Dealing with Incorporate Comorbidity Problem - Essay Example

? Incorporate Comorbidity Problem Question One The abnormalities of the brain and the nervous system are a factor in most of the health conditions, especially mental health conditions (Porth & Matfin, 2009). In schizophrenia, which happens to be a psychiatric disorder, excesses in neurotransmitters, that is glutamate, dopamine and serotonin, which transmit information to the brain, might aid the condition’s development. As a result of the complication of this disorder, the participation of neurotransmitters in schizophrenia is probably part of a larger mental illness base that also comprises brain structure abnormalities, environmental stressors and genetic predisposition (Porth & Matfin, 2009). Neurons, which are brain cells, are responsive to distinctive types of neurotransmitters having receptors built purposely for them (Porth & Matfin, 2009). Those neurons that tend to be sensitive to certain neurotransmitters cluster together, thereby forming circuits in the brain, responsible for processing certain types of information. Neurotransmitters are discharged from a neuron at the time it signals another brain cell; these neurotransmitters are discharged to the small space amid the two neurons known as the synapse (Porth & Matfin, 2009). Inside the synapse, the neurotransmitters tend to attach to the receptors at the ending of another neuron, thereby affecting the action of the new neuron. Consequently, the new neuron absorbs as much of the neurotransmitter as it possibly can and then discharges the excess back to the synapse. After that, the first neuron goes ahead to reabsorb the excess; this process through a process is referred to as reuptake (Porth & Matfin, 2009). In the brain, there are various neurotransmitters, two of which are involved in schizophrenia symptoms, that is dopamine and glutamate (Craft, Gordon, & Tiziani, 2011). Dopamine happens to be primarily responsible for movement and thoughts, while, at the same time being related with novelty seeking, or concern in new experiences, as well as reward. Apparently, illegal drugs such as cannabis, cocaine and methamphetamine act by affecting the function of dopamine in the brain; therefore, dopamine is related with feelings of not only pleasure but also well-being (Craft et al., 2011). Dopamine paths within the brain tend to be extremely specialized, thereby being capable of influencing different types of behavior or thinking. Thus, people with high intensities of dopamine in parts of the brain might also suffer from psychotic symptoms or even paranoid thinking that are symptoms of schizophrenia (Craft et al., 2011). Glutamate happens to be other neurotransmitter, which might play a significant role in schizophrenia. Glutamate plays a key part in learning, formation as well as encoding of memory (Craft et al., 2011). There are hallucinogenic drugs such as PCP used in blocking glutamate receptors; however, amphetamines, PCP are capable of causing paranoia, which apes schizophrenic symptoms. In instances where people suffer from schizophrenia and use PCP, it worsens their symptoms (Craft et al., 2011). Research shows that an interaction between dopamine and glutamate happens to be the center of schizophrenia; nonetheless, dopamine receptors are capable of reducing glutamate action; in case there are unusually many dopamine receptors, the effects of glutamate will be blocked. Question Two Reports by the American Psychological Association (2001) assert that users of marijuana often express the experience of marijuana smoking as firstly relaxing and mellow, forming a feeling of haziness as well as light-headedness. The eyes of the user might dilate, making colors seem to be intense with other senses becoming enhanced (Porth & Matfin, 2009). Afterwards, the user might feel paranoia and panic; these feelings happen as a result of the interaction between the THC and the brain. In understanding the manner in which marijuana affects the brain, the American Psychological Association (2001) explains that there is a need of knowing the brain parts affected by THC; firstly, the brain has neurons, which are the cells responsible for processing information in the brain with chemicals called neurotransmitters allowing neurons to communicate with one another. Secondly, neurotransmitters fill up a synapse between two neurons, thus binding to protein receptors responsible for enabling various functions (American Psychological Association, 2001). Thirdly, some neurons comprise thousands of receptors, which are specific to certain neurotransmitters. Fourthly, foreign chemicals such as THC have the capability of mimicking or blocking actions of neurotransmitters and interfering with typical functions. The brain has groups of cannabinoid receptors clustered in various places; these cannabinoid receptors tend to affect various mental and physical activities