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Pharm > Intro to Neuropsychopharmacology Part 1 > Flashcards

Intro to Neuropsychopharmacology Part 1 Flashcards

1
Q

Biogenic Amine Pathways in the Brain:

A
  1. Neurons containing norepinephrine are located in the locus coeruleus
    • innervate nearly every part of the CNS
  2. Neurons containing serotonin are located in two groups of raphe nuclei
    • project to most of the brain
  3. Neurons containing dopamine are located in the substantia nigra and the ventral tegmental area of the midbrain
  4. Neurons containing ACh are located in the basal forebrain complex
    • ​includes the septal nuclei and nucleus basalis
    • project to the hippocampus and the neocortex
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2
Q

Dopamine pathways in the brain include:

A
  1. Nigrostriatal
  2. Tubero-infundibular
  3. Mesolimbic
  4. Mesocortical
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3
Q
  • GABA localization:
  • Limbic Structures:
A
  • GABA Localization: Substantia Nigra, Globus Pallidus, Hippocampus
  • Limbic structures: Amygdala, Hypothalamus, Spinal cord
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4
Q

AFFECTIVE DISORDERS:

A
  1. Major Depressive Disorder
    1. Unipolar
    2. Bipolar
  2. Dysthymic Disorder
  3. Mania
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5
Q

Monoamine Theory of Depression

A

Based on pharmacological evidence:

  1. the ability of known antidepressant drugs (TCAs and MAO inhibitors) to facilitate monaminergic transmission
  2. drugs such as reserpine that depletes amines to cause depression
  • Other pharmacological evidence (ie. delay in onset of effects) fails to support the traditional monoamine hypothesis
  • But, pharmacological manipulation of monoamine
    transmission remains the most successful approach to treating depression
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6
Q

Neurochemical Effects of Tricyclic Antidepressants:

A
  1. Blockade of transmitter uptake
    • NE and 5–HT
  2. Receptors and second messengers​​
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7
Q

Drugs Used in the Treatment of Depressive Disorders:

A
  1. Serotonin Specific Reuptake Inhibitors – SSRIs
  2. Serotonin – Norepinephrine Reuptake inhibitors – SNRIs
  3. Atypical Antidepressants – Mirtazapine and Bupropion
  4. Monoamine Oxidase Inhibitors
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8
Q

SSRI:

Pharmacokinetics and metabolism

A
  • Most commonly used anti-depressants
  • Favored because of side effect profile
  • Both long and short half-life compounds available
  • Fluoxetine has a long half-life active metabolite
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9
Q

**SSRI: **

Pharmacological properties and side effects

A
  • Antidepressant actions similar in efficacy and time- course to TCAs
  • Common side effects include:
    1. Nausea and vomiting
    2. Insomnia
    3. Nervousness
    4. Sexual dysfunction
  • Acute toxicity is less than with TCAs and MAO inhibitors ⇒ Less risk of overdose
  • Serotonin reaction can occur in presence of MAO inhibitors
    • Includes hyperthermia, muscle rigidity and cardiovascular collapse
  • Black box warning for use in teens
  • SSRI discontinuation syndrome
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10
Q

SSRI Discontinuation Syndrome:

A
  • Symptoms occur within 1 to 7 days after stopping an SSRI
  • Most common with shorter acting drugs like sertraline and fluvoxamine
  • Not with fluoxetine
  • Symptoms can include: dizziness, light-headedness, vertigo, anxiety, fatigue, headache, tremor, visual disturbances, etc.
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11
Q

SSRIs:

Clinical uses

A

Approved clinical uses include:

  • Major depressive disorder
  • Obsessive-Compulsive disorder
  • Panic disorder
  • Social phobia
  • PTSD
  • Generalized anxiety disorder
  • PMS
  • Hot flashes associated with menopause
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12
Q

SSRI Drugs (2):

A
  1. Fluoxetine
  2. Sertraline
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13
Q

Fluoxetine:

A
  • First SSRI on market
  • Effects on drug metabolism
  • Active metabolite with long half-life
    • ​7 days or more
  • Available as sustained released product
    • PMS
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14
Q

Sertraline:

A
  • Similar in action to fluoxetine with less effects on drug metabolism
  • Shorter half-life
    • OCD, PTSD, Panic attacks
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15
Q

SNRI drugs:

