As Future Allied Health or Complementary Medicine Practitioners - Case Study Example

Clinical Pharmacology of Hypertension Student’s Name: Institution: Clinical Pharmacology of Hypertension Introduction The case study presents a patient with hypertension (high blood pressure), a disease that it known for affecting a large part of human population globally. According to Association (2009), this disease causes approximately 1 billion deaths. All these deaths are associated to be caused by cardiovascular disease. In his writing, Carretero & Opari (2000) argues that death does not occur by hypertension alone but by several acute-linked diseases including renal failures, strokes, and Myocardia Infraction. Being the dominant cause of morbidity and mortality, hypertension possesses significant health challenges, while the cost associated in its treatment and lessening other risk factors remain at the top of the list. The scope of this paper is to analyze the underlying causes and pathophysiology of hypertension with the help of the details of the patient. Classification A human normal blood pressure is rated to be 115/75 mmHg, thereby the 115 represents the systolic pressure while the 75 represents the diastolic pressure (Dreisbach & Sharma, 2000). A person is treated with hypertension usually when their blood pressure is consistently over 135/90 mmHg, only that nowadays, medical professionals have become cautions and resort to treating the patient the moment such a patient hits 130/80 mmHg. As notified by Khabunde (2007), cardiovascular risk increases for every 20/11 mmHg increment. Research by McPhee, Papadakis & Tierney (2008) classifies hypotension into two broad categories; essential (primary) and secondary hypertension. Close to 90-95% of the population diagnosed with the disease possesses primary type, characterized by the fact that the disease may not be fully known and may be more prevalent while a person ages. On the other hand, secondary hypertension is caused by an underlying medical condition that has distorted the homeostatic passageway of regulating blood pressure. Usually, secondary type of hypertension is more easily treatable since the underlying cause can be identified. Some of the commonly recognized diseases that are considered causal agents of hypertension include tumors, kidney diseases, and Cushing’s disorder. Another significant cause is the genetic abnormality occurring in the aorta (McPhee, Papadakis & Tierney, 2008). Signs and Symptoms Characterizing Hypertension From the case presented about the 60-year-old male plumber, it is obvious that some of the mentioned signs suggest that the patient is suffering from hypertension. Moderate hypertension starts from 140/90, a condition termed as asymptomatic. Sudden and prolonged enhanced blood pressure is associated with visual disturbances, sleepiness, and headaches; which could easily lead to frequent nausea. Of key to note is that, though hypertension is known to be more dominant in the elderly (in this case, a 60-year old), children are likely to be affected by the disease whereby the symptoms could be more acute including bell palsy and epistaxis (Oparil & Weber, 2005). The symptoms and signs of secondary hypertension rely on the kind of ailment that is causing it, implying that the indicators for Cushing’s syndrome would be different from the drug induced one or genetic one. Primary Diagnosis The evaluation of hypertension entails correctly measuring the patient’s blood pressure, conducting a detailed medical history together with physical examination, and acquiring results of routine lab results. Williams (2010) advises that a 12-lead electrocardiogram should be used. By virtue of incorporating these steps, the medical practitioner will be assured of accurately determining the following:1) baseline values for judging biochemical effects resulting from therapy; 2) cardiovascular risk factors; 3) potential causes of hypertension; and presence of end-organ disease. Other studies may be acquired on the grounds of clinical findings or in persons suspected with secondary hypertension as well as evidence of target-organ disease including urine microalbumin, uric acid, chest radiograph, and CBC. Pathophysiology In his point of view, Supiano(2001) acknowledges that the exact cause of hypertension is not known. There are various risk factors such as race, metabolic, genetics, age, and “sedentary lifestyle that can cause obesity.” According to Williams (2010), it has been estimated that close to 88% of the causes of hypertension have a higher BMI than 20. The vascular irregularities and pathophysiologic mechanism have proven to be speculative, throwing a challenge for more research to be conducted over the same. Blood pressure is actually the combined consequence of vascular resistance and cardiac output, meaning that either one can in combination or independently cause hypertension (Williams, 2010) ). Several studies show that various factors may work conjointly or independently turn the neuro-humoral systems either on or off. In individuals with a hyper-responsive system caused by “changed vascular properties”, Williams (2010) sees the need for observi9ng an aggravated pressure flow. It has been established that there is a natural evolution of the disease, therefore, most research has proven that one of the reasons of the early elevations of the cardiac output or blood volume may be explained