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Brain and Behaviour Year 2 > Depression and Antidepressants > Flashcards

Depression and Antidepressants Flashcards

1
Q

Define depression

A

 A state of low mood and avoidance of activity that can affect a person’s behaviour
and feelings.

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2
Q

Name 4 types of depression from the DSM-IV class-action and describe them

A
  • Major depression = this is a continuous low mood for 2 weeks or longer
  • Bipolar disorder = this is a cycle of depression and then manic highs
  • Dysthymic disorder = this is depression that has lasted for around 2 years
  • Depressive disorder = this is depression that is otherwise unspecified
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3
Q

Name the difference types of depression from DSM V

A

sion of the system DSM V
- Depressive disorders
- Disruptive Mood Dysregulation Disorder
- Major Depressive Disorder, Single and Recurrent Episodes
- Persistent Depressive Disorder (Dysthymia)
- Premenstrual Dysphoric Disorder
- Substance/Medication-Induced Depressive Disorder
- Depressive Disorder Due to Another Medical Condition
- Other Specified Depressive Disorder
Unspecified Depressive Disorder

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4
Q

name some symptoms of depression

A
  • Psychomotor retardation
  • Fatigue or loss of energy
  • Diminished ability to concentrate
  • Diminished interest in social activity
  • Psychomotor agitation
  • Depressed mood
  • Feelings of guilt and worthlessness
  • Suicidal ideation
  • Insomnia
  • Weight loss and decreased appetite
  • Lack of interest and anhedonia(lack of pleasures)
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5
Q

define anhedonia

A

lack of interest and pleasure

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6
Q

there is a strong….

A

genetic link to depression

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7
Q

Describe how depression and genetics can be linked

A

depression has a strong genetic component
- there is also a shared genetic risk between forms of depression for example if you are related to a patient with major depression disorder you can have a chance of developing that or something like bipolar disorder

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8
Q

Name some genes that are linked to depression

A
  • HTR2A
  • GRIK4
  • CRHR1
  • HTR1A
  • MAOA
  • all these genes code for monoamines such as serotonin, noradrenaline and dopamine
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9
Q

describe how noradrengic pathways and serotonergic pathways are linked to depression

A

depression can be linked to a decrease in transmission of noradrenaline and serotonin as these are linked to the emergence of depression

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10
Q

What brain regions are associated with depression

A
  • Amygdala
  • Ventrolateral prefrontal cortex
  • Dorsolateral prefrontal cortex
  • Medial prefrontal cortex
  • Striatal regions (ventral striatum)
  • Hippocampus

These areas have shown decreased metabolism due to significant reductions in
glucose consumption.

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11
Q

in terms of inflammation what does depression also show a link to

A

Depression is associated with an increase in cortisol and pro-inflammatory cytokines
such as IL-6.

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12
Q

how are depression and mean grey matter linked

A
  • The mean grey matter volume of the subgenual anterior cingulate cortex is reduced in patients with major depressive disorder and bipolar disorder
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13
Q

what area is important in the default mode network

A

left subgenual cingulate cortex

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14
Q

what is the default mode network (DMN)

A

network of brain regions active when the brain is at wakeful rest

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15
Q

How is the DMN linked to depression

A
  • if we look at studies looking at depressed subjects we can access hot spots in the brain that have areas of activity that are different from control subjects
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16
Q

what does DMN stand for

A

default mode network

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17
Q

what polymorphism is associated with a higher risk of major depression after signciant life events

A

5-HT transporter polymorphism is associated with a higher risk of major depression
after significant life events

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18
Q

describe how genes can lead us to getting depression

A
  • some genetic weakness exposes us to depression for example it can reduce our ability to be able to deal with stress
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19
Q

what is another word for negative thoughts

A

rumination

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20
Q

what can cause rumination (negative thoughts)

A
  • When rumination (negative thoughts) occurs this is due to hyperactivity of the amygdala and hippocampus which causes hyperactivity in the VLPFC and DLPFC
21
Q

name 4 main antidepressant drugs

A

Tricyclic antidepressants
MAO inhibitors
SSRIs – selective serotonin reuptake inhibitors
Reversible MAO inhibitors

