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Tavalin - Antidepressants Flashcards

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1
Q

What are the TCA’s?

A
  • Amitriptyline
  • Nortriptyline
  • Protriptyline
  • Imipramine
  • Clomipramine
  • Desipramine
  • Trimipramine
  • Doxepin
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2
Q

What are the SSRI’s?

A
  • Citalopram
  • Escitalopram
  • Fluoxetine
  • Paroxetine
  • Sertraline
  • Fluvoxamine
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3
Q

What are the atypical antidepressants?

A
  • Venlafaxine
  • Duloxetine
  • Bupropion
  • Mirtazapine
  • Maprotiline
  • Vortioxetine
  • Amoxapine generic
  • Trazodone
  • Nefazodone generic
  • Vilazodone
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4
Q

What are the MAOI’s?

A
  • Tranylcypromine
  • Isocarboxazid
  • Phenelzine
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5
Q

What are the mood stabilizers?

A
  • Lithium
  • Valproate
  • Carbamazepine
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6
Q

What is depression?

A
  • Heterogeneous affective disorder that manifests itself in emotional, cognitive, behavioral, and somatic regulation
  • Interfere with ability to work, study, sleep, eat, and enjoy once pleasurable activities
  • Disabling episodes may occur only once, but more commonly occur several times in a lifetime
  • Lifetime prevalence of 17%
  • 15% of prescriptions in US are for depression
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7
Q

What are the symptoms of depression?

A
  • CORE SYNDROME + “VITAL SIGNS”

- NOTE: symptoms may occur to varying severity

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8
Q

What are the symptoms of the depressive core syndrome?

A
  • Persistent sad, anxious, tense, or empty mood
  • Feelings of hopelessness, pessimism, guilt, worthlessness, and helplessness
  • Persistent physical symptoms that do not respond to tx, like headaches, digestive disorders, and chronic pain
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9
Q

What are the “vital signs” of depression?

A
  • Difficulty concentrating, remembering, making decisions
  • Loss of interest or pleasure in hobbies or activities that were once enjoyed, incl. sex
  • DEC energy, fatigue, being “slowed down”
  • Insomnia, early morning awakening, or oversleeping
  • Appetite and/or weight loss or overeating and weight gain
  • Thoughts of death or suicide; suicide attempts
  • Restlessness, irritability
  • NOTE: reflective of somatic disturbances
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10
Q

What are the 3 classifications of depression?

A
  • Reactive (secondary): about 60%
  • Major depressive disorder (endogenous; unipolar): about 25%
  • Bipolar disorder (manic depression): 15%
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11
Q

What are the features of reactive (secondary) depression?

A
  • 60%
  • Associated w/loss (adverse life events), physical illness, drugs (anti-HTN, alcohol, hormones), or other psychiatric disorders (senility)
  • Consists of CORE depressive syndrome
  • May remit spontaneously, or in response to drugs
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12
Q

What are the features of major depressive disorder (endogenous; unipolar)?

A
  • 25%
  • Typically recurrent; consists of core syndrome and vital symptoms
  • Precipitating life event not adequate for the severity, and may be unresponsive to life events (autonomous)
  • Any age, but peak onset 20-40 yrs
  • More common in F; INC risk +/- 3 months childbirth
  • Family hx of depressive disorder is common, i.e., genetic
  • Responsive to anti-depressant drugs and ECT
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13
Q

What are the features of bipolar disorder (manic depression)?

A
  • 15%
  • Characterized by alternating episodes of depression and mania
  • Misdiagnosed as endogenous depression if manic episodes missed
  • Treated with mood stabilizers (and possibly antipsychotics), in addition to anti-depressants
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14
Q

What are the symptoms of mania?

A
  • Abnormal or excessive elation
  • Unusual irritability
  • DEC need for sleep
  • Grandiose notions
  • INC talking
  • Racing thoughts
  • INC sexual desire
  • Markedly INC energy
  • Poor judgment
  • Inappropriate social behavior
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15
Q

What is the biogenic amine hypothesis for depression? How are AD’s involved?