by scarce elimination of sodium by kidneys. High levels of sodium can considerably increase the osmotic pressure, leading to expanded blood volume. It can be inferred that hypertension is maintained by the boost in vascular resistance as well as a decrease in elastic of the walls, especially when the patient has been following a medically unhealthy lifestyle. Another factor that has been proven by different studies relate to the decrease in sensitivity of receptors in the blood vessel. Usually, the decrease in receptors sensitivity tends to modify central nervous system (CNS) manipulation as well as sympathetic nervous system (SNS) distribution, consequently leading to two major expressions. Firstly, having an insensitive receptor needs a larger change in blood pressure in order to generate a similar response, as the receptor is not activated. Secondly, decreased receptors sensitivity leads to superior SNS activity for a particular level of arterial blood pressure. In the case of the patient suffering from hypertension, -shows evidence that changes in VEF (vascular endothelial function) can considerably obstruct normal vascular tone of individuals with hypertensive hypertension. Vascular tone is changed by increase in circulation of angiotensin II as well as the increased sympathetic activity. The already distorted sympathetic activity resultantly leads to a decrease in production of nitric oxide, which is a vasodilator. In the words of Williams (2010), ‘type 2 diabetes causes endothelial dysfunction by enhanced oxygen free radical mediated damage as well as decreased nitric oxide bioavailability’. In his investigation, Rodriguez-Cruz (2009) notes that other factors that maintain hypertension are caused by dysfunction in electrolyte homeostasis, specifically deviations in potassium, calcium, and sodium concentrations. For instance, calcium increases vascular contractility by stimulating rennin release. Renin functions by synthesizing epinephrine, coupled with the activity of the sympathetic nervous system that can be associated with abnormalities in the vascular tone. On the other hand, potassium assists in decreasing the blood pressure by suppressing the release of rennin (Dreisbach & Sharma, 2010). In a hypertension patient in this case study, cardiac output is usually normal and peripheral resistance tends to sustain hypertension by the decrease in lumen or dysfunction in vascular function. In different persons, sometimes it can be difficult to comprehend which systems are operational and therefore designing appropriate treatments could be difficult. In this case, treatments are more often designed to affect the regulatory factors instead of the cause (Peralta, Hicks, Chertow, Ayanian, Vittinghoff, Lin & Shlipak, 2005). Review of existing interventions Two generally known approaches for the primary prevention of hypertension include– population-based interventions and individual-based interventions. Individual-based interventions seek to identify high-risk hypertensive persons and provide them with pharmacologic treatment. Rationale for Pharmacologic Treatment of Hypertension Patients suffering from primary hypertension should be treated with drugs that 1) lessen blood volume, thus allowing reduction of CNS cardiac output and venous pressure, 2) lessen systemic vascular resistance, and 3) lessen cardiac output through depressing stroke volume and heart rate. Patients with secondary hypertension are recommended by removing or controlling the underlying pathology or disease, though they might still need antihypertensive drugs. Rationale for Reducing Arterial Pressure Arterial pressure can be controlled by decreasing central nervous pressure, systemic vascular resistance, or cardiac output. An inexpensive and effective way of reducing venous pressure is by use of drugs that lessen blood volume. Such drugs essentially act on the kidney to enhance water and sodium excretion. Reduction of blood volume will slowly reduce central venous pressure and further reduce cardiac output with the help of the Frank-Starling mechanism, which happens after the reduction in ventricular preload. Usage of these drugs is an added benefit since they lessen the systemic vascular resistance (Rodriguez-Cruz, 2009). Most of the antihypertensive drugs exert their primary action on systemic vascular resistance. Some even generate vasodilatation by distorting sympathetic adrenergic vascular tone or by blocking the formation of vascular receptors or angiotensin II. Though less commonly used due to a high incidence of side effects, there are drugs that function on regions in the brain and majorly control sympathetic autonomic outflow. By lessening sympathetic efferent activity, the presence of acting drugs tends to decrease arterial pressure by lessening cardiac output and systemic vascular resistance. As noted by Peralta, Hicks, Chertow, Ayanian, Vittinghoff, Lin & Shlipak (2005), some antihypertensive drugs (especially beta–blockers) function by depressing heart rate and contractility (an action that lessens stroke volume). This is done by blocking the influence caused by sympathetic nerves on the patient’s heart. In addition, calcium-channel blockers, specifically those that are more cardio selective, also reduce cardiac output by lessening contractility and heart rate. Secondly, some of the calcium-channel blockers (including dihydropyridines) are more selective in the presence