Problem description:
The human body needs a lot of trace elements, which will lead to many diseases. For example, iron deficiency can lead to anemia. Zinc deficiency will affect brain development. Calcium deficiency can lead to osteoporosis. Lack of iodine will lead to a great chance of being commonly known as "big neck disease". Does anyone know what diseases can be caused by magnesium and potassium deficiency? How to pay attention to maintenance and treatment?
Analysis:
Magnesium deficiency:
The effect of 1. on nerve-muscle Under normal circumstances, under the influence of depolarization phase of action potential, a large number of vesicles containing acetylcholine move towards axonal membrane. Through effervescence, a large amount of acetylcholine is released into the gap of neuromuscular joints. The release of vesicles is not only affected by the changes of axonal membrane potential, but also related to the concentrations of Ca2+ and Mg2+ in intercellular fluid. The depolarization phase of action potential can lead to the opening of Ca2+ channels on the membrane, and the amount of Ca2+ entering also determines the release amount of vesicles. Mg2+ can competitively enter the axon and counteract Ca2+. In hypomagnesemia, the entry of Ca2+ increases, so the release of acetylcholine also increases. In addition, Mg2+ can also inhibit the sensitivity of acetylcholine receptor on the endplate membrane. In hypomagnesemia, this inhibitory effect is weakened. Therefore, the transmission of excitement at the neuromuscular joint is enhanced. In addition, Mg2+ can also inhibit the stress of nerve fibers and skeletal muscles. In hypomagnesemia, the stress of nerve fiber and skeletal muscle increases, and a series of manifestations of nerve-muscle stress increase can appear in clinic, such as contraction tremor of small bundle muscle fiber, positive Chvostek sign, Trousseau sign, tetany and so on. Mg2+ also inhibits the central nervous system. This inhibition is weakened in hypomagnesemia, so there may be symptoms such as hyperreflexia, overreaction to sound and light, anxiety and excitability. Mg2+ can also inhibit smooth muscle, and the excitement of smooth muscle in hypomagnesemia can lead to vomiting or diarrhea.
2. Effects on metabolism
(1) Hypocalcemia: Moderate and severe hypomagnesemia can often cause hypocalcemia, and its mechanism involves parathyroid dysfunction. It has been found that in hypomagnesemia, the immunoreactive parathyroid hormone (IPTH) in the circulating blood of patients decreases. If magnesium is injected intravenously into the patient, the concentration of IPTH can increase significantly within a few minutes, which indicates that PTH secretion is impaired rather than synthesis. The decrease of blood calcium stimulates PTH secretion through adenylate cyclase bound to parathyroid cell membrane. This enzyme needs to be activated by Mg2+, and at this time, the concentration of Mg2+ in plasma decreases, so it is not easy to activate this enzyme. Therefore, although the blood calcium has been initially reduced, it can not stimulate the parathyroid gland to secrete PTH, and the blood calcium is further reduced, resulting in hypocalcemia.
At this time, the response of PTH target organs such as skeletal system and renal tubular epithelium to PTH is also weakened. This is because PTH must also be mediated by adenylate cyclase to promote the functional activities of target organs. In hypomagnesemia, adenylate cyclase in the target organ can not be activated, so the mobilization of bone calcium and the reabsorption of calcium by renal tubules are hindered, and blood calcium can not be supplemented. This is also an important cause of hypocalcemia.
⑵ Hypokalemia: Hypokalemia often occurs due to magnesium deficiency. Experiments show that limiting magnesium content in rat diet can increase urinary potassium excretion and reduce skeletal muscle content. If only potassium is supplemented without magnesium in time, it is difficult to recover blood potassium. Therefore, low magnesium will make low potassium difficult to correct. Clinically, it can also be seen that in some cases, low magnesium is the cause of persistent refractory low potassium. In these cases, hypokalemia will not be corrected if only potassium is supplemented without magnesium.
3. In vitro perfusion experiments on the heart showed that magnesium can stabilize the bioelectric activity of isolated animal myocardial tissue. Removal of Mg2+ from perfusate can significantly reduce the negative resting potential of myocardial cells, indicating that magnesium deficiency can increase the excitability of myocardium. In addition, magnesium can also block the slow and continuous sodium influx of fast-responding autonomous cells such as Purkinje cells, which is a basis for the automatic depolarization of these cells. In hypomagnesemia, this blocking effect is weakened, and the influx of sodium ions is relatively accelerated, so the automatic depolarization of myocardial rapid response autonomic cells is accelerated and the autonomy is improved. Because the excitability and self-discipline of myocardium increase when magnesium is deficient, arrhythmia is prone to occur.
In addition to the direct effect, magnesium deficiency can also lead to arrhythmia by causing hypokalemia, because hypokalemia can also increase the excitability and autonomy of myocardium, shorten the effective refractory period and prolong the abnormal period.
Arrhythmia may be very serious in hypomagnesemia, and even ventricular fibrillation may occur.
