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PA20023 > Mood disorders and their treatment > Flashcards

Mood disorders and their treatment Flashcards

1
Q

What is mood?

A

The conscious state of mind or predominant.

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2
Q

What are mood disorders?

A

Psychological abnormal elevation or lowering of mood. They are the leading cause of psychiatric disability and suicide.

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3
Q

What does it mean that mood disorders are disorders of emotion and not cognition?

A

They can still think and reason.

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4
Q

What are the most common brain disorders?

A

Anxiety disorders, headaches, addiction and sleep disorders.

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5
Q

What is the normal state of mood called and what does it involves?

A

Euthymia. Normal state of mood also includes happiness and sadness at different times.

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6
Q

What is dysthymia?

A

It includes mild depression that those without mood disorders can experience due to bereavement. They individual is still able to function and interact with the environment.

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7
Q

What is cyclothymia?

A

Switching between depressed states and mania.

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8
Q

What is the difference between type II and type I bipolar?

A

Type II experiences hypomania whereas type I experiences a full manic episodes.

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9
Q

What is the difference between sadness and depression?

A

Sadness is a normal human emotion that is usually triggered by an event. When adjusted, the sadness fades. Depression is an abnormal mental condition involving feelings of adequacy and guilt and lack of energy. It can be progressive and unremitting.

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10
Q

What is the prevalence of mood disorders?

A

7%.

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11
Q

What is the ratio of depression, in terms of gender?

A

Female:male 2.5:1.

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12
Q

What is the difference between reactive depression and endogenous depression?

A

Reactive depression makes up 75% of cases. It is non-familial and associated with stressful events. It is usually temporary. Endogenous depression makes up 25% of cases and is usually inherited. It is not related to external stressors and is more likely to be episodic and chronic.

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13
Q

Despite the differences, what is similar for reactive and endogenous depression?

A

The treatment for both conditions is the same.

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14
Q

What are some of the emotional components of depression?

A

Misery, apathy, pessimism, negative thoughts, loss of self-esteem, lack of motivation.

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15
Q

What are some of the biological components of depression?

A

Retardation of thought, slowness of action, loss of appetite.

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16
Q

What are some of the diagnostic criteria for the diagnosis of depression?

A

Depressed mood for most of the day or diminished pleasure in everyday activities, weight loss/gain, insomnia/hypersomnia, fatigue and loss of energy, impaired concentration.

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17
Q

What are the cause of mood disorders?

A

Genetic factors, neurotransmitter dysfunction e.g. monoamines, neuroendocrine, neurogenesis, glutamate and psychosocial/environmental factors such as life events.

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18
Q

What are the brain areas involved in mood regulation?

A

The frontal cortex, the hippocampus, the nucleus accumbens, the amygdala, the hypothalamus, ventral tegmental area, dorsal raphe nuclei and the locus coeruleus.

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19
Q

What is the frontal cortex involved in?

A

Cognitive function and attention.

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20
Q

What is the hippocampus involved in?

A

Cognitive function and memory.

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21
Q

What is the nucleus accumbens involved in?

A

Reward and aversion.

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22
Q

What is the amygdala involved in?

A

Responses to emotional stimuli.

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23
Q

What is the dorsal raphe nuclei involved in?

A

5HT input to other areas.

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24
Q

What is the locus coeruleus involved in?

A

Noradrenaline input to other areas.

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25
Q

What is the monoamine theory of depression?

A

That there is a functional deficit of 5HT and/or noradrenaline in the brain.

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26
Q

How was the monoamine theory of depression thought of?

A

Originally from observations that reserpine depletes NA/5HT vesicular stores and causes depression like behaviour in mice, isoniazid used for TB caued elevated ood and bloced MAO and that ECT for psychosis elevated mood caused increased amine metabolites.

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27
Q

What was the result of tryptophan on the brain?

A

It caused increased 5HT and resulted in an elevated mood.

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28
Q

What does tryptophan hydroxylase cause?

A

It caused a blockage of tryptophan and caused a depressed mood.

