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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, that is, normal blood chloride metabolic acidosis. AG metabolic acidosis, normal class, the patient plasma [Cl-] levels are elevated, that is, high blood chloride metabolic acidosis
Respiratory acidosis is the primary value of PCO2 increased and pH reduced to characteristics of hypercapnia.
Dysfunction due to alveolar ventilation. A. respiratory center is common in depression, such as narcotics overdose; b. respiratory tract obstruction, such as laryngospasm, bronchospasm, respiratory tract burns, foreign bodies, drowning, neck hematoma, or mass compression of the trachea, etc.; c. lung disease, such as shock lung, pulmonary edema, atelectasis, pneumonia, etc.; d. thoracic injuries: such as surgery, trauma, pneumothorax, pleural effusions.
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First, metabolic acidosis
Metabolic acidosis (Metabolic Acidosis) is characterized by a plasma [HCO-] primary reduction.
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etabolic 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 metabolic acidosis (see Figure 6-2). During this period the relationship between the tail section in this chapter is not clearly described.
Figure 6-2 Normal metabolic acidosis and anion gap changes in the type(1) Lactic acidosis: lactic acidosis (Lactic Acidosis) is found in a variety of causes hypoxia, its pathogenesis is to enhance glycolysis during hypoxia, lactate production increases, due to insufficient accumulation of the oxidation process, resulting in blood lactate levels. This acidosis is common. Patients in clinical shock associated with hypoxia, severe anemia, apnea, cardiac arrest, CO poisoning, cyanide poisoning, seizures and too strenuous exercise, the heart as alcohol poisoning respiratory depression, severe liver disease when liver lactate metabolic disorders, diabetes sugar oxidation disorders, leukemia, malignant cells may occur when both glycolysis and strengthening, and so often encountered.
Characteristics of lactic acidosis:
Blood lactate concentration, for example, patients with severe shock, arterial blood lactate levels increased more than 10 times.
Blood [lactate -] / [pyruvate -] ratio increases (normal plasma lactate concentration of approximately 1mmol / L, pyruvate concentration of about 0.1mmol / L, both the ratio of 10:1).
AG increased, blood chloride normal. It belongs to increase the class of AG on behalf of normal blood chlorine thank acidosis. Plasma lactate concentration of such acidosis can often exceed 6mmol / L, the higher up to 12mmol / L. [Lactate -] was not one of determination of negative ions, which increases when the anion gap increased. Such patients also increased pyruvate.
(2) Ketoacidosis: Ketoacidosis (Ketoacidosis) is the body fat lot of use cases, such as diabetes, starvation, pregnancy, a longer reaction time, symptoms of vomiting, alcoholism and vomiting for several days less into the food, is the enhance fatty acid oxidation in the liver, ketone bodies increased and generated more than extrahepatic utilization, resulting in ketonemia. Ketones including acetone, -hydroxybutyric acid, acetoacetic acid, the latter two organic acids, resulting in metabolic acidosis. This acidosis is also a class of normal blood chloride increased AG metabolic acidosis.
Due to insulin deficiency and diabetes patients can be severe ketoacidosis, and even death. Because normal human insulin hormone against lipid solution, so that solutions remain constant. When insulin deficiency, lipolytic hormones such as ACTH, cortisol, glucagon and growth hormone to enhance the role of such a large number of active lipase within the fat cells, so that triglycerides broken down into glycerol and fatty acids in the process of strengthening, a large number of fatty acids into the liver, the liver is a significant increase in ketogenic.
Increased hepatic ketogenesis and carnitine acyltransferase (Acylcarnitine transferase) activity related to the rise. Because the normal enzyme when compared with the inhibition of insulin regulation, lack of time when the islet toxin significantly enhanced this activity. At this time the formation of fatty acids into the liver coenzyme A (Fatty acyl-CoA), the large quantities of this enzyme into the mitochondria, the -oxidation and generates a large number of acetyl coenzyme A, acetyl coenzyme A synthesis of ketone bodies is the basis of material . Under normal circumstances, acetyl coenzyme A catalyzed by citrate synthase and oxaloacetate entering the citric acid cycle citric acid reduced synthesis or acetyl coenzyme A carboxylase by the role of malonyl coenzyme A and generated synthesis of fatty acids, so Synthesis of acetyl coenzyme A is a small amount of ketone bodies, extrahepatic can use. In addition, diabetes increased the fat cells in the liver coenzyme A can inhibit citrate synthase and acetyl coenzyme A carboxylase activity, the acetyl coenzyme A into citric acid cycle pathway poor, but also easily synthesized fatty acids. This allows a large number of acetyl coenzyme a synthesis of ketone bodies reduce the liver.
