Metabolic hypokalemia

Introduction Potassium in the human body depends on the outside world. The daily intake of potassium from food is about 50-100mmol, and 90% is absorbed by the small intestine. The kidney is the main organ for potassium excretion and potassium balance regulation. The potassium in the glomerular filtrate is completely absorbed in the proximal renal tubules. Later, the distal tubular cells and collecting duct cells secrete excess potassium from the urine. Discharge, so that potassium maintains balance in the body. However, when the body's intake of potassium is insufficient, the kidneys can not significantly reduce potassium excretion, so that potassium remains in the body, so it is easy to cause potassium deficiency. The serum potassium concentration was 3.5-5.5 mmol/L with an average of 4.2 mmol/L. Hypokalemia is usually referred to as serum potassium <3.5 mmol/L.

Cause

1. The reduction of potassium intake is generally rich in potassium in the diet. Therefore, as long as it can eat normally, the body will not be deficient in potassium. Patients with digestive tract obstruction, coma, and fasting after surgery for a long time cannot eat. If these patients are given intravenous nutrition without potassium supplementation or potassium supplementation, it can lead to potassium deficiency and hypokalemia. However, if the lack of intake is the only cause, the degree of potassium deficiency in a certain period of time may not be very serious due to the potassium-sparing function of the kidney. When the potassium intake is insufficient, the urinary potassium excretion can be reduced to less than 20mmol/L within 4 to 7 days, and can be reduced to 5-10mmol/L within 7 to 10 days (normally, the urinary potassium excretion is 38-150mmol). /L).

2. Excessive potassium discharge

(1) Loss of potassium through the gastrointestinal tract: This is the most important cause of potassium loss in children. It is common in patients with severe diarrhea, vomiting and other loss of digestive juice. The concentration of K+ in the feces during diarrhea can reach 30-50 mmol/L. At this time, the potassium lost with the feces can be 10 to 20 times more than normal. The increase in fecal potassium content is due to the reduction of potassium absorption in the small intestine due to diarrhea. On the other hand, the decrease in blood volume due to diarrhea can increase the secretion of aldosterone, and aldosterone can not only increase the discharge of urinary potassium. It can strengthen the role of potassium secretion in the colon. Since 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, and a large amount of potassium is lost through the kidney with urine, because metabolic alkalosis caused by vomiting can cause Increased renal potassium excretion (details later), blood volume reduction caused by vomiting can also promote renal potassium excretion through secondary aldosterone increase.

(2) Loss of potassium through the kidney: This is the most important cause of potassium loss in adults. Common factors that cause increased potassium excretion in the kidney are:

1 long-term continuous use or excessive use of diuretics: for example, a diuretic that inhibits the proximal tubule sodium and water reabsorption (carbonic anhydrase inhibitor acetazolamide), inhibits the thick section of the medullary ascending branch, Cl- and Na+ reabsorption The diuretics (furosemide, diuretic acid, thiazide, etc.) can increase the flow of the original urine to the distal renal tubule, and the increase in the flow rate here is an important reason for promoting the increase of renal tubular potassium secretion. The above diuretic can also increase the amount of Na+ reaching the distal convoluted tubules, thereby enhancing the loss of potassium by the Na+-K+ exchange. Many diuretics also have a common mechanism that causes an increase in renal potassium excretion: an increase in aldosterone production due to a decrease in blood volume. The role of furosemide, diuretic acid, and thiazide is to inhibit the reabsorption of Cl- by the thick segment of the medullary ascending branch and also inhibit the reabsorption of Na+. Therefore, long-term use of these drugs can lead to both hyponatremia and hypochloremia. It has been shown that hypochloremia caused by any cause can increase potassium excretion in the kidney. One of the possible mechanisms is that hypochloremia seems to directly stimulate the potassium secretion of the distal renal tubules.

2 Certain kidney diseases: In the case of distal renal tubular acidosis, due to the hydrogen dysfunction of the distal convoluted tubules, H+-Na+ exchange is reduced and K+-Na+ exchange is increased, resulting in potassium loss. In proximal renal tubular acidosis, the reabsorption of HCO3- in the proximal convoluted tubule is reduced, and the increase in HCO3- reaching the distal convoluted tubule is an important reason for promoting the increase of potassium excretion in the distal convoluted tubule (detailed later). In the polyuria phase of acute tubular necrosis, osmotic diuresis due to increased urea in renal tubule fluid, and the function of reabsorption of water and electrolyte by neonatal tubular epithelium may result in increased potassium excretion.

