Urinary, Fluid, and Acid/Base Balance

Q1. Explain glomerular filtration rate

Glomerular filtration rate (GFR) is understood as a test used in checking how well the kidneys are functioning. The test achieves this by estimating the amount of blood that flows through the glomeruli every minute. Glomeruli act as filters in the kidney as their function is to filter any waste from the blood. The waste and fluid that are not absorbed by the kidney are eliminated from the body as urine. Therefore, the rate at which the kidneys filter blood is known as the glomerular filtration rate (Delanaye, Krzesinski, & Moranne, 2012) . 

The blood that should be filtered enters the glomerulus, which is nested within a cup-shaped sac at the end of each nephron (glomerular capsule). Glomerular capillaries look like sieves because their walls have small pores. The glomerulus is situated between arterioles- incoming arteriole and outgoing arteriole, which deliver and carry away blood, respectively. The function of the two arterioles is to regulate blood pressure in the glomerular by increasing and decreasing in size. The features of the glomerular capillary wall help in determining what and how much should be filtered into the Bowman’s capsule. 

Many equations have been created to help in determining the glomerular filtration rate (GFR). Several laboratories are currently reporting the test automatically, and they shift the responsibility of interpreting the results to the primary care providers. It is, therefore, necessary for healthcare professionals to be trained on how to estimate the GFR value and recognize when the value is not accurate. The results of the test assist health care professionals in determining problems with the kidney. The equation for determining the GFR helps in earlier detection of chronic kidney disease. Early detection of the disease helps in managing the disease before it reaches a level that it will be hard to control (Rule & Turner, 2013) . 

Q2. Explain the renin-angiotensin-aldosterone system (RAAS) and its effect on blood pressure.

Renin-angiotensin-aldosterone system (RAAS) is understood as a hormone system responsible for regulating fluid, blood pressure, and electrolyte balance, including systemic vascular resistance. When the blood pressure goes down, juxtaglomerular cells located in the kidneys change precursor prorenin in the blood into renin, which is secreted into the circulation. On the other hand, plasma renin converts angiotensinogen, excreted by the liver to angiotensin I. Subsequently, the angiotensin-converting enzyme located on the vascular endothelial cells converts angiotensin I to angiotensin II (Giestas & Ramos, 2010) . 

Angiotensin II is considered as a potent vasoconstrictive peptide known for causing the blood vessels to narrow, which leads to increase blood pressure. It is also considered as a stimulant for the secretion of aldosterone, a hormone found in the adrenal cortex. Consequently, aldosterone facilitates the reabsorption of water and sodium by the renal tubules into the blood. At the same time, aldosterone leads to the excretion of potassium in order to keep electrolytes in balance. This increases the amount of extracellular fluid within the body, and it also leads to high blood pressure. The hormone directly impacts the heart, and after a heart attack, the hormone leads to the abnormal heart enlargement and scar tissue development, which may cause heart failure (Giestas & Ramos, 2010) . 

When RAAS is abnormally active, the blood pressure of an individual will be too high. Many drugs can be used to interrupt various steps within the system in order to lower blood pressure. The drugs are the only way that heart failure, kidney failure, high blood pressure, effects of diabetes can be controlled. High blood pressure can be treated by targeting the renin-angiotensin-aldosterone system. Diuretics help in increasing the release of water in the body, thus reducing the amount of blood. Also, the ACE inhibitors prevent the enzyme needed for the development of angiotensin II, which interrupts the signaling pathway (Khatib, Yusuf, & Healey, 2013) . 

Q3. Explain tubular reabsorption along the renal tubule and collecting duct

The fluid that moves out from the Bowman's capsule and glamorous is similar to the blood plasma, which has no proteins. If the filtrate is allowed to flow to the bladder and finally eliminated from your body, it is expected that you will lose over 10-times the total volume of your body fluids each day. With the help of tubular reabsorption mechanisms located in the nephrons of the kidney, water and solutes are returned into the circulatory system. It is considered as reabsorption because the fluids are beings absorbed into the bloodstream for the second time (Tojo & Kinugasa, 2012) . 