22
Q

Tricyclic antidepressants

  • examples
  • mechanism of action
  • side effects
  • other notes
A

Examples; - clomipramine, imipramine, desipramine, amitriptyline, nortriptyline, protriptyline
Mechanism of action;
- Inhibit reuptake of amines (noradrenaline and serotonin)
Side effects;
• Adverse effects: dry mouth, blurred vision, constipation, urinary retention, aggravation of narrow angle glaucoma, fatigue, sedation, weight gain, postural hypotension, dizziness, loss of libido, arrhythmias = mainly due to binding of cholinergic receptors
• Dangerous in overdose – they can cause cardiotoxicity

Characteristics
• Different degree of selectivity for amines between them (5-HT vs. noradrenaline)
• Have affinity for H1, muscarinic, α1 and α2 adrenoceptors

23
Q

MAO inhibitors

  • examples
  • mechanism of action
  • side effects
A

Examples; phenelzine, tranylcypromine, iproniazid
- Treatment of atypical depression is what they are more effective in

Mechanism of action;
• Non-selective MAOA versus MAOB
• Interaction with pethidine and sympathomimetic compounds

Side effects
• Cheese reaction - Interactions with tyramine-containing food (mature cheese, pickled fish and meat, red wine, beer, broad bean pods, yeast extract)- restrictions continue at least 2 weeks after discontinuation = can cause hypertensive crisis
• Hepatotoxicity

24
Q

Selective serotonin reuptake inhibitors

  • examples
  • mechanism of action
  • positives about the drug
  • side effects
A

Examples; Clitalopram, fluoxetine, paroxetine
- Efficacy comparable to tricyclic compounds

Mechanism of action

  • Increased selectivity for serotonin reuptake (citalopram the most selective)
  • Inhibit serotonin reuptake increasing the amount of serotonin

Positives;

  • No anticholinergic activity
  • No cardiotoxic effects
  • Safe in overdose

Side effects
- Adverse effects: nausea, headaches, gastrointestinal problems, increased aggression, insomnia, anxiety, sexual dysfunction

25
Q

what is a recently introduced drug

A

More recently introduction of S-isomer of citalopram; escitalopram

26
Q

reversible monamine oxidase inhibitors

  • examples
  • mechanism of action
  • side effects
A

Examples = Moclobemide

Mechanism of action;
• Increased selectivity for MAOA
• Safer than irreversible MAOIs
• Efficacy comparable to MAOIs

Side effects
• Adverse effects: nausea, agitation, confusion
• can start medication straight away
• Reduced cheese effect as they have less time present in body

27
Q

What is another name for reversible monamine oxidase inhibitors

A

RIMA

28
Q

name a serotonin noradrenaline reuptake inhibitor

A

Venlafaxine

- Block monoamine reuptake but they have no affinity for other targets

29
Q

name a noradrenaline reuptake inhibitor

A

Reboxetine

30
Q

name a noradrenergic and specific serotonergic antidepressant

  • mechanism of action
  • side effects
  • other
A

Mirtazapine

Mechanism of action
- Antagonist at alpha-2 adrenergic receptors

Side effects

  • Cause drowsiness as they have an affinity for H1 receptors
  • Sedation
  • Dry mouth
  • Constipation

Other
Exert antagonist effects at 5HT2 and 5HT4 receptors

31
Q

name a serotonin agonist and reutpake inhibitor

A

mainly antagonism at 5-HT2 receptors and serotonin reuptake inhibition) = trazodone

Tianeptine (enhancer or positive allosteric modulator of 5-HT uptake; also atypical mu opioid receptor agonist)

