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Pharmacology > Renal - EMILY > Flashcards

Renal - EMILY Flashcards

1
Q

What ion controls the movement of water into and out of the nephron?

A

Sodium

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2
Q

What are some reasons we’d use diuretics?

A

-To mobilize tissue fluid
-To reduce blood volume
-To protect kidney function

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3
Q

What are the 5 major classes of diuretics?

A
  1. Carbonic anhydrase inhibitors
  2. Osmotic diuretics
  3. Loop diuretics
  4. Thiazide diuretics
  5. Potassium sparing diuretics
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4
Q

What is the ultimate goal of using diuretics?

A

Increase excretion of sodium followed by water

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5
Q

All diuretics (except for osmotic diuretics) inhibit specific ________ that play a role in renal tubular _________ reabsorption

A

Targets; sodium

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6
Q

The biggest impact on modifying sodium absorption occurs where?

A

The loop of Henle

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7
Q

Carbonic anhydrase inhibitors act mainly in the:

A

Proximal convoluted tubule

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8
Q

Osmotic diuretics act mainly in the:

A

Descending limb of the loop of Henle

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9
Q

Loop diuretics act mainly in the:

A

Thick ascending limb of the loop of Henle

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10
Q

Thiazide diuretics act mainly in the:

A

Distal convoluted tubule

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11
Q

Potassium-sparing diuretics act mainly in the:

A

Collecting duct

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12
Q

All diuretics (except spironolactone) are active in the tubular _______

A

Lumen

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13
Q

What must diuretics reach to be effective?

A

Adequate concentration in the urine

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14
Q

What is the primary MOA of carbonic anhydrase inhibitors?

A

Interacts with enzymes

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15
Q

What is the primary MOA of osmotic diuretics?

A

Osmotic effects in water-permeable regions of the nephron

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16
Q

What is the primary MOA of loop diuretics?

A

Interact with specific membrane transport proteins

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17
Q

What is the primary MOA of thiazide diuretics?

A

Interact with specific membrane transport proteins

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18
Q

What is the primary MOA of potassium-sparing diuretics?

A

Interact with hormone receptors

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19
Q

What 2 drugs are carbonic anhydrase inhibitors? Which ones work systemically and which or topical?

A

Acetazolamide (systemic)

Dorzolamide (topical)

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20
Q

Carbonic anhydrase inhibitors are (non-competitive/competitive) and (reversible/irreversible)

A

Non-competitive; reversible

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21
Q

What condition are carbonic anhydrase inhibitors (specifically acetazolamide) usually used for?

A

Acute glaucoma management in dogs to reduce production of aqueous humor

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22
Q

Acetazolamide has self-limiting diuretic effects: T or F?

A

True. Systemic acidosis makes H+ available in the cell again

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23
Q

Which carbonic anhydrase inhibitor should be used in cats first? Why?

A

Dorzolamide, because cats are more susceptible to the adverse effects of carbonic anhydrase inhibitors so topical would eliminate systemic effects

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24
Q

What are some adverse effects of acetazolamide?

A

-Drowsiness and disorientation
-Hypersensitivity
-Hypokalemia and metabolic acidosis
-Worsening of hepatic disease/encephalopathy

25
Q

What drug is an osmotic diuretic?

A

Mannitol

26
Q

What is the MOA of mannitol?

A

Mannitol increases the osmolarity of the fluid in the nephron when it’s in there, which makes the osmolarity similar to interstitial fluid and reduces passive water diffusion out of the nephron. This means that less sodium is reabsorbed, so more water is excreted.

27
Q

How is mannitol administered?

A

As an IV solution

28
Q

What are the pharmacokinetics of mannitol?

A

-Mostly not metabolized*
-Half-life is dose-dependent
-Rapid elimination by the kidneys

29
Q

What are the pharmacodynamics of mannitol?

A

-Increased cardiac output
-Decreased rigidity of RBC membranes (enhanced blood flow)
-Reduced hematocrit

30
Q

What are the 2 main therapeutic indications for mannitol?

A
  1. Increased intracranial pressure
  2. Renal failure (not recommended for anuric patients though)
31
Q

What are some considerations for using mannitol?

A

-Give IV only
-Use a test dose
-Is the tissue barrier intact? (Nephrotoxic agents and renal ischemia damage make osmotic diuretics ineffective)

32
Q

What are the adverse effects of mannitol?