including short-term memory, problem solving, coordination and learning (Davis, Rees, Lovitt, & Bebee, 2000). The cannabinoid receptors are activated through a neurotransmitter known as anandamide; anandamide comes from a group of chemicals known as cannabinoids with THC also being a cannabinoid chemical (Davis et al., 2000). Apparently, THC tends to mimic the acts of anandamide; this implies that THC binds with cannabinoid receptors while activating neurons, thereby causing adverse consequences on the mind and the body. Therefore, when a person inhales marijuana smoke, its chemicals are distributed all over the body (Porth & Matfin, 2009). Excessive concentrations of cannabinoid receptors are present in the hippocampus, cerebellum, and basal ganglia. Apparently, the hippocampus is in the temporal lobe and is essential for short-term memory; therefore, when the THC attaches with the cannabinoid receptors in the hippocampus, it obstructs the recollection of current events. Moreover, THC also influences coordination controlled in the cerebellum (Davis et al., 2000). The basal ganglia are responsible for controlling unconscious muscle movements. This is another basis why motor coordination tends to be impaired due to the influence of marijuana. Question Three There are five subtypes of schizophrenia contained in the DSM-IV; a person is diagnosed with a schizophrenia subtype depending on its leading symptoms since symptoms are capable of changing over the course of the disease, thereby leading to the changing of the subtype diagnosis as well (Craft et al., 2011). These subtypes comprise: 1. Paranoid Schizophrenia: In this case, patients are capable of taking care of themselves, with their behavior and their physical appearance remaining unaffected. Their main symptoms comprise delusions and hallucinations (Healy, 2005). Apparently, these patients do not go through any negative symptoms and hence, do not lose their ability of talking clearly. This schizophrenia normally develops later than other types of schizophrenia, and typically responds well to medication. 2. Disorganized Schizophrenia: This schizophrenia normally develops slowly at a younger age compared to other subtypes. Patients in this case happen to be the most psychotic. They tend to be difficult in understanding, with their appearance making them easy to identify. Patients with the type of disorganized schizophrenia are capable of dressing in weather, i.e. inappropriate clothing or appearing disheveled and unkempt (Martini, 2004). 3. Catatonic Schizophrenia: Patients with this schizophrenia might have symptoms comparable to patients with other subtypes; however, their physical movements differentiate them. Catatonic behavior is normally extremely slow, and these patients might appear as if they are going in slow motion (Fitzgerald, Gruener, & Mtui, 2005). 4. Undifferentiated Schizophrenia: This is a grouping used for patients who do not attain the norm for any other subtype. Apparently, these patients are capable of meeting the general minimum criteria for schizophrenia but do not show a pattern of symptoms, which is coherent with any subtype. Undifferentiated schizophrenia might be diagnosed in people who have fluctuating or atypical symptoms (Elder, Evans, & Nizette, 2005). 5. Residual Schizophrenia: Patients with this schizophrenia have symptoms that include positive symptoms that are less severe compared to those experienced in acute schizophrenia (Rinamhota & Marshall, 2000). Question Four The majority of schizophrenia medication has a lot of side effects, thus making it difficult for patients to remain on a treatment plan; nonetheless, schizophrenia’s antipsychotic medications are getting better day by day, thus creating room for improvement (Porth & Matfin, 2009). According to the condition suffered by Sandy, which is schizophrenia, there are several medications that can be used in alleviating her symptoms. They include: 1. Clozapine: This is an antipsychotic medication that acts by modifying the chemical actions inside the brain (Fitzgerald et al., 2005). It is used in treating acute schizophrenia, in addition to reducing the danger of suicidal behavior in people suffering from schizophrenia or related disorders. Apparently, clozapine is normally given after other medications become unsuccessful in the treatment of symptoms. Although clozapine happens to be highly effectual for most of the people who fail in responding to other drugs, it is capable of critically affecting white blood cell count within a small group of people. It is necessary to undertake weekly blood tests for anyone taking the medication. Unfortunately, people lacking the time, resources, or even the capacity of getting themselves to a clinic weekly might be unable to get this prospective lifesaving drug (American Psychological Association, 2001). 