Diabetes - General Features and Complications

• Diabetes is raised blood glucose level due to problems with insulin.

  • Type 1 = insulin dependent, juvenile onset. Due to autoimmune destruction of beta cells.
  • Type 2 = non-insulin dependent, maturity onset. Due to combination of insulin resistance and relative insulin lack.
  • Other types = gestational or secondary to other condition
• Symptoms of Type I diabetes:

  • Polyuria - pass a lot of urine
  • Polydipsia - get very thirsty (drink more to replace urine that has been lost)
  • Weight loss - because cells can't take up glucose and the glucose is then getting lost in the urine
  • Blurred vision
• Blurred vision in Type I diabetes:

  • Because you're dehydrated, because cells can't take up glucose and the glucose is then getting lost in the urine
  • This causes osmotic changes in the fluid in the vitreous of the eye, causing it to shrink slightly
  • Therefore you get blurred vision due to a temporary change in the shape of the eye
  • Temporary; when glucose level is controlled, the eye should re-adjust
• Symptoms of Type 2 diabetes:

  • May be asymptomatic
  • Predisposition to infections - candida, urine
  • Can present in same way as type 1
  • Can present with long term complications - since type 2 diabetes can be asymptomatic for so long
• Diagnosis of Type 2 diabetes involves the 75g oral glucose tolerance test

  
• Glycated haemoglobin is abbreviated to HbA1c. Haemoglobin in red cells is in the circulation for 120 days. Glucose sticks to it, so HbA1c level is a measure of average glucose over several weeks.

  • Normal is less than 42 mmol/mol
  • Pre-diabetes is 42-47 mmol/mol
  • Diabetes is 48 mmol/mol or over
• Aims of diabetes treatment:

  • Control symptoms
  • Prevent complications
  • Lead a normal life
  • Key element is patient education and self-management
• Glucose control:

  • Type 1 always needs insulin
  • Type 2:
  • Diet alone - less sugar/carbohydrates
  • Diet plus tablets/injected drugs
  • Diet plus insulin
• Glucose balance:

  • Things that raise glucose:
  • Food
  • Glucagon (from alpha cells in islets of langerhans), adrenaline, cortisol, growth hormone
  • Illness/stress
  • Things that lower glucose:
  • Starvation
  • Insulin, anti-diabetic drugs
  • Exercise
• Insulin secretagogues (oral hypoglycaemic drugs)

  • Mechanism of action = increase insulin secretion
  • Classes:
  • Sulphonylureas e.g. Gliclazide
  • DPP4 inhibitors - e.g. Sitagliptin and vildagliptin
  • GLP-1 binders - e.g. Exanetide and liraglutide (injected)
• Insulin sensitizers (oral hypoglycaemic drugs):

  • Mechanism of action = increase the action of insulin
  • Classes:
  • Biguanides (metformin)
  • Thiazolidinediones ('glitazones' e.g. Pioglitazone)
• Glucose monitors:

  • 'Flash' - only give readings when interrogated
  • 'Continuous' - transmits results and can give warnings of high/low glucoses
• Acute complications of diabetes:

  • Ketoacidosis (Type 1)
  • Hyperosmolar hyperglycaemic state (Type 2)
  • Hypoglycaemia - complication of treatment
• Chronic complications of diabetes - damage done to the body by having diabetes:

  • Microvascular damage - damage done to the body by having diabetes
  • Macrovascular damage - (essentially atherosclerosis)
  • Neuropathy
  • Foot problems - get bad circulation and numbness from neuropathy - can often result in amputations
• Chronic complications of diabetes - damage done to the body by having diabetes:

  • Microvascular damage - damage done to the body by having diabetes
  • Retinopathy - blood vessels that supply the retina
  • Neuropathy - blood vessels that supply the nerves
  • Nephropathy - blood vessels that supply the kidneys
• Chronic complications of diabetes - damage done to the body by having diabetes:

  • Macrovascular damage - (essentially atherosclerosis)
  • Peripheral vascular disease - results in gangrene/claudication of the legs - most strongly associated with diabetes
  • Coronary heart disease - results in angina/heart attacks
  • Cerebrovascular disease - results in strokes/TIAs
• Chronic complications of diabetes - background diabetic retinopathy:

