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Psyc-2020 > Antidepressants, Mood Stabilizers, and Medications to Treat Anxiety > Flashcards

Antidepressants, Mood Stabilizers, and Medications to Treat Anxiety Flashcards

1
Q

What features of depression might make you want to learn more towards psychotherapy than pharmacotherapy?

A
  1. Presence of personality disorders

2. Psychosocial stressors -> medication cannot fix this

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2
Q

What features of depression might make you want to learn more towards pharmacotherapy than psychotherapy?

A
  1. History of response to medications in the past
  2. Family history of major depressive disorder
  3. Moderate to severe depression -> medications will always be needed
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3
Q

What is the mechanism by which antidepressants take 4-8 weeks to fully work?

A

Inhibitory 5-HT1A receptors are over-expressed on dendrites of serotonergic neurons in depression. Thus, they do not adequately release serotonin.

Over time of SSRI treatment, the 5-HT1A receptors become downregulated due to large amounts of serotonin in the area. This downregulation allows the increased release of 5-HT to the synapse.

This is called neuronal disinhibition

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4
Q

Other than for elderly patients, when should you start out with a low dose of antidepressant?

A

Patients with anxiety -> initial few doses can cause anxiety

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5
Q

What condition, if left untreated, can decrease the effectiveness of an antidepressant and must be addressed?

A

Insomnia

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6
Q

What are some of the withdrawal symptoms of SSRIs?

A

Dizziness, nausea, paresthesias, anxiety, insomnia

-> must be tapered over 2-4 weeks

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7
Q

What is the black box warning on antidepressants?

A

They increased suicidal thoughts and behavior (suicidality) in all people under age 24 in short term MDD / other psych disorder.

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8
Q

What is the only SSRI which has a recommendation of not being safe in pregnancy? What can it cause?

A

Paroxetine - can cause cardiac malformations in 1st trimester

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9
Q

List the four major SNRIs - only one of these you are unlikely to know?

A

Venlafaxine
Desvenlafaxine
Duloxetine
Levomilnacipran - Fetzima

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10
Q

List the atypical antidepressants. There is one which you are new to.

A 
Bupropion
Mirtazapine
Trazodone
Vilazadone
**Vortioxetine**
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11
Q

What medication class are doxepin and amoxapine in? What do other ones in this class end in?

A

Tricyclic antidepressants

-Others end in -amine, tyline, or tiline

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12
Q

What class is isocarboxazid in and what are some others in this class?

A

MAOIs

Phenelzine
Tranylcypromine
Selegiline

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13
Q

In regards to dosing, why are SSRIs preferred to other classes of antidepressants?

A
  1. They have a wide therapeutic window -> no need to closely titrate.
  2. They can be started at therapeutic dose (vs TCAs / MAOIs which need titration)
  3. They are safe in overdose
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14
Q

Which is the top SSRI known to be activating or sedating and what should be done to minimize this side effect? What drug is associated with the most weight gain?

A

Activating - Fluoxetine (one with longest halflife) -> dose in morning when you need the energy

Sedating - Paroxetine - give at bedtime

Weight gain - Paroxetine

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15
Q

What should be done to curb sexual side effects of SSRIs?

A

Lower the dose or add medication (bupropion, except in anxiety)

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16
Q

Which SSRI has the most CYP interactions, and which SSRIs are known to interfere with opiates?

A

Fluvoxamine - most interactions

Fluoxetine and paroxetine - interferes with effectiveness of opiates like codeine via CYP2D6 interference blocking conversion to active form

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17
Q

What additional functionality do SNRIs have and what side effect does this add?

A

NE reuptake blockade which is good for management of chronic pain syndromes

Added side effect - hypertension

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18
Q

Why does bupropion not have any sexual side effects? Is it useful in anxiety or any other conditions?

A

It is an NDRI, with no serotonergic effects which cause sexual dysfunction

Bad in anxiety -> can exacerbate

Useful in smoking cessation

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19
Q

What is the side effect of concern for bupropion / contraindication?

A

Seizures at higher doses

-> contraindicated in bulimics and anorexics likely to have underlying electrolyte imbalances

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20
Q

What is the mechanism of action of mirtazapine? Include all relevant receptors and their effects

A

Noradrenergic and specific serotonergic antagonist (NaSSA)

  • blocks 5-HT2 and 5-HT3 receptors (increases 5-HT1 agonism overall), with fewer sexual / GI side effects
  • blocks alpha2 receptors - increases NE in the synapse
  • histamine antagonism - increases weight gain and sedation
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21
Q

What is the mechanism of action of Vilazodone? What is its increased side effect?

