Jeef First Aid Renal Part 1-9

Front 1

193. Dialysis cysts?

Back 1

a. Cortical and medullary cysts resulting from long-standing dialysis.

Front 2

194. Simple cysts of kidney?

Back 2

a. Benign, common (>40% of elderly)
b. Incidental finding.
c. This, nonenhancing, cortical, fluid filled.

Front 3

195. Medullary cystic disease?

Back 3

a. Medullary cysts sometimes lead to fibrosis and progressive renal insufficiency with urinary concentrating defects.
b. Ultrasound shows SMALL kidney.
c. Poor prognosis.

Front 4

196. Mannitol MOA?

Back 4

a. Osmotic diuretic
b. ↑ tubular fluid osmolarity, producing ↑ urine flow.

Front 5

197. Clinical use of Mannitol?

Back 5

a. Shock
b. Drug overdose
c. ↑ ICP or intraocular pressure

Front 6

198. Mannitol toxicity?

Back 6

a. Pulmonary oedema
b. Dehydration

Front 7

199. When is mannitol contraindicated?

Back 7

a. Anuria
b. CHF.

Front 8

200. MOA of Acetazolamide?

Back 8

a. Carbonic anhydrase inhibitor.
b. Causes self-limited NaHCO3 diureses and reduction in total-body HCO3 stores.

Front 9

201. Clinical use of acetazolamide?

Back 9

a. Glaucoma
b. Urinary alkalinization
c. Metabolic alkalosis
d. Altitude sickness.

Front 10

202. Toxicity of acetazolamide?

Back 10

a. Hyperchloremic metabolic acidosis
b. Neuropathy
c. NH3 toxicity
d. Sulfa allergy.
e. “ACIDazolamide causes ACIDOSIS”.

Front 11

203. Furosemide MOA?

Back 11

a. Sulfonamide loop diuretic.
b. Inhibits cotransport of Na-K-2Cl of thick ascending limb.
c. Abolishes hypertonicity of medulla, preventing concentration of urine.
d. ↑ Ca2+ excretion. Loops Lose Calcium.

Front 12

204. Clinical uses of furosemide?

Back 12

a. Oedematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary oedema)
b. HTN
c. Hypercalcemia

Front 13

205. Toxicity of Furosemide?

Back 13

a. Oto and renal (interstitial nephritis- bc it’s a sulfonamide derivative)
b. Hypokalaemia
c. Allergy (sulfa)!!!!
d. Gout
e. Dehydration

Front 14

206. Ethacrynic acid MOA?

Back 14

a. Phenoxyacetic acid derivative (NOT a sulfonamide).
b. Essentially same MOA as furosemide.

Front 15

207. Clinical use of Ethacrynic acid?

Back 15

a. Diuresis in pts allergic to sulfa drugs.

Front 16

208. Tox of ethacrynic acid?

Back 16

a. Similar to furosemide but can be used in pts w/hyperuricemia and acute gout (never used to treat gout).

Front 17

209. HCTZ MOA?

Back 17

a. Inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron.
b. ↓ Ca excretion (so retains calcium).

Front 18

210. Clinical use of HCTZ?

Back 18

a. HTN
b. CHF
c. Idiopathic hypercalciuria
d. Nephrogenic diabetes insipidus.

Front 19

211. Tox of HCTZ?

Back 19

a. Hypokalemic metabolic alkalosis
b. Hyponatremia
c. Hyperglycemia
d. Hyperlipidemia
e. Hyperuricemia
f. Hypercalcemia.
g. Sulfa allergy.

Front 20

212. K+ sparing diuretics listed (4)?

Back 20

1. Spironolactone
2. Triamterene
3. Amiloride
4. Eplerone

Front 21

213. MOA of Spironolactone?

Back 21

a. Competitive aldosterone receptor antagonist in the cortical collecting tubule.

Front 22

214. How does the MOA of Triamterene and amiloride differ from Spirinolactone?

Back 22

a. They act at the same part of the tubule by blocking Na channels in the CCT.

Front 23

215. Clinical use of spironolactone?

Back 23

a. Hyperaldosteronism
b. K+ depletion
c. CHF

Front 24

216. Tox of Spironolactone?

Back 24

a. Hyperkalemia- arrhythmias
b. Gynecomastia
c. Impotence

Front 25

217. Effect of all diuretics on Urine NaCl?

Back 25

a. All diuretics ↑ urine NaCl.
b. Serum NaCl may ↓ as a result.

Front 26

218. Effect of all diuretics except for K-sparing on urine K+?

Back 26

a. All ↑ urine K (save for K sparing).
b. Serum K may ↓ as a result.

Front 27

219. Which diuretics ↓ blood pH (causing acidemia)?

Back 27

a. Carbonic anhydrase inhibitors- HCO3- reabsorption.
b. K+ sparing aldosterone blockade prevents K+ and H+ secretion.
c. Additionally, hyperkalemia leads to K+ entering all cells (via H+/K+ exchanger in exchange for H+ exiting cells.

Front 28

220. Which diuretics ↑ pH (causing alkalemia)?

Back 28

a. Loop diuretics and thiazides cause alkalemia through several mechanisms:
1. Volume contraction: ↑ ATII-> ↑ Na/H+ exchanger in proximal tubule -> ↑ HCO3 (“contraction alkalosis”.
2. K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells.
3. In low K+ state, H+ (rather than k+) is exchanged for Na in cortical collecting tubule, leading to alkalosis and “paradoxical aciduria”.

Front 29

221. How do Loops ↑ urine Ca?

Back 29

a. Abolish lumen-positive potential in thick ascending limb-> ↓ paracellular Ca2+ reabsorption -> hypocalcemia and ↑ urinary Ca2+.

Front 30

222. How do thiazides ↓ urine Ca?

Back 30

a. Volume depletion -> ↑up-regulation of sodium reabsorption -> enhanced paracellular Ca reabsorption in proximal tubule and LOH.
b. Thiazides also block luminal Na/Cl cotransport in distal tubule ->↑ Na+ gradient -> ↑ interstitial Na/Ca exchange -> hypercalcemia.

Front 31

223. MOA of ACE inhibitors?

Back 31

a. Inhibit ACE, reducing levels of AG II and PREVENTING INACIVATION of bradykinin, a potent vasodilator.
b. Renin release is ↑ due to loss of feedback inhibition.

Front 32

224. Clinical uses of ACE inhibitors?

Back 32

a. HTN
b. CHF
c. Diabetic real disease.

Front 33

225. Toxicity of ACE inhibitors?

Back 33

a. Dry cough
b. Angioedema
c. Proteinuria
d. Taste changes
e. Hypotension
f. Pregnancy problems (fetal renal damage)
g. Rash
h. Increased renin
i. Lower angiotensin II.
j. Hyperkalemia!

Front 34

226. When should you avoid ACE inhibitors?

Back 34

a. Pregnancy
b. Hyperkalemia
c. Bilateral renal artery stenosis bc ACE inhibitors significantly ↓ GFR by preventing constriction of efferent arterioles.

Front 35

227. Complete

Back 35

227. Complete