Diabetes Mellitus Flashcards
What is diabetes mellitus?
Metabolic hyperglycaemic condition caused by lack of insulin production by the pancreatic islet cells
What is the aetiology of diabetes mellitus?
Pancreatib B cell malfunction is caused by autoimmune destruction in 90% of the patients. This is linked to certain MHC genotypes (ie. HLA DQB) but also linked to environmental triggers.
B cell autoantigens play a role in initiation and progression of this destruction (ie. GAD, insulin, insulinoma associated protein 1 IA-2.
What is the epidemiology of diabetes mellitus?
One of the most common chronic diseases of childhood in the UK. Prevalence of 0.35% in UK
What would be found in the history and exam of diabetes and mellitus?
Onset usually <30y
Polyuria and nocturia (caused by osmotic glycosuria)
Tiredness, fatigue, weight loss
What are the signs of DKA?
Diabetic ketoacidosis: Confusion, abdominal pain, polyuria, polydipsia, Kussmal breathing ( deep andrapid), ketotic breath, nausea and vomiting, dehydration.
What are the signs of complications in DM?
Signs of complications: fundoscopy revealing changes in retinopathy (ie, cotton wool spots, blot haemorrages) Examination of feet (senation)
What are the signs of associated AI conditions?
Signs of associated autoimmune conditions (ie. Vitiligo, Addisons etc)
What investigations would you do for DM?
Blood glucose: FBG>7mmol/l or random BG >11mmol/l
Hb1AC: assessment of glycaemic control of past 2-3 months
FBC: reticulocyte count (high = high erythrocyte turnover leads to misleading high Hb1AC)
U&E / urine dip: to monitor nephropathy (glycosuria, ketnouria, proteinuria)
Suspected DKA: blood (FBC shows high WCC, UE shows high U/Creat, LFt, CRP, amylase may be high)
CXR (exclude infection) ECG (ischaemic changes)
What is the management for DKA?
- Insulin: begin with IV, when consciousness regained switch to SC. Only remove IV after SC has commenced
- Dextrose + Fluids: to restore BP and monitor glucose fall. Aim for SBP100mmHg and CBG <7mmol/l
- Potassium replacement: Start in the second bag of fluid id passing urine, monitor electrolytes as this is being given. This is because insulin leads to increased K uptake in cells therefore risk of hypokalaemia in response to insulin
- BG monitoring
- Thromboprophylaxis, antibiotics if infection is suspected, NBM for 6h, NG tube if GCS is reduced
May require ICU if severely dehydrated, hypotensive or oliguric.
How do you manage glycaemic control for DM?
- Advice and patient education: by dietologists and specialist
- SC insulin: Short acting (lispro) 3xdaily before meals and long acting (detemir) 2x daily
- Insulin pumps: better coverage but more expensive
- Monitor symptomsL control thirst, regular Hb1AC monitoring
- Regular fundoscopy, diabetic foot exam and renal function tests
- Treatment of hypos with IM glucagon and glucose
- Screning and management of CVS risk factors
How does DKA happen?
Decreased insulin leading to increased gluconeogenic hormone release by the liver. This initially leads to massive glucose release and decreased uptake by tissues (leading to glucosuria and massive oliguria). Longer term, this leads to increased lipolysis and ketone generation. This leads to metabolic acidosis.
Common causes include infection, management errors, new diagnosis of diabetes, other medical causes or unidentified causes
What are the micro and macrovascular complications?
Diabetic retinopathy, nephropathy, neuropathy and diabetic foot
PVD, CAD, lacunar infarctions
What are the other complications of DM?
Infection susceptibility
Insulin side effects (weight gain, overdosage à nausea, side effects, hypoglycaemia)
Overdose symptoms can be masked by: B blockers, autonomic neuropathy, and adaptation to recurrent episodes
What does prognosis depend on?
Depends on glycaemic control
