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Animal Medicines > CNS drugs > Flashcards

CNS drugs Flashcards

1
Q

what is consciousness?

A

the state of being aware of + responsive to one’s surroundings.

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2
Q

how is sensory input relayed to the brain?

A

sensory input from peripheral receptors. transmitted via peripheral nerves to spinal nerves to the brain

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3
Q

what happens in the brain when we lose consciousness?

A

still receiving communication from peripheral receptor. not processed = not perceived.

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4
Q

why is the blood-brain barrier important?

A

for drug to have effect within CNS, needs to cross blood-brain barrier

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5
Q

what is the blood-brain barrier?

A

‘wall’ that separates blood + CSF - offer extra layer of protection against contaminants in the blood.

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6
Q

use of CSF?

A

fluid that surrounds brain and spinal cord

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7
Q

what is a synapse?

A

junction between neurons

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8
Q

what can a synapse be?

A

inhibitory / excitatory - both important for homeostasis

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9
Q

main neurotransmitters + where they bind and have an effect?

A

GABA - bind with GABA receptor - inhibition effect
Glutamate - bind with NMDA receptor - excitation effect

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10
Q

other neurotransmitters that affect CNS?

A

noradrenaline
dopamine
5-hydroxytryptamine (5-HT / serotonin)
acetylcholine
histamine

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11
Q

veterinary medicines that have action on CNS?

A

anaesthetics
sedatives
anti-convulsants
(behaviour modifiers) - generally target other neuro receptors (not GABA/glutamate) within CNS
analgesics

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12
Q

define anaesthesia

A

loss of sensation

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13
Q

difference between local and general anaesthesia?

A

local - loss of sensation in local area
general - loss of consciousness

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14
Q

what does a drug need to do to induce anaesthesia?

A

supress CNS function, therefore drugs that potentate effect of GABA / inhibit effect of glutamate will achieve this.

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15
Q

examples of anaesthetic drugs + administration route?

A

isoflurane / sevoflurane = inhaled
propofol / alfaxalone / ketamine = injected

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16
Q

pharmacokinetics of isoflurane + sevoflurane?

A

absorbed by blood from alveoli, distributed to CNS, minimal metabolism, mostly eliminated by lungs

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17
Q

pharmacodynamics of isoflurane + sevoflurane?

A

enhanced activation of GABA receptors

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18
Q

pharmacokinetics of propofol?

A

given IV so no absorption phase. highly protein bound. metabolised by liver and excreted in urine + faeces.

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19
Q

pharmacodynamics of propofol?

A

activates GABA receptors

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20
Q

pharmacokinetics of alfaxalone?

A

given IV/IM. IM route delay onset of action due to absorption phase. not highly protein bound (only 30-50%). Metabolised by liver and excreted in urine + faeces

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21
Q

pharmacodynamics of alfaxalone?

A

activates GABA receptors

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22
Q

pharmacokinetics of ketamine?

A

given IV/IM/SC. absorbed into blood stream for distribution. metabolised by liver + excreted in urine.

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23
Q

pharmacodynamics of ketamine?

A

antagonise NMDA receptor, therefore blocks action of glutamate

24
Q

why is ketamine known as a dissociative anaesthetic?

A

has no action on GABA.

25
Q

effect of sedative?

A

no loss of consciousness - generally still aware of surroundings

26
Q

examples of sedatives?

A

phenothiazines
a-2 agonists
benzodiazepines

27
Q

why are sedatives often given in combination with an opioid?

A

synergistic effect = lower dose of each drug can be given but with same degree of sedation achieved.

28
Q

example of phenothiazine?

A

acepromazine

29
Q

administration route of acepromazine?

A

injection / oral

30
Q

pharmacodynamics of acepromazine?

A

antagonises dopamine - anti-emetic effect and causes peripheral vasodilation via antagonism of a-1 receptors.

31
Q

example of a-2 agonist?

A

medetomidine

32
Q

administration route of medetomidine?

A

injection (IV/IM/SC), also absorbed across mucous membranes.

33
Q

pharmacodynamics of medetomidine?

A

act on a-2 receptors in CNS. leads to inhibition of noradrenaline release.

34
Q

why are a-2 agonists avoided in unhealthy animals?

A

cardiovascular side effects (peripheral vasoconstriction) seen.

35
Q

example of a benzodiazepine?

A

diazepam

36
Q

administration route of diazepam?

A

IV / oral.

37
Q

pharmacokinetics of diazepam?

A

highly protein bound. metabolised by the liver and mostly eliminated in the faeces.

38
Q

pharmacodynamics of diazepam?

A

facilitate the binding of GABA to its receptor

39
Q

why is sedation unreliable in healthy animals given diazepam?

A

can cause excitation (GABA is excitatory)

40
Q

why can diazepam be used in unhealthy patients?

A

little to no effect on cardiovascular / respiratory system.

41
Q

what is a seizure?

A

an uncontrolled excess of electrical activity in the brain.

42
Q

use of anti-convulsants?

A

stop a seizure / lower seizure threshold and reduce likelihood of seizure activity.

43
Q

examples of anti-convulsants + when to give them?

A

benzodiazepines (during seizures.
barbiturates / bromide (longer term management.

44
Q

example of benzodiazepine?

A

diazepam

45
Q

pharmacokinetics of diazepam?

A

rectally / IV. blood vessels rectally do not drain into portal vein so not subject to first pass metabolism. good blood supply = absorption rapid with onset of action comparable to IV route.

46
Q

pharmacodynamics of diazepam?

A

enhanced effect of GABA has inhibitory effect on CNS

47
Q

why is diazepam not suitable for long-term seizure control?

A

short half-life

48
Q

example of barbiturates?

A

phenobarbitone

49
Q

pharmacokinetics of phenobarbitone?

A

given orally. high bioavailability. metabolised by liver and excreted in urine.

50
Q

pharmacodynamics of phenobarbitone?

A

potentiate effect of GABA and inhibit glutamate

51
Q

side effects of phenobarbitone?

A

polyphagia thought to be seen due to suppression of satiety centre of hypothalamus.
polyuria due to inhibitory effect in ADH release.
sedation seen as side effect - dogs often become tolerant of this.

52
Q

example of bromide?

A

potassium bromide

53
Q

pharmacokinetics of potassium bromide?

A

given orally. not metabolised. excreted in urine.

54
Q

pharmacodynamics of potassium bromide?

A

hyperpolarises neuronal membranes which potentiate GABA

55
Q

which drug is potassium bromide often given with?

A

phenobarbitone - synergistic effect

Animal Medicines (20 decks)

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