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Veterinary Pharmacology > Renal Pharmacology & The Urinary System, Pt. 2 > Flashcards

Renal Pharmacology & The Urinary System, Pt. 2 Flashcards

1
Q

What are the 3 most common high ceiling diuretics? Where do they act?

A
  1. Furosemide*
  2. Bumetanide
  3. Ethacrynic acid
    (most common, highly effective)

acts at Henle’s loop (mTAL), binding and impairing the function of NKCC and reducing 25% of sodium reabsorption

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2
Q

What are 3 common effects of Furosemide? What effect does it have at low doses?

A
  1. increased sodium and chloride excretion in urine and out of the ECF
  2. blocks tubuloglomerular feedback
  3. disrupts countercurrent multiplier system (blocked NKCC decreases osmolality of interstitial fluid, interrupting its opposite flow of the blood from the vasa recta)

antioxidant free radical scavenger

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3
Q

How does Furosemide travel to and absorb into the kidneys? Where is it well absorbed? In what species is there an exception?

A

high plasma protein binding —> not filterable, enters via active secretion into the lumen to affect apical NKCC

GIT

horses - slowly absorbed, IV administration recommended

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4
Q

What are 4 possible side effects of Furosemide? In what animals is usage not recommended?

A
  1. excretion of calcium, magnesium, and potassium causes decrease of concentrations in the blood
  2. lethargy
  3. decreased appetite
  4. ototoxicity - inner ear endolymph affected by impaired electrolyte transport

pregnant or lactating animals

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5
Q

What is the primary indication of Furosemide usage?

A

general edema - udder, pulmonary, liver disease, cardiovascular

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6
Q

What is a common usage of Furosemide in horses? How does this disease develop?

A

lowers pulmonary vascular pressure to treat exercise-induced pulmonary hemorrhage

  • exercise causes cardiac output to increase 6-8x
  • increased left atrial pressure causes pulmonary hypertension
  • blood vessels dilate to decrease resistance and eventually rupture
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7
Q

What are some common signs of exercise-induced pulmonary hemorrhage? What breed is it especially common in?

A
  • pulmonary hypertension
  • edema
  • rupture of pulmonary capillaries
  • intra-alveolar hemorrhage
  • presence of blood in the airways

Thoroughbreds

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8
Q

What are 6 other indications of Furosemide?

A
  1. udder edema
  2. diuresis with acute renal failure
  3. hypertension
  4. hydrocephalus
  5. ascites from liver failure
  6. hypercalcemia (decreases Ca reabsorption)
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9
Q

What are the 2 types of potassium-sparing diuretics? Where do they act?

A
  1. Na+ channel blockers (ENaC) - Amiloride, Triamterene
  2. mineralocorticoid receptor antagonist - Spironolactone, Eplerenone

late DT and CD

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10
Q

What are the 2 common ENaC blockers used as potassium-sparing diuretics? What is their mechanism of action? What makes them less effective?

A
  1. Triamterene
  2. Amiloride

impairs the electrogenic sodium reabsorption late in the DT and CD (ENaC), causing less potassium to leave the cell

limited elimination of sodium at this point in the kidney - commonly combined with other diuretics

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11
Q

What is a possible side effect of Triamterene and Amiloride? In what patients is usage contraindicated?

A

hyperkalemia

  • hyperkalemia
  • NSAID treatment —> nephrotoxicity
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12
Q

What aldosterone antagonist is commonly used as a potassium-sparing diuretic? What is its mechanism of action? What additional effect does it have?

A

Spironolactone

antagonizes cytoplasmic aldosterone receptors in the late DT and CD responsible for molecular ENaC and Na/K ATPase production

calcium excretion in the urine

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13
Q

What makes Spirinolactone distribution unique?

A

does not require active secretion at the PT to reach its site of action —> diffused into cells from the blood to act on the cytoplasmic MR

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14
Q

What are 7 side effects of Spironolactone? When is usage contraindicated?

A
  1. hyperkalemia
  2. metabolic acidosis
  3. gastritis
  4. diarrhea
  5. drowsiness
  6. lethargy
  7. ataxia

gastric ulcers

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15
Q

What are 5 common indications of Spironolactone?

A
  1. ascites
  2. diuretic
  3. heart failure
  4. primary hyperaldosteronism
  5. hepatic insufficiency
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16
Q

What is a common drug combined with Spironolactone? When is this usage indicated?

A

Hydrochlorothiazide

diuretic, antihypertensive

17
Q

What 3 conditions commonly use diuretics for treatment? What diuretics are used in each?

A
  1. CHF - thiazide and loop diuretics (check potassium!)
  2. liver cirrhosis resulting in ascites and hyperaldosteronism - Spironolactone
  3. nephrotic syndrome (hypoalbuminemia, proteinuria, edema) - Furosemide
18
Q

What commonly affects the efficacy of diuretics used in nephrotic syndrome?

