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Therapeutics > Depression and Anxiety > Flashcards

Depression and Anxiety Flashcards

1
Q

How significant is depression as a contributor to the global burden of disease and disability?

A

Depression is a significant contributor to the global burden of disease and disability.

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2
Q

According to the WHO, how many people suffer from depression worldwide?

A

The WHO estimates that more than 280 million people of all ages suffer from depression.

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3
Q

How does the prevalence of depression differ between females and males?

A

Females are affected by depression at twice the prevalence of males.

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4
Q

How many deaths annually are a result of suicide linked to depression?

A

Around 700,000 deaths annually are a result of suicide linked to depression.

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5
Q

What is the rank of suicide as a cause of death in the age group 15-29 years?

A

Suicide is the 4th leading cause of death in the age group 15-29 years.

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6
Q

What are some risk factors for the development of depression?

A

Risk factors for the development of depression include environmental factors, social stressors, adverse events in early life, and genetic predisposition (increased risk with a first-degree family history).

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7
Q

DSM 5 Diagnostic Criteria: Major depressive disorder

A

A. ≥5 symptoms on most days for 2 weeks; that represent a change from previous functioning:
-Depressed mood and/or loss of interest must be present
-Weight loss/gain; insomnia or hypersomnia; psychomotor agitation/retardation; fatigue; feelings of worthlessness/guilt; decreased concentration; suicidal ideation

B. Symptoms must cause significant clinical impairment in functioning

C. Episode not attributable to direct physiological effects of a substance or underlying general medical condition

D. The occurrence of the major depressive episode is not better explained by presence of schizophrenia, delusional disorder or any other psychotic disorder

E. No history of a manic or hypomanic episode

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8
Q

What is the DSM-5 used for in relation to depression?

A

The DSM-5 is used to diagnose Major Depressive Episodes (MDE) and other depressive disorders.

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9
Q

Can depressive symptoms that do not meet the criteria for Major Depressive Episode still be significant?

A

Yes, depressive symptoms that don’t meet the criteria for MDE can still be distressing, disabling, and warrant intervention.

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10
Q

What other disorders may require treatment if depressive symptoms are present but do not meet MDE criteria?

A

Depressive symptoms that do not meet MDE criteria may meet diagnostic criteria for other disorders such as dysthymia or adjustment disorder with depressive symptoms, requiring treatment.

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11
Q

How do depressive disorders occur according to the DSM-5?

A

Depressive disorders occur along a spectrum, meaning they can vary in severity and presentation.

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12
Q

Is the exact pathophysiology of depression known?

A

No, the exact pathophysiology of depression is not known and likely involves the interplay of different mechanisms and genetic predisposition.

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13
Q

What are some hypotheses that explain the mechanisms contributing to depression?

A

Some hypotheses include the monoamine hypothesis, the neurotrophic hypothesis, and neuroendocrine factors.

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14
Q

What are the three most important neurotransmitters involved in depression?

A

The three most important neurotransmitters involved in depression are noradrenaline, serotonin, and dopamine.

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15
Q

How are monoamines classified?

A

Monoamines can be classified into catecholamines (dopamine, adrenaline, noradrenaline) and indolamines (serotonin, histamine).

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16
Q

What happens when a nerve impulse arrives at a 5-HT or noradrenergic nerve terminal?

A

The neurotransmitter is released from synaptic vesicles through exocytosis into the synaptic cleft.

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17
Q

What occurs after the neurotransmitter is released into the synaptic cleft?

A

The neurotransmitter binds to specific receptors on the post-synaptic membrane, and the nerve impulse is either propagated or inhibited, depending on the receptor type

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18
Q

How are 5-HT and noradrenaline molecules removed from their receptors?

A

5-HT and noradrenaline molecules are taken back into the nerve terminal via serotonin or noradrenaline re-uptake transporters

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19
Q

Which enzymes degrade neurotransmitters, and where are they found?

A

Neurotransmitters can be degraded by the enzymes MAO (monoamine oxidase) and COMT (catechol-o-methyltransferase), which are found in both the synaptic cleft and the nerve terminal.

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20
Q

Are the functions of different neurotransmitters and monoaminergic circuits in the CNS isolated or integrated?

A

The functions of different neurotransmitters and monoaminergic circuits in the CNS are closely integrated and overlap.

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21
Q

What does the monoamine hypothesis of mood postulate?

A

The monoamine hypothesis postulates that brain amines, specifically norepinephrine (NE) and serotonin (5-HT), are important in the pathways responsible for the expression of mood.

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22
Q

According to the monoamine hypothesis, what results from a functional decrease in the activity of brain amines?

A

A functional decrease in the activity of brain amines is thought to result in depression.

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23
Q

According to the monoamine hypothesis, what results from a functional increase in the activity of brain amines?

A

A functional increase in the activity of brain amines results in mood elevation.

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24
Q

What is the monoamine hypothesis mainly based on?

A

The hypothesis is mainly based on studies showing that drugs capable of alleviating symptoms of major depressive disorder (MDD) enhance the actions of these neurotransmitters.

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25
Q

What biological changes are hypothesized to be important in depression according to the monoamine theory?

A

The hypothesized biological changes include low levels of monoamine neurotransmitters, upregulation of inhibitory presynaptic and somatodendritic autoreceptors that control monoamine release, and upregulation of postsynaptic monoamine receptors.

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26
Q

What is one of the hypothesized biological changes in depression according to the monoamine theory?

A

One hypothesized change is low levels of monoamine neurotransmitters.

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27
Q

What is another hypothesized biological change in depression according to the monoamine theory?

A

Another hypothesized change is the upregulation of inhibitory presynaptic and somatodendritic autoreceptors that control monoamine release.

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28
Q

What is a third hypothesized biological change in depression according to the monoamine theory?

A

A third hypothesized change is the upregulation of postsynaptic monoamine receptors.

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29
Q

What problem does the monoamine hypothesis face regarding post-mortem studies?

A

Post-mortem studies do not show decreases in levels of 5-HT or NE.

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30
Q

What problem does the monoamine hypothesis face regarding the timing of antidepressant therapy effects?

A

Although amine activity changes within hours after starting antidepressant therapy, the clinical response can take up to 6-8 weeks

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31
Q

What problem does the monoamine hypothesis face with the use of Bupropion?

