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Psych > Psychopharmacology for psychiatry > Flashcards

Psychopharmacology for psychiatry Flashcards

1
Q

Types of treatment

A

Chemicals - drugs/meds
electrical stimulation - ECT for depression
structural rearrangement - surgery/orthopaedics
talking (psycho) therapies - CBT

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2
Q

What are three ways of classifying drugs?

A

Chemical Structure,
Illness Treated,
Pharmacology (what they do e.g. dopamine blocker)

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3
Q

What is a pro and con of classifying by chemical structure?

A

Each drug can be uniquely classified // no use in clinical decision making

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4
Q

What is a pro and 2 cons of classifying by illness treated?

A

Easy for doctors to choose // some medicines have multiple functions, some illnesses need multiple symptoms treated

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5
Q

What are the two GABA receptors?

A

GABA A & GABA B

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6
Q

What is an example of GABA-A agonist?

A

Alprazolam
treats GAD, anxiety and alcohol withdrawal
muscle relaxant, anticonvulsant, sleep promoting

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7
Q

What is an example of GABA-B agonist?

A

Baclofen
treats spasticity
decreases alcohol craving

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8
Q

What are the 4 target sites for psychiatry medications?

A

Receptors,
Neurotransmitter Reuptake Sites,
Ion Channels,
Enzymes

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9
Q

What is the general action of enzyme targeting medications?

A

Block enzyme activities

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10
Q

What are three examples of enzyme targeting medicines?

A

Monoamine Oxidase Inhibitors (anxiety)
Acetylcholinesterase inhibitors (dementia)
Lithium blocking glycogen synthase kinase (mood stability

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11
Q

What are 3 examples of receptor antagonists?

A

Dopamine antagonist (schizophrenia),
serotonin antagonist (depression),
histamine antagonist (sleep)

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12
Q

What are two examples of receptor agonists?

A

Benzodiazepines enhance GABA (sleep),
Guanfacine enhance Noradrenaline (ADHD)

mimic endogenous neurotransmitter to stimulate activity

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13
Q

Action of reuptake site targeting medicines

A

Most block reuptake sites to increase NT conc in the synapse to enhance post-synaptic receptor action
Some switch reuptake site direction to enhance release

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14
Q

What are three examples of Reuptake transporter blockers?

A

Citalopram (serotonin, depression),
Desipramine (noradrenaline, depression), Methylphenidate (dopamine, ADHD)

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15
Q

What is an example of Reuptake transporter enhancer?

A

Amfetamine - ADHD

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16
Q

What are 2 examples of sodium channel blockers?

A

Sodium Valproate - epilepsy // Carbamazepine - epilepsy

17
Q

What are 2 examples of calcium channel blockers?

A

Gabapentin and Pregabalin - epilepsy

18
Q

Fast acting NT - 95% of neurons

A

Excitatory - glutamate. 80% of neurons, pyramidal cells
Inhibitory - GABA. Inter-neurons

affect content e.g. memory, movement, vision

19
Q

Slow acting (modulators) - 5% of all neurons

A

dopamine/serotonin/NA/acetylcholine
endorphins and other peptides

controls emotions, drives etc

20
Q

For glutamate neurotransmitter system, is the change in neurotransmitter an excess or deficiency, and what disorder can it lead to?

A

Excess,
epilepsy, treated with Perampanel

alcoholism, treated with Acamprosate, Ketamine (blocker)

21
Q

For GABA neurotransmitter system, is the change in neurotransmitter an excess or deficiency, and what disorder can it lead to?

A

Deficiency,
anxiety, Benzodiazepines, GABA enhancer

22
Q

For 5-HT neurotransmitter system, is the change in neurotransmitter an excess or deficiency, and what disorder can it lead to?

A

Deficiency,
depression/anxiety
treated with SSRIs and NSSRIs, MAOIs, serotonin enhancers

23
Q

For dopamine neurotransmitter system, is the change in neurotransmitter an excess or deficiency, and what disorder can it lead to?

A

Excess,
psychosis, treated with Dopamine receptor blockers

24
Q

For noradrenaline neurotransmitter system, is the change in neurotransmitter an excess or deficiency, and what disorder can it lead to?

A

Excess,
nightmares, treated with Prazosin blockers

25
Q

For acetylcholine neurotransmitter system, is the change in neurotransmitter an excess or deficiency, and what disorder can it lead to?

A

Deficiency,
amnesia/dementia treated with Acetylcholinesterase enzyme blockers

26
Q

How do partial agonists work?

A

Lower efficacy than full agonists, will only illicit response sometimes upon receptor binding

27
Q

What are the advantages of partial agonists?

A

Improved safety if overdose
can act as antagonists in high neurotransmitter

28
Q

Which neurotransmitter system do most drugs act on?

A

5HT system

29
Q

Aripiprazole

A

Used instead of haloperidol
Prevents total destruction of dopamine activity. THis prevents parkinsonian motor symptoms. dampened dopamine activity

30
Q

Inverse agonists

A

a drug that binds to the same receptor as an agonist but induces the opposite pharmacological response.

Used on GABAergic neurons to create pro cognitive effects in dementia

31
Q

Receptor subtypes

A

5 proteins make up a receptor -> multiple different combinations
different subtypes have different actions

32
Q

How does allosteric modulation work?

A

Drug binds to a different site of the protein to the neurotransmitter and can cause its effects - Benzodiazepines and enhancing GABA action

33
Q

GABA and allosteric modulation

A

GABA-A receptor is an ion-channel linked receptor
GABA binds at the orthosteric site (target site), enhances Cl- conductance -> neuron inhibition and calm brain

Benzodiazepines, alcohol, neurosteroids act on allosteric sites, enhance GABA action -> sedation, reduced anxiety etc

34
Q

Compare the selectivity and function of haloperidol and clozapine

A

Both dopamine receptor blockers for schizophrenia

Haloperidol is very selective
Clozapine is non-selective, causes systemic adverse effects like weight gain and sedation

35
Q

Compare the selectivity and function of amitriptyline and citalopram

A

Both 5-HT reuptake blockers for depression

Citalopram is an SSRI (selective)
Amitriptyline is non-selective, causes adverse effects from blocking histamine and ACh receptors

Psych (9 decks)

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