32
Q

what is the mechanism of action of agomelatine and what does the treatment do

A

Mechanism of action

  • agonist at melatonin MT1 and MT2 receptors and antagonist at 5-HT2c receptors
  • (may act as a noradrenaline/dopamine disinhibitor);
  • onset of effect in the first week of treatment;
  • improves sleep quality;
  • less sexual dysfunction than SSRIs;
  • anxiolytic effects; no discontinuation syndrome
33
Q

why do antidepressant drugs have a delayed onset of action

A

 Antidepressants have a delayed onset of action.
 This is believed to be because of somatic neuronal auto receptors.
 Their activation by the drugs causes decreased neuronal firing.
 It takes some time for these auto receptors to de-sensitize, but when they do the
neurones will return to firing at a normal rate.
 Inhibition of reuptake continues, and the level of amines rises.

34
Q

why might some patients stop taking antidepressants in the first few weeks

A
  • only feel the negative effects of the drug first until the auto receptors become densistise and then they feel the positive effects
35
Q

what is antidepressant drug discontinuation syndrome

A
  • A condition that can occur after a decrease in the dose of drug taken, an interruption of treatment or abrupt cessation of treatment; it can be prevented by a very gradual discontinuation of treatment, by using a very slow tapering of the doses taken by the patient
  • see the symptoms
36
Q

What are the symptoms of antidepressant drug discontinuation

A
  • Insomnia
  • Anxiety
  • Nausea
  • Headaches
  • Electric shock sensations
  • Agitation
  • Mood swings
  • Diarrhoea/abdominal cramps
37
Q

what is the definition of bipolar

A

– A mood disorder characterised by cycles of depression and mania

38
Q

what is the main choice of drug for bipolar disorder

A

lithium

39
Q

describe how lithium works and the characterises of it

A
  • Used as maintenance treatment in bipolar disorder (and also acute mania and drug-resistant depression) – gets rid of the bipolar cycles
  • Narrow therapeutic margin (0.6-1 mM)
40
Q

what are the adverse effects of lithium

A
  • Renal and thyroid function must be checked before treatment (and then at regular intervals during maintenance treatment)
  • Adverse effects: thirst, nausea, fine tremor, polyuria, weight gain, oedema, acne
41
Q

name some mood stabilisers that can be used in bipolar

A

carbamazepine

sodium valproate

42
Q

what is important to note for antidepressant drugs used in bipolar

A
  • they can precipitate the manic episodes or mixed affective states
  • can also increase the frequency in mood change cycles
43
Q

what are the order of risk for mania switch

A

TCAs > SNRIs > MAOIs > SSRIs

44
Q

What are the phases of treatment for depression

A

Acute treatment

  • First 6-12 weeks of treatment; aims at remission (control of symptoms)
  • Inadequate early response is associated with poor prognosis

Continuation treatment
- for 6 months after full symptom control; to maintain remission status and prevent relapse

Maintenance treatment

 - Aims at prevention of recurrence of a further episode of depression. 
 - Indicated when higher risk of these recurrence; “maintenance dose”.
45
Q

What is the criteria for choosing an antidepressant drug

A
  • The clinical characteristics of depression
  • The adverse effects profile
  • The danger of suicide/overdose
  • The response to previous treatments
46
Q

How do you define resistance to drugs treatment in depression

A
  • Lack of clinical response after adequate pharmacotherapy has been prescribed (at least two different antidepressant drugs)
  • Affects a large number of patients (conservative estimate: 25-30%)
47
Q

What are the non pharmacological approaches for depression treatment

A
  • electroconvulsive therapy (treatment-refractory severe depression with suicide risk)
  • Cognitive behavioural therapy (CBT) (can augment the effects of pharmacological treatment)
  • Vagal nerve stimulation (especially in chronic depression)
  • Deep brain stimulation (subcallosal cingulate white matter – Brodmann area 25)
48
Q

Describe how deep brain stimulation can be used to treat depression

A
  • Focuses on areas 25 the subgenual cingulate cortex –

- Links of this area to striatium, dorsal frontal cortex, orbitofrontal cortex

49
Q

name a scale that can be used to rate depression

A

Hammerton depression scale

Brain and Behaviour Year 2 (36 decks)

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