Diuretics Flashcards
Osmotic diuretic:
Mannitol is an example of this.
What is the use of mannitol?
How does it work?
To lower ICP and intraocular pressure
Mannitol is an osmotic diuretic that is metabolically inert in humans and occurs naturally, as a sugar or sugar alcohol, in fruits and vegetables. Mannitol elevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma.
Loop diuretics:
Where do they act?
Give 2 examples - F, B
What cotransporter does it inhibit, therefore reducing water absorption due to lower solute concentration within the tubule?
What are they used in?
Side effects:
- Why does it cause hypokalaemia and metabolic alkalosis?
- Why do they get muscle cramps?
- Why are they more likely to get kidney stones?
- What part of the body is it toxic to?
Oedema (in HF or ascites)
Thick ascending loop of Henle (Hence LOOP diuretic)
Furosemide
Bumetanide
NaK2CL cotransporter
More unabsorbed Na reaches the distal tubule where Na is reabsorbed with the exchange of potassium and H+.
https://in.pinterest.com/pin/643944446691869326/
Diuretics often cause a loss of potassium, calcium, and magnesium, which can also cause cramps. - basically a loss of electrolytes - that is why athletes drink water with electrolytes to make sure their muscles don’t hurt
Due to increased calcium excretion - think about the anatomy
Less calcium is reabsorbed in the TA Loop of Henle
The ear - ototoxicity
Thiazide and thiazide-like diuretics:
Give an example of thiazide D? - B
Give an example of thiazide-like D? - C, I
It acts on the distal convoluted tubule. What cotransporter do they block preventing sodium reabsorption?
Side effects:
- Why do they get hypokalaemia?
- What other electrolytes is lowered?
- Why does it cause hypercalcaemia?
- Why should you be careful prescribing this to someone with gout?
- Why is it used in care with those who have DM?
Due to Na left in the DCT then NaK ATPase removes some in exchange for K.
Bendroflumethiazide
Chlorthalidone
Indapamide
NaCl cotransporter in the distal convoluted tubule
Because loop and thiazide diuretics increase sodium delivery to the distal segment of the distal tubule, this increases potassium loss (potentially causing hypokalemia) because the increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine.
Magnesium - same reason as below - affects all transporters in the DCT!
Thiazides enhance Ca reabsorption in the distal convoluted tubule, by increasing Na/Ca exchange (which makes thiazides useful in treating the calcium-subtype of kidney stones).
It reduces uric acid excretion
Glucose tolerance impaired - MOA unknown
Potassium-sparing diuretic:
IT IS CALLED POTASSIUM-SPARING AS IT STOPS THE LOSS OF POTASSIUM WHICH THE OTHER DIURETICS DON’T DO!!!!
It has mechanisms of action!!
Amiloride:
- Where does it act?
- What transporter does it inhibit?
Spironolactone:
- What hormone does it inhibit that prevents sodium reabsorption, therefore, lowering BP?
What electrolyte is likely to increase?
Why do men get gynecomastia with spironolactone?
DCT
ENaC - this absorbs sodium so amiloride prevents reabsorption - K is not involved so it is saved!
Aldosterone which acts on the NaK ATPase and ENac
Hyperkalaemia - USUALLY - The pump acts to re-absorb sodium and water in exchange for potassium, which is then eliminated in the urine. If this doesn’t happen, then more potassium is ‘SAVED.’
Due to spironolactone’s oestrogenic effects
General side effects:
What is the main one? - Think Grandma!!
URINARY FREQUENCY
Useful info:
https://www.cvpharmacology.com/diuretic/diuretics
https://www.cvpharmacology.com/diuretic/diuretics
