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Medical Pharmacology Exam 2 > Antidepressants and Stimulants > Flashcards

Antidepressants and Stimulants Flashcards

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USMLE® Step 1 flashcards
1
Q

There are 3 types of depression. What are they?

A

Major depression
Dysthymia (less sever than major)
Bipolar disorder (cycling moods)

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2
Q

Characterized by enthusiasm, rapid thoughts and speech patterns, extreme self-confidence and impaired judgement. This describes _

A

Mania

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3
Q

The current hypothesis regarding mood disorders is that they are related to the levels of _. High levels correlate with _ while low levels correlate with _

A

Biogenic amines (5HT and NE)
Mania
Depression

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4
Q

What is the serotonin metabolite measured to detect its levels? Where is it measured from? What is a postmortem finding in depressed patients indicative of low 5HT?

A

5-hydroxyindoleacetic acid
CSF
High receptor levels

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5
Q

What is the norepinephrine metabolite measured to detect its levels? What is the effect of norepinephrine depletion on mood

A

3-methoxy-4-hydroxyphenylglycol

Low NE, likely depression

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6
Q

In general, what is the net effect of drugs used for the treatment of depression?

A

Increase the monoaminergic neurotransmission (5HT, NE and maybe DA)

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7
Q

What is the major effect of the tri-cyclic antidepressants? What are they used for? What is the prototype?

A

Block monoamine reuptake
Major depression
Imipramine

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8
Q

The side effects of TCAs arise from their non-specific actions at what 3 receptor signaling systems?

A

Muscarinic
Adrenergic
Histamine

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9
Q

Four examples of TCAs were provided. They are _

A

Imipramine
Amoxapine
Amitriptyline
Nortriptyline

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10
Q

Regarding TCAs, where are they primarily absorbed? How long till they start working? Where / What are they metabolized? How are they excreted?

A

Small intestines
up to 2 weeks
Metabolized by liver microsomal enzymes
Primarily Kidneys

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11
Q

3 major side effects of TCAs include:

A

Antimuscarinic effects
Cardiovascular effects
Orthostatic hypotension

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12
Q

SSRIs are the most widely prescribed antidepressant in the US. What is a major advantage over TCAs? What is another condition beyond depression that SSRIs are used for?

A

No cardiotoxic effects

Anxiety disorders

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13
Q

What are 4 examples of SSRIs provided?

A

Fluoxetine
Citalopram
Escitalopram
Sertraline

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14
Q

What is the mechanism by which SSRIs work?

A

Selectively block 5HT reuptake

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15
Q

While SSRIs start working immediately, why do their effects take up 2 weeks to show?

A

Neurogenesis has to occur (e.g. in hippocampus)

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16
Q

Regarding SSRIs, where are they primarily absorbed? How do they interact with P450 enzymes? How are they eliminated?

A

Small intestines
Block these enzymes
Eliminated via kidneys

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17
Q

Fluoxetine is metabolized to what active metabolite? Where does this occur? How does this metabolism affect its half-life?

A

Nor-fluoxetine
Liver
It can increase half life up to 30 days

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18
Q

A commonality between TCAs and SSRIs regarding plasma proteins is _

A

They both bind highly (up to 90%) to plasma proteins

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19
Q

What are 3 early onset (but transient) side effects of SSRIs?

A

Nausea
Anxiety
Insomnia

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20
Q

What are 3 late onset side effects of SSRIs?

A

Anorexia
Sexual dysfunction
Mania (in bipolar patients)

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21
Q

What are the 3 CYP enzymes blocked by SSRIs?

A

2D6
1A2
3A4

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22
Q

What are 4 known drug interactions of SSRIs? i.e. these drugs can increase to toxic levels if used with SSRIs

A

TCAs
Neuroleptics (haloperidol)
Antiarrhythmics (some)
Beta adrenergics (some)

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23
Q

What are the 2 examples of serotonin-NE reuptake inhibitors (SNRI) provided? What group of patients are they used for?

A

Venlaflaxine
Duloxetine
Patients refractory to SSRIs

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24
Q

Of the 2 SNRIs, which is more likely to bind plasma proteins? Less likely? Which enzymes metabolize these drugs? Which is contraindicated in patients with liver insufficiency?

A 
More - Duloxetine (97%)
Less - Venlaflaxine (27%)
2A6 - Venlaflaxine
1A2 and 2A6 - Duloxetine
Duloxetine not for kidney insufficiency patients
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25
Q

What are 4 major side effects of SNRIs?

A 
Nausea
Anxiety
Insomnia
Sexual dysfunction
(Same as SSRIs, except anorexia)
26
Q

What are the 3 examples of atypical antidepressants provided?

A

Bupropion
Nefazodone
Mirtazapine

27
Q

What is the mechanism of action of bupropion? What is it used to treat?

A

Inhibits DA reuptake

Bipolar disorder

28
Q

What is the mechanism of action of nefazodone? What specific receptor does it block?

A

Inhibits reuptake of 5HT

Block 5HT2 receptors

29
Q

What is the net effect of mirtazapine? What receptor is targeted?

A

Increases NE and 5HT

Blocks alpha-2 receptor

30
Q

When/how are atypical antidepressants likely to be used?

A

In combination with TCAs when others don’t work.

