Trachte drugs Flashcards
(41 cards)
What are the major loop diuretics?
Lasix (furosemide)
Bumetanide
Ethacrynic acid
If you have a sulfa allergy can you take Lasix?
No
What should you take if you have a sulfa allergy for a loop diuretic?
Bumetanide
What is a common side effect of long term Loop diuretic use? what should you give to compensate?
Hypomagnesium (We are blocking NKCC here which makes the interstium very positive and paracellularly pushes 20% of Mg through)
Give Mg2+
Hypocalcemia is rare
What does low salt in the interstium lead to?
Increase in Cox 2
-Which increases prostaglandins, increases RPF and GFR, which potentiates the drug
What are loop diuretics good to treat?
- Pulmonary edema
- Edema
- Hyperkale
- Acute renal failure
- Anion overdoes with Bromide, flouride and iodide
- Acute HF
- Ascites
What are the 5 common AE of loop diuretics?
- Hypokale (Na gets exchanged for K in the collecting duct)
- Hearing loss
- Lasix (allergy can lead to Acute interstitial nephritis)
- Hyperurecemia
- Contraction Alkalosis
What stimulates ADH secretion?
Increased osmolarity
Decreased volume
Why would we get hyperuricemia in loop diuretic pts?
Cauese hypovolumic state
- induces ADH secretion
- Cause upregulation of UT1 which leads to increase absorption of Urea!
What causes contract alkalosis in pts whom are on a loop diuretic?
Multifold:
- Increase in RAAS–> increase aldosterone which upregulates K+/H+ anti-porter in the alpha intercalated cell in the collecting duct
- Increased RAAS–> increased AgII leads to increase in Na+/H+ anti-porter in the PCT
both lead to increased H+ in the filtrate. Leading to an alkalosis.
What are the major Thiazide diuretics? What is their MOA?
- Chlorithalidone
- Hydrochlorothiazide
- Metalazone
- block NCC channel in DCT
What are some of the major uses of thiazides?
- HTN–> 1st line
- HF–> adjunctive treatment with 1st line Loopers
- Nephrolithiasis by Hypercalcemia
- Nephrogenic diabetes insipidus
- Osteoporosis
How do thiazides lead to hypercalemia?
There is an Na/Ca antiporter on the basolateral side of the endothelial cells. This is driven by concentration gradients.
- Since Thiazides block Na into cell this increase the pump
- Ca is going out of the cell and Na is coming in
- Increasing the pump thus decreases the intracellular Ca which leads to a greater conc. gradient
- Ca flows faster down the TRPV5 channel into the cell
- leads to hypercalcemia
- treats calcium related stones
Can one with a sulfa allergy take thiazides?
No
What are some major AE of Thiazides?
- Hyperglycemia
- Hyperuricemia
- Hypokale
- Hyperlipidemia–> 5-15% increase in LDL’s
- Hyponatremia
- allergic rxns
- Contraction alkalosis
- Lithium pt monitored
What causes the hyperglycemia in Thiazide use?
- There are potassium pumps on Beta-Cells in the pancreas
- When these are closed–> leads to more positive membrane potential inside cell which depolarizes and causes Calcium channels to open
- Calcium rushes and cause insulin vesicle release
- Sulfonyureas inhibit Potassium pumps
- Increases K+ intracellular
What are the 2 mechanisms of Potassium sparing diuretics?
- Inhibit aldosterone receptors
2. Inhibit Na exchange for K and H in the cortical collecting duct
What are the aldosterone inhibitors?
- Spironolactone (aldactone
2. Eplerenone (inspra)
What are the Na exchange inhibitors potassium sparring diuretics?
- Amiloride (Midamor)
2. Triamterene (Dyrenium)
What is Amiloride used to treat
Li+ induced nephrogenic diabetes insipitus
What is the MOA of Potassium sparing diuretics?
Blocks absorption of Na in the collecting duct for the exchange of K+
Where does aldosterone bind and what are its affects?
Intracellular SRE
- Increase K+ excretion
- Increase Na+ resorption
- Increase H+ excretion
- Upregulates Na/K ATPase of basolateral membrane
What is the MOA of Elperenone?
Mineralcorticol receptor antagonist
what is the MOA of Amlodipine?
inhibits ENAC thus decreases Na resorption