A

Bupropion, an antidepressant, has no activity on brain NE or 5-HT, which challenges the monoamine hypothesis.

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32
Q

Why is it a problem for the monoamine hypothesis that post-mortem studies do not show decreases in levels of 5-HT or NE?

A

It is a problem because the monoamine hypothesis predicts that depression is associated with low levels of these neurotransmitters, but post-mortem studies do not support this prediction, challenging the validity of the hypothesis.

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33
Q

What does the time course of changes with antidepressant drugs depict?

A

It depicts the different time courses and changes in effects of antidepressant drugs, including clinical changes, neurotransmitter changes, and receptor sensitivity changes.

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34
Q

How quickly do antidepressant drugs increase CNS monoamine concentrations?

A

Antidepressant drugs increase CNS monoamine concentrations rapidly.

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35
Q

How long can the full clinical response be delayed after the initiation of antidepressant therapy?

A

The full clinical response can be delayed until 6-8 weeks after the initiation of therapy.

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36
Q

Does the improvement in clinical condition mirror the increase in neurotransmitters?

A

No, the improvement in clinical condition does not mirror the increase in neurotransmitters.

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37
Q

What might the delay in full clinical response indicate?

A

The delay in full clinical response may suggest that other factors, such as the downregulation of receptors or the synthesis of new neurotrophic factors, are involved.

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38
Q

How might receptor changes contribute to the clinical response to antidepressants?

A

The clinical response may coincide with the downregulation of receptors.

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39
Q

What role might neurotrophic factors play in the clinical response to antidepressants?

A

The synthesis of new neurotrophic factors may be involved in achieving the full clinical response.

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40
Q

What does the neurotrophic hypothesis of depression postulate?

A

The neurotrophic hypothesis postulates that depression arises from abnormalities in neurotrophic pathways involving brain-derived neurotrophic factors (BDNF).

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41
Q

What are neurotrophic factors?

A

Neurotrophic factors are nerve growth factors that promote cellular growth, differentiation, and survival of nerves.

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42
Q

How is BDNF expression related to depression?

A

BDNF expression is reduced when monoamine transmission is impaired and in conditions of stress with increased serum cortisol, which is associated with depression.

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43
Q

What are the effects of decreased BDNF expression on the brain?

A

Decreased BDNF expression adversely affects neuronal plasticity, leading to loss of neuronal circuitry, atrophy, and structural changes in the hippocampus, medial frontal cortex, and anterior cingulate areas

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44
Q

What structural changes are associated with major depressive disorder (MDD)?

A

Structural imaging studies show that MDD is associated with a 5-10% loss of hippocampal volume.

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45
Q

What changes are associated with the successful treatment of depression?

A

Successful treatment of depression is associated with increased BDNF expression, restoration of hippocampal function, increased synaptic connectivity, and improved neuroendocrine regulation.

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46
Q

What neuroendocrine factors are associated with depression?

A

Depression is associated with the hypersecretion of corticotropin-releasing hormone (CRH) and cortisol.

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47
Q

How do CRH and cortisol affect the brain in depression?

A

CRH and cortisol have detrimental effects on neuroplasticity and neurogenesis, and may contribute to the suppression of BDNF.

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48
Q

How does elevated CRH affect serotonergic neurotransmission?

A

Elevated CRH depresses serotonergic neurotransmission.

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49
Q

How does antidepressant treatment affect BDNF and the hypothalamic-pituitary axis?

A

Antidepressant treatment improves chronic activation of monoamine receptors, increases BDNF transcription/expression, downregulates the hypothalamic-pituitary axis, and normalizes its function.

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50
Q

What is the TrkB receptor?

A

TrkB (Tropomyosin receptor kinase B) is a transmembrane receptor protein that is a receptor for brain-derived neurotrophic factors (BDNF).

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51
Q

How to antidepressants increase neurotransmitters in the synaptic cleft (MOA)

A
  1. Blocking the degradation of neurotransmitters
  2. Blocking neurotransmitters reuptake
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52
Q

How do antidepressants increase neurotransmitter levels in the synaptic cleft?

A

Antidepressants increase neurotransmitter levels in the synaptic cleft by blocking degradation of neurotransmitters or blocking neurotransmitter reuptake.

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53
Q

How do Monoamine Oxidase Inhibitors (MAOIs) work?

A

MAOIs work by blocking the degradation of neurotransmitters.

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54
Q

How do Selective Serotonin Reuptake Inhibitors (SSRIs) work?

A

SRIs work by blocking the reuptake of serotonin, resulting in more serotonin in the synaptic cleft.

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55
Q

How do Tricyclic Antidepressants (TCAs) work?

A

TCAs work by blocking the reuptake of neurotransmitters like serotonin and noradrenaline.

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56
Q

How do Serotonin and Noradrenaline Reuptake Inhibitors (SNRIs) work?

A

SNRIs work by blocking the reuptake of both serotonin and noradrenaline, increasing their levels in the synaptic cleft.

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57
Q

What is the result of blocking neurotransmitter degradation or reuptake?

A

The result is more neurotransmitter in the synaptic cleft for longer periods, allowing it to exert its effect.

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58
Q

What is another mechanism by which antidepressants can work?

A

Antidepressants can also work by inhibiting negative feedback via antagonism of autoreceptors, which normally stop the nerve from producing and releasing serotonin or noradrenaline.

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59
Q

Is there a significant difference in efficacy between antidepressants acting on different pathways (serotonergic, noradrenergic, dopaminergic)?

A

There is little difference in efficacy between drugs acting on different pathways, but their side effect profiles will differ.

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60
Q

How do SSRIs, SNRIs, and TCAs increase noradrenergic and/or serotonergic neurotransmission?

A

SSRIs, SNRIs, and TCAs increase neurotransmission by blocking the norepinephrine (NET) and serotonin (SERT) transporters at presynaptic terminals.

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61
Q

How do Monoamine Oxidase Inhibitors (MAOIs) work?

A

MAOIs inhibit the catabolism of norepinephrine (NE) and serotonin (5-HT), preventing their breakdown.

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62
Q

How do trazodone and related drugs contribute to their antidepressant effects?

