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CNS > Pharma 6: Antidepressant And Antipsychotic Drugs > Flashcards

Pharma 6: Antidepressant And Antipsychotic Drugs Flashcards

1
Q

Selective Serotonin Reuptake Inhibitors

A

Fluoxetine Citalopram

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2
Q

Fluoxetine Citalopram Selectivity to serotonin transporter

A

300-3000 greater for serotonin than noradrenaline

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3
Q

Fluoxetine, citalopram Adverse effects

A

Safer than TCAs and MAOI so they’ve replaced them

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4
Q

Fluoxetine, citalopram Therapeutic uses

A

-Very effective in treating “moderate” depression - Less effective than TCAs in treating severe depression -Treats bulimia nervosa, OCD, anorexia nervosa, panic disorder.

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5
Q

Pharmacokinetics of Fluoxetine, Citalopram

A
  • Absorbed orally - Fluoxetin—>potent inhibitor of CYP2D6 (metabolized TCAs, antipsychotics, antiarrythmatics, B antagonists) - If pt has hepatic impairment—> reduce dose of SSRI
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6
Q

Fluoxetine, Citalopram Adverse effect

A

-nausea -anxiety -insomnia -anorexia -weight loss -tremors -sexual dysfunction

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7
Q

Antidepressants and <18 years

A

CAUTION! Possibly causes excitement, insomnia aggression in first few weeks Possibly increased suicidal ideation Lower seizure thresholds

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8
Q

Serotonin syndrome Caused by: S/S:

A

All SSRI can potentially cause this especially when used with MAOI Characterized by: tremor, hyperthermia, CV collapse—>death

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9
Q

Discontinuation syndrome Caused by S/S

A

Potentially caused by SSRI after their abrupt withdrawal ((Fluoxetine—>lowest risk due its longer T1/2 and active metabolite)) S/S: headache, malaise, flu like, agitation, irritability, nervousness, sleep difficulties

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10
Q

Venlafaxine, Duloxetine (SNRI) MOA

A

-Inhibit serotonin and noradrenaline reuptake -Little activity at a-adrenergic, muscuranic, histamine receptor—> less of the side effects resulting from these receeptors

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11
Q

Venlafaxine Pharmacokinetics

A

Minimal inhibition or CYP450 Substrate for CYP2D6

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12
Q

VENLAFAXINE Side effects

A

-Nausea -Headache -Sexual Dysfunction -Disziness -Insomnia -Sedation -Constipation High dose—> HTN, TACHYCARDIA

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13
Q

Duloxetine Metabolism

A

Highly metabolized in liver—> inactive metabolites !Avoid in pt with liver dysfunction

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14
Q

Duloxetine side effects

A

Gi (common); nausea, dry mouth, constipation Others: insomnia, dizziness, somnolence, sweating, sexual dysfunction. May increase bp and hr

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15
Q

Duloxetine drug-drug interaction

A

Moderate inhibitor of CYPD26–> increase conc of drugs (antipsychotics) metabolized by it

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16
Q

Tricyclic antidepressants

A

Imipramine

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17
Q

Imipramine MOA

A

TCA Therapeutic —>Inhibit serotonin and noradrenaline reuptake +block serotonergic, a adrenergic, histaminic, muscarinic receptors—> adverse effects?

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18
Q

Imipramine Therapeutic uses

A

Moderate-severe depression Some anxiety disorders eg anxiety attacks

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19
Q

Imipramine Pharmacokinetics

A

Well absorbed orally Metabolized by hepatic microsomal system—> sensitive to agents that induce/inhibit CYP450?

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20
Q

Imipramine Adverse effects

A

Antimuscarinic: blurred vision, dry mouth, urinary retention and constipation A adrenergic block: Orthostatic hypotension, dizziness, reflex tachy CV: arrhythmia and SD Sedation: in first few weeks of use Weight gain

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21
Q

Imipramine Precautions

A

If bipolar pt—> antidepressants may cause a switch to manic behavior Suicidal pt—> LIMITED QUANTITIES OF TCA cuz low TI there4 lethal imipramine dose is 5-6 maximal dose.

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22
Q

TCA Interaction with MAOI

A

Mutual enhancements—> htn, hyperpyrexia, convulsions, coma

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23
Q

TCA Interaction with direct acting adrenergic drugs

A

Potentiate effects of biogenic amine drugs by preventing their removal from synaptic cleft

24
Q

TCA Interaction with ethanol and cns depressants

A

Toxic sedation

25
Q

TCA Interaction with indirect acting adrenergic drugs

A

Block effects of indirect acting sympathomimetic drugs by preventing the drugs from reaching their intracellular sites or action

26
Q

MAOI

A

Phenelzine

27
Q

Phenelzine MOA

A

Inactivate reversibly/irreversibly MAO—> accumulation of serotonin, NA and dopamine in synaptic cleft

28
Q

Function of MAO

A

Inactivates monoamines like norepinephrine, serotonin and dopamine from synaptic vesicle

29
Q

Phenelzine Consequences of inhibiting MAO

A

Inhibits MAO in the liver and gut that catalyze oxidative deamination of drugs and toxic substances like tyramine → increase in concentration of tyramine and other drug-drug or food-drug interactions

30
Q

Phenelzine

Therapeutic uses

A
  1. used in patients who are depressed and are unresponsive or allergic to TCA and SSRI or patients with strong anxiety
  2. Patients with atypical depression
  3. LAST LINE because of risk of drug driug and drug food interractions.
31
Q

Phenelzine

Pharmacokinetics

A

Well abosorbed orally

Metabolized in liver

Excreted rapidly in urine

32
Q

Phenelzine

Adverse effects

A
  • Drowsiness
  • orthostatic hypotension
  • blurred vision
  • dry mouth
  • dysuria
  • constipatiopn
  • tremors
  • OD→Convulsions
33
Q

Phenelzine when used with other anti-depressants (SSRI) causes

A

SEROTONIN SYNDROME

34
Q

Significance of tyramine

A
  • found in aged cheese and meats, chicken liver red wine smoked fish etc
  • inactivated by MAO in gut
  • tyramine causes release of large quantities of CATECHOLAMINES from stores in nerve terminals→HYPERTENSIVE CRISIS

ie. occipital headache, stiff neck, tachycardia, nausea, hypertension, arrhthmias, seizures, stroke??

