Discuss with your peers what was surprising to you as a psychology student and a consumer. What aspects of these drugs were comforting to you? What aspects did you find disturbing? Why?
After viewing this week’s video, look up information on a particular drug used to treat a neurological or psychiatric disorder in the APUS online library and/or other online sources (see below). Please be sure that the information is relatively new (no more than three to five years old). Write your discussion summary of what you found focusing on the components below:
the class of the drug
the mechanism of action
receptor sites the drug targets
the drug’s main affect
and side effects and drug interactions
non-FDA uses of the drug
I chose to discuss Risperdal because I have never heard of it and was curious how anti-psychotic drugs work within the human body. Risperdal, or Risperidone, is an antipsychotic, and is used to treat symptoms of psychotic disorders, such as schizophrenia. It belongs to the chemical class of benzisoxazole derivative and it works by changing the chemicals in the brain. It can also be used in autistic children to treat irritability. Risperidone is a second-generation atypical antipsychotic. It is a dopamine antagonist possessing anti-serotonergic, anti-adrenergic and anti-histaminergic properties.
The exact mechanism of action of risperidone is not known, but is believed that it affects the way the brain works by interfering with communication among the brain’s nerves. Nerves communicate with each other by making and releasing chemicals called neurotransmitters. The neurotransmitters travel to other nearby nerves where they attach to receptors on the nerves. The attachment of the neurotransmitters either stimulates or inhibits the function of the nearby nerves. Like any medication, it is basically trial and error with the patient. Some people do well with certain drugs and others don’t. It all depends on your body.
Risperidone blocks several of the receptors on nerves including dopamine type 2, serotonin type 2, and alpha 2 adrenergic receptors. It is believed that many psychotic illnesses are caused by abnormal communication among nerves in the brain and that by altering communication through neurotransmitters, risperidone can alter the psychotic state. This drug was finally approved by the FDA in December 1993.
Adverse effects of risperidone include significant weight gain and metabolic problems such as diabetes mellitus type 2, as well as tardive dyskinesia and neuroleptic malignant syndrome. Risperidone and other antipsychotics also increase the risk of death in people with dementia. The other symptoms that are usually present in most drugs include; fever, confusion, sweating, stiff muscles, drooling, tremors, seizures and many more.
Like I said, this drug appealed to me because I never knew how these types of medications cured psychotic diseases. It is crazy to think that one little pill can change the chemicals so much in your brain that you act like a normal person. As a student and consumer I am always alarmed with the amount of adverse effects these drugs can have on your body. You are trying to treat one symptom or disorder, while causing your body to possibly obtain other horrible side effects. Sometimes you have to ask yourself what’s worse, the disorder or the medication. With anything, you should always consult your doctor and try out different medications to find the right fit.
Lithium is a psychoactive drug utilized to reduce abnormal brain activity and primarily used to treat bipolar disorder but is also prescribed to treat and schizophrenia. It is an antimanic class agent, meaning it is designed to stabilize mood my controlling symptoms of mania. Lithium salts have been studied over the last 70 years of its use despite researchers only recently being able to pinpoint how the drug specifically works. There are several mechanisms of action that allow lithium to have the therapeutic effect of reducing symptoms of mania. Lithium modulates signals impacting neural plasticity involved in mood recovery and stabilization, creating a more “balanced” effect in the user. Lithium also modulates neurotransmitters that balance or express excitatory and inhibitory activities. This is similar to the idea of preventing the higher “highs” and lower “lows”, a symptom indicative of bipolar, or manic depressive disorder. A third mechanism of action for lithium is to adjust gene expression.
This adjustment of gene expression targets G-protein couplings as well as glutamine, NMDA, and GABA receptors. G-protein couples are responsible for mediating the post synaptic actions of depression following a manic episode. In short, G-proteins are somewhat responsible for the roller coaster effect of manic and depressive episodes and autopsies revealed increased G-protein coupling in bipolar patients. Glutamine receptors also are elevated during mania, and both NDMA and GABA receptors assidt in the regulation of dopamine and glutamate receptor. The overall main effect identified in people prescribed the drug is to create a balanced overall demeanor, particularly in the long term, by mitigating the potential mood swings and dramatic changes experienced by bipolar patients.
One unexpected side effect of lithium was the increase of the overall brain volume, namely in the hippocampus and the amygdala. The reduction of brain volume in these areas that is in essence shored up by lithium supplements assists in limiting the duration of bipolar disorder. While lithium is not considered a “cure” for the disorder, it continues to be an effective treatment. Some of the side effects include similar concerns for many medicines including indigestion and appetite issues, joint pain, or increased sensitivity to temperatures. More severe side effects include difficulty with fine motor control leading to issues controlling movement or loss of coordination. Other severe symptoms may include hallucinations or slurred speech.
Due to the serious potential for death due to over-ingestion of lithium, it is not considered at high risk for use as a recreational drug. There have been recalls for specific, non FDA-approved forms of lithium carbonate, and for portions of time lithium was not provided. When initially used as medicine, lithium was prescribed to treat symptoms of gout. In 1975 its use was re-invigorated to treat symptoms of mania. The FDA has not approved its use for treating symptoms of depression, but it occasionally prescribed. The ambiguity regarding lithium use in the last 70 years was surprising to me. Given the long standing nature of its use, I was surprised that the greater scientific and psychological community really had little idea how it worked.
I suppose it was a good thing that people understood how much was too much and avoid toxic and fatal poisonings, but it is still surprising to me. Oddly enough, I find that more comforting than disturbing given the unequivocal usefulness of the drug. Imagine the people who benefitted from the treatment who would not have been helped had the drug not been provided to people some 70 years. The methods used to determine just how the drug worked were a little bizarre, however. In some experiments, urine was injected into lab rats to create increased levels of urea in the body. These subjects were then given lithium treatments to counteract or at least effect the imbalance.
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