Drugs for Mania and Schizophrenia Flashcards by Ninong Balduds

Alternating between periods of EXTREMELY low mood and euphoric/irritable mood

Strong familial component, genetically determined

Manic-Depressive Disease

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Elevated, expansive or irritable mood accompanied by
hyperactivity, pressure of speech, flight of ideas,
grandiosity, hyposomnia, and distractibility.

Mania

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MOA of Lithium Carbonate

Inhibits recycling of phosphoinositide leading to decreased levels of IP3 and DAG

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Pharmacokinetics of Lithium Carbonate

Not metabolized in the liver

Sodium competes with Lithium for renal tubular
reabsorption and thereby can increase the
excretion of Lithium

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Adverse effects of Lithium Carbonate

Fine tremors at therapeutic doses (one of the most
common adverse effect

Polyuria (interferes with the action of ADH)

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Limitation of Lithium Carbonate

Not effective in the management of RAPID CYCLING
→is a term used when a person with bipolar disorder experiences four or
more mood swings (episodes) within a 12-month period.

An episode may consist of depression, mania, or a condition known as mixed-state
in which depression and mania are co-occurring

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Drug better than lithium in the management of rapid cycling

Valproic Acid

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Drug used in the management and prophylaxis of mania

Alternative for patients who did not respond to lithium therapy

Carbamazepine

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Examples of Antipsychotics

Aripiprazole

Risperidone

Ziprasidone

Olanzapine

Quetiapine

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Causes of Schizophrenia

Genetic & Ecological

Dopamine & Serotonin Hypothesis

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Evidences of Dopamine Hypothesis

Abnormalities in DA neurotransmission.

Most antipsychotic drugs block D2 receptors.

Drugs that act by increasing neuronal release of DA or by
blocking the neuronal reuptake of DA can induce psychotic
behavior that resembles the behavior of schizophrenic
patients.

Post-mortem studies have reported increase in dopamine
receptor density in brain of schizophrenics who were not
treated with antipsychotic drugs.

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Description of Serotonin Hypothesis

5HT2A and 5HT2C stimulation leads to inhibition of cortical
and limbic DA release.

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Positive Psychotic Symptoms (D,H,C,A)

Delusions

Hallucinations

Catatonia

Agitation

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Disorganized Psychotic Symptoms (CT, DS, DB,DP)

Confused thinking

Disorganized speech

Disorganized behavior

Disorganized perceptions

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NEGATIVE-deficit Symptoms (EF, Al, Av, An)

Emotional flattening

Alogia – limited speech

Avolition – lack of motivation

Anhedonia – lack of interest and pleasure

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Cognitive Symptoms (DA, IM, DAF)

Decreased attention

Impaired memory

Decreased abstractive functions

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Mood Symptoms (D,S,H)

Dysphoria

Suicidality

Hopelessness

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Three Schizophrenia Phases

Prodromal

Psychotic (acute)

Residual (chronic)

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Prodromal Phase (D,S,H,I,PC)

Dysphoria

Suicidality

Hopelessness

Decline in functioning
that precedes 1st
psychotic episode

Socially withdrawn

Irritable

Physical complaints

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Psychotic (acute) Phase (DHCA,PD,D,DT)

Positive symptoms

Perceptual disturbance

Delusions

Disorganized thought

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Residual (chronic) Phase

Occurs between episodes of psychosis
Marked by negative symptoms

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Increased activity in this pathway may
cause delusions, hallucinations, and
other positive symptoms.

Mesolimbic Pathway

Decreased activity in this pathway can
cause apathy, withdrawal, lack of
motivation and pleasure, and other
negative symptoms.

Mesocortical Pathway

Inhibition of this pathway causes
extrapyramidal side effects of
antipsychotic drugs.

Nigrostriatal Pathway

Inhibition of this pathway leads to elevated serum prolactin levels.

