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.
prevention and treatment of DKA
Prevention:
NEVER omit insulin – education of patient and doctors (and dentists). If an IDDM patient cannot eat, should still take insulin, monitor closely and take carbohydrate in liquid form. If unable to keep liquids down, needs hospital admission for i-v treatment (GKI) before DKA occurs.
treatment: Medical emergency. Intravenous insulin, rehydration with saline, potassium replacement, and treatment of any underlying cause
signs of DKA
Clinical features Thirst, polyuria, malaise, confusion, coma. Deep breathing (‘Kussmaul respiration). Smell of acetone on breath.
hyperosmostic ketoacidiosos
Also known as HONK (hyperosmolar non-ketotic coma). Same as DKA, but without the ketoacidosis. Slower onset over a few days. Treatment similar to DKA, but dehydration and electrolyte disturbance can be severe, and must be corrected slowly.
diabetes principles before surgery
- Check control beforehand – glucose record book, HbAIc, contact doctor
- Check for relevant complications, e.g. angina, heart failure
- Minimise disruption to normal meals and medication – first on list in morning, allow mid-morning snack, take usual medication
- Monitor glucose pre-procedure and before leaving surgery
- Be prepared to diagnose and treat hypoglycaemia
- Remember increased risk of infection, but no need for prophylactic antibiotics
surgery fasting for diabetcis
- Short procedures – ‘fast and check’ – omit morning insulin/medication, do procedure, then give a late breakfast with normal medication. Monitor glucose before and after.
- Longer or major procedures – glucose/insulin/potassium infusion – ‘GKI’. Diet-controlled patients may not need insulin, but stress of illness may raise glucose levels, so still monitor
GKI- whats in it and how much do you give depending on……
Various recipes, but all contain glucose, insulin and potassium in one bag. Common starting dose: • 10% dextrose 500ml • 10mmol KCl • 16u soluble (short-acting) insulin • Rate 100ml/hour
Monitor glucose hourly, and aim to keep between 4 and 10. If > 10 and rising, replace bag with one containing 4 more units of insulin. If <6 and falling, replace with one containing 4 less units of insulin.
NB – infusion rate is constant, it is the insulin content which is adjusted.