The nephrons are designed in a manner they are capable of maintaining body fluid homeostasis. In other words, they help in maintaining the stability of extracellular body fluid and at the same time, maintaining a balance of the minerals and salts significant for the normal functioning of your organs and tissues regardless of how active you are or how much you eat (Peters & Wetzels, 2013) . The different segments of nephrons are responsible for absorbing different substances, as shown in the diagram below.

The nephron’s walls are made of cube-like cells, which are single-layered known as cuboidal epithelial cells. The ultrastructure changes of these cells depend on the segment they are located in and its function. For instance, walls of the cells opposite to the lumen are covered in tiny finger-like structures known as microvilli. The surface is understood as the brush border. The features of the wall of the cells increase the surface area necessary for reabsorption of fluids into the blood. The cells are also densely packed with cell’s energy generators (mitochondria), which provide energy for fueling the transport system leading to efficient reabsorption (Tojo & Kinugasa, 2012) . 

Q4. Explain countercurrent multiplication and its benefits

Concentrated urine production is achieved through osmotic equilibration luminal fluid in the collecting duct with the medullary interstitium. The concentration of urine is made possible by countercurrent multiplication, which occurs in the inner medulla. Within the outer medulla, a single effect is NaCI absorption from the ascending limb. In the outer medulla, the single effect is not established. Countercurrent multiplication often occurs within the loops of Henle located in the kidney, and it is responsible for producing urine in the nephrons. Chloride ions and sodium are pushed from the ascending limb, but water is retained because the limb is impermeable to water. As a result, the concentration gradient is created in the medulla, where the concentration of chloride and sodium is highest. The fluid moving to the distal tubule from the loop of Henle is less concentrated than the liquid entering the loop (Mount, 2014) . 

The steep osmotic gradient within the renal medullary interstitium is critical for the creation of concentrated urine. In addition, the structural organization of the blood vessels and renal tubes within the medulla consists of counterflow systems essential for creating and maintaining a higher osmotic pressure. The kidney manages to produce a high osmotic gradient as the loop hairpin that turns and folds back by itself (Koulouridis & Koulouridis, 2015) . The ascending and descending flows are combined to produce a countercurrent system enabling the flows to interact with each other. The osmotic gradient is achieved through three separate flows. First, active transport pumps Na away from the ascending tubule. Second, water flows out of the descending tubule through osmosis. Finally, as a result of blood pressure, glomerular filtration pushes fluid into the tubule. The figure below shows how the countercurrent multiplication works.

Q5. Compare and contrast respiratory acidosis/alkalosis states

Acidosis and alkalosis are similar in that they both explain the abnormal conditions which occur as a result of pH imbalance of the blood as a result of too much acid or alkali (base). Some diseases or underlying conditions often cause pH imbalance. It is essential to maintain a normal blood PH, which is 7.35-7.45, in order to ensure the metabolic process is functioning correctly, and the right amount of oxygen is delivered to the tissues. Acidosis and alkalosis are different in that acidosis is associated with an excess of acids, which makes the pH to reduce below 7.35, while alkalosis is associated with excess base in the blood, which leads to arise in pH above 7.45 (Adrogué & Madias, 2014) . Various diseases and conditions can interfere with the control of pH in the body leading to blood pH imbalance (Strayer, 2014) . 

An increase or decrease in the amount of carbon dioxide (CO2) in the body alters the pH level of blood. Normal body functions produce excess acid in the body, which must be eliminated or neutralized to keep the pH at the right level. The acid in the body is carbonic acid, and this is because it is formed after the combination of carbon dioxide (CO2) and water. When the body uses fat for energy or when it uses glucose, CO2 is produced (Adrogué & Madias, 2014) . It is the responsibility of the lungs to regulate blood pH. Through the exhalation of CO2, the lungs flush acid out. Therefore, lowering and raising the rate of respiration changes the amount of CO2 breathed out, which can affect the blood pH.

