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.

Cause

Etiology classification

(1) Insufficient intake

Potassium is abundant in food, and potassium deficiency is seen in hunger. Patients with coma, long-term fasting after surgery, digestive tract obstruction, difficulty swallowing esophageal lesions, anorexia nervosa, and partial eclipse.

(2) Excessive discharge

Potassium loss

Vomiting, diarrhea, gastrointestinal drainage, and intestinal epidemics cause a large amount of potassium loss, which is quite common in the clinic. Clinically rare, but can also cause a large number of potassium loss in the digestive tract: 1Verner--Morrison syndrome, also known as non-insulin secreting islet cell tumor, islet non-B cell tumor, intestinal vasoactive peptide tumor and islet vasculature Peptide, the disease is characterized by watery diarrhea, low potassium, gastric acid deficiency, excessive secretion of vasoactive intestinal peptide by tumor cells. 2 villous adenoma, a tumor that occurs in the colon and rectum area, the potassium content of the secreted colon fluid is as high as 100-140mmol / L. The patient lost a lot of potassium due to chronic diarrhea.

2. Excessive potassium loss in the kidney

That is, a large amount of potassium is lost from the urine, which is also the cause of the common hypokalemia in the clinic. Seen in long-term use of potassium-sparing diuretics such as miso-salt, chlorophyll, etc., or a large number of solute diuretics such as mannitol, sorbitol, hypertonic glucose, etc. In kidney disease, it can be seen in acute renal failure, polyuria, renal tubular acidosis and chronic renal insufficiency. In addition, diseases that can cause massive potassium loss in the kidneys are clinically rare, including Liddle syndrome (which is a hereditary renal tubular defect) and Fanconi syndrome (a proximal tubule transport dysfunction that leads to bicarbonate, potassium, sodium, and calcium. Waiting for the absorption barrier).

3. Excessive secretion of the adrenal cortex

Hyperaldosteronism is mainly caused by excessive secretion of salt corticosteroids, while excessive secretion of glucocorticoids such as Cushing syndrome or ectopic ACTH secretion syndrome also causes an increase in urinary potassium excretion, as glucocorticosteroids also have weak salt corticosteroids. active. In addition, trauma, surgery, infection, hypoxia, due to stress stimulation, adrenocortical hormone secretion, can also promote increased urinary potassium excretion.

(3) Abnormal potassium distribution

Refers to the transfer of potassium into cells, seen in alkalosis (alkaline), increased insulin glycogen synthesis, and familial periodic paralysis. Poisoning, cottonseed oil poisoning, etc.

mechanism

Potassium is ubiquitous in various foods. In addition to special conditions such as fasting, it is generally rare for people with hypokalemia due to insufficient intake. The role of the kidney on cations is mainly to preserve sodium and potassium, and the mechanism of potassium preservation in the body is far less perfect than the mechanism of sodium preservation. Generally, when the potassium intake is cut off, the urinary potassium excretion is reduced, but it takes a few days for the urinary potassium to be discharged to the minimum limit, and at the lowest limit, there is still 10-20 mmol of potassium lost every day. Potassium loss is most common in the digestive tract and kidney in clinical disease. Respiratory alkalosis has little effect on serum potassium. Metabolic alkalosis is often accompanied by pathogenic factors such as diuretics, vomiting, and aldosterone. In addition to alkali poisoning, the extracellular fluid H+ concentration decreases, intracellular H+ is released, and K+ in the extracellular fluid enters the cell, and abnormal potassium distribution occurs. In addition, when the alkali poisoning, the renal tubular epithelial cell line H+ decreased, so the exchange of H+ and Na+ decreased and the exchange of Na+ and K+ increased, resulting in an increase in urinary potassium excretion. All of the above are factors that cause hypokalemia during alkalosis.

In hypokalemia, the extracellular fluid is hypokalemia. Therefore, the cations (Na+, K+, H+) inside and outside the cell will be exchanged and redistributed. Three K+s in the cell are transferred out and two Na+ and two H+ metastases in the extracellular fluid are transferred. Entering the cell, the H+ in the extracellular fluid is reduced, and it is easy to produce low-potassium metabolic alkalosis. The increase in K+ in the intracellular fluid and the increase in Na+ will have a significant effect on the activity of the enzyme in the cell. If the liver tissue section is placed in a high-sodium glucose medium, no glycogen production is observed, but in a medium similar to the intracellular fluid with high potassium and magnesium and less sold, glycogen production is exhibited. It is indicated that the balance of electrolytes, especially K+ and Na+, is of great significance for maintaining normal cell function and metabolic activity.