A

Trazodone and related drugs have direct effects on serotonin (5-HT) receptors that contribute to their antidepressant effects.

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63
Q

Antidepressant drug classes

A
  1. Tricyclic antidepressants (TCA)
  2. Selective serotonin reuptake inhibitors (SSRI)
  3. Serotonin and noradrenaline reuptake inhibitors (SNRIs)
  4. Monoamine oxidase inhibitors (MAOi)
  5. Atypical antidepressants (NDRI)
  6. Noradrenaline Reuptake Inhibitors (NRIs)
  7. Serotonin Receptor Antagonist
  8. Tetracyclic antidepressants
  9. Melatonin Receptor Agonist + Serotonin Receptor Antagonist
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64
Q

Serotonin and noradrenaline reuptake inhibitors (SNRIs)

A

block serotonin reuptake at lower doses, at higher doses also block NA reuptake.

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65
Q

Monoamine oxidase inhibitors (MAOi)

A

reversible or irreversible inhibition of MAO A and B enzymes, leading to reduced degradation of NTs. Nice physiology so we will discuss in a little more detail.

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66
Q

Atypical antidepressants (NDRI)

A

noradrenaline and dopamine reuptake inhibitor. Mechanism of action for this drug still controversial. It displays weak reuptake blocking properties, and has no serotonergic effects. It is used for smoking cessation, with a low weight gain potential but is highly epileptogenic. Least likely sexual side effects.

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67
Q

Noradrenaline Reuptake Inhibitors (NRIs)

A

Inhibits NA reuptake only, but also able to enhances serotonergic neurotransmission via increased stimulation of somatodendritic alpha 1 receptors.

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68
Q

Serotonin Receptor Antagonist

A

Antagonism of the postsynaptic serotonin receptors in frontal cortex, increasing dopamine and noradren
aline. Antagonism of these serotonin receptors is associated with antidepressant effect.

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69
Q

Tetracyclic antidepressants

A

tetracycline antidepressants, act as antagonists at presynaptic alpha 2 receptors reducing negative feedback inhibition on serotonin and noradrenaline release, improving NT production/transmission. Enhances norepinephrine and 5hydroxytryptamine

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70
Q

Melatonin Receptor Agonist + Serotonin Receptor Antagonist

A

agonist of melatonin receptors, improving sleep quality, and a weak antagonist at serotonin receptors, increasing dopamine and NA release in frontal cortex.

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71
Q

Tricyclic antidepressants (TCA) drugs

A

Amitriptyline
Nortriptyline
Imipramine

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72
Q

Selective serotonin reuptake inhibitors (SSRI) drugs

A

Fluoxetine
Citalopram
Sertraline
Paroxetine
Escitalopram

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73
Q

Serotonin and noradrenaline reuptake inhibitors (SNRIs) drugs

A

Venlafaxine
Duloxetine

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74
Q

Monoamine oxidase inhibitors (MAOi) drugs

A

Selegiline
Phenelzine

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75
Q

Atypical antidepressants (NDRI) drugs

A

Bupropion

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76
Q

Noradrenaline Reuptake Inhibitors (NRIs) drugs

A

Reboxetine

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77
Q

Serotonin Receptor Antagonist drugs

A

Trazadone

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78
Q

Tetracyclic antidepressants drugs

A

Mianserine
Mirtazapine

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79
Q

Melatonin Receptor Agonist + Serotonin Receptor Antagonist drugs

A

Agomelatine

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80
Q

What can trigger a hypertensive crisis in a patient taking a monoamine oxidase inhibitor (MAOI) like phenelzine?

A

A hypertensive crisis can be triggered by the consumption of foods high in tyramine, such as aged cheese and certain wines.

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81
Q

Mechanism of action of MAOi

A
  1. MAO inhibition
  2. Tyramine accumulation
  3. Release of norepinephrine
  4. Vasoconstriction and increased blood pressure
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82
Q

How does MAO inhibition by phenelzine contribute to a hypertensive crisis?

A

Phenelzine inhibits the enzyme monoamine oxidase (MAO), which normally breaks down neurotransmitters and tyramine. When MAO is inhibited, tyramine is not efficiently metabolized and can be absorbed into the bloodstream.

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83
Q

What happens to tyramine in the body when MAO is inhibited?

A

Tyramine is not broken down efficiently and can accumulate in the bloodstream.

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84
Q

What effect does excessive tyramine have on norepinephrine?

A

Excessive tyramine causes the release of large amounts of norepinephrine from nerve terminals.

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85
Q

What are the effects of a sudden surge of norepinephrine in the bloodstream?

A

The sudden surge of norepinephrine leads to intense vasoconstriction and a rapid, significant increase in blood pressure, resulting in a hypertensive crisis.

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86
Q

What symptoms might a patient experience during a hypertensive crisis caused by MAOIs?

A

The patient might experience severe headache and elevated blood pressure, such as 200/100 mmHg, after consuming tyramine-rich foods or beverages.

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87
Q

Why have monoamine oxidase inhibitors (MAOIs) fallen out of favor as antidepressants?

A

MAOIs have fallen out of favor due to their adverse effects and interactions with certain foods and drugs.

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88
Q

What is the role of monoamine oxidase (MAO) enzymes?

A

MAO enzymes are responsible for the metabolism of monoamines, which are neurotransmitters located mostly in the CNS, with type A also found in the gut.

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89
Q

What are the two types of MAO enzymes, and what do they metabolize?

A

Type A metabolizes norepinephrine (NE), serotonin (5-HT), and tyramine, while Type B metabolizes dopamine

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90
Q

What is the specific role of MAO-A in neurotransmitter metabolism?

A

MAO-A is responsible for the metabolism of NE and 5-HT after they are reuptaken by their respective transporters (NET/SERT) into the nerve terminal.

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91
Q

How does inhibition of MAO enzymes in the brain produce the desired clinical effect?

A

Inhibition of MAO enzymes leads to the accumulation of monoamine neurotransmitters in the presynaptic neuron, increasing stores for release when the nerve is stimulated.

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92
Q

What are the types of MAO inhibitors, and what do they inhibit?

A

MAO inhibitors can be irreversible inhibitors of both type A and type B, or reversible inhibitors of type A only.

