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5. HDS Neuro Psych > Anti-depressants > Flashcards

Anti-depressants Flashcards

1
Q

Trimonoaminergic System

A

Neurotransmitters in pathophysiology and tx of mood disorders:

  • Serotonin, norepinephrine > dopamine
    • Many areas receive input from all 3 systems
    • All known treatments for mood disorders act on one or more of these neurotransmitter systems
  • Serotonin neurons in CNS originate in the raphe nucleus
    • Projections to spinal cord
      • Pain perception, visceral regulation, and motor control
    • Projections to the Forebrain
      • Mood, cognition, and neuroendocrine function
  • Noradrenergic neurons originate in the locus coeruleus
    • Projections to spinal cord
      • Regulate pain pathways
    • Projections to the forebrain
      • Mood, arousal, and cognition
  • Serotonin and NE released 1° from varicosities
    • Large amounts of neurotransmitter into the projection area
    • Feedback inhibition ⇒ fairly constant amount released & concentrations stays in a narrow range
    • Maintains a baseline tone for the target areas
    • Specific stimuli elicit rapid bursts ⇒ superimposed on baseline
  • Dopamine system projections much more discrete
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2
Q

Catecholamines

Synthesis, Storage, and Release

A
  • Tyrosine → L-dihydroxyphenylalanine (L-DOPA) by tyrosine hydroxylase (rate limiting)
    • Feedback inhibition by NE via pre-synaptic α2 -adrenergic receptors
      • ⊕ α2 Ad-R (GPCR) ⇒ ↓ cAMP ⇒ ↓ cAMP activated protein kinase ⇒ normally ℗ and ⊕ this enzyme
  • L-DOPA → Dopamine by aromatic L-amino acid decarboxylase (AAADC) (aka L-DOPA decarboxylase)
    • Found in neuronal and non-neuronal cells in CNS and peripheral tissues
    • Exogenous L-DOPA ⇒ ↑ catecholamines in catecholamine neurons and serotonergic neurons
  • DA → synaptic vesicles → norepinephrine by dopamine-β-hydroxylase
    • NE concentrated within vesicles and ready for release
    • DA and NE transport into vesicles by vesicular monoamine transporter (VMAT)
      • Inhibited by reserpine
    • Degradation of DA & NE by cytoplasmic monoamine oxidase
  • In the adrenal medulla, NE → epinephrine by phenylethanolamine N-methyltransferase (PNMT)
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3
Q

Catecholamines

Reuptake

A
  • NE released into the synaptic cleft
  • Taken back up into synaptic terminal by norepinephrine reuptake transporter (NET)
    • Specific for norepinephrine
    • Inhibited by cocaine
  • Stored in the vesicles for reuse
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4
Q

Catecholamines

Metabolism

A
  • Norepinephrine → aldehyde (DOPGAL) by monoamine oxidase (MAO)
    • Two forms ⇒ MAO-A and MAO-B
      • On outer membranes of MΦ within neurons, glia, liver and GI tract
      • Distribution of isozymes differs among cells and tissues
        • Intestines ⇒ 75% MAO-A
        • Liver ⇒ 50/50 split b/t MAO-A and MAO-B
        • 1° metabolic barriers vs dietary tyramine and other circulating substrates
      • Tyramine is metabolized by both isozymes
      • MAO-A catabolizes 5-HT, NE, and dopamine
      • MAO-B preferentially catabolizes dopamine
  • Aldehyde → acidic metabolites by aldehyde dehydrogenase
  • Norepinephrine further metabolized by catechol-O-methyltransferase (COMT)
    • Methylation can occur on parent compound or acid metabolite
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5
Q

Catecholamine

Receptors

A
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6
Q

Serotonin

Synthesis, Storage and Release

A
  • Dietary L-tryptophan → 5-hydroxytryptophan (5-HTP) by tryptophan hydroxylase (rate limiting)
    • Only in cells that synthesize 5-HT in the brain and periphery
    • Feedback inhibition via serotonin receptors located pre-synaptically (5HT1B/D) and somatodendritic receptors (5HT1A)
      • ⊕ GPCR ⇒ ↓ cAMP ⇒ ↓ cAMP activated protein kinase ⇒ normally ℗ and ⊕ this enzyme
  • 5-HTP → serotonin (5-HT) by aromatic L-amino acid decarboxylase (AAADC)
  • Transported into synaptic vesicles by non-specific vesicle monoamine transporter (VMAT)
  • Stored, protected from monoamine oxidase, and ready for release on demand
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7
Q

