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Brain and Behaviour 2 PBL > PBL 4 > Flashcards

PBL 4 Flashcards

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1
Q

what is the definition of depression

A

being persistently sad for weeks or months rather than a few days

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2
Q

definition of citalopram

A
  • Citalopram – type of antidepressant that is known as an SSRI
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3
Q

definition of mirtazapine

A
  • Mirtazapine- alpha adrenoreceptor antagonist increasing noradrenergic and serotonergic neurotransmission
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4
Q

definition of CBT

A
  • CBT- this is a therapy that is psychosocial intervention in order to improve behaviours, finds different ways of thinking
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5
Q

definition of mental state exam

A
  • Mental state exam – this is a structured way of observed and describing a patients current state of mind, attitude, behaviour, mood speech, thought processes
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6
Q

name 4 different types of depression

A
  • Major depression:
  • Bipolar Disorder:
  • Dysthymic Disorder:
  • Depressive Disorder:
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7
Q

describe 4 different types of depression

A

• Major depression: at least two weeks of low mood present across all situations.
• Bipolar Disorder: switching between episodes of severe depression and manic highs.
• Dysthymic Disorder: serious state of chronic depression, which persists for at least two years.
• Depressive Disorder: depression that does not fit into other category.
o Disruptive Mood Dysregulation Disorder.

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8
Q

name some other types of depression

A

o Disruptive Mood Dysregulation Disorder.
o Premenstrual Dysphoric Disorder.
o Depressive order due to another medical condition (e.g. PD).

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9
Q

what are the DSMIV symptoms of depression

A

• Lowering of mood.
• Fatigue/loss of energy
• Diminished ability to concentrate
• Anhedonia: decreased enjoyment/interest in all or almost all activities.
o Loss of libido.
• Decreased appetite, weight loss or weight gain.
• Feelings of guild/worthlessness
• Thoughts about suicide, negative thoughts about the future.

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10
Q

define anhedonia

A

decreased enjoyment/interest in all or almost all activities. = loss of pleasure

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11
Q

name the ICD symptoms

A

ICD symptoms

  • Depressed mood
  • Loss of interest and enjoyment
  • Reduced energy leading to increased fatigability, diminished activity
  • Reduced concentration and attention
  • Reduced self-esteem and self-confidence
  • Ideas of guilt and unworthiness
  • Bleak and pessimistic views of the future
  • Ideas of – self harm, suicide
  • Disturbed sleep
  • Diminished appetite
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12
Q

what are the key symptoms of depression in the ICD

A

At least one of these, most days, most of the time for at least two weeks:
• Persistent sadness/low mood.
• Loss of interest or pleasure.
• Fatigue or low energy.

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13
Q

describe the ICD-10 classication

A

• Not Depressed: <4 symptoms

• Mild Depression: 4 symptoms
o Patient usually distressed by these but will probably continue most ordinary activities.

• Moderate Depression: 5—6 symptoms.
o Patient has great difficulty in continuing with ordinary symptoms.

• Severe Depression: 7 < symptoms, with or without psychotic symptoms.

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14
Q

describe the epidemiology of depression

A

• 12-month prevalence of major depression: 2-5 percent.
• Lifetime risk: 10-20 percent.
• Mean age of onset: about 27 years.
• High comorbidity with other disorders (anxiety, substance misuse).
(!) Twice as great in women as men (suicide more common in men).

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15
Q

who is suicide more common in

A

men

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16
Q

what is associated with high risk major depression

A

: 5-HT transporter polymorphism: associated higher risk major depression (after significant life events).

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17
Q

how might genetics cause depression

A

Genetic: may be expressed
• Directly through modification of relevant cortical circuitry.
• Indirectly through effects on psychological coping mechanisms.

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18
Q

how does adverse early life experiences cause depression

A

• Affect the development of the hypothalamus-pituitary-adrenal (HPA) axis and affect the neurobiological response to stress in adulthood.

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19
Q

How do current life experiences cause depression

A
  • Unemployed, divorced, poor social support.

* Physical illness (especially chronic/severe/painful).

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20
Q

describe the neurobiology changes that leads to depression

A

• Changes in activity monoamine neurons (reduced 5-HT, dopamine, noradrenaline), changes in HPA
o Involved in mood regulation.
• Endocrine disorders (e.g. hypothyroidism/Cushing’s) that can increase risk of developing depression.

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21
Q

what is non pharmacological treatment for depression

A

Electroconvulsive theraphy
• Treatment-refractory depression with suicide risk.

Cognitive Behavioral Theraphy
• Talking theraphy
• Looks at how we think about a situation and how this affects the way we act.
o The way we act impacts the way we think and feel.
• CBT tries to change this.

Inter-Personal Psychotherapy (IPT)
• Psychological symptoms (such as depressed mood), can reflect a response to current difficulties in relationships/affect the quality of these.
• IPT focuses on inter-personal conflicts, life changes and how you feel about yourself/other/grief/loss.

