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Association Task Force On Clinical Guidelines

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Discuss About The Association Task Force On Clinical Practice Guidelines.

 

Answer:

Introduction

A body height of 185cm, weight of 95kg and a waist circumference of 100cm is not proportional because his body mass index (BMI) is above the standard recommendation of 18.5-24.9 (Flegal, Kit, Orpana, and Graubard, 2013).

 BMI = weight (kg)/height in metres2

         = 95kg/1.8m2

         = 95/3.24

        = 29.32kg/m2

 

A BMI of 29.32 implies that Brodie is overweight.

An ideal body shape and size for Brodie with a height of 185cm is 65kg, representing a BMI of 19.0kg/m2.

 The increase in weight of Brodie is the cause for his life style complications such as a high blood pressure of 150/95mmHg, high cholesterol levels and upper respiratory infection. A blood pressure of 130/80mmHg is considered high (Roberts and Hedges, 2013). High blood pressure is also as a result of lack of psychology activity, extra salt in the diet, and older age (Whelton et al., 2018). All these characteristics are evident in Brodie.

Increase in body weight cause the blood pressure to increase as well. This is because the increase in weight is associated with increase in total body fat, as a result the capillaries, which are responsible for blood transportation in the entire body, become thin due to fat deposits. As the heart pumps blood, the restrictive nature of the capillaries forces it to increase pumping pressure, hence little amount of blood reaches the heart muscle. This causes high blood pressure in the body (Mamun et al., 2009).

For Brodie to lower his health risks such as high blood pressure and high cholesterol levels, he has to lower his body weight to recommended standard levels. Additionally, Brodie has to adopt a healthy lifestyle. These can be achieved through choosing foods high in fiber such as fruits, vegetables, beans and whole-grain (Rosner, Cook, Daniels, and Falkner, 2013). The patient also needs to prefer whole-wheat to processed starches. Limiting serving size and minimizing the intake of foods with high calorie such as cheeses and higher-fat-meats. Exercise is one of the best way to reduce weight and lower the risk of heart diseases (Chudyk and Petrella, 2011).

Aerobic Respiration

During body exercise, the mitochondria of muscle fibers generates ATP (Adenosine Triphosphate) through the process of aerobic respiration. Aerobic respiration needs oxygen in order to breakdown food energy so as to produce ATP for muscle movements. Large amounts of ATP are produced by during aerobic respiration and is a faster way of producing ATP. For example, 38 ATP molecules can be produced for each glucose molecule that is synthesized. It is the most appropriate method of production of ATP by body cells. Aerobic respiration demands a lot of oxygen for it to take place and it can occur over an extended period of time (Cheuvront, Kenefick, Montain, and Sawka, 2010). The increase in levels of activity raises the breathing rate which causes an increase in the supply of more oxygen for more production of ATP. The process of aerobic respiration takes place in four main stages namely glycolysis, production of acetyl coenzyme, the citric acid cycle, and the chain of electron transport.

 

Anaerobic Respiration

Under intensive exercise, muscle contraction takes place very fast and as a result oxygen cannot travel to the muscles cells quickly enough to keep up with the demands of the muscles for ATP.  During this stage, muscle fibres can shift to a haltering process that doesn’t need oxygen. Energy stores are broken down in the absence of oxygen to produce ATP through anaerobic respiration.

Anaerobic respiration produces only two ATP molecules for each molecule of glucose, thus making it less efficient process compared to aerobic respiration. Nonetheless, anaerobic respiration produces ATP twice faster than aerobic glycolysis. Glycolysis can supply large amounts of ATP that is required during short periods of intensive activity. Anaerobic also requires large amounts of glucose to produce comparatively low amount of ATP. Furthermore, lactic acid is produced in large amounts during glycolysis process. The faster accumulation of lactic acid than it can be eliminated from the muscle causes muscle fatigue. The process of anaerobic respiration can only last for approximately 30 to 60 seconds.  Modern studies have shown that mitochondria found in the muscle fibers have the ability to synthesize lactic acid to generate ATP and that intensive training leads to increased uptake of lactate by the mitochondria to generate ATP.