A

SPARI - Serotonin partial agonist / reuptake inhibitor

SSRI + 5HT1A agonist -> possible increased efficacy for anxiety / depression

May make GI side effects worse

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22
Q

What is the mechanism of action of trazodone?

A

SARI - Serotonin antagonist / reuptake inhibitor

  • SSRI plus antagonizes 52 - 5HT-2 receptors
  • also has anti alpha-1 (lighter) and anti-histamine (beeswatting on the bench) effects
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23
Q

What is the usefulness of trazodone and its side effect profile?

A

Useful for insomnia due to anti-histamine effects

Alpha-1 blockade - can cause orthostatic hypotension (coach fainting)
Also causes priapism (erect trombone)

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24
Q

What is the mechanism of action of Vortioxetine and why is it potentially better than other antidepressants?

A

SSRI + a number of agonist / antagonist effects

  • 5HT7 blockade my confer some advantage to patients with cognitive complains over other SSRIs
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25
Q

What is the overall mechanism of tricyclic antidepressants?

A

Inhibition of NE reuptake, with varying degrees of SRI activity

ALL antagonize alpha1, histamine, and muscarinic ACh receptors

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26
Q

What syndromes might TCAs be particularly useful for?

A

Pain syndromes: migraines / neuropathy, due to NRI effects

Enuresis: Due to anticholinergic effects

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27
Q

Which TCAs are thought of as primarily NRIs? Primarily SRIs?

A

Nortriptyline (tripping child) and desipramine (imprint) - primarily NRIs

Clomipramine - primarily SRI -> has a specific usefulness

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28
Q

What cardiac side effects does a patient need to look out for when starting a TCA? What should be done when starting a patient?

A

Look out for chest pain / shortness of breath

Need baseline EKG if older than 40 or history of CVD
-> can cause tachycardia / prolonged QT / ST depression even at therapeutic doses

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29
Q

What are the drug interactions of concerns with TCAs?

A

They do not interact with CYP system, but should be not combined with other things potentiating their offtarget effects (anticholinergics, antihypertensives, CNS depressants)

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30
Q

What are the 3 C’s of TCA overdose?

A

Coma
Convulsions (seizures)
Cardiotoxicity (QT prolongation, arrhythmias)

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31
Q

What is the specific mechanism of action of all MAOI antidepressants in the US?

A

All MAOIs are irreversible and nonselective (block both A and B, take 2 weeks to reproduce the enzyme)

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32
Q

What type of depression are MAOI’s useful for?

A

Atypical depression, characterized by sleeping too much, eating too much, leaden paralysis, mood reactivity, and rejection sensitivity

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33
Q

What are the possible overdose side effects of MAOIs which limit their use?

A 
Hypertensive crisis (tyramines broken down by MAO-A primarily in gut, + NE breakdown blockade)
Serotonin syndrome
34
Q

What are the common side effects of MAOIs?

A

Edema
Insomnia
Sexual dysfunction and orthostatic hypotension (alpha1 blockade)
Weight gain (think of eating too much cheese)

35
Q

What is the definition of a hypertensive crisis and what is the treatment? What are a few symptoms?

A

Diastolic blood pressure is greater than 120 mmHG

Alpha-antagonist phentolamine is treatment

Symptoms: Occipital headache, neck stiffness, dilated pupils, and abnormal heart rate

36
Q

What drugs should be avoided with MAOIs and what can they cause?

A

Any drugs with sympathomimetic activity, including decongestants, stimulates, and antidepressants with NRI activity

Can cause hypertensive crisis

37
Q

How long do you have to wait after stopping a MAOI to start another 5HT agent? How longer after stopping fluoxetine to start a MAOI?

A

2 weeks after MAOI - enzyme turnover time

5 weeks after fluoxetine - has a long halflife

38
Q

What are the features of serotonin syndrome?

A

Hyperthermia, hypertension (think of overheating boss with smoke coming from his ears), autonomic instability, hypertonicity and myoclonus (think of boss taping his food excessively)

39
Q

What are the tricyclic compounds, opioids, and migraine medications which can precipitate serotonin syndrome when taken with MAOIs?

A

Tricyclic compounds

  • > cyclobenzaprine
  • > carbamazepine

Migraines
-> triptans (5HT1b/d)

Opioids (4 M’s + 1 other)

  • > tramodol
  • > methadone
  • > dextromethorphan (oh god memo)
  • > mepiridine
  • > Propoxyphene
40
Q

Why should MAOIs be given cautiously with anesthesia?

