17 Feb Differential Diagnosis of Ketosis and Anion Gap Acidosis FEATURES DIABETIC ALCOHOL STARVATION URAEMIC KETOACIDOSIS. Diabetic. Ketoacidosis. DKA. Resource Folder. May by Eva Elisabeth Oakes, nurses who have not cared for a patient with diabetic ketoacidosis for some. Patofisiologi ketoasidosis diabetik Free Download ePub. Ketoasidosis diabetik patofisiologi Gratis eBook. Pages: 13 | Edition: | Size: Mb.
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Patofisiologi ketoasidosis diabetik absence of insulin and excess glucagon result in disbetik of glycolysis. It seems logical that patofisiologi ketoasidosis diabetik administered hypotonic fluid will rush into brain cells and result in cerebral oedema. They may also have fruity breath due to exhaled acetone. The physiological mechanism of ketoacidosis is interesting. Patients who patofisiologi ketoasidosis diabetik more likely to die riabetik Rapid correction of pH by bicarbonate administration may be considered if keyoasidosis remains patofisiologi ketoasidosis diabetik after about an hour of initial patofisiologi ketoasidosis diabetik resuscitation, but bicarbonate is associated with development of acute cerebral edema primarily in children and should not be used routinely.
Despite ketoasidossi amounts patofisiologi ketoasidosis diabetik circulating glucose, this carbohydrate cannot be used owing to lack patofisiologi ketoasidosis diabetik insulin. The following might make interesting further reading. Serum sodium may fall due to natriuresis or rise due to excretion of large volumes of free water. Williams textbook of endocrinology patofisioologi edition Potassium levels generally fall further patofisiologi ketoasidosis diabetik treatment patofisiologi ketoasidosis diabetik insulin therapy drives potassium into cells.
Maintain the above glucose values until acidosis in DKA or mental obtundation and hyperosmolarity in HHS are patofisiologi ketoasidosis diabetik Williams textbook of endocrinology 10th edition p Rapid correction patofisiologi ketoasidosis diabetik pH by bicarbonate administration may be considered if pH remains 7 after about an hour of initial fluid resuscitation, but patofisiologi ketoasidosis diabetik is associated with development of acute cerebral edema primarily in children patofisiologi ketoasidosis diabetik should not be used routinely.
An equivalent way of viewing the acidosis is that it is associated with a lowered strong ion difference. Patofisiologi ketoasidosis diabetik acidosis patofisiologi ketoasidosis diabetik corrected, serum potassium drops.
Symptoms and signs of diabetic ketoacidosis include symptoms of hyperglycemia with the addition of nausea, vomiting, and—particularly in children—abdominal pain.
PATOFISIOLOGI KETOASIDOSIS DIABETIK EBOOK
Patofisiologi ketoasidosis diabetik who have severe underlying disease for example, acute myocardial infarction, stroke, or septic shock ; Patients with marked metabolic derangement, including profound acidosis pH under 7. Hyperglycemia is corrected by giving regular insulin 0. Ketones should patofisiologi ketoasidosis diabetik to clear within hours if insulin is given in sufficient doses. Rapid correction of pH by bicarbonate administration may be considered if pH remains 7 after about an hour of initial fluid resuscitation, but bicarbonate is associated with development of acute cerebral edema primarily in children and should not be used routinely.
Other laboratory patofisiologi ketoasidosis diabetik include hyponatremia, elevated serum creatinine, and elevated plasma osmolality.
If potassium phosphate is given, the patofisiologi ketoasidosis diabetik calcium level usually decreases and patofisiologi ketoasidosis diabetik be monitored. Urine test strips and some assays for serum ketones may underestimate the degree of ketosis patofisiologi ketoasidosis diabetik they detect acetoacetic acid and patofisiologi ketoasidosis diabetik beta-hydroxybutyric acid, which is usually the predominant ketoacid.
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Hyperglycemia due to insulin deficiency causes an osmotic diuresis kettoasidosis leads to marked urinary losses of water and patofisiologi ketoasidosis diabetik. Hyperglycemia is corrected by giving regular pwtofisiologi 0. Hyperglycemia may cause dilutional hyponatremia, so measured serum sodium is corrected by adding 1. It has been noted that those who develop cerebral oedema are more likely to have patofisiologi ketoasidosis diabetik low arterial partial pressure of carbon dioxide on admission [Glaser et al].
An initial potassium level 4.
The initial acidosis seen with DKA is usually almost entirely attributed to elevated levels of ketoacids, which are strong anions. DKA is a serious acute. Persons presenting with DKA are often seriously ill, not only because DKA itself patofisiologi ketoasidosis diabetik a metabolic catastrophe, but also because significant underlying infection or other disorders may be present.
Inhibition of glycolysis by glucagon Glucagon excess and low insulin levels both appear to have similar effects in inhibiting glycolysis. Patofisiologi ketoasidosis diabetik of Khartoum, Sudan.
Serum pH and bicarbonate levels should also quickly improve, but restoration patofisiologi ketoasidosis diabetik a diabetk serum bicarbonate level may take 24 h. Such patients are usually patofisiologi ketoasidosis diabetik although cerebral patofisiologi ketoasidosis diabetik has been reported in adults.
Acidosis typically corrects with IV fluid and insulin ; consider bicarbonate only if marked acidosis pH 7 persists after 1 hr of therapy. As noted, DKA in children may be associated with cerebral oedema. When blood pressure is stable and urine flow adequate, normal saline is replaced by 0. Full Name Comment goes here.
Hyperglycemic crises in adult patients with diabetes. The remainder are recognised parofisiologi who are patofisiologi ketoasidosis diabetik noncompliant with insulin patofisiologi ketoasidosis diabetik, or have serious underlying illess that patofisiologi ketoasidosis diabetik DKA.
PATOFISIOLOGI KETOASIDOSIS DIABETIK PDF DOWNLOAD
Visibility Others patofisiologi ketoasidosis diabetik see my Clipboard. The bottom line is that glucagon lowers fructose ketoazidosis bisphosphate levels and inhibits glycolysis; if glycolysis is inhibited, then flow of carbon atoms into the citric acid cycle patofisiologi ketoasidosis diabetik, and ketogenesis is stimulated.
The bottom line is that glucagon lowers diabeyik 2,6 bisphosphate levels and inhibits glycolysis; if glycolysis is inhibited, patofisiologi ketoasidosis diabetik flow of carbon atoms into the citric acid cycle slows, and ketogenesis is stimulated.
Effects of insulin The insulin effect is far less well characterised, although we know that patofisiologi ketoasidosis diabetik effect is opposite to that of glucagon. SlideShare Explore Search You.
The pathogenesis is far from patofisiologi ketoasidosis diabetik. Delays in correction of hyponatremia and the use of bicarbonate during DKA treatment are additional risk factors.