Applied Biological Principles in Mental Health - Essay Example

Unipolar depression also referred to, as major depression is a medical illness that affects approximately 15 million American adults (National Alliance on Mental Illness, NAMI, 2007). It is normal to experience sadness, loss or a passing case of the blues. Major depression is different in that the feelings of sadness are persistent and significantly alter an individual's thoughts, behavior and mood affecting activity and health. (NAMl, 2007) Depression is more common in women than men with double the incidence rate in women, compared to men. Those who experience one episode of depression go on to have more episodes. In the absence of treatment, the patient deteriorates further with an increase in frequency of episodes and severity of the illness. Sometimes the patients commit suicide. The symptoms of depression include feeling of worthlessness, hopelessness and emptiness, lack of interest and pleasure in activities that the individual once enjoyed, decreased or increased need for sleep, poor appetite, persistent sadness, suicidal ideation, presence of physical symptoms that fail to respond to treatment and whose etiology cannot be identified and difficulties in concentrating and thinking and poor memory or memory lapses. (NAMI 2007). When some of these symptoms occur together and last for a period longer than two weeks and cause disturbances in normal functioning such as inability to go to work, to care for children, the individual is diagnosed as having Unipolar depression (DSMLV) The etiology of unipolar depression is not exactly known. A mix of psychological, biological and environmental factors contributes to development of depression. Though the specific cause is unknown scientific research has proven major depression to be a biological medical illness. A biological explanation for unipolar depression lies in alterations in the structure of the brain, imbalances in neurochemicals, genetic predisposition and endocrine involvement in some cases. The brain can be divided into several functional and developmental areas when explaining it structure. The cerebrum is at the top and is the biggest and most developed region of the brain. It performs all cognitive and conscious process. The limbic cortex is found beneath it and it controls processes involved in self-preservation; emotions like fear, behaviour like eating is controlled here. Beneath the limbic cortex, the basal ganglia and the cerebellum are found. They control movement. At the base of the brain, the brain stem found, it satisfaction is to keep one alive physiologically through control of circulation and respiration. (Martini, 2007) The areas of the brain are made of grey matter composed of cell bodies of nervous or white matter made from axons of neurons. Grey matter is mostly found in the outer parts of the brain while white matter is in the inner part. The surfaces of the brain are folded into gyri and sulci so that surface area is increased to enable unpacking of neurons. Cell bodies found deep inside the white matter are called ganglia (as in the basal ganglia). Nuclei refer to grey matter found in patches, which usually have a specific function. An example is the cranial nuclei found in the brainstem. Meninges are membranes that cover the brain. They are in 3 layers starting from the innermost, pia matter, arachnoids mater and dura mater. The arachnoid and pia mater have a sub arachnoid space that contains cebrospinal fluids. CSF is formed in the ventricles of brain (cavities of the brain) from blood plasma and fills the two lateral ventricle, the third ventricle and the fourth ventricle before flowing into the sub arachnoids spare from the where it will circulate over the brain and be absorbed via villi of the arachnoid mater. CSF provides buoyancy for the brain, reduces brain injury accidents when head experiences trauma and is a medium for nutrition of the brain and excretion. The cerebrum is divided into two hemispheres (left and right), which are each divided into four lobes. These are parietal lobe, temporal lobe, occipital lobe and frontal lobe. The frontal lobes are found behind the forehead. They are responsible for language, motor function, problem solving, reasoning and memory. The parietal lobes lie behind the frontal lobes and are responsible for integrating sensory information, reading and arithmetic. The occipital lobes lie at the back and are responsible for visual processing. The temporal lobes are found under the parietal and are important for memory, hearing, perception and recognition functions. Observations of depressed individuals have led to the conclusion that there must be underlying compromise of normal physiological function, especially when these patients respond to medication. From Magnetic Resonance Imaging techniques, patients with unipolar depression have been