Metabolic acidosis.

metabolicis characterized by a decrease in the primary origin of plasma ( HCO-) .metabolic acidosis can be divided into two categories according to whether AG increase: AG increase metabolic acidosis, the patient plasma level is normal, that is, the normal blood chlorine metabolic acid often mentioned in the literature in the poison. AG normal metabolic acidosis, patient plasma levels increased, that is, the literature often mentions high blood chlorine metabolic acidosis. The relationship between these is clear at the end of this chapter.(i) Causes and mechanisms 1. Excessive acidic substances (1) lactic acidosis: Lactic acidosis (Lactic Acidosis) can be seen in various causes of hypoxia, the pathogenesis is hypoxia when the process of glycation is strengthened, lactic acid production increases, due to insufficient oxidation process and accumulation, resulting in elevated levels of lactic acid. This acidosis is common. Clinically accompanied by hypoxia patient shock, severe anemia, apnea, cardiac arrest, CO poisoning, cyanide poisoning, seizures and excessive exercise, heart respiration inhibition when poisoning, liver-to-lactic acid metabolism disorders in severe liver disease, diabetic patients with sugar oxidation disorders, leukemia may appear malignant cell sugar enzymes and strengthening and so on are often encountered.characteristics of lactic acidosis:of lactic acid in the blood, such as severe shock patients with arterial lactic acid levels increased by more than 10 times.increased the ratio of lactic acid in the blood (normal plasma lactic acid concentration of about 1mmol/L, acetone acid concentration of about 0.1mmol/L, the ratio of the two is 10:1). . AG enlarges and blood chlorine is normal. Therefore belongs to AG increase class normal blood chlorine sex represents thank-you acidosis. The concentration of lactic acid in this acidic plasma can often exceed 6mmol/L, and the highest can reach 12mmol/L. The lactic acid root-) is one of the undetested negative ions, and its increase when the negative ion gap is increased. There was also an increase in acetone acid in this patient. (2) Ketoacidosis: Ketoacidosis is a case of high use of ontology lipids, such as diabetes, hunger, long-term pregnancy reaction with vomiting symptoms, alcohol poisoning vomiting and several days less food, fatty acids in the liver oxidation strengthened, ketone production increased and exceeded the amount of extra-liver use, resulting in ketoemia. Ketones include acetone, β-hydroxybutyric acid, and acetylacetic acid, both of which are organic acids, leading to metabolic acidosis. This acidosis is also AG-like normal blood chlorine metabolic acidosis.who develop diabetes due to insulin deficiency can develop severe ketoacidosis and even die. Because normal time the body's insulin against
the
hormone, so that the finger solution to maintain a constant. When insulin is lacking, the role of lipolytic hormones such as ACTH, cortisol, glucoglycerin and growth hormone is strengthened, a large number of activation of lipase in fat cells, so that triglycerides break down into glycerin and fatty acids process strengthened, fatty acids into the liver, the liver ketones significantly increased.increase in ketogenic ketones in the liver is associated
increased activity
acylcarnitine transferase, a carnitine metastase. Because insulin contrast enzymes have inhibitory regulation under normal conditions, the activity of this enzyme is significantly enhanced when islet toxicity is lacking. At this time into the liver fatty acids to form fatty acyl coenzyme A (Fatty acyl-CoA), under the action of this enzyme into the mitochondrial, through β-oxidation to produce a large number of acetyl coenzyme A, acetyl coenzyme A is the basis of synthetic ketones.
Under normal circumstances, acetyl coenzyme A is catalyzed by citric acid synthase and oxalic acid shrinks into the triacetic acid cycle, or by the role of acetyl coenzyme A pyrethromase to produce propylene coenzyme A and synthesize fatty acids, so the amount of acetyl coenzyme A synthesizing ketones is very small, the liver can be fully used. In addition, the increase in fatty coenzyme A in liver cells in diabetic patients can also inhibit the activity of citric acid synthase and acetyl coenzyme A carbase, so that acetyl coenzyme A into the triacetic acid cycle path is not smooth, but also not easy to synthesize fatty acids. This results in a large number of acetyl coenzyme a liver intracted synthesis of ketones.of non-diabetic patients is a lack of glycogen consumption supplementation, the body and then a large amount of fat caused by hunger.. 2. Renal acidophylactic dysfunction can cause renal metabolic acidosis regardless of the reduction of renal tube epithelyl cell H-plus excrement and bicarbonate production or a serious decrease in renal filtration rate, regardless of acute or chronic renal failure. Because the kidney is the ultimate guarantee of the body's acid-base balance regulation, the acidosis of kidney failure is more serious, and it is also one of the clinical critical conditions that have to take hemodialysis measures. (1) Renal failure: if renal failure is mainly caused by renal tube dysfunction, then metabolic acidosis at this time is mainly due to the small tube epithal cell production NH3 and H-plus reduction. Normal renal tube epithyl cell glutamine and
amino acids
are supplied by the blood, in the glutamine enzyme and amino acidase catalytic action to continuously produce NH3, NH3 dispersion into the tube cavity and renal tube epithyl cell secretion of H-plus binding to form NH4-plus, so that the urine pH increased, which can make H-plus continuous secretion into the tube cavity, complete the process of excrete. The na-plus in the original urine is constantly exchanged by NH4-plus, and with HCO3-along with the re-entry into the blood becomes NaHCO3.