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93
Q

Why have tricyclic antidepressants (TCAs) like imipramine and amitriptyline fallen out of favor?

A

TCAs have fallen out of favor due to poorer tolerability compared to newer agents and their potential lethality in overdose.

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94
Q

In what situations are TCAs currently used?

A

TCAs are used primarily in cases of depression unresponsive to SSRIs or when sedation/analgesia is also required.

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95
Q

What are the multiple effects of TCAs due to their interactions with various receptors?

A

TCAs are considered promiscuous molecules with effects including:

-Antagonism at alpha1 adrenoceptors (causing hypotension)
-Antagonism at histamine (H1) receptors (causing sedation, increased appetite, and weight gain)
-Antagonism at muscarinic receptors (causing dry mouth and urinary retention)
-Blockage of voltage-gated sodium channels in the heart (responsible for lethality in overdose)

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96
Q

How do TCAs increase neurotransmitter levels?

A

TCAs inhibit the reuptake of monoamine neurotransmitters by blocking norepinephrine transporters (NET) and, in some cases, serotonin transporters (SERT).

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97
Q

What are some common adverse effects of TCAs due to their receptor antagonism?

A

Adverse effects include hypotension (from alpha1 adrenoceptor antagonism), sedation and weight gain (from histamine receptor antagonism), dry mouth and urinary retention (from muscarinic receptor antagonism), and increased risk of cardiac issues (from sodium channel blockage).

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98
Q

What are some anticholinergic side effects associated with tricyclic antidepressants (TCAs)?

A

Anticholinergic side effects include urinary retention, blurred vision, dry mouth, constipation, and tachycardia.

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99
Q

What rhyme can help memorize anticholinergic effects of TCAs?

A

The rhyme is: “blind as a bat (loss of accommodation), mad as a hatter (confusion), red as a beet (flushing), hot as a hare (atropine fever), dry as a bone (blocking sweating).”

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100
Q

How can tolerance to anticholinergic side effects of TCAs be managed?

A

Tolerance can occur over time, and gradual dose increases may help reduce the incidence of these effects.

101
Q

What are the anti-histaminic effects of TCAs, and what are their consequences?

A

The anti-histaminic effects of TCAs cause sedation, stimulate appetite, and may lead to weight gain.

102
Q

What issues are associated with the alpha-blocking effects of TCAs?

A

The alpha-blocking effects can cause postural hypotension, which is especially problematic in the elderly.

103
Q

What cardiac issues are associated with TCA overdose?

A

Cardiotoxicity includes sinus tachycardia, refractory hypotension, impaired myocardial contractility, and cardiac conduction abnormalities like increased arrhythmia risk, prolonged QTc, and QRS complex prolongation.

104
Q

How is TCA overdose treated based on QRS complex width?

A

The width of the QRS complex guides treatment with sodium bicarbonate in TCA overdose.

105
Q

What are the CNS toxic effects of TCA overdose?

A

CNS toxicity includes delirium, coma, and seizures, related to sodium channel inhibition, GABA receptor antagonism, and anti-histaminic effects.

106
Q

What are some contraindications for using TCAs?

A

Contraindications include acute closed angle glaucoma, benign prostatic hyperplasia (BPH), and recent myocardial infarction or arrhythmias.

107
Q

What symptoms might occur with sudden withdrawal from TCAs?

A

Sudden withdrawal can lead to agitation, headache, malaise, sweating, and gastrointestinal upset. Gradual dose reduction over 4 weeks is recommended to avoid these symptoms.

108
Q

How do SSRIs increase synaptic serotonin concentration?

A

SSRIs increase synaptic serotonin concentration by inhibiting the reuptake of serotonin.

109
Q

Which SSRI may exhibit norepinephrine (NE) reuptake inhibition at high doses?

A

Fluoxetine may display some norepinephrine reuptake inhibition at high doses.

110
Q

Why do SSRIs generally have a more favorable side effect profile compared to TCAs?

A

SSRIs have a more favorable side effect profile because they have low affinity for alpha-1, histamine, and muscarinic receptors.

111
Q

Why are SSRIs considered relatively safe in overdose?

A

SSRIs are considered relatively safe in overdose because they have low affinity for alpha-1, histamine, and muscarinic receptors.

112
Q

Why does fluoxetine have a long duration of action?

A

Fluoxetine has a long duration of action due to its long half-life of 23 - 75 hours and its active metabolite, norfluoxetine, which has a half-life of 6 days.

113
Q

Why must fluoxetine be discontinued for 4 weeks or more before starting an MAOI?

A

Fluoxetine must be discontinued for 4 weeks or more to avoid the risk of serotonin syndrome due to its long half-life and active metabolite.

114
Q

Which enzymes are inhibited by SSRIs and which SSRIs have the strongest inhibition?

A

SSRIs inhibit CYP2D6, with fluoxetine and paroxetine being the most potent inhibitors. Fluoxetine and fluvoxamine also inhibit CYP3A4.

115
Q

How might SSRIs affect haemostasis?

A

SSRIs inhibit serotonin uptake by platelets via SERT, potentially increasing the risk of bleeding, especially when used with other drugs that affect haemostasis, like aspirin or warfarin.

116
Q

Which SSRI has notable antimuscarinic effects, and what are the general antimuscarinic effects of SSRIs?

A

Paroxetine has notable antimuscarinic effects. Generally, SSRIs have few antimuscarinic effects, cause little sedation or weight gain, and are not cardiotoxic in overdose.

117
Q

SSRI adverse effects

A
  1. Insomnia
  2. Anxiety
  3. Sexual dysfunction
  4. Drug interaction
  5. Nausea
118
Q

What is serotonin syndrome, and what causes it?

A

Serotonin syndrome is a life-threatening condition characterized by neuromuscular hyperactivity, autonomic dysfunction, and altered mental state due to excessive serotonin levels in the peripheral and central nervous systems. It often occurs due to interactions between serotonergic drugs or an increase in SSRI dosage.

119
Q

When do symptoms of serotonin syndrome typically arise?

A

Symptoms usually arise within 24 hours after an increase in SSRI dosage or when using two or more serotonergic drugs together, such as SSRIs with MAOIs, TCAs, or other serotonergic agents like tramadol or St. John’s wort.

120
Q

What are the signs of neuromuscular hyperactivity in serotonin syndrome?