During inhalation, air is taken into the lungs through the nasal cavity, passing through the trachea, bronchi, bronchioles and then to the alveoli in the lungs through simple diffusion (Gupta, Lin. and Chen, 2010). Here oxygen travel from the alveoli in the lungs, through the capillary walls into the blood. Once the blood has become rich in oxygen and is purified, it travels back to the left atrium through the pulmonary veins and the coronary arteries supply blood to the heart muscle. Contraction of the atrium causes blood to flow from the left atrium to the left ventricle through open mitral valve which closes the moment the ventricle is full, thus preventing backward flow of blood into the atrium. Once the blood is inside the heart, through the simultaneous working of the atria and ventricles through contraction and relaxation, blood is pumped out of the heart in a synchronised and periodic management. The blood then leaves the heart chambers passing through a valve. The four heart valves include mitral valve, aortic valve, pulmonic valve, and tricuspid valve. These valves prevent backward flow of blood. Contraction of the atrium causes blood to flow from the right atrium to the right ventricle through the tricuspid valve which shuts once the ventricle is full and thus preventing back flow of blood into the atrium. Blood leaves the heart through the pulmonic valve after the contraction of the ventricle. Blood leaves the heart through the aortic valve during the contraction of the ventricle. The oxygenated blood then travels to the smaller arteries and lastly to the capillaries. Oxygen diffuses from the alveoli into the red blood cells in the capillaries. The red blood cells contain haemoglobin which combines with oxygen to form oxyhaemoglobin (Triebel,  2012). Then the oxygen molecules move into the blood cells through diffusion (Hendgen-Cotta, Kelm, and Rassaf, 2014). 

Sodium

Sodium is the most common electrolyte in extracellular fluid. The standard content is between 135 and 145 mEq/L. The major function of sodium is in regulating the distribution of water and balance of fluid in the body. Sodium is followed by water, so increased sodium levels in a solution creates high affinity for water. Sodium is also useful in promoting transmission of nerves impulses, balancing intracellular osmolality, enzyme activation, maintaining acid-base equilibrium, and fostering contractility of skeletal, myocardial and smooth muscles. The intestines absorb sodium and kidneys excrete it. The commencement of the increase of sodium levels causes the body to make changes by stimulating a thirst mechanism so that the individual takes more water. The antidiuretic hormone (ADH) influences the levels of sodium. The increase in ADH secretions causes reabsorption of more water in the kidneys and low levels of ADH secretion enables increased excretion of water. The aldosterone hormone also influences the secretion of sodium levels. The increase in the production of aldosterone hormones increases the reabsorption of sodium in the distal tubules in the kidney. The combination of sodium with bicarbonate and chloride ions (Ziomber et al., 2008). Extracellular sodium combines with intracellular potassium to maintain equilibrium in extracellular and intracellular fluids through the sodium-potassium pump.

Sodium levels that are below 135 mEq/L results in a condition called hyponatremia which can be caused by excess water comparative to the amount of sodium or low levels of sodium (Upadhyay, Jaber, and Madias, 2009). A drop in sodium concentration triggers cellular edema which impacts the central nervous system and results to depression and cerebral edema. Low sodium levels of 115 mEq/L or much less, causes twitching and muscle tremors, focal weakness and even death.

High levels of sodium of 145 mEq/L and above causes hypernatremia which is commonly related with a hyperosmolar state characteristic of fluid volume deficit. The rise in extracellular sodium makes the intracellular fluid to move out of the cells into the extracellular spaces which leads to cellular dehydration. This leads to symptoms like muscle weakness and twitching, anxieties, and low levels of consciousness.     

 

Potassium

Potassium is a significant element in intracellular fluid. The recommended standard range for potassium levels in the blood is 3.5 to 5.0 mEq/L. Potassium has a significant function in cellular metabolism, more so in protein and glycogen synthesis and in the processes of enzyme function that is required for cellular energy. It also assists in sustaining cellular electrical neutrality and osmolality. Potassium also plays a role in acid-base equilibrium, nerve impulse conduction, sustenance of normal cardiac rhythm, and contraction of smooth and skeletal muscle (He and MacGregor, 2008).

Potassium has to be synthesized on a daily basis because the body doesn’t have an effective way of storing it. The levels of potassium are monitored by kidney excretion with high amounts of potassium eliminated through sweat and feces. The levels of extracellular potassium is regulated by sodium-potassium levels through the pumping of sodium out of the cells and permitting potassium to enter back into the cells. There is an inverse association between potassium and sodium in the kidneys.  Aldosterone prompts the secretion of potassium and reabsorption of sodium by acting on the distal tubules. The kidneys do not have a mechanism of detecting deficiency in potassium and will therefore continuously excrete potassium even at low levels (Gumz, Rabinowitz, and Wingo, 2015).