Tuberofundibular Pathway

MOA of Typical/1st Generation Antipsychotics Antipsychotics AKA "Neuroleptics/ Major tranquilizers" usually take several weeks for their effects to fully develop

Blockade of Dopamine Target: Mesolimbic neurons, Nigrostriatal neurons, Tuberofundibular neurons Effect: Alleviate Positive symptoms, Extrapyramidal side effects, Hyperprolactinemia

MOA of Typical/2nd Generation Antipsychotics

Blockade of Serotonin Target: Mesocortical neurons Effect : Alleviate Negative symptoms

Examples of First generation Phenothiazines ("ZINE")

CHLORPROMAZINE PROMAZINE TRIFLUPROMAZINE FLUPHENAZINE PERPHENAZINE ACETOPHENAZINE TRIFLUOPERAZINE PROCHLORPERAZINE THIORIDAZINE MESORIDAZINE *PIMOZIDE PIPERACETAZINE

Examples of First generation Butyrophenone ("PERIDOL")

* HALOPERIDOL DROPERIDOL

Examples of First generation Thioxanthines ("XENE" | "XOL")

THIOTHIXENE CHLORPROTHIXENE FLUPENTIXOL

Nervous system disorder that involves repetitive movement or unwanted sounds (tics) that can’t be controlled, caprolalia, and echolalia.

Tourette Syndrome

Examples of Second Generation ("PINE" | "ONE" | "OLE" | "PRIDE")

OLANZAPINE - As effective as Haloperidol in alleviating positive symptoms CLOZAPINE - First atypical neuroleptic; lowers the risk of suicide and tardive dyskinesia - Use us limited because of adverse effects QUETIAPINE - Indicated for mania and adjunctive therapy for MDD ARIPRIPRAZOLE - Indicated for Tourette Syndrome LOXAPINE RISPERIDONE PRALIPERIDONE ZIPRASIDONE SERTINDOLE AMILSUPRIDE

Adverse effects of clozapine

Seizures Agranulocytosis - requires monitoring of leukocyte during the first 6 months of therapy.

Adverse effects of risperidone

QT prolongation

Adverse effects of Thioridazine

Pigmentary retinopathy Cardiac toxicity

Adverse effects of Chlorpromazine

Corneal Deposits

General adverse effects of Antipsychotics

Alpha-1 adrenoceptor blockade Muscarinic receptor blockade Histamine receptor blockade (CNS) Neuroleptic Malignant Syndrome

A severe form of drug toxicity that occurs in 0.5% to 1% of patients treated with antipsychotics A life-threatening condition characterized by muscle rigidity, hyperthermia, and autonomic dysfunction (tachycardia, diaphoresis, tachypnea, and urinary and fecal incontinence)

Neuroleptic Malignant Syndrome

Management of Neuroleptic Malignant Syndrome

Discontinue antipsychotic drug Administer DANTROLENE Provide supportive care

Adverse effects of dopamine blockade: inhibition of the dopamine receptors in the striatal pathway

Extrapyramidal Syndrome Tardive Dyskinesia

Adverse effects of dopamine blockade: inhibition of the dopamine receptors in the tuberofundibular pathway

Hyperprolactinemia

General management of Extrapyramidal Syndrome

Decrease the dose of the antipsychotic drug Change into atypical antipsychotic Administration of drug that can counteract it

Extrapyramidal Syndrome Manifestations

Akathisia Pseudo parkinsonism Dystonia

motor restlessness; most difficult to treat compelled to pace, shuffle their feet, shift positions, unable to sit quietly

Akathisia

Management of Akathisia

Administration of BZD (Benzodiazepines)

tremors, rigidity, and bradykinesia

Pseudo parkinsonism

Management of Pseudo Parkinsonism

Administration of anticholinergic agents

abnormal muscle tension of the neck and face (oculogyric crisis, gloss spasm, tongue protrusion, torticollis) difficulty to move

Dystonia

Management of Dystonia

Diphenhydramine, anticholinergic agents

Abnormal involuntary movements occurring with CHRONIC antipsychotic therapy (months to years). Abnormal movements of the face and tongue with widespread choreoathetosis. “superdensity phenomenon”

Tardive Dyskinesia

Management of Tardive Dyskinesia

Lower the dose or discontinue and give atypical agents

Prevention of Tardive Dyskinesia

Lowest dose for the shortest period of time required to control symptoms of schizophrenia. The drug should be discontinued periodically to assess the need for continued treatment and possibly to reduce dopamine super sensitivity.

Manifestations of Hyperprolactinemia

Galactorrhea - milk production from the breast unrelated to pregnancy or lactation Amenorrhea - the absence of menstruation Gynecomastia in men