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Pharm > Anti-Depressants > Flashcards

Anti-Depressants Flashcards

1
Q

Depressed Mood most of the time for at least 2 weeks and/or loss of interest or pleasure in most activities

A

Major Depressive Disorder

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2
Q

Anti-depressant drug usage

A
  • Antidepressant drugs were the most commonly prescribed medications in the USA.
  • Their primary indication is for treatment of MDD. It has received FDA approvals for the treatment of:
  • panic disorder
  • generalized anxiety disorder (GAD)
  • post-traumatic stress disorder (PTSD)
  • obsessive-compulsive disorder (OCD).
  • Commonly used to treat pain disorders such as:
  • neuropathic pain
  • pain associated with fibromyalgia.
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3
Q

Mono-Amine Hypothesis:

A

Depression results from a deficiency in ammount or function of cortical and limbic Serotonin, Norepinephrine and dopamine

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4
Q

Neurotrophic hypothesis:

A

Brain derived neurotropic factor (BDNF) is critical for regulation of neural plasticisty and neurogenesis. In depression there is loss of BDNF in hippocampus

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5
Q

MAOI

A

work at the presynaptic nerve terminal to prevent the breakdown of dopamine, NE and Seratonin

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6
Q

What is the lag time between initiation of therapy and response to anti-depressants?

A

1-4 weeks

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7
Q

SSRIs

A 
➢	Fluoxetine 
➢	Fluvoxamine
➢	Sertraline 
➢	Paroxetine
➢	Citalopram
➢	Escitalopram
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8
Q

Pharmacodynamics of SSRIs

A

➢ SSRIs inhibit serotonin transporter (SERT)

➢ Block only serotonin (not NE) reuptake- Elevated serotonin levels

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9
Q

Depression results from a deficiency in ammount or function of cortical and limbic Serotonin, Norepinephrine and dopamine

A

Mono-Amine Hypothesis

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10
Q

Which SSRIs are CYP inhibitors?

A
  • Fluoxetine (CYP2D6 inhibitor)
  • paroxetine (CYP2D6 inhibitor)
  • fluvoxamine (CYP3A4 inhibitor)
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11
Q

A/E and DI of SSRIs

A

➢ Sexual Dysfunction (↓libido) in up to 40% of all patients→reason for non compliance
➢ Nausea, diarrhea
➢ Weight gain—Paroxetine
➢ Drug Interactions:
• Fluoxetine, paroxetine: CYP2D6 inhibitors → possible drug interactions
• Fluvoxamine CYP3A4 inhibitor
• sertraline, citalopram and escitalopram no DI
➢ Serotonin Syndrome (with MAOIs)

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12
Q

Pharmacokinetics of SSRIs

A

➢ Fluoxetine is metabolized to active norfluoxetine long elimination half life.
• Hence it has to be discontinued 4 weeks or longer before an MAOI can be administered to reduce risk of serotonin syndrome
➢ Fluoxetine and paroxetine are CYP2D6 inhibitors
➢ Fluvoxamine CYP3A4 inhibitor
➢ Modest CYP interactions:
• sertraline
• citalopram
• escitalopram

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13
Q

SSRIs with modest CYP interactions

A
  • sertraline
  • citalopram
  • escitalopram

these have no drug interactions

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14
Q

Brain derived neurotropic factor (BDNF) is critical for regulation of neural plasticisty and neurogenesis. In depression there is loss of BDNF in hippocampus

A

Neurotrophic hypothesis

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15
Q

SSRI that causes weight gain

A

Paroxetine

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16
Q

What drug combination puts a patient at risk for serotonin syndrome

A

SSRIs and MAOIs

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17
Q

Selective Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)

A
  • venlafaxine
  • desvenlafaxine
  • duloxetine
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18
Q

Seratonin-NE Reuptake Inhibitors

A

a) SNRIs (Selective Seratonin-NE Reuptake Inhibitors

b) TCAs

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19
Q

TCAs

A
  • Amitriptyline
  • Desipramine
  • Doxepin
  • Imipramine
  • Nortriptyline
  • trimipramine
  • clomipramine
  • protriptyline
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20
Q

