The ordinary diet is rich in potassium. Therefore, as long as you can eat normally, your body will not be short of potassium. Patients with postoperative digestive tract obstruction, coma and long-term fasting can't eat it. When these patients are given intravenous nutrition, if potassium is not supplemented at the same time or is insufficient, potassium deficiency and hypokalemia can be caused. However, if insufficient intake is the reason, the degree of potassium deficiency in a certain period of time can not be very serious because of the potassium preservation function of the kidney. When potassium intake is insufficient, urinary potassium excretion can be reduced to less than 20mmol/L within 4 ~ 7 days and 5 ~ 10 mmol/L within 7 ~ 10 days (normal urinary potassium excretion is 38 ~ 150 mmol/L).

2. Excessive potassium excretion

⑴ Potassium loss through gastrointestinal tract: This is the most important cause of potassium loss in children, which is common in patients with severe diarrhea and vomiting accompanied by a large amount of digestive juice loss. When diarrhea occurs, the concentration of K+ in feces can reach 30 ~ 50mmol/L, and at this time, the potassium lost with feces is 10 ~ 20 times more than normal. The reason for the increase of potassium content in feces is that diarrhea reduces the absorption of potassium in small intestine, and on the other hand, the decrease of blood volume caused by diarrhea can increase aldosterone secretion. Aldosterone can not only increase urinary potassium excretion, but also strengthen the role of colon in secreting potassium. Because the potassium content in gastric juice is only 5 ~ 10 mmol/L, the loss of gastric juice is not the main cause of potassium loss during severe vomiting, but a large amount of potassium is lost through kidney and urine, because metabolic alkalosis caused by vomiting can increase the potassium excretion of kidney (see later), and the decrease of blood volume caused by vomiting can also promote the potassium excretion of kidney through the increase of secondary aldosterone.

⑵ Potassium loss through kidney: This is the main reason for potassium loss in adults. Common factors leading to increased renal potassium excretion are:

① Long-term continuous use or excessive use of diuretics: such as diuretics (carbonic anhydrase inhibitor acetazolamide) that inhibit the reabsorption of sodium and water in proximal convoluted tubules and diuretics (furosemide, uric acid, thiazides, etc.) that inhibit the reabsorption of Cl- and Na+ in ascending branches of medullary loops. ) can increase the original urine flow to the distal renal tubule, where the increase in flow is an important reason for promoting the increase of potassium secretion in renal tubules. The above diuretics can also increase the amount of Na+ reaching the distal convoluted tubule, and lead to potassium loss by strengthening Na+-K+ exchange. Many diuretics also have the same mechanism of increasing renal potassium excretion: decreased blood volume leads to increased aldosterone secretion. The effects of furosemide, uric acid and thiazide are to inhibit the reabsorption of Cl- by the thick segment of ascending branch of medullary loop, thus inhibiting the reabsorption of Na+. Therefore, long-term use of these drugs can lead to hyponatremia and hypochloremia. It has been proved that hypochloremia caused by any reason can increase the amount of potassium excretion in the kidney. One of the possible mechanisms is that hypochloremia seems to directly stimulate the potassium secretion function of distal renal tubules.

② Some kidney diseases, such as acidosis of distal convoluted tubule, due to the dysfunction of hydrogen secretion of distal convoluted tubule, H+-Na+ exchange decreased and K+-Na+ exchange increased, resulting in potassium loss. In proximal renal tubular acidosis, the reabsorption of HCO3- in proximal convoluted tubule decreases, and the increase of HCO3- in distal convoluted tubule is an important reason for promoting the increase of potassium excretion in distal convoluted tubule (see later). In the polyuria stage of acute renal tubular necrosis, osmotic diuresis caused by the increase of urea in renal tubular fluid and the insufficiency of the function of newborn renal tubular epithelium to reabsorb water and electrolyte can increase the excretion of potassium.

③ Hyperadrenocortical hormone: In primary and secondary aldosteronism, the Na+-K+ exchange between renal distal convoluted tubule and collecting duct increases, thus playing the role of potassium removal and sodium preservation. In Cushing's syndrome, the secretion of glucocorticoid cortisol is greatly increased. Cortisol also has a certain mineralocorticoid-like effect. Long-term increase of cortisol can also promote Na+-K+ exchange between distal convoluted tubule and collecting duct, resulting in increased renal potassium excretion.

