The purpose of the experiment was to help us better understand how water, Coke and Gatorade effected the renal system. The goal was to test and see if my hypothesis were correct regarding the urine specific gravity, urine flow rate, and presents of reagents using the Labstix. My hypothesis for this experiment was that the Gatorade drinkers will have the highest urine flow rate and that non-drinkers would have the highest urine specific gravity. Water is hypo-osmotic and coke contains a high amount of sugar making it hyperosmotic relative to plasma. Gatorade consists of large amounts of electrolytes making it iso-osmatic relative to the plasma. Based on these characteristics of the consumed substances, we are able to study the hormonal effects on the average UFR and USG.
The patient in “The Red Hat Hikers” scenario is suffering from hyponatremia. Hyponatremia is defined as a serum sodium level of less than 136mEq/L. Sodium is an electrolyte that is found predominately in the extracellular fluid, and it is the chief regulator of water in the body. Sodium is also important for muscle contraction, nerve impulses, acid-base balance and chemical reactions that occur inside the cell (McCance & Huether, 2014). Normal sodium levels in the body are maintained by the kidneys and the hormone aldosterone. Aldosterone is secreted by the adrenal cortex at the completion of the renin-angiotensin-aldosterone system, and it helps stimulate the proximal tubules of the kidneys to reabsorb sodium and water. The anti-diuretic hormone (ADH) also indirectly affects sodium levels because it regulates water balance in the body (McCance & Huether, 2014).
After drinking water, the control and test subjects had gradual increase of urine flow, reaching a peak then decreasing again, whereas the desmopressin subject had decreased urine flow after taking the hormone, thereafter plateauing. According to the Dunnett’s t test between the urine flow of the subjects, the urine flow of the treatment subjects was significantly different to that of the control.
Consequently, the efferent arteriole, which filters blood away from the glomerulus, is tinier in diameter than the afferent arteriole, which carries blood into each glomerulus. This puts blood under high pressure in the glomerulus; thus it forces tiny molecules and liquid out of the capillary and into the Bowman’s capsule. Soon afterwards, the tiny and liquid molecules cross the epithelium of the Bowman’s capsule, the basement membrane and capillary wall in order to get into the Bowman’s capsule and to arrive in the nephron tubules. The consequence of this is that the filtrate (the tiny and liquid molecules) pass along the remainder of the nephron and helpful substances are reabsorbed along the route. Last of all, “the filtrate flows through the collecting duct and passes out of the kidney along the ureter” as mentioned by (Parson’s, R: p128).
“Diabetes Insipidus (DI) is a disorder of insufficient activity of ADH, leading to polyuria (frequent urination) and polydipsia (frequent drinking)” (Huether & McCance, 2012, P.449). There are two forms, neurogenic or central DI can occur with injury or some drug to posterior pituitary gland interferes with abnormalities in ADH secretion. Second nephrogenic is failure of the renal tubes to concentrate urine in respond to ADH. In DI the individual has difficulty concentrating urine whether partial or total. The lack of ADH allows filtered water to be excreted in the urine instead of reabsorbed. Results in excretion of large volumes of dilute urine, leading to increase plasma osmolality. The disorder triggers excessive urination and thirst and fluid intake. Urine output can range from 1 to 2 liter/day averaging 8 to 12 liter/day with low specific gravity. Loss of fluid output without replacement the individual can rapidly develop dehydration. The individual that is unable to maintain the appropriate water balance hypernatremia and hyperosmolality will occur. Laboratory test a 24hour urine, serum electrolyte and glucose level. Urine
Since the body is unable to use the glucose which is present, the blood sugar levels increase. The kidney will start to filter the glucose into the urine to lower the blood sugar levels. Glucose however also pulls along water and solutes with it into the urine, this event is called osmotic diuresis (Wolfsdorf et al., 2007).
As shown in table 1, No significant changes in plasma sodium, potassium, chloride, bicarbonate, creatinine, and blood urea nitrogen were observed among all the studied groups. Aldo., EPL+Aldo., and Apocynin+Aldo. groups caused no alterations in urine electrolyte parameters. Moreover, all groups did not significantly alter the ratio of plasma sodium to potassium as compared with the sham group (sham = 42.19 + 3.77; Aldo. = 39.62 + 1.87, p = 0.57; EPL+Aldo. = 43.08 + 3.84, p = 0.96; Apocynin+Aldo. = 41.12 + 3.80, p = 0.94). In addition, the ratio of urinary sodium to potassium in Aldo. (0.29 + 0.02, p = 0.94), EPL+Aldo. (0.28 + 0.01, p = 0.99) and Apocynin+Aldo. (0.29 + 0.02, p = 0.89) were comparable to sham group
However, loop diuretics can initiate or further exacerbate thiamin deficiency. This relationship was first described in 1980 when the administration of loop diuretics in rats increased urinary excretion of thiamin after 4 weeks, suggesting that long-term therapy promotes deficiency (Yiu, Itokawa & Kuwai, 1980). The renal excretion of thiamin is directly dependent on urine flow, which is increased with diuretic medication (Wooley, 2009). Further, thiamin is not protein-bound, and is therefore easily filtered at the site of the glomerulus. A particular diuretic called furosemide decreases thiamin uptake by cardiac myocytes A particular diuretic called furosemide not only hyper-excretes thiamin, but it also minimizes thiamin’s entry into heart cells (Dinicolantonio et al., 2013). Therefore, administration of this medication may further affect heart contractility since myocardial cells are deprived of thiamin, preventing the decarboxylation reaction necessary in pyruvate’s conversion to acetyl CoA and slowing energy
The history of Gatorade starts in 1965 when University of Florida’s assistant football coach Dwayne Douglas question Florida’s kidney disease specialist Robert Cade about why the players lost so much weight during practices and games, went to the bathroom so little. Cade then directed Florida’s College of Medicine’s renal and electrolytes division. They soon found out that players sweat so much that they didn’t have enough fluid to urinate. Then the research started. Cade and his colleagues took samples of Ten University of Florida freshmen football players. They had some eye-opening results, the player’s electrolytes were completely out of order, their blood sugar was low and their Blood volume was also low. Electrolytes are salts and minerals that can conduct electrical impulses in the human body. Their solution was water with salt in it to replace the salt they were losing in sweat. They gave them sugar to keep their blood sugar up. The first product of Gatorade was so bad none of the scientist could take it. Then Cade’s wife Mary suggested adding lemon juice. It was then when Gatorade was born. There first flavor was lemon lime quickly followed by orange and grape. Gatorade continued fixing their creation in the beginning of the 1966 season. Gatorade began to be the number one drink on the sideline.