Diuretics/raas/adh

Front 1

Xanathine Oxidase Inhibitor

Back 1

Allopurinol

Hint 1

Tx Tophagous gout. May precipitate acute gout attack on initiation of therapy.

Front 2

More specific Xanathine Oxidase Inhibitor

Back 2

Febuxostat

Hint 2

Less Hypersensitivity, but may cause cardiovascular adverse effects

Front 3

Mamalian recombinant uricase. IV infusion.

Back 3

Pegloticase

Hint 3

Pegylated. Rapidly reduction in serum urate. Oxidizes urate to alltoin.

Front 4

Impairs chemotaxis of granulocytes in gouty joints.

Back 4

Colchicine

Hint 4

acute tx or with probenecid. N/V in 30% of patients.

Front 5

High doses increase urate excretion, low urate reabsorption by competitive inhibition.

Back 5

Probenecid

Hint 5

ASA is contraindicated because it prevents actions on urate. Low dose produces paradoxical urate secretion. Can cause kidney stones. Uicosuric.

Front 6

If a patient is hypersensitive to Probenecid, this metabolite of phenylbutazone can be used.

Back 6

Sulfinpyrazone

Hint 6

MOA same as probenecid, more GI problems, less hypersensitivity. Uricosuric.

Front 7

Inhibition of Na/K/Cl pump and thus their reabsorption in the Thick Ascending Loop.

Back 7

Furosemide

Hint 7

Site 2. Acts only on tubular side of cell. DECREASES urinary excretion of Urate (competition) and Lithium (loss of Na+, a competitive inhibitor of Li+ reabsorption). CI in patients with Hyperlipidiemia.

Front 8

NKCC2 Blocker that is 4x as potent as furosemide. Useful in Diabetic patients or patients that are allergic to Fuorsemide.

Back 8

Bumetanide

Hint 8

Less Hyperglycemia.

Front 9

NKCC2 Blocker WITHOUT a sulfonamide group. Useful for patients that have sulfa allergies.

Back 9

Ethacrynic acid

Hint 9

High ceiling, site 2 diuretic. More GI problems, less hyperglycemia.

Front 10

Greater bioavailability and longer half life than furosemide permits once a day dosing.

Back 10

Torsemide

Hint 10

The Newest NKCC2 blocker.

Front 11

Drug interactions in common for all Site 2 Diuretics (Furosemide, Bumetanide, Ethacrynic acid, Torsemide)

Back 11

K+ loss; ASA/Ibuprofen decrease effectiveness; Propanolol concentration increased by Furosemide; Secreted organic acids, especially probenecid, reduce tubular concentration of furosemide.

Hint 11

Other uses besides for edema include, for Hypercalcemia (with Na+) and hypertension in patients with low renal blood flow.

Front 12

Site 3 Diuretics and their action.

Back 12

Hydrochlorothiazide, Chlorthalidone, Metolazone, Indapamide, Benthiazide, Chlorothiazide

Hint 12

Inhibit NaCl reabsorption at DCT site 3. Effect on NCC co-transporter. Does not lead to countercurrent washout and tend to decrease renal blood flow. Increases urinary excretion of K+, but NaCl diet restriction reduces the possibility of hypokalemia. Decreases urinary excretion of Ca+ (OPPOSITE of site 2 diuretics).

Front 13

Aldosterone receptor antagonist. Strong action in CHF or with liver disease. K+ protection.

Back 13

Spironolactone

Hint 13

K+ sparring. SE include hyperkalenmia.

Front 14

Mineralocorticoid receptor antagonist. K+ sparing.

Back 14

Eplerenone

Hint 14

Hyperkalemia

Front 15

Physiological antagonists of aldosterone, faster acting than spironolactone. Inhibit Na+ influx through channel. Dissipates transepithelial potential. Removes drive to transport K+ across cell.

Back 15

Amiloride and Triamterone

Front 16

Site 1 Diuretic. Carbonic Anhydrase inhibitor.

Back 16

Acetazolamide

Hint 16

Effective for tx of Glaucoma, and reduction of DSF volume. Treat mountain sickness.

Front 17

Renal vasodilator at low doses. Increases GFR. Increases renin production. Frequently combined with dobutamine in treating post-infarct patients with poor renal blood flow.

