Acidosis diabetic ketoacidosis

Lactic acidosis Diabetic ketoacidosis Lactic acidosis... 

Diabetic ketoacidosis A reversible but life-threatening short-term complication primarily seen in patients with type 1 diabetes caused by the relative or absolute lack of insulin that results in marked ketosis and acidosis. 

Hyperosmolar hyperglycemic state A potentially fatal short-term complication most commonly seen in older patients with type 2 diabetes caused by an insufficiency of insulin action that leads to alterations of osmolality and hyperglycemia, but without the ketosis and acidosis seen in diabetic ketoacidosis. 

The following factors have been suggested as alternatives to consider when presented with a potential case of exposure to carbon monoxide diabetic ketoacidosis, hypothyroidism and myxedema coma, labyrinthitis, and lactic acidosis toxic exposures resulting in methemoglobinemia ingestion of alcohols or narcotics and diseases that cause gastroenteritis, encephalitis, meningitis, and acute respiratory distress syndrome. 

The manifestations of acute severe metabolic acidemia (pH less than 7.15 to 7.20) involve the cardiovascular, respiratory, and central nervous systems. Hyperventilation is often the first sign of metabolic acidosis. Respiratory compensation may occur as Kussmaul s respirations (i.e., deep, rapid respirations characteristic of diabetic ketoacidosis). 

Renal disease or renal dysfunction (eg, as suggested by serum creatinine levels greater than or equal to 1.5 mg/dL [males], greater than or equal to 1.4 mg/dL [females], or abnormal Ccr) that may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction (Ml), and septicemia CHF requiring pharmacologic treatment hypersensitivity to metformin acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. Treat diabetic ketoacidosis with insulin. 

Examples of conditions that can lead to production of excess acid include diabetic ketoacidosis, lactic acidosis, sepsis, and renal failure. 

The answer is C. Ingestion of an acid or excess production by the body, such as in diabetic ketoacidosis, may induce metabolic acidosis, a condition in which both pH and HCOj become depressed. In response to this condition, the carbonic acid-bicarbonate system is capable of disposing of the excess acid in the form of CO2. The equilibrium between bicarbonate and carbonic acid shifts toward formation of carbonic acid, which is converted to COj and HjO in the RBC catalyzed by carbonic anhydrase, an enzyme found mainly in the RBC. The excess CO2 is then expired by the lungs as a result of respiratory compensation for the acidosis (Figure 1-2). The main role of the kidneys in managing acidosis is through excretion of H" rather than CO2. 

Acute complications of diabetes include diabetic ketoacidosis, hyperglycaemic non-ketotic hyperosmolar coma, lactic acidosis and hypoglycaemia. 

Normally, the sum of the cations exceeds the sum of the anions by no more than 12-16 mEq/L (or 8-12 mEq/L if the formula used for estimating the anion gap omits the potassium level). A larger-than expected anion gap is caused by the presence of unmeasured anions (lactate, etc) accompanying metabolic acidosis. This may occur with numerous conditions, such as diabetic ketoacidosis, renal failure, or shock-induced lactic acidosis. Drugs that may induce an elevated anion gap metabolic acidosis (Table 58-1) include aspirin, metformin, methanol, ethylene glycol, isoniazid, and iron. 

Acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma... 

Ition of the ketone bodies may be as high as 5000 mg/24 hr, and the blood concentration may reach 90 mg/dl (versus less than 3 mg/dL in normal individuals). A frequent symptom of diabetic ketoacidosis is a fruity odor on the breath which result from increased production of acetone. An elevation of the ketone body concentration in the blood results in acidemia. [Note The carboxyl group of a ketone body has a pKa about 4. Therefore, each ketone body loses a proton (H+) as it circulates in the blood, which lowers the pH of the body. Also, excretion of glucose and ketone bodies in the urine results in dehydration of the body. Therefore, the increased number of H+, circulating in a decreased volume of plasma, can cause severe acidosis (ketoacidosis)]. Ketoacidosis may also be seen in cases of fasting (see p. 327). 

Takaike H, Uchigata Y, Iwasaki N, Iwamoto Y. Transient elevation of liver transaminase after starting insulin therapy for diabetic acidosis or ketoacidosis in newly diagnosed type 1 diabetes mellitus. Diabetes Res Clin Pract 2004 64 27-32. 

