CNS drugs Flashcards
what is consciousness?
the state of being aware of + responsive to one’s surroundings.
how is sensory input relayed to the brain?
sensory input from peripheral receptors. transmitted via peripheral nerves to spinal nerves to the brain
what happens in the brain when we lose consciousness?
still receiving communication from peripheral receptor. not processed = not perceived.
why is the blood-brain barrier important?
for drug to have effect within CNS, needs to cross blood-brain barrier
what is the blood-brain barrier?
‘wall’ that separates blood + CSF - offer extra layer of protection against contaminants in the blood.
use of CSF?
fluid that surrounds brain and spinal cord
what is a synapse?
junction between neurons
what can a synapse be?
inhibitory / excitatory - both important for homeostasis
main neurotransmitters + where they bind and have an effect?
GABA - bind with GABA receptor - inhibition effect
Glutamate - bind with NMDA receptor - excitation effect
other neurotransmitters that affect CNS?
noradrenaline
dopamine
5-hydroxytryptamine (5-HT / serotonin)
acetylcholine
histamine
veterinary medicines that have action on CNS?
anaesthetics
sedatives
anti-convulsants
(behaviour modifiers) - generally target other neuro receptors (not GABA/glutamate) within CNS
analgesics
define anaesthesia
loss of sensation
difference between local and general anaesthesia?
local - loss of sensation in local area
general - loss of consciousness
what does a drug need to do to induce anaesthesia?
supress CNS function, therefore drugs that potentate effect of GABA / inhibit effect of glutamate will achieve this.
examples of anaesthetic drugs + administration route?
isoflurane / sevoflurane = inhaled
propofol / alfaxalone / ketamine = injected
pharmacokinetics of isoflurane + sevoflurane?
absorbed by blood from alveoli, distributed to CNS, minimal metabolism, mostly eliminated by lungs
pharmacodynamics of isoflurane + sevoflurane?
enhanced activation of GABA receptors
pharmacokinetics of propofol?
given IV so no absorption phase. highly protein bound. metabolised by liver and excreted in urine + faeces.
pharmacodynamics of propofol?
activates GABA receptors
pharmacokinetics of alfaxalone?
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
pharmacodynamics of alfaxalone?
activates GABA receptors
pharmacokinetics of ketamine?
given IV/IM/SC. absorbed into blood stream for distribution. metabolised by liver + excreted in urine.
pharmacodynamics of ketamine?
antagonise NMDA receptor, therefore blocks action of glutamate
why is ketamine known as a dissociative anaesthetic?
has no action on GABA.
effect of sedative?
no loss of consciousness - generally still aware of surroundings
examples of sedatives?
phenothiazines
a-2 agonists
benzodiazepines
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.
example of phenothiazine?
acepromazine
administration route of acepromazine?
injection / oral
pharmacodynamics of acepromazine?
antagonises dopamine - anti-emetic effect and causes peripheral vasodilation via antagonism of a-1 receptors.
example of a-2 agonist?
medetomidine
administration route of medetomidine?
injection (IV/IM/SC), also absorbed across mucous membranes.
pharmacodynamics of medetomidine?
act on a-2 receptors in CNS. leads to inhibition of noradrenaline release.
why are a-2 agonists avoided in unhealthy animals?
cardiovascular side effects (peripheral vasoconstriction) seen.
example of a benzodiazepine?
diazepam
administration route of diazepam?
IV / oral.
pharmacokinetics of diazepam?
highly protein bound. metabolised by the liver and mostly eliminated in the faeces.
pharmacodynamics of diazepam?
facilitate the binding of GABA to its receptor
why is sedation unreliable in healthy animals given diazepam?
can cause excitation (GABA is excitatory)
why can diazepam be used in unhealthy patients?
little to no effect on cardiovascular / respiratory system.
what is a seizure?
an uncontrolled excess of electrical activity in the brain.
use of anti-convulsants?
stop a seizure / lower seizure threshold and reduce likelihood of seizure activity.
examples of anti-convulsants + when to give them?
benzodiazepines (during seizures.
barbiturates / bromide (longer term management.
example of benzodiazepine?
diazepam
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.
pharmacodynamics of diazepam?
enhanced effect of GABA has inhibitory effect on CNS
why is diazepam not suitable for long-term seizure control?
short half-life
example of barbiturates?
phenobarbitone
pharmacokinetics of phenobarbitone?
given orally. high bioavailability. metabolised by liver and excreted in urine.
pharmacodynamics of phenobarbitone?
potentiate effect of GABA and inhibit glutamate
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.
example of bromide?
potassium bromide
pharmacokinetics of potassium bromide?
given orally. not metabolised. excreted in urine.
pharmacodynamics of potassium bromide?
hyperpolarises neuronal membranes which potentiate GABA
which drug is potassium bromide often given with?
phenobarbitone - synergistic effect