Serotonin

Reuptake and Metabolism

A
  • Reuptake back into the synaptic terminal by the selective serotonin reuptake transporter
    • Specific transporter for serotonin
    • Transporters also exist on platelets and in enterochromaffin cells in the GI tract
      • Non-neuronal transporters responsible for some side effects of SSRIs/SNRIs
  • 5-HT → aldehyde of 5-HT by monoamine oxidase (MAO)
  • Aldehyde → 5-hydroxyindoleacetic acid (5-HIAA) by aldehyde dehydrogenase
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8
Q

Serotonin Receptors

A
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9
Q

Monoamine and Serotonin

Interaction

A

Reciprocal relationship:

NE ⇒ ⊗ serotonin release via α2 adrenergic heteroreceptors on serotonergic terminals

Serotonin ⇒ ⊗ norepinephrine release via 5HT2A receptors on noradrenergic neurons

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10
Q

Monoamine Hypothesis of Depression

A

Depression results from a decrease in serotonin and norepinephrine transmission.

  • Drugs to tx other diseases found to have a strong antidepressant effect via serotonergic and noradrenergic neurotransmitter systems
    • Imipramine (tx schizophrenia) ⇒ ⊗ serotonin reuptake
      • Its active metabolite ⇒ ⊗ reuptake of norepinephrine
    • Iproniazid (tx tuberculosis) ⇒ ⊗ monoamine oxidase ⇒ responsible for degradation of monoamines
      • Has antidepressant effects
    • Reserpine (antihypertensive) ⇒ ⊗ VMAT ⇒ caused depression in some pts
      • VMAT responsible for uptake of monoamines into storage vesicles
      • Allows monoamines to be degraded by monoamine oxidase
      • Subsequent ↓ in monoamine release thought to lead to depression
  • Pts responsive to a serotonin reuptake inhibitor will relapse w/ low tryptophan diet (precursor for serotonin)
  • Most available antidepressants ∆ monoamine neurotransmission in some way
  • Hypothesis still incomplete b/c little e/o actual ∆ in monoamine levels during depression
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11
Q

Neurotrophic Hypothesis of Depression

A

Depression is associated w/ a loss of neurotrophic support

&

Antidepressants will increase neurogenesis and synaptic connectivity in areas such as the hippocampus.

Brain derived neurotrophic factor (BDNF) ⇒ most important factor

  • Pain and stress ⇒ ↓ BDNF ⇒ atrophic changes in areas of the brain relevant to depression
  • Direct injection of BDNF in animals ⇒ antidepressant effects
  • Chronic treatment w/ antidepressants ⇒ ↑ BDNF ⇒ correlates w/ onset of therapeutic effect
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12
Q

Neuroendocrine Factors

A

Depression associated w/ a number of hormonal abnormalities including:

  • Elevated cortisol, suggesting a disruption of the HPA
  • Thyroid dysregulation
  • Sex hormone deficiency
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13
Q

Antidepressants

Basic Pharmacology

A
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14
Q

Ketamine

A
  • Has been used to tx severe resistant depression
  • No therapeutic lag
  • Thought to work by ↑ synaptogenesis
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15
Q

Selective Serotonin Reuptake Inhibitors (SSRI)

Drugs

A
  • Fluoxetine (Prozac)
  • Sertraline (Zoloft)
  • Citalopram (Celexa)
  • Fluvoxamine (Luvox)
  • Paroxetine (Paxil)
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16
Q

SSRIs

Mechanism of Action

A

⊗ reuptake of serotonin into the presynaptic terminal

  • Pharmacological effect occurs shortly after dosing
  • Therapeutic effect occurs over 2 to 4 weeks
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17
Q

SSRIs

“Therapeutic lag”

