RESULTS
Effect of the interventions on urine volume and pH
The chronic administration of 0.75% (v/v) EG aqueous solution to the rats caused a significant increase in the urine volume (p < 0.001). On the day 30, urine output was 4.75 ± 0.35 ml/day in the control group, and 9 ± 1.21 ml/day in the EG group. HAEP increased further urine output when compared to the EG group during weeks 2nd, 3th and 4th week intervals and to the cystone group during 3th and 4th week intervals (Figure 1).
The effect of HAEP on the urine pH level is presented in Figure 2. The urine pH level in EG group was higher than the control group. On the other hand, cystone and HAEP did not cause significant changes in the urine pH as compared to the control group when they were used along with EG.
Effects of the interventions on the urinary excretion of calcium, phosphate and magnesium
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However, HAEP increased urinary excretion of creatinine at both doses as compared to the EG group and the control. Higher dose of HAEP showed higher effect than cystone (Figure 4). EG increased significantly urinary excretion of uric acid while HAPE and cystone decreased it. Regarding urinary protein excretion, EG increased urine protein excretion while cystone and HAPE decreased urinary protein excretion. The higher dose of HAEP has the higher effect on urinary protein and it was more effective than cystone.
Effects of the interventions on the urinary electrolytes and creatinine clearance
The effects of the interventions on urinary excretion of sodium, chloride and potassium are summarized in Figure 5. EG significantly decreased urinary excretion of potassium, sodium and chloride. Cystone and HAPE counteracted the effect of EG and elevated the excretion of potassium, sodium and chloride as compared to the EG group. Furthermore, EG
Potassium works with sodium to regulate the body’s water balance. The kidneys help to control the blood pressure by controlling the amount of fluid stored in the body. Therefore, the more fluid then the higher the blood pressure is. The kidneys do this by filtering out the blood and extracting any extra fluid, which then is stored in the bladder as urine. This is done very delicately as both sodium and potassium pull the water across the wall of the cells from the bloodstream into a collecting channel that leads to the bladder. When eating to much salt, the amount of sodium in the bloodstream will be imbalanced compared to the amount of potassium and thus reducing the ability of the kidneys remove the extra fluid. Eating more fruit and vegetables, the potassium levels increase and can help restore the chemical imbalance. However, there is a possibility of too much potassium, also known as hyperkalemia, which can lead to other issues like renal failure.
In the creatinine colorimetric assay the absorbance of the yellow creatinine-picric complex, which is formed from the reaction between creatinine and picric acid, is read spectrophotometrically. Using spectrophotometric data one can determine the relationship between creatinine concentration and absorbance by fitting an equation to the creatinine and absorbance data. The equation sets a standard which can be used to determine the concentration of creatinine in solutions, such as blood and urine, which contain creatinine.
When using different methods to measure pH levels there are some tools that can be useful. Some more than others but by putting into action the different methods it may determine which tools will work best and give the best results when testing the pH within a solution. The pH, which stands for the proportion of hydrogen ions in a solution, could be acidic (acidosis), neutral or basic (alkaline). The pH scale goes from numbers 1 through 14. A pH of 7 is neutral;
Introduction: Blood pH is between 7.35 to 7.45. This range is strict, and those who have blood with a pH outside of the range are in danger of illness and death. In order for blood to maintain its pH within a one-tenth range, it uses a bicarbonate buffering system. The buffer resists pH change. Materials and Methods: For this lab, we titrated HCl into Na2CO3 while keeping a pH probe in the solution throughout the process.
There are links between high serum urate, hyperuricemia, and many inflammatory diseases, yet the mechanism is obscure. For humans, purine and ATP are broken down to urate, which builds up in plasma because we lack the enzyme uricase to promote its excretion as allantoin. Urate may benefit our health by acting as an antioxidant that scavenges reactive oxygen species. Yet, hyperuricemia is associated with gout, metabolic syndrome and cardiovascular disease. These inflammatory diseases are characterized by inflammation and oxidative stress. During oxidative stress urate is oxidized to several reactive electrophiles including urate hydroperoxide. This novel oxidant could promote the pro-oxidant effects of urate.
