Neuro Pharmacology Flashcards

1
Q

Patho of epilepsy?

A

Tissues from an epileptic focus have less synaptic inhibition leading to cells becoming easily excitable increasing the firing rate and a subsequent seizure

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2
Q

Adverse effects of midazolam?

A

Sedation, headache, blurred vision, hypotension, nausea/vomiting, respiratory depression.

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3
Q

How does neuronal communication work?

A

traveling wave of electrical excitation known as an action potential that is orchestrated by the opening and closing of ion channels

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4
Q

What is GABA?

A

inhibitory neuron that inhibits or slows down excitatory impulses

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5
Q

Too little of what neuron can lead to seizures?

A

GABA

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6
Q

Describe the MOA of Anti-Epileptic drugs, and the four ways they work.

A

MOA: lower neuronal excitability and enhance neuronal inhibition.
1- blocking of voltage gated sodium channel -> reduces NA in neuron
2- blocking of high and low voltage gated calcium channels
3- enhancing of GABA system
4- blocking of calcium channel and binding of SV2a protein

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7
Q

Seizure pathology? How should the brain act normally?

A

Abnormal excessive synchronous electrical activity. Normally neuronal firing is regulated by a balance between inhibitory and excitatory synaptic input. Brain cells generate action potentials.

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8
Q

What is the patho of status?

A

failure of mechanism to terminate a seizure either due to an increase in the excitatory mechanism or a decrease in the inhibitory mechanism.

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9
Q

Whats important to note about a prolonged seizure?

A

Difficult to abort

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10
Q

Treatable causes of seizure in the pre hospital field and their treatments?

A

Hypoglycemia - D10
Eclampsia - Magnesium

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11
Q

What is the doze for Midaz in the Adult ACP World for seizures?

A

2-5mg IV/IO to effect, 5-10 mg IM titrate to effect, MAX DOSE 30 MG

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12
Q

Describe the MOA of Midaz

A

Midaz increases the affinity for GABA to GABA binding sites, GABA binds to gaba-a receptors, increasing the frequency of anion channel opening (chorlide), influx of chloride rushes in bringing the cell negative and further hyperpolarizing the cell, this hyperpolarizing prolongs the depolarization phase and their ability to conduct action potentials quick thus increasing inhibition.

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13
Q

What is a hypnotic used for?

A

used to initiate and maintain sleep

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14
Q

What is an anxiolytic used for?

A

to treat acute anxiety

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15
Q

How does midaz work in an anxious patient

A

It increases inhibition which inhibits the SNS which is firing the action potentials that is giving the feelings of fear and anxiousness, net result is increased calmness and decreased anxiety

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16
Q

What do AMPA receptors permit entry of?

A

Sodium Ions

17
Q

What do NMDA receptors permit entry of?

A

Calcium Ions

18
Q

What does the gaba-a subunit a1 control?

A

Sleep

19
Q

What does the gaba-a subunits a2-a3 control?

A

Anxiety

20
Q

Where in the brain controls fear and anxiety?

A

Amygdala

21
Q

How does anxiety occur?

A

In times of stress excitatory neurons in the amygdala fire rapidly, sending excitatory signals to other parts of the brain.

22
Q

What regulates fear and anxiety?

A

Inhibitory neurons in the amygdala by releasing GABA and inhibiting the excitatory signals, GABA allows for the calming tranquilizing effect and prevents us from becoming overwhelmed in stressful situations.

23
Q

What is the difference between benzos and barbs

A

Benzos increase opening frequency of ion channels, barbs increase opening duration.

24
Q

What do barbiturates do?

A

Decrease activity of the excitatory neurotransmitters acetylcholine and glutamate.

25
Q

Adverse effects of barbs?

A

Dizzy, lightheaded, sedation, memory and attention deficits. Small OD can lead to coma and death due to respiratory depression

26
Q

Therapeutic uses for anxiolytics or hypnotics

A

1- anxiety and related conditions
2- sleep disorder
3- pre operative sedation and anxiety
4- etoh withdrawal
5- epilepsy and status
6- muscle spams

27
Q

What is important to note about the duration of midaz?

A

It is short acting

28
Q

What is important to note about benzos regarding CNS?

A

The greater the dose the more CNS depression you will have, due to decreased action potentials

29
Q

How does midaz affect the body ie hr rr etc?

A

Decreases HR thus decreases BP and decreases RR overall CNS depression

30
Q

How to hypnotic agents work?

A

agonists at gaba sites, gaba inhibits excitatory impulses allowing anxiety to stop and bringing calm to the patient

31
Q

What is glutamate?

A

Excitatory neuron

32
Q

How does a cell generate action potentials faster and cause a seizure?

A

Cell becomes +++ as voltage gated channels open along the ion which leads to propogation of depolarization down the axon = depol and generation of action potentials. Increased glutamate leads to increased activity of NMDA and AMPA receptors leading to more ++++ and more depol leading to more action potentials generated and thus seizure

33
Q

What are the four dopaminergic pathways in the brain?

A

Mesolimbic - memory and emotional behaviours
mesocorticol - cognition/motivation
nigrostriatal - controls movement
tuberoinfundibular - controls prolactin secretion

34
Q

What dopaminergic receptor is the main target for anti-psychotics?

A

D2 receptor

35
Q

What do 1st generation or typical drugs do?

A

block d2 receptors in all areas of the brain

36
Q

Anti-Psychotic Impacts on the pathways

A

Mesocorticol - dopamine blockade leads to more neg symptoms
Nigrostriatal - parkinsonian like side effects
Tuberoinfundibular - increased prolactin secretion
Mesolimbic - decrease positive symptoms associated with schizo (this is where we want it to work)