Q6. Compare and contrast metabolic acidosis/alkalosis states

Metabolic acidosis occurs when the balance of bases and acids in the body is thrown off. In this case, the body might be producing too much acid, or it is not getting rid of excess acid, or it may not be having enough base to neutralize the excess acid. The occurrence of any of any of these will affect the processes and reactions in the body. Metabolic acidosis mostly affects people with diabetes as the body does not get enough insulin, and it becomes dehydrated. In this case, the body burns fat as fuel instead of carbohydrates. In addition, metabolic acidosis is caused by less oxygen in the body, which leads to the formation of lactic acid. The symptoms of the condition include headache, breathing fast, feeling tired, loss of appetite, and throw up. Treatment of the condition can be achieved through detoxification, insulin, IV fluids, and sodium bicarbonate (Kraut & Madias, 2010) . 

On the other hand, metabolic alkalosis is associated with the increase in bicarbonate (HCO3−) without an associated increase in Pco2 (carbon dioxide partial pressure), which may alter the body pH. The most common causes of metabolic alkalosis include diuretic use, hypokalemia, and prolonged vomiting. HCO3's renal impairment needs to be available so as to sustain alkalosis. The symptoms of the condition include tetany, lethargy, and headache. Diagnosis is achieved through clinical and serum electrolyte and arterial blood gas measurements. The condition is treated using hydrochloric acid, or IV acetazolamide (Halperin & Kamel, 2012) . 

It is the responsibility of the kidneys to regulate blood pH. The kidneys eliminate acids in the urine, thus regulating bicarbonate (HCO3-, a base) concentration in the blood. A change in Acid-base is as a result of the increase or decrease of HCO3- concentration, which occurs more slowly, unlike changes in CO2. The right pH level can be maintained by drinking a lot of fluid and maintaining a healthy weight (Adrogué & Madias, 2014) . 

  References

Adrogué, H. J., & Madias, N. E. (2014). Respiratory acidosis, respiratory alkalosis, and mixed disorders. SPEC–Comprehensive Clinical Nephrology, 5e eBook (12-Month Access), 169.

Delanaye, P. S., Krzesinski, J. M., & Moranne, O. (2012). Normal reference values for glomerular filtration rate: what do we really know?. Nephrology Dialysis Transplantation, 27(7), 2664-2672.

Giestas, A. P., & Ramos, M. H. (2010). Renin-angiotensin-aldosterone system (RAAS) and its pharmacologic modulation. Acta medica portuguesa, 23(4), 677-88.

Halperin, M. L., & Kamel, K. S. (2012). Metabolic alkalosis. In Nephrology Secrets (pp. 595-604). Mosby.

Khatib, R. J., Yusuf, S., & Healey, J. (2013). Blockade of the renin–angiotensin–aldosterone system (RAAS) for primary prevention of non-valvular atrial fibrillation: a systematic review and meta analysis of randomized controlled trials. International journal of cardiology, 165(1), 17-24.

Koulouridis, E., & Koulouridis, I. (2015). Molecular pathophysiology of Bartter’s and Gitelman’s syndromes. World Journal of Pediatrics, 11(2), 113-125.

Kraut, J. A., & Madias, N. E. (2010). Metabolic acidosis: pathophysiology, diagnosis and management. Nature Reviews Nephrology, 6(5), 274.

Mount, D. B. (2014). Thick ascending limb of the loop of Henle. Clinical Journal of the American Society of Nephrology, 9(11), 1974-1986.

Peters, H. P., & Wetzels, J. F. (2013). Tubular reabsorption and local production of urine hepcidin-25. BMC nephrology, 14(1), 70.

Rule, A. D., & Turner, S. T. (2013). Estimating the glomerular filtration rate from serum creatinine is better than from cystatin C for evaluating risk factors associated with chronic kidney disease. Kidney international, 83(6), 1169-1176.

Strayer, R. (2014). Acid-base disorders. Rosen’s Emergency Medicine. 8th ed. Philadelphia: Mosby, 1604-14.

Tojo, A., & Kinugasa, S. (2012). Mechanisms of glomerular albumin filtration and tubular reabsorption. International journal of nephrology, 2012.