A

-Hypertonic dehydration**
-Cardiac arrhythmias due to electrolyte loss
-Acute hyponatremia
-CHF or pulmonary edema
-Volume overload in oliguric patients
-Hyperosmolar state/osmotic compensation

33
Q

What is the most commonly used loop diuretic in vet med?

A

Furosemide

34
Q

What is the MOA of loop diuretics?

A

They block the action of the Na+/K+/2Cl symporter in the thick ascending limb of the loop of Henle and prevents normal concentration of urine

35
Q

How does furosemide activate the RAAS?

A

It alters the chloride equilibrium leading to renal hypotension

36
Q

Furosemide has a _______ onset and a _________ duration of action

A

Rapid; short

37
Q

Which organ is the major site of action, metabolism and excretion of furosemide?

A

Kidney

38
Q

What is furosemide used for?

A

-Mobilizing edema of cardiac, renal or hepatic origin
-Reducing exercise-induced pulmonary hemorrhage in race horses
-Renal failure
-Hypercalcemia

39
Q

What are the pharmacodynamics of furosemide?

A

-Potassium-wasting
-Has hemodynamic effects (decreased pulmonary artery pressure; increased renal blood flow and GFR)

40
Q

What are the pharmacokinetics of furosemide?

A

-Primarily excreted by the kidneys
-Can be given IV or orally to dogs
-Usually given IV to horses

41
Q

What are the main adverse effects of furosemide?

A

-Volume depletion and hyponatremia
-Electrolyte abnormalities
-Cardiac effects
-Renal effects in at-risk patients
-Many drug interactions

42
Q

When should you reduce the furosemide dose being given and why?

A

When also giving ACE inhibitors at the same time. This increases the risk of renal damage due to hypotension/ischemia

43
Q

What is the MOA of thiazide diuretics?

A

-Inhibit Na/Cl co-transporters in the distal convoluted tubule
-Increase Ca2+ reabsorption

44
Q

Which 3 drugs are thiazide diuretics?

A
  1. Chlorothiazide
  2. Hydrochlorothiazide
  3. Trichlormethiazide
45
Q

What are the pharmacodynamics of thiazide diuretics?

A

-Moderate diuresis
-Blood pressure reduction in hypertensive individuals

46
Q

What are the pharmacokinetics of thiazide diuretics?

A

-Incomplete GI absorption in vet species
-Extensively protein-bound**
–>Not filtered at glomerulus
—>Get into tubules via proximal tubular secretion
-Renal excretion (+/- biliary)

47
Q

What are the adverse effects of thiazide diuretics?

A

-Potassium wasting (increased risk of arrhythmias)**
-Hyperglycemia
-Hypercalcemia
-Hyponatremia
-Hypochloremia
-Sulfonamide hypersensitivity

48
Q

What type of patients is the use of thiazide diuretics contraindicated in?

A

Patients with severe renal disease or hepatic disease

49
Q

What are 2 types of potassium-sparing diuretics?

A
  1. Mineralocorticoid receptor antagonists
  2. Epithelial sodium channel blockers
50
Q

Which drug is a mineralocorticoid potassium-sparing diuretic?

A

Spironolactone

51
Q

Which 2 drugs are epithelial sodium channel blockers (potassium-sparing)?

A
  1. Amiloride
  2. Triamterene
52
Q

What is the MOA of spironolactone?

A

Blocks binding of aldosterone in late distal tubule and collecting duct. This reduces sodium absorption and potassium excretion.

53
Q

What is the MOA of epithelial sodium channel blockers?

A

They block sodium channels in the luminal epithelium and prevent sodium reabsorption

54
Q

What is spironolactone usually administered with and why?

A

A thiazide or loop diuretic to increase diuresis while sparing potassium

55
Q

Spironolactone is most effective in the presence of what?

A

Hyperaldosteronism (happens in cardiac failure, liver disease, and nephrotic syndrome)

56
Q

Why should you use spironolactone with an aldosterone antagonist in patients with liver failure?

A

Secondary hyperaldosteronism (due to decreased aldosterone metabolism) causes increased sodium and water retention and acsites

57
Q

What is the main adverse effect of potassium-sparing diuretics?

A

Hyperkalemia

58
Q

Why shouldn’t you use potassium-sparing diuretics with ACE inhibitors?

A

Can cause hyperkalemia

59
Q

What is the purpose of using diuretic combinations?

A

-To achieve adequate diuresis while minimizing adverse effects
-To increase efficacy in acute renal failure
-To treat refractory edema

Pharmacology (11 decks)

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