A
  • Functional deficit of MA’s (esp. NE and 5-HT) thought to be involved in depression pathophys
  • Example: Reserpine disrupts MA storage and causes symptoms of depression -> AD’s act to INC level of MA’s
    1. THERAPEUTIC LAG: NE and 5-HT INC immediately after AD admin, but takes weeks (2-8) to see clinical effects -> suggests adaptive changes underlie response
    2. Changes in β-receptor coupling, cAMP and serotonergic neurotransmission, SN alterations, and neurogenesis via brain-derived neurotropic factor -> acute effects appear to be required
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16
Q

What is therapeutic lag?

A
  • NE and 5-HT INC immediately after AD admin, but takes weeks (2-8) to see clinical effects, suggesting adaptive changes underlie response
  • Changes in β-receptor coupling, cAMP and serotonergic neurotransmission, SN alterations, and neurogenesis via brain-derived neurotropic factor -> acute effects appear to be required
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17
Q

What is the stress hormone hypothesis for depression?

A
  • Stress hormones CRH and cortisol dysregulated
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18
Q

What is the most recent hypothesis for depression?

A
  • Mistrafficking of 5HT1c receptors via p11

- p11 is an IC trafficking protein important for controlling responsiveness to AD agents

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19
Q

Should depressed people take NSAID’s?

A
  • NSAIDs DEC cytokines, so they may be CONTRA in some forms of depression
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20
Q

Describe the presynaptic packaging and release of NE and 5-HT, and their targets.

A
  • NE and 5-HT presynaptically synthesized from AA precursors L-tyrosine and L-tryptophan, respectively
  • Packaged in vesicles by vesicular monoamine transporter
  • Upon invasion of presynaptic AP to terminals, depolarization drives voltage-dependent Ca channels to open, and fusion of vesicles with presynaptic membrane —> opening of fusion pore and release of NT into synaptic cleft
  • NE, 5-HT can activate post-synaptic receptors and initiate signaling cascades that modulate neuronal excitability and other cell function
  • Can act presynaptically at auto- and hetero-receptors to suppress release
  • NE receptors on 5-HT terminals, and vice versa: mechanism for them to cross-modulate each other
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21
Q

How is NE and 5-HT synaptic transmission terminated? What drugs affect this termination?

A
  • Action terminated by action of presynaptic transporters called NET and SERT that recycle transmitter back to their respective presynaptic terminals, where they may be re-packaged, or degraded by monoamine oxidases (MAO’s)
    1. TCA’s and SNRI’s act to block reuptake and prolong residency of these transmitters in synaptic cleft
    2. SSRI’s act selectively to prolong serotonergic action (at SERT)
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22
Q

What is the basic action of the MAOI’s?

A
  • MAOI’s prevent presynaptic degradation of NE and 5-HT, INC their availability for release
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23
Q

What is the BBW for the anti-depressants?

A
  • Potential INC of suicidal thinking or attempts in kids and young adults (up to 24 years)
  • Pts should be closely monitored, esp. during the initial weeks of tx
  • NOTE: comprehensive review recommends that benefits outweigh risks for kids and adolescents with severe depression and anxiety disorders
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24
Q

What kinds of things do you need to monitor in a pt on anti-depressants?

A
  • Worsening depression
  • Suicidal thinking or behavior
  • Any unusual changes in behavior, like sleepiness, agitation, or withdrawal from normal social situations
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25
Q

What is the role of the placebo effect in anti-depressant tx?

A
  • Strong placebo effect associated with emotional disorders, incl. generalized anxiety disorder
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26
Q

Is St. John’s Wort clinically effective? What else do you need to worry about with pts on this med?

A
  • Maybe
  • Recent NIH study found that it was no more effective in treating major depressive disorder than placebo, and worse than an SSRI
  • CYP450 inducer: 2000 FDA warning that SJW interferes with various meds, esp. for HIV, heart disease, seizures, some cancers, and organ transplant reduction
  • NOTE: trials currently under way for mild-moderate depression (extract of hypericum perforatum)
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27
Q

Describe the pharmacogenomics of resistance to AD tx. Which drugs are most affected?