A

Signs include tremor, sustained clonus (pathognomonic sign), hyperreflexia, and rigidity.

121
Q

How does serotonin syndrome affect mental state?

A

It can cause agitation and confusion.

122
Q

What are the symptoms of autonomic hyperactivity in serotonin syndrome?

A

Symptoms include hyperthermia, fever, sweating, tachycardia, tachypnea, and diarrhea.

123
Q

What is the primary treatment for serotonin syndrome?

A

Treatment involves withdrawing the offending drug(s) and providing symptomatic care with benzodiazepines and supportive measures.

124
Q

What is the first-line treatment for Major Depressive Disorder (MDD) during pregnancy and breastfeeding?

A

The first-line treatment is Cognitive Behavioural Therapy (CBT).

125
Q

What are the second-line “safe” medication options for MDD during pregnancy?

A

The second-line “safe” medications include citalopram, escitalopram, and sertraline.

126
Q

What risks are associated with antidepressant use during pregnancy?

A

Antidepressant use can be associated with the syndrome of poor neonatal adaptation and persistent pulmonary hypertension of the newborn (PPHN). Both antidepressant use and untreated depression carry their own risks.

127
Q

What is the risk of teratogenicity with antidepressants in pregnancy?

A

The risk of teratogenicity is generally low for most antidepressants. However, paroxetine has been associated with an increased risk of cardiovascular malformations. Citalopram, escitalopram, and sertraline are recommended based on their efficacy and safety

128
Q

What are the risks of untreated depression during pregnancy?

A

Untreated depression during pregnancy can have significant adverse effects on both the mother and the infant, including the risk of relapse and complications.

129
Q

What is the risk of neonatal adaptation syndrome with SSRI exposure during the third trimester?

A

About 15-30% of fetuses exposed to SSRIs in the third trimester are at elevated risk of developing a syndrome of poor neonatal adaptation, marked by jitteriness, irritability, tremor, and excessive crying. These symptoms typically resolve within days with supportive care.

130
Q

What is the risk of persistent pulmonary hypertension of the newborn (PPHN) associated with SSRIs?

A

SSRIs taken late in pregnancy may be associated with an increased risk of PPHN, with an absolute risk of 2.9 to 3.5 per 1000 infants compared to a general population risk of 2 per 1000.

131
Q

What are the recommended antidepressant treatments for breastfeeding women?

A

For breastfeeding women, recommended treatments include citalopram, escitalopram, and sertraline. These medications have data supporting their effectiveness during the postpartum period and minimal risk during lactation.

132
Q

What is the significance of the Relative Infant Dose (RID) for antidepressants during breastfeeding?

A

Medications with a RID of <10% are generally considered safe. All tested SSRIs meet this criterion, with exposure via breastfeeding being 5-10% lower than in utero.

133
Q

How should decisions be made regarding the management of MDD in pregnancy and breastfeeding?

A

Decision-making should be collaborative with the patient, weighing the benefits and risks of treatment options.

134
Q

What does the choice of antidepressants depend on

A
  • Efficacy similar
  • Advocate for monotherapy
  • Safety and tolerability
  • Cost
  • Comorbidities
  • Pregnancy and breastfeeding intentions
135
Q

Antidepressants used in special situations

A

Mianserin
Venlafaxine
Mirtazapine
Bupropion

136
Q

What is the mechanism of action of mianserin and mirtazapine?

A

Mianserin and mirtazapine are antagonists at the presynaptic alpha-2 receptor, reducing negative feedback via auto-receptors

137
Q

What are the notable side effects of mianserin and mirtazapine?

A

They are generally free of anticholinergic side effects, not associated with sexual dysfunction or cardiotoxicity, but can cause sedation and weight gain. They also have a serious risk of bone marrow depression and agranulocytosis, requiring monitoring of FBC and differential count.

138
Q

Why are mianserin and mirtazapine useful in patients with prostatic enlargement or closed-angle glaucoma?

A

They are free of anticholinergic side effects, which makes them safer for patients with these conditions.

139
Q

What should be monitored during treatment with mianserin or mirtazapine?

A

Monitoring of full blood count (FBC) and differential count is required due to the risk of bone marrow depression and agranulocytosis.

140
Q

How does venlafaxine affect neurotransmitter reuptake?

A

At lower doses, venlafaxine primarily has serotonergic effects. At higher doses, it inhibits norepinephrine (NE) reuptake.

141
Q

What is the half-life of venlafaxine and its active metabolite?

A

The half-life of venlafaxine is approximately 4 hours, while its active metabolite has a half-life of about 10 hours.

142
Q

What withdrawal symptoms can occur if venlafaxine is missed?

A

Withdrawal symptoms can include paresthesias, ataxia/dizziness, lethargy, insomnia, anxiety, and agitation.

143
Q

When is venlafaxine considered for use?

A

Venlafaxine is considered primarily for patients who are poorly responsive to other antidepressants

144
Q

How should venlafaxine discontinuation be managed?

A

Discontinuation should occur gradually to minimize withdrawal symptoms.

145
Q

What is the primary use of bupropion?

A

Bupropion is used to assist in smoking cessation and is also useful in reducing weight gain.

146
Q

How does bupropion help with SSRI-related sexual dysfunction?

A

Bupropion may be useful for patients who experience sexual dysfunction related to SSRI use.

147
Q

What neurotransmitters does bupropion affect?

A

Bupropion inhibits the reuptake of dopamine and norepinephrine (NE).

148
Q

Approach to poor response to first line antidepressants

A

A full clinical response may take 6-8 weeks or longer

If no response after 8 weeks at optimal dose
- Re-evaluate symptoms
- Review adverse effects
- Review adherence
- Switch to another class
- Refer psychiatry

149
Q

What are some key differences between Bipolar Mood Disorder (BPMD) and Major Depressive Disorder (MDD) in terms of age of onset?

A

BPMD is often associated with an earlier age of onset compared to MDD.

150
Q

How does the recurrence rate of BPMD compare to MDD?

A

BPMD typically has more frequent recurrences than MDD.

151
Q

What types of depression are more commonly seen in BPMD?

A

BPMD is more commonly associated with atypical or mixed depression compared to MDD.