In addition, magnesium deficiency can also cause changes in myocardial morphology and structure. For example, because magnesium is an essential cofactor in many enzyme systems, severe magnesium deficiency can cause metabolic disorder of myocardial cells, lead to myocardial necrosis, and may lead to the destruction of myocardial cell integrity due to excessive potassium deficiency. In animal experiments, myocardial necrosis caused by magnesium deficiency diet may be related to coronary artery spasm caused by hypomagnesemia.
Prevention and control principle
1. Prevent and treat primary diseases, and prevent or eliminate the causes of hypomagnesemia.
2. Magnesium supplementation is a severe hypomagnesemia with symptoms, especially various types of arrhythmia. Magnesium supplementation must be timely. Other therapies are often ineffective for severe arrhythmia caused by magnesium deficiency. Only slow intravenous injection or drip of magnesium salt (usually magnesium sulfate) can be effective. Intravenous magnesium supplementation should be cautious, especially in patients with impaired renal function. In the process of magnesium supplementation, serum magnesium concentration should be determined frequently to prevent magnesium supplementation from turning into hypermagnesemia. Children should also pay special attention to prevent hypotension when injecting magnesium intravenously because magnesium can dilate peripheral arterioles and other blood vessels. For mild hypomagnesemia, magnesium can also be supplemented by intramuscular injection. The dosage of magnesium supplement depends on the degree of magnesium deficiency and the severity of symptoms.
3. Correcting the metabolic disorder of water and other electrolytes includes supplementing water, especially potassium and calcium, because hypomagnesemia is often accompanied by dehydration, hypokalemia and hypocalcemia.
The effects of hypokalemia on the body are as follows:
The main effect of 1. on skeletal muscle is hyperpolarization block. In hypokalemia, the ratio of [K+]i/[K+]e increases, so the negative value of resting potential of muscle cells increases. When the distance between resting potential and threshold potential increases, the excitability of cells decreases, and even can not be excited in severe cases, that is, cells are in hyperpolarization block state. Myasthenia first appeared in clinic. Then there will be flaccid paralysis. This change is most obvious in the muscles of limbs, and respiratory muscle paralysis can occur in severe cases, which is one of the main causes of death in patients with hypokalemia.
2. Effects on the heart
⑴ Influence on excitability: Theoretically, it is speculated that when the extracellular potassium concentration decreases, the intracellular K+ outflow should increase due to the increase of the difference of K+ concentration inside and outside the cell membrane, which will increase the negative resting potential of myocardial cells and lead to hyperpolarization. But in fact, when the serum potassium concentration decreases, especially below 3mmol/L, the negative value of resting potential decreases, which may be due to the decrease of potassium conductance of myocardial cell membrane when the extracellular potassium concentration decreases.
Conductivity) decreased, thus reducing the outflow of intracellular potassium, while alkaline inward sodium current partially depolarized the membrane. The decrease of the negative value of resting potential reduces the distance between resting potential and threshold potential, so the stimulation required to cause excitement is also smaller, so the excitability of myocardium increases. When the extracellular potassium concentration decreases, the inhibition of calcium influx is weakened, so the calcium influx is accelerated, shortening the second phase of repolarization (plateau period) and the effective refractory period of myocardium. The decrease of potassium conductance in myocardial cell membrane leads to the decrease of potassium outflow and the extension of 3-phase repolarization time. In recent years, it has also been observed that the three-phase repolarization time is prolonged from the action potential of myocardial cells recorded at the apex of right ventricle in patients with hypokalemia. The prolongation of phase 3 repolarization time also means the prolongation of myocardial supernormal period. The above changes prolong the time of the whole action potential, so the next zero-phase polarization wave can arrive before the previous repolarization. S-T segment depression reflecting 2-phase repolarization can be seen on ECG. It is equivalent to the depression and broadening of T wave in the third phase of repolarization, and obvious U wave can appear at its end, which is equivalent to the prolongation of Q-T interval of ventricular action potential time.
⑵ Influence on autonomy: After the third phase of repolarization reaches the maximum repolarization potential (-90mV), the outflow of potassium in the cell gradually decreases due to the progressive decrease of the permeability of Ik channel on the membrane, and sodium ions slowly and continuously enter the cell from outside the cell (background current), so the positive charge entering the cell gradually exceeds the positive charge escaping from the cell, and the membrane gradually depolarizes. This is the automatic depolarization of fast response cells. In hypokalemia, the conductance of potassium ions decreases, so after reaching the maximum repolarization potential, the outward flow of potassium ions in cells is slower than normal, while the inward flow of sodium ions is relatively fast. Therefore, the automatic depolarization of these fast-acting autonomous cells is accelerated and their autonomy is improved.
⑶ Effect on conductivity: In hypokalemia, the negative value of myocardial resting potential becomes smaller, and the velocity of sodium inflow slows down in depolarization. Therefore, the rising speed and amplitude of 0-phase membrane potential are slowed down, the spread of excitement is slowed down, and the myocardial conductivity is reduced. The prolongation of P-R interval on ECG indicates that the time required for depolarization wave to conduct from atrium to ventricle is prolonged, and QRS complex is widened, indicating that ventricular conductivity is reduced.