Diabetes Key Points

Glucagon Cortisol Epinephrine/adrenaline Growth hormone

The term diabetes mellitus describes a metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism. Resulting from defects in insulin secretion, insulin action or both.

‘Long term bloods’ Formed by non-enzymatic attachment of glucose to haemoglobin A Formed slowly and continuously Normally less than 42 (6%) but in diabetics it can increase 2-3 times Can be used diagnostically if over 6.5% or 48mmol/mol

Fasting glucose equal to or between 6.1 and 7

OGTT between 7.8 and 11.1

Autoimmune destruction of pancreatic cells, usually occurs early in life Characterised by low insulin output, high blood glucose, glucose in urine, excess urine flow, switch to fat metabolism Treated with insulin injections, careful balance of diet and exercise 10% of diabetics

Associated with obesity, usually starts later in life. Insulin may be normal, but is ineffective (insulin resistance) Many of symptoms the same, but less severe

Genetic defects of beta-cell function Genetic defects in insulin action Diseases of the exocrine pancreas (endocrinopathies) Drug-or chemical induced Infections Uncommon forms of immune-mediated diabetes Other genetic syndromes sometimes associated with diabetes

Acute with symptoms of polyuria, polydipsia, lethargy, weight loss, nausea, vomiting, abdominal cramps, blurred vision and superficial infection

A group of metabolic diseases characterised by hyperglycaemia resulting from defects in insulin secretion, insulin action or both The chronic hyperglycaemia of diabetes is associated with long-term damage, dysfunction and failure of various organs, especially the eyes, kidneys, nerves, heart and blood vessels

Insidious presentation with symptoms of polyuria, polydipsia, lethargy, weight loss, nausea, vomiting, abdominal cramps, blurred vision and superficial infection

Coronary artery disease (MI) Cerebrovascular disease (stroke) Peripheral vascular disease

Retinopathy Nephropathy Neuropathy

Neuropathy (nerve damage) -> impotence is commonly a presenting symptom Cataracts Kidney damage (nephropathy) Arthritis -> damage to collagen in joints Capillary damage -> circulatory defects and damage to retina Abnormal plasma lipoprotein metabolism -> increased risk of cardiovascular disease

Damage to a-crystallin protein

Glucose is converted to sorbitol by aldose reductase - Sorbitol accumulates in tissues -> disturbs control of intracellular osmotic pressure Glucose is converted into ketones Glycation of collagen - stiffening of the collagen in the blood vessel walls leading to high bp

If a diabetic lets their blood glucose get too high he may develop ketoacidosis, a life-threatening emergency Most of the problems in ketoacidosis are due to: - Dehydration (due to excessive urine production) - Low pH (due to excessive lipid metabolism) - Large amounts of ketoacids in the blood (also due to excessive lipid metabolism)

Patient has diabetes if OGTT 2h greater than 11.0 and or a fasting glucose of greater than/equal to 7.0 mmol/L Patient has IGT if OGTT 2h between 7.8 and 11.1 and a fasting glucose less than 7.0 mmol/L

Fructosamine is a glycation product that forms when glucose binds to proteins1. It measures average blood glucose levels over the past two to three weeks and is used to help manage diabetes It is an earlier indicator of diabetes control compared to haemoglobin A1c (HbA1c), which measures average blood sugar over the previous two to four months

The excretion of a small amount of albumin in urine Diabetic nephropathy is a major complication in 35-45% of IDDM which may progress to end stage renal failure Microalbuminuria is the excretion of 50-200mg albumin in 24 hours Its detected by sensitive immunoassays (using antibodies directed against human albumin) Early detection can allow reversal of nephropathy through good glycaemic control, hypotensives and a low protein diet However once proteinuria has developed then improving glycaemic control may transiently slow down progression but will not reverse it What are four acute metabolic complications of diabetes mellitus

Diabetic ketoacidosis (DKA) Hyperosmolar non-ketotic coma (HNC) Lactic acidosis (LA) Hypoglycaemia

Altered lipid metabolism Increased concentrations of total lipids, cholesterol, triglycerides and free fatty acids Free fatty acids are shunted into ketone body formation due to lack of insulin The rate of formation of these ketone bodies exceeds the capacity for their peripheral utilisation and renal excretion leading to accumulation of ketoacids and therefore metabolic acidosis Caused by: Not enough insulin Skipping insulin Stress, trauma Insulin resistance

Dehydration Acidosis Hyperosmolality Diminished cerebral oxygen utilisation Consciousness becomes impaired Ultimately patient becomes comatose

Early manifestations are mild and include vomiting, polyuria and dehydration More severe cases include Kussmaul respirations (acetone breath) Abdominal pain or rigidity may be present and mimic acute appendicitis or pancreatitis Cerebral dehydration and coma ultimately ensure