A

General and local anesthetics often contain epinephrine

41
Q

Are dietary restrictions needed with selegiline? By what route will you not need it?

A

Yes, but not needed if given as EMSAM (transdermal patch)

-> only inhibits MAO-B at these doses, so an ineffective antidepressant

42
Q

What nonpharmacologic therapy can be used alone or in combination with drugs for seasonal / nonseasonal depression?

A

Light therapy

43
Q

What is ketamine good for and its main side effect of risk?

A

Good for 72-hour antidepressant action (Aside from its general anesthetic properties)

  • > may cause hypertensive crisis
  • > does not lead to lasting maintenance of antidepressant effects without further injections
44
Q

When is ECT considered and how is it done?

A

With 2+ medication failures (generally more)
Patients who are acutely suicidal

Works via inducing seizures, works in 70% of treatment-resistant

45
Q

What are the contraindications of ECT and side effects of concern?

A

Contraindications:
Recent MI (causes SANS / PANS discharge)
Space occupying / hemorrhagic cranial lesion (increases ICP)

Side effect:
Memory problems

46
Q

What confers the greatest mortality risk in ECT?

A

Use of general anesthesia

47
Q

What is used as an alternative to ECT in treatment-resistant patients which has less efficacy? Side effect?

A

Transcranial magnetic stimulation (TMS)
-> Electrical current depolarizes neurons over dorsolateral prefrontal cortex

-> can cause headache

48
Q

What drugs / combinations are used to treat acute bipolar depression?

A

Atypical antipsychotic alone
Atypical antipsychotic / antidepressant (olanzapine / fluoxetine)
Lamotrigine
Lithium

49
Q

What drugs are used to treat acute bipolar mania?

A

Atypical / typical antipsychotics
Carbamazepine / Valproic Acid
Lithium

50
Q

What drugs are used for maintenance treatment of bipolar?

A

Atypical antipsychotics
Carbamazepine / Valproic Acid
Lamotrigine
Lithium

51
Q

Can you summarize the therapeutic uses of lithium, anticonvulsants, atypical / typical antipsychotics for BPAD?

A

Lithium: Good for all three
Anticonvulsants (carbamazepine / valproic acid) -> sedating, good for mania and maintenance
Atypical antipsychotics - good for all three, often as adjuunct
Typical antipsychotics - only used in acute bipolar mania

52
Q

What medication is known to decrease suicidality in bipolar patients, and what is its mechanism of action?

A

Lithium

Depletion of PIP to stop second messaging systems via G-protein

53
Q

What is the therapeutic concentrations of lithium and when should this concentration be measured?

A

0.6 - 1.2 mEq/L

Should be measured 12 hours after last dose, every 6 months after maintenance has begun

54
Q

How long does it take for lithium effects to be seen and what should be done in the meantime?

A

10-14 days, use antipsychotics or benzodiazepines to control agitation / insomnia

55
Q

What levels of lithium are considered deadly and when should hemodialysis begin?

A

> 2.5 mEq/L

>2.0 = acute renal failure, need to begin hemodialysis. Seizures can occur far before this point

56
Q

What drugs increase lithium levels? Where is it cleared?

A 
NCAT - think MCAT but NCAT
N - NSAIDs
C - Calcium channel blockers
A - ACE inhibitors
T - Thiazide diuretics

N/A - reduce GFR via reduced blood flow or volume
T - reduce sodium levels, thus increasing reabsorption of lithium in PCT

It is 95% kidney-cleared, 80% is reabsorbed so 20% of lithium clearance approximates GFR

57
Q

What drugs / conditions decrease lithium levels?

A

Theophylline / caffeine (increase GFR)
High sodium (larger Vd, less reabsorption of lithium)
Pregnancy (large Vd)

58
Q

List the minor CNS, cardiovascular, dermatological, endocrine / metabolic, fetal, GI, hematologic, and renal side effects of lithium?

A 
CNS - hand tremor / cognitive blunting
Cardiovascular - Edema
Dermatologic - alopecia, acne, psoriasis
Endocrine / metabolic - weight gain
Fetal - Ebstein's anomaly
Hematologic - Benign leukocytosis
Renal - Polyuria, polydipsia, nephrogenic diabetes insipidus
59
Q

What are the more medically serious side effects of lithium?

A

Hypothyroidism is common
Irreversible kidney disease
ECG changes - SA node blockade and sick sinus syndrome

60
Q

What is the mechanism of action of valproic acid and what is it used for in BPAD?