**Duloxetine **(Cymbalta®)

A
  • 12-18 hour half-life
  • Side effect profile is more SSRI-like than TCA-like
  • Use with caution in patients with liver disease
  • Also approved for use in fibromyalgia, diabetic neuropathy, back pain, and osteoarthritis pain
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16
Q

Atypical antidepressants:

A
  • Drugs without typical tricyclic structure or SSRI action
  • May or may not block catecholamine uptake
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17
Q

Atypical antidepressants drugs (2):

A
  1. Bupropion
  2. Mirtazapine
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18
Q

Bupropion:

A
  • Weakly blocks norepinephrine and dopamine uptake
  • Also approved for nicotine withdrawal and seasonal affective disorder
  • No weight gain or sexual dysfunction
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19
Q

Mirtazapine:

A
  • Blocks presynaptic alpha2 receptors in brain
  • Increases appetite
  • AIDS patients
20
Q

Tricyclic Antidepressants:

A
  • First highly effective drugs for the treatment of depression
  • Block NE and 5-HT reuptake
  • Now used secondarily to SSRIs and other newer compounds
21
Q

Tricyclic Antidepressants:

Pharmacokinetics and Metabolism

A
  • Rapidly absorbed after parenteral or oral administration
    • Relatively high concentrations are found in the brain and heart
  • Imipramine and amitriptyline are demethylated to active metabolites which are used as drugs by themselves
  • Long plasma half-life: 8 to 100 hours
22
Q

Tricyclic Antidepressants:

Pharmacological Properties and Side Effects

A
  • Produces elevation of mood in depressed patients after about 2 to 3 weeks
  • Decreases REM and increases stage 4 sleep
  • Prominent anticholinergic effects
    • Cardiac abnormalities
  • Sedation
  • Cardiac abnormalities
  • **Overdoses: **acute toxicity
    • Symptoms include hyperpyrexia, hyper- or hypotension, seizures, coma and cardiac conduction defects
23
Q

Tricyclic Antidepressants:

Drug interactions

A
  • Guanethidine - blocks guanethidine uptake
  • Sympathomimetic drugs - particularly indirect acting ones
  • Effects on absorption and metabolism of other drugs
24
Q

Tricyclic Antidepressants:

Therapeutic uses

A
  1. Treatment of major depression
    • replaced by SSRIs as primary treatment
  2. Enuresis in childhood – Imipramine
  3. Chronic pain – amitriptyline
  4. Obsessive-compulsive disorders – clomipramine and SSRIs
  5. Other tricyclic antidepressants – amoxapine, desipramine, doxepin, nortriptyline
25
Q

Monoamine Oxidase Inhibitors:

A
  • Block the oxidative deamination of naturally occurring biogenic amines, such as NE, DA and 5-HT and ingested amines
  • Monoamine oxidase is found in the mitochondrial fraction of neurons
  • It is also found in liver, lung and other organs
  • Two forms of MAO - A and B
    • Antidepressant action probably due to inhibition of MAO-A
26
Q

Phenelzine:

A

irreversible inhibitor of MAO

27
Q

Monoamine Oxidase Inhibitors:

  • Pharmacological Properties:
  • Drugs and Food Interaction:
  • Therapeutic Use:
A
  • Pharmacological Properties:
    • Antidepressant action takes about 2 weeks
    • Produces mood elevation in depressed patients
      • May progress to hypomania, particularly in bipolar disease.
    • Acute toxicity can produce agitation, hallucinations, hyperpyrexia, convulsions and changes in blood pressure
  • Drugs and Food Interaction:
    • ​Tyramine from food ⇒ can produce
  • *hypertensive crisis**
  • Therapeutic Use:
    • ​Major depression
      • not drug of first choice
28
Q

Psychosis:

A
  • A general term for major mental disorders characterized by:
    • derangement of personality
    • loss of contact with reality
    • delusions
    • hallucinations
  • prototype is Schizophrenia
29
Q

Etiology of Schizophrenia:

A
  • cause(s) of schizophrenia are yet unknown
  • DOPAMINE HYPOTHESIS:
    • ​Schizophrenia results from hyperactivity of
      dopaminergic neurons or their receptors,
      particularly those with terminals in limbic areas
      of the brain
30
Q

What do all anti-psychotic drugs interact with?