Deep Brain Stimulation
• Subcallosal cingulate cortex (area 25).

vagal nerve stimulation

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22
Q

in deep brain stimulation what area of the brain is stimulated

A

• Subcallosal cingulate cortex (area 25

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23
Q

what are the risk factors for suicide

A
  • Male Gender
  • Unemployed
  • Concurrent Mental Disorders
  • Previous Suicide Attempt
  • Alcohol/drug abuse.
  • Significant Life Events.
  • Low socio-economic
24
Q

name the brain regions that are associated with depression

A

• Amygdala
• Ventrolateral prefrontal cortex and dorsolateral prefrontal cortex.
o (!) There is decreased cortical thickness.
• Medial prefrontal cortex.
• Striatal regions.
• Hippocampus.

25
Q

what is the default mode network

A

• Network of brain regions active when the brain is at wakeful rest.
o Increased activity in depression.
• (!) Difference in the importance of the left subgenual cingulate area.

26
Q

describe the interaction between key structures involved in depression

A

• Amygdala/hippocampus = processing of emotional stimuli.
• In depression, hyper activation (RED) correlates with increased activity in subgenual cingulate cortex and MPFC (medial prefrontal cortex).
• In depression, there is decreased activation (BLUE) in PFC.
The balance between these causes an increase in rumination.

27
Q

what is CBT

A

CBT looks at how we think about a situation and how this affects the way we act. In turn our actions can affect how we think and feel. The therapist and client work together in changing the client’s behaviours, or their thinking patterns, or both of these. (1 mark for thinking and 1 mark for acting components in the answer)

28
Q

to what class of antidepressant does mirtazapeine belong and how is it thought to act as an antidepressant and through what mechanism does mirtazapine cause drowsiness as a side

A

i. It is a Noradrenergic and specific serotonergic antagonist (NaSSA) (1 mark)
It increases central noradrenergic and serotonergic transmission (1/2) through antagonism of presynaptic alpha2 adrenergic auto and heteroreceptors (1/2)

ii. Antagonism of the H1 histamine receptor (1 mark)

29
Q
  1. What is the “cheese effect” and why does it occur? What are its symptoms, and what class of drugs can induce this adverse effect? (3 marks)
A

The “cheese effect” manifests as severe headaches, and also a massive hypertensive crisis may occur (1 mark)

It is a reaction which reflects the interaction of irreversible monoamine oxidase inhibitors with food containing high levels of tyramine. (1 mark)

Normally tyramine is broken down in the gut and liver, but if this is prevented then tyramine can lead to elevated levels of noradrenaline in the synaptic cleft (1 mark)

30
Q
  1. Name two risk factors for depression-associated suicide. (1 mark)
A

Male gender, older age, unemployed, concurrent mental disorders, previous suicide attempt, alcohol and drug abuse, low socio-economic status, previous psychiatric treatment, certain professions - doctors, students, low social support, living alone, significant life events…

31
Q

name examples of tricyclic antidepressants and their mechanism of action

A 
Examples 
•	Clomipramine
•	Imipramine
•	Desipramine
•	Amitriptyline
•	Nortriptyline
•	Protriptyline

Mechanism of action
• Inhibit reuptake of amines.
o Different degree of selectivity for amines between them (mainly 5-HT vs noradrenaline).
• Have affinity for various other receptors e.g. H1, muscarinic alpha-1 and alpha-2 adrenoceptors.

32
Q

describe the adverse effects of tricyclics antidepressants

A
  • Dangerous in overdose (cardiotoxicity).

* Adverse effects: dry mouth, constipation, urinary retention, weight gain, postural hypotension, sedation etc…

33
Q

name some examples of MOA inhibitors and how they work

A 
Examples 
•	Phenelzine
•	Tranylcypromine
•	Iproniazid
MOA
•	Irreversible Inhibition of MOA
•	Non-selective MOAA versus MOAB.
- they are used in treatment of atypical depression (depression with anxiety, phobia and hypochondria)
34
Q

name the side effects of MAO inhibitors

A

• Cheese effect: tyramine (found in various cheese, red wine, beer etc…) is metabolised by MOA. Build up if inhibited.
o Causes severe headaches/hypertensive crisis.
• Interacts with pethidine (painkiller) and sympathomimetics.
• Hepatotoxicity.

35
Q

name an example of reversible MOA inhibitors (RIMA) and there mechanism of action

A

• Moclobemide

MOA
•	Increased selectivity for MOAA
•	SAFER than irreversible MOAIs
o	(!) Can switch to another medication almost immediately while in MOAs must wait. 
•	Higher efficacy vs MOAIs.
36
Q

What are the side effects of RIMA/reversible MOA inhibitors

A

• Adverse Effects: nausea, agitation, confusion

37
Q

name some examples of SSRIs and how they work

A 
Examples
•	Citalopram (active enantiomer is escitalopram
•	Fluoxetine
•	Paroxetine 
•	Sertraline

How they work

• Increased selectivity for serotonin reuptake
o (!) Citalopram the most selective: longer time for serotonin to be removed from synaptic cleft.
• NO anticholinergic activity.
• NO cardiotoxic effects.
• SAFE in overdose.

