ChemPath - Diabetes Cases Flashcards
What is needed for a diabetes diagnosis
Symptoms + 1 test result
Asymptomatic + 2 test results
What are the thresholds for diagnosing impaired glucose tolerance and diabetes mellitus
Diabetes
Fasting > 7
Random >11.1
OGTT 2h >11.1
HbA1c > 48 (6.5%)
Impaired
Random 7.8-11.1
HbA1c 40-48
What is the formula for osmolality
2(Na+K)+ U+G
What is the formula for anion gap
Na+K−Cl−bicarb
What is the osmolar gap
measured osmolarity – calculated osmolarity:
Measured (frozen plasma)
Normal <10
If >10 = unaccounted ions → should check anion gap to see if these are charged ions
What can cause a high anion gap
Presence of other anions in the blood
Ketones - DKA
Ethylene glycol poisoning (anti-freeze)
Methanol
Ethanol
Lactate
Metformin
What is the role of calcium in hyperventilation
pH increases → plasma protein stick to calcium → plasma calcium becomes unionised → less free ionised calcium (although plasma calcium appears normal) → tetany from hypocalcaemia → more hyperventilation
What abnormalities does hyperosmolar hyperglycaemic state (HHS) cause
High osmolality (pt is very dehydrated)
Acidosis
What is the management for hyperosmolar hyperglycaemic state (HHS)
0.9% saline (500-1,000mL/hour) slowly
What cautions do you have to take in treating hyperosmolar hyperglycaemic state (HHS)
Do not give fluids too quickly → lots of fluid quickly cerebral oedema and death
Do not give insulin immediately (as insulin will pull glucose into cells and dehydrate them even more)
What is the Cori cycle and why does it explain how lactic acidosis occurs with metformin overdose
The metabolic pathway by which lactate is produced by anaerobic glycolysis in the muscles
- Lactate moves to the liver and is converted to glucose
- Glucose returns to the muscles and is metabolised to lactate
Metformin inhibits hepatic gluconeogenesis → excess lactate
The excess lactate is usually cleared by the kidneys, but in pts with renal failure, the kidneys cannot handle the excess lactic acid
Explain how COPD patients develop respiratory acidosis
CO2 is a potent stimulus for respiration
As the lungs slowly fail, there is less CO2 breathed out → CO2 levels increase
High CO2 → high stimulation the breathe → CO2 is breathed out
Pink puffers are sensitive to the raised CO2 and continue to hyperventilate
Eventually the brain becomes less responsive to CO2 → you become a blue bloater where you do not hyperventilate but CO2 continues to rise
What is the role of alanine-aminotransferase (ALT)
Transfers an amine group away from alanine and the amine group becomes urea
The rest of the molecule feeds into gluconeogenesis
Therefore for gluconeogenesis to occur, this enzyme must be produced and activated i.e. during starvation
It should be within the hepatocytes
Describe the synthesis and circulation of bile salts
- Unconjugated bilirubin is produced from the break down of RBCs
- Bilirubin is metabolised in the liver to produce conjugated bilirubin
- CB is stored in the gall bladder, which secretes CB into the duodenum
- 90% of bile salts are absorbed in the ileum
- Bacteria in the SI convert a small amount of bilirubin into urobilinogen → urine
- 10% of the bile salts are lost in faeces, and the rest of the bilirubin is in the faeces as stercobilinogen
What are the clinical features of obstructive jaundice
Pale stools and dark urine
Scratch marks due to presence of bile salts
Bile salts and bile acids present in the blood
Urobilinogen negative (as bilirubin is not reaching the gut bacteria)
