diabetes Flashcards
type 1 and type 2
and secondary diabetes
Type 1 – autoimmune destruction of beta cells in islets of Langerhans. Insulin-dependent (IDDM). Ketosis-prone. Onset childhood to 40’s.
Type 2 – combination of insulin resistance and relative insulin lack. Non-insulin-dependent (NIDDM). Onset after 40; associated with obesity; familial. Prevalence in UK is 2% known and 2% undiagnosed.
Secondary (rarer) e.g. due to pancreatectomy, cortisol excess, acromegaly. Important secondary cause is gestational diabetes – in pregnancy.
diagnosis
check gluscoe the do a oral glucose tolerance test: overnight fast, 75g glucose and measure plasma glucose fasting and at 2 hours
how to measure diabetes long term
Glycated haemoglobin (hbA1c) (2-3 months)
HBA1c diabetes level
over 48 mol/mol
things that raise glucose
food,
Glucagon, adrenaline, cortisol, growth hormone,
illness/stress
what causes lower glucose
Starvation
Insulin, anti-diabetic drugs
Exercise
insulins use description
Many types with different lengths of action, all injected subcutaneously. Common to have twice daily short/medium mix or once daily long acting with 3 x short acting before meals. Use of continuous subcutaneous infusions of soluble insulin from pumps is increasing.
acute complications of diabetes
Ketoacidosis (type 1)
Hyperosmolar hyperglycaemic state (hyperosmolar non-ketotic coma ‘HONK’)
Hypoglycaemia - complication of treatment, does not occur with diet alone.
chronic
Microvascular – retinopathy and nephropathy
Macrovascular – coronary, peripheral, cerebral
Neuropathy
Mixed complications – diabetic foot, erectile dysfunction
Increased susceptibility to infection – skin, mouth, general
prevention of chronic conditions
Good control of blood glucose – diet, insulin, drugs. Self-glucose monitoring.
Control of blood pressure – drugs and diet
Control of lipid abnormalities – drugs and diet
Regular (annual) screening for complications – early detection
Retinopathy – laser photocogulation
Nephropathy – aggressive blood pressure control, ACE inhibitors( some pt with autonomic neuropathy can lose the ability to get some hypo warning signs)
Foot ulcers – careful foot care, chiropody, good footwear, avoiding trauma, education.
treatment of advanced complications
Retinopathy – vitro-retinal surgery
Nephropathy – dialysis and transplantation
Foot problems – vascular bypass surgery, amputation
Impotence – Viagra, surgery.
acute complications- hypoglycaemia
Complication of glucose-lowering treatment, not of diabetes per se.
Common with insulin – inevitable consequence of good control. Can occur with insulin secretagogues, often unrecognised and of slower onset.
Symptoms begin when blood glucose <3.5.
warning syptoms of hypoglycaemia
Warning symptoms (adrenergic) – tremor, sweating, anxiety, palpitations, hunger, dry mouth
Neuroglycopaenic symptoms – confusion, aggression, slurred speech, inco-ordination (ALWAYS check glucose in a suspected drunk) leading to coma, convulsions and death.
Some patients, e.g. those with autonomic neuropathy from long term diabetes, lose the warning symptoms which allow them to take action before they get too confused.
how to treat hypoglycaemia
Confirm diagnosis by checking glucose, if possible. IF IN DOUBT – TREAT ANYWAY: transiently raising the glucose too high will do no permanent harm.
• Oral glucose e.g. 100ml lucozade, carton of fruit juice, warm milk with 2 teaspoons of sugar, 3 dextrose tablets.
• Glucose gel squeezed into mouth in patient refusing/unable to swallow
• 1mg glucagon intramuscularly – acts by releasing glucose from liver glycogen stores – may fail in liver disease or malnutrition
• Intravenous glucose 10-30ml via large bore cannula in large vein. Flush with saline.
• Emergency hospital admission if the above fails within 15 minutes
if pt ok within 1hr with normal blood glucose then don’t need gp admittance
diabetic ketoacidiosis
Diabetic ketoacidosis
Occurs in type 1 diabetes. Caused by intercurrent illness (usually infection) or omitting insulin. Onset over 12-24 hours.
What is it? Insulin lack causes high glucose. Osmotic diuresis causes severe dehydration with loss of Na and K. Insulin lack also stimulates breakdown of fat into ‘ketone bodies’ (stupid term) – aceto-acetic acid, and 3 hydroxybutyric acid. This causes fall in blood pH, which stimulates breathing, to get rid of dissolved CO2 (i.e. carbonic acid) and raise the pH.