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Eye and CNS case discussion > CNS case discussion > Flashcards

CNS case discussion Flashcards

1
Q

What is the main excitatory neurotransmitter in brain?

A

Glutamate

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2
Q

What is the main inhibitory neurotransmitter in the brain?

A

GABA

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3
Q

How is neurotransmitter release triggered?

A

Action potential depolarises membrane and causes calcium channels to open. Ca2+ influx causes exocytosis of neurotransmitter from presynaptic cleft

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4
Q

What happens to a neurotransmitter after acted on post-synaptic terminal? Why?

A

Reuptake
Or degradation by enzymes
Prevent constant neurone stimulation

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5
Q

What are the 3 mechanism by which AEDs have their seizure suppressing action?

A

Enhance action of GABA
Reduce action of glutamate
Modulate movement of ions

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6
Q

What is the MOA for phenobarbital?

A

Enhance action of GABA

Also has glutamate and Ca channel effects

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7
Q

What do you need to be aware of when administering drug treatments whilst on phenobarbital?

A

Highly protein bound
Enhances metabolism
Decreases effect of many drugs (e.g. corticosteroids, B blockers)

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8
Q

What are the 3 pathways for pain transmission?

A

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

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9
Q

What is the pathway for pain transition in the spinothalamic pathway?

A

From spine to thalamus

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10
Q

What is the pathway for pain transmission in the spinoreticular pathway?

A

Spinal cord - reticular formation - thalamus

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11
Q

What is the pathway of pain transmission in the spinocervicular pathway?

A

Thalamus subnuclei - cerebellum - medial meniscus - lateral cervical nucleus

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12
Q

Which class of sedatives are often administered to seizing patients? Why is this drug classed not used as a 1st choice in healthy animals?

A 
Benzodiazepines
Paradoxical excitement (hyperactive) and not licensed
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13
Q

What drug would be used for premedication of an epileptic patient?

A

Alpha 2 agonist - analgesic effect. Antagonists can be used to reverse

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14
Q

What is the MOA of alpha 2 agonists in the CNS and PNS?

A

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)

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15
Q

What is the MOA of phenothiazines?

A

Antagonist of a2, histamine, dopamine, serotonin and more

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16
Q

Why is phenothiazine not given to brachycephalic breeds?

A

Very sensitive to these drugs - cause blood pressure drop

17
Q

How do local anaesthetics work?

A

Sodium channel blockers

18
Q

How can local anaesthetics be given?

A

Topical
Nerve block
Epidural (may appear ability to toilet after)

19
Q

What happens to propofol in the body?

A

Redistribution to VRGs - vessel rich organs THEN metabolised

20
Q

How is isoflurane removed from the body?

A

Breathed out due to pressure gradient in alveoli

21
Q

Nuclear sclerosis reduces the ability to of the lens to accommodate. What is accommodation of the lens and how is it achieved?

A

Changing shape of lens

Ciliary body muscle contracts and relaxes - tightens or loosens lens fibres

22
Q

What structures are visible in an ocular exam of the normal fundus?

A

Optic disc
Retina and RPE (retina pigmented epithelium)
Retinal blood vessels
Tapetum lucidum

23
Q

What are the signs of canine cognitive dysfunction syndrome?
DISHA

A 
Changes in sleep wake cycle
Changes in activity levels
House soiling
Interaction and social behaviour changes
Disorientation
24
Q

Imbalances in which 2 neurotransmitter are particularly associated with the aggression sometimes seen in patients with CCDS?

A

Serotonin and acetylcholine

25
Q

What changes in gross or microscopic anatomy would you expect to see in the brain of a patient with CCDS?

A

Atrophy
Reduced neurone density
Neurofibrillary tangles

26
Q

What must you consider before using medication as part of treatment to improve emotional health?

A

Physical health status
Environment - is the feeling justified in that context
Is the behaviour normal duration and intensity?

27
Q

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?

A

MAO breaks down 5-HT NA and dopamine - inhibits MAO-A and B enzymes –> increases longevity of these NTs. More serotonin and dopamine available.

28
Q

What pharmacodynamics does segeline have that make it a good treatment choice for CCDS?

A

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

Eye and CNS case discussion (7 decks)

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