Diabetic ketoacidosis may either result from or be aggravated by infection, surgery, trauma, shock, emotional stress, or failure to take sufficient amounts of insulin. Treatment is focused on reversing the hypokalemia by administering potassium chloride and on offsetting the acidosis by providing bicarbonate. The dehydration and electrolyte imbalance are treated with appropriate measures and crystalline zinc insulin is administered to counter the hyperglycemia. 

Newly diagnosed patients with type 1 diabetes may present with acute metabolic decompensations, ketone production, and metabolic acidosis, a condition known as diabetic ketoacidosis (DKA).Although (J-cell destruction occurs gradually, acute physical or emotional stress can acutely create a demand for increased insulin production. 

Metabolic acidosis involves a build-up of hydrogen ions in the blood, thus lowering blood pH. Under normal physiological conditions, the kidneys excrete excess hydrogen ions, and release more bicarbonate ions into the bloodstream to buffer the excess acid. However, in renal failure, or in diabetic ketoacidosis, this mechanism either fails, or is unable to compensate to an adequate extent. Hence, metabolic acidosis is usually treated with sodium bicarbonate, either intravenously (1.26% or 8.4% i.v. solution) or orally (typically 1 g three times a day). Sodium bicarbonate 1.26% intravenous solution is isotonic with plasma (and with sodium chloride 0.9%), so may be given in large volumes (1-2 L) by peripheral venous catheter to correct metabolic acidosis and provide fluid replacement at the same time. Sodium bicarbonate 8.4% may only be given by central venous catheter. 

The glucagon/insulin ratio can rise under certain pathological conditions (i.e., insulin-dependent diabetes). A small percentage of diabetics develop ketoacidosis, a condition that results from the overproduction and underuhlization of ketone bodies. Increased concentrations of p hydmxybutyrate and acetoacetate, which are acids, can cause a drop in the pH of the blood. This acidification, known as acidosis, can impair the ablLity of the heart to contract and result in a loss of consciousness and coma, which, in rare cases, may be fatal. Diabetic ketoacidosis may manifest as abdominal pain, nausea, and vomiting. A subject may hyperventilate (breathe quickly and deeply) to correct acidosis, as described under Sodium, Potassium, and Water in Chapter 10. It is the responsibility of the clinician, when confronted with a subject whose breath smells of acetone or who is hyperventilating, to facilitate prompt treatment. 

A 41-year-old woman took paraldehyde 20-50 g on three different occasions and developed a metabolic acidosis that mimicked diabetic ketoacidosis (13). 

Secondary gout is a result of hyperuricemia attributable to several identifiable causes. Renal retention of uric acid may occur in acute or chronic kidney disease of any type or as a consequence of administration of drugs diuretics, in particular, are implicated in the latter instance. Organic acidemia caused by increased acetoacetic acid in diabetic ketoacidosis or by lactic acidosis may interfere with tubular secretion of urate. Increased nucleic acid turnover and a consequent increase in catabolism of purines may be encountered in rapid proliferation of tumor cells and in massive destruction of tumor cells on therapy with certain chemotherapeutic agents. 

The transfer of intracellular K" into ECF invariably occurs in acidosis as H shifts intraceHularly and shifts outward to maintain electrical neutrality. As a general rule, K concentrations are expected to rise 0.2 to 0.7 mmol/L for every 0.1 unit drop in pH. When the underlying cause of the acidosis is treated, normokalemia will rapidly be restored. Extracellular redistribution of may also occur in (1) dehydration, (2) shock with tissue hypoxia, (3) insulin deficiency (e.g., diabetic ketoacidosis), (4) massive intravascular or extracorporeal hemolysis, (5) severe burns, (6) tumor lysis syndrome, and (7) violent muscular activity, such as that occurring in status epilepticus. Finally, important iatrogenic causes of redistribution hyperkalemia include digoxin toxicity and P adrenergic blockade, especially in patients with diabetes or on dialysis. ... 

Most metabolic acid-base disorders develop slowly, within hours in diabetic ketoacidosis and months or even years in chronic renal disease. The respiratory system responds immediately to a change in acid-base status, but several hours maybe required for the response to become maximal. The maximum response is not attained until both the central and peripheral chemoreceptors are fully stimulated. For example, in the early stages of metabolic acidosis, plasma pH decreases, but because H ions equilibrate rather slowly across the blood-brain barrier, the pH in CSF remains nearly normal. However, because peripheral chemoreceptors are stimulated by the decreased plasma pH, hyperventilation occurs, and plasma PCO2 decreases. When this occurs, the PCO2 of the CSF decreases immediately because CO2 equilibrates rapidly across the blood-brain barrier, leading to a rise in the pH of the CSF. This will inhibit the central chemoreceptors. But as plasma bicarbonate gradually falls because of acidosis, bicarbonate concentration and pH in the CSF wih also fall over several hours. At this point, stimulation of respiration becomes maximal as both the central and peripheral chemoreceptors are maximally stimulated. 

