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PR3136 > ANTI-DEPRESSANTS > Flashcards

ANTI-DEPRESSANTS Flashcards

1
Q

SSRI examples

A
  1. Fluoxetine (x50 fold)
  2. Citalopram (x1000 fold)

Fluoxetine more widely prescribed

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2
Q

ADR of MAO inhibitors

A
  1. Postural HYPOtension (due to blocked production of NA at cervical neurons leading to sympathetic block)
  2. Insomnia, restlessness (due to increase NA at CNS)
  3. DDI w 5-HT stimulating drugs (SSRI & SNRI)
  4. FDI w food rich in monoamines
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3
Q

ADR of MAO inhibitors

A
  1. Postural HYPOtension (due to blocked production of NA at cervical neurons leading to sympathetic block)
  2. Insomnia, restlessness (due to increase NA at CNS)
  3. DDI w 5-HT stimulating drugs (SSRI & SNRI)
    eg pethidine
  4. FDI w food rich in monoamines
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4
Q

TCA examples (NET & SERT)

A
  1. Imipramine
  2. Amitriptyline
  3. Nortriptyline
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5
Q

TCA examples (NET)

NET = NorEPINEPHRINE

A

Desipramine

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6
Q

NARI examples

A
  1. Reboxetine

2. Maprotiline (earlier NARI similar ADR as TCA)

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7
Q

SNRI (5-HT & NorADRENALINE) examples

A
  1. Venlafaxine
  2. Desvenlafaxine
  3. Duloxetine
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8
Q

DDI risk for Serotonin Syndrome

A
  1. MAO-A inhibitors
  2. SSRI
  3. SNRI
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9
Q

ADR of TCA

A
  1. Sedation (due to H1 receptor antagonist)
  2. Postural hypotension (due alpha-adrenergic antagonism)
  3. Dry mouth, constipation & blurred vision etc (due to muscarinic receptors antagonist)
  4. DDI (high plasma protein binding & hepatic metabolism)

1&2 esp at start of treatment

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10
Q

Mechanism of “cheese” reaction w MAOi

A
  1. MAOi blocked MAO degradation of tyramine in liver & intestines -> increase tyramine (sympathomimetic)
  2. Reuptake of tyramine and preferential storage into vesicles > NA -> increase release of NA into synapse (sympathomimetic)
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11
Q

ADR of SSRI

A
  1. Sedation
  2. Postural hypotension
  3. Dry mouth, blurred vision & constipation
  4. Nausea
  5. Insomnia
  6. Sexual dysfunction
  7. DDI w 5-HT stimulating drugs (MAOi & SNRI)
  • 1,2&3 less than TCA
  • Citalopram still has some histamine receptor antagonism leading to sedation
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12
Q

ADR of NARI

A
  1. Dry mouth, constipation & blurred vision
  2. Insomnia (due to increase NA in CNS)
  3. Tachycardia (due to increase NA in heart)
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13
Q

ADR of SNRI (5)

A

less than TCA

  1. Nausea
  2. Insomnia
  3. Sexual dysfunction
  4. Serotonin Syndrome when combine w other serotoninergic agents & MAOi
  5. Withdrawal effects may be more common & stronger than SSRI & TCA

(( similar to SSRI ))

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14
Q

Advantages of SNRI (3)

A
  1. Faster than other anti-depressant
  2. Good for treatment-resistant patients
  3. Fewer SE than TCA
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15
Q

Advantages of SSRI

A
  1. Reduced SE & safety
  2. Increased tolerability
  3. Increased efficacy
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16
Q

Other anti-depressants (5)

A
  1. Mirtazapine
  2. Buproprion
  3. Agomelatine
  4. Ketamine
  5. Vortioxetine
17
Q

Mechanism of action of Mirtazapine (NaSSA)

A
  • Norepinephrine & selective 5-HT receptor agonist

- BUT 5-HT2c receptor antagonist & alpha2 adrenergic receptor antagonist

18
Q

Mechanism of action of Buproprion (NDRI)

A

Norepinephrine & dopamine reuptake inhibitor

19
Q

Mechanism of action of Agomelatine

A

MT1 & MT2 melatonin receptor agonist

  • helps in sleep disorder
  • BUT 5-HT2c receptor antagonist
20
Q

Mechanism of action of Ketamine

A
  • Glutamate NMDA rceptor antagonist

- anaesthetic properties (IV GA)

21
Q

Mechanism of action of Vortioxetine

A
  • Multimodal 5-HT receptor effects
  • Full agonist of 5-HT1a receptor
  • Partial agonist of 5-HT1b receptor
  • Agonist of 5-HT1d, 5-HT3 & 5-HT7 receptor
  • also increase neurotransmitters (acetylcholines, histamines, dopamine, norepinephrine & 5-HT) in pre-frontal cortex & hippocampus of brain
22
Q

ADR of Vortioxetine

A

Suicidal ideations in children & teens

23
Q

Advantage of Vortioxetine

A
  1. Pro-cognitive

2. Good for treatment-resistant patients

24
Q

MAO inhibitors examples

A

Irreversible, non-selective - phenelzine
Reversible, MAO-A i - moclobemide
MAO-B i - selegiline (Jumex) (anti-parkinson)

25
Q

2 major types of depression

A
  1. Unipolar depression
  2. Bipolar depression or Affective disorder
    - alternate between depression and mania
26
Q

Unipolar Depression causes

A
  1. Reactive Depression
    - 75% of cases
    - associated with life events
  2. Endogenous Depression
    - 25% of cases
    - familial pattern -> genetic predisposition
    - not directly related to external stress
27
Q

Bipolar Depression cause

A
  • strongly familial
28
Q

Monoamine Theory

A
  • reserpine (5-HT and NA inhibition) lead to depressed mood
  • hypothesis mainly formulated for NA only but later shifted to 5-HT
  • monoamine theory alone is unable to explain the pharmacological actions of anti-depressants
  • monoamines are important but there are a complex interactions with other neurotransmitter systems as well
29
Q

Types of MAO enzymes

A

MAO-A
- breaks down 5-HT mainly

MAO-B
- breaks down NA and dopamine mainly

30
Q

Major limitations on the use of MAOi

A

FDI with food rich in monoamines

- Cheese Reaction

31
Q

How to reduce the risk of Cheese Reaction with MAOi

A

Use reversible & selective MAO-A inhibitor

eg Moclobemide

32
Q

Cheese Reaction signs and symptoms

A
  1. Acute HTN
  2. Severe throbbing headache
  3. Intracranial haemorrhage
33
Q

Nortriptyline

A
  • 2nd gen TCA
  • milder SE compared to amitriptyline & imipramine
    hence improve compliance
34
Q

Cheese Reaction = Serotonergic Syndrome ?

A

No.

Cheese reaction due to FDI of MAOi with food rich in monoamines (eg tyramine)

Serotonin Syndrome due to DDI w serotonin enhancing drugs

35
Q

1st drug class developed specifically as anti-depressant

A

SSRI

36
Q

Drugs to treat sexual dysfunction from SSRI

A

Cyproheptadine or other 5-HT2 blockers

37
Q

Serotonin Syndrome signs and symptoms (4)

A
  1. Tremor
  2. Hyperthermia
  3. Cardiovascular collapse
  4. Acute HTN

PR3136 (19 decks)

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