Dehydration Associated with the Use of Diuretics - Research Paper Example

Dehydration Associated with the Use of Diuretics Dehydration Associated with the Use of Diuretics Purpose ment: The purpose of the study is to determine whether teaching African Americans how to monitor diuretic effectiveness will decrease the incidence of dehydration. Hypothesis ACE inhibitors among African Americans appear to be less effectual when administered in low doses when they are recommended as a single medication. Many African Americans have such rigorous hypertension that two or more prescriptions are needed to control their blood pressure. Monitoring the body’s reactions thus becomes vital for hypertensive patients as the intake of diuretics can leave them in a pre-dehydrated state. Significance of the Problem One African-American dies due to high blood pressure on an hourly basis America. This is almost twice as often as their Hispanic and Caucasian counterparts. In spite of having a related African heritage, the citizens of African nationality who live in the West Indies and Africa have lesser rates of hypertension than do African Americans. This means that researches into how diuretics affect African Americans are vital in establishing if the rate of mortality due to hypertension in this ethnic group can be checked. Theory Past researches have indicated that there is a higher incidence of hypertension in African Americans than among Whites. One of the major reasons for this has been given as the higher rate of cardiovascular sicknesses among African Americans. The long list of supposed causes for this frequency suggests that the genuine reasons are still unidentified (Sacks and Campos 2010). Biological disparities in the systems concerned in the environment or blood pressure control, as well as the lifestyle habits of African Americans are viewed as being among the probable causes of high blood pressure. The greater frequency of hypertension in African Americans living in the United States and not Africa seem to indicate that behavioral as well as environmental characteristics can also be considered as reasons for the heightened rates of hypertension among African Americans (Sacks and Campos 2010). They could also imply that there are mechanisms that increase the blood pressure in African Americans that are dormant in the Africans that reside in Africa. Disparities in the individual experiences of the environment between Caucasian and African Americans have also been given as a reason for the difference in the experience of hypertension. Aspects like dietary habits, socioeconomic status, stress, existence of social networks, and health behaviors are also believed to influence the prevalence of hypertension. Among the outcomes of differential nutritional habits, surplus adiposity surfaces as a natural candidate to clarify the higher frequency of hypertension among African Americans, who have a 51% greater incidence of obesity than Caucasians (Sacks and Campos 2010). One theory states that the Africans residing adjacent to the Sahara Desert evolved tremendously proficient systems for the renal re-absorption of sodium. Though this characteristic bestowed on these Africans a survival advantage while living in the extremely harsh climate, it also offered genetic vulnerability to hypertension when such people were began to regularly consume the Western diet that had a lot of salt (Sacks and Campos 2010). In spite of the authenticity of this theory, most researchers have found a bigger incidence of salt-sensitivity among the African American population than among Hispanic and Caucasian Americans matched for gender, age, and blood pressure. For these three ethnicities, salt sensitivity is more common among hypertensives than among those without hypertension. Therefore, a bit of the salt sensitivity may well be the outcome and not the source of the hypertension. In addition, salt sensitivity is twice as common among hypertensive African American citizens as Hispanic or White Americans (Sacks and Campos 2010). Figure 1- statistics on high blood pressure occurrences among American adults (NCHS Data Brief 2010). Figure 2- Assessing the incidence of hypertension among various age groups across different American ethnic groups (NCHS Data Brief 2010). Theoretical Background Problems Aldosterone is the principle mineralocorticoid hormone that is produced by the adrenal cortex. It supports the retention of bicarbonate and sodium, the emission of hydrogen and potassium ions and the secondary preservation of water. Any excessive secretion of this substance can result in plasma volume expansion, hypertension and edema. The connection between aldosterone and rennin takes place in a physiological conduit that controls blood pressure. Renin is an enzyme that is secreted by the kidneys and initiates the production of a protein messenger known as angiotensin. Genetic defects affect