this is the main acid-insulation function of the renal tube. Acidosis can occur when lesions occur in the kidney tubes, which can cause severe impairment of this function. This kind of acidosis due to renal gloculpherine filter function did not change significantly, there is no
alic acid
anions due to filtration disorders in the body retention, which is characterized by AG normal high blood chlorine metabolic acidosis. That is to say, HPO4, SO4, and other anions do not retain, so AG does not increase, and HCO3-re-absorption is insufficient, it is replaced by another easy-to-adjust anion Cl-, so blood chlorine rise.Renal failure if it is mainly glophropathy caused by filtration dysfunction, then generally when the glomary filtration rate is less than 20% of normal, the plasma did not determine anion HPO3, SO4, and some organic acids can be increased due to retention. At this time is characterized by AG increase class normal blood chlorine metabolic acidosis. HPO4-filtering is reduced, which can reduce the discharge of titrated acid, resulting in the retention of H-plus in the body.(2) carbonate enzyme inhibitors: for example, when using acetylamide as diuretic, because the drug inhibits the activity of carbonate enzymes in the epithetular cells of the renal tube, so that CO2-H2O→H2CO3→ At this time, Na, K, HCO3- excreted from the urine higher than normal, can play a diuretic role, long medication time to pay attention to the above-mentioned types of acidosis.(3) Renal tract acidosis: Renal Tubular Acidosis (RENAL Tubular Acidosis, RTA) is AG normal high blood chlorine metabolic acidosis caused by dysfunction of kidney acidified urine. At present, according to its pathogenesis can be divided into four types. type I- far-end renal trachea acidosis (Distal RTA). It is caused by the long-end tube row H-plus barrier. At this time, the remote tube can not form and maintain the normal tube and tube peri-tube fluid H-steep concentration difference. Small tube endocyst cells form H2CO3 disorders, and the tube cavity H-plus can also disperse back to the tube perith fluid. It may be caused by a series of structural, functional, and metabolic abnormality in the epithrine cells of the renal tube. The causes are primary, autoimmune, renal calcification, drug poisoning (sexmycin B, toluene, lithium compounds, certain analgesics and anesthetics), nephritis, urinary obstruction, kidney transplantation, leprosy, genetic diseases, cirrhosis, etc. Type II - Near-end renal tracheal acidosis (Proximal RTA). It is caused by near-end tube re-absorption of HCO3-disorder. At this time there is a large amount of HCO3-discharge in the urine, plasma HCO3-decrease. If we artificially increase the plasma HCO3 in this type of patient to normal levels and maintain it, we can get to 15% of the excess of HCO3-super-
filtration
in the kidneys, which is a large amount. This can lead to severe acidosis. When plasma HCO3 - significantly decreased, acidosis is serious, the patient's urine HCO3 - is very few, the above method can be observed where its obstacles. The pathogenesis of this type of RTA may be due to insufficient energy for active transport, and many hereditary metabolic disorders. III.-I.-II.hybrid type, which has both the functional disorder of the long-end small tube acidifying urine and the obstacle of the near-end crank tube re-absorption of HCO3. IV. type - According to current data, it is believed to be caused by the remote crank tube cation exchange barrier. At this point, the tube cavity membrane has a barrier to the passage of H-plus. Patients have low renin-type low-aldosteroneemia, high blood potassium. When the K-plus is high, competing with H-plus also results in a decrease in renal NH4-plus discharge, and H-plus retention. Commonly caused by aldosterone deficiency, reduced kidney response to aldosterone, or other causes such as type I. or type II. (4) Adrenal cortological dysfuncology (Addison's disease): on the one hand, due to decreased renal blood flow, buffer material filtering is reduced, resulting in less titration acid, on the other hand, due to the reduction of Na-heavy absorption, NH3 and H-plus discharge is also reduced, because there is an exchange relationship between the re-absorption of Na-plus and the discharge of NH3 and H-plus. . 3. The level of HCO3-) in the extra-renal loss intestinal fluid, pancreatic fluid and bile is higher than that in the plasma. Therefore, when diarrhea, intestinal fistula, intestinal decompression attraction, etc. , can be caused by a large number of loss of hCO3-, AG normal high blood chlorine metabolic acidosis. A large amount of HCO3 can also be lost after ureter b colon matching - resulting in this type of acidosis, the structure may be Cl-passive re-absorption and HCO3-mass excretation, that is, Cl-HCO3-exchange caused. . 