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29
Q

How do tricyclic antidepressants work?

A

They were developed for psychosis and cause elevated mood. They block amine re-uptake.

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30
Q

What is electroconvulsive therapy?

A

Using chemically and electrically induced convulsions. There is a muscle relaxant and the electrodes are bilateral or unilateral.

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31
Q

How was electroconvulsive therapy brought about for use in depression?

A

Schizophrenia and epilepsy were considered mutually exclusive so it was thought that inducing convulsions could prevent psychosis. It was found to elevate patients mood too.

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32
Q

What are problems with ECT?

A

Confusion and memory deficits and it is short lasting - it needs repetition.

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33
Q

What drugs can be used to treat depression?

A

Monoamine oxidase inhibitors - they elevate monoamines in the cytoplasm not the vesicles, and spontaneous leakage increases receptor activation.

34
Q

What was the first generation of antidepressants used?

A

Tricyclic antidepressants.

35
Q

How do first gen. antidepressants work?

A

They block the reuptake by nerve terminals. They elevate release of amines in the synaptic cleft.

36
Q

What causes the side effects of tricyclic antidepressants?

A

Postsynaptic receptors are blocked too such as muscarinic, ACh, histamine and 5HT.

37
Q

What are the clinical issues with tricyclic antidepressants?

A

They have major side effects such as sedation, postural hypotension, mania and convulsions. There are issues with confusion, respiratory depression and hypoxia.

38
Q

What drugs to tricyclic antidepressants interact with?

A

Alcohol, hypotensives, NSAIDs, MAOIs.

39
Q

What are SSRIs?

A

Selective serotonin reuptake inhibitors.

40
Q

What are the benefits of SSRIs compared to tricyclic amines?

A

There is a better side effect profile, it is safer in overdose and they may have a more rapid onset.

41
Q

What is the problem with the monoamine theory?

A

There are immediate short-term pharmacological effects but the clinical effects always take 4-8 weeks to onset. This suggests that there are chronic adaptive changes in response to antidepressants rather than acute ones.

42
Q

What does 5HT do in raphe nuclei?

A

They modulate the activity of the forebrain neurones via the multiple receptors.

43
Q

What is 5HT release controlled by?

A

Activation of inhibitory 5HT1aR on the raphe neurons.

44
Q

What happens initially with uptake blockers?

A

5HT release in the forebrain is decreased by increased 5HT1aR inhibiton of raphe neurones and reduced firing.

45
Q

What happens after uptake blockers have been used chronically?

A

Release of 5HT is increased by following desensitisation of 5HT1aR on raphe neurones and increased firing.

46
Q

What can the blockage of noradrenaline cause?

A

An increase of 5HT release as 5HT release is modulated by adrenergic receptors on soma and terminals of raphe neurones.

47
Q

What does block of te alpha1R receptor cause?

A

An increase of 5HT released in the forebrain and increases the NA released in raphe neurones.

48
Q

How is chronic stress thought to be a cause of major depression?

A

It causes increased glutamate and reduced BDNF in the hippocampus and frontal cortex. It results in neuronal damage and reduced neurogenesis, leading to depression.

49
Q

What are some of the limitations of antidepressants?

A

There is low efficacy, side efffects can deter use, there is a delay in onset and some older drugs are cardiotoxic.

50
Q

What might deter people from using antidepressants?

A

Side effects such as detachment and emotional blunting.

51
Q

What is cyclothymia?

A

Brief hypomania that alternates with brief milder depressive states. It is not as long lasting as seen in full mania or depressive episodes.

52
Q

What is mixed bipolar?

A

The occurrence of simultaneous symptoms of opposite mood - high energy, sleeplessness, racing thoughts that are concurrent with hopelessness, despair, irritability and suicidal ideations.

53
Q

What symptoms does mania involve?

A

Jolly, infectious, labile and repetitive moods. It involves distorted, excited and exaggerated thoughts along with hallucinations sometimes. Sleep is short but deep.

54
Q

What is needed to mania and hypomania to be diagnosed?