A
  • Recent study shows many AD’s are substrates for ABCB1 (MDR1; P-gp) at the BBB, limiting the abilities of these drugs to accumulate in brain
  • Single nucleotide (T vs. C) polymorphisms in MDR1 may dictate whether depression will remit in response to AD tx
  • SUBSTRATES: Citalopram, Venlafaxine, Paroxetine, Amitriptyline
  • NOT SUBSTRATES: Mirtazapine, Fluoxetine
  • Pts who are C carriers (CC or CT) tend to have depression that does not remit in response to drugs that are substrates for MDR1, but equal remission rates to drugs that are not substrates -> C-allele dictates overall higher rate of MDR1 transport activity for those drugs that are substrates and a reduced accumulation of these drugs in the brain
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28
Q

What are the indications for the TCA’s?

A
  • Major depression
  • Pain
  • Anxiety disorders (OCD, phobias, panic)
  • ADHD
  • Nocturnal enuresis
  • Depression associated with schizophrenia
  • NOTE: used to be gold standard for clinical trials, but now SSRI’s are (newer drugs have reduced AE’s, but not DEC # of “treatment resistant” pts)
29
Q

What is the MOA of the TCA’s?

A
  • INH reuptake of 5-HT and NE into presynaptic terminals
  • Potentiate and prolong actions of these NT’s
  • Receptor and transporter regulation w/repeated tx
  • Also block mAch, alpha-AR’s, and histamine receptors (correlate with side effects)
30
Q

Describe the general behaviors/clinical effects of the TCA’s?

A
  • ACUTE: drowsiness, dysphoria, anxiety, impaired cognition

- CHRONIC (2-8 weeks): improved clinical symptoms -> NOT euphoria

31
Q

What are the AE’s of the TCA’s?

A
  • Orthostatic hypotension: antagonism of alpha-1-AR’s
  • Blurred vision, worsening of narrow-angle glaucoma, dry mouth, constipation, urinary retention, tachycardia, confusion: antagonism of mAchR
  • Sedation: antagonism of histamine and alpha-1-AR’s
  • Metabolic/endocrine: weight gain, sexual disturbances
32
Q

What does TCA OD look like?

A
  • CV effects, incl. arrhythmias, direct myocardial depression, worsening of CHF
  • Acidoses, delirium, seizures
  • NOTE: low therapeutic index
33
Q

Describe the pharmacokinetics for the TCA’s.

A
  • Most incompletely absorbed due to first pass
  • High lipid solubility, so distribution to brain and fat
  • Highly bound to plasma proteins (high Vd), limiting excretion -> LONG 1/2 LIFE (>1d)
  • Tertiary amines metabolized to secondary active amines by demethylation
    1. Imipramine -> Desipramine, Amitriptyline -> Nortriptyline
  • Tricyclic ring subject to oxidation (CYP2D6) and conjugation
34
Q

What are the drug interactions for the TCA’s?

A
  • Potentiates effects of alcohol and other sedatives, anti-parkinson drugs, antipsychotic drugs, biogenic amines (present in food), competition for plasma protein binding
  • Can block effects of Clonidine, leading to dangerous elevations in BP (if Clonidine being used as anti-HTN)
35
Q

How are Escitalopram and Citalopram related?

A
  • Escitalopram (Lexapro) is an active isomer of Citalopram (Celexa), which is a racemic mixture that has largely supplanted its use
36
Q

What are the indications for the SSRI’s? How are they unique amongst the AD’s?

A
  • FIRST-LINE tx in pts diagnosed with major depression
  • Also used to tx panic, OCD, social-anxiety disorder, ADHD, and some eating disorders
  • Similar efficacy to other AD’s, but typically better compliance due to more tolerable side effects -> negligible activity at mAch, H1, and alpha-1 receptors
37
Q

What is the MOA of that SSRI’s?

