Hyperglycaemia

Question 1

Hyperhlycaemia is ?

Answer 1

Hyperglycaemia (or high blood glucose) is when there is an excess of glucose circulating in the bloodstream. Unlike hypoglycaemia, the symptoms of hyperglycaemia develop slower, as the BGL increases. There are two primary manifestations of severe hyperglycaemia DKA and HHS.

Question 2

DKA is

Answer 2

DKA almost exclusively occurs in type I diabetics, in whom a severe or complete insulin deficiency reduces glucose uptake by cells and causes excessive glycogenolysis (the conversion of glycogen into glucose) in the liver causing hyperglycaemia (>13.8mmol/L). Hyperglycaemia leads to glycosuria, osmotic diuresis, dehydration and loss of electrolytes.
Lack of insulin also leads to the breakdown of triglycerides and mobilisation of fatty acids from adipose tissue (insulin normally prevents fat breakdown). A large share of the initial breakdown of fatty acids occurs in the liver, however the liver only uses a small amount of fatty acids for its own energy needs. The rest are converted into ketones, which are released into the blood. This is known as ketosis.

Question 3

Ketosis

Answer 3

Ketosis is a condition where there are elevated levels of three different molecules called ketone bodies – beta-hydroxybutyric acid, acetoacetic acid and acetone – in the blood and tissues, produced when the store of glycogen in the liver is exhausted. The first two can be used as an energy source but result in metabolic acidosis (ketoacidosis). Acetone cannot be used by the body and is excreted via urine and breath. Excess ketoacids cause metabolic acidosis (a serum pH <7.3). The ketoacids require buffering from sodium bicarbonate. Consequently there is a marked decrease in serum bicarbonate levels.

Question 4

HHS -Hyperosmolar Hyperglycaemic State (HHS)

Answer 4

HHS most commonly occurs in type II diabetics and may be the first sign of diabetes. A partial or relative insulin deficiency reduces the uptake of glucose across cell membranes and allows uninhibited glycogenolysis (the conversion of glycogen into glucose) in the liver. This results in hyperglycaemia (usually over 20mmol/L), glycosuria (glucose in the urine) and osmotic diuresis, causing significant water and electrolyte loss. Concomitant illness such as severe infection and myocardial infarction causes further glucose production, worsening hyperglycaemia and its associated symptoms. Because the body still produces some insulin, fat break down is minimal and ketosis does not occur (as in DKA).If the patient is unable to maintain adequate fluid intake because of concomitant illness or excessive water loss, dehydration develops.