Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmocolgy > P18: Antidepressant Drugs > Flashcards

P18: Antidepressant Drugs Flashcards

1
Q

Give examples for manic symptoms

A
  • Euphoria
  • Over-confidence
  • Grandeur delusions
  • Irritability
  • Anger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give examples for depressive symptoms

A
  • Misery, apathy
  • Pessimism
  • Indecisiveness
  • Loss of appetite
  • Insomnia
  • Avolition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can cause secondary mood disorders?

A
  • Illness

- Medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the classes of primary mood disorders?

A
  • Bipolar

- Unipolar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What symptoms do you show if you have a Bipolar mood disorder?

A

Both mania and depressive symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What symptoms do you show if you have a Unipolar mood disorder?

A

Only depressive symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name some of the genetic risk factors of MDD

A
  • No single genes identified
  • Familial component exists (twins)
  • Genes regulating 5-HT transmission (weak)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name some of the social risk factors of MDD

A
  • Bereavement
  • Financial strain
  • Emotional, physical or sexual abuse
  • Childhood trauma/abuse
  • Social exclusion – e.g. being LGBT in an unsupportive environment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name some of the medical risk factors of MDD

A
  • Alcohol or illegal drug use
  • Serious or chronic ill health
  • Medicinal drugs, e.g. antihypertensive medication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the Monoamine Theory of Depression?

A
  • Deficiency in one or more key monoamines [Serotonin, NorAd, Dopamine]
  • Pre-synaptic neurone upregulates these key MAs
  • Abnormally functioning gene causes depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the evidence for the Monoamine Theory of Depression?

A
  • Treatment of patients with the noradrenaline packaging blocker reserpine for hypertension caused depression
  • Treatment of tuberculosis with the monoamine oxidase inhibitor iproniazid improved patients’ moods
  • Majority of antidepressant drugs potentiate monoamine (noradrenaline, 5-HT, dopamine, adrenaline) signalling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Patients with MDD often show over-activity in which part of the brain?

A

Thalamus, which has strong connections to the amygdala (fear and anxiety)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do Tricyclic Antidepressants (TCAs) work?

A

Inhibit the uptake of both 5-HT and NA, prolonging their synaptic lifespan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give some examples of Tricyclic Antidepressants

I am Despacito

A
  • Imipramine (NA&raquo_space; 5-HT)
  • Amitriptyline (5-HT and NA)
  • Desipramine (NA, active metabolite of imipramine)

slow onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the side effects of TCAs?

A
  • Epilepsy
  • anti-muscarinic - dry mouth, constipation, urinary retention
  • α-adrenoceptor antagonism - postural hypotension
  • Sedation (H1 antagonism)
  • cardiotoxic in overdose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do Monoamine Oxidase Inhibitors (MAOI) work?

A

Inhibit MAO-A, so NA and 5-HT are not broken down.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give some examples of MAOIs

A
  • Phenelzine (non reversible)
  • Tranylcypromine [Non-reversible]
  • Moclobemide ​[MAO-A, Rev]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the side effects of MAOIs?

A
  • Hyperthermia
  • Hypotension
  • Coma
  • Respiratory depression
19
Q

How do Serotonin Selective Reuptake Inhibitors (SSRIs) work?

A

Inhibit reuptake of 5-HT therefore prolong synaptic lifespan of 5-HT

2-3 week onset

20
Q

Give some examples of SSRIs

A
  • Fluoxetine (prozac)
  • Paroxetine
  • Citalopram
  • Fluvoxamine
21
Q

What are the side effects of SSRIs?

A
  • Epilepsy

- Lacks sedative and anti-muscarinic effects of TCAs

22
Q

What causes serotonin syndrome?

A

Use of two (or more) types of monoamine modulators can in rare instances induce an acute toxic reaction

rapid onset

23
Q

What are the symptoms of serotonin syndrome?

A
  • High body temperature (>41C)
  • Agitation
  • Sweating
  • Dilated pupils
  • Diarrhoea
  • Seizures
24
Q

What is Venlafaxine?

