Diagnosis of Diabetes Flashcards
What is the definition of diabetes?
A metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbance in carb/protein/fat metabolism resulting from defects in insulin secretion/action or both.
What are the symptoms of diabetes?
- Polyuria,
- Nocturia,
- Thirst,
- Polydipsia,
- fatigue,
- Change in weight,
- Blurring of vision,
- Genital candidiasis,
- Nausea,
- Vomiting,
- Headache,
- Hyperphagia,
- Mood changes
What is the diagnostic criteria for diabetes?
- Fasting glucose >7mmol/L,
- Random plasma glucose .11.1mmol/L,
- HbA1c .6.5% or 48mmol/mol.
- Either one abnormal value if symptomatic or two if asymptomatic
What may cause a false low HbA1c and what may cause a false high HbA1c?
Low - Sickle cell anaemia or pregnancy (anything that shorted RBC lifespan)
High - Splenectomy or anything that increases red cell life span
What are some different types of diabetes?
- Type 1 (Immune pathogenesis and severe insulin deficiency)
- Type 2 (combination of insulin resistance and deficiency)
- Gestational
- Genetic defects of beta cell function,
- Pancreatic disease and more
Explain the pathophysiology of DKA
With absolute insulin deficiency there is increased lipolysis which increases free fatty acids and glycerol which increases ketogenesis which causes metabolic acidosis
Explain the pathophysiology oh hyperosmolarity in diabetes
- With insulin deficiency there is increased glycogenolysis and gluconeogenesis which causes hyperglycaemia. This causes glycosuria, osmotic diuresis and dehydration which can cause hyperosmolarity.
What is the best investigation for DKA?
Blood testing strips to detect beta hydroxybutyrate as ketonuria/ketonaemia can be found after exercising, repeated vomiting or eating a ketogenic diet.
What do the following capillary ketone values suggest?
- <0.6mmol/L
- 0.6-1.5mmol/L
- 1.5-3.0mmol/L
- >3.0mmol/L
- <0.6mmol/L = normal
- 0.6-1.5mmol/L = metabolic control deteriorating
- 1.5-3.0mmol/L = high risk of DKA, seek medical advice.
- > 3.0mmol/L = suggests DKA
What is the difference between hyperosmolar hyperglycaemic state and DKA?
HHS - Type 2 diabetes, older age, duration of onset is days to weeks, abdo pain uncommon, more volume depleted and relative insulin deficiency.
DKA - Type 1 diabetes, younger age, presetns within hours to days, abdo pain is common and they have absolute insulin def
What is the definition of DKA?
- Hyperglycaemia and hyperketonaemia/ketonura 2+ and metabolic acidosis (bicarb <15 or pH <7.3)
What is the definition of hyperosmolar hyperglycaemia state
- Hyperglycaemia (usually >30mmol/L) and hyperosmolality ( >320mOsm/kg) without significant ketonaemia/ketoneuria or metabolic acidosis
What is the pathogenesis of type 1 diabetes
- Autoimmune destruction of insulin producing beta cells in islets of Langerhans.
- Genetic susceptibility + environmental trigger (viral infection, diet/diet toxin, vitamin D def or immune checkpoint inhibitors)
What are the autoimmune markers associated with T1DM?
- Anti-GAD,
- Anti-IA-2,
- Anti-ZnT8
What is a useful marker of endogenous insulin secretion?
C-peptide as it is cleaved from pro-insulin to form insulin. Useful as it is not a constituent of synthetic insulin.
- can be measured in blood or urine but needs paired blood glucose.
- <200mmol/L is seen in T1D, pancreatic diabetes and MODY. Shows severe insulin deficiency.
- >900mmol/L due to increased insulin because of resistance so seen in T2.
Compare type 1 and type 2 diabetes
Type 1 - Age of onset under 40, family history of diabetes is less common, autoimmune disease, ketoacidosis is common, c peptide is less than 200 and autoantibodies are +ve, other autoimmune diseases are common.
Type 2 - Age onset over 50, usually overweight, family history is more common, ketoacidosis is uncommon, there is partial insulin def but resistance, C peptide is usually over 900 and negative for autoantibodies
Describe features of pancreatic diabetes
- Can be caused by pancreactectomy, pancreatitis, haemochromatosis, carcinoma or CF.
- Higher risk of hypos than in T1D due to loss of alpha cells that produce glucagon,
- May have ketones and acidosis,
- C peptide is low/undetectable,
- Pancreatic autoantibodies are negative,
- Treat with SU and insulin
What is MODY?
Maturity onset diabetes of the young. It is an autosomal dominant mutation in HNF1-A that presents under age 25. Managed by diet, sulphonylureas or insulin