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MOD 4 > Depression and Drugs > Flashcards

Depression and Drugs Flashcards

1
Q

Half life of drug associated with probability of experience discontinuation syndrome

A

The shorter the half-life, the greater probability (short so gets removed fast, so more dramatic drop)

Most common with Venlafaxine and Paxil (Paroxetine)

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2
Q

SSRIs vs TCAs

A

SSRIs are much safer than TCAs

  • not lethal on overdose
  • no anticholinergic and other autonomic effects)
  • minimal sedation (Because no histamine activity)
  • no cardiac toxicity
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3
Q

Explain the actions of a tricyclic antidepressant (imipramine)

A

TCAs are hydrophobic so they are not very selective, thus they interact with many targets. There is a narrow theraputic index, and can become toxic quickly.

At low [] it inhibits neuronal uptake of NE, but then it blocks alpha receptors, histamine receptors, Ach receptors, and 5HT receptors and its uptake.

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4
Q

Side effects associated with TCAs: cardiotoxicity

A

conduction block, arrhythmias, can be lethal

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4
Q

Why is mirtazapine generally not used as first line treatment?

A

Causes a lot of NE release. Also nonspecific for inhibiting other post synpatic serotonin receptors. Biggest problem is ++++ sedation.

[Also causes reduction in white blood cells in small in small number of patients, produces appreciable sedation and weight gain due to antihistamine properties.]

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5
Q

Side effects associated with TCAs: blockage of histamine H1 receptors

A

sedation, weight gain (causes increase in appetite)

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5
Q

What are some potential side effects of SSRIs? (6)

A
  • sexual dysfunction
  • GI disturbances
  • weight gain on long term use
  • metabolic syndrome
  • liver toxicity
  • increased hemorrhage during surgery
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5
Q

What is akathisia?

A

Movement disorder -inner restleness, need to be in constant motion. Symptom of Serotonin syndrome (mild)

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5
Q

Which drugs inhibit Cytochrome p450 isozyme CYP2D6? (4 main ones)

A

Fluoxetine, Paroxetine, Sertraline, and Vortioxetine.

CYP2D6 metabolizes antidepressant, antipsychotics, antiarrhythmias, B-blockers, opiates, and many other drugs. Thus you get drug interaction

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6
Q

What is the percentage of patients with major depressive disorder that respond to an inidtal anti depressant (with adequate dose and duration)?

A

50-60%

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6
Q

What is a drug good for weakly blocking serotonin reuptake and sedatitve effect?

A

Trazodone - weak blocker and potent anti-histamine. Sometimes you desire thie effect if pt has trouble sleeping (“trazure your sleep”)

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7
Q

1) Treatment for serotonin syndrome
2) treatment for abrupt serotonin discontinuation

A

1) remove the drug
2) put pt back on drug and slowly taper off

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8
Q

What is the new drug that doesnt inhibit cytochrome p450 isozyme

A

Escitalopram (escited that its such a good drug)

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10
Q

Etiology of Depression: What is the Monoamine Deficiency Hypothesis?

A
  • deficiency of NE and/or serotonin causally related to symptoms
  • depletion of brain amine by reserpine or reduction in braine NE can precipitate depressive episodes
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11
Q

What do you need to monitor with ongoing care with SNRIs?

A

BP

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12
Q

what is unique about bupropion

A

blocks dopamine reupta,e and has an active metabolite that weakly blocks NE reuptake. But it has NO ABILITY to block serotonin reuptake pump.

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13
Q

What are the classes of antidepressants used to treat unipolar depression?

A
  1. TCAs (tricyclic antidepressants)
  2. MOAIs (monoamine oxidase inhibitors)
  3. Serotonin Selective Reuptake Inhibitors (SSRIs)
  4. Combine Serotonin-Norephinephrine Reuptake Inhibitors (SNRIs)
  5. 2nd and 3rd generation heterocyclic atypical antidepressants
14
Q

Even though SSRIs are first line therapy, what are its side effects? (6)

A
  1. sexual dysfucntion
  2. GI disturbances
  3. weight gain on long term use
  4. metabolic syndrome
  5. liver toxicity
  6. increased hemorrhage during surgery
16
Q

The two main tricyclic antidepressants

A

Imipramine

Desipramine

17
Q

What are the four targets that cause side effects associated with TCAs use? (4)

A
  1. blocks alpha 1 adrenergic receptors
  2. Blocks histamine (H1) receptors
  3. Blocks muscarinic acetylcholine receptors
  4. Cardiotoxicity
18
Q

what causes serotonin syndrome?

A

too high of sertonin when on an SSRI and an MAOI. These extremely elevated levels of serotonin

19
Q

Currently approved SSRIs -most known one

A

Fluoxetine (Prozac)

20
Q

What are 4 pieces of evidence for serotonergic dysfunction in depression?