31
Q

What are 5 common side effects for atypical antidepressants?

A 
Headache
Nausea*
Tinnitus
Insomnia*
Nervousness* - *same as SSRI/SNRI/TCA
32
Q

True or False, MAOIs are widely used drugs for the treatment of depression.

A

False. Third line treatment because of severe and unpredictable side effects

33
Q

What is the function of MAO-A? MAO-B

A

MAO-A - Deaminates NE, 5HT and DA

MAO-B - Deaminates DA

34
Q

What is the net effect of MAOIs on monoamine levels?

A

It increases presynaptic levels of monoamines

35
Q

What are three examples of MAOIs provided? Which is specific to MAO-B (except at high levels)

A

Phenelzine
Tranylcypromine
Selegiline - MAO-B selective

36
Q

What type of inhibition do MAOIs exert on MAOs? What is the practical repercussion on enzyme activity if a patient stops using the drug?

A

Irreversible Inhibition

Need several weeks after stopping drug for levels to return to normal

37
Q

Which of the MAOIs can be administered transdermally? How are they eliminated?

A 
Selegiline
Mainly kidneys (like other antidepressants)
38
Q

hallucinations, agitation, hyperreflexia, convulsions, orthostatic hypotension and constipation. These are all possible side effects of _

A

MAOIs

39
Q

What content of certain foods can be potentially problematic for patients on MAOI? Why?

A

Tyramine

It is metabolized by MAOs, if levels are high, then it can cause great release of catecholamines

40
Q

What is serotonin syndrome? What drug combination can cause it?

A

Potentially fatal condition (fever, diarrhea, excitement, hypomania, ataxia, hyperreflexia, hyperthermia and COMA)
MAOIs and SSRIs

41
Q

What is the drug of choice for prophylactic treatment of bipolar disorder? What makes this drug unsafe? What is the mechanism of its toxic side effects?

A

Lithium salts
Low therapeutic index
It substitutes for sodium ions

42
Q

What is lithium’s interaction with plasma proteins? What group of patients are at risk for toxicity when using lithium?

A

No binding to plasma proteins

Patients with kidney problems (how its cleared)

43
Q

Tremors, mental confusion, convulsions and arrthymias are all potential side effects of _

A

Lithium

44
Q

What are 2 drug classes with known drug interactions with lithium?

A

Thiazide diuretics

NSAIDs

45
Q

In addition to lithium, what other 3 drug classes can be used to treat bipolar disorder?

A

Antidepressants
Antipsychotics
Anticonvulsants

46
Q

What are the three examples of stimulants provided? Which has no medical use? Which 2 are psychomotor stimulants (fight fatigue)?

A

Dextroamphethamine (psychomotor stimulant)
Methylphenidate
Methamphetamine (psychomotor stimulant, no medical use)

47
Q

Which of the stimulants can be used to treat narcolepsy and ADHD? (2) How are these drugs excreted?

A

Dextroamphethamine
Methylphenidate
Urine

48
Q

What are three ways that stimulants increase the levels of DA and NE in the brain?

A
  • Increase vesicular monoamine transporter (VMAT) activity, increase release of vesicles
  • Block MAO, less metabolism
  • Increase non-vesicular release of DA and NE (reuptake channels)
49
Q

What are the 3 main traits of ADHD?

A

– Inattention
– Hyperactivity
– Impulsivity

50
Q

In addition to stimulants, what other drug can be used to treat ADHD? What is its mechanism? What is a potential advantage over other options?

A

Strattera
NE reuptake inhibitor
Non-habit forming

51
Q

In addition to dextroamphetamine and methylphenidate, what other 2 drugs can be used to treat narcolepsy? What are advantages of modafinil?

A

Amphetamine

Modafinil (less psychoactive and euphoric effects)

52
Q

What are 5 potential CNS side effects of amphetamines?

A 
Euphoria
Anxiety
Vertigo
Insomnia
Confusion
53
Q

What are 2 GI and 2 cardiovascular side effects of amphetamines?

A

Cardiovascular - Arrythmias, hypertension

GI - Nausea and diarrhea

54
Q

True or false: Amphetamines have addiction / abuse potential

A

True

55
Q

A major problem associated with using TCAs in the elderly is _. A major area of drug-drug interactions with TCAs are _

A

Orthostatic hypertension

Binding within plasma proteins

56
Q

Why are SNRIs an improvement over TCAs?

A

They are less dirty (no muscarinic, adrenergic or histamine receptor actions) so less side effects

57
Q

Of the MAOs, which can be used for the treatment of Parkinson’s disease? How is its formulation altered for this purpose?

A

Selegiline

Used as pills, vs. Patch for depression

58
Q

MAOIs need to be used carefully to avoid the cheese effect (increased tyramine). What MAOI is an exception and why?

A

Selegiline

Transdermal patch, bypasses GI where a lot of tyramine is released

59
Q

What is the proposed mechanism by which lithium works? What class of receptors is affected by this?

A

Blocks formation of phosphoinositol

Blocks activity of the metabotropic receptos (GPCRs)

60
Q

Why can lithium cause / precipitate diabetes insipidus?

A

Too much urination because of non-responsiveness to ADH because ADH receptor is a metabotropic receptor and lithium blocks synthesis of its second messenger

Medical Pharmacology Exam 2 (16 decks)

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