A

Increases GABA levels in the brain, along with Na+ channel inactivation, used for acute mania and maintenance treatment

61
Q

What is the most likely drug-drug interaction of valproic acid, and should plasma concentration be monitored?

A

Most likely to interact with highly protein-bound meds like warfarin, digitalis, and other anticonvulsants

Should be monitored and held to 50-100 mg/mL

62
Q

What blood-related and toxicity-related side effects differentiate valproic acid from lithium toxicity?

A

Valproate - will cause leukopenia / thrombocytopenia (vs lithium increases leukocytes), possible agranulocytosis

Valproate can also cause hemorrhagic pancreatitis (hemorrhagic sponge) and hepatotoxicity

63
Q

What tests should be ordered for valproate which are not ordered for lithium?

A

Liver function tests (metabolized by liver, can cause hepatotoxicity)
Platelets (agranulocytosis is a concern)

Lithium is more thyroid / kidney oriented since it is metabolized by kidney

64
Q

What is the mechanism of action of carbamazepine and its therapeutic window which requires monitoring?

A

Inhibition of voltage-gated Na+ channels

Therapeutic level is 8-12 mg/mL (Valproate was 50-100)

65
Q

What are some of the more common and rarer side effects of carbamazepine?

A

Common:
Diplopia, ataxia, nausea

Less common but serious: Stevens-Johnson syndrome (along with lamotrigine), pancytopenia, hepatic / pancreatic failure (like valproate)

66
Q

What is the teratogenicity of lithium, carbamazepine, valproate, and lamotrigine?

A

Lithium: Epstein’s anomaly (malformation of tricuspid valve)
Carbamazepine: NTDs
Valproate: NTDs
Lamotrigine: None

67
Q

What symptoms are very worrying of SJS and what should be done if this occurs?

A

Rash which is associated with sore throat and fever or diffuse facial / mucosal involvement
-> go to the ER

68
Q

What phases of bipolar disorder is lamotrigine indicated for? Its mechanism of action?

A

Inhibition of Na+ channels / glutamate channels

Approved for maintenance of BPAD, and sometimes treatment of bipolar DEPRESSION

69
Q

What interactions and side effects does lamotrigine have?

A

Carbamazepine -> decreases lamotrigine levels by inducing CYP

Valproate -> increases lamotrigine levels by blocking CYP

70
Q

What are the common and severe side effects of lamotrigine? who is most susceptible?

A

Common - Headache, nausea, dry mouth, ataxia, diplopia

Severe: SJS (toxic epidermal necrolysis) -> beningn rash is common early, but can be serious, titrate slowly especially if with valproic acid.

Kids more susceptible to SJS

71
Q

Why is antidepressant use risky and BPAD, and what should be used to prevent these sequellae?

A

Can lead to manic episode (Reversal)

Use lamotrigine for depresison, or olanzapine / fluoxetine

72
Q

What is the treatment for OCD?

A

HIGH dose SSRI or clomipramine (mostly SRI tricyclic) -> need that serotonin

73
Q

What are the benzos with the most rapid onset and shortest half lives?

A

Rapid onset - Diazepam

Shortest halflife - Alprazolam

74
Q

What are the side effects of benzos, especially as they relate to the elderly?

A

Cognitive problems / falls in elderly

Decreased respiration in prexisting pulmonary dysfunction

Anterograde amnesia

75
Q

What benzos are the safest to use with the elderly and why?

A

Lorazepam, Oxazepam
-> glucuronidation is only required (phase 2 metabolism does not slow with age)

-> others require oxidation (phase 1) which does slow with age

76
Q

What is the teratogenicity of benzos?

A

Has been associated with cleft palate in first trimester

77
Q

What is the largest drug interaction of benzos?

A

Benzos and opiates -> combined respiratory depression, sleepiness, coma, and death

78
Q

What beta-blocker is used in anxiety, what for, and how does it work?

A

Propanolol - for social anxiety disorder / social phobia, right before meeting that situation

Works by reducing peripheral manifestations of anxiety (tachycardia, tremor, sweating) to prevent conscious thought of it

79
Q

What is one medication which is only approved for GAD? How does it work?

A

Buspirone - 5HT-1a agonist

80
Q

What are the side effects of buspirone? Do you tolerize?

A

Mostly GI upset, drowsiness / dizziness

SEROTONIN SYNDROME IS POSSIBLE

-> cannot tolerize like benzos, but takes much longer to work (4-6 weeks)

Psyc-2020 (41 decks)

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