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Antidepressant ✔️ Flashcards

(103 cards)

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1
Q

What are the main groups of antidepressants?

A

• Tricyclic Antidepressants (TCAs)
• Selective Serotonin Reuptake Inhibitors (SSRIs)
• Serotonin/Noradrenaline Reuptake Inhibitors (SNRIs)
• Monoamine Oxidase Inhibitors (MAOIs)
• Atypical Antidepressants

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2
Q

Give examples of Tricyclic Antidepressants (TCAs).

A

Imipramine, Amitriptyline

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3
Q

What is the mechanism of action of TCAs?

A

Inhibit the neuronal reuptake of NA and 5-HT into presynaptic nerve terminals, increasing concentrations of monoamines in the synaptic cleft

(Inhibit the neuronal reuptake of NA and 5-HT )

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4
Q

Which additional receptor blockades are thought to be mainly responsible for the side effects of TCAs?

A

The blockade of serotonergic, α-adrenergic, histaminic, and muscarinic receptors.

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5
Q

What are the antimuscarinic side effects of TCAs?

A

Blurred vision, dry mouth, urinary retention, constipation.

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6
Q

What cardiovascular side effects are associated with TCAs?

A

Arrhythmias and sudden death

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7
Q

What effects result from α-adrenergic blockade by TCAs?

A

Orthostatic hypotension, dizziness, and reflex tachycardia.

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8
Q

What common side effects occur especially during the first weeks of TCA treatment?

A

Sedation

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9
Q

True or False:

TCAs can cause weight gain as a side effect.

A

True

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10
Q

What are the therapeutic uses of TCAs?

A

• Moderate to severe depression
• Some panic disorders (e.g., anxiety attacks)
• Neuropathic pain

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11
Q

What precautions should be taken when prescribing TCAs?

A

• Avoid use in manic-depressive/bipolar disorder patients (they may unmask manic behavior)

• TCAs have a narrow therapeutic index (lethal dose is 5–6 times the maximal daily dose)

• Suicidal patients must be given limited quantities of TCAs

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12
Q

True or false

TCAs should be avoided in manic-depressive/bipolar disorder patients because they may unmask manic behavior.

A

True

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13
Q

True or false

TCAs have a wide therapeutic index, making them safe in high doses.

A

False

(They have a narrow therapeutic index; lethal dose is 5–6 times the maximal daily dose.)

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14
Q

Suicidal patients must be given limited quantities of TCAs.

A

True

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15
Q

How do TCAs interact with direct-acting adrenergic drugs?

A

They prevent removal of biogenic amine drugs, potentiating their effects.

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16
Q

How do TCAs interact with indirect-acting adrenergic drugs?

A

They prevent the drugs from reaching their intracellular sites of action, blocking their effects.

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17
Q

What is the interaction between TCAs and ethanol or other CNS depressants?

A

Toxic sedation.

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18
Q

What occurs when TCAs are combined with monoamine oxidase inhibitors?

A

Mutual enhancement of hypertension, hyperpyrexia, convulsions, and coma.

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19
Q

What is the mechanism of action of SSRIs like fluoxetine and citalopram?

A

They selectively inhibit serotonin reuptake (300–3000 fold more selective for serotonin than noradrenaline transporter).

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20
Q

Which receptors does fluoxetine antagonize, and what effect can this have?

A

5HT2C receptors; it may cause activation/arousal (e.g., insomnia, nervousness at the start of treatment).

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21
Q

What should be taken into consideration when prescribing fluoxetine to a patient with anxiety?

A

Its 5HT2C antagonism may cause activation/arousal symptoms like insomnia and nervousness.

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22
Q

Does fluoxetine affect noradrenaline reuptake?

A

Yes, but it is a weak NA reuptake inhibitor and only relevant at high doses.

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23
Q

Why are SSRIs considered safer than TCAs and MAOIs?

A

Because they cause fewer anticholinergic and cardiotoxic effects and are less dangerous in overdose.

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24
Q

What is the most commonly prescribed class of antidepressants?

