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Veterinary Pharmacology > Renal Pharmacology & The Urinary System, Pt. 3 > Flashcards

Renal Pharmacology & The Urinary System, Pt. 3 Flashcards

1
Q

What are the most common causes of acute renal failure?

A

nephrotoxicity and infectious disease

  • ethylene glycol
  • lilies (cats)
  • grapes and raisins (dogs)
  • aminoglycosides
  • amphotericin B
  • cisplatin
  • contrast agents
  • NSAIDs
  • ACE inhibitors
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2
Q

What is the most common cause of renal ischemic injury?

A

reperfusion injury following dehydration, shock, hypotension, cardiac output failure, or thrombosis

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3
Q

Renal ischemic reperfusion injury:

A
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4
Q

What is renal ischemia? Reperfusion? How do each cause injury?

A

ISCHEMIA = interruption of blood supply to the tissue that the cells may adapt to

REPERFUSION = re-establishments of blood flow that tends to cause injury due to the overwhelming oxygen supply

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5
Q

Significant changes following reperfusion:

A
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6
Q

What are the 5 key events in acute renal failure resulting in ischemic reperfusion injury? What does this result in?

A
  1. inflammatory cells infiltrate the injured tubular cells resulting in the release of cytokines
  2. generation of ROS, like NO, ONOO-, OH, superoxide
  3. disruption of cytoskeleton
  4. translocation of carriers causing loss of function
  5. damaged cells activate apoptotic pathways via caspases and MAP kinase

impaired renal function

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7
Q

What are the major ROS and RNS produced by acute renal failure?

A

ROS: superoxide, peroxynitrite, hydrogen peroxide, hydroxyl radical

RNS: NO from arginine and nitric oxide synthase

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8
Q

What ROS causes the most damage?

A

hydroxyl radical generated from fenton reactions converting hydrogen peroxide, resulting in the oxidation of DNA, proteins, and lipid membranes

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9
Q

What are the 2 major generators of ROS?

A
  1. mitochondrial complexes
  2. hypoxanthine
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10
Q

What is the proposed mechanism for the formation of ROS during ischemic reperfusion injury with hypoxanthine?

A
  • as ischemia prolongs ATP is converted into AMP, adenosine, inosine, then hypoxanthine
  • as reperfusion and reoxygenation occurs, released Ca and proteases convert xanthine dehydrogenase into xanthine hydrogenase
  • xanthine hydrogenase converts hypoxanthine into superoxide, hydrogen peroxide, and hydroxyl radical
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11
Q

What are the 5 main steps to the pharmacological management of acute renal failure?

A
  1. treat or minimize underlying disease
  2. manage systemic complications (other organs affected)
  3. correct fluid, electrolyte, and acid-base balance
  4. initiate diuresis
  5. establish a prognosis depending on recovery, chronic disease, and permanent damage
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12
Q

How is the fluid deficit measured to properly relace it?

A

% dehydration x BW = liters required (volume)

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13
Q

What fluids are recommended for acute renal failure fluid therapy? In what situation should this be altered?

A

0.9% NaCl - physiological level will not alter osmolality

HYPERNATREMIA/CARDIAC INSUFFICIENCY - use low sodium fluids, like 0.45% NaCl in 2.5% dextrose or LRS in 2.5% dextrose

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14
Q

What should be measured during fluid therapy treatment for acute kidney failure?

A
  • urine output via catheter (1-2 mL/kg/hr)
  • BW
  • hematocrit
  • plasma protein concentration
  • sodium concentration
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15
Q

What 4 treatments are preferred for urine production enhancement during acute kidney failure?

A
  1. Furosemide*
  2. Dopamine
  3. 10-20% Mannitol**
  4. 10-20% Dextrose
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16
Q

What can Furosemide exacerbate during treatment?

A

gentamicin toxicity

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17
Q

How does dopamine act as a urine production enhancer? What are 3 common adverse effects?

A

it is a positive inotrope and vasodilator that increases cardiac activity to increase renal blood flow and GFR

  1. tachycardia
  2. hypertension
  3. vomiting
18
Q

How do mannitol and dextrose act as urine output enhancers? What additional effects do each have?

A

osmotic diuretics

  • MANNITOL = decreases cellular edema, ROS scavenger
  • DEXTROSE = caloric support, increased insulin
19
Q

How is hyperkalemia cause by acute renal failure typically treated? What are 2 possible options if this fails?

A

normally improves after fluid therapy and diuresis

  1. calcium gluconate - cardioprotective
  2. (insulin) dextrose - increases intracellular movement of K
20
Q

What is typically used to treat metabolic acidosis caused by acute renal failure?

A

sodium bicarbonate alkalinizes ECF

21
Q

What 4 drug classes are commonly used to treat nausea/vomiting caused by acute renal failure?

A
  1. H2 antagonists - Famotidine, Ranitidine
  2. SR antagonists - Dolasetron
  3. dopamine antagonists - Metoclopramide
  4. PG analogs - Misoprostol
22
Q

In what species is chronic kidney disease most common? What is it?

