CNS case discussion Flashcards
What is the main excitatory neurotransmitter in brain?
Glutamate
What is the main inhibitory neurotransmitter in the brain?
GABA
How is neurotransmitter release triggered?
Action potential depolarises membrane and causes calcium channels to open. Ca2+ influx causes exocytosis of neurotransmitter from presynaptic cleft
What happens to a neurotransmitter after acted on post-synaptic terminal? Why?
Reuptake
Or degradation by enzymes
Prevent constant neurone stimulation
What are the 3 mechanism by which AEDs have their seizure suppressing action?
Enhance action of GABA
Reduce action of glutamate
Modulate movement of ions
What is the MOA for phenobarbital?
Enhance action of GABA
Also has glutamate and Ca channel effects
What do you need to be aware of when administering drug treatments whilst on phenobarbital?
Highly protein bound
Enhances metabolism
Decreases effect of many drugs (e.g. corticosteroids, B blockers)
What are the 3 pathways for pain transmission?
Spinothalmic
Spinoreticular
Spinocervicular (not humans)
Nociceptor sends transmission to spinal cord, enter spine via dorsal root ganglia. Not heavily myelinated tracts. They decussate. Always travel through thalamus
What is the pathway for pain transition in the spinothalamic pathway?
From spine to thalamus
What is the pathway for pain transmission in the spinoreticular pathway?
Spinal cord - reticular formation - thalamus
What is the pathway of pain transmission in the spinocervicular pathway?
Thalamus subnuclei - cerebellum - medial meniscus - lateral cervical nucleus
Which class of sedatives are often administered to seizing patients? Why is this drug classed not used as a 1st choice in healthy animals?
Benzodiazepines Paradoxical excitement (hyperactive) and not licensed
What drug would be used for premedication of an epileptic patient?
Alpha 2 agonist - analgesic effect. Antagonists can be used to reverse
What is the MOA of alpha 2 agonists in the CNS and PNS?
In CNS acts as sympatholytic - binds to presynaptic receptors, not postsynaptic –> sedation effect
In PNS act as sympathomimetic –> vasoconstriction –> reduced HR due to baroreflex (try to reduce BP)
What is the MOA of phenothiazines?
Antagonist of a2, histamine, dopamine, serotonin and more
Why is phenothiazine not given to brachycephalic breeds?
Very sensitive to these drugs - cause blood pressure drop
How do local anaesthetics work?
Sodium channel blockers
How can local anaesthetics be given?
Topical
Nerve block
Epidural (may appear ability to toilet after)
What happens to propofol in the body?
Redistribution to VRGs - vessel rich organs THEN metabolised
How is isoflurane removed from the body?
Breathed out due to pressure gradient in alveoli
Nuclear sclerosis reduces the ability to of the lens to accommodate. What is accommodation of the lens and how is it achieved?
Changing shape of lens
Ciliary body muscle contracts and relaxes - tightens or loosens lens fibres
What structures are visible in an ocular exam of the normal fundus?
Optic disc
Retina and RPE (retina pigmented epithelium)
Retinal blood vessels
Tapetum lucidum
What are the signs of canine cognitive dysfunction syndrome?
DISHA
Changes in sleep wake cycle Changes in activity levels House soiling Interaction and social behaviour changes Disorientation
Imbalances in which 2 neurotransmitter are particularly associated with the aggression sometimes seen in patients with CCDS?
Serotonin and acetylcholine
What changes in gross or microscopic anatomy would you expect to see in the brain of a patient with CCDS?
Atrophy
Reduced neurone density
Neurofibrillary tangles
What must you consider before using medication as part of treatment to improve emotional health?
Physical health status
Environment - is the feeling justified in that context
Is the behaviour normal duration and intensity?
Segeline is the drug most commonly used in CCDS. It is a MAOBI (monoamine oxidase B inhibitor) - what is their MOA? How does this potentially reduce anxiety?
MAO breaks down 5-HT NA and dopamine - inhibits MAO-A and B enzymes –> increases longevity of these NTs. More serotonin and dopamine available.
What pharmacodynamics does segeline have that make it a good treatment choice for CCDS?
Increases dopamine and noradrenaline (enhances learning)
Scavenges free radicals that do oxidative damage (cause of CCDS - slows damage)
Enhances nerve growth factor
Reduces ischaemic damage
