Drug Treatment Of Psychosis PPT | Drug Addiction | Drug Induced Psychosis | Drug Psychosis | Drug Treatment | Drug Treatment Of Psychosis | Schizophrenia Positive Symptoms : Slideworld Medical PPT Search Engine

Drug Treatment of Psychosis

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Notes

Show Notes

Slide 1 :

DRUG TREATMENT OF PSYCHOSIS Martha I. Dávila-García, Ph.D. Howard University Department of Pharmacology Spring 2002

Slide 2 :

Psychosis Psychosis is a thought disorder characterized by disturbances of reality and perception, impaired cognitive functioning, and inappropriate or diminished affect (mood). Psychosis denotes many mental disorders. Schizophrenia is a particular kind of psychosis characterized mainly by a clear sensorium but a marked thinking disturbance.

Slide 3 :

Psychosis Producing Drugs Levodopa CNS stimulants Cocaine Amphetamines Khat, cathinone, methcathinone Apomorphine Phencyclidine

Slide 4 :

Schizophrenia Pathogenesis is unknown. Onset of schizophrenia is in the late teens early twenties. Genetic predisposition -- Familial incidence. Multiple genes are involved. Afflicts 1% of the population worldwide. May or may not be present with anatomical changes.

Slide 5 :

Schizophrenia It is a thought disorder. The disorder is characterized by a divorcement from reality in the mind of the person (psychosis). It may involved visual and auditory hallucinations, delusions, intense suspicion, feelings of persecution or control by external forces (paranoia), depersonalization, and there is attachment of excessive personal significance to daily events, called “ideas of reference”.

Slide 6 :

Schizophrenia Positive Symptoms. Hallucinations, delusions, paranoia, ideas of reference. Negative Symptoms. Apathy, social withdrawal, anhedonia, emotional blunting, cognitive deficits, extreme inattentiveness or lack of motivation to interact with the environment. These symptoms are progressive and non-responsive to medication.

Slide 7 :

Etiology of Schizophrenia Idiopathic Biological Correlates Genetic Factors Neurodevelopmental abnormalities. Environmental stressors.

Slide 8 :

Etiology of Schizophrenia Schizophrenia is not characterized by any reproducible neurochemical abnormality. However, structural and functional abnormalities have been observed in the brains of schizophrenic patients: Enlarge cerebral ventricles. Atrophy of cortical layers. Reduced volume of the basal ganglia.

Slide 9 :

Dopamine Theory of Schizophrenia Many lines of evidence point to the aberrant increased activity of the dopaminergic system as being critical in the symptomatology of schizophrenia.

Slide 10 :

Dopamine Theory of Schizophrenia Dopamine Correlates: Antipsychotics reduce dopamine synaptic activity. These drugs produce Parkinson-like symptoms. Drugs that increase DA in the limbic system cause psychosis. Drugs that reduce DA in the limbic system (postsynaptic D2 antagonists) reduce psychosis. Increased DA receptor density (Post-mortem, PET). Changes in amount of homovanillic acid (HVA), a DA metabolite, in plasma, urine, and CSF.

Slide 11 :

Pharmacodynamics Anatomic Correlates of Schizophrenia... Frontal cortex Amygdala Hippocampus Nucleus accumbens Limbic Cortex Areas Associated with Mood and Thought Processes: DA DA DA DA DA

Slide 12 :

Dopamine Theory of Schizophrenia Evidence against the hypothesis Antipsychotics are only partially effective in most (70%) and ineffective for some patients. Phencyclidine, an NMDA receptor antagonist, produces more schizophrenia-like symptoms in non-schizophrenic subjects than DA agonists. Atypical antipsychotics have low affinity for D2 receptors. Focus is broader now and research is geared to produce drugs with less extrapyramidal effects.

Slide 13 :

Dopamine System There are four major pathways for the dopaminergic system in the brain: The Nigro-Stiatal Pathway. The Mesolimbic Pathway. The Mesocortical Pathway. The Tuberoinfundibular Pathway.

