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(UNI) Neuropharmacology (3rd Year) > Depression and Bipolar > Flashcards

Depression and Bipolar Flashcards

1
Q

How many patients, being served by a typical pharmacy serving 5000 patients, will be suffering from a mental health problem?

A

750.

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2
Q

How many patients, being served by a typical pharmacy serving 5000 patients, will suffer from mixed anxiety and depression?

A

300.

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3
Q

How many patients being served by a typical pharmacy serving 5000 patients, will suffer from depressive symptoms?

A

500.

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4
Q

How many patients, being served by a typical pharmacy serving 5000 patients, will suffer from undiagnosed depressive symptoms?

A

250.

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5
Q

How many patients, being served by a typical pharmacy serving 5000 patients, will suffer from bipolar disorder?

A

20

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6
Q

How many patients, being served by a typical pharmacy serving 5000 patients, will attempt suicide every year?

A

8.

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7
Q

How many patients, being served by a typical pharmacy serving 5000 patients, will successfully commit suicide every year?

A

At least once every 2 years.

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8
Q

What is the most common of the affective disorders?

A

Depression.

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9
Q

How can depression vary?

A

It varies in severity from mild (dysthymia: low grade but long term) to major depression, where delusions may occur (psychotic depression).

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10
Q

Define the term unipolar when it comes to affective disorder.

A

Low mood which alternates with normality.

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11
Q

Define the term bipolar when it comes to affective disorders?

A

Low mood which alternates with mania.

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12
Q

What is the prevalence of major depression?

A

Major depression has a lifetime prevalence of 2-4% in males and 5-9% in females.

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13
Q

What is the general age of onset for severe depression?

A

Mid to late 30s.

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14
Q

How long does most antidepressant therapy last for?

A

At least 6 months and up to 12 months after acute response to therapy.

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15
Q

In how many patients who recover from a single depressive episode is recurrence seen?

A

> 50%.

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16
Q

What percentage of depression cases are classified as reactive depression?

A

75%.

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17
Q

Define reactive depression.

A

Depression in response to external events.

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18
Q

What percentage of depression cases are classified as endogenous depression?

A

25%.

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19
Q

Define endogenous depression.

A

Depression caused by biological systems.

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20
Q

Do the available antidepression drugs differentiate between reactive and endogenous depression?

A

No.

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21
Q

What is the main criteria for the diagnosis of depression?

A

The DSM-IV Criteria for Major Depressive Disorder (MDD).

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22
Q

What does the DSM-IV Criteria for Major Depressive Disorder (MDD) include?

A
  • Depressed mood or a loss of interest or pleasure in daily activities for more than two weeks.
  • Mood represents a change from the person’s baseline.
  • Impaired function: social, occupational, educational.
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23
Q

Give some depression symptoms, of which 5 or more are required for a diagnosis of depression.

A
  • Depressed mood or irritable most of the day, nearly every day, as indicated by either subjective report. (Misery, apathy, pessimism.)
  • Decreased interest or pleasure in activities. Loss of motivation – Anhedonia.
  • Significant weight change (5%) or change in appetite.
  • Change in sleep patterns: Insomnia or hypersomnia.
  • Change in activity: Psychomotor agitation or retardation.
  • Fatigue or loss of energy.
  • Guilt, low self-esteem, feelings of inadequacy or worthlessness.
  • Diminished ability to think or concentrate, or more indecisiveness.
  • Loss of libido.
  • Suicidal thoughts.
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24
Q

What brain region is implicated in anhedonia and reduced drive in depression?

A

Reward system (VTA, NAcc).

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25
Q

What brain region is implicated in reduced energy seen in depression?

A

HPA axis.

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26
Q

What brain region is implicated in memory problems seen in depression?

A

The hippocampus.

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27
Q

What brain regions are implicated in attention and cognitive impairment seen in depression?

A

The prefrontal cortex and anterior cingulate.

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28
Q

What brain regions are implicated in anxiety seen in depression?

A

The limbic system, PAG, and the amygdala.

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29
Q

What brain region is implicated in the immune system issues seen in depression?

