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Pharm Human Behavior Paragraph Pharm Human Behavior Paragraph Antipsychotics Typical Atypical Chlorpromazine Clozapine Haloperidol Olanzapine Thioridazine Apiprazole Fluphenazine Risperidone Antipsychotics can all be thought of as “anti‐schizophrenia drugs.” as a general model. Remember that schizophrenia has positive symptoms (things that are there that shouldn’t, stimulation) such as hallucinations or voices, as well as negative symptoms (things that should be there but aren’t, depression) such as affective blunting or anhedonia. This causes a major problem for pharmacological management. Essentially, schizophrenia and other psychotic‐like symptoms are caused by excess dopamine in the mesolimbic‐mesocortical region of the CNS. Thusly, the administration of dopamine antagonists limits the symptoms of schizophrenia. However, treating the positive symptoms of psychosis can exacerbate the negative symptoms. Remember for a bit how we treated Parkinson’s disease. There was a lack of dopamine in the nigro‐ striatal pathway that caused Parkinsonian symptoms. If we now block dopamine in the brain, we block dopamine everywhere. That means these drugs can lead to parkinsonian symptoms. More importantly, dopamine antagonism treats only positive symptoms of schizophrenia. Since schizophrenia was discovered, new insight has lead to the activity of serotonin receptors. As the drugs become newer, they do a better job of treating both the positive and negative symptoms and limiting their depressive side effects. Therefore, these drugs are separated by their ability to target positive and negative symptoms, on their side effects, and on which receptors they either antagonize or agonize. Major side effects of antipsychotics are extrapyramidal symptoms. In the acute phase they cause pseudoparkinsonism, dystonia, or akathisia. In this case, the patients don’t move much. In the chronic phase they suffer from tardive dyskinesia that presents like a chorea or Huntington’s presentation caused by a hypersensitivity to dopamine stimulation. The only way to fix these symptoms is to withdraw the drug (which can push the patient back into psychosis) or switch to an atypical antipsychotic. Another major side effect is seen particularly in strong Dopamine Antagonists is neuroleptic malignant syndrome (NMS) characterized by temperature dysregulation, muscle rigidity, and potential for renal failure. In addition another major side effect is that of muscarinic and alpha blockade leading to orthostatic hypotension (α), dry mouth (M), constipation(M), and urinary retention(M). ALL antipsychotics can produce a prolonging of the QT interval The typical antipsychotics are the older drugs that target dopamine and are prone to tardive dyskinesia. The atypical antipsychotics block dopamine and serotonin and are devoid of tardive dyskinesias. We should mention that all of these drugs inhibit multiple receptors to some degree, but for a second year medical student, you can safely learn “dopamine” or “dopamine and serotonin” and forget about most of the minutia. 1 | Owl Club Review Sheets Pharm Human Behavior Paragraph TYPICALS – Block Dopamine Chlorpromazine, Thioridazine, Fluphenazine. These are the phenothiazines. They contain sulfur, so you must be cautious for sensitivity reactions. These are the oldest and the cheapest of the antipsychotics and are used as the prototype for others. They block dopamine receptors without much specificity, and therefore effect the entire brain. These have the largest alpha and muscarinic blockade and suffer from side effects involving sedation, orthostatic hypotension, dry mouth, constipation, and other anti‐ACh side effects. These really aren’t great drugs, but they are first choice since they are cheap, and not everyone suffers from the side effects. These are taken PO daily, and are for chronic management of psychosis. Haloperidol. This is a high potency dopamine antagonist usually used either within the hospital setting or for controlled injected dosages. You don’t start someone off on haloperidol, but this is usually is what is in the syringe in movies where a psych patient is “freaking out” and has to be sedated by men in white suits. It is a very potent dopamine antagonist. It causes significant sedation. Unfortunately it has two major side effects in addition to those shared with all antipsychotics. It has the capacity to lower the seizure threshold and highest risk for NMS. It is used in the non‐emergent setting in noncompliant patients who can receive an injection that lasts for weeks. This way, even if they don’t take their meds, they have some dosage of antipsychotics to limit their symptoms. ATYPICALS – Block Dopamine and Serotonin, Now Considered FIRST LINE DRUGS Clozapine. Clozapine is the prototype for atypical antipsychotics. It