Depression & its treatment Flashcards

1
Q

What are neurotransmitters:

A

Neurotransmitters are released from the nerve ending by a nerve impulse. They diffuse across the synapse (junction) and by interacting with post-synaptic receptors, effects the transfer of the impulse from one neuron to another

Noradrenaline
Serotonin

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2
Q

Basic Processes involved in neurotransmission:

A
  • Synthesis
  • Storage
  • Release
  • Inactivation/Reuptake
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3
Q

Noradrenaline Synapse:

A
Tyrosine
 (tyrosine hydroxylasae) Dopa
(Aromatic amino acid decarboxylase)
Dopamine 
(Dopamine B hydroxylase) 
Stored in vesicles
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4
Q

How can we increase noradrenaline?

A

We can block the reuptake
We can inhibit ezymes, meaning
We can inhibit breakdown
We can inhibit receptors also

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5
Q

Noradrenaline - Pathways:

A

Locus coeruleus noradrenergic projections

  • Alertness
  • Arousal
  • Sensory perception
  • Motor tone
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6
Q

Serotonin synapse:

A
-Tryptophan
(tryptophan hydroxylase) 
- 5 hydroxy tryptophan 
(aromatic amino acid decarboxylase)
- 5 hydroxy tryptamine 
- Vesicular monoamine transporter 
- Exocytosis into cleft
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7
Q

Serotonin pathway:

A

Serotonin pathways have a regulatory function in certain things:

  • Sleep
  • Food intake
  • Thermoregulation
  • Sexual behaviour
  • Pain
  • Motor tone

Raphe serotoninergic projections - projects throughout the CNS

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8
Q

Types of depression:

A

Unipolar:

  • Major Depressive Disorder
  • Dysthymia
  • Seasonal Affective Disorder
  • Postnatal Depression

Bipolar:
- Alternating periods of depression and mania

Characterised by duration – i.e. long term anxiety (everyone gets anxiety at some point)

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9
Q

Difference between mild and major depression:

A

In its mildest form, depression can mean being in low spirits. It doesn’t stop you leading your normal life, but makes everything harder to do and seem less worthwhile

At its most severe, major depression (clinical depression) can be life-threatening, because it can make you feel suicidal or simply give up the will to live

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10
Q

Brief overview of depression treatment;

A

CBT
Antidepressants
Exercise
ECT

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11
Q

Depression - Causes:

A
  • Life Events
  • Childhood Experience
  • Genetics
  • Chemical Imbalance
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12
Q

Relationship between neurotransmitter and symptoms of depression:

A

Emotional–>
- Loss of pleasure, interestest and motivation:
Dorso-lateral: PFC, DA

Sadness and suicide:
Ventro medial: PFC, 5HT, NE and DA

Somatic–>
- Fatigue, loss of energy:
DA, NE, 5HT

  • Sleep, appetite, libido etc:
    Nuceleus accumbens and hypothalamus: 5HT, NE, DA

Cognitive–>
- Attention, concentration, problem solving:
Dorso lateral: PFC, DA (D1), Ach, 5HT, NE , GABA, Histamine.

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13
Q

Antidepressant Drugs:

A
TCAs
SSRIs 
NaRIs
SNRIs
MAOIs
Atypical
Ketamine
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14
Q

Psychotherapy includes:

A
  • Talking therapy
  • Cognitive Behavioural Therapy
  • Counselling
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15
Q

Physical Interventions:

A
  • ElectroconvulsiveTreatment
  • Electromagnetic Therapy
  • Deep Brain Stimulation
  • Vagal Stimulation
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16
Q

Main problem with MAOI drugs ?

A

interactions with foods (and other drugs), which can be very severe
“Cheese reaction”

Dietary tyramine (found in particularly high levels in cheese and marmite) is absorbed as normal, but it is precursor for monoamine synthesis

As the MAO enzyme is inhibited —- huge rises in transmitter levels can occur when these foods are eaten

Large hypertensive response, often enough to cause haemorrhages, occurs. Very dangerous, and difficult to control patients’ protein intake levels/tyramine levels, so a major problem

Main reason MAOIs rarely used

17
Q

Depression treatment time scales:

A

Antidepressant Drugs: 2-4 weeks

Psychotherapy- weeks, months, years

Physical Interventions: immediately

18
Q

What is the mono amine hypothesis?

A

Depressive disorders are due to a depletion and mania to an excess provision of monoamine neurotransmitters at one or more CNS sites

Antidepressants correct this depletion by increasing the availability of monoamines at post-synaptic receptors

BUT
Effects on transmitters are immediate & antidepressant effects take several weeks to arise

Important to consider what secondary changes the altered monoamine levels have in the brain; these secondary changes may explain “antidepressant drugs” effects

19
Q

Stress, Neurogenesis and Antidepressants:

A

Stress can reduce neurogenesis
Good evidence that AD’s can increase neurogenesis but obviously takes time to make the new neurons and to migrate to a particular part of the brain
You can label markers and track them .

20
Q

SSRI’s physiology:

A

Serotinin acutely blocks the reuptake
Activation of receptors
Reduced serotnieric release

When you consistently block the reuptake you get a down regulation of all the receptors .
Ultimately you get restored release