A serum potassium level less thatn 3.5 mEq/L leads to hypokalaemia, mostly caused by gastrointestinal loss. Loss of extracellular potassium through diarrhoea, vomiting etc. triggers the body to compensate the loss by shifting potassium from intracellular spaces. Kidney excretion, metabolic alkalosis, and hyperaldosteronism can also result in potassium loss. Potassium levels below 3 mEq/L can cause complications with the cardiovascular and neuromuscular function leading to ineffective respiratory function. Extensive low levels of potassium weaken the ability of the kidney to concentrate urine thus leading to polyuria and a low specific gravity urine. Hypokalemia inhibits the secretion of insulin from the pancreas causing glucose intolerance (Greenlee, Wingo, McDonough, Youn, and Kone, 2009).

Serum potassium levels higher than 5.0 mEq/L leads to hyperkalemia which is mostly associated with kidney failure as a result of ineffective kidney function. Excessive production of potassium can be caused by severe infections, burns, and in painful crush harms.

Calcium

Calcium plays a significant part in the function of all body cells, and is vital in the nervous system. The peripheral nerve is open to extracellular fluid and the central neurones are submersed with calcium, most of which is free. The variations in extracellular calcium have a deep impact on neuron function. A fall in calcium results in a decrease in the threshold for nerve excitation, and may trigger impulsive electrical activity. On the other hand, a rise in calcium results in low excitability 30. These effects are as a result of external calcium binding to the K channels through its ‘gates’ and drags their opening 6. Parallel experiments with zinc show that external extracellular calcium may influence sodium channels by the same direct effect.  The entrance or exit of calcium from the cell is made possible through the cytoplasmic pool, and the changes in the levels of free calcium is important for intracellular signalling and control. An extensively large calcium concentration gradient across the plasma membrane fosters the entry of calcium through on channels. The entrance of calcium into cells has to be disposed of in order for the termination of any signal and restoration of any free calcium levels (Brini, Calì, Ottolini, and Carafoli, 2014).  

Venous return is the flow of blood to the right side of the heart through the vena cava. During rest, almost 70% of total volume blood is contained in the vena cava. This implies that a lot of blood can be returned to the heart depending on the need. The amount of blood flowing back to the heart increased during exercise. However, blood pressure in the veins is at minimum making it difficult to return blood to the heart. Furthermore, the wide lumen of the vein produces low resistance to blood flow. This implies that there is need for an active mechanism to assist in venous return. It is vital to maintain venous return during exercise to make sure that the skeletal muscles are supplied with sufficient oxygen to meet the activity needs. In a restful position, the valves and smooth muscles in the veins are adequate to sustain venous return. This is not the case during exercise. There is high demand of oxygen during exercise and the heart bit is high, thus prompting the vascular system to assist. The maintenance of the venous return requires the help of both skeletal muscle pump and respiratory pump.  This is possible during exercise due to the continuous contraction of the skeletal muscles and increase breathing rate (Magder, 2016).

The respiratory infection of Brodie is likely to affect his oxygenation because the infection affects the lung thus inhibiting sufficient flow of oxygen into the blood. Thus respiratory infection impairs gas exchange. As a result, there will be no effective elimination of carbon dioxide from the blood, whose increase might negatively affect major body organs such as heart.

 


The body has mechanisms to cope with cold such as vasoconstriction and shivering. Cold triggers the human body to exhibit vasoconstriction. This results in the decrease in peripheral blood flow which further lowers convective heat movement between the body trunk and the skin. This increases insulation by the shell of the body (Parsons, 2014). Then the loss of heat from the exposed surface of the body will happen much faster than it is replaced, thus the temperature of the skin and underlying tissues will reduce. In cases of cold exposure of the entire body, the response of vasoconstriction takes place in the peripheral shell and limbs of the whole body. Humans also experience cold-induced thermogenesis which is related to contractile activity of the skeletal muscles.  This thermogenesis in humans is triggered through automatic shivering or by behaviour modification such as increasing physical activity. Shivering comprises of instinctive, repeated, rhythmic muscle contractions that spreads throughout the whole body (Castellani, and Young, 2016).

Coronary heart disease plaques the inner walls of arteries making them more rigid and narrowed. This limits the flow of blood to the heart muscle causing oxygen starvation. The plaque may also make the inner walls of the blood vessels gummy causing other inflammatory cells in the blood to mix with the plaque. An addition of cholesterol to this plaque causes an in increase in the plague which pushes further the artery walls outward and growing inward, constricting the vessels. This can cause a rupture of the plaque leading to a blood clot that may block blood supply to the heart causing heart attack (Gottlieb et al., 2010).  

Severe coronary artery disease decreases the supply of oxygen which is required in large amount during aerobic respiration. Coronary artery disease impairs the arteries restricting blood flow to the heart and as a result increasing levels of carbon dioxide due to inability of the heart to eliminate the gas. This will make the body opt for anaerobic respiration which doesn’t require oxygen. However, this may not last for more than a minute due to the large amount of lactic acid which it produces and whose accumulation is faster than elimination, due to absence of oxygen, causes muscle fatigue.