A

HPA axis.

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30
Q

What is the monoamine hypothesis of depression based upon?

A

It was based upon the recognition that patients taking reserpine for BP control became depressed and patients taking isoniazid for tuberculosis treatment became happier.

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31
Q

Define the monoamine hypothesis of depression.

A

From this it was postulated that a lack of amines leads to depression and too many amines lead to mania.

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32
Q

What class of drug is reserpine?

A

A monoamine reuptake inhibitor.

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33
Q

What class of drug is isoniazid?

A

An MAO inhibitor.

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34
Q

Based on the monoamine hypothesis for depression, drugs affecting which neurotransmitters may elevate mood?

A

NA/5HT.

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35
Q

Outline some pharmacological support for the monoamine hypothesis of depression.

A

Inhibiting reuptake and degredation of monoamines increases their concentration in the synaptic cleft. Reserpine, which depletes monoamines, exacerbates depression.

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36
Q

Outline some problems with the monoamine hypothesis.

A
  • The pharmacological effects are correlated with the blood plasma concentrations, but the therapeutic effects are delayed 3-4 weeks.
  • Some effective atypical antidepressants do not modulate amine levels in the synaptic cleft.
  • Cocaine potently inhibits the uptake of NADR but is not an effective antidepressant.
  • Precursor amino acids increase levels of amines but are not generally effective antidepressants.
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37
Q

What other hypothesis about depression have been proposed?

A

Genetic vulnerability, Stress triggers.

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38
Q

Describe the genetic vulnerability seen in some patients with depression.

A

Polymorphisms in the 5-HT transporter and the enzyme COMT show positive correlations with depressive symptoms.

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39
Q

Describe the changes seen in the HPA axis when someone has depression.

A
  • High levels of circulating cortisol.
  • Elevated levels of CRH in CSF.
  • Increased number of CRH-secreting neurons.
  • CRH binding sites reduced in frontal cortex.
  • Dysregulated circadian cortisol patterns.
  • Reduced hippocampal volume.
  • Increased amygdala sensitivity.
  • Blockade of CRF-1 receptors reduces anxiety and depressive symptoms.
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40
Q

What is the dexamethasone supression test?

A

Cortisol levels are generally high in depressed patients and fail to respond to challenge with a synthetic steroid, dexamethasone, which, in normal patients produces a decrease in cortisol levels.

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41
Q

Why is mild depression generally not treated?

A

Because the risk-benefit ratio is poor.

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42
Q

What psychotherapies are used to treat mild depression?

A
  • Cognitive behavioural therapy (CBT).
  • Self-help.
  • Talking therapies.
43
Q

What is important to remember when starting pharmacological therapy for the treatment of depression?

A

That the therapeutic effects of the drug may take a while to kick in. Some patients may in fact experience a mood dip before the drugs kick in.

44
Q

When may electroconvulsive therapy be used for the treatment of depression?

A

To treat the most severe, life-threatening depression.

45
Q

What other non-pharmacological interventions may be used to treat depression?

A

Electroconvulsive therapy (ECT), transcranial magnetic stimulation.

46
Q

What drug classes are used to treat depression?

A

Tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, atypicals (alpha-2-antagonists).

47
Q

Give some examples of tricyclic antidepressants used to treat depression.

A

Amitriptyline, chlomipramine, imipramine.

48
Q

Give some examples of irreversible monoamine inhibitors used for the treatment of depression.

A

Isocarboxazid, phenelzine, tranylcypromine.

49
Q

Give some examples of reversible monoamine inhibitors used for the treatment of depression.

A

Moclobomide.

50
Q

Give some examples of selective serotonin reuptake inhibitors used for the treatment of depression.

A

Citalopram, fluoxetine, fluvoxamine, paroxetine, sertraline.

51
Q

Give some examples of atypicals (alpha-2-antagonists) used to treat depression.

A

Mirtrazepine.

52
Q

How are atypicals thought to help in the treatment of depression?

A

They may increase the release of amines by blocking presynaptic receptors.

53
Q

What guides clinical judgement for the treatment of depression, as defined by NICE?

