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BSP Midterm > Antidepressants And Mood Stabilizers > Flashcards

Antidepressants And Mood Stabilizers Flashcards

1
Q

What are some other indications for antidepressants?

A

Nicotine withdrawal (bupropion)
Enuresis (imipramine)
Diabetic peripheral neuropathy, fibromyalgia, and chronic MSK pain (duloxetine)
Stress incontinence (duloxetine)

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2
Q

What are serotonin-selective reuptake inhibitors (SSRI’s)?

A

They selectively inhibit pre-synaptic reuptake of serotonin via SERT
Result in enhanced, prolonged serotonergic neurotransmission to post-synaptic receptors

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3
Q

Name SSRI’s

A 
Citalopram
Escitalopram
Fluoxetine
Paraoxetine
Sertraline
Vilazodone
Vortioxetine
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4
Q

Describe common side effects of SSRI’s

A

As a class, much less impact on histamine, muscarinic, and adrenergic receptors. Fewer SE vs TCA’s
Examples:
CNS (sedation or insomnia/agitation/nervousness)
Sexual dysfunction (libido/impotence)
Weight gain (adults)/weight loss (mild; adolescents)
Acute withdrawal reactions (like with all categories): flu-like symptoms (malaise, lethargy, generalized aches)

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5
Q

Describe rare (toxic) side effects of SSRI’s

A

QT prolongation
Hyponatremia

Serious:
Serotonin syndrome
-Increased risk when given concurrently with other serotonin-affecting agents
-sweating, hyperreflexia, akathisia/myoclonus, shivering/tremors

Suicidality (attempts/completions)
-highest risk in children/adolescents/young adults

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6
Q

What precipitates neuroleptic malignant syndrome?

A

Dopaminergic agents (antipsychotics)

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7
Q

What are identical features of neuroleptic malignant syndrome and serotonin syndrome?

A

HTN, tachycardia, tachypnea, hyperthermia (>40C)

Hypersalivation

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8
Q

What are overlapping features of neuroleptic malignant syndrome and serotonin syndrome?

A

Diaphoresis, pallor (neuro)
Coma
Stupor and alert (neuro); agitation (sero)
Lead-pipe rigidity in all muscle groups (neuro); increased tone esp in LE (sero)

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9
Q

What are distinct features of neuroleptic malignant syndrome and serotonin syndrome?

A

Neuro:
Hypo-reflexia
Normal pupils
Normal or decreased bowel sounds

Serotonin:
Hyper-reflexia
Clonus
Dilated pupils
Hyperactivity of bowel sounds
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10
Q

Describe drug-drug interactions with SSRI’s

A

High risk of drug-drug interactions

  • *Most is fluoxetine (broad and strong inhibitor)
  • *Least is citalopram and sertraline (mild inhibitors)
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11
Q

What are serotonin-noradrenergic reuptake inhibitors (SNRI’s)? Tertiary vs secondary amine TCA’s?

A

Include TCA’s
Selectively inhibit presynaptic reuptake of serotonin via SERT and norepinephrine via NET
Tertiary TCA’s inhibit both NE/5-HT relatively equally (except clomipramine/amitriptyline, which impact 5-HT>NE)
Secondary TCA inhibit NE>5-HT

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12
Q

Name SNRI’s

A 
All TCA's
Desvenlafaxine
Duloxetine
Venlafaxine
Levomilnacipran

SNRI’s + dopamine antagonist: amoxapine

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13
Q

**Only TCA-based SNRI’s have impact on what 3 key non-efficacy-related receptors?

A

Histamine (H1)
Muscarinic (cholinergic)
Alpha1 (adrenergic)

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14
Q

Name the tertiary amine TCA’s

A

amitriptyline
Clomipramine
Doxepin
Imipramine

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15
Q

Name the secondary amine TCA’s

A

Amoxapine
Desipramine
Nortriptyline

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16
Q

*What are the 3 key TCA system side effects?

A

CV (alpha):
Tachycardia, orthostatic hypotension, dysrhythmias

Anticholinergic (muscarinic):
Dry mouth, urinary retention/constipation, blurred vision/increased IOP

CNS (histamine):
Sedation/fatigue, dizziness/seizures

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17
Q

What are the 3 C’s from toxic ingestion of TCA’s?