152
Q

What is the significance of family history in diagnosing BPMD?

A

A strong genetic predisposition exists for BPMD. If both parents have bipolar disorder, there is a 50-75% risk that their child could inherit it. If one parent has bipolar disorder, the risk is about 25%.

153
Q

How does family history of suicide relate to BPMD?

A

A family history of suicide can be a significant indicator of BPMD, reflecting the strong genetic component and higher risk.

154
Q

How is the diagnosis of Bipolar Mood Disorder (BPMD) typically established?

A

The diagnosis of BPMD is not made at a single point in time but is established over a period, observing the pattern and frequency of mood episodes.

155
Q

What defines Bipolar Type 1 Disorder?

A

Bipolar Type 1 Disorder is defined by the occurrence of at least one manic or mixed episode (full mania and full depression simultaneously).

156
Q

Are major depressive episodes necessary for diagnosing Bipolar Type 1 Disorder?

A

While patients with Bipolar Type 1 Disorder typically experience major depressive episodes, these are not necessary for the diagnosis.

157
Q

What characterizes Bipolar Type 2 Disorder?

A

Bipolar Type 2 Disorder is characterized by the occurrence of one or more major depressive episodes and at least one hypomanic episode.

158
Q

How does Bipolar Type 2 differ from Bipolar Type 1 in terms of episode severity?

A

Bipolar Type 2 includes hypomanic episodes rather than full manic episodes, which are seen in Bipolar Type 1 Disorder.

159
Q

Symptoms necessary for diagnosis of maniac episode

A
  1. elevated/ expansive mood
  2. irritable mood
160
Q

Other symptoms associated with maniac episode

A
  1. inflated self esteem/ grandiosity
  2. increased goal directed activity or agitation
  3. risk taking
  4. decreased need for sleep
  5. distractible/ concentration
  6. more talkative pressured speech
  7. flight of ideas/ racing thought
161
Q

What is required for a diagnosis of a manic episode according to DSM-IV?

A

Diagnosis requires at least one week of elevated or irritable mood plus at least three of the following symptoms if the mood is elevated, or four symptoms if the mood is only irritable

161
Q

Can mania present with other symptoms?

A

Yes, mania can also present with psychosis, including hallucinations or delusions, which impacts daily functioning.

162
Q

What is required for a diagnosis of a hypomanic episode?

A

Hypomania requires at least 4 days of elevated mood or irritability.

163
Q

How does hypomania differ from mania in terms of impact on daily life?

A

While hypomania also impacts daily life, the impairment is not as severe as in mania and does not involve hallucinations or delusions. Hypomania can be harder to detect due to its less severe impact

164
Q

Categorization of BPMD treatment

A
  • Antimaniac agent
  • Maintenance agent
  • Bipolar depression agent
165
Q

What is the role of anti-manic agents in the treatment of BPMD?

A

Anti-manic agents are used to treat the acute manic or hypomanic phases of BPMD

166
Q

Can you give an example of an anti-manic agent?

A

Examples include lithium, valproate, and certain antipsychotics.

167
Q

What is the purpose of maintenance agents in BPMD treatment?

A

Maintenance agents are used during the euthymic (stable mood) phase to prevent relapse and provide prophylactic efficacy.

168
Q

Can you provide an example of a maintenance agent?

A

Lithium is commonly used as a maintenance agent.

169
Q

How do bipolar depression agents differ from traditional antidepressants?

A

Bipolar depression agents are specifically effective in treating bipolar depression and are not the same as traditional antidepressants.

170
Q

Can you name a type of medication used for bipolar depression?

A

Atypical antipsychotics and certain mood stabilizers are used to treat bipolar depression.

171
Q

What are mood stabilizers and how are they used in BPMD treatment?

A

Mood stabilizers are effective in managing all phases of bipolar illness, including manic, hypomanic, and depressive episodes

172
Q

Can you provide examples of mood stabilizers?

A

Examples include lithium, valproate, and lamotrigine.

173
Q

What other types of medications may have mood stabilizing properties?

A

Some antipsychotics and anti-epileptic drugs also have mood stabilizing properties.

174
Q

What are the first-line treatments for acute mania?

A

The first-line treatments for acute mania are lithium or valproate.

175
Q

Which antipsychotics are commonly used in the treatment of acute mania?

A

Commonly used antipsychotics include olanzapine, risperidone, quetiapine, haloperidol, and aripiprazole

176
Q

What should be considered when choosing an antipsychotic for treating acute mania?

A

Consider efficacy, tolerability, adverse effects, and the likelihood of continuing the medication into the maintenance phase.

177
Q

What is the advantage of combination therapy in managing acute mania?

A

Combination therapy, such as lithium plus an antipsychotic or valproate plus an antipsychotic, is more effective than monotherapy.

178
Q

What should be added to a mood stabilizer if a patient with acute mania has psychotic features?

A

An antipsychotic should be added to the mood stabilizer.

179
Q

When should you avoid lithium

A

In patients with renal disease

180
Q

When should you avoid valproate

A

In liver disease and females of child bearing age

181
Q

What are the first-line monotherapy options for managing acute bipolar depression?

A

Monotherapy options include quetiapine, lamotrigine, olanzapine, lithium, and valproate.

182
Q

Why is it important to use these specific medications for bipolar depression?

A

These medications are effective for bipolar depression and are not standard antidepressants, which may not be suitable

183
Q

What are some second-line treatment options for acute bipolar depression?

A

Second-line options include:

  • Olanzapine plus fluoxetine
  • Lithium plus valproate or lamotrigine
  • Lithium or valproate plus an antidepressant
184
Q

When considering second-line treatments, what should be taken into account?

A

Consider the combination’s efficacy, tolerability, and the individual patient’s history.

185
Q

Why should unopposed SSRI or antidepressant monotherapy be avoided in bipolar depression?

A

Unopposed SSRI or antidepressant monotherapy may trigger a manic episode, which is why it’s important to use these medications with caution and usually in combination with a mood stabilizer

186
Q

What is the general approach to selecting maintenance therapy for BPMD?

A

The same medication that was successfully used for the acute phase is typically selected for maintenance treatment.

187
Q

What are the first-line mood stabilizers for maintenance therapy in BPMD?

