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Renal > Renal Pharmacology > Flashcards

Renal Pharmacology Flashcards

1
Q

What is the mechanism of mannitol?

A

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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2
Q

What are the clinical uses of mannitol?

A
  • Drug overdose

- Elevated intracranial/intraocular pressure

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3
Q

What are the toxicities associated with mannitol?

A
  • Pulmonary edema (can pull too much water out of cells and into the interstitial space)
  • Dehydration
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4
Q

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

A
  1. Anuria (failure of kidneys to produce urine)

2. HF

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5
Q

What is the mechanism of Acetazolamide?

A

Carbonic anhydrase inhibitor in the PCT

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

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6
Q

What are the clinical uses of Acetazolamide?

A
  • Glaucoma
  • Urinary Alkalinization
  • Metabolic Alkalosis
  • Altitude Sickness (**tested a lot!)
  • Pseudotumor cerebri
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7
Q

What toxicities are associated with Acetazolamide?

A
  • Hyperchloremic metabolic acidosis
  • Paresthesias
  • NH3 toxicity
  • Sulfa allergy

Think: “ACID”azolamide causes ACIDosis

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8
Q

What are three examples of loop diuretics?

A

Furosemide, Bumetanide, Torsemide

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9
Q

What is the mechanism of loop diuretics/furosemide?

A
  • 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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10
Q

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

A

INCREASE Ca2+ excretion

Think: “Loops Lose Ca2+”

These drugs can be dangerous in patients with osteoporosis

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11
Q

What drug inhibits the action of loop diuretics/furosemide?

A

NSAIDS

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12
Q

What are the clinical uses of loop diuretics/furosemide?

A
  • Edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema)
  • Hypertension
  • Hypercalcemia
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13
Q

What are the toxicities associated with loop diuretics/furosemide?

A

Think: “OH DANG!”

Ototoxicity 
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout
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14
Q

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

A

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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15
Q

What are the toxicities associated with Ethacrynic Acid?

A

Similar to furosemide (OH DANG!)

Can cause hyperuricemia (NEVER use to treat gout!)

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16
Q

What are two examples of Thiazide diuretics?

A
  1. Chlorthalidone

2. Hydrochlorothiazide

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17
Q

What is the mechanism of Thiazide diuretics?

A

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

18
Q

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

A

DECREASE Ca2+ excretion

19
Q

What are the clinical uses of thiazide diuretics?

A
  • Hypertension
  • HF
  • Idiopathic hypercalciuria
  • Nephrogenic Diabetes Insipidus
  • Osteoporosis
20
Q

What are the toxicities associated with thiazide diuretics?

A 
Think: "HyperGLUC":
HyperGlycemia
HyperLipidemia
HyperUricemia
HyperCalcemia

Also:
Hypokalemic metabolic alkalosis
Hyponatremia
Sulfa Allergy

21
Q

What are some examples of K+ Sparing Diuretics?

A

Think: “The K+ STAys”

Spironolactone and eplerenone
Triamterene
Amiloride

22
Q

What is the mechanism of Spironolactone and Eplerenone?

A

They are competitive aldosterone receptor antagonists in the cortical collecting tubule

23
Q

What is the mechanism of Triamterene and Amiloride?

A

They block Na+ channels in the cortical collecting tubule

24
Q

What are the clinical uses of K+ Sparing Diuretics?

A
  • Hyperaldosteronism
  • K+ depletion
  • HF
25
Q

What are the toxicities associated with K+ Sparing Diuretics?

A
  • Hyperkalemia (can lead to arrhythmias)

- Endocrine effects with Spirolactone (eg. gynecomastia, anti androgen effects)

26
Q

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

A

INCREASES with all diuretics except acetazolamide

Serum NaCl may decrease as a result

27
Q

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

A

INCREASE with loop and thiazide diuretics

Serum K+ may decrease as a result

28
Q

Which diuretics decrease the blood pH causing acidemia?

A
  • 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
29
Q

Which diuretics increase the blood pH causing alkalemia?

A

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”
30
Q

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

A

Increases with loop diuretics: decrease in paracellular Ca2+ reabsorption causing hypocalcemia

Decreases with thiazides: enhanced Ca2+ reabsorption in DCT so less in the urine

31
Q

What are some examples of ACE inhibitors?

A

Captopril, Enalapril, Lisinopril, Ramipril

32
Q

What is the mechanism of ACE inhibitors?

A

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

33
Q

What are the clinical uses of ACE inhibitors?

A
  • 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)
34
Q

What are the toxicities associated with ACE inhibitors?

A

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

35
Q

What are some examples of Angiotensin II receptor blockers?

A

Losartan, candesartan, valsartan

36
Q

What is the mechanism of Angiotensin II receptor blockers?

A

Selectively block binding of angiotensin II to AT1 receptor

Effect similar to ACE inhibitors, but ARBs do not increase bradykinin

37
Q

What are the clinical uses of Angiotensin II receptor blockers?

A
  • Hypertension
  • HF
  • Proteinuria
  • Diabetic Nephropathy if intolerant to ACE inhibitors (eg. cough, angioedema)
38
Q

What are the toxicities associated with Angiotensin II receptor blockers?

A
  • Hyperkalemia
  • Decreased Renal Function
  • Hypotension
  • Teratogen
39
Q

What is the mechanism of Aliskiren?

A

Direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I

40
Q

What is the clinical use of Aliskiren?

A

Treats hypertension

41
Q

What toxicities are associated with Aliskiren?

A
  • Hyperkalemia
  • Decreased Renal Function
  • Hypotension
42
Q

When is Aliskiren contraindicated?

A

Contraindicated in diabetics taking ACE inhibitors or ARBs

Renal (4 decks)

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