Clinical Endocrinology Flashcards
Type 1 diabetes
destruction of pancreatic beta cells - cannot get insulin released
- immune reaction
- usually occurs in children
Main actions of insulin
Activates stimulates the GLUT4 transporter to get -Glucose uptake into muscle and adipose tissue -glycolysis -glycogen synthesis -protein syntehsis -uptake of ions
Inhibits
- Gluconeogensesis (making glucose)
- Glycogenolysis (breakdown of glycogen)
- Lipolysis (breakdown of fat)
- Ketogenesis (breakdown of ketones)
- Proteloysis (breakdown of protein)
How are ketones made
When there is no glucose left in blood or body, then fat can be broken down into ketone bodies
-is stimulated by glucagon (when there is low blood sugar)
What happens when there is an insulin deficiency?
- get activated lipolysis, and increase plasma FFA - increase liver fatty acids
- if have excess glucagon same thing can happen
- overall can get accelerated ketogenesis
-this could be bad if there already is glucose because dont need to make more
Ketones - acetoacetate, acetone, beta hydroxybutyrate
What happens in mitochondria
-free fatty acids get broken down to acetyl coa and then ketones
What can happen to the anion gap when there is ketoacidsos
- beta hydroxybutyric acid and acetoacetic acid can dissocaite
- get an excess of H+ and decrease of HCO3-
- this will increase the anion gap (metabolic acidosis)
what happens when b-hydroxybutyric acid is dissociated
and what do we give?
- H+ is converted to co2 and h2o
- na-beta hydroxybutyrate and cl- is left over
- na-b-hydroxybutyrate is lost in urine
- however cl remains in ECF
- Na is lost in the urine
- and can give NACL
- however can get hyperchloraemia afterwards
How can we test for acetoacetate in urine?
- ketone strips used
- if reagent contains glycine then will go purple
- does not detect beta hydroxybutyrate
Criteria to diagnose diabetic ketoacidosis
- hyperglycaemia
- low bicarb
- ketonuria
- low pH
What are the two things that DKA requires
-stress and lack of insulin and fat
Feedback controls for Potassium
Feedback - slow and overshoot (raise in ecf, get increase secretion)
Feedforward - sensors in gut - can then get increase potassium excretion (so we dont die from one meal)
How does insulin effect K?
after a meal
-insulin will stimulate Na/K atpase pump and get more K uptake into cells
How does aldosterone effect K?
- increase K uptake by cells
2. increases potassium secretion from kidney vis Na/K atpase pump, and get more Na absorebd
Other controls of potassium ?
B2 adrenergic stimulation - gets K from ECF–> ICF so get vasodilation
- acidosis - get increase potassium extracellularly, because H and K compete for going into cell so in acidosis get H plus excreted and more going into cell and more K plus absorbed and out of cell
- exercise promotes release of potassium from muscle
- beta blockers - increase serum potassium
- diabetes - have high blood sugar, and get increase ecf osmolarity, brings water out of cells - so get an increase in potssium conc in icf and increase in ecf
Where is potassium absorbed and secreted?
early reabsorption (proximal tubule), late secretion (DCT and collecting duct)
- max secretion can be greater than GFR
- kidney is slow to conserve K
- K depletion with hypokalemia can result when K intake is restricted