found to have increased ventricle size. Soures reports that these finding are interpreted as atrophy of central white matter. (Soures, 2003). The frontal lobe has been demonstrated to be smaller in volume in depressed patients compared to controls. The prefrontal cortex is decreased in patients with depression and continues to decrease with increase in severity of the illness. When specific regions of the prefrontal cortex are observed, a decrease in the grey matter in the subgenus area is noted. This finding is in line with a decrease in blood flow to the area. (Soures, 2003). Cognitive deficits seen in depression are a reflection of decreased function in the lateral cortex while active manifestations are evidence of paralimbic activity that is disordered. The ventral striatum hypo function results in anhedonia which is characteristic of unipolar depression patients, while psychomotor agitation and retardation are evidence of an interface of motor systems with the thalamus (Soures, 2003) The functional unit of the nervous system is the neuron. Nerve impulse come from neurons and travel along its extended cytoplasm called an axon to the place in the brain where the impulse initiates certain actions for example triggering muscle contraction, secretion by a gland o another action potential in a second neuron. Neurons have synapses that form means of communication from the one neuron to another. Neurotransmitters are the chemical agents released into the synaptic cleft from the presynaptic bulb . Neurotransmitters are in 3 main groups amino, amino acids and peptides. (Blows, 2003). The neurotransmitters released bind to receptors. This binding results in a specific activity. Examples of neurotransmitters include Acetycholine, Norepinephrine, GABA, and Dopamine. Each neurotransmitter binds to a specific receptor. Most biological theories of depression advance a hypothesis of disturbances in central nervous system neurotransmitter. This is especially so for catecholamines. (norepinephrine and epinephrine, serotonin, dopamine and acetycholine. (Davis, Millon and Blaney, 1999) Upregulation refers to a process whereby the sensitivity of binding of receptors is increased or there is an increase in the number of receptors. Downregulation is a process that results in decreased receptor sensitivity or decreased number of receptors. Neurons containing norepinephrine arise from the brainstem and projects to the cerebral cortex, limbic system, basal ganglia, thalamus and hypothalamus. This projection is in line with norepinephine's function of maintaining arousal and altering function of other neurotransmitters. Projections to adrenal gland through the sympathetic nervous system control release of NE that triggers the fight or flight response. When there is pathological increased activity in the brainstem as is the case in depression anxiety, agitation, decreased appetite, insomnia and poor concentration result (Davis et al, 1999) Serotonergic systems arising from the brainstem project to the cerebral cortex, hypothalamus, thalamus, basal ganglia, septum and hippocampus. Serotonergic transmission has effects of inhibition and facilitation. Serotonin is a regulator of sleep, appetite and libido and also regulates other neurotransmitter activity (Davis et al). From this, one can conclude that pathologic decreases of serotonin contribute to appetites, sleep, and libido disturbance (Davis et al, 1999). In depression the serotonin levels are lowered hence the clinical manifestation of insomnia, lack of interest is sex and poor appetites. Davis et al state that recent evidence shows that chronic stress down regulates S. HT serotonin receptors leasing to reduced transmission. Dopamine is also thought to be involved in the pathogenesis of depression. McLean et al report that dopamine depletion contributes to the disrupted affect seen in clinical unipolar depression (McLean et al, 2003) The endocrine system is also involved in the pathophysiology of depression. Hormones released into the body regulate reaction to stress and sexual development among other physiological processes. The endocrine system is connected with the brain at the hypothalamus, which controls bodily function like sleep, appetite and sexual drive. The hypothalamus controls the pituitary glands, which in turn controls glandular secretion of hormones. Some of the neurotransmitters associated with depression are used in the hypothalamus to maintain homeostasis of the endocrine system. The neurotransmitters, serotonin, norepinephrine and dopamine perform a role in management of the endocrine system. Development t of clinical depression is sometimes a symptom of disorder in the function of hormone producing organs Thyroid disorders, Cushing's syndrome and Addison's disease are among the conditions included (www.allaboutdepression.com/). In clinically depressed individuals, approximately 