Diabetic Ketoacidosis — Applied Clinical Biochemistry

Biochemistry · Basic Sciences

How it begins

Análisis exhaustivo de la fisiopatología molecular, cascadas bioquímicas, alteraciones electrolíticas, desequilibrio ácido-base y fundamentos bioquímicos del tratamiento. Nivel experto con correlaciones clínicas de UCI.

What it covers

1. Definition, Epidemiology and Diagnostic Criteria
2. · Epidemiology and Mortality
3. Molecular Physiopathology: Insulinopenia and Counterregulation
4. · The Insulin-Glucagon Axis: Critical Molar Ratio
5. · Role of Glucagon in DKA
6. · Role of Catecholamines
7. · Role of Cortisol and GH
8. Accelerated Lipolysis: Activation of Hormone Sensitive Lipase
9. · Lipolytic Adipocyte Enzymes
10. · Transport of FFA to the Liver
11. Hepatic Ketogenesis: Detailed Biochemistry
12. · The Control Point: CPT-I and Malonil-CoA
13. · The HMG-CoA Pathway: Synthesis of Ketone Bodies
14. Ketone Bodies: Chemistry, Metabolism and Detection
15. · The BHB/AcAc Ratio: Mitochondrial Redox Index
16. · Peripheral Use of Ketone Bodies
17. Hyperglycemia: Uncontrolled Gluconeogenesis and Glycogenolysis
18. · Accelerated Hepatic Gluconeogenesis
19. · Hepatic Glycogenolysis
20. · Reduction of Peripheral Capture
21. · The Renal Glucose Threshold and Glucosuria
22. Electrolyte Alterations: Detailed Pathophysiology
23. · Potassium (K⁺): The Most Dangerous Electrolyte
24. · Sodium (Na⁺): Real Deficit vs. Apparent
25. · Phosphorus (PO₄³⁻): The Forgotten Electrolyte
26. · Magnesium (Mg²⁺) and Calcium (Ca²⁺)
27. Acid-Base Balance: Anion Gap and the Triple Complexity of CAD
28. · The Anion Gap and its Calculation
29. · Delta-Delta (ΔAG/ΔHCO₃⁻): Unmasking the Underlying Disorder
30. · Common Mixed Disorders in DKA
31. · Winter's Formula in CAD
32. Laboratory Diagnosis: Complete Biochemical Panel
33. Biochemical Fundamentals of Treatment
34. · Pillar 1 — Volume Replacement (Priority)
35. · Pillar 2 — Insulinotherapy: The Biochemistry of the Ketogenic Brake
36. · The "Anion Gap Closing": Ketogenic Resolution Signal
37. · Bicarbonate: Controversy and Evidence
38. Biochemical Complications of Treatment
39. · Cerebral Edema
40. · Hypoglycemia and Hypokalemia
41. · Post-SF Hyperchloremic Acidosis
42. Euglycemic CAD: The Role of SGLT2 Inhibitors
43. · Molecular Mechanism of CAD by iSGLT2
44. Differential Diagnosis: CAD vs. Hyperglycemic Hyperosmolar Syndrome (HHS)
45. Biochemical Criteria for Resolution and Transition to Subcutaneous Insulin
46. · Recommended Biochemical Monitoring During Treatment
47. Biochemical Integration: CAD as a Model of Extreme Catabolism