The function of hypokalemia may be characterized by loss of appetite, sparse hair, stagnant development, and progressive muscle spasm. This may be due to the fact that both are low and the ratio of the two remains unchanged. Renal function can be significantly changed in chronic chronic potassium deficiency, and it shows interstitial nephritis, renal tubular damage, and urinary concentrating dysfunction in the kidney.

Deficiency of potassium on myocardial damage and myocardial function disorders can have serious consequences and can lead to a variety of arrhythmias, such as premature beats, ventricular tachycardia, atrioventricular block, and even cardiac arrest. The effect of hypokalemia on myocardial function depends not only on the extent of hypokalemia but, more importantly, on the rate and duration of hypokalemia. In the case of slow onset, potassium deficiency can reach severity and clinical symptoms are not necessarily significant. On the contrary, if the onset of rapid clinical symptoms can occur rapidly and to a serious extent. In addition, potassium deficiency is often accompanied by disturbances of other electrolytes that can affect each other. The symptoms of early potassium deficiency are not obvious, and are often masked by the symptoms of the primary disease.

an examination

Related inspection

Buffer base (BB) Adrenal MRI examination of adrenal cortical imaging glycosylated hemoglobin component (GHb, HbA1c)

(1) medical history

Attention should be paid to the various causes of potassium loss, such as inadequate intake, excessive potassium loss through the gastrointestinal tract or kidney, and various possibilities for abnormal potassium distribution. Should pay attention to the treatment of medication, endocrine disorders and family history.

(2) Physical examination

Patients with mild hypokalemia often have no obvious clinical signs, and may have weakness, weak limbs, weakened or disappeared biliary reflexes, severe respiratory paralysis and cardiac dysfunction, heart rhythm disorders, and enlarged heart.

(3) Laboratory inspection

When clinically suspected hypokalemia, the following tests should be performed to determine the diagnosis.

1. Determination of serum potassium: patients with hypokalemia have serum potassium <3.5 mmol / L. Patients with acidosis or dehydration are deficient in potassium but serum potassium may not be low.

2. Determination of urinary potassium: urinary potassium in patients with non-nephrotic potassium loss <20 mmol / L, and urinary potassium in renal-derived potassium loss >20 mmol / L.

3. Blood pH measurement: The blood pH of patients with simple hypokalemia often increases or is normal. However, renal tubular acidosis, severe diarrhea, diabetic ketotoxicosis and other patients with hypokalemia, blood pH often decreases.

4. Plasma renin activity and aldosterone determination: patients with decreased plasma renin activity and elevated aldosterone should consider primary aldosteronism, both of which should consider secondary aldosteronism, both The decrease is mostly caused by taking licorice extract.

(four) device inspection

Mainly based on ECG examination. In the early stage of hypokalemia, the electrocardiogram showed T flat, followed by U wave and T wave, forming a double peak with U wave. When the potassium was severely low, the T wave was inverted, the U wave was prominent, and the ST segment was decreased. Changes in the ECG tend to appear earlier and more reliably than clinical symptoms. The electrocardiogram changes in patients with hypokalemia mainly depend on the proportion of potassium ion concentration in the intracellular fluid, so the change of acute hypokalemia electrocardiogram is more obvious than chronic hypokalemia. The electrocardiogram changes gradually recovered when serum potassium was restored after hypokalemia treatment. However, it should be noted that changes in the ECG can only be used as evidence for hypokalemia, which can produce similar ECG changes due to elevated blood pH, HCO3, and Na+.

Differential diagnosis

The prominent symptom in the early stage of hypernatremia is thirst. In severe cases, the brain cells are dehydrated and mainly manifest symptoms of the nervous system such as irritability, lethargy, hyperreflexia, increased muscle tone, and later convulsions, convulsions, and coma.

Hyperkalemia: serum potassium is higher than 5.5mmol / L. Muscle weakness can occur in the early stage, severe abdominal reflexes disappear, muscle paralysis, and even respiratory muscles are paralyzed. The early circulatory rate of the circulatory system is slow, severe arrhythmia, and even ventricular fibrillation leads to cardiac arrest.