(2012) highlighted a key difference in long term use of monthly GhRH antagonist degarelix (240/80 mg) over LHRH agonist goserelin (3.6mg) in a study that included (n=175) patients completing the trial over 12 weeks. Goserelin treated patients were given bicalutamide (50 mg) in combination on a daily basis for the first 28 days to control hormone flares and related side effects. This study was a randomized parallel-arm, open label, multicenter trial that found the short term efficacy to be the same in both when controlling the total prostate volume (TPV) and relief of lower urinary tract symptoms (LUTS), but more favorable over long term treatment in degarelix patients for LUTS relief. These findings potentially extrapolated the different overall effects on the GnRH receptors in the bladder and prostate with efficacy favoring degarelix in long term
Different treatment plans were assessed, either for nocturia by itself or that occurring in association with BPH. As, BPH is a potential risk factor for nocturia, α blockers are considered a potential treatment for nocturia (11). The α1-blockers are the most common treatment for LUTS/BPH and all currently available α1-blockers have similar efficacy and improve symptoms by approximately 35% and Qmax by 1.8–2.5 mL/s (12, 13). Many studies assessed the effect of α1-blockers, either alone or in combination with 5-α reductase inhibitors on nocturia associated with BPH. Tamsulosin OCAS 0.4 was evaluated in BPH patients with ≥ 2 night voids and was proved to significantly improve the mean IPSS when compared to placebo (14). However, the reduction in nocturnal voids was associated with a minimal difference between tamsulosin and placebo with a mean change of 3.1 to 2.0 night voids for tamsulosin and
The urine sample provided was clear and yellow with no frothing indicating that there was little or no protein in the urine. The sample contained no cells or crystals but did contain a small number of hyaline casts. The lack of cells indicates the filtration membrane is at least partially intact, the casts are not necessarily associated with pathology and are more likely due to exercise or dehydration although can be due to renal failure (Serafini-Cessi, Malagolini and Cavallone 2003). Dehydration and exercise decrease the urine output due to vasoconstriction of the renal arteries, stimulating the release of Tamm-Horsfall protein to help protect against calcium crystallisation and UTIs (Serafini-Cessi, Malagolini and Cavallone 2003).
Hydrochlorothiazide 25mg PO: Antihypertensive, Diuretics. Increases excretion of sodium and water by inhibiting sodium reabsorption in the distal tubule. Lowering BP in hypertensive patients and diuresis with mobilization of edema. Nursing Considerations: Monitor BP, intake, output, and daily weight and assess legs, feet and sacral area for edema. Monitor electrolyte balances to assess hypokalemia.
First, the rate of urea production is just not constant. Urea can be grossly modified by a high protein intake, critical illness (i.e. sepsis, burns, and trauma), gastrointestinal hemorrhage, or drug therapy such as the use of corticosteroids or tetracycline. On the other hand, patients with chronic liver disease and low protein intake can have lower urea levels without noticeable changes in GFR. Second, the rate of renal clearance of urea is not constant. Approximately 40–50% of filtered urea is passively reabsorbed by proximal renal tubular cells. Moreover, in states of decreased effective circulating volume (i.e. volume depletion, low cardiac output), there is certainly enhanced reabsorption of sodium and water in the proximal renal tubular cells along with a corresponding increase in urea reabsorption. As a result, the concentration of serum urea may increase out of proportion with changes in S.Cr and be under representative of
Amiloride is a selective inhibitor of sodium transport in the nephron, which function as interfering with the distal renal tubular and collecting duct in the epithelial sodium channel, in the proximal renal tubular inhibition of sodium-hydrogen and sodium-potassium exchange, resulting in depression of potassium secretion. Amiloride is a potent diuretic drug, excreting sodium without changing serum potassium level, and the excretion can function in the absence of aldosterone, it acts on the distal renal tubules, blocking the sodium-potassium exchange mechanism, to promote sodium and chlorine excretion but still keeping potassium and hydrogen secretion on normal state, promoting a more alkaline urine. Amiloride itself has relative weak sodium
Gastric juice (1ml) was taken in to a 100 ml conical flask, to this 2-3 drops of Topfer's reagent was added and titrated with 0.01 N sodium hydroxide until all traces of red color disappears and the color of the solutions turns yellowish orange (end point). 2. The volume of alkali added was noted. This volume corresponds to free acidity. 3.
Diuretic therapy is important for treatment of patients who require it but to CHF but it can also cause an imbalance in electrolytes. Depletion of magnesium and potassium can lead to cardiac arrhythmias and cardiac arrest. The risk of hypokalemia can be minimized by slow diuresis, lower diuretic dos, potassium supplementation, or combined being used with potassium-sparing diuretics
Haller, C. A., Jacob, P., & Benowitz, N. L. (2002). Pharmacology of ephedra alkaloids and