Diabetes Key Points Flashcards
What four hormones can increase blood glucose
Glucagon
Cortisol
Epinephrine/adrenaline
Growth hormone
Define diabetes mellitus
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.
Define HbA1c
‘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
What would indicate impaired fasting glycaemia
Fasting glucose equal to or between 6.1 and 7
What would indicate impaired glucose tolerance
OGTT between 7.8 and 11.1
Define type 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
Define type 2 diabetes
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
What conditions may be associated with type 4
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
How does type 1 present
Acute with symptoms of polyuria, polydipsia, lethargy, weight loss, nausea, vomiting, abdominal cramps, blurred vision and superficial infection
What is the pathophysiology behind type 2
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
How does type 2 present
Insidious presentation with symptoms of polyuria, polydipsia, lethargy, weight loss, nausea, vomiting, abdominal cramps, blurred vision and superficial infection
What are the three macrovascular complications of diabetes
Coronary artery disease (MI)
Cerebrovascular disease (stroke)
Peripheral vascular disease
What are the three microvascular complications of diabetes
Retinopathy
Nephropathy
Neuropathy
What are the five complications of poor glycaemic control
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
How does diabetes cause cataracts
Damage to a-crystallin protein
What are the three mechanisms of damage in hyperglycaemia
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
Why is ketoacidosis an emergency
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)
How is the OGTT interpreted
(2
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
What is fructosamine and how is it measured
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
What is microalbuminaemia
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
What are four acute metabolic complications of diabetes mellitus
Diabetic ketoacidosis (DKA)
Hyperosmolar non-ketotic coma (HNC)
Lactic acidosis (LA)
Hypoglycaemia
What cause DKA
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
Symptoms of DKA
Dehydration
Acidosis
Hyperosmolality
Diminished cerebral oxygen utilisation
Consciousness becomes impaired
Ultimately patient becomes comatose
How does someone present if they have DKA
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
What is a hyperosmolar non-ketotic coma
Presence of relative insulin deficiency and hyperglycaemia with associated elevated serum osmolality, dehydration and stupor progressing to coma if uncorrected without the presence of ketosis or acidosis
These patients have sufficient circulating insulin to prevent lipolysis and ketosis
Caused by:
Dehydration
Medications such as steroids and thiazides
Acute illness
Cerebral vascular disease
Advanced age
What is lactic acidosi
Elevated lactic acid with acidosis and without ketoacidosis
There may be low levels of ketones present
Half of the reported cases of LA have been in diabetics
Rarely seen in diabetic patients particularly since the withdrawal of phenformin from the market
What causes LA
Hypoxia
Medications such as phenoformin
What is hypoglycaemia
Common in insulin-treated diabetics and occasionally seen in those treated with oral hypoglycemic sulfonylurea agents
Can range from very mild (3.3 to 3.9) with minimal or no symptoms
To severe (<2.2 mmol/L) where there is neurologic impairment
Associated with insulin therapy, may be related to errors in dosage, delayed or skipped meals, exercise and/or intensity of glycaemic control