4. Acid or acidic drugs ingest or import too much ammonium chloride in the liver can break down to produce ammonia and hydrochloric acid, with this sputum agent can cause acidosis. NH4Cl → NH3 plus H.C.-. High blood chlorine metabolic acidosis for AG normal class. The use of calcium chloride for a long time can also lead to such acidosis, the mechanism is that Ca is less absorbed in the intestines, and Cl- and H-plus are accompanied by absorption, the amount of more than Ca, Ca, can be in the intestines with one of the buffer alkali HPO4, so that HPO4-absorption is reduced. Ca plus can also be combined with H2PO4-to produce non-absorbent Ca3 (PO4)2 and H-plus, while H-plus is absorbed with Cl-. Saliolic acid preparations such as aspirin (acetyl saliolic acid) can be quickly broken down into saliolic acid in the body, it is an organic acid that consumes plasma HCO3-, causing AG to increase class normal blood chlorine metabolic acidosis. methanol poisoning due to methanol metabolism in the body to produce formic acid, can cause serious acidosis, some cases reported blood pH can be reduced to 6.8. Misuse of industrial alcohol containing methanol or the use of methanol as an alcohol drinker can cause poisoning. There were a large number of cases of poisoning in China in 1987. In addition to other poisoning hazards of methanol, AG increased normal blood chlorine metabolic acidosis is one of the important causes of death of acute poisoning. This is the reason for the positive effect of NaHCO3 rescue. acidic foods such as
protein
metabolism can eventually form sulphuric acid, ketoic acid, etc. , of course, in normal people there is no problem. But when the kidneys are low, a high-protein diet can lead to metabolic acidosis. This is also AG increased class normal blood chlorine metabolic acidosis. too much amino acid solution or hydrolytic protein solution, it can also cause metabolic acidosis, especially the hydrochloric acid of amino acids, which break down HCl in metabolism. The pH was adjusted to 7.4 when these solutions were prepared, but it remains to be noted that hydrochloric acid can break down hydrochloric acid in metabolism. This is the reason for clinically supplementing patients with a certain amount of NaHCO3. . 5. Diluted acidosis is imported into physiological saline in large quantities, which can dilute HCO3-and increase Cl-in the body, thus causing AG normal high blood chlorine metabolic acidosis. (ii) the body's compensation regulation when metabolic acidosis occurs in the body, the aforementioned set of regulatory mechanisms will play the role of compensation regulation. If the pH value can be maintained in the normal range is called compensation metabolic acidosis, pH lower than the normal lower limit is non-compensation metabolic acidosis. . 1. Extracellular fluid buffer acidosis when the extracellular fluid is raised, immediately causing a buffer chemical reaction. Taking HCO3- the largest number of buffer bases as an example, the reaction is as follows: H-HCO3-→H2CO3→H2O-CO2-CO2 is discharged by breathing strengthening, HCO3-reduced. . 2. When the respiratory compensation is raised, it stimulates the chemical receptors of the cerebral respiratory center, the cervical artery and the aortic body, causing the breathing to deepen and accelerate, the albacle intake increases, and more CO2 is emitted. . 3. Extracellular ion exchange H-plus enters the cell, and K-plus goes out of the cell. The H-ions are buffered in cells in combination with the buffer substances Pr-, HPO4, Hb-, etc. H-plus can also be buffered by the exchange of cations in the bone. . 4. Kidney compensation metabolic acidosis is not caused by kidney dysfunction, can be compensated by the kidneys. All three forms of renal acid excretation are strengthened. (1) row H-plus increase, HCO3-re-absorption strengthened: acidosis when the nephrotic tube epithyroid cells increased carbon anthene enzyme activity, the generation of H-plus and HCO3-increase, H-secretion into the tube cavity, in return for Na-plus and HCO3-accompanied by re-absorption. Obviously this is a process of acidic acid preservation. (2) NH4-plus discharge increased: acidosis when the renal tube epithetry cells produced NH3 increased, may be the production of NH3 substrates such as glutamine at this time easy to enter.