Slide 14 :

THE DOPAMINERGIC SYSTEM

Slide 15 :

Catecholamines Tyrosine ? Tyrosine hydroxylase L-Dopa ? Dopa decarboxylase Dopamine (DA) ? Dopamine ? hydroxylase Norepinephrine (NE) (Noradrenaline) Phenylethanolamine- ? -N-methyltransferase Epinephrine (EPI) (Adrenaline)

Slide 16 :

Dopamine Synapse DA L-DOPA Tyrosine Tyrosine

Slide 17 :

Dopamine System DOPAMINE RECEPTORS There are at least five subtypes of receptors: Receptor D1 D2 D3 D4 D5

Slide 18 :

Slide 19 :

Dopamine System DOPAMINE RECEPTORS Receptor 2o Messenger System D1 ?cAMP D2 ?cAMP,?K+ ch.,?Ca2+ch. D3 ?cAMP,?K+ ch.,?Ca2+ch. D4 ?cAMP D5 ?cAMP

Slide 20 :

Dopamine Reuptake System

Slide 21 :

Antipsychotic treatments SCHIZOPHRENIA IS FOR LIFE There is no remission

Slide 22 :

Antipsychotic treatments Schizophrenia has been around perhaps, since the beginning of humankind, however, it was not until the last century that it was established as a separate entity amongst other mental disorders. Many treatments have been devise: Hydrotherapy: “The pouring of cold water in a stream, from a height of at least four feet onto the forehead, is one of the most certain means of subsiding violent, maniacal excitement that we have ever seen tried”... wrote an anonymous physician in the early 1800’s.

Slide 23 :

Antipsychotic treatments Lobotomies (Egaz Moniz received the Nobel Prize). In 1940’s Phenothiazenes were isolated and were used as pre-anesthetic medication, but quickly were adopted by psychiatrists to calm down their mental patients. In 1955, chlorpromazine was developed as an antihistaminic agent by Rhône-Pauline Laboratories in France. In-patients at Mental Hospitals dropped by 1/3.

Slide 24 :

Antipsychotics treatment Antipsychotics/Neuroleptics Antipsychotics are the drugs currently used in the prevention of psychosis. They have also been termed neuroleptics, because they suppress motor activity and emotionality. ** These drugs are not a cure ** Schizophrenics must be treated with medications indefinitely, in as much as the disease in lifelong and it is preferable to prevent the psychotic episodes than to treat them.

Slide 25 :

Antipsychotics/Neuroleptics Although the antipsychotic/neuroleptics are drugs used mainly in the treatment of schizophrenia, they are also used in the treatment of other psychoses associated with depression and manic-depressive illness, and psychosis associated with Alzheimer’s disease. These conditions are life-long and disabling.

Slide 26 :

Antipsychotics/Neuroleptics NON-compliance is the major reason for relapse.

Slide 27 :

Antipsychotic/Neuroleptics Three major groups : 1) Phenothiazines 2) Thioxanthines 3) Butyrophenones OLDER DRUGS

Slide 28 :

Antipsychotics/Neuroleptics Old antiphsychotics /neuroleptics are D2 dopamine receptor antagonists. Although they are also effective antagonists at ACh, 5-HT, NE receptors. dopamine receptor antagonist D2

Slide 29 :

Antipsychotics/Neuroleptics It appears that the specific interaction of antipsychotic drugs with D2 receptors is important to their therapeutic action. The affinities of most older “classical” agents for the D2 receptors correlate with their clinical potencies as antipsychotics.

Slide 30 :

Antipsychotic/Neuroleptics Correlations between therapeutic potency and affinity for binding D2 receptors. [3H]Haloperidol binding IC50 (mol/L) Clinical dose of drug [mg d-1] haloperidol clozapine thiothixene chlorpromazine promazine spiroperidole

Slide 31 :

Antipsychotics/Neuroleptics Both D1 and D2 receptors are found in high concentrations in the striatum and the nucleus accumbens. Clozapine has a higher affinity for the D4 receptors than for D2. Recently it has been found that most antipsychotic drugs may also bind D3 receptors (therefore, they are non-selective).