Back 17

Dopamine

Hint 17

Alters renal blood flow. Increases blood flow and GFR, and decreases countercurrent exchange.

Front 18

Osmotic Diuretics.

Back 18

Mannitol, Isosorbide.

Hint 18

Prevent water absorption in kidney, countercurrent washout via increased renal blood flow. Reduces intracranial and intra ocular pressures osmotically. Prophylaxis of acute renal failure. SE include HA, nausea and vomiting due to increased CSF osmolarity.

Front 19

3 Actions of Angiotensin

Back 19

1. Fast Pressor Response: Constricts areteriole smooth muscle, including renal arteries (causing decreases in GFR but increases FF), 2. Slow Pressor Response: Increases sympathetic outflow to the heart, blood vessels and JG cells, 3. Via AT-1 receptors, induces cardiac hypertrophy and the deposition of matrix proteins causing increased stiffening.

Front 20

Peptidyldipeptidase inhibitor (ACEi), and the only member of this group to contain a sulfhydryl group.

Back 20

Captopril

Hint 20

Hyperkalemia due to REDUCING ALDOSTERONE SECRETION. Very useful in diabetic nephropathy. CI for use with TRIAMTERENE or AMILOIRIDE. Helps prevent diuretic hypokalemia.

Front 21

Peptidyldipeptidase with a carboxyl rather than a sulfhydryl group. Bioavailability not affected by food.

Back 21

Enalapril

Hint 21

Fewer side effects than captopril.

Front 22

Longer acting, once a day dosage Peptidyldipeptidase. Also not affected by food.

Back 22

Lisinopril

Front 23

Angiotensin II receptor antagonist. Imidazole derivative.

Back 23

Losartan K (Cozaar)

Hint 23

Blocks AT-II binding to AT-1 receptors.

Front 24

Me, too ARB. Food markedly decreases absorption.

Back 24

Valsartan (Diovan)

Front 25

Non-peptide inhibitor of renin.

Back 25

Aliskiren (Tekturna)

Hint 25

SE Diarrhea and Hyperkalemia.

Front 26

Aldosterone agonists. Stimulate Na+ reabsorption, K+ secretion. Contributes to cardiac and vascular remodeling, vascular fibrosis and myocardial damage.

Back 26

Fludrocortisone (drug of choice), Deoxycorticosterone acetate (DOCA)

Hint 26

Tx is for Adrenal Insufficiency

Front 27

Aldosterone Receptor Antagonists. For CHF and Htn. One is more specific than the other (2 total here, one we've already seen).

Back 27

Spironolactone, Eplerenone (much more specific)

Front 28

MOA of ADH

Back 28

(1) V1a receptors on smooth muscle and brain tissue, causes contraction through PIP hydrolysis. (2) V2 receptors on the apical surface of tubular cells in the collecting ducts and DCT. Causes increased intracellular cAMP. (3) induction and transport of aquaporin II.

Front 29

Effects of ADH

Back 29

Vasoconstriction, Water abstraction, Decreased inner medullary blood flow, Increased thirst and salt apetite, Increased ACTH release, Increase production of Coagultion Factor VIII (i.e. off label use in Von Willebrand's Disease).

Front 30

Factors that increase ADH secretion

Back 30

(1) elevated serum osmolality. (2) decrease in extracellular volume. (3) angiotensin II. (4) clofibrate

Front 31

ADH agonist, intranasal administration, Acts on V2 receptors in the DCT and CD. used for Diabetes Insipidous, GI bleeding. (looking for two drugs here).

Back 31

Desmopressin (Stimate). Tannin Vasopressin (Pitressin).

Hint 31

interactions with clofibrate. Not useful in nephrogenic diabetes insipidous. Diabetes insipidous (pituitary) is due to a lack of ADH or a neurogenic mechanism. Nephrogenic DI is due to a mutation in ADH V2 receptors or Aq2.

Front 32

ADH Antagonist. Does NOT interfere with cAMP production. Interferes with water permeability.

Back 32

Demeclocycline.

Hint 32

For SIADH

Front 33

ADH Antagonist. Antagonizes ADH mediated increases in cAMP.

Back 33

LIthium

Hint 33

interferes with Aquaporin