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Animal Medicines > CNS drugs > Flashcards

CNS drugs Flashcards

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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?

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A

antagonise NMDA receptor, therefore blocks action of glutamate

24
Q

why is ketamine known as a dissociative anaesthetic?

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A

has no action on GABA.

25
effect of sedative?
no loss of consciousness - generally still aware of surroundings
26
examples of sedatives?
phenothiazines a-2 agonists benzodiazepines
27
why are sedatives often given in combination with an opioid?
synergistic effect = lower dose of each drug can be given but with same degree of sedation achieved.
28
example of phenothiazine?
acepromazine
29
administration route of acepromazine?
injection / oral
30
pharmacodynamics of acepromazine?
antagonises dopamine - anti-emetic effect and causes peripheral vasodilation via antagonism of a-1 receptors.
31
example of a-2 agonist?
medetomidine
32
administration route of medetomidine?
injection (IV/IM/SC), also absorbed across mucous membranes.
33
pharmacodynamics of medetomidine?
act on a-2 receptors in CNS. leads to inhibition of noradrenaline release.
34
why are a-2 agonists avoided in unhealthy animals?
cardiovascular side effects (peripheral vasoconstriction) seen.
35
example of a benzodiazepine?
diazepam
36
administration route of diazepam?
IV / oral.
37
pharmacokinetics of diazepam?
highly protein bound. metabolised by the liver and mostly eliminated in the faeces.
38
pharmacodynamics of diazepam?
facilitate the binding of GABA to its receptor
39
why is sedation unreliable in healthy animals given diazepam?
can cause excitation (GABA is excitatory)
40
why can diazepam be used in unhealthy patients?
little to no effect on cardiovascular / respiratory system.
41
what is a seizure?
an uncontrolled excess of electrical activity in the brain.
42
use of anti-convulsants?
stop a seizure / lower seizure threshold and reduce likelihood of seizure activity.
43
examples of anti-convulsants + when to give them?
benzodiazepines (during seizures. barbiturates / bromide (longer term management.
44
example of benzodiazepine?
diazepam
45
pharmacokinetics of diazepam?
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
pharmacodynamics of diazepam?
enhanced effect of GABA has inhibitory effect on CNS
47
why is diazepam not suitable for long-term seizure control?
short half-life
48
example of barbiturates?
phenobarbitone
49
pharmacokinetics of phenobarbitone?
given orally. high bioavailability. metabolised by liver and excreted in urine.
50
pharmacodynamics of phenobarbitone?
potentiate effect of GABA and inhibit glutamate
51
side effects of phenobarbitone?
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
example of bromide?
potassium bromide
53
pharmacokinetics of potassium bromide?
given orally. not metabolised. excreted in urine.
54
pharmacodynamics of potassium bromide?
hyperpolarises neuronal membranes which potentiate GABA
55
which drug is potassium bromide often given with?
phenobarbitone - synergistic effect

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