A

“Therapeutic lag” ⇒ correlates w/ desensitization of presynaptic receptors, ↑5-HT release, ↑ ⊕ of postsynaptic 5HT1A receptors

  • Initial admin of SSRI ⇒ modest ↑ in 5HT at the
    • Synapse
    • Somatodendritic 5HT1A receptors in the raphe nucleus
    • Presynaptic receptor
  • Over time, somatodendritic receptors and presynaptic receptors desensitize
  • Removes feedback inhibition on serotonergic neuron ⇒ large ↑ in neuronal activity ⇒ ↑↑↑ release of serotonin
  • Post-synaptic:
    • 5HT1A receptors DO NOT desensitize
    • 5HT2 receptors DO desensitize
      • Desensitization of 5HT2A ⇒ some degree of side effect tolerance and may play a role therapeutically
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18
Q

SSRIs

Therapeutic Uses

A
  • Major depression (typical)
  • Generalized anxiety disorder
  • Post-traumatic stress disorder
  • Obsessive compulsive disorder
  • Panic disorder
  • Premenstrual dysphoric disorder
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19
Q

SSRIs

Pharmacokinetics

A
  • Fluoxetine ⇒ longest half-life
    • Norfluoxetine (active metabolite) ⇒ half-life of almost 8 days
      • Needs to be discontinued 4 weeks before switching to an MAO inhibitor
        • Avoid the potential for serotonin syndrome
  • Some of these drugs are potent inhibitors of cytochrome p450 ⇒ potential for drug interactions
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20
Q

SSRIs

Common Adverse Effects

A
  • Nausea
    • ⊕ of 5HT3 receptors in area postrema and on vagal afferent to the CNS
  • Diarrhea
    • ⊕ of 5HT4 receptors in GI tract
  • Sexual dysfunction
    • ⊕ of 5HT2A and 5HT2C receptors in spinal cord ⇒ ⊗ spinal reflexes of orgasm and ejaculation
    • ⊕ of 5HT2A receptors in mesocortical tract ⇒ ↓ dopamine release ⇒ apathy and ↓ libido
  • Anxiety, agitation, insomnia
    • ⊕ of 5HT2A receptors in the various areas of brain and spinal cord
  • Discontinuation syndrome
    • Sudden discontinuation of short half-life SSRI’s (ex. paroxitine and sertraline) can lead to this syndrome
    • Dizziness, and tingling or numbing in the skin
    • Starts 1-2 days after stopping and may persist for a week
  • Serotonin syndrome
    • Can occur w/ any drug that ↑ serotonin (incl. opioids)
    • More likely to occur when drugs used in combo (ex. MAOi & SSRI)
    • Wash out period is necessary when switching meds
    • Hyperthermia, muscle rigidity, cardiovascular collapse, flushing and diarrhea
  • Reduced platelet aggregation
    • ⊗ of 5-HT uptake by platelets ⇒ inadequate availability 5-HT for hemostatic mechanisms
    • SSRI’s ↓ risk of clotting and repeat MI in cardiac pts for post-MI depression
    • SSRI’s ↑ risk of bleeding, esp. when combined w/ ASA or other NSAID’s (benefits in pts at risk for thrombosis)
  • Sweating
  • Suicide
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21
Q

Neuroleptic Malignant Syndrome

vs

Serotonin Syndrome

A
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22
Q

Serotonin Syndrome

Treatment

A

Tx depends on severity:

  • Discontinue SSRI
  • Treat w/ a benzodiazepine
  • 5HT2 blocker (cyproheptadine)
23
Q

SSRIs

Drug Interactions

A

Most common interactions are pharmacokinetic

  • Paroxetine and fluoxetine are potent inhibitors of cytochrome p450 CYP2D6 that metabolizes the tricyclics ⇒ sign. ↑ and toxicity
  • Fluvoxamine inhibits cytochrome p450 CYP3A4 that metabolizes other drugs such as diltiazem
  • Citalopram is relatively free of interactions
  • The most serious interaction is w/ MAOI’s to produce serotonin syndrome
24
Q

Selective Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)

