Endo Flashcards
Addison’s disease: recall the synthesis of adrenocortical steroids
There’s three arms:
Mineralocorticoid arm: aldosterone
Glucocorticoid arm: Cortisol
Sex steroids (although majority of sex steroids are created in gonads, it is important to remember that a small proportion are produced in the adrenal gland, as adrenal disorders will disrupt this balance)
List the clinical features of Addison’s disease
Posteral hypotension - lack of aldosterone (regulates blood pressure as we stand up)
Pigmentation in mucous membranes, pigmentation of scars - lots of ACTH means lots of pre-cursor POMC
Vitiligo - destrucion of melanocytes, means patient is prone to autoimmune disease
List specific features of Addison’s disease
Extreme fatigue Vomiting Weight loss Postural hypotension Hyponatraemia Hyperkalaemia
Congenital adrenal hyperplasia: explain the hormonal consequences of specific adrenal enzyme deficiencies,
No aldosterone, no cortisol
Excess of sex steroids
Congenital adrenal hyperplasia: explain the clinical features and investigation of congenital adrenal hyperplasia with reference to specific enzyme deficiencies.
Virilisation due to excess sex steroids
Salt-losing addisonian crisis
Death after 24 hours
Measure levels of 17α-hydroxyprogesterone for diagnosis
What do you do when a patient shows up with an Addisonian crisis?
First thing: intravenous saline solution
Second thing: Intravenous hydrocortisone
Third thing: Dextrose
What’s the definition of Type I and Type II diabetes?
Type 1: complete lack of insulin
Type 2: relative lack of insulin and insensitivity
Explain the basis of the immunological mechanisms responsible for b-cell loss.
The immunological destruction of islet cells is relapse-remitting (meaning it worsens over time). Reaches a “honeymoon phase” which is the last time islet cells produce a non-hyperglycaemic response.
Alleles HLA-DR3 and HLA-DR4 deletions pose a significant risk to chance of getting T1DM. HLA-DR1 and DR5 slight risk,.
What are the principles of insulin treatment in type 1 diabetes?
In healthy individuals, there is always a basal level of insulin so this means two types of treatment are needed:
- Background level of insulin (long-acting)
- Increased doses when meals are had (short-acting, can be human or analogue)
Insulin pumps or islet cell transplantation (requires life-long immunosuppressants)
Capillary monitoring for insulin levels can also be done by a permanent pump or constant finger-pricks.
Explain the physiology of diabetic ketoacidosis.
! A feature of T1DM ! (In T2DM, insulin production is sufficient to supress ketone production. CAN happen in T2DM)
Lack of insulin -> breakdown of muscles to produce ketone bodies -> excess of ketones acetoacetate and hydroxybutarate
Outline treatment of diabetic ketoacidosis.
Intravenous fluids and insulin.
Explain the physiology of hypoglycaemia.
Defined as a glucose level of less than 3.6 mmol/litre and is a consequence of TREATING diabetes. Too little glucose present, will start to impair mental processes ar 3 mmol and consciuousness at 2 mmol
Due to eating too infrequently, too little or alcohol or an inappropriate insulin regime.
Outline the treatment of hypoglycaemia.
Glucose (as tablets or solution), then long-term complex carbohydrate to maintain blood glucose levels
What are the actions of insulin?
Inhbits protein breakdown and amino acid transport to liver.
Inhibits glycerol transport from adipocytes to liver.
Promotes glucose entering muscle.
This means a lack of insulin promotes protein breakdown in muscles and glycerol transport out of adipocytes = cachexia and weight loss.
What are the signs and symptoms of hypoglycaemia?
Increased autonomic activation: Palpitations. Tremor. Sweating. Pallor/cold extremities. Anxiety.
Impaired CNS functions:Drowsiness, confusion and altered behaviour. Coma.