3 Excessive adrenal cortex hormone: When the original and secondary aldosterone increase, the exchange of Na+-K+ in the renal distal convoluted tubule and collecting tube increases, thus acting as a potassium-sparing sodium. In Cushing syndrome, the secretion of corticosteroid cortisol increased significantly. Cortisol also has a certain mineralocorticoid-like effect. A large number of long-term increases in cortisol can also promote Na+-K+ exchange between the distal convoluted tubules and the collecting duct, resulting in an increase in renal potassium excretion.

4 The number of anions that are not easily reabsorbed in the far-curved tubules is increased: HCO3-, SO42-, HPO42-, NO3-, -hydroxybutyric acid, acetoacetic acid, penicillin, etc. belong to this. When they increase in the distal convoluted tubule fluid, the negative charge of the original urine is increased because it cannot be reabsorbed, so K+ easily enters the luminal fluid from the renal tubular epithelial cells and is lost with the urine.

5 magnesium deficiency: magnesium deficiency often causes hypokalemia. Potassium reabsorption of the ascending sputum depends on the Na+-K+-ATR enzyme in the renal tubular epithelial cells, which in turn requires activation of Mg2+. In the absence of magnesium, the enzyme may be inactivated due to the loss of intracellular Mg2+, and thus potassium reabsorption occurs and potassium is lost. Animal experiments have also shown that magnesium deficiency can also cause an increase in aldosterone, which may also be the cause of potassium loss.

6 alkalosis: In the case of alkalosis, the renal tubular epithelial cells have a decrease in H+, so the H+-Na+ exchange is strengthened, so the potassium is increased with the urine.

(3) Loss of potassium through the skin: sweat contains only 9mmol/L of potassium. Under normal circumstances, sweating does not cause hypokalemia. However, when heavy physical labor is performed in a high temperature environment, a large amount of sweating may also cause loss of potassium.

3. Extracellular potassium transfer to the cells: When extracellular potassium is transferred to the cells, hypokalemia may occur, but the total potassium content in the body is not reduced.

(1) hypokalemic periodic paralysis: extracellular potassium is transferred to the cells during seizures, which is a familial disease.

(2) Alkalosis: Intracellular H+ moves to the outside of the cell to act as a compensatory effect, while extracellular K+ enters the cell.

(3) Excess insulin: When using high-dose insulin to treat diabetic ketoacidosis, there are two mechanisms for hypokalemia:

1 Insulin promotes cell glycogen synthesis, potassium is required for glycogen synthesis, and plasma potassium enters cells with glucose to synthesize glycogen.

2 Insulin may directly stimulate Na+-K+-ATPase on the skeletal muscle cell membrane, so that Na+ excretion in myocytes increases and extracellular K+ enters myocytes.

(4) cockroach poisoning: During the Anti-Japanese War period, a large number of cases of rickets occurred in a certain place in Sichuan. The clinical manifestations were mainly muscle weakness and paralysis, and severe cases often died due to respiratory muscle paralysis. According to research by Chinese scholar Du Gongzhen, the cause of the disease is sputum poisoning. However, the mechanism by which cockroaches caused poisoning has not yet been elucidated. It has been confirmed that the mechanism of sputum poisoning caused by sputum poisoning is that sputum poisoning causes hypokalemia. When the cockroach is poisoned, the Na+-K+-ATPase on the cell membrane continues to move. Therefore, potassium in the extracellular fluid continuously enters the cells. However, the pores from which potassium flows out of the cells are specifically blocked, and hypokalemia occurs. Some of the bismuth salts which are soluble in acid such as cerium acetate, cerium carbonate, cerium chloride, cerium hydroxide, cerium nitrate and strontium sulfide.

4. Crude cotton oil poisoning: In the past two or three decades, a hypokalemia has occurred in some cotton producing areas in China, and it has been called soft disease in some provinces. Its main clinical features are extremely weak muscles or flaccid paralysis of the limbs. In severe cases, death is often caused by respiratory muscle paralysis, and serum potassium concentration is significantly reduced. Many people are often ill in the same area. The cause is closely related to the consumption of crude cottonseed oil.