of the systemic vasculature, thus reducing systemic vascular resistance. Treatment The best treatment should be the one that seeks to regulate the various factors that maintain hypertension. Non- pharmacological treatment comprises of lifestyle changes such as decrease (or halt) in cigarette and alcohol consumption, and where necessary, weigh reduction with practice of a more active lifestyle. Caffeine intake should be wholly minimized because it increases the pulse rate. As put by Uren & Rutherford (2004), lifestyle interventions can considerably reduce blood pressure by close to 10mmHg among 4-6 people with hypertension. Most often, adoption of pharmacological interventions assists in effectively regulating blood pressure. Based on Supiano’s information, there are six distinct classes of pharmacological medications that actively perform different levels to subsidize blood pressure to norm (Supiano , 2004). It is recommended that the patient in the case study should be treated with one or several of the below listed medications. ACE inhibitors: Function by inhibiting the congregation of angiotensin II, resultantly making the vessels to expand and improve the blood pressure. What follows is that tension in the blood circulation is regulated to normalcy by increasing kidney filtration. The decrease in levels of fluids assists in reducing blood pressure. It is important to note that this kind of medication is taken only when other medications are dysfunctional. Angiotensin-II receptor antagonists: These medications function in an analogous approach to ACE inhibitors. Rather than stopping the generation of angiotensin II, they prevent its action on the involved receptors. This will allow expansion of vessels in bid to improve blood flow and thus reduce blood pressure. Beta-blockers: They work best by blocking the effects of sympathetic nervous system together with hormone epinephrine. This action tends to decrease the cardiac output while the heart relaxes, slowing down the pulse rate. In the process, the blood pressure is lowered. Alpha-blockers: They trigger the vessels to enable them ease and expand. They work well when they are combined with beta-blockers to release a greater effect. Calcium-channel blockers: They function by expanding the arteries and reducing the muscle tension and decreasing the cardiac output. They ensure that there is complete relation of the heart muscle and that the heart pumps more slowly and blood pressure is reduced. Diuretics: They assist in clearing the unnecessary water and sodium through kidneys, a move that decreases the osmotic pressure. They further relax the blood vessels and reduce the strain on them (McPhee, Papadakis & Tierney, 2008). Most importantly, treatment for hypertension is done all through an individual's life and not curable at once. Nevertheless, all the drug classes mentioned above assist in maintaining the blood pressure and keeping it within a normal range. Summary The complexity involved in pathophysiologic mechanisms responsible for high blood pressure is in such a manner that selective antihypertensive treatment is barely possible, and various drugs and lifestyle changes are needed in order to trigger worthwhile change. Hypertension remain a widespread challenge among the elderly and middle-aged, and attempting to control their blood pressure sometimes proves difficult because there are less sophisticated machinery that can allow proper understanding of the underlying causes of essential (primary) hypertension. References Association, B. P. (2009, March 4). High Blood Pressure. Retrieved March 8, 2010, from Patients UK: http://www.patient.co.uk/health/High-Blood-Pressure-(Hypertension).htm Carretero, O. A., & Opari, l. S. (2000, Jan 25). Essential hypertension. Part I: definition and etiology. Circulation, 3(101), 329-335. Dreisbach, A. W., & Sharma, S. (2010, Feb 19). Hypertension and Kidney. Retrieved March 8, 2010, from Emedicine: http://emedicine.medscape.com/article/241381-overview Khabunde, R. E. (2007, January 04). Primary (essential) hypertension. Retrieved March 8, 2010, from Cardiovascular Physiology Concepts: http://www.cvphysiology.com/Blood%20Pressure/BP024.htm McPhee, S. J., Papadakis, M. A., & Tierney, L. M. (2008). Current Medical Diagnosis and Treatment 2008. United States: McGraw-Hill. Oparil, S., & Weber, M. A. (2005). Hypertension: A Companion to Brenner and Rector's The Kidney (2nd ed.). United States: Elsevier. Peralta C.A., Hicks L.S., Chertow G.M., Ayanian J.Z., Vittinghoff E., Lin F., Shlipak M.G. (2005). Control of hypertension in adults with chronic kidney disease in the United States. Hypertension. 45(4) 1119– 1124. Rodriguez-Cruz, E. (2009, Nov 16). Hypertension. Retrieved March 8, 2010, from eMedicine: http://emedicine.medscape.com/article/889877-overview Supiano, M. A. (2001, Dec 2). Hypertension: Classification, Epidemiology, Diagnosis, Evaluation and Treatment. Retrieved March 8, 2010, from Armenian Health Nework: http://www.health.am/hypertension/hypertension/#Pathophysiology Uren, N., & Rutherford, D. (2004, Sept 24). High blood pressure (hypertension). Retrieved March 8, 2010, from Net Doctor: http://www.netdoctor.co.uk/diseases/facts/hypertension.htm Williams, B. (2010, Feb 10). Secondary Hypertension. Retrieved March 8, 2010, from Hypertension: Overview, Causes, Symptoms, Risk factors, Treatment: http://www.health.am/hypertension/secondary-hypertension/ Read More