Mental disorders Flashcards

1
Q

What are the different anxiety related conditions?

A
  • Generalised anxiety disorder (GAD): worries about wide range of events
  • Panic disorder: reoccurring unforeseen panic attacks.
  • PTSD
  • Acute stress disorder
  • Specific phobias
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2
Q

What diagnositic tool can be used to diagnose anxiety?

A
  • GAD7

- PHQ9

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3
Q

What managements can be used for anxiety?

A
  • CBT (notice the thought and consequence in different circumstances - focus on the thoughts and how much you believe it).
  • beta blockers (can be used to lower HR and treat palpitations that patients experience)
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4
Q

What is the glucocorticoid receptor hypothesis?

A

During depression cortisol is found to be very high due to negative feedback mechanisms being dysfunctional. This causes changes to the neurons in the hippocampus.

50% of Cushing’s syndrome patients suffer from depression. and 50% patients with moderate depression show increased cortisol levels

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5
Q

What is the neurotrophic hypothesis?

A

Increased glutamate in depression causes cellular atrophy and decrease brain derived neurotrophic factor (BDNF) which usually protects neurons

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6
Q

What is the immunological hypothesis?

A

Depression can mimic the sick role due to raised inflammatory cytokines and interleukins.

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7
Q

What is the monoamine hypothesis?

A

Patients with depression have low levels of monoamines which are required for regulating mood.

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8
Q

How does Citalopram work?

A

Limits monoamine reabsorption into the pre-synaptic cell, therefore increasing the levels of monoamines available to the post-synaptic receptor. This means it works based on the monoamine hypothesis.

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9
Q

What are the two main tool used to assess the degree of depression?

A
  • Hospital Anxiety and Depression (HAD) scale
  • Patient health questionnaires (PHQ-9)
  • NICE use the DSM-IV criteria to grade depression
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10
Q

What is the delivery of individual CBT for patients with depression?

A
  • typically 16-20 sessions over 3-4 months
  • consider 3-4 follow-up sessions over the next 3-6 months
  • for moderate or severe depression, consider 2 sessions per week for the first 2-3 weeks
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11
Q

What is the delivery of interpersonal therapy (IPT) for patients with depression?

A
  • typically 16-20 sessions over 3-4 months

- for severe depression, consider 2 sessions per week for the first 2-3 weeks

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12
Q

What is the delivery of behavioural activation for the patients with depression?

A
  • typically 16-20 sessions over 3-4 months
  • consider 3-4 follow-up sessions over the next 3-6 months
  • for moderate or severe depression, consider 2 sessions per week for the first 3-4 weeks
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13
Q

What is the delivery of behavioural couples therapy?

A

typically 15-20 sessions over 5-6 months

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14
Q

What is SSRIs used to treat for?

A

Depression, PTSD, Anxiety and OCD

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15
Q

What is the mechanism of SSRIs?

A

Block serotonin re-uptake transporters (SERT)

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16
Q

Examples of SSRIs?

A
  • Citalopram
  • Escitalopram
  • Fluoxeline
  • Fluoxamine
  • Paroxeline
  • Sertaline
17
Q

Side affect of SSRIs - with excess stimulation in brain

A
  • Insomnia
  • Irritability
  • Anxiety
18
Q

Side affect of SSRIs - with excess stimulation of spinal serotonin receptors

A
  • Sexual side affects: erectile dysfunction
19
Q

Side affect of SSRIs - with excess stimulation in serotonin receptor in GI tract

A

Nausea
vomiting
diarrhoea

20
Q

What is the mechanism of SNRIs?

A

Block serotonin and norepinephrine re-uptake transporters = thus increase serotonin and norepinephrine levels

21
Q

What is SNRIs used for?

A
  • depression

- reduce pain e.g fibromyalgia and other neuropathic pain

22
Q

Examples of SNRIs

A
  • Venlafaxin
  • Desvelfaxine
  • Duloxeline
  • Levomilnacipram
23
Q

What are the side affects of SNRIs?

A

Same as SSRIs but due to its affect on noradrenergic receptors, it can increase BP and HR.

24
Q

What is the mechanism of tricyclic antidepressant (TCA)?

A

Blocks serotonin and norepinephrine transporters HOWEVER different ones have different selectivity.

TCAs also block alpha 1 receptor, histamine receptor and muscarinic receptors

25
Examples of TCAs
- Amitriptyline - Amoxapine - Clomipramine - Desipramine - Doxepine - Imipramine - Maprotiline - Nortriptyline - Protriptyline
26
Side affects of TCAs: inhibition of alpha 1 receptor
decreased BP and dizziness
27
Side affects of TCAs: inhibition of histamine receptor
sedation
28
Side affects of TCAs: inhibition of muscarinic receptor
leads to anti-cholinergic affects such as blurred vision, dry mouth, constipation and urinary retention
29
TCAs can also block sodium channels, what affect can this cause?
affects similar to anti-arrhythmic agents such as quinidine - leading to cardiac conduction abnormalities
30
What are the two subtypes of Monoamine oxidase ?
MOA-A - metabolise serotonin (5-HT), and a little of norepinephrine (NE) and dopamine (DA) MAO-B - mainly metabolise dopamine
31
What does MOAIs do?
stops the breakdown of serotonin, norepinephrine and dopamine
32
Examples of MAOIs
- Isocarboxazide - Phenelizine - Tranglcypromine - seleginline (type B - used for parkinsons)
33
mechanism of MAOIs in the gut
Stops the metabolism of tyramine which is in food that is aged or fermented - building of tyramine release catecholamines - this leads to hypertensive crises - STROKE. SO.... patients advised to avoid tyramine rich foods
34
Mechanism of Atypical Anti-depressant: Bupropion
stops NET and dopamine re-uptake transporter (DAT)
35
Mechanism of Atypical Anti-depressant: Mirtazapine
alpha 2 antagonist - used for sedation
36
Mechanism of Atypical Anti-depressant: Trazodone and Nefazadone
blocks SERT and 5-HT receptors, histamine and alpha 1 receptors. Used for sedation
37
Mechanism of Atypical Anti-depressant: Vilazadone
stimulating serotonin receptors (5-HT) and block SERT
38
Mechanism of Atypical Anti-depressant: Vortiaxeline
Inhibit SERT