Slide 32 :

Antipsychotics/Neuroleptics Antipsychotics produce catalepsy (reduce motor activity). BLOCKADE OF DOPAMINE RECPTORS IN BASAL GANGLIA. Antipsychotics reverse hyperkinetic behaviors (increased locomotion and stereotyped behavior). BLOCKADE OF DOPAMINE RECPTORS IN LIMBIC AREAS. Antipsychotics prevent the dopamine inhibition of prolactin release from pituitary. BLOCKADE OF DOPAMINE RECEPTORS IN PITUITARY. ? hyperprolactinemia

Slide 33 :

Pharmacokinetics Absorption and Distribution Most antipsychotics are readily but incompletely absorbed. Significant first-pass metabolism. Bioavailability is 25-65%. Most are highly lipid soluble. Most are highly protein bound (92-98%). High volumes of distribution (>7 L/Kg). Slow elimination. **Duration of action longer than expected, metabolites are present and relapse occurs, weeks after discontinuation of drug.**

Slide 34 :

Pharmacokinetics Metabolism Most antipsychotics are almost completely metabolized. Most have active metabolites, although not important in therapeutic effect, with one exception. The metabolite of thioridazine, mesoridazine, is more potent than the parent compound and accounts for most of the therapeutic effect.

Slide 35 :

Pharmacokinetics Excretion Antipsychotics are almost completely metabolized and thus, very little is eliminated unchanged. Elimination half-lives are 10-24 hrs.

Slide 36 :

Antipsychotic/Neuroleptics Phenothiazines Chlorpromazine Thioridazine Fluphenazine Trifluopromazine Piperacetazine Perfenazine Mesoridazine Acetophenazine Carphenazine Prochlorperazine Trifluoperazine Aliphatic Piperidine Piperazine* * Most likely to cause extrapyramidal effects.

Slide 37 :

Antipsychotic/Neuroleptics [Drug dose] Effect Piperazine Aliphatic Piperidine

Slide 38 :

Antipsychotic/Neuroleptics 2) Thioxanthines Thiothixene Chlorprothixene Closely related to phenothiazines

Slide 39 :

Antipsychotic/Neuroleptics 3) Butyrophenones Haloperidol Droperidol* *Not marketed in the USA

Slide 40 :

Antipsychotic/Neuroleptics [Drug dose] Effect Phenothiazine d. Thioxanthene d. Butyrophenone d.

Slide 41 :

Antipsychotics/Neuroleptics Newer drugs have higher affinities for D1, 5-HT or ?-AR receptors. NE, GABA, Glycine and Glutamate have also been implicated in schizophrenia.

Slide 42 :

Antipsychotics/Neuroleptics The acute effects of antipsychotics do not explain why their therapeutic effects are not evident until 4-8 weeks of treatment. Blockade of D2 receptors ? Short term/Compensatory effects: Firing rate and activity of nigrostriatal and mesolimbic DA neurons. DA synthesis, DA metabolism, DA release

Slide 43 :

Antipsychotics/Neuroleptics Presynaptic Effects Blockade of D2 receptors ? Compensatory Effects Firing rate and activity of nigrostriatal and mesolimbic DA neurons. DA synthesis, DA metabolism, DA release. Postsynaptic Effects Depolarization Blockade Inactivation of nigrostriatal and mesolimbic DA neurons. ? Receptor Supersensitivity

Slide 44 :

Antipsychotic/Neuroleptics Pimozide Molindone Loxapine Clozapine Olanzapine Qetiapine Risperidone Sertindole Ziprasidone Olindone Newer Drugs

Slide 45 :