Crude raw cotton oil is produced in some small oil mills and mills in rural areas. The production processes of these plants are out of specification. Cottonseed is not fully steamed or even used to extract oil, and the extracted oil is not refined according to regulations. Therefore, many toxic substances in cottonseed are stored in the oil. The occurrence of "soft disease" and subsequent series of studies are gossypol. The mechanism of hypokalemia in "soft disease" has not been elucidated. The discovery of "soft disease" and the subsequent series of studies were carried out by Chinese scholars. So far, there are no records of the disease in foreign books.

an examination

Related inspection

Serum potassium (K+, K) electrocardiogram

Mainly based on medical history and clinical manifestations. Serum potassium determination of blood K+ electrocardiogram, more sensitive to reflect hypokalemia, the main manifestations of ECG are prolonged QT interval, ST segment decline, T wave low, widened, biphasic, inverted or U wave Wait.

Differential diagnosis

(a) primary aldosteronism

Clinically, hypertension and hypokalemia are the main manifestations, and periodic paralysis, hand, foot and ankle can occur. Aldosterone was significantly elevated in plasma and urine, and plasma renin and angiotensin activity were decreased. The disease is caused by a large amount of aldosterone secretion due to a tumor or hyperplasia of the adrenal cortical spheroidal zone, which can be diagnosed according to the above characteristics and laboratory examination. However, attention should be paid to the identification of hypokalemia in patients with essential hypertension due to the application of potassium-sparing diuretics or chronic diarrhea. It should also be differentiated from patients with acute hypertension and renal artery stenosis due to secondary aldosteronism combined with hypokalemia.

(B) Cortisol

It is caused by excessive secretion of cortisol for adrenal hyperplasia or tumor. Patients exhibit central obesity, hypertension, purple lines and acne, often accompanied by hypokalemia and metabolic alkalosis. Urine 17-hydroxycorticosteroids increased, plasma cortisol increased, and diurnal secretion rhythm disappeared. Typical diagnosis is not difficult.

(C) 17a-hydroxylase deficiency and 11p-hydroxylase deficiency

17a - Lack of hydroxylase can lead to insufficient synthesis of glucocorticoids (cortisol) and sex hormones, and 11p hydroxylase deficiency only causes cortisol synthesis disorders. Both of them can cause an increase in ACTH compensatory secretion, resulting in excessive synthesis and secretion of deoxycorticosterone (mineral corticosteroid), leading to hypertension and hypokalemia. 17a-hydroxylase deficiency patients have insufficient synthesis of sex hormones, so men and women have secondary sexual development disorders, and 11p-hydroxylase deficiency is accompanied by excessive androgen secretion, so female patients appear masculine, male The patient has precocious puberty and can be identified.

(four) renal tubular acidosis

In addition to type IV, other types of type 3 (type I, type II, type III) have marked hypokalemia, hyperchloremia and metabolic acidosis, while urine is alkaline (urinary pH is above 6). ). Often accompanied by blood sodium, calcium, phosphorus and other reductions, urine routine examinations are often no abnormal findings.

(5) hypokalemia periodic paralysis

There is a family history, often in the diet, alcoholism, sleep after strenuous exercise or wake up in the morning, more men than women. Limbs often start from the lower extremities and are bilaterally symmetrical. Each episode can last for hours or even days. The performance is soft, the key reflection disappears, but it feels normal. The electrocardiogram showed a change in hypokalemia. The disease should be differentiated from primary aldosteronism, which can also have periodic paralysis. Periodic paralysis is not all hypokalemia, but also normal or hyperkalemia patients.

(6) Hereditary diseases

Hereditary diseases characterized by hypokalemia are relatively rare. For example, Bartter syndrome is autosomal recessive, and a large amount of potassium is lost due to defects in potassium transport of renal tubules. In addition to hypokalemia, aldosterone secretion should be differentiated from primary aldosteronism; Fanconi syndrome is also autosomal recessive, which is a functional defect of renal proximal convoluted tubules, and multiple substances are absorbed back. It is characterized by amino acid urine, diabetes, proteinuria, depletion, sodium, calcium, phosphorus, and often accompanied by metabolic acidosis; Liddle syndrome is a hereditary disease, which increases the absorption of the renal distal convoluted tubules, resulting in potassium The discharge increased. In addition to hypokalemia, clinical manifestations include hypertension, metabolic alkalosis, and decreased plasma renin activity. The aldosterone content in blood and urine is significantly reduced.

In addition, some rare tumors can also exhibit hypokalemia, such as nephromas, which are tumors of the paraventricular cells of the renal afferent arterioles. A large amount of renin secretion leads to hypokalemia; islet vaso-intestinal peptide, secreting a large amount of vasopressin (VIP), which can cause severe hypokalemia due to massive watery diarrhea; colon and rectal villus adenoma, its secretory new The liquid contains a lot of potassium, and a large amount of grade liquid can cause hypokalemia.

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