Renal Flashcards
Osmotic Diuretics: MOA: increases renal tubular filtration. Clinical use: used to lower IOP and ICP. Contraindicated in Px with CHF or Anuria.
Mannitol
Which receptor can be stimulated to increase the release of Renin?
Beta 1 receptor
MOA: inhibits Na/K/2Cl in the thick ascending loop of Henle. Stimulates the release of PGE –> action inhibited by NSAIDs. Clinical use: Acute pulmonary edema. SE: Ototoxicity, hypokalemia, dehydration, sulfa-drug allergy, interstitial nephritis, and Gout.
Loop Diuretics: Furosemide (contains sulfur)
Ethycrynic Acid (does not contain sulfur)
MOA- inhibits carbonic anhydrase in proximal convoluted tubule. Causes increased bicarbonate in the lumen (so you pee it out). Clinical uses: acute mtn sickness and metabolic alkalosis. SE: metabolic acidosis and sulfa drug allergy.
Carbonic anhydrase inhibitor: Acetazolamide
What is the first line drug used for the treatment of Gout? What is the second line treatment?
For chronic Gout (2)?
First line: Endomethacin
Second line: Colchicine
Chronic: Probenacid (prev. UA reuptake) and Allopurinol (Xanthine oxidase inhibitor)
Clinical use: hypertension, CHF, calcium stones (still get them, but less stones), nephrogenic diabetes insipidus (it decreases diluting capacity of the kidney-urine becomes more concentrated). SE: hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, hypokalemic metabolic alkalosis, hyponatremia (thus cells are more likely to depolarize). Describe MOA:
Thiazide Diuretics - Hydrochlorothiazide
MOA: Inhibits Na/Cl Reabsorption in early distal convoluted tubule.
***nephrogenic DI –> not responding at the nephron, vs. neurogenic…
MOA: competitive antagonist of Aldosterone Receptor in the Cortical Collecting Tubule. Clinical use: hyperaldosteronism, CHF. SE: hyperkalemia–> possible arrhythmias.
Spironolactone - treatment for hirsutism as it has anti-androgenic effects, gynecomastia.
MOA: Inhibits Na channels in the Cortical Collecting Tubule. Clinical use: hyperaldosteronism, CHF, K+ depletion. SE: hyperkalemia –>can cause arrhythmias.
Name both drugs:
Potassium Sparing Diuretics- Triamterene/Amiloride
MOA: Inhibit Angiotensin Converting Enzyme (therefore decreases Angiotensin II). Also prevents bradykinin, decreased GFR (no constriction of efferent arteriole). Clinical use: CHF, hypertension, renal disease due to diabetes. SE: cough, angioedema, teratogen (fetal renal abnormalities), hypotension, hyperkalemia, increased creatinine (decreased GFR). 3 drugs:
Ace Inhibitors: Captopril, Enalapril, and Lisinopril.
***Most of the drugs that end in -pril.
MOA: Block Angiotensin II Receptor - action similar to ACE inhibitors. These drugs do NOT increase kallikrein. Clinical use: Hypertension, CHF, Renal disease due to diabetes. SE: least amount of side effects, but similar to ACE inhibitors (except no cough, no angioedema-due to not increasing kallikrein). This drug is also a teratogen.
Angiotensin Receptor Blocker- Candesartan–> most drugs that end in -sartan.
***Sweet as CANDY-sartan, thus has less side effects.
What is the mechanism of action of an ACE inhibitor?
Inhibits Angiotensin Converting enzyme –> therefore decreases angiotensin II. Also decr. GFR and prevents bradykinin.
Where do potassium sparing diuretics work on?
Cortical collecting tubules - inhibits Na channels.
Where do drugs like Furosemide and Ethycrynic acid work on?
Loop of Henle - inhibits Na/K/2Cl
Where do carbonic anhydrase inhibitor drugs work on?
Proximal convoluted tubule
Where do thiazide diuretics work on?
Early distal convoluted tubule - inhibits Na/Cl- resorption.