enzymes involved in aldosterone metabolism. This leads to an increase in aldosterone, salt and water re-absorption and plasma volume which results in hypertension Aldosterone and renin are facets of a mechanism of physiological feedback that controls cardiac output and blood volume by affecting vascular resistance, particularly where arterial blood pressure is concerned. They are elements of the renin-angiotensin-aldosterone coordination system (RAAS) (Zillich, Garg, Basu, Bakris and Carter, 2006). The enzyme rennin is distributed by the juxtaglomerular structures of the kidneys. It is released in reaction to indicators from the body’s sympathetic nervous system, when the blood volume is low. When angiotensin is activated, it stimulates the adrenal glands to produce the steroid hormone known as aldosterone. When this messenger is distributed in the bloodstream, it stimulates the kidneys to reabsorb water and sodium. Potassium is also released, and this results in an increased blood volume. The major result of increased blood pressure which results from aldosterone and renin working together is improved by this occurrence. Occasionally the sympathetic nervous system also increases the heart rate through the synchronized release of epinephrine. The standardization of renal mineral replacement with hormones such as aldosterone and rennin is a particularly vital step in the regulation of blood pressure. Kidney cells work with the sympathetic nervous system in controlling the pathway. Neurological responses delay the renal emission of water and sodium, while the regional sensors located in the juxtaglomerular apparatus react by secreting even more renin. The maintenance of sodium in the human body does not only take place within the kidneys (Sacks and Campos, 2010). Aldosterone also stops the elimination of sodium through sweat while also stimulating a substitution with potassium ions. Aldosterone and rennin laboratory tests are employed to determine if adequate or surplus quantities of hormone are being secreted (Zillich, Garg, Basu, Bakris and Carter, 2006). These tests also help in identifying the reasons for malfunctions in the control of blood pressure. The consumption of foods that have too much sodium, as well as obesity can put undue strains on this system; as can disorders that compel the adrenal glands to emit too much aldosterone (Teiwes and Toto, 2007). This characteristics cause hypertension or high blood pressure. Some of the prescriptions used to manage this condition actually obstruct aldosterone receptors, thereby causing a reduction in arterial pressure and decreasing the outcomes of the feedback pathway. Arterial hypertension materializes when qualities that change the relationship between total peripheral resistance and blood volume develop. Renovascular hypertension develops when renal artery stenosis results in reduced glomerular pressure and flow in the glomerulus’ afferent arteriole; which then stimulates juxtaglomerular cells to secrete renin (Verdecchia, Reboldi, Angeli, Borgioni, Gattobigio, Filippucci, Norgiolini, Bracco, and Porcellati, 2004). This reaction also instigates increased peripheral resistance and angiotension II-induced vasoconstriction. By using the aldosterone mechanism, it also results in increased blood volume and sodium re-absorption. Catecholamines in adrenal medula tumors and in pheochromocytoma trigger episodic vasoconstriction and therefore induce hypertension. Mutations affect proteins that influence sodium re-absorption, and, therefore, result in the occurrence of salt sensitivity hypertension It is believed that hypertension essentially comes from an interaction of environmental and genetic and factors that influence cardiac output. Blood pressure, some scholars believe, is a constantly circulated variable and hypertension is simply an extreme of this circulation and not a disease (Zillich, Garg, Basu, Bakris and Carter, 2006). Genetic factors obviously have a role in deciding the levels of blood pressure, as has been shown in the past by researches that investigate the occurrence of hypertension in families. Even though single-gene mutations may be the cause of hypertension in rare cases, the variety of hypertension they cause is not likely to be essential hypertension (Turnbull, 2003). It is more probable that essential hypertension is a heterogeneous and polygenic disorder in which the collective effects of polymorphisms or mutations at numerous gene loci affect the blood pressure (McAdams, Maynard, Baer, Gelber, Young, Alonso and Coresh, 2012). The rarer kinds of hypertension are the ones caused by single gene disorders through several mechanisms. The gene defects that cause rarer forms of hypertension are found in enzymes that are a part of aldosterone metabolism. These usually trigger an adaptive increase in the emission of aldosterone, increased salt and finally hypertension (Onusko, 2003). There