation rate
  • Concentration is not altered by metabolism unlike intravenous
49
Q

What does the stage of anaesthesia depend on?

A

Concentration of the general anaesthetic in the brain

50
Q

When is the use of inhalational anaesthetics problematic?

A

When patients have diseased/damaged lungs

51
Q

Why do inhalational anaesthetics need to be lipid soluble?

A

Can easily cross alveolar membrane

52
Q

How does blood and lipid solubility of inhalational anaesthetics affect speed of induction and recovery? (3)

A
  • Inhalational anaesthetics have low solubility in blood but high solubility in lipid
  • Alveolar concentration equilibrates quickly with the blood, readily delivered to tissues due to high lipid solubility
  • Can accumulate in fat but usually doesn’t because of poor perfusion
53
Q

How is the concentration of inhalational anaesthetics in the CNS controlled? (2)

A
  • To increase = increase conc. in inspired air and increase ventilation rate
  • To decrease = decrease conc. in inspired air and increase ventilation rate
54
Q

What problem can halogenated general anaesthetics cause?

A
  • Can trigger malignant hyperthermia
  • Rise in body temp, increase in heart rate, increased muscle contractions, hypertension
  • Halogenated GAs activate ryanodine receptors causing increased Ca2+ in skeletal muscle, rapid production of heat
55
Q

What is malignant hyperthermia?

A

Inherited mutation in ryanodine receptors on sarcoplasmic reticulum of skeletal muscle

56
Q

What drug is used to treat malignant hyperthermia? (2)

A
  • Intravenous dantrolene
  • Ryanodine receptor inhibitor
57
Q

Why aren’t intravenous anaesthetics used for maintenance of anaesthesia?

A

Reversal relies on the patient’s metabolism which is more difficult to control than ventilation rate

L2 pharmacology (9 decks)

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