Renal Drugs Flashcards

1
Q

What is the name of the CA Inhibitor?
Where does it work?
What does it do?

A

Acetazolamide
Proximal Tubule
Inhibits CA so that Na wont be reabsorbed bc H can’t be exchanged to go out into lumen

Leads to Acidosis with HypoK. Only drug that does this.

Also bc HCO3- isnt being reabsorbed, Cl- will to keep things neutral…hyperCl-emia

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2
Q

What can acetazolamide be used for?

SEs?

A

Glaucoma
Alkanalize the urine
Metabolic Alkalosis (ie in altitude sickness)
pseudomotor cerebri

SEs?
Sulfa allergy, parasthesia, metab acidosis
NH3 tox

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3
Q

What kind of diuretic is mannitol?
Where does it work?
What does it do?

A

Osmotic
Proximal
It draws water out into the lumen (no Na or anything else) by increasing the tubular osmo. This increases urine flow, relieving the high Ps in the eye and cranium

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4
Q

What can Mannitol be used for?

A

Drug OD

To decrease IOP and ICP

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5
Q

What are the two loop diuretics?
Where do they work?
MOA?

A

Furosemide, Ethacrynic Acid
Thick Asc Loop
INHIBIT Na/K/2Cl transporter
-blocks Na, K, and Cl from leaving the tubule so medulla not so salty, so now can’t concetrate the urine (bc this creates the gradient for water to leave out of the thin descending

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6
Q

Where else do the Loops work, and what other ion does it excrete?

A

Work on AFFERENT arteriole causing vasodilation (blocked by NSAIDs)

Excretion of Ca2+

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7
Q

What is the difference btwn Furosemide and Ethacrynic acid?

A

They do exactly the same but etha used for ppl with a sulfa allergy

Etha is a Phenoxyacetic acid derivative

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8
Q

What are the loops used for?

A

Edema! EDEMA!! EDEMA!!!

CHF, Cirrhosis, nephOtic syndrome, pulm edema, HTN, hyperCa2+emia

So this can be used for HTN

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9
Q

SEs of loops?

A
OH DANG
Ototoxicity
HypoKalemia
Dehydration
Allergy (sulfa)
Nephritis (Interstitial)
Gout (due to hyperuricemia)
Never use to treat gout or in patients with gout
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10
Q

What is the Thiazide diuretic and where does it work?

MOA?

A

It is hydrochlorothiazide
Early Distal Tubule

Block the Na/Cl cotransporter, so they are prevented from being reabsorbed. Stay in the tubule

This also means that the nephron cant dilute as well

This one DECREASES Ca2+ excretion, so can cause HyperCa2+emia

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11
Q

What is hydrochlorothiazide used for?

A

HTN!!
CHF, hyperCa2+URIA (so if someone always have high Ca in their blood for no good reason, ie people with kidney stones)
Nephrogenic diabetes insipidus, Osteoporosis (bc ur keeping Ca in)

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12
Q

SEs of thiazides?

A
HypoKemia (so dont use with digoxin)
Metab Alkalosis
Hyponatremia
HyperGLYCEMIA (so no diabetic pts, use ACEI or ARBs for them)
HyperLIPIDEMIA
HyperURICEMIA
HyperCALCEMIA
Sulfa Allergia
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13
Q

What are the K+ sparing diuretics? Where do they work, and MOA?

A

The K+ STAEs

Spironolactone & Eplerenone
Triamterene
Amiloride

Work in the Cortical Collecting Tubule

Spironolactone & Eplerenone are COMPETITIVE aldo receptor ANTAGONISTS

Amiloride & Triamterine both block Na channels in CCT

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14
Q

What are the K+ sparing used for?

SEs?

A

Hyperaldo
K+ depletion
CHF

SEs:
HyperK+emia (arrythmias, elevated T waves)
Endocrine effects with spironolactone (ie gynecomastia, antiandrogen effects so can fix hirsutism in females, but makes men womanly)

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15
Q

What is spironolactone best used for?

A

Improving mortality in CHF, not HTN

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16
Q

What is the difference btwn spironolactone and eplerenone?

A

Spironolactone is a NON SELECTIVE androgen receptor antagonist, so in men helps their CHF, but gives them boobs

Eplerenone is a SELECTIVE aldo receptor antagonist, so you get anti CHF, but no androgen issues

17
Q

What are the ACE Inhibitors and how do they work? What’s the difference btwn ACE I and ARBs?

A

Captopril, Enalapril, Lisinopril

Inhibit ACE, so no Angio II. Which means…
DECREASE GFR bc no constriction of efferent arterioles, but bc of this Renin will INCREASE!!

Also no bradykinin breakdown so you get angioedema

ACEIs and ARBs do the same thing but with ARBs bradykinin still broken down so no cough or angioedema

18
Q

What are ACEIs and ARBs used for?

A
HTN
CHF
Proteinuria
Diabetic Nephropathy
Prevent heart remodeling due to chronic HTN
19
Q

SEs of ACEIs and ARBS?

A
CATCHH
Cough
Angioedema
Teratogen
Creatinine (Increased, bc GFR went down)
HyperKalemia
HypoTN

Dont give to patients with bilateral renal artery stenosis bc these drugs will further decrease GFR and kidney function will fall off

20
Q

DDIs with Loops?

A

Aminoglycosides (mycins, amikacin) because increase the ototox

Li+–>Loops increase Li+ clearance bc it looks like Na

Digoxin: Loops cause K excretion–>Hypokalemia. Digoxin competes with K for a spot on ATPase. Without K, get digoxin toxicity

21
Q

What are the DOCs in acute pulmonary edema? (ie CHF)

A

Loops for diuresis
Digoxin (increased contractility)
ACEIs/ARBs

22
Q

What other way can loops help with HTN?

A

Loops also vasodilate by increasing PGs. PGs vasodilate the afferent arteriole. NSAIDs block this bc they block PGs

THEREFORE NSAIDS WILL BLOCK(!!!) THE HTN LOWERING EFFECTS OF LOOPS

23
Q

Why do loops cause gout or hyperuricemia?

A

Bc urate has its own pump in the proximal tubule, it can be excreted. but if there is a weak acid ie penicillin, cephalosporin, loops, they will compete for that weak acid pump thats for urate and win. therefore urate will be reabsorbed

24
Q

How do thiazides treat nephrogenic diabetes insipid?

A

The free water created in the thin limb is rejoined with the salt from distal tubule that the thiazides prevented from being absorbed. Kidney adapts to this and will create an increase in aldo which then create more Na reabsorption; then as a consequence, water will follow the Na.

So basically the aldo creates another door for water to go thru bc its own door is messed up.

25
Q

What is the change seen in Ca2+ with loops and thiazides?

A

Loops–>Increase it in urine, decrease in serum

Thiazide–>Decreased in urine, incr in serum