A
  • Selective INH of SERT

- Potentiate and prolong action of 5-HT

38
Q

What is the clinical effect of the SSRI’s?

A
  • ACUTE: CNS stimulation, anxiety, agitation

- CHRONIC: improvement of most or all clinical symptoms, CNS activation remains

39
Q

What are the AE’s for the SSRI’s?

A
  • Nausea, DEC libido, sexual dysfunction
  • Fewer AE’s relative to other AD’s
  • Low incidence of CV and anticholinergic effects
  • Higher therapeutic index (DEC risk of OD)
  • INC risk of BIRTH DEFECTS with PAROXETINE (2005)
40
Q

Describe the pharmacokinetics of the SSRI’s.

A
  • Moderate bioavailability (about 50%); better than TCA’s
  • High protein binding; LONG 1/2 LIFE -> 1-4d
  • Norfluoxetine, active metabolite of Fluoxetine has 1/2 life of 7-9d, so FLUOXETINE can be formulated for WEEKLY ADMIN
  • Most agents metabolized by CYP2D6, CYP2C19, and 3A4, and can exhibit strong INH of CYP2D6 and CYP2C19
  • Drug choice may be influenced by pt-specific parameters (incl. age and other meds)
41
Q

What are the drug interactions for the SSRI’s?

A
  • MAOI’s are CONTRA -> must wait at least 2 WEEKS
  • MOAI’s or SSRI overdose can lead to SEROTONIN SYNDROME (onset w/in 24hrs of OD or concurrent MAOI)
    1. Due to overstimulation of 5-HT1A receptors in central grey (midbrain) and medulla
    2. Characterized by: hyperpyrexia, hyperreflexia, tremor, shivering, myoclonus, agitation, seizures, confusion, delirium, CV collapse, and coma
    3. Can be fatal, but good prognosis when med discontinued (recovery in about 24hrs)
    4. Can also be triggered by INC 5-HT release (amphetamines, MDMA) or via 5-HT agonists (LSD, Buspirone, L-tryptophan)
42
Q

What are the indications and the pharmacokinetics for the atypical AD’s?

A
  • INDICATIONS: all used for tx of major depression, but exhibit heterogeneous MOA’s
  • PHARMACOKINETICS: generally similar to TCA’s, but usually shorter 1/2 life
43
Q

What are the MOA, 1/2 life, and AE’s for Venlafaxine?

A
  • MOA: INH 5-HT and NE reuptake (SNRI), and is devoid of antihistaminergic, anticholinergic, and antiadrenergic props (does NOT have TCA-like AE’s)
  • Short 1/2 life: 4-10hrs
  • Produces small, sustained HTN, sweating, dizziness, nausea, anxiety
44
Q

What are the MOA, metabolism, and 1/2 life for Duloxetine?

A
  • MOA: most potent SNRI (INH SERT and NET), about 100x more potent than Venlafaxine
  • 50% bioavailability
  • Highly bound to plasma proteins (95%)
  • Metabolized by CYP2D6 and CYP1A2
  • 1/2 life: 12hrs
45
Q

What are the MOA, use, and AE’s for Amoxamine?

A
  • MOA: mixed INH of NET > SERT = DAT (analog of antipsychotic drug, Loxapine)
  • May be used for depression in psychotic pts
  • Risk of extrapyramidal AE’s due to DA receptor antagonism: various mvmt disorders, like acute dystonic rxns, pseudo-parkinsonism, tardive dyskinesia, or akathisia (agitation, distress, restlessness)
46
Q

What are the MOA, AE’s, 1/2 life, and use for Bupropion?

A
  • MOA: weak blocker of DAT, SERT, and NET (active metabolite is an NE reuptake blocker)
  • AE’s: agitation, anxiety, restlessness, risk of SEIZURE
    1. REMEMBER: bulimics may have risk of seizures due to electrolyte imbalances -> do not give them this drug, or others that may facilitate seizures
  • Admin as divided doses or slow-release formulation (medium 1/2 life)
  • Also used to aid in SMOKING CESSATION
47
Q

What are the MOA and AE’s for Maprotiline?