A
  • less protein binding of the drug and reduced distribution to action site
  • binding to albumin in the tubular lumen reduces action

(aldosterone antagonists not indicated —> decreases renal response)

19
Q

What stimulates the ADH-thirst system? What are the 2 outcomes?

A

increased ECF osmolality or decreased blood volume stimulates hypothalamic osmoreceptors

  1. ADH release - stimulates water reabsorption by the kidneys (concentrates urine)
  2. stimulates thirst center - promotes fluid intake
20
Q

What are the 3 classes of ADH receptors? Where are they located? How do they work?

A
  1. V1a - glomerulus, renal medulla
  2. V1b - inner medulla
  3. V2 (AQP2) - mTAL, DCT, CD; responds to ADH

tunnel-like channels that use asparagine to recognize water and repel other ions based on size and charge

21
Q

What drugs act as ADH stimulants? Inhibitors?

A

STIMULANTS = vinca alkaloids, cyclophosphamide, tricyclic antidepressants, isoproterenol

INHIBITORS = ethanol, mineralocorticoids, glucocorticoids

22
Q

What is the therapeutic treatment for diabetes insipidus centralis? How can it be used as a diagnostic? What should be monitored?

A

recombinant ADH, Desmopressin acetate (off-label for increasing von Willebrand factor)

  • centralis = responsive
  • nephrogenic = no response

USG

23
Q

What test is used for diagnosing the type of diabetes insipidus?

A

Carter-Robbins test

  • water is administered, where a functional kidney will dilute urine
  • NaCl is later administered, where a functional kidney will concentrate urine
  • with diabetes insipidus centralis, urine concentration will not change, but will be concentrated upon ADH administration (Desmopressin)
24
Q

When do uroliths form? What is the most common treatment?

A

concrement-forming substances reach a concetration above the metastable range and solubility threshold

solubilization/dissolving crystals by altering urine pH below the metastable range

25
Q

What are the 4 most common types of uroliths in domestic species?

A
  1. calcium oxalate (50%)
  2. calcium phosphate/magnesium ammonium phosphate (30%)
  3. uric acid/urate (25-30%)
  4. xanthine/cystine (<5%)
26
Q

What is cystine urolithiasis? When do they form?

A

oxidized form of cysteine formed when cysteine dimerizes by forming a disulfide bond

solubility decreases as urine acidity increases —> soluble in ammonia, insoluble in acetic acid

27
Q

What is the structure of cystine crystals?

A

hexagonal and flat colorless crystals

28
Q

What is the most common kidney stone in dogs and cats? What is its structure like? In what urine does it form?

A

magnesium ammonium phosphate (struvite) - also in rabbits and guinea pigs

long, flat, colorless coffin lid

forms in alkaline urine with a pH of 7-9 —> soluble in acetic acid

29
Q

What is the second most common kidney stone in cats? What is its structure like? In what urine does it form?

A

calcium oxalate (also in dogs and horses)

short, square, colorless envelope shape

produced in acetic, neutral, and alkaline urine —> insoluble in acetic acid

30
Q

What is the shape of urate crystals? In what urine does it form?

A

(sodium/ammonium urate) red round or amorphous shapes —> red-colored urine

acidic or neutral urine in large amounts

31
Q

What are the 3 causes of urolithiasis?

A
  1. PRE-RENAL - increased filtration of stone-producing substances (hypercalcinuria, phosphaturia), increased mobilization from bone (increased PTH or calcitriol)
  2. RENAL - abnormal renal reabsorption, ADH release (enhanced urine concentration)
  3. POST-RENAL - pH of urine (phosphates dissolved in acidic urine, uric acid dissolved in alkaline urine)
32
Q

What are the 4 major effects of urolithiasis?

A
  1. urinary tract blockage
  2. stretching of ureters (renal colic)
  3. growth of pathogens (NH3 formation by bacteria further alkalinizes urine)
  4. hydronephrosis
33
Q

How can acute cases of urolithiasis be treated?

A

surgical removal

34
Q

What are 3 possible treatments of cystine urolithiasis?

A
  1. dietary management (low methionine and cyteine diet)
  2. solubilization
  3. urine alkalinization (sodium bicarbonate, potassium citrate)
35
Q

What is the most common treatment of calcium oxalate urolithiasis?

A

difficult to treat - stimulation of calcium absorption by thiazide diuretics or potassium citrate

36
Q

What are 3 possible treatments of urate urolithiasis?

A
  1. low protein diet
  2. urine alkalization by sodium bicarbonate or potassium citrate
  3. Allopurinol - xanthine oxidase inhibitor

Veterinary Pharmacology (35 decks)

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