PK and PD of SNRIs and TCAs

A

➢ Pharmacodynamics:
• Both TCAs and SNRIs bind both the serotonin (SERT) and the norepinephrine transporters (NET)
• and inihibit reuptake of serotonin and NE
➢ The SNRIs differ from the TCAs in that they lack:
• the potent antihistamine
• α adrenergic blocking
• antimuscarinic effects of the TCAs.
• As a result, the SNRIs tend to be favored over the TCAs in the treatment of MDD and pain syndromes because of their better tolerability.
➢ Among TCAs, clomipramine has more affinity to bind to SERT.
• This selectivity for the serotonin transporter contributes to clomipramine’s known benefits in the treatment of OCD.

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21
Q

Side Effects of SNRIs and TCAs

A

➢ SNRIs: serotonergic A/E (diarrhea, vomiting) and noradrenergic effects- ↑ BP and HR, and CNS activation, such as insomnia, anxiety, and agitation.
➢ TCAs-
➢ Alpha-1 Blockade: orthostatic hypotension, sexual dysfunction, cardiac conduction delays (QT prolongation)
➢ Histamine Blockade: weight gain, sedation
➢ Anti cholinergic: Dry mouth, Blurred vision, constipation, urinary hesitancy
➢ Sexual Dysfunction
➢ Lowers seizure threshold – seizures may occur (especially in overdoses)
• TCA Over dose = 3 C’s:
• Coma, Convulsions, Cardiac arrythmias (Rx- IV NaHCO3)

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22
Q

Side effects of histamine blockade

A

Weight gain and sedation

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23
Q

How do SNRIs differ from TCAs

A 
SNRIs lack:
•  the potent antihistamine
•  α adrenergic blocking
•  antimuscarinic effects of the TCAs. 
•  As a result, the SNRIs tend to be favored over the TCAs in the treatment of MDD and pain syndromes because of their better tolerability.
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24
Q

clomipramine

A

a) a TCAs
b) has more affinity to bind to SERT.
c) used to treat OCD
d) This selectivity for the serotonin transporter contributes to clomipramine’s known benefits in the treatment of OCD.

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25
Q

TCAs and SNRIs affect which transporters

A

Both bind to SERT and NET and inhibit repute of Seratonin and NE

26
Q

When are SNRIs preferred over TCAs and why?

A

SNRIs tend to be favored over the TCAs in the treatment of MDD and pain syndromes because of their better tolerability.

Remember: SNRIs lack:
• the potent antihistamine
• α adrenergic blocking
• antimuscarinic effects of the TCAs.

27
Q

TCA Over dose symptoms and treatment

A

Coma, Convulsions, Cardiac arrythmias

Rx- IV NaHCO3

28
Q

side effects of alpha 1 blockade

A
  1. serotonergic A/E (diarrhea, vomiting) and
  2. noradrenergic effects:
    a) ↑ BP and HR,
    b) CNS activation, such as insomnia, anxiety, and agitation.
29
Q

anti-cholinergic symptoms

A

Dry mouth, Blurred vision, constipation, urinary hesitancy

30
Q

Trazodone

A

5-HT2 antagonist (block 5-HT2A receptor)

a) rapidly absorbed and undergos extensive hepatic metabolism
b) Trazodone forms a metabolite (m-cpp) that blocks the 5-HT2A/2C receptors
c) has modest H1 receptor blockade

A/E: mainly causes sedation and priapism

31
Q

TCA and Unicyclic anti-depressants

A
  • bupropion
  • mirtazapine
  • amoxapine
  • maprotiline
32
Q

Nefazodone

A

5-HT2 antagonist (block 5-HT2A receptor)

a) potent inhibitor of CYP3A4 –> drug interactions
b) rapidly absorbed and undergos extensive hepatic metabolism

33
Q

bupropion

A

Tetracyclic and Unicyclic Anti-depressant

causes increased NE and DA activity
• no effect on 5-HT
• (No sexual dysfunction)
• Used for smoking cessation