A

cats older than 12 y/o —> most common cause of death in cats older than 5 y/o

complex mixture of disorders that cause irreversible loss of nephrons, decreasing GFR

23
Q

What are the histological hallmarks of chronic kidney disease? What is commonly generated? What systemic change is most commonly seen?

A

tubulointerstitial nephritis and fibrosis

ROS - NO, ONOO, OH, O2-

angiotensin II is released, resulting in hypertension

24
Q

What is the main cause of nephron destruction in chronic kidney disease? What 3 things most commonly lead to this?

A

generation and accumulation of ROS

  1. glomerular hypertension and hyperfiltration
  2. angiotensin II release
  3. anemia
25
Q

What role does angiotensin II play in the formation of ROS?

A

ANGII indices NADPH oxidase, which is responsible for generating superoxide that is able to combine with nitric oxide into ONOO-

26
Q

What are the 3 major steps of pharmacological management of CKD? What else is done?

A
  1. stage
  2. renoprotection
  3. manage sequelae - hypertension, anemia, metabolic acidosis, ulceration
  • intervention
  • monitoring and follow-ups
27
Q

What are the 3 major dietary strategies of managing CKD?

A
  1. low high-quality protein diet that is low in phosphorus to reduce nitrogen waste, acid formation, and mineral deposition
  2. moderate sodium restriction, especially in hypertensive patients
  3. control lipid intake to reduce hypercholesterolemia, inflammation, and protect renal hemodynamic function
28
Q

What phosphorus binders can be added into the diet to control CKD?

A
  • aluminum hydroxide
  • calcium acetate
  • calcium carbonate
29
Q

How is dietary calcitriol used to treat CKD?

A

increases serum calcium levels and decreases serum PTH levels

30
Q

How can additional alkalinization therapy necessity be calculated in metabolic acidosis caused by CKD?

A

blood gas analysis

  • serum total CO2 < 15-17 mmol/L = PO
  • serum total CO2 < 10-12 mmol/L = parenteral
31
Q

What 2 options are commonly used for alkalinization therapy in CKD? What needs to be checked before they are used?

A
  1. sodium bicarbonate
  2. potassium citrate

serum Na and K levels

32
Q

What causes the GI effects of CKD? What ones are most common?

A

uremia - mucosal irritation, impaired GI mucosal barriers, hypergastrinemia —> vomiting, diarrhea

33
Q

What are the main 3 classes of drugs used for the GI effects of CKD?

A
  1. H2 antagonists - Cimetidine, Famotidine, Ranitidine
  2. PPIs - Omeprazole
  3. mucosal protectants - Sucralfate (produces a layer that protects ulcers)
34
Q

What 5 drugs are used to treat anorexia-vomiting-hypertension syndrome of CKD?

A
  1. Metoclopramide
  2. Maropitant - neurokinin type 1 selective receptor antagonist for motion sickness
  3. Misoprostol - synthetic PG analog that inhibits gastric acid and pepsin secretion and protects gastric mucosa
  4. Enalapril, Benazepril - ACE inhibitors for hypertension (RAAS and low vasodilator production)
  5. Furosemides, Spironolactone - diuretics for hypertension
35
Q

How is calcium homeostasis controlled by PTH?

A
  • in response to low concentrations of plasma calcium, PTH is secreted
  • PTH mobilizes calcium from bones, reduces loss of calcium by the kidney, and increases calcitriol in the plasma to increase calcium absorption from the intestine
  • this results in the normalization of plasma calcium levels
36
Q

What hormones are involved in phosphate homeostasis? What regulates its renal reabsorption?

A

calcitriol and PTH

PTH - increases movement of HPO4 from the bones and increases its absorption from the intestines, allowing vitamin D to induce its excretion from the kidney

37
Q

What are 3 causes of secondary hyperparathyroidism? What does this result in? What are the 2 treatments?

A
  1. hypocalcemia
  2. hyperphosphatemia
  3. impaired vitamin D

increased PTH mobilizes calcium and phosphate from bone, causing soft tissue mineralization

dietary restruction of phosphorus and calcium supplementation; calcitriol supplementation

38
Q

What hormone is necessary for erythropoiesis? How is it produced?

A

erythropoietic (EPO)

low tissue oxygen tension causes the kidney to produce hypoxia-inducible factor 1, which causes the synthesis of EPO, which induces red blood cells proliferation, maturation, and release due to activation of EPO receptors on the plasma membrane of erythroid precursor cells

39
Q

What anemia results from CKD? What causes this? What are some clinical signs?

A

progressive, non-regenerative

lack of EPO production and GI blood loss

apathy, lethargy, poor appetite, poor body condition

40
Q

What treatment is used for anemia caused by EPO? What causes resistance?

A

recombinant human EPO —> check hematocrit, may increase too much (doping)

antibody production

Veterinary Pharmacology (35 decks)

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