Diabetic Ketoacidosis
Download as PPTX, PDF3 likes1,228 views
The document discusses three serious acute complications of diabetes: diabetic ketoacidosis, hyperglycaemic hyperosmolar state, and lactic acidosis. It focuses on diabetic ketoacidosis (DKA), which results from a combination of insulin deficiency and excess of counterregulatory hormones like glucagon. This leads to increased gluconeogenesis and lipolysis, reduced glucose utilization, and ultimately ketonemia, ketonuria and metabolic acidosis as the liver produces ketone bodies from free fatty acids at a rate the body cannot buffer. While rare in type 2 diabetes, DKA is more common in type 1 diabetes due to higher insulin levels in type 2 patients. The document also briefly discusses hyperglycaem
Diabetic Ketoacidosis
- 1. 1 3 Most Serious Acute Complications Of Diabetes. 1. Diabetic Ketoacidosis 2. Hyperglycaemic Hyperosmolar State 3. Lactic Acidosis www.medicinemcq.com
- 2. 2 Diabetic ketoacidosis Serious complication of T1 DM. Less common in T2 DM. www.medicinemcq.com
- 3. 3 Type 2 diabetes Ketoacidosis rare - higher portal vein insulin levels in type 2 diabetics than in type 1 diabetics. Keeps the formation of ketone bodies in check. Type 2 - Hyperosmolar nonketotic state. www.medicinemcq.com
- 4. 4 Insulin/glucagon ratio is decreased. Marked insulin deficiency. Glucagon excess. www.medicinemcq.com
- 5. 5 Effect of decreased Insulin/glucagon ratio Decreased peripheral utilization of glucose. Increased gluconeogenesis. Osmotic diuresis and dehydration. Dehydration is characteristic of DKA. www.medicinemcq.com
- 6. 6 Activation of the ketogenic machinery The second major effect of decrease in the insulin:glucagon www.medicinemcq.com
- 7. 7 DKA Due to combination of insulin deficiency and counter regulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone). Insulin deficiency and glucagon excess - necessary for DKA to develop. www.medicinemcq.com
- 8. 8 Hyperglycemia of DKA 1. Due to increased hepatic glucose production 2. Impaired peripheral glucose utilization. www.medicinemcq.com
- 9. 9 Hypercortisolaemia Increases protein breakdown. Provides increased amino acid precursors for gluconeogenesis. Glucose production is thus increased. www.medicinemcq.com
- 10. 10 Glucose utilisation in peripheral tissues Decreased insulin deficiency insulin resistance Blood glucose levels rise glycosuria, osmotic diuresis and dehydration www.medicinemcq.com
- 11. 11 Insulin deficiency stimulates lipoprotein lipase. Excessive breakdown of adipose stores Increase in FFA. Esterified to acyl CoA. www.medicinemcq.com
- 12. 12 Lipoprotein lipase is exquisitely sensitive to inhibition by insulin. Lipoprotein lipase stimulates the breakdown of stored triglycerides in adipose tissue. www.medicinemcq.com
- 13. 13 Ketonemia and ketonuria Liver - Oxidation of acyl CoA produces ketone bodies www.medicinemcq.com
- 14. 14 Systemic metabolic ketoacidosis Plasma hydrogen ion concentration increases www.medicinemcq.com
- 15. 15 Excessive breakdown of adipose stores Large amounts of glycerol and FFA released into the circulation. www.medicinemcq.com
- 17. 17 Ketone bodies Strong organic acids. Buffered by bicarbonate. www.medicinemcq.com
- 18. 18 Systemic metabolic acidosis The rapid increase in ketone body production outstrips the bodies buffering capacity provided by bicarbonate www.medicinemcq.com
- 19. 19 Ketoacidosis is rare in type 2 diabetes Much more common in T1 DM. Higher portal vein insulin levels in T2 DM than in type 1 diabetics. Keeps the formation of ketone bodies in check. T2 DM - hyperosmolar nonketotic www.medicinemcq.com
- 20. 20 Hyperosmolar nonketotic state Severe dehydration Result from osmotic diuresis For rest of the slides, visit www.medicinemcq.com > Diabetes Mellitus