Renal Pharmacology Flashcards by Clare Burke

What is the mechanism of mannitol?

Osmotic diuretic b/c its a sugar that is freely filtered by the glomerulus, but then not reabsorbed

Increases tubular fluid osmolarity –> increased urine flow and decreased intracranial/intraocular pressure

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What are the clinical uses of mannitol?

Drug overdose

- Elevated intracranial/intraocular pressure

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What are the toxicities associated with mannitol?

Pulmonary edema (can pull too much water out of cells and into the interstitial space)
Dehydration

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What are two conditions in which administration of mannitol is contraindicated?

Anuria (failure of kidneys to produce urine)

2. HF

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What is the mechanism of Acetazolamide?

Carbonic anhydrase inhibitor in the PCT

Causes self-limited NaHCO3 diuresis and a decrease in total body HCO3- stores

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What are the clinical uses of Acetazolamide?

Glaucoma
Urinary Alkalinization
Metabolic Alkalosis
Altitude Sickness (**tested a lot!)
Pseudotumor cerebri

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What toxicities are associated with Acetazolamide?

Hyperchloremic metabolic acidosis
Paresthesias
NH3 toxicity
Sulfa allergy

Think: “ACID”azolamide causes ACIDosis

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What are three examples of loop diuretics?

Furosemide, Bumetanide, Torsemide

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What is the mechanism of loop diuretics/furosemide?

Sulfonamide loop diuretics inhibit cotransport system (Na+/K+/2Cl-) in thick ascending limb of the loop of henle
Abolish hypertonicity of medulla, preventing concentration of urine
Stimulate PGE release (vasodilatory effect on afferent arteriole) –> increases the GFR

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Do loop diuretics/furosemide increase or decrease the excretion of Ca2+?

INCREASE Ca2+ excretion

Think: “Loops Lose Ca2+”

These drugs can be dangerous in patients with osteoporosis

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What drug inhibits the action of loop diuretics/furosemide?

NSAIDS

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What are the clinical uses of loop diuretics/furosemide?

Edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema)
Hypertension
Hypercalcemia

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What are the toxicities associated with loop diuretics/furosemide?

Think: “OH DANG!”

Ototoxicity 
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout

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What is the mechanism of Ethacrynic Acid and what is its main clinical use?

Phenoxyacetic acid derivative (NOT a sulfonamide)

Essentially the same action as Furosemide

Clinical Use: diuresis in patients allergic to sulfa drugs

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What are the toxicities associated with Ethacrynic Acid?

Similar to furosemide (OH DANG!)

Can cause hyperuricemia (NEVER use to treat gout!)

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What are two examples of Thiazide diuretics?

Chlorthalidone

2. Hydrochlorothiazide

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What is the mechanism of Thiazide diuretics?

Inhibit NaCl reabsorption in early DCT, which DECREASES the diluting capacity of the nephron, therefore more ions are excreted

Do thiazide diuretics increase or decrease the excretion of Ca2+?

DECREASE Ca2+ excretion

What are the clinical uses of thiazide diuretics?

Hypertension
HF
Idiopathic hypercalciuria
Nephrogenic Diabetes Insipidus
Osteoporosis

What are the toxicities associated with thiazide diuretics?

Think: "HyperGLUC":
HyperGlycemia
HyperLipidemia
HyperUricemia
HyperCalcemia

Also:
Hypokalemic metabolic alkalosis
Hyponatremia
Sulfa Allergy

What are some examples of K+ Sparing Diuretics?

Think: “The K+ STAys”

Spironolactone and eplerenone
Triamterene
Amiloride

What is the mechanism of Spironolactone and Eplerenone?

They are competitive aldosterone receptor antagonists in the cortical collecting tubule

What is the mechanism of Triamterene and Amiloride?

They block Na+ channels in the cortical collecting tubule

What are the clinical uses of K+ Sparing Diuretics?

Hyperaldosteronism
K+ depletion
HF

What are the toxicities associated with K+ Sparing Diuretics?

- Hyperkalemia (can lead to arrhythmias) | - Endocrine effects with Spirolactone (eg. gynecomastia, anti androgen effects)

How does urine NaCl change when a patient is taking diuretics?

INCREASES with all diuretics except acetazolamide Serum NaCl may decrease as a result

How does urine K+ change when a patient is taking diuretics?

INCREASE with loop and thiazide diuretics Serum K+ may decrease as a result

Which diuretics decrease the blood pH causing acidemia?

- Carbonic anhydrase inhibitors b/c they increase HCO3- lost - K+ sparing diuretics b/c aldosterone blockade prevents K+ secretion and H+ secretion. Additionally, hyperkalemia leads to K+ entering the cells (via H+/K+ exchanger) in exchange for H+ leaving the cells and making the blood more acidic

Which diuretics increase the blood pH causing alkalemia?

Loop diuretics and thiazides cause alkalemia through several mechanisms: - Volume contraction --> increased AT II --> increased Na+/H+ exchanger in PCT --> increased HCO3- reabsorption ("contraction alkalosis") - K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) - In low K+ state, H+ (rather than K+) is exchanged for Na+ in the cortical collecting tubule --> alkalosis and "paradoxical" aciduria"

How does urine Ca2+ change when a patient is taking diuretics?

Increases with loop diuretics: decrease in paracellular Ca2+ reabsorption causing hypocalcemia Decreases with thiazides: enhanced Ca2+ reabsorption in DCT so less in the urine

What are some examples of ACE inhibitors?

Captopril, Enalapril, Lisinopril, Ramipril

What is the mechanism of ACE inhibitors?

Inhibit ACE --> decreases AT II --> decreased GFR by preventing the constriction of efferent arterioles Levels of increased renin as a result of loss of feedback inhibition Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator

What are the clinical uses of ACE inhibitors?

- Hypertension - HF - Proteinuria - Diabetic nephropathy (in diabetic nephropathy, decreased intraglomerular pressure, slowing the GBM thickening) - Prevent unfavorable heart remodeling as a result of chronic hypertension (not really used in hypertensive emergencies, more a long term treatment option)

What are the toxicities associated with ACE inhibitors?

Think: Captopril's "CATCHH" ``` Cough Angioedema (contraindicated in C1 esterase inhibitor deficiency) Teratogen (fetal renal malformations) Creatinine increases (decreasing GFR) Hyperkalemia Hypotension ``` **Avoid in bilateral renal artery stenosis because ACE inhibitors will further decrease GFR and this may lead to renal failure

What are some examples of Angiotensin II receptor blockers?

Losartan, candesartan, valsartan

What is the mechanism of Angiotensin II receptor blockers?

Selectively block binding of angiotensin II to AT1 receptor Effect similar to ACE inhibitors, but ARBs do not increase bradykinin

What are the clinical uses of Angiotensin II receptor blockers?

- Hypertension - HF - Proteinuria - Diabetic Nephropathy if intolerant to ACE inhibitors (eg. cough, angioedema)

What are the toxicities associated with Angiotensin II receptor blockers?

- Hyperkalemia - Decreased Renal Function - Hypotension - Teratogen

What is the mechanism of Aliskiren?

Direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I

What is the clinical use of Aliskiren?

Treats hypertension

What toxicities are associated with Aliskiren?

- Hyperkalemia - Decreased Renal Function - Hypotension

When is Aliskiren contraindicated?

Contraindicated in diabetics taking ACE inhibitors or ARBs