Drugs and MOA

A

Duloxetine ⇒ ⊗ serotonin and norepinephrine transporter

Venlafaxine ⇒ ⊗ serotonin transporter @ low doses and also ⊗ norepinephrine transporter @ higher doses

Do not bind histamine, α__-adrenergic, and muscarinic receptors ⇒ better tolerated than TCAs

25
Q

SNRIs

Therapeutic Uses

A
  • Major depression
  • Atypical depression (venlafaxine)
  • Generalized anxiety
  • Stress urinary incontinence
  • Vasomotor symptoms of menopause
  • Pain of diabetic peripheral neuropathy (duloxetine)
26
Q

SNRIs

Pharmacokinetics

A
  • Venlafaxine → desvenlafaxine (active metabolite) by cytochrome p450 enzyme
    • Both have a T½of 11 hours
    • Desvenlafaxine is marketed separately ⇒ does not undergo additional oxidative metabolism
  • Duloxetine is extensively metabolized in liver by cytochrome p450 CYP2D6
    • Contraindicated w/ hepatic insufficiency
    • Also highly protein bound
27
Q

SNRIs

Adverse Effects

A
  • Relatively mild compared to TCAs
  • Some overlap w/ SSRIs (Nausea)
  • Noradrenergic effects:
    • ↑ BP / HR
    • CNS activation such insomnia, anxiety, and agitation
  • High doses of venlafaxine more likely to have adverse cardiac effects
  • Discontinuation syndrome
  • Serotonin syndrome
28
Q

SNRIs

Drug Interactions

A
  • Compared to SSRIs, interactions w/ cytochrome p450 are mild
  • Venlafaxine is a substrate but not an inhibitor
  • Duloxetine is a moderate inhibitor of CYP2D6 ⇒ ↑ TCAs
  • The most serious interaction is w/ MAOI’s to produce serotonin syndrome
29
Q

Tricyclic Antidepressants

Drugs

A
  • Amitriptyline
  • Nortriptyline
  • Imipramine
  • Desipramine
  • Clomipramine
30
Q

TCAs

Mechanism of Action

A

⊗ norepinephrine and serotonin reuptake

Considerable variation

  • Tertiary amines: Amitriptyline, Imipramine, Clomipramine (CIA)
    • Proportionally more effect in boosting 5-HT > NE
    • Produces more sedation, anticholinergic effects, and orthostatic hypotension
    • Clomipramine ⊕ primarily serotonin reuptake
  • Secondary amines: Nortriptyline, Desipramine
    • More effect on NE levels
    • Produces more irritability, overstimulation, and sleep disturbance
    • Desipramine more selective for norepinephrine
31
Q

TCAs

Therapeutic Uses

A
  • Not commonly used d/t adverse effects and toxicity
  • Used for refractory depression
  • At lower doses, may be used to treat pain
  • Imipramine has been used for enuresis (bed wetting)
  • clomipramine has been used for OCD
  • No longer preferred treatments
32
Q

TCAs

Pharmacokinetics

A
  • Most are dosed once a day and at night d/t sedating effects
  • Extensively metabolized by the CYP2D6
  • Can interact w/ other drugs that inhibit this system such as fluoxetine
33
Q

TCAs

Adverse Effects

A
  • Sedation
  • Anticholinergic: dry mouth, tachycardia, urinary retention etc
    • More common w/ tertiary amines such as amitriptyline and imipramine
  • α-Adrenergic Blockade: postural hypotension
  • Antihistamine H1 Receptors: weight gain and sedation
  • Sexual Side Effects
    • H1 & sexual side effects more common w/ clomipramine which is fairly specific for serotonin reuptake transporter
  • Discontinuation Syndrome
    • Because of cholinergic rebound
  • Serotonin Syndrome if combined w/ SSRI’s or MAOi
34
Q