A

SSRIs

(Selective Serotonin Reuptake Inhibitors)

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25
What are common side effects of SSRIs?
• Nausea • Anxiety • Insomnia • Anorexia • Weight loss • Tremors • Sexual dysfunction
26
What caution should be taken when using SSRIs in physiotherapy patients?
SSRIs can cause bleeding due to effects on platelet aggregation; patients may bruise easily if not handled gently.
27
What can SSRI overdose cause?
Seizures
28
What are the therapeutic uses of SSRIs?
• Depression (moderate degree; less effective than TCAs and MAOIs for severe depression) • Bulimia nervosa & Anorexia nervosa • Obsessive-compulsive disorder (OCD) • Panic disorder
29
True or False: SSRIs can cause serotonin syndrome, especially when combined with MAOIs or other drugs that affect serotonin reuptake.
True
30
What are symptoms of serotonin syndrome?
Mental confusion, tremor, hyperthermia, cardiovascular collapse (may lead to shock or death)
31
What can increase the risk of serotonin syndrome when taking SSRIs?
Concurrent use with MAOIs or drugs that affect 5-HT reuptake (e.g., some antibiotics, tramadol)
32
What are symptoms of SSRI discontinuation syndrome?
Headache, malaise, irritability, flu-like symptoms, agitation, and changes in sleep pattern
33
Which SSRI has the lowest risk of discontinuation syndrome and why?
Fluoxetine — due to its longer half-life and active metabolite
34
True or False: SSRIs can cause BOTH serotonin syndrome and discontinuation syndrome.
True
35
What is the mechanism of action of SNRIs like venlafaxine and duloxetine?
They inhibit serotonin and noradrenaline reuptake.
36
Why do SNRIs cause fewer side effects than TCAs?
Because they have little activity at α-adrenergic, muscarinic, or histamine receptors.
37
What are two examples of SNRIs (Serotonin-Noradrenaline Reuptake Inhibitors)?
Venlafaxine and duloxetine.
38
In which patients can SNRIs be effective when SSRIs fail to work?
In patients with depression unresponsive to SSRIs.
39
What type of physical symptoms associated with depression are SNRIs effective in treating?
Chronic painful symptoms like backache and muscle aches.
40
What pain condition can SNRIs be used to treat?
Neuropathic pain
41
What syndrome can occur if SNRIs are stopped abruptly, similar to SSRIs?
Discontinuation syndrome.
42
What is an example of a monoamine oxidase inhibitor (MAOI)?
Phenelzine
43
Where is the MAO enzyme found in the body?
Neural, gut, and liver tissues
44
What is the mechanism of action of MAO inhibitors?
IRREVERSIBLY inactivates MAO enzyme, leading to accumulation of neurotransmitters (NA, DA, 5-HT) in the synaptic cleft and enhancing their action.
45
How do MAOIs affect the liver and gut?
They inhibit MAO in the liver and gut, blocking the breakdown of drugs and toxic substances like tyramine.
46
Why do MAOIs show a high incidence of interactions?
Due to inhibition of MAO in the gut and liver, they cause drug-drug and drug-food interactions.
47
What are common side effects of MAOIs?
• Drowsiness • Orthostatic hypotension • Blurred vision • Dry mouth • Dysuria • Constipation • Tremors • Convulsions in overdose
48
What dangerous condition can occur if MAOIs are combined with SSRIs?
Serotonin syndrome
49
What causes hypertensive crisis in patients taking MAOIs?
Ingestion of tyramine-rich foods (a.k.a. the ‘cheese reaction’).
50
What are symptoms of a hypertensive crisis due to MAOIs?
Occipital headache, tachycardia, nausea, hypertension, cardiac arrhythmias, seizures, and possibly stroke.
51
What dietary instruction must be given to patients on MAOIs?
Patients must be taught to avoid tyramine-containing foods. Ex: cheese
52
Why are MAOIs considered last-line agents?
Due to high risk of drug-drug and drug-food interactions.
53
What kind of dietary restrictions do patients on MAOIs require?
They must avoid foods containing tyramine because MAO normally degrades it.
54
What is tyramine and where is it found?
Tyramine is a substance found in aged cheeses, meats, chicken liver, pickled or smoked fish, and red wine.
55
Why is tyramine dangerous in patients taking MAOIs?
It causes release of large amounts of stored catecholamines from nerve terminals, leading to hypertensive crisis.
56
What normally inactivates tyramine in the body?
Monoamine oxidase (MAO) in the gut.
57
Why must caution be taken when prescribing MAOIs to severely depressed patients with suicidal tendencies?
Because they may intentionally consume tyramine-rich foods, risking a hypertensive crisis.
58
Why should MAOIs not be co-administered with SSRIs?
Co-administration can lead to life-threatening serotonin syndrome.
59
What is Trazodone primarily classified as?
An atypical (mild) antidepressant
60
What is a very useful side-effect of Trazodone?
Sedation (it initiates sleep)
61
What is the presumed mechanism of action of Trazodone?
Unknown, but thought to increase 5-HT in synapses by blocking uptake.
62
How does the effect of Trazodone vary by dose (low vs high)?