Alcohol taken in excess tends to prevent gluconeogenesis from lactate in the liver, because oxidation of ethanol to acetaldehyde competes for the NAD" that is necessary for the conversion of lactate to pyruvate. Severe acidosis, such as diabetic ketoacidosis, may suppress lactate conversion and cause a shift in the lactate-pyruvate equilibrium with the accumulation of H. This shift may, in part, be responsible for the lactic acidosis seen in diabetics. 

Intracellular phosphate may be lost in acidosis as a result of the catabolism of organic compounds within the cell. Diabetic ketoacidosis is associated initially with high-normal to increased serum phosphate. Treatment of the ketosis and acidosis with insuhn and intravenous fluids, however, results in a rapid reduction in the serum phosphate concentration. Consequently, patients being treated for diabetic ketoacidosis may have both intracellular phosphate depletion and hypophosphatemia. 

Oral or intravenous administration Phosphate-containing laxatives or enemas Increased extracellular phosphate load Transcellular shift Lactic acidosis Respiratory acidosis Untreated diabetic ketoacidosis Cell lysis... 

Treatment is by correction of the cause of the acidosis (e.g., insulin administration in diabetic ketoacidosis) and neutralization of the acid with NaHCOs, sodium lactate, or TRIS [tris(hydroxymethyl)aminomethane] buffer. Problems that may occur following alkali replacement therapy include development of respiratory alkalosis, particularly if the low CO2 tension persists, and further decline in the pH of CSF, which may decrease consciousness. The alkaline overshoot results from resumption of oxidation of organic anions (e.g., lactate, acetoacetate) with resultant production of bicarbonate from CO2. Severe acidosis should be corrected slowly over several hours. Potassium replacement therapy frequently is needed because of the shift of intracellular K" " to extracellular fluid and loss of K+ in the urine. 

Acid-base disturbances frequently coexist with two or more simple disorders (Table 39-2). In these settings, blood pH is either severely depressed (e.g., a patient with metabolic acidosis and respiratory acidosis) or normal. Both plasma HCOj and pH may be within normal limits when metabolic alkalosis and metabolic ketoacidosis coexist, as in a patient with diabetic ketoacidosis who is vomiting. In this situation, an elevated anion gap may be the initial abnormality that can be detected in the underlying mixed acid-base disturbance. 

Acid-base disorders such as lactic acidosis and diabetic ketoacidosis can release endogenous intracellular phosphorus and cause... 

Severe metabolic acidosis is usually associated with acute processes. The manifestations of severe acidemia (pH <7.15 to 7.20) involve the cardiovascular, respiratory, and central nervous systems. Hyperventilation is often the first sign of metabolic acidosis. At a pH of 7.2, pulmonary ventilation increases about fourfold and an eightfold increase has been noted at a pH of 7. Respiratory compensation may occur as Kussmaul s respirations—the deep, rapid respirations seen commonly in patients with diabetic ketoacidosis. In extremely severe acidosis (pH <6.8), central nervous system (CNS) function is disrupted to such a degree that the respiratory center is depressed. 

D-Fructose is the sweetest natural sugar. Its use as a natural sweetener is, therefore, increasing rapidly. It is absorbed slowly from the intestine, and thus does not cause abrupt changes in the serum levels of carbohydrates. It has little, if any, effect on insulin secretion. Thus, it exerts beneficial effects as a component of diets for mild and well-balanced diabetes, but should be taken within caloric restriction,445 as obesity impairs D-glucose tolerance and increases the insulin resistance of peripheral tissue.446 Use of D-fructose in the direct treatment of diabetic ketoacidosis does not offer advantages over routine, fluid therapy, and may even be dangerous on the basis that rapid infusion of large amounts of D-fructose may cause lactate acidosis. 

In the conditions discussed above (diabetic ketoacidosis, lactic acidosis, uremia, and ingestion of salicylate, ethylene glycol, or methanol) metabolic acidosis is associated with an increased anion gap. In the face of excess metabolic acids, bicarbonate is depleted in the process of buffering excess hydrogen ions. Provided that the renal functions is normal, the kidney attempts to compensate by secreting an acid urine and retaining bicarbonate. 

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