Renal

Question 1

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

Answer 1

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

Tx: Drug OD, ^ IOP/ICP,

ADRs: Pulmonary Edema, Dehydration
CI: Anuria, HF

Question 2

Acetazolamde: 
MOA? 
Therapeutic Use (5)? 
ADRs? 
CI?

Answer 2

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

Question 3

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

Answer 3

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

Question 4

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?

Answer 4

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

Question 5

Which diuretics can be used to treat nephrogenic DI?!

How does this work?

Answer 5

Thiazide diuretics:

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

Question 6

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?

Answer 6

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

Question 7

What are the 4 K sparing diuretics?

Answer 7

“Take a SEAt, Potassium”

• Spironolactone
• Eplerenone
• Amiloride
• Triemterine

Question 8

What is the shared MOA between spironolactone and Epleronone?

Answer 8

These are aldosterone receptor antagonists in the collecting duct

Question 9

What is the shared MOA between triamterine and amiloride?

Answer 9

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

Question 10

What are the therapeutic uses for K sparing diuretics?

5–2 are for specific drugs

Answer 10

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

Question 11

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

Answer 11

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

Question 12

How does urine NaCl change with ALL diuretics?

Answer 12

INCREASES

Question 13

How does urine K+ change with ALL diuretics?

Answer 13

INCREASES (unless coadmin w K sparing)

Thiazides and Loops deplete K the most

Question 14

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

Answer 14

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

Question 15

How does urine Ca change depending upon the diuretic used?

Answer 15

Thiazides: DECREASE urine Ca
Loops: INCREASE urine Ca

Question 16

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

Answer 16

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)

Question 17

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

Answer 17

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

Question 18

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

What are three CI circumstances?

Answer 18

CATCHH

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

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

Question 19

LoSARTAN, CandeSARTAN, ValSARTAN

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

Answer 19

These are Angiotensin II Receptor Blockers (ARBs)!!

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

Question 20

What are the clinical uses for ARBs?

How about the ADRs?

Answer 20

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!!!

Question 21

Aliskiren:
MOA?
Clinical use?
ADRs?

Answer 21

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