is atypical for two reasons. Firstly, it has extremely reduced extrapyramidal symptoms. Secondly, it also blocks 5HT receptors. Inhibition of 5HT2 Receptors then treats the negative symptoms of schizophrenia. How is not really important, but just to let you know, inhibition of the presynaptic, inhibitor 5HT2 receptor causes an increase in the release of serotonin which treats the negative symptoms. Clozapine is able to limit its extrapyramidal symptoms because of its selectivity for D2c receptors, found primarily in the mesolimbic‐mesocortical pathway, unlike the D2A receptors found in the nigro‐striatal pathway. Unfortunately, it has also been known to cause agranulocytosis with a significant compromise of WBC and the immune system, requiring weekly blood tests (which also suffer from noncompliance). Also causes weight gain. Olanzapine. Since Clozapine had the trouble with agranulocytosis, drug companies had to look elsewhere. An analogue of Clozapine, Olanzapine has lower selectivity for D2C receptors than Clozapine, but strongly antagonizes 5HT2 receptors. Most importantly, it does not suffer from agranulocytosis. Therefore, Olanzapine is not as good as treating psychosis as Clozapine, but does not have that major complication. It still suffers from orthostatic hypotension, muscarinic blockade, and causes weight gain. Risperidone. This is a different class of drug than the “‐apines” but is still considered atypical because of its stronger antagonism of 5HT2. This drug, while although it is an atypical, has an increased risk for tardive dyskinesias. Apiprazole. You will see commercials for this drug on TV. It was mentioned in our class, which means it is going to get more play in future years. It’s an atypical that is also a partial dopamine agonist. 2 | Owl Club Review Sheets Pharm Human Behavior Paragraph ANTIPSYCHOTICS Drug Unique Feature Unique Side Effect Typicals Chlorpromazine Prototype for antipsychotics, large side effects, but cheap Extrapyramidal Side Effects to use Haloperidol Super Strong Dopamine Antagonist Greatest Risk for NMS Atypicals Clozapine Selective for D2C Receptors without EPS symptoms Agranulocytosis Equipotent antagonist for 5HT2 receptors Olanzapine Weak selectivity for D2C receptors, increased affinity for No Agranulocytosis 5HT2 receptors Risperidone 5HT2 Receptor Increased risk for Tardive Dyskinesia Apiprazole Dopamine Agonist None Known Yet ANTIPSYCHOTIC SIDE EFFECTS Symptom Character Receptor that Causes It Extrapyramidal Found in the acute phase of dopamine antagonism. Dopamine Antagonism Symptoms – Parkinsonian symptoms caused by inhibition of Dyskinesia dopamine outside the psychosis center Extrapyramidal Found in the chronic phase of dopamine antagonism. Dopamine Antagonism Symptoms – Huntington’s symptoms caused by remodeling and Tardive Dyskinesia hypersensitivity to dopamine Orthostatic Get dizzy when you stand up Alpha Blockade Hypotension Neuroleptic Thermal dysregulation (patient gets hot) Severe Dopamine Antagonism Malignant Muscle Rigidity, ↑Heart Rate, ↓BP Syndrome Renal Failure Antimuscarinic Dry mouth, constipation, urinary retention Acetyl Choline Antagonism Symptoms Sedation Sedation Histamine Blockade Prolonged QT All antipsychotics carry this potential Alpha and Muscarinic Blockade ANTIPSYCHOTIC SIDE EFFECTS BY DRUG AND RECEPTOR Drug D2 α M H1 EPS symptoms Chlorpromazine ++ ++++ +++ +++ ++ Haloperidol ++++ + + + ++++ Clozapine ++ +++ ++ + ‐ Olanzapine + ++ + + ‐ Risperidone ‐ ++ ‐ ++ + Apiprazole + ? ? ? ? Effectiveness Orthostatic Dry Mouth, Sedation and EPS Hypotension Constipation, symptoms Urine Retention 3 | Owl Club Review Sheets Pharm Human Behavior Paragraph Antidepressants SSRIs MAO‐Is TCAs Atypicals Lithium Phenylzine Amitriptyline Bupropion Li Fluoxitine Tranylcypromine Imipramine Venlafaxine Citalopram Selegiline Trazodone Sertraline Mocolbemide Paroxetine Depression can be explained by the monoamine hypothesis. Essentially, there is not enough Norepi, serotonin, and/or dopamine in the brain. Whatever the underlying cause (insufficient production, release, activation, or response), by increasing neurotransmitter concentration we can eliminate depressive symptoms. Well that is all well and good, but it turns out that despite the increase in local levels of neurotransmitters immediately, it takes 2‐3 weeks for depressive symptoms to decline. This indicates that there is some neuronal plasticity in effect, requiring remodeling of synapses before therapeutic effect can be seen. Likewise, it takes 2‐3 weeks once a drug has been removed for the effects to wear off. It is important to ensure this length of time before switching to a different antidepressant to ensure there are no drug interactions. Much like the neurology CNS block, this block is very class‐heavy.
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