A

Potent blocker of both serotonin and noradrenaline reuptake (SNaRI)

25
Q

What is Nefazodone?

A
  • Potent 5-HT2 receptor antagonist, with weak SNaRI activity
  • More sedating than venlafaxine
  • Causes nausea
26
Q

What is Mirtazapine?

A
  • α2, 5-HT2 and 5-HT3 receptor antagonist

- Increases both noradrenaline and serotonin transmission

27
Q

What is Reboxetine?

A
  • Selective noradrenaline reuptake inhibitor
  • Anti-muscarinic and pro-sympathetic side effects (e.g. dry mouth, insomnia, constipation, urinary retention, tachycardia)
28
Q

What are the structural changes to the brain with someone with Bipolar affective disorder?

A

Increased volume of the pallidum and lateral ventricles

29
Q

What are the functional changes to the brain with someone with Bipolar Affective Disorder?

A

Abnormal modulation of the amygdala is likely to underlie emotional and mood regulation

30
Q

How does Lithium work as a drug to treat MDD?

A
  • Mood stabilising drug, more effective in bipolar than unipolar affective disorder
  • Reduces the frequency and severity of relapses by half, reduces the likelihood of suicide
31
Q

What is the Lithium Mechanism of Action?

A
  • Affects the Inositol cascade
  • Li+ inhibits inositol recycling, limiting actions of Gq-coupled receptors
  • Reduces CNS glutamate, GABA, glycine, 5-HT, ACh, dopamine and noradrenaline signalling
32
Q

What are the 2 major categories of depressive disorder

A

dysthymia - mild

major depressive disorder (MDD) - severe

33
Q

What are the major flaws of the monoamine theory of depression

A
  • Treatment with monoamine interacting drugs has an immediate neurochemical effect, but behavioural effects take 3-4 weeks to appear
  • No evidence for a primary deficit in monoamine transmission in MDD patients
  • Atypical antidepressants do not target the monoamine systems but are effective
34
Q

How might the Hypothalamo-Pituitary-Adrenal Axis result in depression

A
  • Adapts to stressors over time and releases more GCs
  • GCs in patients with MDD can’t regulate their own production
  • Evidence that HPA axis is over active in MDD patients
  • GC over-exposure thought to damage serotonergic pathways in the brain, leading to neuronal retraction
35
Q

What classes of drugs and treatments are used to treat MDD

A

Tricyclic antidepressants (TCAs)
Serotonin Selective Re-uptake Inhibitors (SSRIs)
Serotonin & Noradrenaline RIs, Noradrenaline Selective RIs
Monoamine Oxidase Inhibitors (MAOIs)

Cognitive Behavioural Therapy - milder forms
Electro-convulsive therapy - severe forms

36
Q

Why are TCAs not suitable for suicidal patients

A

Easy and severe effects of overdose

37
Q

How do TCAs interact with alcohol

A

Strongly potentiates its sedative properties

38
Q

What are the 2 isoforms of MAO and how they differ

A

MAO-A - noradrenaline and serotonin

MAO-B - noradrenaline, dopamine and serotonin

39
Q

What is the cheese reaction

A

When irreversible MAOIs interact with tyramine in foods like blue cheese, smoked fish and cured meats - caises acute hypertension

40
Q

How do MAOIs interact with drugs like barbiturates and alcohol

A

reduces the metabolism of them and prolongs and exaggerates their effects.

41
Q

In which patients are SSRIs used

A

first line treatment for patients who don’t respond to CBT

42
Q

How is serotonin syndrome treated

A

Treatment is cessation of monoamine modulators, and administration of a serotonin antagonist, e.g. cyproheptadine

43
Q

How is Electroconvulsive Therapy carried out

A

Induction of an epileptic seizure

Electric current applied through two electrodes attached to the anterior temporal areas of the scalp

Performed under general anaesthetic, and after administration of a muscle relaxant - prevents injury during the fit

Pharmocolgy (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions