Reply to classmates’ post. At least 125 words each and 1 scholarly reference within last 5 years for each.

POST 1

Hypokalemia or potassium deficiency develops when the serum potassium concentration decreases to les than 3.5 mEq/L. Potassium is lost from extracellular fluid ECF, the change in the concentration moves potassium from the cell to the ECF. That is why generally, low serum potassium levels indicate a loss of total body potassium. Low levels of potassium include reduced intake of potassium, increased entry of potassium into the cells, and increased losses of body potassium. Dietary deficiencies are rare but it could happen in elderly with lower consumption of protein and inadequate intake of fruits and vegetables. Dietary deficiency due to dietary deficiency could occur in patients with alcoholism or anorexia nervosa. ECF hypokalemia can also happen because of redistribution between the ECF and intracellular fluid. Respiratory alkalosis can make shifts of this kind because the hydrogen moves out of ECF to try to correct the alkalosis which moves the potassium inside the cell. Insulin and folate promote movement of potassium inside the cell, decreasing ECF potassium. Renal loses can promote movement of ICF potassium to ECF. Like in diabetic ketoacidosis where hydrogen ions are increased in the ECF and causes hydrogen ions to go inside the cell in exchange of potassium, but diuresis is happening at the same time. Then potassium is loss in the urine and if you add insulin treatment and hydration the potassium depletion would be more evident. Diarrhea can cause hypokalemia, because we can lose 100 to 200mEq of potassium and several liters of fluid each day. Normally 5 to 10mEq of potassium and 100ml of water in lost in stool each day. Vomiting and continuous nasogastric suction can cause hypokalemia because of the loss of gastric fluid and also because of renal compensation for volume loss and metabolic alkalosis that happens because of sodium, chloride and hydrogen ion losses. The use of diuretics, excessive aldosterone secretion, increase distal tubular flow rate, and low plasma magnesium concertation contrite to renal losses of potassium through urine. To compensate aldosterone is secreted if sodium loss is also severe with can cause secondary hyperaldosteronism which lower potassium even more. Primary hyperaldosteronism also causes potassium wasting. In many renal diseases the kidneys have a reduced ability to keep sodium which causes a diuretic effect and increased distal tubule flow rate which causes potassium depletion. Magnesium depletion with hypokalemia increase distal potassium excretion. Antibiotics that can cause hypokalemia are amphotericin B, gentamicin, and carbenicillin (McCance & Huether, 2018). Alterations in potassium levels can affect cardiac cell conduction that could result in decreased cardiac output and peripheral perfusion presenting as arrhythmias and hypotension which can lead to cardiac and respiratory arrest (Iqbal et al., 2019).

Patient education that could be given is to encourage foods high in potassium like avocados, broccoli, dairy products, dried fruit, cantaloupe, bananas, juices, melon, lean meats, milk, whole grains, and citrus fruits. Also, it is important to teach the patient ways to prevent a decrease in potassium by excessive use of diuretics and laxatives(Henry et al., 2018).

POST 2

Diabetes Insipidus is a disease that results in an imbalance of fluids in the body. When diabetes insipidus occurs, the kidneys are unable to hold on to water thus excreting large amounts of water(urine) leading to electrolyte imbalances i.e. hypernatremia. The anti-diuretic hormone (ADH) helps to regulate the amount of fluid in the body.

ADH is produced by the posterior pituitary and released into the blood supply via the inferior hypophyseal arteries. Subsequently, ADH targets the kidney and binds to V2 receptors on the renal collecting tubule. this leads to a signaling cascade of Gs-adenyl cyclase system activation which increases cyclic 3′,5′-adenosine monophosphate (cAMP), leading to the phosphorylation of preformed AQP2 water channels. The AQP2 channels translocate to the cell membrane and promote water flow by an osmotic gradient from the lumen into the cells of the collecting duct (Radbel, 2020, p. 2).

The excess amount of urine that becomes excreted due to Diabetes Insipidus can lead to dehydration if not treated appropriately. “The serum sodium concentration is strictly controlled by water homeostasis, which is mediated by thirst, antidiuretic hormone (ADH), and the renin-angiotensin-aldosterone system. A disruption in the water balance leads to abnormality in the serum sodium concentration (hyponatremia, with serum sodium <135 milliequivalent) or hypernatremia (serum sodium >145 milliequivalents)” (Zain et al., 2018, para. 2)

Education is very important for patients with DI. People with DI can become dehydrated very easily so it is very important to educate people on the importance of hydration and replacing electrolytes that may be excreted through urine (Radbel, 2020). Patients should also be warned about traveling and be prepared to manage diarrhea and vomiting so as to avoid dehydration (Radbel, 2020, p. 3). People with DI should not travel unless there condition is treated but if they have to should stay away from traveling to hot destinations and to places where medical care may not be available (Radbel, 2020).