are also mutations in proteins that have an effect on sodium re-absorption. For instance, epithelial sodium protein mutations result in more sodium re-absorption in the distal tubular which is stimulated by aldosterone and results in a salt-sensitive variety of hypertension known as the Liddle syndrome (Zillich, Garg, Basu, Bakris and Carter, 2006). Hereditary blood pressure variations could also be reliant on the growing effects of allelic characteristics in different genes that influence blood pressure. For instance, the predilection to acquiring essential hypertension has been linked to heterogeneity in the genes encoding qualities of the angiotension-renin system (Krause, Lovibond, Caulfield, McCormack and Williams, 2011). There is a connection between polymorphism and hypertension in both the angiotensin II type I receptor and angiotensinogen locus. Gene variations in the angiotension-renin systems may also be a major factor in the known racial disparities in the regulation of blood pressure. Environmental Factors Environmental factors are believed to contribute to the expression of the genetic determinants where increased pressure is concerned. The environmental role is depicted by the lower prevalence of hypertension among Chinese citizens residing in China as compared to Chinese-Americans living in mainland US. Obesity, stress, physical activity, excessive consumption of salt and smoking have all been named as exogenous aspects that contribute to hypertension. Increase re-absorption of sodium thereby increasing blood volume Filtration is an operation where passive transport is stimulated through the force of blood pressure and flow. This usually takes place all through the whole nephron system. The activity is centered in the Bowman’s capsule and Glomerulous where nitrogenous wastes, water, amino acids, glucose, minerals, vitamins, hormones and bicarbonate ions are all found. The large quantity of plasma that passes the Glomerulous is the outcome of existing high blood pressure present that is present in this organ. Active transport carries the constructive substances that replenish the human body from the kidney tubules and reinstalls them in the body’s capillaries. Figure Three: Kidney Fluid Exchanges. Adapted From Virtual Chembook, by C. Ophardt, 2013, Retrieved from http://www.elmhurst.edu/~chm/vchembook/253fluidkidneys.html In the proximal colvoluted tubule, the process of re-absorption takes place when bicarbonate ions are reabsorbed and the pH is preserved. Amino Acids, Glucose, and Potassium ions are all useful to the body and so are also transported through the bloodstream. Chlorine as well as Sodium ions are also conveyed back into the blood vessels so that a measure of salt regulation can take place. Conversely, elements like toxins and hydrogen ions are actively emitted from the bloodstream and into the tubule. Inside the loop of henle, the downward channel facilitates the re-absorption of water via osmosis while the ascending branch permits the active as well as passive transportation of salts like sodium so that they can be removed from the tubules re-absorbed. The distal convoluted tubule is the place where the concluding modifications are made to the transitory urine that is in held within the tubule systems. Here, highly selective re-absorption occurs; facilitating the small changes to be made particularly between the presence of Sodium and Potassium. The principal mechanism by which the kidneys control blood volume is by changing the secretion of sodium and water into the urine. There are numerous mechanisms by which this control is initiated. For instance, increased blood volume results in the occurrence of more arterial pressure, a greater glomerular filtration rate, and increased renal perfusion. This results in an increase in the renal excretion of sodium and water that is recognized as pressure natriuresis ( Psaty, Lumley, Furberg, Schellenbaum, Pahor, Alderman and Weiss, 2003). In some varieties of renal ailments, the pressure natriuresis connection is changed so that the kidneys preserve more water and sodium at a definite pressure, thus increasing blood volume. The activation of the angiotensin-renin-aldosterone coordination results in increased sodium preservation which also causes less loss of water in urine (Kokubo and Kamide, 2009). Both aldosterone and angiotensin inspire distal tubular sodium re-absorption through different ways and reduce water and sodium loss in kidneys. The activation of the angiotensin-renin-aldosterone system takes place in renal artery stenosis, which is a source of secondary hypertension (Kaplan and Ronald, 2009). The medicines that obstruct the creation of angiotensin II augment water and sodium loss, and thus decrease the blood volume. Hence, any medicine or mechanism that changes the operations of the angiotensin-renin-aldosterone system will have an effect on blood volume (Zannad, 2007). Another critical hormone that features in the process of controlling water balance is vasopressin. This hormone is discharged by the posterior pituitary (August, 2004). One of its functions is to motivate water re-absorption in the kidney’s collecting duct, and in so doing reduces the level of water loss and boosts the blood volume. Adjustments in the blood volume influence arterial pressure by altering the cardiac output. Any incidence of increased blood volume results in more central venous pressure. This then boosts the right ventricular end-diastolic pressure, the right atrial pressure, and the blood volume. This increase in the ventricular preload increases, by the Frank-Starling means, the ventricular stroke volume.  Figure Four: The description of Arterial Pressure. Adapted From Lexic.us, 2013, Retrieved from, http://www.lexic.us/definition-of/arterial_pressure The Problem with a High dosage of diuretics Various medicines are used to contain hypertension. These medicines are usually based on the main causes of the condition. The different medications that are used include beta blockers, diuretics, angiotensin II receptor blockers, ACE inhibitors, and calcium channel blockers. Moreover, physicians normally propose the use of diuretics as the first prescription when dealing with new cases of hypertension. Figure Five: Information about Diuretics. Adapted From Pharmacy, by A. Gbemudu, 2013, Retrieved from http://www.rxlist.com/script/main/art.asp?articlekey=94169&page=3 Diuretics function by reducing plasma volume in the blood as well as vascular resistance within the body. A decrease in extracellular fluid will result in less pressure on the blood vessels. Diuretics are not a distinct drug class but are of three types; each of which have vital roles in the treatment of most hypertensive patients. Diuretic drugs allow the kidneys to excrete more urine and thus promote diuresis. Diuretics attain this by changing how kidneys handle sodium. If a kidney expels more sodium, then the excretion of water will also increase. Most diuretics create diuresis by restraining the re-absorption of sodium at various places in the renal tubular system. Sometimes a mixture of two diuretics is recommended to hypertension patients as the combined effect is better than the synergistic effect of just one compound. This is because a single nephron section can compensate for changed sodium re-absorption at different nephron segment; consequently, obstructing numerous nephron sites considerably improves efficacy. The majority of hypertension patients, most of whom have essential hypertension, can be efficiently contained with diuretics. Anti-hypertensive therapy using diuretics is especially effective when combined with a decreased intake of dietary sodium. The efficiency of these drugs is resultant from their facility to decrease blood volume and cardiac output. When treating patients who suffer from heart failure with diuretics, health workers have to be careful to not unload too much volume as this can negatively affect the cardiac output. The majority of people who experience heart failure are advised to use loop diuretics as they are more efficient in unloading water and sodium than thiazide diuretics. In cases of mild heart failure, a patient may be prescribed a thiazide diuretic. It is generally believed that the obesity epidemic and metabolic syndrome are the consequence of an excessive caloric intake and decreased physical exercise. However, the real causes of hypertension in the metabolic syndrome remains are not well comprehended. Factors like the starting of the renin angiotensin coordination system, greater insulin secretion, obesity, elevated serum uric acid, and the reduced production of nitric oxide in vascular endothelial cells have been suggested as the instigators of hypertension. Some past researches have indicated that the impairment of endothelial nitric oxide production, sodium retention, or the activation of the sympathetic nervous system are contributing factors to the emergence of hypertension. A recent report stated that the increased frequency in mesangial cells of angiotensin II type 1 receptors plays a significant part in the emergence of hypertension in metabolic syndrome. Other researches state that stress reactions with a basic anomaly in the enzyme 11beta-hydroxysteroid dehydrogenase (HSD1), is a causative factor in the development of hypertension. The sharp rise in fructose consumption compares with the increased incidences of metabolic syndrome and the incidence of hypertension in developed nations. Processed foods are usually lacking in potassium. The frequent consumption of potassium is vital in regulating factors that stop hypertension from developing. With the increased intake of salt and fructose in modern diets, it remains to be established if the increased consumption of salt and fructose affects the increase of