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(A) etiology
1. High chlorine normal AG metabolic acidosis
(1) Lactic acidosis: Lactic acidosis is a common metabolic acidosis causes, normal lactate dehydrogenase by pyruvate in lactate (LDH) under the action made by the hydrogenation NADH, NADH is changing as NAD, lactic acid can also be under the LDH NAD into NADH when transforms to pyruvate, it was decided the direction of the reaction of pyruvate and lactate mainly as a reaction between the substrate concentration and the ratio of NADH and NAD case, the normal Grape glycolysis can produce NADH, but the resulting mitochondrial NADH can be generated to NAD, also pyruvate dehydrogenase in the pyruvate (PDH) into acetyl-CoA under the action of A, which then converted to CO2 via the citric acid cycle and H2O (Figure 1).Under normal oxidative conditions, lactate can enter the liver or kidney mitochondria within the cell, after
Acidosis: the blood and tissue accumulation of acidic substances, characterized by increased blood hydrogen ion concentration, PH value decreased. First, metabolic acidosis metabolic acidosis (Metabolic Acidosis) is characterized by a plasma [HCO-] primary reduction. Metabolic acidosis can be divided into two categories based on whether to increase AG: AG metabolic acidosis increased class patient plasma [Cl-] levels were normal, which is often referred to the literature of normal blood metabolic acid chloride poisoning. AG metabolic acidosis, normal class, the patient plasma [Cl-] levels are elevated, which is often referred to the literature of high blood chloride II metabolic acidosis, respiratory acidosis respiratory poisoning (Respiratory Acidosis) is characterized by plasma [H2CO3] primary increased. (A) the causes and mechanisms 1. Respiratory center inhibition of central nervous system diseases such as the extension of brain tumors, cerebral extension of polio, encephalitis, meningitis, vertebral artery embolism or thrombosis, intracranial pressure, brain trauma, the respiratory center activity can be inhibited, so that ventilation to reduce the CO2 accumulation. In addition, some drugs such as narcotics, tranquilizers, sedatives (morphine, barbital sodium, etc.) have the role of inhibition of respiration, excessive doses can cause hypoventilation. Carbonic anhydrase inhibitors such as acetazolamide can cause metabolic acidosis mentioned before. It also inhibits carbonic anhydrase in red blood cells leaving CO2 released from red cells in the lung decreased, which led to increased arterial Pco2. The sick and wounded have a tendency to acidosis the drug should be used with caution. 2. Respiratory nerve and muscle dysfunction seen in polio, acute infectious polyneuritis (Guillain-barre syndrome) botulism, myasthenia gravis, hypokalemia, or familial periodic paralysis, spinal cord injury, etc. In severe cases, paralysis of respiratory muscles can be. 3. Thorax thoracic abnormalities of respiratory motion abnormalities are common after spinal, scoliosis, flail chest (Flail Chest), between ankylosing spondylitis (Ankylosing Spondylitis), cardiopulmonary obesity syndrome (Picwick syndrome) and so on. 4. The common airway obstruction foreign body obstruction, laryngeal edema and inhalation of vomit. 5. Diffuse lung disease is respiratory acidosis the most common cause. It includes chronic obstructive pulmonary disease, bronchial asthma, severe interstitial lung disease. These diseases can seriously impede the alveolar ventilation. 6.CO2 inhalation means high concentration of CO2 gas inhalation, such as trenches, tanks and other small space with poor ventilation of the environment. At this point does not reduce alveolar ventilation. First, metabolic alkalosis metabolic alkalosis (Metabolic Alkalosis) is characterized by a plasma [HCO3-] primary increased. (A) the causes and mechanisms 1. Hydrogen ions losing too much (1) loss of gastric juice: is common in high intestinal obstruction pyloric obstruction or vomiting when the direct loss of gastric acid (HCl). Loss of gastric juice may be accompanied by a large number of Cl, K loss and reduction of extracellular fluid volume, these factors also at this time related to the occurrence of low Xie alkalosis. (2) excessive renal row of H: H excessive renal excretion was mainly due to increase in aldosterone secretion caused. Aldosterone can promote distal convoluted tubules and collecting pipe from H and K, and enhance Na reabsorption. H emission