A

Coma
Cardiotoxicity (conduction abnormalities) (quinidine-like effect)
Convulsions

18
Q

What do class 1 antiarrhytmics do?

A

In ventricular cells, slows phase 0 depolarization and conduction velocity (slows conduction), alters QRS complex

Subclass-specific changes in repolarization (Na+ channel blockade)
Class IA: moderate Na+ channel block and prolonged repolarization
Class IB: mild Na+ channel block and shortened repolarization
Class IC: marked Na+ channel block and no change in repolarization

19
Q

Describe side effects of non-TCA SNRI’s

A

Relatively similar to SSRI’s with less risk (in general) of sexual dysfunction
Higher with venlafaxine

20
Q

What are serotonin-adrenergic receptor antagonists (SARAs)?

A

Trazodone and nefazodone act like SSRI’s and also selectively block post-synaptic alpha1 receptors on noradrenergic (NE) neurons and post-synaptic 5-HT2A (and H1 blockade (sedation))

Mirtazapine selectively blocks presynaptic alpha2 receptors on NE and 5HT neurons. Blocks postsynaptic 5HT 2a/2b/3 receptors, no SERT/NET activity. H1 blockade (sedation)

21
Q

What are side effects (H1/alpha1) of SARA’s?

A 
CNS (sedation) (most with trazodoe/mirtazapine)
Orthostatic hypotension (most with trazodone)
Weight gain (most with mirtazapine)
22
Q

What are noradrergic-dopamine reuptake inhibitors (NDRI’s)?

A

Bupropion

Selectively inhibits presynaptic reuptake of NE via NET and dopamine via DAT. Results in enhanced, prolonged NE and DA neurotransmission to postsynaptic receptors

May also enhance presynaptic release of NE and DA. Also shown to have effects on VMAT2

23
Q

What are side effects of NDRI’s?

A

Agitation/insomnia (stimulating) (hypertension, tachycardia, tremors)
Weight loss
**Seizures (dose-dependent or those at risk)

24
Q

What are monoamine oxidase inhibitors (MAOI’s)?

A

Inhibition of MOA (A/B) increases levels of monoamines in neuronal vesicles and increase amounts of NE, 5-HT, and DA released
All oral agents are irreversible (avg 14 days recovery. Tranylcypromine shortest at 3-5 days)
All agents Nonselective except selegiline (B-selective, becomes non-selective at high doses; antidepressant form is patch)

Tranylcypromine (stimulant analog) increases neurotransmitter release

25
Q

Name MAOI’s

A

Isocarboxazid
Phenelzine
Selegiline
Tranylcypromine

26
Q

What are side effects of MAOI’s?

A

Orthostatic hypotension
Sexual dysfunction
Weight gain
Insomnia/agitation/nervousness

27
Q

Describe drug-drug interactions of MAOI’s with 5HT/NE affecting drugs

A

Some anti-hypertensives, amphetamines, SSRI’s/TCAs/SNRI’s
*2 week wash-out period (fluoxetine; 5 wks)

Risk of serotonin syndrome
Risk of hypertensive crisis

28
Q

*The major risk of MAOI’s is hypertensive crisis. Explain

A

Non-selective MAOI’s inhibit MAO-A necessary in GI for tyramine metabolism
Increased tyramine can induce significant catecholamine release and hypertensive crisis
Selegiline (especially topical) minimally blocks MAO-A in GI tract at low doses; blockade increased to significant-blockade at high doses
Dose-dependent inhibition

Low risk with low dose selegiline patch

29
Q

*What are the signs and symptoms of hypertensive crisis due to MAOI’s?

A 
Severe headache
Nausea/vomiting
Sweating/severe anxiety
Nosebleeds
Tachycardia
Chest pain
Changes in vision
Shortness of breath
Confusion
30
Q

What are examples of tyramine containing foods/beverages?

A

Aged cheeses esp. those not pasteurized
Fava/broad/soy beans or snow peas
Fermented or pickled eats/poultry/fish (lox/salmon/herring)
Processed, pickled, or cured meats/sausages (bologna, pepperoni, salami, summer sausage)
Tap beer/beers not pasteurized, red wine, sherry, and liqueurs
Yeast or protein extracts/spreads
Over-ripe or spoiled fruit/foods
Soy/fish/shrimp sauces

31
Q

Describe treatment modalities of depression

A 
Pharmacotherapy (antidepressants, antipsychotics, mood stabilizers)
Psychosocial therapies (pt and family)
Electroconvulsive therapy (ECT)
Deep brain stimulation (DBS)
Transcranial magnetic stimulation (TMS)
Light therapy
32
Q

What are the 5 R’s for general antidepressant efficacy?

