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mental health modified > treatment of mood disorders > Flashcards

treatment of mood disorders Flashcards

1
Q

Heritability approximately _______________

A

Heritability approximately 35%

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2
Q

What is a monoamine synapse?

A

A monoamine synapse is a type of chemical synapse in the brain that utilizes monoamine neurotransmitters such as serotonin, dopamine, and norepinephrine to communicate between neurons.

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3
Q

What is the strategy of antidepressant drugs?

A

The strategy of antidepressant drugs is to increase extracellular levels of neurotransmitters such as 5HT and NA in the brain, with varying degrees of selectivity for particular neurotransmitter systems.

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4
Q

What are the three main classes of antidepressant drugs?

A

The three main classes of antidepressant drugs are tricyclic antidepressants (TCAs), selective NA/5HT reuptake inhibitors (SS/NRIs), and monoamine oxidase inhibitors (MAOIs).

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5
Q

How do antidepressant drugs relieve depression?

A

Antidepressant drugs relieve depression by blocking the reuptake of neurotransmitters from the synapse, which allows more of them to remain in the synaptic cleft and continue to activate the postsynaptic neuron.

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6
Q

Why do antidepressant drugs take weeks to bring about clinical antidepressant effects?

A

Although antidepressant drugs immediately increase extracellular levels of neurotransmitters, they take weeks to bring about clinical antidepressant effects because they need to restore the balance of neurotransmitters in the brain and activate certain brain circuits that are involved in regulating mood and emotional processing.

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7
Q

What are the three stages of treatment regimen for depression?

A

The three stages of treatment regimen for depression are an acute stage where the aim is to induce remission, a maintenance stage where the aim is to prevent relapse into the existing episode, and a prophylaxis stage to avert recurrence after full remission from an episode of depression.

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8
Q

What is major depressive disorder (MDD)?

A

Major depressive disorder (MDD) is a mental illness that is characterized by persistent feelings of sadness, hopelessness, and loss of interest in activities that were once enjoyable.

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9
Q

What causes MDD?

A

The exact causes of MDD are not fully understood, but research suggests that imbalances in the monoamine neurotransmitter systems may play a role.

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10
Q

What is the theory behind how antidepressant drugs can help treat MDD?

A

One theory is that MDD is caused by a deficiency of serotonin, dopamine, or norepinephrine in certain areas of the brain. Antidepressant drugs can help treat MDD by increasing the levels of these neurotransmitters in the brain.

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11
Q

What is the aim of the maintenance stage of treatment regimen for depression?

A

The aim of the maintenance stage of treatment regimen for depression is to prevent relapse into the existing episode.

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12
Q

What are Tricyclic Antidepressants (TCAs)?

A

Tricyclic Antidepressants (TCAs) are a class of antidepressant drugs that are useful in the treatment of a number of conditions such as depression, migraine prophylaxis, neuropathic pain, obsessive-compulsive disorder, enuresis, panic disorder, sleep disorders, and attention deficit/hyperactivity disorder.

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13
Q

What are some examples of TCAs?

A

Some examples of TCAs include clomipramine, amitriptyline, doxepin, imipramine, desipramine and mirtazapine

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14
Q

What are the preferred uses of TCAs?

A

The preferred uses of TCAs include depression with pain, fibromyalgia, migraine, and insomnia.

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15
Q

What are the least preferred uses of TCAs?

A

The least preferred uses of TCAs include patients in whom anticholinergic effects would be problematic, overweight patients, suicidal patients, cardiac patients, and patients with dementia.

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16
Q

What is the mechanism of action of TCAs?

A

The mechanism of action of TCAs involves blocking the reuptake of the neurotransmitters norepinephrine and serotonin, leading to increased extracellular levels of these neurotransmitters and ultimately improving mood.

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17
Q

What is fibromyalgia?

What is neuropathic pain?

What is obsessive-compulsive disorder (OCD)?

What is enuresis?

What is attention deficit/hyperactivity disorder (ADHD)?

A

Fibromyalgia is a condition characterized by widespread pain, fatigue, and tender points on the body.

Neuropathic pain is a type of chronic pain that results from damage or dysfunction in the nervous system.

Obsessive-compulsive disorder (OCD) is a mental illness characterized by recurring, unwanted thoughts (obsessions) and repetitive behaviors or mental acts (compulsions).