A
  • MOA: selective INH of NE reuptake (NRI)

- AE: INC risk of seizures (also seen with TCA’s at high doses)

48
Q

What are the MOA and AE’s of Mirtazepine?

A
  • MOA: enhances release of 5-HT and NE by antagonizing presynaptic alpha-2AR’s and antagonizes 5-HT2 receptors (analog of Mianserin, a TCA)
  • AE’s: potent antihistaminic (sedating), INC weight gain, less GI and sexual disturbances than SSRI’s
  • Tetracyclic AD
49
Q

What are the 2 SARI’s? Describe their MOA’s, uses, and half-lives.

A
  • TRAZODONE: moderate INH of 5-HT reuptake, but mainly acts as a 5-HT2a antagonist and 5-HT1a partial agonist
    1. Useful in tx of depression characterized by anxiety and sleep disturbances
    2. Short 1/2 life: 2-9hrs
    3. INH CYP3A4
  • NEFAZODONE: similar, but largely discontinued due to HEPATOTOXICITY (still exists in generic form)
50
Q

What are the 2 SMS’s? Describe their MOA’s.

A
  • VILAZADONE: potent 5-HT1a partial agonist and SSRI
  • VORTIOXETINE: serotonin modulator and stimulator -> potent blocker of SERT and high efficacy partial agonist at 5-HT1a and 5-HT1b
    1. Antagonist at 5-HT1d, 3a, and 7 receptors
    2. Weaker block of NET and B1-AR
  • NOTE: similar pharmacologic profiles to the SARI’s
51
Q

What are the indications of the MAOI’s?

A
  • Typically, only used in pts unresponsive to tx w/other AD’s and for whom ECT is not suitable
  • Also used for panic disorder and agoraphobia
  • NOTE: have largely been discontinued
52
Q

What is the MOA of the MAOI’s?

A
  • Block oxidative metabolism of monoamines by IRREVERSIBLE INH of MAO-A and MAO-B in NN terminals
  • MAO-A metabolizes primarily NE, 5-HT, and tyramine
  • MAO-B mostly DA selective
53
Q

What are the acute and chronic clinical effects of the MAOI’s?

A
  • ACUTE: CNS stimulation, agitation, possibly euphoria

- CHRONIC (2-6wks): improvement of most or all symptoms, CNS activation remains

54
Q

What are the AE’s for the MAOI’s?

A
  • Sleep disturbances (INC arousal)
  • Orthostatic hypotension
  • Weight gain
  • Some sex dysfunction
55
Q

What are the pharmacokinetics of the MAOI’s?

A
  • Generally well absorbed from GI tract
  • Daily dosing required in spite of irreversible enzyme INH
  • Inactivated by acetylation (pharmacogenomic differences)
  • Because block of MAO is irreversible, DRUG EFFECT PERSISTS 1-3wks -> discontinue substantially before switching drug regimens
56
Q

What are the drug interactions of the MAOI’s?

A
  • Foods containing high amounts of tyramine (cheese, wine, chocolate)
  • Sympathomimetic drugs (cold remedies, diet aids, stimulants) -> acute HTN reaction
  • Meperidine (OPIOD), Dextromethorphan -> hyperpyrexia, delirium, convulsions, coma, DEATH
  • SSRI’s: CONTRA due to ability to produce SEROTONIN SYNDROME
57
Q

What are the indications for the mood stabilizers?

A
  • Maintenance of manic depression -> bipolar affective disorder
  • Acute mania is typically treated with antipsychotic and/or BNZ
  • NOTE: do NOT take away mania (i.e., not anti-manics), but prevent cycling between manic states and severe depressive states
58
Q

What is the MOA of lithium?

A
  • Poorly understood
  • Most favored hypothesis: INH of post-synaptic inositol phosphate signaling + INH of NT-stimulated adenylyl cyclase activity
  • NOTE: effective in 60% of pts
59
Q

What are the pharmacokinetics for lithium?