increase was due H2COH3 H + HCO3-reaction, HCO3-generated more, and accompanied by the reabsorption of Na also increased, causing metabolic alkalosis, but also associated with hypokalemia. Aldosterone secretion found in the following cases: primary aldosteronism. Cushing syndrome (Cushint's Syndrome congenital adrenal hyperplasia - can be divided into two types, 17 - hydroxylase deficiency type (non-masculine) and 11 - hydroxylase deficiency type (masculine). Bartter syndrome - a hyperplasia is a nearly spherical device is characterized by an increase in renin secretion syndrome. ball device near the tumor, the cells can secrete large amounts of renin, causing high blood pressure and metabolic alkalosis. long-term heavy use of licorice and its preparation, because glycyrrhizic acid (Glycyrrhizic Acid) has mineralocorticoid activity, it can cause similar aldosteronism when metabolic alkalosis. when extracellular fluid volume reduction caused by increased secretion of aldosterone to enhance Na reabsorption and security capacity, can cause metabolic alkalosis. common in furosemide, loop diuretics marrow Lee uric acid in urine loss of time or when a large number of gastric juice. In this case, extracellular fluid is reduced by 1 liter of plasma [HCO3-] increased by about 1.4mmol / L. furosemide and Lee acid addition can reduce the extracellular fluid, its inhibition of renal medullary loop of the ascending branch of the Cl-, Na reabsorption can lead to reach the more remote leaving Na PIPE PIPE row H for remote process to enhance Na It is also related to the occurrence and metabolic alkalosis. trauma and surgical stress response when there is increased secretion of adrenal hormones, often accompanied by metabolic alkalosis. 2. excessive intake of alkaline substances (1) carbonate Hydrogen excessive salt intake: for example, sodium bicarbonate overdose of ulcer patients, and gastric acid in the intestinal NaHCO3 significantly increased after the lead, especially patients with impaired renal function because the kidneys regulate the ability of HCO3-down can lead to alkalosis . In addition, correct acidosis, the input can also cause excessive sodium bicarbonate alkalosis. (2) excessive intake of sodium lactate: by the liver produce HCO3-. is seen to correct acidosis lose excess sodium lactate solution. (3) Excessive intake of sodium citrate: blood transfusion more than when using liquid sodium citrate anticoagulation. per 500 milliliters of blood in sodium citrate 16.8mEq, can be generated by the liver metabolism of HCO3-. so massive blood transfusion (for example, enter 3000 and quickly 4000 ml) can occur in metabolic alkalosis. 3. potassium deficiency caused by a variety of reasons to reduce serum potassium can cause an increase in plasma NaHCO3 and metabolic alkalosis. The mechanism has serum K falls, the renal tubular epithelial cell row K row of H corresponding reduction in the increase in exchange for Na, HCO3-increased. metabolic alkalosis at this time, unlike when the row alkalosis alkaline urine, it ranked acidic urine, known as the anomalous acidity of urine. decreased serum potassium , due to ion exchange, K moved to supplement the extracellular fluid extracellular K, and H is inside the cell to maintain electrical neutrality, thus lead to metabolic alkalosis (when cells are acid poisoning, of course, the cell buffer material can be washed into the cells of the H). 4. lack of chlorine: Cl-is the only easy and tubular Na reabsorption of anions have been, when the original urine [Cl-] is lowered, will strengthen the tubular H, K of the discharge in exchange for Na, HCO3-reabsorption increased, thus generating NaHCO3. Therefore, when the loss of low chlorine hyperlipidemia H, K and NaHCO3 reabsorption had increased, it can lead to metabolic alkalosis. At this point the patient Urine Cl-is decreased. In addition, the aforementioned benefits of furosemide and uric acid can inhibit the medullary thick ascending limb loop segment of the active Cl-reabsorption resulting in lack of Cl-. At this point the remote curved pipe reinforced platoon H, K in exchange Back up the remote control too much song Na. it also can lead to metabolic alkalosis. At this point is the urine of patients with elevated Cl-. vomiting lose HCl, is the loss of Cl-, Cl-in plasma and urine fall through the above Cl-reduced the original mechanism of urine to promote metabolic alkalosis occurs.


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