Enuresis is a medical term for bedwetting, or involuntary urination, that occurs during sleep.

Attention deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, hyperactivity, and impulsivity.

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18
Q

What are the antagonist activities of TCAs?

A

TCAs have antagonist activity at mACh receptors, histamine H1 receptors, and 𝛼1-adrenoceptors.

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19
Q

What are the atropine-like side effects of TCAs? What causes it?

A

The antagonist activity at mACh receptors results in atropine-like side effects.

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20
Q

What are the adverse effects of histamine H1 receptor antagonism?

A

The antagonist activity at histamine H1 receptors can cause weight gain, drowsiness, and sedation.

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21
Q

What are the adverse effects of 𝛼1-adrenoceptor antagonism?

A

The antagonist activity at 𝛼1-adrenoceptors can produce postural hypotension, syncope in some patients, and sedation.

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22
Q

What is the treatment for TCA overdose?

A

The treatment for TCA overdose includes removal of the remaining drug in the stomach, anticonvulsant agent (diazepam), antiarrhythmic drugs, and further cardiac support to prevent or treat ventricular arrhythmias.

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23
Q

What is the onset of a clinically significant antidepressant effect for SSRIs?

A

It takes 4-6 weeks before a clinically significant antidepressant effect is observed for SSRIs.

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24
Q

What are the main advantages of SSRIs over TCAs and MAOIs?

A

The main advantages of SSRIs over TCAs and MAOIs are that they are generally better tolerated, possess less anticholinergic and cardiovascular side effects, and have low acute toxicity in overdose.

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25
Q

What are some examples of SSRIs?

A

Some examples of SSRIs include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), fluvoxamine (Luvox), citalopram (Celexa), and escitalopram (Lexapro).

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26
Q

What are the uses of SSRIs?

A

The uses of SSRIs include depression, social phobia, panic disorder, obsessive-compulsive disorder, bulimia nervosa, post-traumatic stress disorder, and premenstrual dysphoric disorder (Sarafem).

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27
Q

What is the least preferred use of SSRIs?

A

The least preferred use of SSRIs is in patients with sexual dysfunction, nocturnal myoclonus, consistent agitation, and consistent insomnia.

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28
Q

How do SSRIs work?

A

Pharmacodynamics: Serotonin, or 5-hydroxytryptamine (5-HT), is a neurotransmitter responsible for a range of functions, including mood regulation. Normally, after serotonin is released into the synaptic cleft (the gap between two neurons), it is taken back into the presynaptic neuron (the neuron that originally released it) in a process called reuptake. SSRIs block the serotonin reuptake transporter (SERT), hence the name “Selective Serotonin Reuptake Inhibitors”. This increases the concentration of serotonin in the synaptic cleft, enhancing its activity at the postsynaptic receptors.

Pharmacokinetics: SSRIs are orally active and are typically taken once daily. They are well absorbed from the gastrointestinal tract. Once absorbed, they are metabolized in the liver primarily by the cytochrome P450 system. SSRIs have varying half-lives, depending on the specific drug. For example, the half-life of fluoxetine is 1-3 days for the drug and 4-6 days for its active metabolite, norfluoxetine. SSRIs are excreted in the urine.

29
Q

What are some common gastrointestinal adverse effects of SSRIs?

A

Nausea, vomiting, and diarrhea are common gastrointestinal adverse effects of SSRIs.

30
Q

What is sexual dysfunction and what is its association with SSRIs?

A

Sexual dysfunction is a side effect of SSRIs that can include decreased libido, difficulty achieving orgasm, and erectile dysfunction.

31
Q

What are some potential anticholinergic side effects of SSRIs?

A

Some potential anticholinergic side effects of SSRIs include dry mouth, blurred vision, and constipation, especially with paroxetine.

32
Q

What are some other common side effects of SSRIs?

A

Other common side effects of SSRIs include headache, insomnia, long-term weight gain, occasional aggressive and violent behaviors, fatigue, and akathesia and dystonic reactions.

33
Q

How can 5HT affect dopamine (DA) levels?

A

Increased activation of serotonin receptors by SSRIs can lead to a decrease in dopamine (DA) levels in the brain.

34
Q

What is discontinuation or withdrawal syndrome associated with SSRIs?