A
  1. Response =/> 50% reduction in symptoms from baseline
    Not well. Just better. Partial response =/>25% reduction but <50% in symptoms from baseline
  2. Remission = symptom-free (very low-to-no symptoms).
    Not only better but well. Healthy state of functioning
  3. Recovery = 2-6 months of ongoing remission.
    Not cured
  4. Relapse = return of symptoms after remission but before recovery
  5. Recurrence = return of symptoms after recovery
33
Q

Describe general antidepressant efficacy

A

All agents effect but take 3-8+ weeks depending on disease severity/duration and dose.
Majority see 50% reduction in first 3-4 weeks (response).
Goal is remission/recovery.
Minority reach remission on single agent.
If pt does not respond in 8 weeks, switching to different MOA reasonable.
If partial response, other drugs may be added.
Mono-therapy with antidepressants only for unipolar depression, not depressive phase of bipolar disorder

34
Q

**Describe treatment of depression

A

ALL antidepressants either are or can be associated with withdrawal syndrome.
Slow titration downward is recommended for most agents (t1/2)
Symptoms include dizziness, headaches, nervousness, nausea, insomnia, and flu-like aches
Lower risk with long-acting agents (fluoxetine, amitriptyline), yet even possible with XR-type products (venlafaxine xR)

35
Q

Describe proposed mood stabilizer action of Lithium

A

Inhibits calcium-dependent and depolarization-provoked release of NE & DA
Inhibits inositol monophosphatase leading to decreased cerebral inositol (valproate decreases inositol via inhibition of myoinositol-1-phosphate synthase)
Decreases functioning of protein kinases in brain like PKC (valproate, too)
Long-term Li+ decreases cytoplasm-to-membrane translocation of protein kinase-C and reduces PKC stimulation-induced release of 5-HT (disrupts prefrontal cortical regulation of behavior. Valproate, too)
Reduces expression of MARCKS protein (valproate, too)
Inhibits GSK-3B activity (Increases B-catenin)(valproate, too)
Facilitates 5-HT release (augments effects of antidepressants)

36
Q

What is the major side effect of lithium? Describe

A

Polyuria (polydipsia)
Clinical picture of *nephrogenic diabetes insipidus

Lithium is a monovalent ion and handled by kidneys similar to Na+/K+. Li+ competes with Na+ for kidney reabsorption.
chronic Li+ ingestion can lead to resistance to ADH, resulting in in polyuria/polydipsia. Li+ enters principal cells of collecting duct via Na+ channels in luminal membrane. Accumulation in these cells interferes with ADH-mediated effects

37
Q

What are other side effects of Lithium?

A

Tremor
Mental confusion/dizziness/sedation (take at bedtime)
Thyroid goiter (hypothyroidism) (inhibits iodination of thyroid hormone)
Leukocytosis (stimulates M-CSF, increasing granulocytes)
Seizures and serotonin syndrome (rare but can be severe)

38
Q

**Describe drug interactions of lithium wth other agents impacting Na+/K+

A

Diuretics via preferential Na+ loss and Li+ reabsorption, especially thiazides (hydrochlorothiazide)
ACEIs especially lisinopril (renally eliminated)
NSAIDs through alteration of renal perfusion

Narrow therapeutic agent (monitored at trough phase)
0.6-1.0 mEq/mL (up to 1.5 mEq/mL in refractory cases)

39
Q

What are indications for lithium?

A

Acute & maintenance treatment of mania/bipolar I disorder
Augmentation in unipolar depressive pts with inadequate response to antidepressant therapy
Off label: reduced risk of suicide and all-cause mortality in pts with mood disorders

40
Q

Describe uses/indications for mood stabilizers (anti-seizures) agents

A

Divalproex used for acute bipolar I (with or without psychotic features): 50-125 McGill/mL
Carbamazepine used for acute and maintenance treatment of acute mania and mixed episodes (bipolar I). Major CYP450 inducer
Lamotrigine used for maintenance of bipolar disorder I and II

BSP Midterm (6 decks)

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