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BRS Year 2 > Psych - Pyschopharmacology: medicines in pyschiatry > Flashcards

Psych - Pyschopharmacology: medicines in pyschiatry Flashcards

1
Q

types of treatments in psych (4)

A
  • chemical (+/- immunotherapy) e.g. drugs for depression
  • Electrical stimulation
    e. g. ECT for depression (neurostimu for pain syndromes)
  • Structural rearrangement
    e. g. psychosurgery/deep brain stimulation for severe depression
  • Talking (psycho therapies)
    e. g. CBT e.g. exposure for phobias
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2
Q

How to classify psychiatric drugs? (3)

A
  1. based on chemical structure (prodrug/active drug)
    - -> not useful in clinical decision making
  2. Based on the illnesses they treat
    - -> problem as many meds work in several disorder e.g. antidepressants work for anxiety and OCD
    - -> most psych disorders have multiple symptoms and a single medicine mighn’t treat them all. Likely have different NT mechanisms
  3. Based on their pharmacology e.g. dopamine blocker, serotonin enhancer (GABA enhancer insteaf of hypnotic)
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3
Q

The 4 different sites that drugs act upon

A
  1. receptors
  2. NT reuptake sites
  3. Ion channels
  4. enzymes
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4
Q

enzymes of which organ can be particularly affected by psych drugs?

A

the liver

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5
Q

What is the only NT that isnt taken back up again?

A

ACh -> peptides broken down outside terminal

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6
Q

Examples of enzyme- targeting meds (3)

A
  1. MAOIs for anxiety/depression
  2. AChesterase inhibitors for dementia
  3. lithium
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7
Q

how does lithium help mood stability

A
  1. blocks glycogen synthase
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8
Q

Examples of receptor-blocker treatments (3)

A
  1. dopamineR blockers for schiz
  2. serotoninR subtype antagonists for depression (repuake?)
  3. histamineR antagonists for sleep
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9
Q

Examples of receptor-simulating treatments

A
  1. benzodiazeptines enhance GABA (Sleep)

2. guanfacine enhance NA (ADHD)

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10
Q

what does citalopram do?

A

enhances serotonin by inhibiting serotonin reuptake

-> for depression/anxiety

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11
Q

Give an example of a tricyclic antidepressant and what they do

A

Desipramine
Inhibitors of serotonin reuptake transporters (SERTs) and norepinephrine transporters (NETs)
This enhances noradrenaline and serotonin

Desipramine is a secondary TCA so only inhibits NETs and enhances noradrenaline

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12
Q

Give an example of a psychomotor stimulant drug

A

methylphenidate
enhances dopamine by inhibiting dopamine reuptake
Treatment for depression

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13
Q

what is an example of a drug that switches the reuptake site direction to enhance release?

A
  • amfetamine for ADHD

- > lack of dopamine for reward centre in ADHD?

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14
Q

what type of receptor is the 5HT receptor?

A

an inhibitory receptor

-> increased stim of this receptors dampens activity of neurons where that receptor is

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15
Q

what conditions are thought to be related to the 5HT receptor?

A
  • involved in conditions like schiz

- > also regulation of sleep and eating

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16
Q

drugs that block Na channels

A

sodium valporate
carbamazepine
-> both for epilepsy and mood stabilisation

17
Q

drugs that block Ca channels?

A

gabapentin
pregabalin
-> both for epilepsy and anxiety

18
Q

examples of fast acting NTs

A
  1. excitatory (glutamate) -> 80% of all neurons (pyramidal cells)
  2. inhibitory (GABA) -> 15%: interneurons
19
Q

examples of slow acting NTs

A
  1. dopamin, serotonin, NA, ACh
  2. endorphins and other peptides

emotions, drives, valence of memory

20
Q

what can XS glutamate cause?

A

epilepsy

alcoholism

21
Q

treatment for XS glutamate? (3)

A

perampanel - blocker
acamprosate - blocker- helps with alcohol craving
ketamine - blocker

22
Q

what can GABA deficiency cause?

A

anxiety

23
Q

treatment for GABA deficiency

A

Benzodiazepines - GABA enhancer

24
Q

what can 5-HT deficiency cause?

A

depression

anxiety

25
Q

treatment for 5-HT deficiency

A

SSRIs and MAOIs - serotonin enhancer

26
Q

what can XS dopamine cause?

A

psychosis

27
Q

treatment for XS dopamine?

A

dopamine receptor blockers

28
Q

what can XS NA cause?

A

nightmares

29
Q

treatment for XS NA?

A

Prazosin - blocker

30
Q

what can ACh deficiency cause?

A

impaired memory

dementia

31
Q

treatment for ACh deficiency?

A

AChesterase enzyme blockers

32
Q

benefits of partial agonists?

-> these have lower max efficacy than full agonists

A
  1. improved safety, esp in overdose

2. in states of high NT or excess agonist med, can act as an antagonist

33
Q

examples of partial agonists

A

buprenorphine -safer than heroin
aripiprazole - safer than haloperidol (is used in the treatment of schizophrenia, tics in Tourette syndrome, mania in bipolar disorder, delirium, agitation, acute psychosis, and hallucinations in alcohol withdrawal.)
varenicline- safer than nicotine

34
Q

how can you reverse amnestic effect of alcohol in humans?

A

give alpha51A inverse agonist

-> works in the hippocampus

35
Q

what in an inverse agonist?

A

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

36
Q

what is allosteric modulation?

A

a group of substances that bind to a different site on the receptor ( allosteric site) to enhance the effects of the neurotransmitter that binds to the orthosteric site of the receptor (normal binding site for the NT)

37
Q

where does GABA binds to it’s receptor?

A

on the orthosteric site

-> the GABA-A receptor is an ion-channel linked

38
Q

what happens when GABA binds to its receptor?

A
  • enhances Cl- conductance -> inhibits neurons -> calms the brain
39
Q

where do the benzodiazepines, barbiturates , alcohol and neurosteroids bind?

A

on the allosteric sites of the GABA-A receptor

  • > enhance its action
  • > leads to reduced anxiety, sleep, anti-epilepsy

BRS Year 2 (110 decks)

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