Summary Of The Red Hat Hikers

Hyponatremia is a common electrolyte imbalance seen by medical professionals. The cause is a disruption of sodium water homeostasis usually maintained by “complex multi-system physiological mechanism” explained Soiza et al (2014).

Together, increased vasopressin and decreased ANP prompts water and sodium retention. Sodium excretion is hindered by a decreased glomerular filtration rate (GFR), caused by lowered glomerular basement membrane permeability, and increased reabsorption of sodium in the distal tubule. In cases of relapse, compensatory efforts cause sodium retention resulting in hypervolemia, decreased COP, and increased GFR. However, as the disease state progresses, GFR decreases again due to glomerular membrane permeability (Vande Walle & Donckerwolcke, 2001). Sodium reabsorption in the distal tubule occurs when Na,K-ATPase pulls sodium at the basolateral membrane, rather than performing ATP hydrolysis. The active pull of sodium at the basolateral membrane also allows for sodium’s passive passage through the apical membrane with the aid of epithelial sodium

The serum sodium levels appear to be higher than normal because the water is shifting from the ECF into the intracellular compartments (ICF).

A study entitled “Determinants of water and sodium intake and output” explained that as plasma volume increased, the same atrial stretch vessels of the heart that caused ANH secretion also contributed to thirst for water in the participants of the study. They concluded that this occurs in order to increase the plasma volume towards a more homeostatic state before the body is completely dehydrated (Stanhewicz and Kenney, 2015). Studying this hormonal effect can give key insight on the many homeostatic mechanisms hormones

antidiuretic hormone (ADH) in the distal convoluted tubules. Therefore, resulted into ANP pathway turning off ADH, renin and aldosterone. At T=30 to T=90, there was increase in urine flow rate for drinking group which increased in plasma volume and blood, decreased in aldosterone concentration and plasma vasopressin (Evans, et al., 2009). Additionally, increment in urine flow rate, Atrial natriuretic peptide (ANP) attributed to the increase in the Glomerular filtration rate (GFR) and glomerular permeability; Atrial natriuretic peptide (ANP) had a direct contribution to the increase of radius and the large glomerular pores (Theilig, Wu. 2015). The Glomerular filtration rate (GFR) rate increased as the surface area of the capillaries increased.

Multiple medical problems, including mixed connective tissue disease with esophageal reflux, Raynaud's, and joint pains, thrombocytopenia, anemia, history of pericarditis, and history of hemoptysis possibly related to previous injury and fibrosis. However, his conditions need to be worked up by hematologist, gastroenterologist, cardiologist, and pulmonologist simultaneously to get a better picture of individual organ disease process ongoing.

Hyperkalemia is a common electrolyte imbalance characterized by elevated serum potassium. Hyperkalemia is defined as serum potassium concentrations greater than 5.5 mmol/L (normal range is 3.5 to 5.0 mmol/L). In the body, ninety-eight percent of potassium is intracellular, and the 2 % left is extracellular which is needed for nerve conduction and muscle contraction. For this reason, extracellular potassium concentration is tightly regulated through renal potassium excretion. Up to 90% of dietary intake of potassium is excreted by the kidney. As kidney function declines, the kidney compensates and aldosterone levels increase in order to boost potassium excretion. However, compensatory mechanisms may become overwhelmed, and result in hyperkalemia (Raymond & Wazny, 2010).

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

Most common electrolyte abnormality is from low or high sodium level in the body. Kidneys maintain the volume and composition of extracellular and intracellular fluid by continuously exchanging water and solutes across their cell membranes. This mechanism occurs with the help of hormone and by body’s feedback mechanism. Antidiuretic hormone produced by hypothalamus and stored in posterior pituitary gland. Osmoreceptor of hypothelamas creates a feedback control system for ADH secretion. Normal osmolality of the body fluid range between 280mOsm/kg to 295mOsm/kg. According to Terpstra (2000), when the osmolality rises to 295 mOsm/kg, osmosis of water occurs which causes the cell to shrink. Osmoreceptor then triggers to secretion of ADH. On the other hand, low osmolality of extracellular fluid such as <280mOsm/kg, can causes cell to swell; swelling cuts the triggering rate of the osmoreceptor cells, therefore slows down the production of ADH. One of the mechanism of ADH is to rise permeability of renal tubules to increase water reabsorption. It occurs by a water channel protein calls aquaporin-2, which permits the tubular luinal membrane to rises water reabsorption by the kidneys. The key factors of SIADH are the result of increased retention of water by kidney because of excessive amount of ADH. Low serum sodium concentration such as hyponatremia and low concentrated serum osmolality such as

The mechanism of hypotonic imbalance is the decrease in serum sodium levels as a result of factors such as diuresis or profuse sweating (Huether & McCance, 2012, p. 103). This results in less extracellular fluid concentration than salt solution (0.9 %), leading the swelling of cells.

The kidneys play an extremely important role in maintenance of potassium. They are responsible for excretion, via feces and sweat. Due to the renin-aldosterone system controlled

The potential cause of hypernatremia and other electrolyte imbalance in patients results from changes in fluid level, either

In the body, sodium and water balance are regulated separately but are closely related. Indeed, changes in serum sodium concentration are often a reflection of an abnormal water balance. Abnormal serum sodium concentration is a common electrolyte disorder encountered in clinical practice with small animals. Though many cases are mild or asymptomatic, hyponatremia and hypernatremia are both clinically important because of the potential for substantial morbidity and mortality. Both conditions should be corrected promptly and early correction may lead to positive outcomes. I will, however, emphasize that chronically abnormal sodium concentration should be carefully corrected, as overly rapid changes of the serum sodium concentration may also result

i. Explain, using water potential terminology, the control of the water content of the blood, with reference to the roles of the kidney, osmoreceptors in the hypothalamus and the posterior pituitary gland

Sodium is the major cation (positively charged ion) which is present in the ECF. The normal range for sodium is 135-145mEq/L. Sodium plays a role in fluid balance, osmotic pressure, muscle contraction and can be regulated by a sodium-potassium pump. When there are deficiencies in sodium (i.e. 145mEq/L) are known as hypernatremia. The kidneys try to counteract this by secreting ADH to retain water. Hyperaldosteronism (increased aldosterone levels which increase sodium reabsorption) can be another cause of hypernatremia. Other causes can include excessive fluid loss, high salt intake and increased kidney reabsorption. Symptoms of hypernatremia include dehydration, fever or coma.