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BRS YEAR 2 > Pschopharmacology > Flashcards

Pschopharmacology Flashcards

1
Q

Classification of treatments

A
  • Chemical
  • e.g. drugs, medicines, immunotherapy
  • Electrical stimulation
  • e.g. ECT, neurostimulation
  • Structural rearrangement
  • e.g. surgery, deep brain stimulation, psychosurgery
  • Talking (psycho) therapies
  • e.g. CBT, exposure therapy
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2
Q

Classification of psychiatric drugs

A

Based on chemical structure
- Every drug has unique structure
- Not useful for clinical decision making, more for data and synthesis
Based on what illnesses they treat
- Easy for doctors to choose a drug based on diagnosis
- Some drugs may work in different disorders
- Many psychiatric disorders have multiple symptoms, and one medicine may not treat them all
Based on pharmacology
- E.g. instead of antipsychotic, dopamine blocker
- E.g. instead of antidepressant, serotonin / noradrenaline / dopamine enhancer
- E.g. instead of hypnotic or anxiolytic, GABA enhancer

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3
Q

GABA receptors

A

GABA-A - ion channel which spans nerve membrane
- benzodiazepines, alcohol, anaesthetics, and barbiturates enhance GABA
Is the major inhibitory neurotransmitter in the cns so when activated it conducts cl- causing hyperpolarization

GABA-B - G protein coupled receptor
- GHB binds with a low affinity via GIRK CHANNELS,when activated causes k+ extrusion so hyperpoloarization. Weak agonist propoerty of GHK seen centrally only not in spinal chord as has no affinity there for BDZ or alcohol

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4
Q

Chemical treatments in psychiatry

A

Work on one (occasionally two) of the following systems:

  • Receptors
  • Neurotransmitter reuptakes sites
  • Ion channels
  • Enzymes

Targets are in the brain, but can affect systems elsewhere in the body - particularly in the liver if the target is an enzyme

Most neurotransmitters reuptaken into neurones via transporters, some limit further release of neurotransmitter, some broken down enzymatically.

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5
Q

Enzyme targeting medicines

A
  • Monoamine oxidase Inhibitors for treatment of depression and anxiety
  • Acetylcholinesterase inhibitors for dementia
  • Lithium as a mood stabiliser (blocks glycogen synthase kinase, to prevent cyclical dysregulation seen in bipolar disorder)
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6
Q

Receptor targeting medicines

A
  • Receptor blockers (antagonists)
  • Dopamine receptor blockers for schizophrenia
  • Serotonin receptor subtype blockers for depression
  • Histamine receptor blockers for sleep
    Antagonists block endogenous agonist binding to the receptor
  • Receptor stimulators (agonists)
  • Benzodiazepines for sleep (enhances GABA)
  • Guanfacine for ADHD (enhances noradrenaline)
    Agonists mimic the endogenous agonist, stimulating the receptor
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7
Q

Reuptake site targeting medicines

A
  • Citalopram (serotonin reuptake inhibitor - SRI) for depression and anxiety
  • Desipramine (noradrenaline reuptake inhibitor - NRI) for depression
  • Methylphenidate (dopamine reuptake inhibitor - DRI) for ADHD
  • Some medicines switch the reuptake site direction to enhance release of neurotransmitters
  • e.g. amfetamine for ADHD (releases dopamine and noradrenaline, and blocks reuptake)
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8
Q

Seratonin neurotransmitter system 5-HT

A
  • 5HT neurones begin in the midbrain, and extend to the hippocampus
  • Serotonin is released, which then works on serotonin receptors on the post synapse
  • There are 15 separate genes which encode for serotonin receptors, which control a variety of functions, including:
  • Cognition
  • Mood
  • Temperature control
  • Carbon dioxide regulation
    Some, such as 5HT1a, are inhibitory, but most are excitatory.
    The coupling to G proteins or ion channels determine if inhibitory or excitatory
  • Serotonin is reuptaken at reuptake channels in the synaptic and axon membrane
  • This process is blocked by SRIs
  • Serotonin may also act on presynaptic receptors to inhibit neurone firing and further serotonin release - homeostatic regulation
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9
Q

Ion channel targeting medicines:

A

blocks channels to reduce neuronal excitability)

  • Sodium channel blockers
  • Sodium valproate for epilepsy and to stabilise mood
  • Carbamazepine for epilepsy and to stabilise mood
  • Calcium channel blockers
  • Gabapentin for epilepsy and anxiety
  • Pregabalin for epilepsy and anxiety
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10
Q

Fast acting Neurotransmitters (on-off switch)

A
  • Excitatory ⇒ glutamate, 80% of all neurons in pyramidal cells
  • Inhibitory ⇒ GABA, 15% of interneurones
  • Roles in core processes involved with memory, movement, vision etc
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11
Q

Slow acting Neurotransmitters (modulators)

A
  • Dopamine, serotonin, noradrenaline, acetylcholine
  • Endorphins and other peptides
  • Roles in emotions, drives and motivations, attention, and valence of memories
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12
Q

Glutamate

A
  1. Causes epilepsy when in excess, may be treated with the blocker Perampanel
  2. Found in high levels in alcoholism, may be treated with the blockers Acamprosate or Ketamine
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13
Q

GABA

A

Causes anxiety when deficient may be treated with enhancer benzodiazepines

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14
Q

5-HT

A

Deficiency of 5-HT results in Depression or anxiety, which may be treated with serotonin enhancers such as SRIs or MAOIs