A
  • RAPID (30min-2hr peak) and complete absorption (6-8hrs)
  • Distributes to TBW, some concentration in bone
  • Cleared in the urine
  • 1/2 life of 20hrs
  • NO METABOLISM
60
Q

What are the AE’s and drug interactions for lithium?

A
  • VERY NARROW therapeutic window -> target 0.5-1.0 mEq/L (toxic effects at >1.5 mEq/L)
  • Neuro/psych: tremor, ataxia, hyperactivity, aphasia (can’t communicate), sedation, fatigue
  • Glandular: edema, mild hypothyroidism
  • Renal: polydipsia, polyuria (nephrogenic diabetes insipidus)
  • Cardiac: bradycardia-tachycardia (“sick sinus:” ability of Li to block N/K ATPase that maintains resting potential in cardiac tissue)
  • Other: acne, folliculitis, and exacerbates psoriasis
61
Q

What are the drug interactions for lithium?

A
  • Sensitive to diuretics and NSAID’s
62
Q

What anticonvulsants may be used to treat depression? How do they compare to lithium?

A
  • Valproate and Carbamazepine now frequently used in mgmt of bipolar disorder
    1. May be used alone, in combo w/Li, or w/other antipsychotics (most frequently Quetiapine or Olanzapine)
    2. Appear effective in either phase of manic depression, esp. Valproate
  • ADVANTAGES compared to Li: INC dose faster, quicker response, better therapeutic index
  • DISADVANTAGES compared to Li: less experience, efficacy questionable in severe disease
63
Q

Which of the mood stabilizers is first-line for bipolar disorder?

A
  • LITHIUM

- Milder forms may be treated with anticonvulsants (i.e., Carbamazepine, Valproate)

64
Q

What are the indications and MOA for Valproic Acid (Valproate)?

A
  • INDICATIONS: used as mono therapy or in combo with Li of antipsychotics to manage bipolar disorder
  • MOA: INH voltage-gated Na channels by stabilizing inactivated state of the channel -> block of channel activity is use-dependent
    1. Also blocks T-type Ca channels to lesser extent
    2. Can stimulate GABA synthesis, and INH GABA degradation
    3. At high doses, may INC resting K conductances
  • In general, these lead to REDUCED EXCITABILITY
65
Q

What are the drug interactions and toxicity for Valproic Acid?

A
  • DRUG INTERACTIONS: INH its own metabolism and that of other drugs (CYP2C) -> dosing needs to be DEC with repeated admin due to this INH
  • TOXICITY: nausea, abdominal pain, and heartburn common
    1. Sedation may be a problem
    2. HEPATOTOXICITY can be common -> careful MONITORING of liver function recommended
66
Q

What are the indications and MOA of Carbamazepine?

A
  • INDICATIONS: used as mono therapy or in combo with Li of antipsychotics to manage bipolar disorder
  • MOA: predominantly INH of Na channels, prolonging recovery from inactivation
67
Q

What are the pharmacokinetics for Carbamazepine?

A
  • Absorption from GI tract 100% (bioavailability), but rate varies with pt
  • Time to peak = 6-8hrs
  • Poor solubility, and distributes and clears slowly
  • 70% bound to plasma proteins (albumin), but does not extensively displace other drugs bound to plasma proteins
  • Metabolized primarily by CYP3A4 to active metabolite (10,11-epoxide), and varies by pt
  • 1/2 life 36hrs after initial dose, but may DEC to 20hrs due to enzyme induction (induces its own metabolism)
68
Q

What are the drug interactions and toxicity for Carbamazepine?

A
  • DRUG INTERACTIONS: broad spectrum inducer of CYP2C and 3A families + UGT’s, enhancing metabolism of many drugs (dosage needs to be INC with repeated tx)
  • TOXICITY: diplopia (double vision) and ataxia common
    1. Mild GI upset, unsteadiness
    2. At high doses, drowsiness
    3. Rash common idiosyncratic rxn
    4. Some occurrences of aplastic anemia

Psych (11 decks)

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