35
Q

Atypical Antidepressant

A

MIRTAZAPINE

36
Q

Mirtazapine

MOA

A
  • Antagonizes presynaptic a2-adrenoreceptors→ enhances serotonin and noradrenaline NT
  • May also antagonize 5-HT2 receptors…antidepression
  • Potent antihistamine effect →sedating useful for depressed pt with difficulty sleeping
  • NO ANTIMUSCURANIC (vs TCA)
  • NO SECUAL DYSFUNCTION (vs SSRI)

+increase apetie→weight gain

37
Q

Schizophrenia

Pathophysiology

A

possibly dysfunction of the mesolimbic or mesocortical dopaminergic neuronal pathways

38
Q

Dopamine hypothesis of schizophrenia

A
  • ANTIpsychotic properties are explained by post synaptic dopamine antagonism
  • Drug induced psychosis is a high risk with drugs that incerease dopamine availability like cocaine, amphetamines, L dopa
  • Potential complication of PD pt on L dopa
39
Q

Limitations of Dopamine Theory

A
  • doesn’t explain cognitive deficits
  • D-lysergic acid, 5-HT2A agonist also produces psychotic symptoms ie not just dopamine
40
Q

First Generation Antipsychotics

A

Chlorpromazine

Thioridazine

Haloperidol

41
Q

FGA

MOA

A
  • Block D2 dopamine receptors→ lower dopaminergic NTion in the four dopamine pathways→ antipsychotic effects
  • Competetive antagonist of H1, M1, a1 adrenoreceptors
42
Q

FGA and extrapyramidal symptoms

A

Particulary HALOPERIDOl→bind tighlty to dopaminergic neuroreceoptors

Less likely with CHLORPROMAZINE→bind weakly

43
Q

SGA drugs

A

Aripiprazole

Clozapine

Olanzapine

44
Q

Second generation antipsychotics

MOA

A

“atypical antipsychotics”

Antagonize dopamine, srotonin and other receptors

45
Q

SGAs and extrapyramidal symptoms

A

Lower incidence of EPS than FGA→FIRST LINE

46
Q

SGAs are associated with..

A

Metabolic side effects:

  • diabetes
  • hyperchol
  • weight gain
47
Q

Antipsychotic effects (on positive symptoms)

A

All antipsychotics can reduce hallucinations and delusions associated with schizophrenia

ie they reudce the postive symptoms by blocking D2R in the mesolimbic system

!NOTE: Blocking D2R in the nigrostriate pathway—> EPS—> dystonias, parkinson like symptoms, akathisia and tardige dyskinesia. Less so in SGA

48
Q

Negative symptoms of schizophrenia are mostly responsive to

A

SGA eg Clozapine

49
Q

Antiemetic effect of antipsychotics

A

All antipsychotics have antiemetic effect due to blocking D2R of the chemoreceptor trigger zone

!EXCEPT aripiprazole

50
Q

Anitcholonergic effects of antipsychotics

A

CHLOROPROMAZINE, CLOZAPINE, OLANZAPINE

produce anticholinergic effects like blurred vision, confusioj and inhibiiot of Gi and ut

!anticholinergic effect—> decrease risk of EPS

51
Q

Other effects of antipsychoyics

A
  • Block a adrenergic receptors—> orthostatic hypotension and lightheadedness
  • alter temperature regulating mechanisms—>poikilothermia
  • block D2R in pituitary—>hyperprolactin
  • potent antagonists of H1 histamine receptors chlorpromazine, olanzapine, clozapine—> sedation
  • some cause sexual dysfunction
52
Q

Statistics on the adverse effects of antipsychotics

A

Can occur in virtually all patients and can be significant in 80% of cases

53
Q

Adverse effect—> EPS

A

Extrapyramidal motor effects

due to disturbance in balance between dopaminergic and cholinergic system

  • HIGH RISK* haloperidol, fluphenazine—> preferentially block D2R
  • LOW RISK* THIORIDAZIN—> strong anticholinergic activity
54
Q

Adverse effect—> tardive dyskinesia

A
  • Due to long term treatment
  • giving up antipsychotics may reduce symptoms
  • may be permanent
55
Q

Neuroleptic malignant syndrome

A
  • Potentially fatal
  • reaction to antipsychotics
  • must discontinue
56
Q

Other adverse effects of antipsychotics

A
  • drowsines
  • confusion
  • dry mouth
  • urinary retention
  • constipation
  • loss of visual accomodation
  • hypotension
  • orthostatic hypotension
  • impaired thermoregulation
  • amennorrhea
  • galctorrhea
  • gynecomastia
  • infertility
  • ed
  • weight gain
  • exacerbate DM hyperlipidemia
  • QT prologation thioridazine
57
Q

Cautions and contraindications of antipsychotics

A
  • lower seizure threshold
  • elderly pt with dementia related psychosis→ increased risk of mortality
  • pt ith mood disorders→monitored for worsening of symptoms and suicidal ideation or behaviors

CNS (28 decks)

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