A
  • Previous response to treatment.
  • Tolerability of adverse effects.
  • Likely side-effect profile with regard to co-morbid conditions.
  • Lethality if history indicates suicide risk.
  • Cost.
54
Q

What class of antidepressants are used for the initial treatment of depression in adults? Why?

A

SSRIs. Because of better patient compliance.

55
Q

What are the initial pharmacological effects of tricyclic antidepressants?

A

They initially inhibit amine (NA and 5-HT) reuptake increasing concentration in the synaptic cleft.

56
Q

What are the later pharmacological effects of tricyclic antidepressants?

A

Later, further changes occur; reduction of presynaptic alpha-2 receptor sensitivity which enhances release and increased postsynaptic beta-1 receptor sensitivity which increases the efficacy of released neurotransmitters.

57
Q

Which effects, the beginning effects or later effects, are the most important to the pharmacological action of tricyclic antidepressants?

A

The later effects.

58
Q

What are the side effects of tricyclic antidepressants?

A

Blurred vision, dry mouth, urinary retention, constipation, excessive perspiration, postural hypotension, tachycardia, palpitations, sedation, weight gain.

59
Q

What drugs do tricyclic antidepressants interact with?

A

Alcohol, anaesthetics, hypotensive drugs, NSAIDs.

60
Q

What class of antidepressants must tricyclic antidepressants not be given with?

A

MAO inhibitors.

61
Q

At what times the therapeutic dose are tricyclic antidepressants toxic?

A

10x.

62
Q

Because fatalities may occur in tricyclic antidepressant overdose, how long of a treatment regimen should be given at one time?

A

One week.

63
Q

Do MAO-B selective inhibitory drugs have an antidepressant affect?

A

No.

64
Q

Give an example of a MAO inhibitor which is selective for MAO-A.

A

Moclobemide.

65
Q

What are the side effects of MAO inhibitors?

A

Hypertensive crisis, postural hypotension, weight gain, insomnia, restlessness, convulsions.

66
Q

What drugs should MAO inhibitors not be given with?

A

TCAs, SSRIs, or pethidine.

67
Q

How do SSRIs compare to TCAs or MAOis?

A

They are similar in efficacy and time course to TCAs however their acute toxicity less than TCAs or MAOis.

68
Q

What are SSRIs designed to target?

A

5-HT re-uptake.

69
Q

What are the side effects of SSRIs?

A

Nausea, insomnia, sexual dysfunction, increases in anxiety particularly during the first phases of treatment.

70
Q

What drugs, when used in combination with SSRIs, can lead to serotonin syndrome?

A

MAOis and MDMA.

71
Q

What are the symptoms of serotonin syndrome?

A

Confusion, hypothermia, muscle rigidity, cardiovascular collapse.

72
Q

Response to antidepressants is unlikely if the patient sees no response in how long?

A

4 weeks.

73
Q

What can be seen if antidepressant treatment is stopped abruptly?

A

Discontinuation symptoms.

74
Q

Continuation of antidepressant medication for how long can halve the relapse rate for depression?

A

> 6 months.

75
Q

What are the symptoms for antidepressant withdrawal?

A
  • Dizziness.
  • Numbness and tingling.
  • GI disturbances.
  • Headache.
  • Sweating.
  • Anxiety and sleep disturbances.
76
Q

In what percentage of the population does bipolar occur?

A

1%.

77
Q

How is bipolar disorder characterised?

A

It is characterised by dramatic mood swings, from overtly ‘high’ to the ‘low’ of very sad and hopeless.

78
Q

Define hypomania?

A

Hypomania is a reduced level of mania which may last for a few days.

79
Q

When do bipolar symptoms typically develop?

A

Symptoms typically develop in late adolescence/early adult hood, with half of cases being seen below the age of 25.

80
Q

Who show an increased incidence in developing bipolar? Men or women?

A

Women.

81
Q

Does bipolar show a genetic link?

A

Bipolar disorder shows a strong genetic component however the specific genes are unknown.

82
Q

Why may diagnosis of bipolar be difficult?