2. Zyprexa (Olanzapine): This is an antipsychotic medication used orally or as an injection, which affects chemicals inside the brain. Olanzapine is used in the treatment of the psychotic condition symptoms such as schizophrenia and bipolar disorder in both adults and children under 13 years old (Elder et al., 2005). Sometimes, olanzapine is used alongside other antipsychotic medications or even antidepressants. The side effects of olanzapine include allergic reaction comprising hives, breathing troubles and swelling in the throat, lips, face and tongue. 3. Haldol (Haloperidol): This is an antipsychotic medication that acts by changing the actions of chemicals inside the brain. Haloperidol is used when treating schizophrenia and controlling motor and speech tics in people with Tourette's syndrome (Zillmer, 2008). Some of the side effects include dizziness, pounding heartbeat, fainting or fast and restless muscle movements inside the eyes, neck, tongue or jaw, seizure and jaundice. Question Five According to the American Psychological Association (2001), regular cannabis use along with psychotic disorders such as schizophrenia is related to the general population 1,2, while heavy cannabis users are overrepresented amongst the latest cases of schizophrenia 3-5 (Craft et al., 2011). Consequently, these findings, together with rising levels of cannabis use amongst young people in most developed countries, have provoked debates concerning whether cannabis use might be a contributory root of psychosis that is capable of precipitating schizophrenia within vulnerable individuals (Craft et al., 2011). Apparently, there are other likely explanations of the relation; common causes might increase the threat of cannabis use, as well as psychosis, devoid of the two having a direct relation. The dependable finding of an association linking cannabis use and psychosis makes possible an unlikely account of the association with there being various prospective studies indicating that cannabis use regularly precedes psychosis (Martini, 2004). The strongest proof that cannabis usage happens to be a contributory root of schizophrenia hails from longitudinal studies of astronomical representative samples of the population followed over time to observe whether cannabis users are at a greater threat of developing schizophrenia. The first such study happens to be a 15-year prospective study of cannabis use, along with schizophrenia in 50,465 Swedish conscripts, which found out that those trying cannabis by the age 18 were 2.4 times more likely to be diagnosed with schizophrenia compared to those who were under 16, and the danger of this diagnosis rose with the regularity of cannabis use (Zillmer, 2008). Other proofs of this include Rinamhota and Marshall (2000) stating a 27-year record of the Swedish cohort, which found a dose-response relation between regularity of cannabis use at baseline and threat of schizophrenia throughout the follow-up. The relation between cannabis usage and schizophrenia continued when the authors statistically controlled the outcomes of other drug usage and other possible confounding issues including a history of psychiatric symptoms at baseline. Imagining a causal relationship and considering current use patterns, they approximated that it is possible to avert 13% of cases of schizophrenia if all cannabis use were thwarted. In one German and two New Zealand group studies, Healy (2005) described a 4-year follow-up of a group of 2,437 adolescents, along with young adults in 1995 and 1999 in Munich. According to the study, there is a dose-response relation between the use of self-reported cannabis at baseline and the probability of reporting psychotic symptoms during the follow-up. Apparently, young people reporting psychotic symptoms at baseline happened to be much more probable in experiencing psychotic symptoms during follow-up in case they used cannabis (Fitzgerald et al., 2005). References American Psychological Association. (2001). Publication manual of the American Psychological Association (5th ed.). Washington: APA. Craft, J., Gordon, C., & Tiziani, A. (2011). Understanding pathophysiology. Sydney: Elsevier. Davis, R., Rees, N., Lovitt, H., & Bebee, R. (2000). Mosby medication guide. Melbourne: Mosby. Elder, R., Evans, K., & Nizette, D. (2005). Psychiatric and mental health nursing. Sydney: Mosby. Fitzgerald, M. J. T., Gruener, G., & Mtui, E. (2005). Clinical neuroanatomy and neuroscience (5th ed.). USA: Elsevier. Healy, D. (2005). Psychiatric drugs explained (4th ed.). London: Churchill Livingstone. Martini, F. (2004). Fundamentals of anatomy and physiology (6th ed.). New Jersey: Prentice Hall . Porth, C. M., & Matfin, G. (2009). Pathophysiology: Concepts of altered health states (8th ed.). Philadelphia: Lippincott. Rinamhota, A., & Marshall, P. (2000). Biological aspects of mental health nursing. London: Livingston. Zillmer, E. S. (2008). Principles of neuropsychology (2nd ed.). USA: Thomson. Read More