TCA

Toxicity

A

Remember the 3 C’s: coma, convulsions and cardiotoxicity

  • Cardiotoxicity
    • Quinidine-like effect ⇒ conduction delays
      • # 1 cause of mortality in TCA toxicity
      • ⊗ Fast sodium-channel in His-Purkinje system
      • Impairs Na+ entry into myocardial cells
      • Slows depolarization (phase 0)
    • Sodium bicarbonate ⇒ antidote to reverse the cardiac toxicity
      • ↑ # of open Na+ channels ⇒ ↑ Na+ gradient across poisoned channels ⇒ partially reversing fast sodium channel blockade
      • Also pH dependent effects
  • Convulsions
    • ⊗ GABA-A receptor
    • Major cause of seizure in TCA toxicity
  • Confusion and hallucinations can occur in the elderly that are very susceptible to anticholinergic effects
35
Q

TCAs

Drug Interaction

A
  • ↑ [TCA] when administered w/ CYP2D6 inhibitors or in pts w/ polymorphism for the enzyme (~7% of Caucasians)
  • Anticholinergic or antihistamine effects may be additive w/ other OTC meds
  • Antihypertensive medications may exacerbate the postural hypotension
36
Q

Serotonin 5-HT2 Receptor Antagonists

Drugs

A

Trazodone and Mirtazapine

37
Q

Trazodone

MOA

A
  • The major metabolite ⇒ 5-HT2A antagonist & ⊗ serotonin reuptake
    • Enhances 5-HT transmission at postsynaptic 5-HT1A receptors and 5-HT2 receptors other than 5-HT2a
    • Effects only occur at high doses
  • At much lower doses, acts as an antagonist at histamine and α-adrenergic receptors
38
Q

Trazodone

Therapeutic Uses

A

Most common use in current practice is as a hypnotic

Treating insomnia w/ low doses of trazodone may augment effects of other antidepressants

39
Q

Trazodone

Pharmacokinetics

A
  • Rapidly metabolized ⇒ low bioavailability
  • Requires BID dosing if used as an antidepressant
  • Most often, it is administered once a day at a low dose at night for its sedative properties
40
Q

Trazodone

Adverse Effects

A
  • Sedation
  • GI upset (less pronounced than SSRIs and SNRIs)
  • Sexual side effects are uncommon
  • α-adrenergicblockade ⇒ hypotension and priapism (rare)
  • Nefazodone (analogue) ⇒ no longer commonly used because of severe liver toxicity
41
Q

Trazodone

Drug Interactions

A

Trazodone is a substrate for CYP3A4

C__ombo w/ potent inhibitors of cytochrome such as ritonavir or ketoconozole ⇒ ↑↑↑ levels of trazodone

42
Q

Mirtazapine

Mechanism of Action

A
  • ⊗ 5HT2A/2C and 5HT3 receptors and ⊗ presynaptic alpha-2 receptors
    • ⊗ of presynaptic receptors ⇒ ↑ release of norepinephrine and serotonin
    • ↑ serotonergic transmission @ 5HT receptors OTHER than 5HT2 receptors, primarily the 5HT1A receptor
    • ⊗ of 5HT2A/2C and 5HT3 receptors ⇒ eliminates side effects ass. w/ stimulating these receptors
  • Also ⊗ histamine receptors
43
Q

Mirtazapine

Pharmacokinetics & Therapeutic Uses

A
  • harmacokinetics:
    • T ½ is 20-40 hours
    • It is usually dosed once a day in the evening because of the sedating properties
  • Indications:
    • Could be used in melancholic depression
    • Antihistamine properties so sedating ⇒ used in depressed pts that have trouble sleeping
    • Also, mirtazapine will enhance appetite
44
Q

Mirtazapine

Adverse Effects & Drug Interactions

A
  • Adverse Effects:
    • Increased appetite and weight gain
    • Sedating
    • Does not interfere w/ sexual function which is mediated by 5HT2A/2C receptors
  • Drug Interactions:
    • Some cytochrome p450 type interactions
    • Sedating properties may be additive w/ other CNS depressants such ethanol or benzodiazepines
45
Q

Bupropion

Mechanism of Action

A

Unicyclic Antidepressant

  • Drug resembles amphetamine in chemical structure ⇒ CNS activating properties
  • ↑ norepinephrine release > ↑ dopamine release
  • Modest ⊗ of norepinephrine and dopamine reuptake
  • Unique structure leads to a different side effect profile
46
Q