blood pressure. Hypertension usually causes persistent and abnormal changes in Blood Pressure control systems. High dietary salt intake has long been connected with hypertension. In the Western nations most people consume approximately 10 g/day, and the prevalence of hypertension is greater than in the developing nations. A reduction in the ability of kidneys to expel salt would result water as well as salt retention, greater plasma and extracellular volume, and increased blood pressure (Wing, Reid, Ryan, Beilin, Brown, Jennings, Johnston, McNeil, Macdonald, Marley, Morgan and West, 2003). The kidneys sodium excreting capacity declines steadily with age and slight increases in the intake of salt among aging people can trigger an immediate rise in blood pressure. In addition, the rate of glomerular filtration and the operational capacity of nephrons reduce with age (Chobanian, 2009). In some people, sudden changes in salt ingestion or excretion bring about considerable increases in blood pressure. Such people are identified as being salt sensitive. However, a persons daily variation in urinary salt excretion and dietary salt intake add to the complication of defining salt-sensitivity. Figure Six: The use of diuretics in treating hypertension. Adapted From The ESC Council for Cardiology Practice by R. Ferreira, 2010, Retrieved From http://www.escardio.org/communities/councils/ccp/e-journal/volume8/Pages/Thiazide-diuretics-hypertension-Ferreira.aspx#.US_F1zdG21s Table 1. Diuretics such as Thiazides in hypertension  1. The onset of action occurs after 2 to 3 hours for most thiazides.  2. Most Thiazides have a half-life of 8 to 12 hours, just permiting effective once daily dosing  3. Chlorthalidone has an elimination half-life of 50 t0 60 hours, and is twice as potent as hydrochlorothiazide.  4. Initial decreases in blood pressure are attributed to the reductions in extracellular fluid and plasma volumes. The persistent antihypertensive effects are due to an overall reduction in systemic resistance. Table 2. Diuretics such as Thiazide in hypertension- ADVERSE EFFECTS  1. Hypokalemia 2. Hyperuricemia 3. Dysglycemia. Diabetes 4. Hyponatremia 5. Hypomagnesemia Table 3. Thiazides in hypertension - CHOICE OF ANTIHYPERTENSIVE DRUGS 1. The main benefits of antihypertensive therapy are due to lowering of blood pressure, per se, regardless of how it is obtained. 2. Major antihypertensive drugs classes do not differ significantly for their ability to reduce blood pressure  3. Each drug class has contra-indications as well as favourable effects in specific clinical settings. The choice of drugs should be made according to this evidence. Low-Sodium Dietary Approaches to Stop Hypertension (DASH) Diet A large body of evidence endorses the notion that blood pressure can be affected by many dietary factors (Falkner and Daniels, 2004). Well-established dietetic modifications that result in reduced blood pressure include weight loss, less salt consumption, and moderate alcohol consumption. In recent years, the increased intakes of potassium as well as the consumption of foods detailed in the “DASH diet” have emerged as efficient approaches that contribute towards the lowering of the blood pressure. Recent studies conducted on the efficiency of the “DASH" (Dietary Approaches to Stop Hypertension) diet has discovered that high blood pressure can be lowered by simply assiduously following an eating plan that is quite low in cholesterol, saturated fat, and total fat, while rich in vegetables, fruits, and low fat dairy foods. The DASH food plan is rich in potassium, magnesium, and calcium. It also recommends ample servings of foods that are rich in fiber and protein. Dieters who decide to follow the DASH eating chart can pick a sodium intake of either 1500mg or 2300 mg on a daily basis. The DASH eating plan includes foods such as vegetables, fruits, low-fat dairy foods, nuts, whole-grain products, fish, and poultry. Sweets, cakes, red meats and foods that contain sugars are all discouraged. References August, P. (2004). ‘Overview: mechanisms of hypertension: Cells, hormones, and the kidney.’ Am Soc Nephrol, 15, 1971. Chobanian, A. V. (2009). ‘The Hypertension Paradox - More Uncontrolled Disease despite improved Therapy.’ N Engl J Med, 361, 878-887 Falkner, B., & Daniels, S. R. (2004). ‘Summary of the fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents.’ Hypertension, 44 (4), 387-388. Ferreira, R. (2010). The use of diuretics in treating hypertension, Retrieved from http://www.escardio.org/communities/councils/ccp/e-journal/volume8/Pages/Thiazide-diuretics-hypertension-Ferreira.aspx#.US_F1zdG21s Gbemudu, A. (2013). Information about Diuretics, Retrieved from http://www.rxlist.com/script/main/art.asp?articlekey=94169&page=3 Kaplan, N., & Ronald, V. (2009). Kaplans Clinical Hypertension (Clinical Hypertension (Kaplan). 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