  • White part = results in gangrene/claudication of the legs - most strongly associated with diabetes
  • Red splodges = microaneurysms that have formed on the arterioles and have subsequently burst, causing microhaemorrhage - completely asymptomatic - don't now you have them; out of periphery of vision
  • This is background diabetic retinopathy - requires no treatment - does require monitoring

  
• Chronic complications of diabetes - more severe background diabetic retinopathy:

  • More microaneurysms
  • Can also see hard exudates - blood vessels become leaky and leak protein or lipid into the space behind the retina/the vitreous and deposit there - as long as they're not in front of the central vision then they don't cause any symptoms

  
• Chronic complications of diabetes - more severe background diabetic retinopathy:

  • Blood vessels here have burst and caused a more severe haemorrhage - pre-retinal haemorrhage seen at bottom (red splotchy line) - has damaged the retina - moves downwards by gravity (sharp upper margin; it's the fluid level)

  
• Chronic complications of diabetes - more severe background diabetic retinopathy:

  • White dots = laser burns - when these patients are found to have significant proliferative retinopathy that has not yet affected the sight, burning out bits of the retina in the peripheral vision can help to prevent long term damage to the eye - doesn't cause major site loss, stops vessels from continuing to grow and burst to eventually cause a haemorrhage that would impact the central vision + make you go blind
  • Diabetes is still a major cause of blindness

  
• Foot of a diabetic person (LHS):

  • Has small vessel disease - not the main artery going down the leg, just a small digital artery supply the single toe that has been blocked
  • Toe has gone black & dry - infection has not got to it
  • RHS shows that the toe + its bones have been removed surgically
  • Sometimes the black toes can drop off and heal themselves up

  
• This is what happens to people with neuropathy in their feet (can't feel their feet):

  • The skin rubs and becomes thickened - they don't realise it's happening - eventually becomes so thick it necroses because there's no longer enough blood supply to the skin - breaks down to form a punched-out neuropathic ulcer on the part of the foot that you tread on
  • Painless; pt doesn't realise it's there
  • Can become infected -> need to be amputated
  • Management = v good foot care - podiatrists remove thick skin with a scalpel - pads in shoes to prevent shoes from rubbing - well-fitting footwear

  
• Chiroarthropathy - when you've had high glucose for many years - blood glucose sticks onto haemoglobin as well as collagen and other fibrous proteins - the person on the left now has stiff fingers; the collagen in their fingers/pal has become stiff + shrunk due to the effects of glucose binding to collagen over many years.

  Patient can't replicate action on left due to muscle wasting in their hand - neuropathy which has affected the motor system (doesn't just affect sensory system) - therefore can't move the hand v well.

  
• Prevention of long-term complications of diabetes:

  • Meticulous glucose control
  • Control of blood pressure
  • Avoidance/treatment of other risk factors: smoking, hyperlipidaemia, obesity, and inactivity
  • Early detection and management - screening
• Benefits of glucose control:

  • Reducing HbA1c (glycated haemoglobin) by 11mmol/mol reduces:
  • Microvascular complications by 25%
  • Amputations by 43%
  • Heart failure by 16%
  • Cataracts by 19%
  • BUT - too tight control increases risk of hypoglycaemia
• Treatment of established complications of diabetes:

  • Retinopathy - laser photocoagulation
  • Nephropathy - ACE inhibition, dialysis, transplantation
  • Neuropathy - advice about foot care
  • PVD (peripheral vascular disease) - bypass surgery, angioplasty or amputation
  • Foot ulcers - chiropody, protection, surgery
• Hypoglycaemia:

  • Plasma glucose is too low - bad; need glucose to provide energy for all cells to work
  • Only occurs with treatment for diabetes - not a complication of diabetes itself
  • Onset over minutes
  • Common with insulin
  • Can occur with oral hypoglycaemias
• Symptoms of hypoglycaemia:

  • Warning - what pts who take insulin are told to look out for - symptoms of increased adrenaline; body secretes adrenaline to try to raise the glucose level
  • Tremor
  • Anxiety - increase pulse/heart rate
  • Palpitations
  • Hunger
  • Dry mouth
  • Adrenergic urgent warning signs of hypoglycaemia - if recognised then should take glucose to keep the glucose level up - don't always get warning symptoms though - if you get autonomic neuropathy that damages the part of the nervous system that triggers adrenaline release then you no longer get warning signs, just established problems
• Symptoms of hypoglycaemia:

  • Established symptoms
  • Confusion/aggression
  • Slurred speech
  • Incoordination - mimics drunkenness
  • Coma
  • Convulsions
  • Death
  • Neuroglycopenic symptoms - can also lead to irreversible brain damage
• Treatment of hypoglycaemia:

  • Establish diagnosis - blood glucose < 4
  • If in doubt, treat anyway
  • First thing to do is try to give oral glucose - sugary drink (natural fruit juice/Lucozade/Coca Cola) or take a glucose tablet
  • Buccal hypostop gel - glucose gel that can be squeezed into the mouth (messy but can get glucose into someone who's not cooperating otherwise)
• Treatment of hypoglycaemia:

  • Intramuscular glucagon 1mg - glucagon is a hormone that raises glucose - it'll mobilise glycogen in the liver, turn it into glucose and release it into the blood to cure the hypoglycaemic reaction - works in 99% of pts (won't work in cases of severe starvation/patients with liver disease)
  • Intravenous glucose 20-30ml 50% - need a good line into a good vein; if you give concentrated glucose under the skin instead of into a vein then it'ill burn the skin; it's a strong acid & may result in a skin graft being needed - 50% is viscous so it requires a large cannula
• Glucagon comes as dry powder to be drawn up with diluent - poor shelf life in solution

  • Inject diluent into dry powder, shake it up and draw it back up into syringe before injecting
  • Given intramuscularly into a large muscle (outer thigh best place)
• Diabetic ketoacidosis happens due to an insulin lack in Type 1 diabetic pts - it is caused by omitting insulin or intercurrent illness.
• Diabetic ketoacidosis causes:

  • Hyperglycaemia
  • Osmotic diuresis - dehydration
  • Loss of Na in urine
  • Loss of K from cells and then in urine
  • Accumulation of 'ketone bodies' - soluble keto acids that accumulate in the blood - they come from fats, which are mobilised from fat stores when insulin levels are low - these ketones supply energy for the brain when there isn't enough glucose - in a complete lack of insulin they build up in an excessive, uncontrolled way, which is what causes ketoacidosis
• Clinical features of ketoacidosis:

  • Onset over 12-24 hours
  • Thirst, polyuria
  • Dehydration - dry mouth, low blood pressure, etc
  • Confusion/drowsiness/coma
  • Deep breathing - Kussmaul respiration (slow, deep breathing)
  • Can control pH of blood by breathing deeply to try to get rid of carbonic acid
  • Carbon dioxide dissolves in the blood as carbonic acid
  • If you breathe v fast you can make your blood alkaline by blowing off carbon dioxide into the atmosphere
  • Features of underlying cause - infection, myocardial infarction
• Prevention of DKA (diabetic ketoacidosis):

  • NEVER omit insulin in Type 1 diabetes
  • If unwell and off food, still take insulin, monitor carefully and take liquid form carbohydrate
  • If unable to keep any food down, immediate hospital admission for intravenous treatment
  • Education of pt and doctor and dentist
• Treatment of diabetic ketoacidosis:

  • Medical emergency
  • Intravenous insulin infusion
  • Intravenous rehydration and electrolyte replacement
  • Treat underlying cause
  • Secondary prevention
• Hyperosomolar non-ketotic coma (HONK):

  • Now called hyperosmolar hyperglycaemic state - HHS
  • Similar to diabetic ketoacidosis, but without the ketoacid build-up
  • Occurs in type 2 diabetes
  • Usually onset over days
  • Treatment similar to diabetic ketoacidosis, but slower correction and thromboprophylaxis
• Diabetes during dental surgery:

  • Check control and usual treatment
  • Check for relevant complications
  • List first in morning - minimise disruption to routine
  • Check glucose before and after procedure, be prepared to treat hypoglycaemia
  • Give a mid-morning snack before leaving surgery
  • Remember increased infection risk
• Procedures requiring fasting:

  • For short procedures 'fast and check'
  • Omit morning insulin/tablets and breakfast
  • Do procedure first on list
  • Give treatment and breakfast immediately afterwards