 

References

Brini, M., Calì, T., Ottolini, D. and Carafoli, E., 2014. Neuronal calcium signaling: function and dysfunction. Cellular and molecular life sciences, accounting, pp.2787-2814.

Castellani, J.W. and Young, A.J., 2016. Human physiological responses to cold exposure: Acute responses and acclimatization to prolonged exposure. Autonomic Neuroscience, 196, pp.63-74.

Cheuvront, S.N., Kenefick, R.W., Montain, S.J. and Sawka, M.N., 2010. Mechanisms of aerobic performance impairment with heat stress and dehydration. Journal of Applied Physiology, 109(6), pp.1989-1995.

Chudyk, A. and Petrella, R.J., 2011. Effects of exercise on cardiovascular risk factors in type 2 diabetes: a meta-analysis. Diabetes care, 34(5), pp.1228-1237.

Flegal, K.M., Kit, B.K., Orpana, H. and Graubard, B.I., 2013. Association of all-cause mortality with overweight and obesity using standard body mass index categories: a systematic review and meta-analysis. Jama, 309(1), pp.71-82.

Gottlieb, D.J., Yenokyan, G., Newman, A.B., O'connor, G.T., Punjabi, N.M., Quan, S.F., Redline, S., Resnick, H.E., Tong, E.K., Diener-West, M. and Shahar, E., 2010. Prospective study of obstructive sleep apnea and incident coronary heart disease and heart failure: the sleep heart health study. Circulation, 122(4), pp.352-360.

Greenlee, M., Wingo, C.S., McDonough, A.A., Youn, J.H. and Kone, B.C., 2009. Narrative review: evolving concepts in potassium homeostasis and hypokalemia. Annals of internal medicine, 150(9), pp.619-625.

Gumz, M.L., Rabinowitz, L. and Wingo, C.S., 2015. An integrated view of potassium homeostasis. New England Journal of Medicine, 373(1), pp.60-72.

Gupta, J.K., Lin, C.H. and Chen, Q., 2010. Characterizing exhaled airflow from breathing and talking. Indoor air, 20(1), pp.31-39.

He, F.J. and MacGregor, G.A., 2008. Beneficial effects of potassium on human health. Physiologia plantarum, 133(4), pp.725-735.

Hendgen-Cotta, U.B., Kelm, M. and Rassaf, T., 2014. Myoglobin functions in the heart. Free Radical Biology and Medicine, 73, pp.252-259.

Magder, S., 2016. Volume and its relationship to cardiac output and venous return. Critical Care, 20(1), p.271.

Mamun, A.A., O'Callaghan, M., Callaway, L., Williams, G., Najman, J. and Lawlor, D.A., 2009. Associations of gestational weight gain with offspring body mass index and blood pressure at 21 years of age: evidence from a birth cohort study. Circulation, 119(13), pp.1720-1727.

Parsons, K., 2014. Human thermal environments: the effects of hot, moderate, and cold environments on human health, comfort, and performance. CRC press.

Roberts, J.R. and Hedges, J.R., 2013. Roberts and Hedges’ Clinical Procedures in Emergency Medicine E-Book. Elsevier Healthcare Sciences.

Rosner, B., Cook, N.R., Daniels, S. and Falkner, B., 2013. Childhood blood pressure trends and risk factors for high blood pressure: the NHANES experience 1988–2008. Hypertension, 62(2), pp.247-254.

Triebel, H., 2012. The structure of functions. Springer Science & Business Media.

Upadhyay, A., Jaber, B.L. and Madias, N.E., 2009, May. Epidemiology of hyponatremia. In Seminars in nephrology(Vol. 29, No. 3, pp. 227-238). WB Saunders.

Whelton, P.K., Carey, R.M., Aronow, W.S., Casey, D.E., Collins, K.J., Himmelfarb, C.D., DePalma, S.M., Gidding, S., Jamerson, K.A., Jones, D.W. and MacLaughlin, E.J., 2018. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology, 71(19), pp.e127-e248.

Ziomber, A., Machnik, A., Dahlmann, A., Dietsch, P., Beck, F.X., Wagner, H., Hilgers, K.F., Luft, F.C., Eckardt, K.U. and Titze, J., 2008. Sodium-, potassium-, chloride-, and bicarbonate-related effects on blood pressure and electrolyte homeostasis in deoxycorticosterone acetate-treated rats. American Journal of Physiology-Renal Physiology, 295(6), pp.F1752-F1763.

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