A/E: Lowers seizure threshold (contraindicated in epilepsy).
No sexual dysfunction (unlike SSRI)

34
Q

TCA with NET > SERT inhibition

A

amoxapine and maprotiline

35
Q

mirtazapine

A

a) antagonism of presynaptic α2 R ↑ release of NE, 5-HT
b) Also an antagonist of 5-HT2 and 5-HT3 and is a potent H1 antagonist (sedation)

A/E: sedation and weight gain

36
Q

non-selective MAOI

A
  • Phenelzine

* Tranylcypromine

37
Q

Selective MAO –B inhibitors

A

Selegiline

38
Q

Act by inhibiting the MAO enzyme responsible for metabolism of the neurotransmitters (NT)

A

MAOIs

➢ Thus increases vesicular storage of NE and 5-HT
➢ Thus ↑ the brain levels of these Nerotransmitters

39
Q

MAOI toxicity and DI

A
  • Drug- Food: Cheese reaction: Hypertensive Crisis from foods with high tyramine content –> cheese, beer, wines, pickled meat, yeast extract contain large quantities of tyramine which is a indirect acting sympathomimetic
  • Tyramine escapes metabolism in MAO inhibited patients → causes more release of NE leading to hypertensive crisis
  • Treated with intravenous Phentolamine
40
Q

Phenelzine

A

non-selective MAOI

41
Q

Selegiline

A

Selective MAO –B inhibitors

42
Q

MAOIs

A

➢ Act by inhibiting the MAO enzyme responsible for metabolism of the neurotransmitters (NT)
➢ Thus increases vesicular storage of NE and 5-HT
➢ Thus ↑ the brain levels of these Nerotransmitters

43
Q

intravenous Phentolamine

A
  • Treatment for MAOI toxicity (treatment for hypertensive crisis from foods with high tyramine content;
  • Tyramine escapes metabolism in MAO inhibited patients → causes more release of NE leading to hypertensive crisis
44
Q

Tranylcypromine

A

non-selective MAOI

45
Q

Seratonin Syndrome

A

➢ Potentially life-threatening
➢ Results from combination of SSRIs with MAOI
➢ C/F :
• Hyperthermia
• Mental Status Changes, seizures
• muscular rigidity, tremor, restlessness, myoclonus, hyperreflexia
➢ Drugs implicated include MAOIs, TCAs, dextromethorphan, meperidine, and possibly illicit recreational drugs such as MDMA (“ecstasy”).
➢ Antiseizure drugs and muscle relaxants have been used in the management of the syndrome.

46
Q

Drugs used to treat major depressive disorder

A

SSRIs, SNRIs, 5-HT antagonists, preferred over TCAs because of better tolerability

47
Q

Drugs used to treat the depressive phase of bipolar disorder

A

SSRI/TCAs in combination with Lithium (for maniac phase)

48
Q

symptoms of seratonin syndrome

A
  • Hyperthermia
  • Mental Status Changes, seizures
  • muscular rigidity, tremor, restlessness, myoclonus, hyperreflexia
49
Q

Drugs used to treat panic disorder

A
  • SSRIs

* venlafaxine

50
Q

Drugs used to treat OCD

A
  • clomipramine

* SSRI (especially fluvoxamine)

51
Q

Imipramine

A

drug used to treat enuresis (bedwetting)

52
Q

Drugs used to treat ADHD

A
  • TCAs

* Atomoxetine

53
Q

Drugs used to treat neuropathic pain and fibromyalgia

A
  • TCAs

* Duloxetine

54
Q

clomipramine

A

used to treat OCD

55
Q

enuresis

A

bedwetting

56
Q

Atomoxetine

A

used to treat ADHD

57
Q

Duloxetine

A

used to treat neuropathic pain and fibromyalgia

58
Q

SSRI of choice to treat OCD

A

fluvoxamine

59
Q

venlafaxine

A

used to treat panic disorder

60
Q

Things SSRIs can treat

A
  • GAD
  • panic attacks
  • social phobias
  • post-traumatic stress disorder
  • bulimia
  • pre-menstrual dysphoric disorder

Pharm (32 decks)

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