A

Lithium is the first-line mood stabilizer. Other options include anti-epileptic drugs (AEDs) like lamotrigine and valproate.

188
Q

What is the primary role of lithium and AEDs in maintenance therapy?

A

Lithium and AEDs like lamotrigine and valproate are used to maintain mood stability and prevent relapse

189
Q

Why is lamotrigine often preferred for managing bipolar depression?

A

Lamotrigine is usually more effective in managing bipolar depression compared to other mood stabilizers.

190
Q

Which antipsychotics with mood stabilizing effects can be used in maintenance therapy for BPMD?

A

Quetiapine and olanzapine are antipsychotics with mood stabilizing effects that can be used.

191
Q

What is a significant drawback of using olanzapine for maintenance therapy?

A

Olanzapine is associated with poorer tolerability, including serious weight gain and an increased risk of developing diabetes mellitus.

192
Q

What phases of BPMD is lithium effective in managing?

A

Lithium is effective in managing all three phases of BPMD: mania, bipolar depression, and maintenance therapy

193
Q

Why is lithium considered the drug of choice despite its drawbacks?

A

Lithium’s efficacy across all phases makes it the drug of choice, but it has a narrow therapeutic index requiring careful monitoring.

194
Q

What are the target lithium levels for acute and maintenance therapy?

A

For acute therapy, the target level is 0.8 - 1.2 mmol/L; for maintenance therapy, it is 0.6 - 1.0 mmol/L.

195
Q

How frequently should therapeutic drug monitoring (TDM) be performed?

A

TDM should be performed weekly after dose increments, then at 1 month, 3 months, and every 6 months during maintenance. Trough samples should be taken 12 hours after the preceding dose.

196
Q

What other tests should be monitored along with TDM?

A

Annual serum creatinine and thyroid-stimulating hormone (TSH) levels should be monitored due to the risk of nephrotoxicity and thyrotoxicity.

197
Q

What are the signs of lithium toxicity?

A

Lithium toxicity can cause neurotoxic effects such as convulsions, ataxia, dysarthria, and coma, as well as renal dysfunction and electrolyte imbalances.

198
Q

What are common adverse effects of lithium even at therapeutic levels?

A

Common adverse effects include
-neutrophilia,
-weight gain,
-polydipsia and polyuria (SIADH0)
- hypothyroidism, and
-renal toxicity.

199
Q

Which drugs are known to interact with lithium and potentially increase toxicity?

A

Drug interactions that increase lithium toxicity include thiazides, ACE inhibitors, and NSAIDs.

200
Q

How do these drugs affect lithium levels?

A

Thiazides increase lithium reabsorption, ACE inhibitors increase lithium concentrations, and NSAIDs decrease renal excretion of lithium.

201
Q

What is the proposed mechanism of action for lithium in BPMD?

A

Lithium is thought to stabilize intracellular signaling by enhancing basal activity and decreasing maximum activity, thereby reducing the upregulation and downregulation of dopamine, glutamate, and GABA receptors.

202
Q

Why should lithium use be carefully managed in patients with altered salt and water balance?

A

Lithium is reabsorbed in the proximal tubule along with sodium. When the body is depleted of salt and water, increased sodium reabsorption leads to increased lithium reabsorption and potential toxicity.

203
Q

What are the implications of lithium use during pregnancy and breastfeeding?

A

Lithium use during pregnancy should be carefully considered due to potential risks, while lamotrigine, atypical antipsychotics, and valproate are also used. During breastfeeding, valproate, lamotrigine, and atypical antipsychotics may be used.

204
Q

What are the core symptoms of anxiety disorders?

A

The core symptoms of anxiety disorders are intense feelings of worry or fear that are strong enough to interfere with daily activities.

205
Q

How do these core symptoms differ from those of major depression?

A

The core symptoms of anxiety disorders are worry and fear, while major depression is characterized by loss of interest and depressed mood.

206
Q

What are some symptoms that overlap between anxiety disorders and major depression?

A

Common overlapping symptoms include fatigue, sleep difficulties, and problems concentrating

207
Q

Why is it important to recognize the overlap in symptoms between anxiety disorders and major depression?

A

Recognizing the overlap is important for accurate diagnosis and effective treatment, as symptoms can influence and exacerbate each other.

208
Q

Common anxiety signs and symptoms

A
  • Feeling nervous
  • Having a sense of impending danger, panic or doom
  • Palpitations
  • Hyperventilation
  • Sweating
  • Tremor
  • Feeling weak or tired
  • Trouble concentrating or thinking about anything other than the present worry/overthinking
209
Q

What types of symptoms can anxiety disorders present with?

A

Symptoms of anxiety disorders can be both physical and non-physical.

210
Q

Why is it important to exclude underlying medical conditions before diagnosing anxiety?

A

It is crucial to exclude underlying medical conditions to ensure that symptoms are not due to other health issues, which may require different treatment approaches.

211
Q

Can you give examples of medical conditions that should be excluded before ascribing symptoms to anxiety?

A

Examples include thyrotoxicosis, asthma attacks, arrhythmias, pneumothorax, and acute coronary syndrome (ACS).

212
Q

How can underlying medical conditions influence the diagnosis of anxiety disorders?

A

Medical conditions can present with symptoms similar to anxiety and may be treated differently, making it essential to differentiate between primary anxiety and secondary medical causes.

213
Q

Spectrum of anxiety disorders

A
  1. Adjustment disorder with Anxiety
  2. Generalised Anxiety Disorder
  3. Panic Disorder
  4. Post Traumatic Stress Disorder
  5. Obsessive Compulsive Disorder
  6. Social Anxiety Disorder
  7. Anxiety secondary to GMC
214
Q

What is a key non-pharmacological treatment for anxiety disorders?

A

Cognitive Behavioral Therapy (CBT) is a key non-pharmacological treatment for anxiety disorders.

215
Q

What is the primary goal of CBT in managing anxiety disorders?

A

The primary goal of CBT is to help individuals identify and change negative thought patterns and behaviors that contribute to anxiety.

216
Q

What is a common pharmacological treatment for acute anxiety symptoms?

A

Benzodiazepines are commonly used for the acute treatment of anxiety symptoms.

217
Q

Why should benzodiazepines be used with caution?