A

Diagnosis can be difficult since patients often enjoy the manic or hypomanic episodes so may only visit GP when depressed, also symptoms can be confused with anxiety or schizophrenia.

83
Q

A questionnaire may be used to aid diagnosis of bipolar disorder, what questions might this include?

A
  • Have you ever found yourself to be abnormally talkative and speaking very quickly?
  • Have you been so manic that people thought you were not yourself?
84
Q

Give the symptoms of the mania of bipolar disorder.

A
  • Overly good, euphoric mood.
  • Increased energy, activity and restlessness.
  • Racing thoughts, talking fast, jumping from one idea to the next.
  • Provocative, intrusive or aggressive behaviour.
  • Needs little sleep.
  • Unrealistic beliefs in one’s abilities and powers – delusions.
  • Increased sexual drive.
  • Abuse of drugs, particularly cocaine, alcohol and sleeping medications.
  • A denial that anything is wrong.
85
Q

Define cycling when it comes to bipolar disorder.

A

Cycling is the term given to the swinging of moods from lows to highs.

86
Q

At what rate may cycling in bipolar occur?

A

There is no set rate of cycling and it can be days, weeks, or months between swings.

87
Q

What are the treatment aims when it comes to bipolar disorder?

A

The aim of treatment is to suppress the cycling so it is maintained around normal mood.

88
Q

Why shouldn’t antidepressants be given for the treatment of bipolar disorder?

A

One shouldn’t give antidepressants because this will push the cycling profile up to more mania.

89
Q

What are the two principles in the treatment of bipolar disorder?

A
  • Short term control of acute mania.

* Long term (prophylactic) treatment to maximise the time interval between episodes.

90
Q

How is acute/overt mania controlled in bipolar disorder?

A

Overt mania is controlled with the neuroleptic olanzapine (NB: atypical antipsychotics not only block dopamine D2 receptors but also 5-HT2A receptors).

91
Q

If carbamazepine is used for the treatment of mania in bipolar, what should be noted?

A

Note the greater risk of cardiotoxicity and increased propensity for drug interactions.

92
Q

If sedation is a priority when treating mania in bipolar, what class of drugs should be used? Give an example.

A

Benzodiazepines e.g. lorazepam.

93
Q

What is the most commonly used drug for prophylaxis of mania as well as depression?

A

Lithium carbonate.

94
Q

How long does lithium carbonate have to be given for for it to build up in the system?

A

6 months.

95
Q

What classes of drugs can be given as mood stabilising drugs?

A

Anticonvulsants, neuroleptics.

96
Q

How long does complete lithium absorption take?

A

8 hours.

97
Q

Give examples of anticonvulsants which may be used as mood stabilising drugs.

A

Carbamazepine, valporate, gabapentin.

98
Q

What is the elimination half-life of lithium?

A

24 hours.

99
Q

What are the optimum blood levels of lithium when treating bipolar disorder?

A

0.5-1.2 mmol/L.

100
Q

At what blood concentration does severe lithium toxicity occur?

A

2 mmol/L.

101
Q

What percentage of patients can not tolerate the adverse side effects associated with lithium?

A

30%.

102
Q

What are the side effects of lithium used for the treatment of bipolar?

A
  • GI discomfort and nausea.
  • Neurological symptoms (which may dissipate) such as fatigue, malaise, muscle weakness.
  • Decreased water reabsorption by the kidney.
  • Weight gain. This is a frequent cause of non-compliance.
103
Q

At moderate lithium overdose, what adverse drug effects are seen?

A 
o	Vomiting.
o	Abdominal pain.
o	Dry mouth.
o	Ataxia.
o	Dizziness.
o	Slurred speech.
o	Lethargy or excitement.
o	Muscle weakness.
104
Q

At severe lithium overdose, what adverse drug effects are seen?

A 
o	anorexia nervosa.
o	persistent vomiting.
o	Blurred vision.
o	Muscle fasciculation.
o	Clonic limb movements.
o	Convulsions.
o	Delirium.
o	Syncope.
o	Coma.
o	Circulatory failure.

(UNI) Neuropharmacology (3rd Year) (20 decks)

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