When the rate of synthesis of ketone bodies exceeds the rate of utilization, their concentration in blood increases, this is known as ketonemia. This is followed by ketonuria – excretion of ketone bodies in urine. The overall picture of ketonemia and ketonuria is commonly referred to as ketosis.
Mechanism:
- Hyperglycaemia occurs due to decreased glucose uptake in fat and muscle cells due to insulin deficiency Lipolysis in fat cells now occurs promoted by the insulin deficiency releasing
- Free fatty acids (FFA) into the blood which provide substrate to the liver
- A switch in hepatic lipid metabolism occurs due to the insulin deficiency and the glucagon excess, so the excess FFA is metabolised resulting in excess production of acetyl CoA
- The excess hepatic acetyl CoA (remaining after saturation of TCA cycle) is converted to ketone bodies which are released into the blood
- Ketoacidosis and hyperglycaemia both occur due to the lack of insulin and the increase in glucagon and most of the clinical effects follow from these two factors
Summary:
1. ↓ Insulin, ↑Glucogon (glycogen à glucose)
- Glucose 500-700 mg/dl
2. Glucose-derived
osmotic diuresis
3. ↑ Glucagon
- ↑ FFA esterfied à
ketone bodies à
acidosis
|
Diagnostic tests:
- Blood glucose greater than 250 mg/dL
- Blood pH less than 7.3
- Blood bicarbonate less than 15 mEq/L
- Ketones present in blood (exceeds 90 mg/dl)
- Ketones excreted in urine exceeds 5000 mg/24 hrs
Signs and Symptoms:
- Kussmal's respiration
- Fruity odor of breath
- Nausea and abdominal pain
- Dehydration
- Lethargy
- Coma
- Polydipsia, polyuria, polyphagia
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