A

Discontinuation or withdrawal syndrome is a potential side effect of SSRIs after prolonged treatment, which can include symptoms such as dizziness, nausea, headache, fatigue, flu-like symptoms, agitation, impaired concentration, paresthesia and sensations of electric shocks, vivid dreaming, and anxiety.

35
Q

What is serotonin syndrome?

A

Serotonin syndrome is a potentially life-threatening condition that can occur when several serotonergic drugs are combined, including SSRIs, MAOIs, and other serotonergic drugs.

36
Q

What are some symptoms of serotonin syndrome?

A

Symptoms of serotonin syndrome can include altered mental status, autonomic dysfunction, and neuromuscular abnormalities such as clonus.

37
Q

What is the association between SSRIs and suicide?
.

A

SSRIs have been associated with an increased risk of suicide in children, adolescents, and young adults, potentially due to discontinuation or withdrawal symptoms with an increased risk of suicidal ideation if a dose is missed

38
Q

What are some recommendations for prescribing SSRIs in children and young adults?

A

SSRIs with short half-lives should be avoided in children and young adults, and SSRIs should not be prescribed to children and young adults apart from fluoxetine, which has a long half-life.

39
Q

How long does it take for a clinical effect to be observed with selective noradrenaline reuptake inhibitors (NRIs)?

A

It takes 4-6 weeks before a clinical effect is observed with NRIs.

40
Q

What is the mechanism of action of NRIs?

A

NRIs selectively inhibit NA transporters and block the reuptake of noradrenaline, indirectly increasing 5-HT release by an action at presynaptic 𝛼1-adrenoceptors on 5-HT neurons.

41
Q

What is the main NRI that is clinically available in the UK?

A

Reboxetine is the main NRI that is clinically available in the UK.

42
Q

What are some adverse effects of NRIs?

A

Some adverse effects of NRIs include mild atropine-like effects, tachycardia, postural hypotension, and sexual dysfunction.

43
Q

What are serotonin and noradrenaline reuptake inhibitors (SNRIs) and what is their mechanism of action?

A

SNRIs, such as duloxetine and venlafaxine, inhibit the reuptake of both 5-HT and NA. They indirectly increase both 5-HT and NA neurotransmission.

44
Q

What are some potential side effects of SNRIs?

A

SNRIs have a similar side-effect profile to SSRIs, with sustained increases in blood pressure in some patients with venlafaxine.

45
Q

What are noradrenaline and selective serotonin antidepressants (NaSSAs) and what is their mechanism of action?

A

NaSSAs enhance both NA and 5-HT neurotransmission. The main drug in this class that is clinically available is mirtazapine, which is an antagonist at the presynaptic 𝛼2-adrenoceptors and 5-HT2 and 5-HT3 receptors.

46
Q

How does mirtazapine increase the release of NA and 5-HT?

What are some potential side effects of mirtazapine?

How do the antagonist effects of mirtazapine on 5-HT2 and 5-HT3 receptors help prevent certain side effects?

A

Mirtazapine increases the release of NA by its action at presynaptic 𝛼2 adrenoceptors and increases the release of 5-HT.

Some potential side effects of mirtazapine include atropine-like effects, postural hypotension, sedation, and weight gain. More rarely, it may cause blood disorders (agranulocytosis).

The antagonist activity of mirtazapine on 5-HT2 and 5-HT3 receptors prevents sexual dysfunction and insomnia associated with 5-HT2 receptors and nausea associated with 5-HT3 receptors.

47
Q

What are some potential side effects of mirtazapine?

A

Some potential side effects of mirtazapine include atropine-like effects, postural hypotension, sedation, and weight gain. More rarely, it may cause blood disorders (agranulocytosis).

48
Q

How do the antagonist effects of mirtazapine on 5-HT2 and 5-HT3 receptors help prevent certain side effects?

A

The antagonist activity of mirtazapine on 5-HT2 and 5-HT3 receptors prevents sexual dysfunction and insomnia associated with 5-HT2 receptors and nausea associated with 5-HT3 receptors.

49
Q

What is trazodone and what is its mechanism of action?

A

Trazodone is a serotonin antagonist and reuptake inhibitor. It is an antagonist at 5-HT1A and 5-HT2 receptors and inhibits the reuptake of 5-HT.