Bupropion

Therapeutic Uses & Pharmacokinetics

A

Atypical depression and smoking cessation

Extensive first pass metabolism ⇒ short T ½

More than once a day dosing may be required

47
Q

Bupropion

Adverse Effects & Drug Interaction

A
  • Side effects may include agitation, insomnia and anorexia
    • Not associated w/ sexual side effects
  • Some cytochrome p450 type interactions
    • Bupropion should not be combined w/ MAOIs
48
Q

Monoamine Oxidase Inhibitors (MAOIs)

Drugs and MOA

A

Phenelzine, Tranylcypromine, Isocarboxazid, Selegiline

Mechanism of Action:

⊗ MOA ⇒ ↓ monoamine metabolism ⇒ ↑ transmission

  • Phenelzine and tranylcypromine are currently in the US
    • Irreversible non-selective MAOi (MAOA and MAOB)
      • MAO-A preferentially catabolizes NE and 5-HT
  • Selegiline ⇒ selective MAO-B inhibitor
    • Used in treating Parkinson’s disease
    • At usual therapeutic dose, selegiline primarily protects dopamine (DA) from catabolism by MAO-B
    • At higher doses that may have antidepressant properties, selegiline loses isozyme-selectivity
  • ⊗ of MAO-A appears to be more important in antidepressant benefit from MAO inhibitors
  • Other agents in this class referred to as the RIMA class (Reversible Inhibitors of Monoamine Oxidase Type A)
49
Q

Monoamine Oxidase Inhibitors

Therapeutic Uses

A

Now rarely used because of toxicity and the potential for food interactions

  • Used for treatment of depression unresponsive to other agents
  • Effective against atypical depression
  • Have been used to treat anxiety, social anxiety, and panic disorder
  • Selegiline is used as an adjunct in Parkinson’s, at higher concentrations it used for depression
50
Q

Monoamine Oxidase Inhibitors

Pharmacokinetics

A

Extensive first pass effect

Transdermal selegiline avoids this first pass and mitigates some of the food interactions

51
Q

Monoamine Oxidase Inhibitors

Adverse Effects

A
  • Tyramine effects
    • ⊗ of both isozymes ⇒ ⊗ tyramine metabolism
      • Constituent of many foods including aged cheese, some red wines, and beer
    • Tyramine escapes normal enzymatic defenses in the gut, plasma and liver ⇒ reaches sympathetic neurons where it releases NE
      • NE is not degraded because MAO is inhibited
    • Can produce dramatic hypertension
    • Competitive, reversible MAO-A selective drugs are much less likely to produce this type of drug interaction
  • Serotonin syndrome via interactions w/ drugs cause 5-HT release
    • Includes meperidine and other opiates, TCA’s, L-DOPA and SSRI’s
  • Hypertension through interactions w/ sympathomimetics
  • CNS stimulation in overdose
    • Tranylcypromine resembles amphetamine
    • Selegiline has an amphetamine like metabolite
  • Postural hypotension
    • May be due to elevated levels of dopamine in the periphery or to formation of a “false transmitter” called octopamine
  • Weight gain
    • Might involve desensitization of serotonergic satiety mechanisms but this is highly speculative
    • Weight gain can be substantial in some pts
    • Can lead to noncompliance, treatment cessation or a search for an alternative drug
52
Q

Monoamine Oxidase Inhibitors

Drug Interactions

A
  • Pharmacodynamic interactions w/ SSRIs, SNRIs, TCAs, meperidine, others to cause the serotonin syndrome
    • Cognitive: delirium, coma
    • Autonomic: hypertension, tachycardia, sweating
    • Somatic: myoclonus, hyperreflexia, and tremor
  • Allow two weeks after most serotonergic drugs but 4-5 weeks w/ fluoxetine before switching to MAOIs
  • MAOIs must be discontinued 2 weeks before giving another serotonergic agent
  • Second major interaction is w/ tyramine
  • Other sympathetic drugs such as pseudoephedrine are also contraindicated w/ MAOIs
53
Q

Antidepressants

Table

5. HDS Neuro Psych (46 decks)

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