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15
Q

Dopamine

A

Excess dopamine is associated with psychosis, which may be treated with dopamine receptor blockers.
The idea for using these blockers as a treatment for dopamine came from amfetamine psychosis amongst cyclists

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16
Q

Noradrenaline

A

Excess noradrenaline may be found in patients who have nightmares, particularly in PTSD or REM behaviour disorder. These may be treated with blockers, such as Prazosin

17
Q

Acetylcholine

A

Deficiency of Acetylcholine is strongly associated with dementia, and may be treated with acetylcholine esterase enzyme blockers

18
Q

Drug treatments for depression

A

MAOI
TCA
SSRI
SNRI
NRI
DRI
Melatonin agonists
Multimodal drugs
Receptor antagonist

19
Q

MAOI

A
  • Phenelzine
  • Moclobemide
20
Q

TCA

A
  • Clomipramine
  • Imipramine
  • Amitriptyline
21
Q

SSRI

A
  • Paroxetine
  • Fluoxetine
  • Sertraline
  • Fluvoxamine
  • Citalopram
  • Escitalopram
22
Q

Receptor antagonist

A
  • Mirtazapine
  • Trazodone
  • Mianserin
23
Q

SNRI

A
  • Venlafaxine
  • Milnacipran
  • Duloxetine
  • Desvenlafaxine
24
Q

NRI

A

Reboxetine

25
Q

DRI

A

Bupropion

26
Q

Melatonin agonist

A

Agomelatine

27
Q

Multimodal drugs

A
  • Vilazodone - USA - SSRI - 5-HT1a agonist
  • Vortioxetine - SSRI + numerous other 5-HT receptor effects
28
Q

Partial agonists

A

Lower max efficacy, so more safe, especially in overdose

In states of high neurotransmitters or excess agonists then the partial agonists can act as an antagonist

Examples:

  • Buprenorphine → replaces heroin
  • Aripiprazole → used to keep dopamine above the levels that haloperidol would bring it down to, allows patients to feel normal with less motor side effects
  • Varenicline → replaces nicotine in smoking cessation by blocking the nicotine receptor, so effects of smoking aren’t felt
29
Q

Inverse agonists

A

Opposite effects to agonists
Reverse the effects of agonists at receptors

Histamine inverse agonists may be useful for ADHD as they keep you awake

30
Q

Receptor subtypes

A

There are five subunits of GABA receptors, with numerous possibilities, but three are most common

a1b2y2 - most common, located in cortex and helps with sleep

a3b3y2 - second most common, in the limbic system and helps with relaxation

a2b3y2 - third most common, in the limbic system and helps with relaxation

31
Q

Pyramidal cells

A

Pyramidal cells aggregate information from other cells, and are gated in their response by GABA receptors

32
Q

Allosteric modulation

A

GABA-A receptor has a benzodiazepine binding site, alcohol binding and a binding site for barbiturates
- These sites are targets for different drugs and natural substances
- They act at allosteric sites to enhance the action of GABA, which causes sedation, calming, and anti-epileptic effects
- Neurosteroids act on the GABA system, and are regulated by things such as pregnancy or periods, this is why some women may have epilepsy only at certain times of their menstrual cycle
- GABA binds at the orthosteric site, inhibiting the neuron and effectively calming the brain

33
Q

Drug selectivity

A

Most drugs = highly selective

E.g. Haloperidol acts on the D2 receptor, and has mild action on the alpha 1 receptor but is unlikely to have therapeutic effects
- Adverse effects of haloperidol are therefore due to dopamine receptor blocking (extrapyramidal side effects)

Some drugs are less selective

E.g. Clozapine acts on D2 receptor, H1 receptor, Alpha 2 receptor, Alpha 1 receptor, 5-HT1A receptor, M1-4 receptor, and the 5-HT2 receptor with a mix of therapeutic and non therapeutic effects
- lots of adverse effects due to off target effects, such as weight gain and metabolic syndrome

Citalopram effects Only the serotonin transporter, meanwhile Amitriptyline effects the serotonin and noradrenaline transporters, H1, 5HT2, M1-4n and alpha-1 receptors

34
Q

Treatment of alochol depenedence via GABAb

A

GABAB agonists e.g. Baclofen attenuate many of the positive reinforcing aspects of reward
Baclofen safe when given in combination with intoxicating doses of alcohol and has minimal abuse liability.
GABAB receptor agonism therefore has the potential to treat all aspects of alcohol dependence which include:
Alleviating acute withdrawal
Initiating and maintaining abstinence
Reducing craving and craving-related relapse
Since GHB works in a similar manner to Baclofen it may be worth considering as an alternative therapy to Baclofen in the treatment of alcohol dependence.

35
Q

Alprazolam

A

eg xanax
GABA
it is a benzodiazepine receptor agonist (non selective GABA A receptor positive allosteric modulator)
treats generalised anxiety disorder,panic disorder,short term treatment of anxiety and alcohol withdrawal

36
Q

Baclofen

A

GABA
is a agonist
used in spacticity
decreases alcohol craving in alcohol dependant patients

37
Q

Neurone auto receptor

A

Usually inhibitory
Activated by neurotransmitters
Inhibit calcium influx
Reduce neurotransmitter release
Switch of firing of terminal

BRS YEAR 2 (39 decks)

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