Antipsychotic/Neuroleptics Clinical Ex. Py. Drug Potency toxicity Sedation Hypote. Chlorpromaz. Low Medium Medium High Haloperidol High Very High Very High Low Thiothixene High Medium Medium Medium Clozapine Medium Very low Low Medium Ziprasidone Medium Very Low Low Very low Risperidone High Low Low Low Olanzapine High Very Low Medium Very low Sertindole High Very Low Very low Very Low

Slide 46 :

Antipsychotic/Neuroleptics Chlorpromazine: ?1 = 5-HT2 = D2 > D1 > M > ?2 Haloperidol: D2 > D1 = D4 > ?1 > 5-HT2 >H1>M = ?2 Clozapine: D4 = ?1 > 5-HT2 = M > D2 = D1 = ?2 ; H1 Quetiapine: 5-HT2 = D2 = ?1 = ?2 ; H1 Risperidone: 5-HT2 >> ?1 > H1 > D2 > ?2 >> D1 Sertindole: 5-HT2 > D2 = ?1

Slide 47 :

Antipsychotic/Neuroleptics Clinical Problems with antipsychotic drugs include: Failure to control negative effect Significant toxicity Parkinson-like symptoms Tardive Dyskinesia (10-30%) Autonomic effects Endocrine effects Cardiac effects 3) Poor Concentration

Slide 48 :

The Nigro-Striatal Pathway

Slide 49 :

Antipsychotic/Neuroleptics Some antipsychotics have effects at muscarinic acetylcholine receptors: dry mouth blurred vision urinary retention constipation Clozapine Chlorpromazine Thioridazine

Slide 50 :

Antipsychotic/Neuroleptics Some antipsychotics have effects at a-adrenergic receptors: orthostatic hypotension Chlorpromazine Thioridazine Some antipsychotics have effects at H1-histaminergic receptors: sedation Risperidone Haloperidol

Slide 51 :

Antipsychotic/Neuroleptics Blockade of D2 receptors in lactotrophs in breast increase prolactin concentration and may produce breast engorgement and galactorrhea.

Slide 52 :

Antipsychotic/Neuroleptics Neuroleptic Malignant Syndrome Is a rare but serious side effect of neuroleptic (antipsychotic) therapy that can be lethal. It can arise at any time in the course of treatment and shows no predilection for age, duration of treatment, antipsychotic medication, or dose.

Slide 53 :

Antipsychotic/Neuroleptics Neuroleptic Malignant Syndrome Occurs in pts. hypersensitive to the Ex.Py. effects of antipsychotics. Due to excessively rapid blockade of postsynaptic dopamine receptors. The syndrome begins with marked muscle rigidity. If sweating is impaired, a fever may ensue. The stress leukocytosis and high fever associated with this syndrome may be mistaken for an infection. Autonomic instability with altered blood pressure and heart rate is another midbrain manifestation. Creatine kinase isozymes are usually elevated, reflecting muscle damage.

Slide 54 :

Antipsychotic/Neuroleptics Neuroleptic Malignant Syndrome Treatment Vigorous treatment with antiparkinsonian drugs is recommended as soon as possible. Muscle relaxants such as diazepam, dantrolene or bromocriptine may be helpful.

Slide 55 :

Antipsychotic/Neuroleptics Drug Interactions Additive effects with sedatives. Additive effects with anticholinergics. Additive effects with antihistaminergics. Additive effects with ?-AR blocking drugs. Additive effects with drugs with quinidine-like action (thioridazine).

Slide 56 :

REFERENCES Katzung, B.G. (2001) Basic and Clinical Pharmacology, Chapter 29, 8th Ed. Lange. 478-497pp. Kandell, E.R. and Schwartz, J.H. (1981). Principles of Neuroscience. Elsvier/North Holland. N.Y. 3. Wingard et al., (1991) Human Pharmacology. Molecular to Clinical. Mosby Year Book.

	Medslides_PPT 1 Years ago. Category: Psychiatry

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