④ The number of anions in the distal convoluted tubule that are not easily reabsorbed increases: HCO3-, SO42-, HPO42-, NO3-, β-hydroxybutyric acid, acetoacetic acid and penicillin. When they are increased in the distal convoluted tubule fluid, they cannot be reabsorbed, which increases the negative charge of the original urine, so K+ easily enters the lumen fluid from renal tubular epithelial cells and is lost with urine.

⑤ Magnesium deficiency: Magnesium deficiency often causes hypokalemia. Potassium reabsorption in ascending branch of medulla oblongata loop depends on Na+-K+-ATR enzyme in renal tubular epithelial cells, which requires the activation of Mg2+. When magnesium is deficient, the enzyme may be inactivated due to the loss of Mg2+ in the cell, so the potassium reabsorption in this area is blocked and potassium is lost. Animal experiments have also proved that magnesium deficiency can also cause aldosterone increase, which may also be the cause of potassium loss.

⑥ Alkalosis: During alkalosis, the excretion of H+ in renal tubular epithelial cells is reduced, so the exchange of H+-Na+ is strengthened, so potassium increases with urine excretion.

(3) Transdermal potassium loss: The potassium content in sweat is only 9mmol/L. Under normal circumstances, sweating will not cause hypokalemia. However, excessive sweating will also lead to the loss of potassium when heavy physical labor is carried out in high temperature environment.

3. Extracellular potassium is transferred to the cell.

Hypokalemia can occur when extracellular potassium is transferred to cells, but the total potassium content in the body does not decrease.

⑴ Hypokalemic periodic paralysis: Extracellular potassium shifts to intracellular during the attack, which is a family disease.

⑵ Alkalosis: intracellular H+ moves to extracellular compensation, and extracellular K+ enters the cell.

⑶ Excessive insulin: When high-dose insulin is used to treat diabetic ketoacidosis, hypokalemia has two mechanisms:

① Insulin promotes cell glycogen synthesis, which requires potassium, and plasma potassium enters cells with glucose to synthesize glycogen.

② Insulin may directly stimulate Na+-K+-ATPase on skeletal muscle cell membrane, thus increasing Na+ excretion and K+ entry into muscle cells.

⑷ Barium poisoning: During the War of Resistance against Japanese Aggression period, a large number of "paralysis" cases occurred in a certain place in Sichuan. The main clinical manifestations are muscle weakness and paralysis, and severe cases often die of respiratory muscle paralysis. Through the research of Chinese scholar Du, it is determined that the cause of the disease is barium poisoning. However, the mechanism of paralysis caused by barium poisoning has not been clarified. It has been proved that the mechanism of paralysis caused by barium poisoning is hypokalemia caused by barium poisoning. When barium is poisoned, Na+-K+-ATPase on the cell membrane continues to move. Therefore, potassium in extracellular fluid keeps entering cells. However, the channel of potassium flowing out of cells is particularly blocked, leading to hypokalemia. Barium poisoning is caused by some acid-soluble barium salts, such as barium acetate, barium carbonate, barium chloride, barium hydroxide, barium nitrate and barium sulfide.

4. Raw cotton oil poisoning

In recent twenty or thirty years, a kind of hypokalemic paralysis has appeared in some cotton producing areas in China, which is also called "soft disease" in some provinces. Its main clinical feature is extreme weakness of limbs muscles or flaccid paralysis, and severe cases often die of respiratory muscle paralysis, and the serum potassium concentration is obviously reduced. Many people often get sick in the same place. The etiology is closely related to the consumption of crude cottonseed oil. Raw cotton oil is produced by some small oil factories and factories in rural areas. The production technology of these factories is not up to standard. Cotton seeds are used to extract oil without being fully cooked or even shelled, and the extracted oil is not refined with alkali as required. Therefore, many toxic substances in cottonseed are stored in oil. Gossypol is related to the occurrence of rickets and a series of follow-up studies. The mechanism of hypokalemia in "soft disease" has not been clarified. The discovery of "soft disease" and a series of subsequent studies were carried out by China scholars. So far, there is no record of this disease in foreign books and periodicals.