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PCOL 1 > Drug treatment for Depression > Flashcards

Drug treatment for Depression Flashcards

1
Q

Depressed mood most of the time or persists for a long time

A

Mood disorder

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2
Q

Causes of Major Depressive Disorder

A

Endogenous (no apparent external cause)
Reactive (identifiable external cause)

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3
Q

Biochemical basis of Depression

A

Neurotrophic Hypothesis & Monoamine Hypothesis

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4
Q

Explain the Neurotrophic Hypothesis

A

stress and pain are associated with a drop in BDNF levels

Essentially, lower BDNF = depression

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5
Q

What is BDNF (Brain Derived Neurotrophic Factor)

A

responsible for nerve growth factor and emotional regulation

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6
Q

Two evidences that support the Neurotrophic hypothesis

A

Direct infusion of BDNF into the brain of rodents has antidepressant effects

Antidepressants are associated with an increase in BDNF

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7
Q

Explain the Monoamine Hypothesis

A

Deficit in function or amount of biogenic amines

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8
Q

Evidences of Monoamine Hypothesis

A

Reserpine treatment is associated w/ depression

All available antidepressants appear to have significant effects of the monoamine system

Administration of NE synthesis inhibitor is associated with relapse

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9
Q

MOA of TCAs (Amitryptiline, Desipramine, Imipramine, Clomipramine, Nortryptiline, Protryptiline, Doxepin, Lofepramine)

A

Blocks the neuronal reuptake of NE and 5HT

All are equally effective in relieving depression, although some patients respond better to one drug than to another

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10
Q

Side effects of TCAs (Amitryptiline, Desipramine, Imipramine, Clomipramine, Nortryptiline, Protryptiline, Doxepin, Lofepramine)

A

Antihistamine (Sedation)

A-1 adrenoreceptor blocker

Antimuscarinic

Acute poisoning (manifests as suicidal ideation) - generally recommended that no more than a week’s supply should be given at any time to acutely depressed patient

Cardiac arrhythmias

Weight gain (most common)

Confusion, impaired memory and cognition

Lower the seizure threshold

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11
Q

Examples of TCAs

A

AMITRYPTILINE
DESIPRAMINE
IMIPRAMINE
CLOMIPRAMINE
NORTRYPTILINE
PROTRYPTILINE
DOXEPIN
LOFEPRAMINE

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12
Q

MOA of TeCAs (Amoxapine, Quetiapine, Mianserin, Mirtazapine, Maprotiline, Setiptiline)

A

blocks neuronal reuptake of NE and 5HT

Alternative for patients who are unresponsive to other antidepressants

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13
Q

Examples of TeCAs

A

Amoxapine & Quetiapine - four rings are not fused together

Mianserin - First second generation, lacks cardiotoxic and anticholinergic S/E,
sedative, postural hypotension, weight gain, and causes blood dyscrasias

Mirtazapine - derivative of Mianserin that lacks blood dyscrasias and adverse effects,
(Noradrenergic & Specific Serotonergic
Antidepressant)

Maprotiline & Setiptiline - both are NaSSA

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14
Q

MOA of SSRIs (Fluoxetine, Paroxetine, Fluvoxamine, Sertraline, Citalopram, Escitalopram, Vilazodone, Vortioxetine)

A

Selectively block the neuronal reuptake of serotonin and have much less effect on the reuptake of NE

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15
Q

SSRIs are

A

the most widely used drugs of depression an certain anxiety disorders

as effective as TCAs - fewer autonomic side effects and less sedation

safer than TCAs - less likely to cause arrhythmia and seizures

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16
Q

Examples of SSRIs

A

FLUOXETINE
PAROXETINE
FLUVOXAMINE
SERTRALINE
CITALOPRAM
ESCITALOPRAM
VILAZODONE
VORTIOXETINE

17
Q

Side effects of SSRIs

A

N&V
Diarrhea/constipation
Tremor
Dizziness
Sexual dysfunction
HA

18
Q

MOA of SNRIs (Duloxetine, Venlafaxine, Desvenlafaxine, Milnacipran)

A

Block the neuronal reuptake of serotonin and norepinephrine

19
Q

SNRIs tend

A

to be favored over the TCAs in the treatment of MDD

20
Q

Examples of SNRIs

A

DULOXETINE
VENLAFAXINE
DESVENLAFAXINE
MILNACIPRAN

21
Q

MOA of NaRIs (Reboxetine, Atomoxetine, Viloxazine)

A

Block the neuronal reuptake of norepinephrine

*Also indicated for ADHD

22
Q

Examples of NaRIs

A

REBOXETINE
ATOMOXETINE
VILOXAZINE

23
Q

MOA of Unicyclic Antidepressant (Bupropion)

A

Block the neuronal reuptake of NE and DA

*Adjunct therapy for patients who are attempting to quit smoking cigarettes

24
Q

MOA of MAOIs (Moclobemide, Selegiline, Rasagiline, Tranylcypromine, Isocarboxazid, Phenelzine)

A

Inhibits Monoamine Oxidase thereby increasing biogenic amines

25
Q

Substrates of MAO - A

A

Norepinephrine, Epinephrine, Serotonin

26
Q

Substrates of MAO - B

A

Dopamine, Tyramine

27
Q

Examples of MAOIs

A

MOCLOBEMIDE - reversible inhibitor of MAO-A

SELEGILINE & RASAGILINE - irreversible inhibitor of MAO-B

Non selective MAOIs:
TRANYLCYPROMINE
ISOCARBOXAZID
PHENELZINE

28
Q

Examples of serious interactions of MAOIs

A

MAOIs + Tyramine-rich food
MAOIs + Adrenergic Drugs
MAOIs + Serotonergic Drugs

29
Q

MOA of Serotonin Receptor Modulators (Trazodone, Nefazodone)

A

Mild inhibition of serotonin reuptake

30
Q

Examples of 5HT receptor Modulators

A

TRAZODONE
NEFAZODONE

Neither drugs is effective for severely depressed people

Trazodone is strongly sedative which can improve sleep of depressed patients

31
Q

Isolated from Hypericum officinalis/ perforatum

Contains HYPERICIN and FLAVONES

A

St. John’s Wort

32
Q

MOA of St. John’s Wort

A

Blocks neuronal reuptake of 5HT

Have fewer side effects than other antidepressants but is not as effective as prescription antidepressants

33
Q

Adverse effects of Antidepressants

A

Some potential adverse effects
are common to all
antidepressants, most of their
adverse effects are specific to
subclass of agents and to their
pharmacodynamic effects

FDA warning applied to all
antidepressants is the risk of
increased suicidality in patients
younger than 25. Association
with suicidal ideation and
gestures but not completed
suicide

PCOL 1 (10 decks)

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