Mood disorders Flashcards

1
Q

What are the main classes of psychiatric disorder?

A
  • Psychoses (e.g. schizophrenia, bipolar, delusional disorder, drug-induces psychoses)
  • Mood and anxiety disorders (neuroses)
  • Eating disorders
  • Substance use disorders
  • Organic disorders
  • Childhood disorders
  • Personality disorders
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2
Q

What do mood disorders involve?

A

they involve a fundamental disturbance of
mood, usually accompanied by a change in activity level and other resultant symptoms
- They range from mild/bordering normality, to severe psychotic depression with hallucinations and
delusions

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3
Q

What are the two distinct types of mood disorder?

A

Unipolar – where mood changes are always in the same direction

Bipolar – where depression alternates with mania

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4
Q

Symptoms of depression

A

*Depressed mood – pervasive low mood
* Anhedonia
* Lethargy and reduced energy
 Reduced concentration and functional
impairment
 Impaired self-confidence; social withdrawal
 Absence from work, relationship dysfunction
 Ideas of guilt, anxiety, panic
 Ideas/acts of self-harm/suicide
Disturbed sleep (early morning wakening)
 Diminished appetite; reduced libido;
amenorrhoea
 Feelings of hopelessness and helplessness
 ‘Mood-congruent’ delusions and
hallucinations
 Diurnal variations in mood (morning worst)

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5
Q

Symptoms of mania

A
Abnormally elevated/irritable mood
for at least one week
 Inflated self-esteem
 Reduced need for sleep
 Pressure of speech
 Racing thoughts
 Distractibility (useful for carers)
 Increase in goal directed behaviours
 Excessive pleasure seeking (drugs, sex) with harmful consequences
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6
Q

Describe course of illness of unipolar depression

A

average length of episode is 6 months, recovery from individual episodes is expected but
commonly persistent ‘subthreshold’ symptoms. Also 12-20% do not recover, and develop chronic
depression

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7
Q

Describe course of illness of bipolar depression

A

average length of manic episode is about 6 months, recovery from individual episodes is
expected but commonly there are persistent ‘subthreshold’ symptoms which are mainly depressive

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8
Q

Risk factors of unipolar depression

A

Lifetime risk = 10-20%
 Female (2x more common than men)
perhaps as more likely to ‘ruminate’ over
thoughts
 Early adulthood (mean age of onset is 25 yrs)
 Previous episode (60% people experience
recurrence)
~75% is non-familial with a clear association with
stressful life events. Often with symptoms of anxiety
or agitation – reactive depression

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9
Q

Risk factors for bipolar depression

A

Lifetime risk = 0.5-1%
 Equal sex incidence
 Teenage (mean age of onset is 17 yrs)
 Previous episode (90% recurrence)

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10
Q

Discuss monoamine hypothesis of depression

A
  • caused by functional deficit of monoamine transmitters at certain areas of brain, where mania is excess
  • unlikely to be the whole story, complex disease with many interacting factors
    ‘In people not at high risk of depression, monoamine depletion does not cause clinical depression, but in
    those who are at risk (having previously had an episode) then depletion causes clinical recurrence’
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11
Q

Describe links between HPA axis and depression

A
  • depressed patients hypersecerete cortisol
  • patients with Cushing’s have a higher frequency of depression, resolves when cortisol is lowered
  • high cortisol = brain atrophy and cognitive decline
  • It has been proposed that continual exposure to cortisol due to stressful events can cause
    death in hippocampal neurons, and this hippocampal degeneration sets off a vicious cycle
    where the stress response becomes more pronounced and more hippocampal damage
    ensues
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12
Q

Discuss depression and abnormal circuitry

A

fMRI studies of depressive patients suggest an
overactivity of the limbic system (emotional perception and appraisal) and underactivity of cortical
regulatory areas (dorsolateral prefrontal cortex).

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13
Q

Effective psychological treatments for unipolar depression

A

Persistent mild depression – guided self-help programme based on cognitive behaviour therapy
(psychotherapeutic approach that addresses dysfunctional emotions, maladaptive behaviours and
cognitive processes through a number of goal-orientated, explicit systematic procedures)
If not responsive then can have cognitive behaviour therapy, or interpersonal therapy (also couples
therapy if appropriate). Antidepressant drugs can also be prescribed with SSRIs as first line.
Moderate/severe depression should be treated with a combination of antidepressants and a high intensity
psychological intervention

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14
Q

Effective psychological and social treatments for bipolar depression

A

Psychological treatments which have been shown to be effective are CBT, interpersonal therapy and
family-focused therapy. Improves long-term prognosis especially if given early on in illness, as they have a
strong education component.
However in contrast to unipolar, medication plays a more important role. Conventional antidepressants do
not seem to be generally effective and also can cause a manic switch. Lithium treatment (stabilisation of
mood) is still the mainstay but may need to be augmented by atypical antipsychotics.

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15
Q

What are the main classes of antidepressants?

A
  • tricyclics
  • SSRIs
  • MAO inhibitors
  • selective serotonin and noradrenaline reuptake inhibitors (SNRIs)
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16
Q

Example of tricyclic antidepressant

A

Amitrypilline

17
Q

Mechanism and side effects of tricyclics

A

The first class of drug used to manipulate the monoamine levels
 Primary mechanism = inhibit reuptake of NA and 5-HT
 They are still in use today + have proven effective in treating depression
 But have unwanted side-effects
o The anti-muscarinic actions of TCAs can  dry mouth, blurred vision, constipation
and urinary retention
o More seriously, risk of arrhythmias and heart block, which can lead to sudden
cardiac death

18
Q

Example of SSRI

A

Fluoxetine

19
Q

Example of selective serotinin and noradrenaline reuptake inhibitor

A

Venlafaxine

20
Q

Describe SNRIs and SSRIs

A

Relatively mild side-effects

 Decreased overdose toxicity in comparison to TCIs and MAOIs

21
Q

Example of MAO inhibitor

A

Phenelzine

22
Q

What do MAO inhibitors do? Side effects?

A

Block the enzymatic degradation of NA and 5-HT, resulting in increased levels of these NTs
in the synaptic cleft
 Effective
Side effects:
- cheese reaction → normally harmless amines (such as tyramine) are ingested and are
normally broken down by MAO in the gut and liver so only small amounts reach circulation.
However, when MAOIs are present, these are absorbed and can result in acute
hypertension, throbbing headache and can even lead to intracranial haemorrhage due to its
sympathomimetic effect. These amines are commonly found in ripe cheeses.
o Hypertension

 Risk of SEs has been reduced through development of reversible, selective inhibitors
targeting either MAO-A or MAO-B

23
Q

Origin of monoamine theory of depression

A

1965, when it was discovered that substances such as
reserpine, an antihypertensive drug that reduces monoamine levels, administered lead to
some patients developing MDD

24
Q

Discuss lithium

A

Mood stabiliser
Many proposed mechanisms
interacts with a number of neurotransmitters and receptors, decreasing norepinephrine release and increasing serotonin synthesis

25
Q

Classification of anxiety disorders

A
Panic disorder 
Phobias
OCD
PTSD
General
26
Q

List the anxiolytics we need to know

A
GABA potentiation (barbiturates, benzodiazepines) → also have sedative effects 
5HT1 agonists (buspirone is a 5-HT1a agonist → autoreceptor → reduces firing rate of serotonergic neuron) 
B-blockers (propranolol)
27
Q

Side ffects of benzos

A
  • sedating/muscle relaxing
  • drowsiness/dizziness
  • decreased libido and erection
  • hypotension
  • nausea
  • cognitive impairment long term
    dependence!