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TV3001 > Pharmacology - CNS > Flashcards

Pharmacology - CNS Flashcards

1
Q

Define general anaesthesia in clinical applications

A

Loss of consciousness, analgesia, muscle relaxations, amnesia

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2
Q

Name 3 commonly used inhalation anaesthetics

A

Isoflurane, Sevoflurane, Nitrous oxide

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3
Q

What is the general mechanism of action of inhalation anaesthetics?

A

Inhibit glutamate receptors and increase GABA activity

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4
Q

List 5 factors that influence the potency and rate of induction and recovery from inhalation anaesthetics

A
  1. Conc of anaesthetic in inspired air
  2. Alveolar ventilation and resp rate
  3. Solubility of anaesthetic in blood
  4. Cardiac output and lung perfusion
  5. Lipophilicity of anaesthetic
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5
Q

True or false: a higher MAC = lower potency

A

True

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6
Q

List some things that will DECREASE the MAC

A
  • Hypothermia
  • Hyponatraemia
  • Pregnancy
  • CNS depressants
  • Anaemia and hypotension
  • Hypoxia
  • Respiratory acidosis
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7
Q

List some things that will INCREASE the MAC

A
  • Hyperthermia
  • Hypernatraemia
  • CNS stimulants
  • Decreased brain perfusion
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8
Q

Is Isoflurane and analgesic?

A

NO!!!

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9
Q

List some of the unique features of Nitrous oxide as an inhalation anaesthetic

A
  • low potency and high MAC
  • BUT has ANALGESIC properties –> via NMDA receptors
  • minimal direct adverse effects on cardiovasc and resp system
  • prolonged use inhibits methionine synthatase –> folate deficiency and bone marrow defects
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10
Q

List 5 types of injectable anaesthetics with examples

A
  1. Barbituates e.g thiopental, phenobarbital
  2. Propofol
  3. Alphaxalone
  4. Benzodiazepines e.g midazolam, diazepam
  5. Dissociative anaesthetics e.g ketamine, tiletamine
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11
Q

Describe the mechanism of action of injectable anaesthetics (aside from dissociative)

A

Enhance the efficacy of GABA at different sites of GABAa receptors

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12
Q

Describe the mechanism of action of dissociative anaesthetics

A

Glutamate antagonist, binds non-competitively to NMDA receptor to inhibit excitatory effects of glutamate = ANALGESIC

Weak action on GABA receptors

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13
Q

Describe the distribution-redistribution phenomenon of injectable anaesthetics

A
  • Once administration is stopped, rapid dist of drug into vessel rich organs, slowly in poorly vasc tissue
  • Anaesthetic then redistributes out of brain to re-est. equilibrium with plasma conc –> decreasing CNS effects
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14
Q

Why do you need to use ketamine with a muscle relaxant?

A

Dissociative anaesthetics maintain skeletal muscle tone incl. protective reflexes such as coughing and swallowing

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15
Q

Define the following:
Tranquiliser
Sedative
Neuroleptanalgesia

A

Tranquiliser: relieve anxiety w/o undue drowsiness

Sedative: cause sedation or drowsiness

Neuroleptanalgesia: combo of tranquiliser/sedative with an opioid to achieve pain relief

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16
Q

Give examples of tranquilisers and sedatives

A

Tranquiliser
- Phenothiazines e.g Acepromazine
- Benzodiazepines e.g Diazepam, Midozalam

Sedatives
- Alpha-adrenergic agonists e.g Xylazine

17
Q

Describe the mechanism of action of Phenothiazines such as Acepromazine

A
  • Blocks excitatory dopamine (DA2-receptors): alter motor control, suppress CNS, inhibit stim of CRTZ
  • alpha adrenergic blocking effects: decreases BP
18
Q

What are some of the main concerns when using Phenothiazines such as Acepromazine?

A
  • Hypotension
  • Epinephrine reversal (epinephrine contraindicated)
19
Q

Describe epinephrine reversal

A
  • Give drug which binds to alpha-1
  • Give adrenaline
  • As alpha-1 are already occupied, epinephrine will stim Beta-2 –> vasodilation
  • Causes a big drop in blood pressure
20
Q

List some commonly used alpha2-adrenoreceptor agonists

A

Xylazine, Detomidine, Medetomidine, Dexmedetomidine

21
Q

Describe the mechanism of action of alpha2-adrenoreceptor agonists

A

a2 receptors linked to G protein coupled receptor –> decrease cAMP + Ca influx + open K channels –> inhibits norepinephrine release

22
Q

What are some of the adverse effects of using alpha2-adrenoreceptor agonists?

A
  • Hypotension
  • Hypoxemia in ruminants –> pulmonary congestion
  • Decreased insulin release
  • Decreased GIT motility
23
Q

How can you reverse the effects of alpha2-adrenoreceptor agonists?

A

a2- adrenoreceptor antagonist e.g Atipamezole

TV3001 (8 decks)

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