Endocrine Flashcards
What is the function of insulin?
- Suppress hepatic glucose output
- Increase glucose uptake into insulin sensitive tissues
- Suppress lipolysis and breakdown of muscle
What is the function of glucagon?
- Increase hepatic glucose output
- Reduce peripheral glucose uptake
- Stimulate peripheral release of gluconeogenic precursors
- Gluconeogenic precursors = glycerol and AA’s which cause lipolysis and muscle glyconeolysis and breakdown
Define Type I DM
Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency
Epidemiology of Type I DM
- Presents age 5-15
- Accounts for 10% of all diabetes
Risk factors of Type I DM
- HLA DR3-DQ2 or HLA DR4-DQ8
- Northern European
- Autoimmune disease - 90%
Pathophysiology of Type I DM
- Autoantibodies attack Beta cells in Islets of Langerhans
- Creates insulin deficiency
- Leads to hyperglycaemia
- Continuous breakdown of glycogen from liver (gluconeogenesis)
- Leads to glycosuria
Signs and symptoms of Type I DM
- Classic triad = polydipsia, polyuria, weight loss (BMI<25)
- Possible ketosis
Diagnosis of Type I DM
Random plasma glucose > 11mmol/L
Fasting plasma glucose > 7 mmol/L
Treatment of Type I DM
- Insulin
- Short acting insulin (4-6h)
- Longer acting insulin (12-24h)
Aetiology of Type II DM
- gradual insulin resistance/pancreatic beta cells fail to secrete enough insulin OR BOTH
- Cushing’s
- Chronic pancreatitis
Risk factors of Type II DM
- Lifestyle - obesity, exercise, excess calorie/alcohol
- Asian men
- > 40 yrs
- Hypertension
Signs and symptoms of Type II DM
- Polydipsia
- Polyuria
- Glycosuria
- Central obesity
- Slow onset
- Blurred vision
Diagnosis of Type II DM
- Fasting plasma glucose > 7 mmol/L
- Random plasma glucose > 11 mmol/L
- HbA1c > 48 mmol/L
Treatment of type II DM
1st line = lifestyle changes
2nd line = Medications
-Metformin
- If HbA1c remains high; dual therapy of Metformin AND:
-DPP4 inhibitor
-Sulphonylurea
-Pioglitiazone
-If still high triple therapy = above + insulin
Define Diabetic Ketoacidosis (DKA)
Complete lack of insulin -> high ketone production
Aetiology of DKA
- Untreated/undiagnosed T1DM
- Infection/illness
Pathophysiology of DKA
- Absence of insulin -> uncontrolled catabolism -> unrestrained gluconeogenesis and decreased peripheral glucose uptake -> hyperglycaemia
- Hyperglycaemia -> osmotic diuresis -> dehydration
- Peripheral lipolysis for energy -> FFAs in circulation increase -> FFAs turned to Acetyl CoA -> ketone bodies -> acidosis
Signs of DKA
- Kussmaul’s breathing
- Pear drop breath
- Hypotension
- Tachycardia
Symptoms of DKA
- N&V
- Weight loss
- Reduced mental state
- Lethargy
- Abdominal pain
Diagnosis of DKA
- Random plasma glucose > 11 mmol/L
- Plasma ketones > 3 mmol/L
- Blood pH < 7.35 / bicarb < 15 mmol/L
- Urine dipstick: glycosuria & ketonuria
- Serum U&E: Raised urea and creatinine
Treatment of DKA
- ABC management
- 0.9% saline IV
- IV insulin
- Restore electrolytes
Define Hyperosmolar hyperglycaemic state (HHS)
- Marked hyperglycaemia
- Hyperosmolality
- Mild/no ketosis
Aetiology of HHS
- Untreated/undiagnosed T2DM
- Infection/illness
Pathophysiology of HHS
- Low insulin -> increased gluconeogenesis -> hyperglycaemia but enough insulin to inhibit ketogenesis
- Hyperglycaemia -> osmotic diuresis -> dehydration