A

dopamine systems

31
Q

Dopamine receptors:

A
  1. D1 type (D 1 and D 5) – Activate adenylyl cyclase
  2. D2 type (D 2, D 3, D 4) – Inhibit adenylyl cyclase
  3. Autoreceptors
32
Q

Which receptors do atypical antipsychotic drugs target?

A

DA + 5HT2 receptors

33
Q

Treatment of schizophrenia:

A
  • drug treatment is the most common effective therapy
  • it is not curative
34
Q

Actions of Antipsychotic Drugs:

A
  1. Decrease in psychotic behavior - drugs differ only in potency
    • All symptoms of schizophrenia are not equally well treated
    • exception Clozapine and other atypical drugs
  2. Sedation
  3. Extrapyramidal actions - result of dopamine receptor blockade
    • Include, Dystonias Parkinsonism and Akathisia
    • Long-term treatment ⇒ Tardive dyskinesia –
      • Oral-facial dyskinesias, choreoathetoid movements
  4. Neuroendocrine effects - result of dopamine receptor blockade
  5. Orthostatic hypotension - alpha adrenergic receptor blockade
  6. Weight gain - Diabetes related events are more common with atypicals, particularly olanzapine, risperidone, clozapine and quetiapine.
  7. Neuroleptic malignant syndrome – Fever, mutism, EPS, possible death
    • Treatment includes cooling and hydration,
      bromocriptine and dantrolene
35
Q

Prototype available typical antipsychotic drugs classes (2):

A
  1. Phenothiazines
  2. Butyrophenone Derivative
36
Q
  • *Phenothiazines**
    • (3):**
A
  1. Chlorpromazine
  2. Thioridazine
  3. Fluphenazine
37
Q
  • *Chlorpromazine**
  • *:**
A

aliphatic side chain

  • low to medium potency
  • sedative
  • pronounced anticholinergic actions
38
Q

Thioridazine:

A

**piperidine side chain **

  • low potency
  • sedative
  • less extrapyramidal actions
  • anticholinergic
39
Q

Fluphenazine:

A

piperazine side chain

  • high potency
  • less sedative
  • less anticholinergic
  • more extrapyramidal reactions
40
Q

Haloperidol:

A

Butyrophenone Derivative

  • not chemically related to the phenothiazines but is pharmacologically similar to the high potency piperazine derivatives
41
Q

Atypical Antipsychotic Agents (5):

A
  1. Clozapine
  2. Olanzapine
  3. Risperidone
  4. Quetiapine
  5. Aripiprazole
42
Q

Atypical Antipsychotic Agents:

Uses

A
  1. Acute psychotic episodes
  2. Chronic schizophrenia
  3. Manic episodes, bipolar disorder
    • aripiprazole, olanzapine, quetiapine, ziprasidone, risperidone, asenapine, lurasidone
  4. Augmentation of antidepressant action:
    • aripiprazole, olanzapine, quetiapine
  5. Tourette’s syndrome
  6. Antiemesis – not thioridazine
43
Q

Clozapine:

A
  • Blocks D4 and 5-HT2 receptors
  • Little effect on D2
  • Muscarinic antagonist
  • Less extrapyramidal symptoms
  • May cause serious agranulocytosis or other blood dyscrasias in a small percentage of patients
  • Weight gain
  • Improves negative symptoms
44
Q

Olanzapine:

A
  • Related to clozapine
  • More potent as 5-HT2 antagonist
    • ​D1 and 2 antagonist, some D4
  • Few extra pyramidal symptoms
  • No agranulocytosis
  • Weight gain and diabetes risk
  • Less seizure incidence than clozapine
  • Reports of olanzapine abuse
45
Q

Risperidone:

A
  • Combined dopamine and serotonin receptor antagonist
  • Has a low incidence of extrapyramidal side effects
  • Greater reduction in negative symptoms
  • Less seizure activity and less antimuscarinic than
    clozapine
  • Paliperidone (Invega®) is the active metabolite of risperidone
  • Both are also available as intramuscular depot preparations
46
Q

Quetiapine:

A
  • Structurally related to clozapine with **effects on D2 and 5-HT2 receptors **
  • Similar to risperidone and olanzapine in effects on schizophrenia symptoms and side effects
  • Approved for augmentation in depression
  • Has some abuse potential
47
Q

**Aripiprazole (Abilify®): **

A
  • D2 partial agonist and 5-HT2 antagonist
  • adjunct in the treatment of depression

Pharm (16 decks)

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