38
Q

What are the adverse side effects of SSRIs

A

nausea, headaches, gastrointestinal problems, increased aggression, insomnia, anxiety, sexual dysfunction.
o Serotonin is released from platelets (vasoconstriction).

39
Q

name a serotonin noradrenaline reuptake inhibitor and its mechanism of action

A
  • Venlafaxine

* Like TCAs: block monoamine re-uptake BUT they have no affinity for other targets (responsible for adverse effects).

40
Q

name a noradrenaline reuptake inhibitor and its mechanism of action

A
  • Reboxetine

* Block noradrenaline re-uptake. Limited in mild depression.

41
Q

name a serotonin antagonist and reuptake inhibitor and its mechanism of action

A

Trazodone

- antagonism at 5HT2 and alpha 2 adrenergic receptors

42
Q

name a noradrengerci and specific serotonergic antidepressant and its mechanism of action

A

• Mirtazapine.

  • Antagonist at alpha-2 adrenergic receptors
  • Affinity for histamine H1 receptors (causes drowsiness)
  • Exert antagonist effects at 5HT2 and 5HT3 receptors.
43
Q

What are the adverse effects of mirtazapine

A

• Adverse Effects: sedation, dry mouth, constipation.

44
Q

name an atypical antidepressants and its mechanism of action

A
  • Tianeptine

* Acts as an enhancer of serotonin re-uptake, but also has affinity at NMDA/AMPA glutamate receptors

45
Q

what 5HT receptors are responsible for inhibitor and excitatory neurotransmission

A

5HT1A: inhibitory neurotransmission.
5HT2: excitatory neurotransmission.

46
Q

how does agomelatine work

A

• Agonist at melatonin MT1 and MT2 receptors and antagonist at 5-HT receptors.
o Onset within 1 week of treatment
o Improves sleep quality and less sexual dysfunction vs SSRIs.

47
Q

describe the delay of action of antidepressants

A

Beneficial effects of antidepressants occur after a delay of a minimum of 4-6 weeks, while the onset of unwanted effects is much faster (possible reduced compliance)

48
Q

what are the phases of treatment

A

Acute Treatment: first 6-12 weeks.
Continuation Treatment: for 6 months after full symptom control.
Maintenance Treatment: aims at prevention of recurrence.

49
Q

what is the treatment for moderate and severe depression

A

• Combination of antidepressant medication and high-intensity psychological intervention (CBT/IPT).

50
Q

what is the treatment for continuation an in order to prevent relapse

A
  • Patients may need support/encouragement from other patient who has benefited from taking antidepressant, to continue for at least 6 months after remission of depression.
  • Important: reduces the risk of relapse
51
Q

name an adverse effect

A

antidepressant induced hyponatremia

52
Q

how does antidepressant induced hyponatraemia work

A

• Mechanism of this is related to the syndrome of inappropriate antidiuretic hormone (SAIDH).

• Serum sodium should be determined at baseline  2 weeks  4 weeks  3 months for high risk:
o Extreme old age (>80)
o History of hyponatraemia
o Co-theraphy other drugs (NSAIDs, chemotherapy, diuretics).
o Co-morbidity (COPD, diabetes, hypertension etc…)
o Reduced renal function.

53
Q

what are the signs and symptoms of antidepressant induced hyponatremia

A

dizziness, lethargy, nausea, confusion, cramps, seizures.

54
Q

what are the disorders of sexual dysfunction linked to antidepressants and why

A

• Disorders due to sedation, hormonal changes, disturbances of adrenergic/cholinergic balance, inhibition of NO, increased serotonin neurotransmission.
o Reduced libido
o Delayed orgasm
o Erectile dysfunction

55
Q

describe how antidepressants are linked to arrhythmia

A

 Sertraline: RECOMMDED post MI.
 Citalopram, moclobemide, lofepramine, venlafaxine: AVOID in those at risk of serious arrhythmias.

 All TCAs: AVOIDED completely at those at serious risk of arrhythmia.
o Dose related: blocks sodium and potassium channels.

56
Q

describe how antidepressants are linked to diabetes

A

 Depression has negative impact on metabolic control
 Poor metabolic control has impact on depression.

SSRIs = first line treatment (fluoxetine).
SNRIs = do not disrupt glycaemic control and have minimal impact on weight
All TCAs: AVOID (increase appetite, weight gain and hyperglycaemia).

57
Q

what happens in antidepressant discontinuation syndrome

A 
 Can occur after taking many drugs. Divided into:
o Neuromotor (ataxia)
o Vasomotor (diaphoresis = sweating)
o Neurosensory (paraesthesia = tingling)
o Other neurological (insomnia).
o Gastrointestinal (nausea).

Onset occurs usually within 5-days of stopping treatment.
 To avoid: theraphy should be discontinued over a 4-week period.

Brain and Behaviour 2 PBL (6 decks)

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