5% have an excess of cortisol. Cortisol secreted by adrenal glands increases in response to a stressful event. Cortisol is believed to be correlated with clinical depression due to the fact that the increased levels go back to normal when the depression episode disappears. Research reveals that timing of cortisol release may be deranged in depressed persons. Normally cortisol levels are greatest at around 8.00 am and 4.00 pm and lowest at night. The cycling of cortisol is different for a depressed individual resulting some times in an unchanging level of cortisol or levels that are highest at night. The hypothalamus is responsible for initiating secretion of cortisol by adrenal glands and maintaining the hormone within normal levels in the body. In a depressed person, the hypothalamus may continuously cause the pituitary to produce corticotrophin-releasing hormone (CRH) that then causes the adrenal gland to produce adrenocortitotrohphic hormone (ACTH) that leads to production of cortisol. When there is no negative feedback to control production of CRH, cortisol production continues to increase (www.allaboutdepression.com/) Familial tendencies have also been found in major depression while not everyone who has family history of unipolar depression develops the disease; these people are generally at greater risk than the general population. Life crises like death, divorce, chronic stress and physical illness and substance abuse act as precipitating factors for the illness in those with genetic predisposition. However, some depressive episodes occur spontaneously. (NAMI, 2007). Antidepressant medication is used to correct the imbalances in the neurotransmitter dopamine, serotonin and norepinephrine. Selective Serotonin Reuptake Inhibitors (SSRIs) are the most commonly prescribed drugs for depression; they block the reuptake of serotonin. This results in an artificial increase in serotonin levels. Serotonin then becomes available for neurotransmission and effects of reduced serotonin levels are overcome. (NAMI, 2001) Drugs that are SSRIs include fluoxetine (Prozac) sertraline, (Zoloft), paroxetine (paxoil), and infalopram. (Celexa) and fluroxamine (Luvox) (Norman, 1999). Tricylic Antidepressants are hardly used as treatment for depression. TCAs include amitriptyline (Elavin, Limbitrol), desipramine, imipramine (Norpramin), nortriptyline (Pamelor, Aveutyl) and protryptyline. They work by blocking the reuptake of catecholamines thus there is more neurotransmitter available for transmission. (Ryall, 1989) These drugs have stopped being used because of their side effects. Their side effects can be explained by he fact that they potently bin to muscurinic receptors, histaminergic receptors and adrenergic receptors leading to such side effects like a dry mouth, sedation, confusion, restlessness and seizures (www.rxlist.com/). Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) are second in popularity for treatment of depression. They block serotonin and norepinephine reuptake increasing amount of neurotransmitter available for signal transmission. Examples include, venlafaxine (Effexor) and duloxetine (cymbalta) (NAMI, 2007). The Monoamine Oxidase inhibitors are also not used much nowadays. They inactivate the enzymes that break down serotonin, norepinephine and dopamine, resulting in an increase of these neurotransmitters in the brain. They are not used much nowadays due tot the dangers of interaction reactions and three necessity to adhere to a particular diet. They are sometimes for a typical depression that is not responsive to other medication. When taking MAOIs the patients should avoid eating foods with large quantities if tyramine, an amino acid. If tyramine is ingested inn large quantities together with a MAOI blood pressure levels increased to high resulting in a hypertensive crisis that could lead to stroke. Foods with large quantities of tyramine include cheese, yeast and alcoholic beverages (Overcome Depression, 2007) Other drugs that can be used to treat depression include bupropion, which is a Norepinephrine-Dopamine Reuptake Inhibitor (NDRI). Bupropion binds to dopamine and norepinenphrine uptake pumps. The drug is biotransformed by cytochrome P enzymes to metabolites that are pharmacologically active with a slower clearance rate than the parent drug. The effect of the total concentration of bupropion and its metabolites exceeds the concentration of most antidepressants. It thus has a narrow therapeutic index and the likelihood of developing side effects, mainly seizures is high with bupropion (Preskorn, 2000) Mirtazapine is another drug used to treat depression. It is an antagonist of 5-HT2 and 5-HT3 receptors. It also has antagonistic side effect of histamine receptors, explaining its sedation effects. It has moderate antagonistic activity on muscarinic receptors, which explains the low incidence of