• Low dose → Sedation • Higher dose → Antidepressant effect
63
What type of drug is Mirtazapine?
Atypical antidepressant.
64
What is the mechanism of action of Mirtazapine?
• Enhances 5HT and NA release by antagonizing presynaptic α2-adrenoceptors • Antagonist at 5HT2A & 5HT2C receptors • 5HT2C blockade contributes to antidepressant effect • 5HT3 blockade provides antiemetic effect • Sedation due to potent antihistaminic activity at H1
65
What are the side effects of Mirtazapine?
• Increased appetite • Weight gain (frequent) • Very sedating (used as a sleep aid in depressed or insomnia patients)
66
Does Mirtazapine have antimuscarinic side effects?
No, unlike TCAs.
67
Does Mirtazapine cause sexual dysfunction like SSRIs?
No
68
What are the clinical uses of Mirtazapine?
• Major depressive disorder • Anxiety disorders • Emesis • Insomnia • As an add-on to antipsychotics in schizophrenia (negative symptoms)
69
True or False: ALL antidepressants lower the seizure threshold.
True
70
Why should antidepressants be used cautiously in children under 18?
Due to the possibility of excitement, insomnia, and aggression in the first few weeks of treatment.
71
Why is there caution in prescribing antidepressants to people under 25?
Because of the risk of causing or worsening suicidal thoughts.
72
What is the role of glutamate in pain transmission?
It is one of the most important excitatory amino acids (E.A.A) involved in pain transmission.
73
What types of receptors does glutamate act on?
Ionotropic and metabotropic receptors
74
Name two key ionotropic glutamate receptors.
AMPA and NMDA receptors
75
What type of pain is AMPA primarily involved in?
Acute/baseline sensory transmission
76
What type of pain is NMDA primarily involved in?
Chronic pain transmission
77
Review
Done
78
What type of gating does the NMDA receptor exhibit?
Both ligand and voltage-gated
79
Is the NMDA receptor found pre- or postsynaptically?
It is found at both pre- and postsynaptic sites.
80
What is required to activate the NMDA receptor?
Binding of glutamate (Glu) and glycine (Gly), and removal of Mg²⁺ block via repetitive depolarizations.
81
Is magnesium block removal essential for presynaptic NMDAR function?
No, it may not be as important in presynaptic NMDARs.
82
When is the NMDA receptor activated?
Only after repetitive noxious stimuli, not during baseline pain transmission
83
What type of pain is the NMDA receptor involved in?
Chronic pain, not acute pain
84
What other functions is the NMDA receptor involved in?
Development, learning and memory, neuronal injury, and plastic changes in pain transmission
85
Name two NMDA receptor antagonists
Ketamine and memantine
86
Why is clinical use of NMDA antagonists limited?
Due to serious side effects such as hallucinations and motor effects
87
What is the mechanism of action of ketamine in depression?
NMDA receptor antagonist
88
What other medical use does ketamine have besides treating depression?
It can be used as a general anesthetic.
89
What is esketamine?
The S-enantiomer of ketamine, used as a nasal spray for treatment-resistant depression.
90
How is esketamine used in treatment-resistant depression?
As a nasal spray in addition to an oral antidepressant.
91
Why is esketamine availability restricted in the USA?
Due to side effects (sedation, dissociation) and abuse potential.
92
Under what conditions is esketamine administered?
Under healthcare provider supervision; patients cannot take it home, are monitored for 2 hours, and then allowed to leave.
93
How long do the therapeutic effects of esketamine last?
2 weeks
94
How do 2nd generation atypical antipsychotics act on 5-HT₂A and D₂ receptors?
They primarily act as 5-HT₂A antagonists, with a higher affinity than for D₂ receptors, which they block loosely with a fast dissociation constant. (So higher affinity for 5-HT₂A than D₂)
95
What is the effect of 5-HT₁A agonism by some 2nd gen antipsychotics?
Increases dopamine release in the prefrontal cortex and reduces glutamate release.
96
Which 2nd gen antipsychotics are 5-HT₁A agonists?
Clozapine, quetiapine, ziprasidone
97
Which 2nd gen antipsychotic has partial D₂ agonism?
Aripiprazole
98
What additional receptors may be blocked by 2nd gen antipsychotics?
H₁, M₁, and α₁ receptors.
99
What type of depression symptoms can 2nd gen antipsychotics treat?
Depression symptoms found in schizophrenic patients.
100
Can 2nd gen antipsychotics be used in non-schizophrenic mood or anxiety disorders?
Yes, as monotherapy or adjuncts to antidepressants and mood stabilizers.
101
Name 2nd gen antipsychotics used in bipolar manic depression and generalized anxiety disorder.
Aripiprazole, olanzapine, risperidone
102
How are 2nd gen antipsychotics used with SSRIs/SNRIs?
As adjunct or combination therapy for unipolar depression.
103
Which antipsychotics are effective as adjuncts in treatment-resistant depression?
Aripiprazole and risperidone.

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