Calcemia: serum calcium is less than 2.2mmol / L. Increased neuromuscular excitability during hypocalcemia, may occur in hand and foot convulsions, tendons, throat, convulsions, as well as irritability, emotional instability, hallucinations and other mental symptoms. Patients with hypocalcemia can show positive signs of Chvostek and Trousseau, but about one-third of patients can be negative. Hypocalcemia with calcium deficiency in the body can cause bone calcification disorders. Children can develop rickets, hysteresis, skeletal deformities, and can be characterized by osteomalacia, fibrotic osteitis, and osteoporosis.

Hypercalcemia: When serum protein is normal, serum calcium is increased by > 2.75 mmol / L. In addition to the signs of the primary disease, the main signs of hypercalcemia are mood changes, depression, increased reflexes, decreased pain, weakness of the proximal muscles, and gait instability. In addition, attention should be paid to the symptoms of impaired renal function and changes in cardiac function.

Hyponatremia: normal blood sodium is 142 mmol/L (135-145 mmol/L), and blood sodium is lower than 135 mmol/L. Those with mild hyponatremia may have no obvious symptoms, or only fatigue, weakness, anorexia, nausea, and lethargy. In severe cases, there may be unconsciousness, sputum, jet vomiting, convulsions, and coma. Physical examination should pay attention to changes in body weight and skin, such as skin elasticity. Various symptoms of edema or dehydration. If there is a change in heart rate, jugular vein filling and blood pressure, it indicates that there is a disorder of circulatory function, indicating that the condition has progressed to a serious stage.

During the follicular phase of the normal menstrual cycle, the serum testosterone concentration averages 0.43 ng/ml, and the upper limit is 0.68 ng/ml. If it exceeds 0.7 ng/ml (=2.44 nmol/L), it is hyperandrogenemia, also known as high testosterone. Blood. It is a common gynecological endocrine disease. More common are menstrual changes such as menstrual thinning, amenorrhea or dysfunctional uterine bleeding, no ovulation, infertility. Some have masculine changes, such as hairy, enlarged throat, and low pitch. Some obesity, hemorrhoids, breast dysplasia, poor uterine development, ovarian enlargement, a few cases of clitoris hypertrophy.

Phosphorus metabolism disorder caused by lower than normal phosphate concentration in circulating blood. Also known as hypophosphatemia. The table is currently hemolysis, burnout, weakness and convulsions.

Hyperuricemia, also known as gout, is a group of diseases caused by dysbial metabolic disorders. Its clinical features are hyperuricemia and the resulting recurrent attacks of gouty acute arthritis and tophi deposits. Chronic arthritis and joint deformity, often involving the kidney caused by chronic interstitial nephritis and uric acid kidney stones. The disease can be divided into two major categories: primary and secondary. The cause of primary disease is mostly unclear due to a small number of enzyme defects. It is often accompanied by hyperlipidemia, obesity, diabetes, hypertension, arteriosclerosis and crown. Heart disease, etc., is a hereditary disease. Secondary people can be caused by a variety of causes such as kidney disease, blood diseases and drugs.

Systemic atherosclerosis and thrombosis can occur early in patients with homocystinuria and cystathione.

Hyperviscosity (or hyperviscosity) is a clinical pathological syndrome characterized by an increase in blood rheology parameters due to elevated blood viscosity factors, blood transition, and slow blood flow. .

Galactosemia is a toxic clinical metabolic syndrome with increased blood galactose. Most children have lactation, vomiting, nausea, diarrhea, weight loss, hepatomegaly, jaundice, bloating, hypoglycemia, proteinuria, etc., due to galactose in breastfeeding or artificial feeding. The performer should consider the possibility of galactosemia, and the relevant laboratory tests should be carried out. If the measures can be detected and taken in time, cataracts and mental retardation can occur rapidly.

Hypoxemia refers to insufficient oxygen in the blood. The arterial partial pressure of oxygen (pao2) is lower than the normal lower limit of the same age, and the main manifestation is the decrease of blood oxygen partial pressure and blood oxygen saturation. Adult normal arterial oxygen partial pressure (PaO2): 83-108 mmHg. A variety of causes, such as central nervous system disorders, bronchial, pulmonary lesions, etc. caused by ventilation and / or ventilation dysfunction can lead to hypoxia. Due to the degree of hypoxemia, the speed and duration of hypoxia, the impact on the body is also different. Hypoxemia is one of the most common critical illnesses in respiratory diseases and one of the important clinical manifestations of respiratory failure.