Non-diabetic patients with ketoacidosis is the lack of glycogen consumption supplement, body fat, then caused a lot of use, such as hunger.2. Paul acid base renal dysfunction row tubular epithelial cells regardless of H + and bicarbonate excretion decreased production of reduced glomerular filtration rate or severe decline, whether acute or chronic renal failure, can cause renal metabolic acidosis poisoning. Since the kidney is the body regulating the ultimate guarantee of acid-base balance, it is more severe acidosis and renal failure, dialysis is forced to take severe measures in the clinical situation.
(1) renal failure: renal failure if renal dysfunction is mainly caused due, then the time of the metabolic acidosis is mainly produced by tubular epithelial cells and the row of H + NH3 decrease. Normal renal tubular epithelial cells from the blood supply of glutamine and amino acids, enzymes and amino acids in the enzyme's catalytic glutamine of continuous generation NH3, NH3 diffusion into the lumen of tubular epithelial cells secrete H + to form NH4, the urinary solution pH value increased, which can continue to secrete H + into the lumen, complete the row of acid process. The original urine Na is continuously exchange NH4 +, HCO3-concomitant with the re-entry of blood into NaHCO3. This is the main row of renal tubular function of acid base security. When the tubular lesions occur causing a serious obstacle to this feature, you can acidosis. Such acidosis due to no major changes in glomerular filtration rate, there is no acid in the anionic filtration barrier due to retention in the body, which is characterized by the normal class of high blood chloride AG metabolic acidosis. That HPO4 =, SO4 = and so there is no retention of anions, so the AG does not increase, while the lack of HCO3-reabsorption by the easy to adjust the other instead of Cl-anion, which increased serum chloride.
Renal failure if the primary glomerular filtration barrier leaving lesions are generally normal when the glomerular filtration rate of less than 20%, the plasma unmeasured anion HPO3 =, SO4 = and some organic acids may be due to retention and increase. At this time the class is characterized by normal blood chloride increased AG metabolic acidosis. HPO4 = filter out the reduction in titratable acid excretion can be reduced, leading to H + retention in the body.(2) carbonic anhydrase inhibitors: such as the use of acetazolamide as a diuretic, because the drug inhibits renal tubular epithelial cells in carbonic anhydrase activity, so that CO2 + H2O H2CO3 H + + HCO3-reaction weakened, H secretion decreased, HCO3- reabsorption decreased, resulting in the normal class of high blood AG acidosis. At this point Na, K, HCO3-from the urine than normal, can play a diuretic effect, medication for a long time to note these types of acidosis.
(3) renal tubular acidosis: renal tubular acidosis (Renal Tubular Acidosis, RTA) is the acidification of the urine of renal dysfunction caused by the normal class of high blood chloride AG metabolic acidosis. Currently divided into four types according to their pathogenesis.Type - distal renal tubular acidosis (Distal RTA). Is a row of distal tubule H + barrier caused. At this point, and distal tubules can not maintain normal tube formation of peritubular fluid with a steep concentration difference of H +. Tubular epithelial cells to form H2CO3 barriers, and H can diffuse back to the lumen peritubular fluid. Renal tubular epithelial cells it may be a series of row H structure, function and metabolism of unusual cause. The etiology of primary, autoimmune, renal calcification, drug toxicity (amphotericin B, toluene, lithium compounds, some of analgesics and anesthetics), pyelonephritis, urinary tract obstruction, renal transplantation, leprosy, genetic disease, cirrhosis of the liver and so on.
Type - proximal renal tubular acidosis (Proximal RTA). The proximal tubule reabsorption of HCO3-caused barriers. At this time a large number of HCO3-in urine excretion, plasma HCO3-reduced. If we artificially HCO3-in plasma of these patients rose to normal levels and maintain it, then to the renal loss of HCO3-ultrafiltration over 15%, which is a big volume. So can cause serious acidosis. When the plasma HCO3-decreased significantly in severe acidosis, the patient will rarely HCO3-in urine, and the use of such methods to be observed where the barriers. The pathogenesis of this type of RTA active transport system may be attributed to lack of energy, mostly the inherited metabolic disorder.
type - that is, - mixed, both distal tubular dysfunction, urinary acidification, but also curved pipe proximal reabsorption of HCO3-in obstacles.
Type - According to current data suggest that the distal curved pipe system due to ion exchange barrier. At this point luminal membrane H through obstacles. Patients with low renin hyperlipidemia low aldosterone, hyperkalemia. K is high, and H competition, decline in the renal excretion NH4, H retention. Common in aldosterone deficiency, aldosterone response to reduced kidney or other, such as type or type some of the causes.
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