Endocrinology Flashcards
Outline the homeostatic mechanism behind control of elevated blood glucose.
Insulin is produced by beta cells in the Islets of Langerhans in the pancreas, causing a reduction in blood sugar.
It causes cells to:
- Absorb glucose from the blood and use it as energy (glucolysis)
- Store glucose as glycogen in the liver and muscle cells (glycogenesis).
Outline the homeostatic mechanism behind control of decreased blood glucose.
Glucagon is produced by alpha cells in the Islets of Langerhans in the pancreas, causing a rise in blood glucose.
It causes the liver to:
- Break down stored glycogen into glucose (glycogenolysis).
- Convert fats and proteins into glucose (gluconeogenesis).
Outline the mechanism behind ketogenesis.
In prolonged fasting, there is insufficient supply of glucose and glycogen stores are exhausted.
The liver takes fatty acids and converts them to ketones, which can be used as fuel.
Ketones can dissociate into a conjugate acid and base, causing an acidosis.
What is Type 1 diabetes mellitus (T1DM)?
An autoimmune disease where the alpha cells in the Islets of Langerhangs in the pancreas are targeted, reducing the capacity to produce insulin.
This means cells cannot take up glucose, so the level of glucose in the blood rises to cause hyperglycaemia.
Presentation of Type 1 diabetes mellitus.
Triad of hyperglycaemia:
- polyuria
- polydispsia
- weight loss
DKA is the presentation in up to 50% of new diagnoses.
Other less typical presentations include secondary enuresis and recurrent infections.
T1DM aetiology.
- autoimmune
- genetic
- infective trigger
When a new diagnosis of T1DM, what additional bloods should be considered?
Baseline bloods including FBC, U&E and laboratory glucose.
Blood cultures if suspected infection (i.e. fever).
HbA1c
TFTs and TPO to test for associated autoimmune thyroid disease.
anti-TTG and serum IgA to test for associated coeliac disease.
Which antibodies are associated with T1DM?
- insulin antibodies
- anti-GAD antibodies
- islet cell antibodies
General management of T1DM.
Manage via a multidisciplinary team:
- s/c insulin regimes
- dietary carbohydrate intake monitoring
- monitor blood sugar levels on waking, at each meal and before bed
- monitor for and manage complications
Usual insulin prescription in T1DM.
Basal Bolus regime.
Basal refers to an injection of a long acting insulin, typically in the evening.
Bolus refers to an injection of a short acting insulin, typically three times a day before meals.
When is an insulin pump considered in the management of T1DM?
- age >12 years
- difficulty controlling HbA1c
Advantages of insulin pumps.
- better blood sugar control
- more flexibility with eating
- less injections
Disadvantages of insulin pumps.
- difficulty learning to use the pump
- attached all the time
- blockages in the infusion set
- risk of infection
What are the short term complications of T1DM?
- hypoglycaemia
- hyperglycaemia
- DKA
Symptoms of hypoglycaemia.
- hunger
- tremor
- sweating
- irritability
- dizziness
- pallor
Severe hypoglycaemia will lead to reduced consciousness, coma and death.
Treatment of hypoglycaemia.
A combination of rapid acting glucose (e.g. lucozade) and slower acting carbohydrates (e.g. biscuits, toast).
Treatment of severe hypoglycaemia.
IV 10% dextrose if a cannula is in situ.
Otherwise IM glucagon.
Causes of hypoglycaemia.
- insulin overdose
- carbohydrate malabsorption (e.g. vomiting, diarrhoea)
- hypothyroidism
- growth hormone deficiency
- liver cirrhosis
- alcohol
Treatment of hyperglycaemia.
Increase the insulin dose.
It can take several hours to take effect and repeated doses could lead to hypoglycaemia.
Triad of DKA.
- acidosis (pH <7.3; bicarbonate <15mmol/L)
- ketonaemia
- blood glucose >11mmol/L
What are the three key complications of DKA that lead to death?
- Cerebral oedema
- Hypokalaemia
- Aspiration pneumonia
Pathophysiology of DKA.
Absolute deficiency of insulin in T1DM leads to a rise in glucagon.
Under the action of glucagon, the rate of gluconeogenesis and lipolysis increased. The catabolism of adipose tissue results in rising levels of acidic ketone bodies.
The hyperglycaemia and glycosuria causes osmotic diuresis, resulting in dehydration.
Risk factors for DKA.
Lack of insulin:
- non-compliance with insulin treatment
- device failure
- changing insulin requirements during puberty
An excess of glucose:
- increased ingestion of glucose
Intercurrent illness (ie. infection)
Symptoms of DKA.
- lethargy
- N+V
- abdominal pain
Background hx of T1DM symptoms or diagnosis:
- weight loss
- polyuria
- polydipsia