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Flashcards in Renal Deck (21)
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1
Q

Mannitol:
MOA?
Therapeutic Uses?
ADR/CI’s?

A

Osmotic diuretic (^ urine flow, DECREASE intraocular + intracranial pressure)

Tx: Drug OD, ^ IOP/ICP,

ADRs: Pulmonary Edema, Dehydration
CI: Anuria, HF

2
Q
Acetazolamde: 
MOA? 
Therapeutic Use (5)? 
ADRs? 
CI?
A

Carbonic Anhydrase Inhibitor–> Dump HCO3- @ PT

Tx:

  • Glaucoma
  • ALTITUDE SICKNESS
  • PSEUDOTUMOR CEREBRI
  • Uriniary alkalization; metabolic alkalosis

ADRs: PT acidosis, paresthesia, NH3 Toxicity
CI: SULFA ALLERGY

3
Q

List Three Loop Diuretics that are SULFA DRUGS:
MOA?
Tx?
Mnemonic for ADRs?

A

Furosemide, Bumetanide, Torsimide (Furry Bum Tortoise)

MOA:

  • Inhib Na/Cl/K cotransport in TAL –> No Hypertonic Medulla–> No concentration of urine…
  • ^ PGE release
  • Waste CALCIUM

Tx: Edema, HTN, HYPERcalcemia

ADRs: “OH DANG”

  • Ototoxicity
  • HYPOkalemia
  • Dehydration
  • Allergy to sulfa
  • Alkalosis
  • Nephritis (interstitial)
  • Gout
4
Q

What is the one loop diuretic that is NOT a sulfa drug?
How does it work?
What is it used to treat?
What are its ADRs?

A

Ethacrynic Acid

  • MOA same as sofa drug loops
  • Treats edema, HTN, hypercalcemia in patients w sulfa allergy
  • ADRs are same as sulfa but with WORSE OTOTOXICITY
5
Q

Which diuretics can be used to treat nephrogenic DI?!

How does this work?

A

Thiazide diuretics:

Slight dehydration–> DECREASE plasma volume + GFR–> ^ resorption Na, H2O in PT

6
Q
What are our three thiazide diuretics?
What is the MOA? 
What are 5 therapeutic uses? 
What is a mnemonic for 6 ADRs? 
When are these drugs CI?
A

Hydrochloriothiazide, Chorthaladone, Metolazone

MOA:
Inhibit NaCl reabsorption in DT–> Dilute urine, DECREASE Ca Excretion

Tx: HTN, HF, Hypercalcinuria, nephrogenic DI, osteoporosis

ADRs: “HyperGLUC”

  • HYPOkalemic metabolic alkalosis
  • HYPOnatremia
  • HyperGLYCEMIA
  • HYyperLIPIDEMIA
  • HyperURICEMIA
  • HyperCALCEMIA

CI: Sulfa allergy

7
Q

What are the 4 K sparing diuretics?

A

“Take a SEAt, Potassium”

  • Spironolactone
  • Eplerenone
  • Amiloride
  • Triemterine
8
Q

What is the shared MOA between spironolactone and Epleronone?

A

These are aldosterone receptor antagonists in the collecting duct

9
Q

What is the shared MOA between triamterine and amiloride?

A

Block Na channels in the collecting duct to prevent K wasting…

10
Q

What are the therapeutic uses for K sparing diuretics?

5–2 are for specific drugs

A
  • Coadmin w other diuretics: px K depletion
  • Hyperaldosteronism
  • HF
  • Neprhogenic DI (amiloride)
  • Hepatic ascites (spironolactone)
11
Q

What is the one common salient ADR with all K sparing diuretics? Which one has some other weird ADRs?

A

ALL can cause HYPERkalemia; remember spironolactone causes the gynecomastia, etc.

12
Q

How does urine NaCl change with ALL diuretics?

A

INCREASES

13
Q

How does urine K+ change with ALL diuretics?

A

INCREASES (unless coadmin w K sparing)

Thiazides and Loops deplete K the most

14
Q

Which diuretics can induce academia and which can induce alkalemia? Describe the mechanisms by which this can occur.

A

Acidemia:

  • Acetazolamide (CA inhibitors);
  • Aldo-R antagonists (via preventing K and H secretion)

Alkamemia: Loops and thiazides

  • Contraction alkalosis (^ ATII)
  • K depletion–> pump K out of cels in XGE for H
  • Low K–> H replaces K in Na/KATPase of collecting duct
15
Q

How does urine Ca change depending upon the diuretic used?

A

Thiazides: DECREASE urine Ca
Loops: INCREASE urine Ca

16
Q

CaptoPRIL, EnalaPRIL, LisinoPRIL, RamiPRIL are all examples of what type of drug?
Describe the MOA.

A

ACE Inhibitors!!!
ACEi–> STOP AT II–> STOP constrxn efferent arteriole–> DECREASE GFR

  • Will also ^ renin due to DECREASE in (-) feedback
  • Potent Vasodilatory effects (inhib deactivation bradykinin)
17
Q

List some therapeutic uses for ACEi’s. In which diseases do they decrease mortality?

A
  • HTN
  • DECERASE mortality in HF (inhib remodeling)
  • Proteinuria, DM Nephropathy (DECREASE intraglomerular pressure and SLOW GBM thickening)
18
Q

List the ADRs for ACEi’s–what is the helpful mnemonic?

What are three CI circumstances?

A

CATCHH

  • Cough
  • Angioedema (due to ^ bradykinin)
  • TERATOGEN
  • ^ Cr, DECERASE GFR
  • HYPERkalemia
  • HypoTN

CI: C1 ESTERASE DEFICIENCY (angioedema), Preggos, bilateral renal stenosis

19
Q

LoSARTAN, CandeSARTAN, ValSARTAN

What is the common MOA? How are they different from ACEi’s?

A

These are Angiotensin II Receptor Blockers (ARBs)!!

Block AT II-R –> Effects similar yo ACEi’s WITHOUT ^ Bradykinin–> NO COUGH

20
Q

What are the clinical uses for ARBs?

How about the ADRs?

A

All things ACEi for patients intolerant to ACEi’s (i.e w cough or angioedema)

ADRs are the same with exception of COUGH/ C1 Esterase deficiency!!!

21
Q

Aliskiren:
MOA?
Clinical use?
ADRs?

A

Direct inhibition of renin (Stops AT I –> AT II)
Used ONLY to treat HTN

ADR/ CI:

  • Do NOT coadmin w ACEi/ARBs
  • Hyperkamenia
  • HypoTN
  • Low GFR