Cryoglobulinemia: 1. Purpura is the most common skin condition, such as cold urticaria, Raynaud phenomenon, acral cyanosis and reticular bluish, skin necrosis and ulceration. 2. Arthralgia is a common symptom in patients with mixed cryoglobulinemia. It often occurs in the hands and knee joints. It is polyarticular pain, symmetrical or asymmetrical, and occasionally joint swelling. 3. Renal damage can be manifested as acute and chronic nephritis, but also nephrotic syndrome, renal failure. 4. The nervous system is mainly peripheral neuropathy. Others such as hepatosplenomegaly, severe abdominal pain, pericarditis and generalized lymphadenopathy. 5. Laboratory examination of more than 90% of type I and more than 80% of patients with type II cold blood globulin content > 1mg / ml, more than 80% of patients with type III carotenoidemia is a high blood carotene content Caused by yellowing of skin color. Carotene is a lipid pigment that gives normal skin a yellow color.

Toxemia in pregnancy is a syndrome of ketosis, acidosis, hypoglycemia and liver failure. Most occur in the middle and late pregnancy. The symptoms of the milder are not obvious. In severe cases, the spirit is depressed, the breathing is difficult, the urine volume is severely reduced, and the exhaled gas has a ketone smell. Abortion, ataxia, convulsions and coma can occur before death. Hematological examination showed an increase in non-protein nitrogen, decreased calcium, increased phosphorus, and positive acetone test.

There is no hypoxemia during hypercapnia. Although PaCO2 has a lower pH value, there is only a temporary neurological inhibition in the clinic, which is characterized by slow response or coma.

Hypoproteinemia: mainly manifests malnutrition. The proteins in the blood are mainly plasma proteins and hemoglobin contained in red blood cells. Plasma proteins include plasma albumin, various globulins, fibrinogen and a small amount of binding proteins such as glycoproteins, lipoproteins, etc., in a total amount of 6.5 to 7.8 g%. If the total plasma protein is less than 6.0 g%, it can be diagnosed as hypoproteinemia.

Primary hypergastrinemia: CT cells proliferate due to genetic or chronic inflammation and Helicobacter pylori infection, which in turn increases the secretion of gastrin and absorbs blood into the blood, producing hypergastrinemia.

Endotoxemia is a pathophysiological manifestation caused by bacteria in the blood or bacteria in the lesion releasing a large amount of endotoxin to the blood, or by injecting a large amount of liquid contaminated by endotoxin. Clinical manifestations of chills, chills, hyperthermia, white blood cells and neutrophils increased. There is no restriction on a system that tends to or find multiple systems with migratory inflammation and multiple organ dysfunction. There is often a history of infection before the disease. In particular, those who have a basic disease that seriously affects the body's defense function, and who cannot control fever and other signs of systemic infection with general antibacterial drugs, should consider the possibility of endotoxemia. If there are defects or ecchymoses in the skin and mucous membranes, or complicated with septic shock, the clinical diagnosis of endotoxemia is basically established.

Hypermagnesemia: plasma magnesium is higher than 0.85mmol / L for hypermagnesemia, clinically less common, except for renal failure, most of which are iatrogenic, and related to the use of magnesium-containing drugs. This disease is most common in patients with renal dysfunction who have progressed to uremia. Hypermagnesemia mainly causes neuromuscular synaptic block. The early manifestations of neuromuscular disorders are similar to uremia and are easily overlooked. Hypermagnesemia should be considered in the presence of postural pus and blood pressure, bradycardia, weakening of deep reflexes, disappearance, muscle weakness, muscle paralysis, cardiac blockade, cardiac arrest, lethargy, and coma.

Magnesium deficiency: early magnesium deficiency often has nausea, vomiting, anorexia, and weakness. Abnormal magnesium deficiency often causes neuromuscular and behavioral abnormalities, such as fibrillation, tremor, ataxia, convulsions and rigidity, nystagmus, hyperreflexia, and are easily induced by sound, light, and mechanical stimulation. Patients often have significant painful brachiopods, Trousseau or Chvostek. Sometimes the mental disorder is abnormal and the orientation is lost.

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