S3 Group work

Question 1

GW:

• Which electrolyte, particularly, do you need to monitor when prescirbing ACEi, ARBs etc…
• How can ACEi manage CHF?
• Compare the action of Thiazide and Loop Diuretics?
• Why isn’t then loads of Na reabsorbed at DCT (with loop diuretic)? Picked up by macula densa and then activate RAAS?
• Why do both loop and thiazide like diuretics cause hypokalaemia?

Answer 1

• K+ (hyperkalaemia)
• ACEi - reduce hypertension
  Reduce preload and afterload, so reduce workload of the heart -> improve heat failure
• Thiazide: DCT. NaCl
  Loop Diuretics: Loop of Henle. More powerful. Na/2K/Cl.
  More potent because - Reabsorbs more Na+ in the loop compared to the DCT, so if you block it at the loop, will stop more Na reabsorption, so more powerful.
• Compacity: Only a maximum amount of Na can be reabsorbed at DCT (e.g. only a certain number of channels etc).
  yes - pick up by RAAS, but net effect, still lower blood pressure
• Increase in Na+ in the tubules (as less is reabsorbed). More Na+ is then moved through ENaC in collecting duct. This increases the positive charge in the collecting duct cells. This then causes ROMK to be upregulated to balance the positive charge build up in the cell. This means that more K+ is excreted.

Question 2

Causes of secondary hypertension?

See notion for more information

Answer 2

Renal artery stenosis, acromegaly, cushing’s