50
Q

How does trazodone increase the release of 5-HT?

A

Trazodone is an antagonist at 5-HT1A autoreceptors, which increases the release of 5-HT.

51
Q

What are some adverse effects of trazodone?

A

Some adverse effects of trazodone include postural hypotension, sedation, and weight gain.

52
Q

What is bupropion and what is its mechanism of action?

A

Bupropion is a noradrenergic and dopamine reuptake inhibitor. Its main mechanism of action is to inhibit dopamine and noradrenaline transporters and block the reuptake of DA and NA.

53
Q

What are some potential adverse effects of bupropion?

A

Some potential adverse effects of bupropion include nausea, constipation, epigastric distress, dry mouth, agitation, insomnia, and, more rarely, the risk of seizures or induction of psychosis.

54
Q

Mechanism of Action of MAOIs

A

MAOIs work by irreversibly inhibiting the activity of monoamine oxidase (MAO), an enzyme that breaks down monoamine neurotransmitters such as serotonin, dopamine, and norepinephrine in the synaptic cleft.

55
Q

What are the main MAOIs used in the treatment of atypical MDD/anxiety?

A

Phenelzine (Nardil) and Tranylcypromine (Parnate) are the main MAOIs used in the treatment of atypical MDD/anxiety.

56
Q

What is the main risk associated with consuming high tyramine foods or sympathomimetics while taking MAOIs?

A

Consuming high tyramine foods or sympathomimetics while taking MAOIs can lead to a hypertensive crisis.

57
Q

What are some atropine-like side effects of MAOIs?

A

Atropine-like side effects of MAOIs include dry mouth, blurred vision, and constipation.

58
Q

What is the main factor that limits the use of MAOIs?

A

The main factor that limits the use of MAOIs is their potentially fatal interaction with specific food types that are rich in certain amines, especially tyramine.

59
Q

Can irreversible MAOIs cause liver damage?

A

Yes, irreversible MAOIs can cause liver damage and are contraindicated in patients with hepatic impairments.

60
Q

What are the first-line treatments for bipolar conditions according to NICE guidelines?

A

Antipsychotic drugs such as olanzapine, quetiapine, and risperidone.

61
Q

What is the basic pharmacology of lithium carbonate?

A

Lithium is a small monovalent cation related to sodium functionally. Its mechanism of action remains unclear but it affects electrolytes and ion transport, affects the release of neurotransmitters (5HT, NA, DA), and affects second messengers and enzymes that mediate neurotransmitter function.

62
Q

What is the onset of action for lithium carbonate?

A

Lithium carbonate has a slow onset of action (6-12 months) and is more useful as prophylaxis therapy than treatment of the acute phase.

63
Q

What are the clinical uses of lithium carbonate?

A

Lithium carbonate is used in the prophylaxis and treatment of mania, prophylaxis of bipolar disorder (manic-depression), concomitant anti-depressant treatment in patients with incomplete response to treatment for depression in bipolar disorder, and as an augmenting agent in treatment-resistant depression.

64
Q

What are the adverse effects of lithium carbonate?

A

Adverse effects of lithium carbonate include tremor, polyuria, thirst, weight gain, and cognitive impairment. Long-term use can also lead to renal failure, hypothyroidism, and goitre.

65
Q

How does carbamazepine treat bipolar conditions?

A

Carbamazepine is an anticonvulsant drug that reduces the firing rate of neurons by blocking voltage-gated sodium channels. It is used in the treatment of mania and bipolar disorder.

66
Q

What is the mechanism of action of valproate in treating bipolar conditions?

A

Valproate is an anticonvulsant drug that increases the availability of GABA in the brain. It is used in the treatment of mania and bipolar disorder.

67
Q

What are benzodiazepines used for in the treatment of bipolar conditions?

A

Benzodiazepines are only used for acute treatment of mania or insomnia associated with bipolar disorder.

68
Q

Why is lithium carbonate generally superseded by antipsychotics in the treatment of bipolar conditions?

A

Antipsychotics have a faster onset of action and are more effective in treating acute manic episodes than lithium carbonate.

69
Q

What is the potential for lithium carbonate to cause renal failure?

A

Long-term use of lithium carbonate can lead to chronic kidney disease and renal failure due to its effects on the renal tubules.

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