A

Elevated or irritable mood along with at least 3 of other symptoms including psychomotor agitation, excessive talking, flights of ideas, reduced need for sleep, distractibility and excessive involvement in activities with negative consequences e.g. spending sprees.

55
Q

How long do symptoms need to be present for diagnosis of mania?

A

Symptoms lasting a week or require hospitalization.

56
Q

How long do symptoms need to be present for the diagnosis of hypomania?

A

At least 4 days - changes in functioning but impairment is not marked.

57
Q

What is DIGFAST?

A

Distractibility, indiscretion, grandiosity, flight of ideas, activity up, sleep down and talkativeness.

58
Q

What is one of the cycling requirements for bipolar to be diagnosed?

A

Occurrence of four or more mood episodes during the last 12 months. There must be periods separated by full remission or by a switch to an episode of opposite polarity.

59
Q

Where is bipolar most prevalent?

A

Australia, Poland and the Netherlands.

60
Q

What is the average age of onset of bipolar disorder?

A

23-24 years old.

61
Q

What can be used to treat bipolar disorder?

A

Lithium, anticonvulsants and atypical antipsychotics.

62
Q

How does lithium work as a treatment for bipolar disorder?

A

It shows 80% stabilisation of mood and can often be given with antidepressants. It can be used acutely (only to treat mania) or prophylactically (used to treat mania and depression).

63
Q

What are the side effects of using lithium and how can this be monitored?

A

Lithium toxicity and this can be monitored using plasma monitoring.

64
Q

Why might anticonvulsants be used to treat bipolar disorder?

A

They have a faster onset and less side effects than lithium and control neuronal excitability.

65
Q

Why might atypical antipsychotics be used to treat bipolar rather than lithium?

A

They have a faster onset and are safer.

66
Q

What is thought about the link between schizophrenia and bipolar disorder?

A

As antipsychotics can be used to treat bipolar, it is thought there may be an overlap in the underlying mechanism between the two disorders.

67
Q

What are some of the acute side effects of lithium toxicity?

A

Polyuria and polydipsia, weight gain, aggravation/precipitation of skin disorders, tremors, nausea, vomiting, sluggishness.

68
Q

What are some of the chronic side effects of lithium toxicity?

A

Thyroid goitre, nephrotoxicity and hair loss.

69
Q

What is the hypothalamus involved in?

A

Sleep, appetite, energy, sex.

70
Q

What is the ventral tegmental area involved in?

A

Dopamine projections to other areas.

71
Q

What is noradrenaline involved in with mood?

A

Alertness, concentration, energy,

72
Q

What is 5HT involved in with mood?

A

Obsession, compulsion, memory, appetite, aggression, sex, anxiety, impulse, irritability

73
Q

What is dopamine involved in with mood?

A

Reward, motivation, appetite, aggression, sex

74
Q

What are some examples of irreversible non-specific MAOIs?

A

Phenelzine, tranylcypromine, iproniazid.

75
Q

Give an example of a reversible MAOA blocker?

A

Moclobemide.

76
Q

Give examples of a non-selective tricyclic antidepressant.

A

Imipramine, amitryptiline, clomipramine.

77
Q

Give examples of NA selective antidepressants.

A

Nortyptiline, desipramine.

78
Q

Give examples of SSRIs.

A

Fluoxetine, fluvoxamine, paroxetine, citalopram, sertraline.

79
Q

5HT selective SSRIs?

A

Citalopram, sertraline, fluvoxamine, peroxetine, venlafaxine, fluoextin.

80
Q

Give an example of a drug that is a serotonin and noradrenaline uptake inhibitor.

A

Venlafaxine - potentially has more rapid onset, lower side effect profile and is better in refractory patients.

81
Q

Give an example of a drug that is a noradrenaline and dopamine uptake inhibitor.

A

Bupropion - can be used to treat depression with anxiety, nicotine dependence and ADHD.

82
Q

Give examples of antidepressants that block monoamine receptors.

A

Mirtazapine, trazodone, mianserin.

PA20023 (17 decks)

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