A
  1. low serum tryptophan (makes serotonin)
  2. reduced platelt uptake of 5-HT
  3. low CSF 5-HIAA (5-HIAA is main metabolite of serotonin)
  4. reduced 5-HT-2 recceptors in cerebral cortex
21
Q

What should we monitor for initially when administering drugs for treatment of depression? (5)

A
  1. Routine Physical Exam
  2. Complete Blood Count
  3. Serum Electrolytes
  4. Liver Function Studies
  5. Thyroid Function Studies
22
Q

Pt presents with flu-like symptomes, imbalance. Also reports electrical feelings in extremities, sensory distrubances. Pt mentions her is hyperaroused with insomnia, and is experience anxiety, with intesinfiying depressive symptoms. This occurred suddenly. What is the cause (in assoc with this lecture)

A

Serotonin discontinuation

these are the symptoms you see if you abruptly stop taking the drug

23
Q

what is seen in neuroimaging studies in depression? (3)

A
  1. altered structure- reduced hippocampal region
  2. receptor changes - reduced 5-HT-2 receptor concentration in cortical regions
  3. changes in brain activity, hypofrontaility, increased activity in prefrontal and limbic regions
24
Q

What should you monitor with ongoing care with mirtazapine?

A

CBC

26
Q

Administration guidelines for treatment

A
  • Start at low dose and titrate dose up gradually as tolerated.
  • Use enough dose to work
  • allow enough time to work typically atleast 6 weeks
  • avoid abrupt discontinuation to avoid problems with withdrawal reactions
27
Q

what is the correlation between hippocampal volume and duration of untreated depression?

A

length of depressed time without tx and deplation of hippocampus volume had a strong correlation

28
Q

What should you monitor in ongoing care with TCA treatment?

A

EKG

30
Q

What should you monitor with ongoing care with MAOIs?

A

Liver function studies and BP

31
Q

4 main MOA inhibitors

A

PHENELZINE (NARDIL)

TRANYLCYPROMINE (PARNATE)

ISOCARBOXAZID (MARPLAN)

**first 3 are non selective *

SELEGILINE (TRANSDERMAL PATCH)

* Selective for MAOB at lower doses

32
Q

Side effects associated with TCAs:

blockage of alpha 1 adrenergic receptors

A

orthostatic hypotension, erectile dysfunction

34
Q

what types of side effects do you get with SSRIs? Why do they occur?

A

SSRIS block reuptake of serotonin, thus yu have more serotonin around to interact with serotonin receptors. There are lots of receptors with different functions, and SSRIs are not selective.

  • 5HT1: antidepressant and anxiolytic actions
  • 5HT2: agtation, enrvousness, insomnia, sexual dysfunction
  • 5HT3: nausea, vomiting, HA
35
Q

Major depressive episode: conditions and definition

A

depressed mood or anhedonia (loss of the capacity to experience pleasure) for atleast 2 weeks

36
Q

What regulated synaptic plasticity in termes of depression??

A

Modification in synaptic AMPA and NMDA receptor (by insertion, internalization, and trafficking)

37
Q

Side effects associated with TCAs: blockage of muscarinic acetylcholine receptors

A

atropine like effects: blurred vision, dry mouth, constipation, urinary retention, mental confusion

38
Q

With major depressive disorder, what are following conditions you need atleast 5 of for greater than 2 weeks?

A

SIGECAPS

Sleep Disturbance

Interest decreased

Guilt

Energy decreased

Concentration decreased

Appetite disturbed

Psychomotor agitation or retardation

Suicidal Ideation

39
Q

what is the significance of tyramine with MAO inhibitors?

A
  • tyramine is an aa rich in certain foods
  • tyramine is metabolized by both types of MAOs, gets broken down in the gut so doesn’t get to CNS
  • if on an MAO inhibitor, tyramine isn’t broken down, gets into CNS, similar to NE structure, displaces NE,
  • NE sudden release causes hypertensive state and huge spike in BP/hypertensive crises
40
Q

Mechanism of action of TCAs

A

they inhibit the reuptake pumps responsible for recapturing NE and 5HT (serotonin)

41
Q

imipramine is now used as a tricyclic antidepressant. what was it originally used to treat?

A

It was developed as an antihistamine, hence why a side effect now is SEDATION.

42
Q

What is the MOA of mirtazapine and the effect?

A

mirtazapine works not by inhibiting serotonin reuptake pumps but instead inhibits presynaptic alpha 2 receptors. Recall that those receptors are involved in negative feedback loop where NE inhibits further release. Inhibting these receptors leads to an increase release of NE.

MOD 4 (14 decks)

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