A

Benzodiazepines have a high dependency rate and are not suitable for chronic management of anxiety disorders. They are appropriate for short-term use, such as in acute situations like a panic attack.

218
Q

What medications are used for the chronic management of anxiety disorders?

A

For chronic management, Selective Serotonin Reuptake Inhibitors (SSRIs) and Tricyclic Antidepressants (TCAs) are used.

219
Q

Which anxiety disorders are commonly treated with SSRIs and TCAs?

A

SRIs and TCAs are used in the treatment of panic disorder, phobias, Obsessive-Compulsive Disorder (OCD), and Generalized Anxiety Disorder (GAD).

220
Q

Why should benzodiazepines not be used for chronic management of anxiety disorders?

A

Benzodiazepines should not be used for chronic management due to their potential for dependence and addiction.

221
Q

In what situations might benzodiazepines still be appropriate?

A

Benzodiazepines may be appropriate for acute situations, such as during a panic attack or severe anxiety episode.

222
Q

How do benzodiazepines primarily act in the central nervous system (CNS)?

A

Benzodiazepines act by potentiating the actions of GABA, the primary inhibitory neurotransmitter in the CNS.

223
Q

What happens when GABA binds to the GABA-A receptor?

A

When GABA binds to the GABA-A receptor, it increases the influx of chloride into the neuron, causing hyperpolarization of the cell membrane and decreased cell excitability.

224
Q

How do benzodiazepines interact with the GABA-A receptor?

A

Benzodiazepines bind to a site closely related to the GABA-A receptor, inducing a conformational change that enhances the receptor’s affinity for GABA.

225
Q

Do benzodiazepines have a direct action on ion flow?

A

No, benzodiazepines do not have a direct action on ion flow; they only enhance the GABA-mediated opening of the ion channel.

226
Q

What are the effects of increased inhibitory neurotransmission caused by benzodiazepines?

A

Increased inhibitory neurotransmission results in sedation, onset of sleep, anterograde amnesia, anxiolysis (via limbic and hypothalamic systems), anticonvulsant activity, and reduction of skeletal muscle tone.

227
Q

Ulltra short acting benzodiazepines

A

half life - 6 hours
Midazolam

228
Q

short acting benzodiazepines

A

half life- 6-12 hours
oxazepam

229
Q

intermediate acting benzodiazepines

A

half life- 12 -24 hours
lorazepam

230
Q

long acting benzodiazepines

A

half life > 24 hours
Diazepam

231
Q

How is the choice of benzodiazepine determined?

A

The choice is based on the onset and duration of action. For insomnia or preoperative medication, benzodiazepines with a rapid onset and short duration are ideal to prevent a hangover effect.

232
Q

What is tolerance in the context of benzodiazepines?

A

What is tolerance in the context of benzodiazepines?

233
Q

What is dependence with regard to benzodiazepines?

A

Dependence is the physiological adaptation to a drug, manifesting as withdrawal symptoms upon discontinuation

234
Q

Which patients are at higher risk for benzodiazepine dependence?

A

Patients with psychiatric illnesses (e.g., personality disorders, substance use disorders) and those using high doses long-term are at higher risk. Short-acting agents also increase the likelihood of withdrawal.

235
Q

What withdrawal symptoms are associated with benzodiazepines?

A

Symptoms include rebound insomnia, anxiety, and rarely, seizures. Withdrawal is more likely with short-acting agents.

236
Q

How can the risk of benzodiazepine dependence be minimized?

A

Use the lowest possible dose for the shortest duration. Limit use to 4 weeks or less and always have a plan to discontinue the medication.

237
Q

What is the recommended approach for benzodiazepine withdrawal once dependence is established?

A

Discontinue gradually by tapering over 4-8 weeks. Using a longer-acting benzodiazepine with active metabolites, such as diazepam, can help reduce withdrawal symptoms.

238
Q

Indications to use benzodiazepines

A
  • Alcohol withdrawal states
  • Seizures
  • Muscle relaxant
  • Acute sedation
  • Perioperatively
239
Q

Adverse effects of benzodiazepines

A
  • Sedation
  • Respiratory depression
  • Amnesia
  • Tolerance and dependence
  • Potentiation of sedative effects when given with other CNS depressants
  • Paradoxical increase in aggression
240
Q

What is the mechanism of action of flumazenil?

A

Flumazenil is a GABA-A receptor antagonist that competes with benzodiazepines at the GABA receptor.

241
Q

When is flumazenil typically used?

A

Flumazenil is used to reverse procedural sedation in patients who do not use benzodiazepines chronically and for the reversal of inadvertent (postoperative/ICU setting) benzodiazepine overdose.

242
Q

Why is flumazenil rarely used in patients with chronic benzodiazepine use?

A

There is a significant risk of seizures when flumazenil is given to patients with chronic benzodiazepine use, those with an existing seizure disorder, or when co-ingestion with a proconvulsant like a TCA has occurred.

243
Q

Why is flumazenil not routinely used in intentional benzodiazepine overdose?

A

Flumazenil is short-acting, leading to a recurrence of respiratory depression and sedation. Intentional benzodiazepine overdose is better managed with supportive care, including airway control and ventilation support.

244
Q

How are sustained seizures caused by flumazenil managed?

A

Seizures can be managed with a high normal dose of benzodiazepines, phenobarbitone, or propofol. Benzodiazepines remain effective as flumazenil is a competitive antagonist and only partially occupies GABA-A receptors.

245
Q

What are the considerations for using flumazenil in benzodiazepine overdose?

A

Given the low mortality rate of oral benzodiazepine overdose and the high rate of adverse effects associated with flumazenil, its risks may outweigh the benefits, particularly since re-sedation is likely.

246
Q

What is the most important aspect of managing a benzodiazepine overdose?

A

The most important aspect is to control the airway and support ventilation.

247
Q

Does pharmacotherapy have to be the first treatment option for mild depression and anxiety disorders?

A

No, pharmacotherapy does not have to be the first treatment option for mild depression and anxiety disorders.

248
Q

What are some non-pharmacological treatments for depression and anxiety disorders?

A

Non-pharmacological treatments include Cognitive Behavioral Therapy (CBT), interpersonal psychotherapy, exposure response prevention, and psychodynamic therapy.

Therapeutics (15 decks)

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