anticholinergic side effects. Orthostatic hypotension results from the adrenergic antagonist effect of the drug (www.rxlist.com/) Combination of antidepressants with each other is referred to as combination therapy. The aim of this kind of therapy is to restore balance of the neurotransmitters as much as possible. Sometimes augmentation is used, this means that an antidepressant is being combined with a drug which is not an antidepressant. Drugs like this are atypical antipsychotic agents like aripiprazole, olanzapine, buspirone, thyroid hormone, stimulants like methylphenidate, dopamine receptor agonists like lithium, lamotrigine and steroid hormones. (NAMI, 2007) Biological theory uses an interdisplinary approach is explaining and providing management of depression. It incorporates psychopharmacology neuroscience, genetic, physiology and biochemistry as is evident from the explanations above concerning biological etiology of unipolar depression and psychopharmacology of its treatment. Biological theory is especially important in the development of drug-based treatment for mental disorders. Brain imaging technique used in the biological theory have made it possible to detect neurobiological problems associated with psychiatric disorders making biology theory a safe and effective basis for providing care to depressed patients. The 'chemical imbalance hypothesis' of explaining depression has led to development of even safer drugs. (SSR/s. the biological theory does not advocate for drugs the only treatment modality rather diet, physical exercise have been recommended and these work well especially in treating depression triggered by chronic stress. In severe cases, electro convulsive therapy and trans-cranial magnetic stimulation are used for treatment of psychiatric disorders. These are mainly employed only when patients are nit responsive to dug therapy. Though biological theory is criticized many, due to the lack of biomarkers psychiatric conditions, though theory has led to the development of many drugs that work and make life more manageable for the patients and relatives of the patients with depression. Biological theory is relevant due to the fact that it provides the nurse with characteristics that are observable. Due to this the nurse can provide objective interventions depending on the response of a client to medication and other treatment based on biological theory. Sometimes the full therapeutic effect of antidepressant medication takes up to 8weeks to occur and other times a patient may have to try a variety of antidepressants before they find a combination that works for them. This is not an entirely negative thing because regular checking of dosage and effectiveness of the drugs helps the client to understand their condition better and may even increase trust in the health system. The client is also empowered to make informed decisions about their health. The advantage that biological theory has over all other theories is that it is the most objective due to its scientific basis, which have resulted in better treatment outcomes for the client. In terms of progress it shows the most promise as far as explaining the etiology of unipolar depression. References Biological Causes of Depression retrieved from www.allaboutdepression.com/au_02.html. Blows WT, 2003, Biological Basis of Nursing, Ratledge Publisher, ISBN 041524854X pg 1-10, 180-190. Davis RD, Million Blaney PH,(1999) Oxford Textbook of Psychology, Oxford University Press, US, ISBN 0195103076 PP 160-168. Iscid Encyclopedia, 2007, Iscid Encyclopedia of science and Philosophy, Lobes of the Brain, retrieved from www.iscid .org/orglencyclopedia/lobes_of_the_brain.htm McLean A, Rubinszkin Js, Robbins TW, Sahakian BJ. (2005) The Effects of Tyrosine Depletion in normal healthy volunteers: Implications for unipolar depression, Psychopharmacology (B&I). 2003 Sep 4 retrieved from www.biopsychiatry.com/tyroine-html. Mirtazapine, retrieved from www.rxlist.com/cgi/generic/mirtaz-cp.htm#cp Monoamine Oxidize Inhibitors, Overcome Depression retrieved from www.overcomedepression.co.uk/Monoamine Oxidize Inhibitors.html. Soures JC, 2003, Brain Imaging in Affective Disorders, Informa Health Care, ISBN 0824708849 pg 3-55. NAMI (National Alliance on Mental Illness, Major Depression, retrieved from www.nami.org/content/contentGroups Melphine 1/Major-Depression.htm Norman TR, (1999) The new antidepressants -mechanisms of action, Australia Prescriber, retrieved from www.australianoprescriber.com/magazine 122/s/06/8/ Preskorn SH, (2000), Bupropion: What Mechanism of Action Journal of Practical Psychiatry and behavioral Health, January 2000, 272-276. Ryall RW, 1989, Mechanisms of Drug Action on the Nervous System, Cambridge University Press, ISBN 05212724370 PG 146-199. Selective Serotonin Reactive Inhibitors (SRRIS) retrieved from www.mayoclinic.com/health/ssris/MH00066 Read More