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Veterinary Toxicology > Urinary Toxicology > Flashcards

Urinary Toxicology Flashcards

1
Q

What are the 4 main functions of the urinary system?

A
  1. acid-base balance
  2. electrolyte balance
  3. ECF volume regulation
  4. metabolic waste excretion
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2
Q

What are the 4 major reasons that the urinary system is susceptible to toxicants?

A
  1. high blood flow coupled with small size - 25% CO (90% to renal cortex, 6-10% to medulla)
  2. high metabolic demand - 10% of body’s oxygen demand that the active transport of the kidney relies on (PT most susceptible)
  3. processes involved in concentrating urine also concentrate toxicants - countercurrent mechanism
  4. metabolic activation of xenobiotics by enzymes within the renal tubular epithelium
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3
Q

What are the renal function markers? When are they affects?

A

BUN and creatinine

50-70% of nephrons must be damaged before BUN and creatinine elevate

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4
Q

What is the difference between mild renal toxicity and acute renal failure?

A

MILD - renal function continues using reserve capacity with minimal alterations found on urinalysis (isothenuria, proteinuria) and is completely reversible

ARF - decreased GFR manifests with increased BUN and creatinine, glucosuria, azotemia, aminoaciduria, oliguria/anuria, renal enlargement, and pain + PD/PU, nausea, vomiting

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5
Q

What are the systemic sequelae of acute renal failure? Is it reversible?

A

dehydration and metabolic acidosis

YES - with appropriate treatment

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6
Q

What is chronic renal failure? What is it characterized by? Is it reversible?

A

progressive deterioration of renal functions with exhaustion of reserve capacity resulting from long-term exposure to toxicants

PU/PD, isosthenuria, increased BUN and creatinine, uremia, dehydration

frequently irreversible and progresses to end-stage renal disease (ESRD) with permanent loss of renal function

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7
Q

What causes ethylene glycol toxicosis?

A

ingestion of the colorless, odorless, sweet-tasting liquid found in antifreeze, windshield de-icing agents, brake and transmission fluids, polishes, and photographic/paint solutions

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8
Q

When is ethylene glycol toxicosis most common? What species are most affected? Which are the most sensitive?

A

fall, winter, spring

dogs*, cats, birds

CATS - high baseline production of oxalic acid

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9
Q

Why is ethylene glycol toxicity so common?

A
  • abundance in households coupled with lack of public awareness of its high potential for toxicity
  • palatability: somewhat pleasant taste; dogs likely will not consume if water is available
  • low lethal dose
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10
Q

What can delay GI absorption of ethylene glycol?

A

if food is present in the lumen

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11
Q

What are the 4 steps of ethylene glycol metabolism?

A
  1. ethylene glycol is oxidized by alcohol dehydrogenase (ADH) into glycoaldehyde —> 1st rate-limiting step
  2. glycoaldehyde is more toxic than EG, but it dose not accumulate and is readily metabolized by mitochondrial aldehyde dehydrogenase and cytosolic aldehyde oxidase into glycolic acid and glyoxal —> 2nd rate limiting-steps
  3. glycolic acid is more toxic, but has a short half-life and is metabolized into oxalic acid via oxidation of glycolic acid oxidase/LDH, formic acid, glycine, and α-hydroxy-β-ketoadipate by conjugation with α-ketoglutarate
  4. oxalic acid is then excreted in the urine and combine with calcium to form calcium oxalate that is deposited into the renal tubules, brain vasculature, and other tissues
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12
Q

What are the 5 mechanisms of toxicity of ethylene glycol?

A
  1. GI tract irritation by EG and calcium oxalate
  2. CNS depression by EG, glycoaldehyde, and calcium oxalate
  3. induction of metabolic acidosis and electrolyte imbalances
  4. cytotoxicity by the production of ROS due to CYP450 inhibition
  5. mechanical damage by calcium oxalate crystals
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13
Q

What are the 3 stages to ethylene glycol toxicity?

A
  1. CNS
  2. cardiopulmonary/acidotic
  3. renal toxicity
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14
Q

What are the 2 main toxic principles that causes CNS signs in ethylene glycol toxicity?

A

mostly EG and aldehydes, but high levels of glycolic acid may also cause CNS effects

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15
Q

Other than CNS signs, what are 4 other signs of stage I of ethylene glycol toxicosis?

A
  1. mimics acute alcohol toxicosis
  2. GIT irritation
  3. EG increases serum osmolarity, leading to PD/PU
  4. EG has an osmotic diuretic effect (like ethanol) and may inhibit release of ADH
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16
Q

What are the major clinical signs associated with stage I of ethylene glycol toxicosis?

A

CNS EFFECT

  • inebriatioin and belligerance
  • depression, loss of withdrawal and righting reflexes
  • progressive ataxia with knuckling over and stumbling
  • osmotic diuresis, PD/PU
  • hypothermia
  • nausea and vomiting due to gastric irritation
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17
Q

What causes stage II of ethylene glycol toxicosis?

A

CADIOPULMONARY/ACIDOTIC

  • accumulation of acidic metabolites, especially glycolic acid
  • calcium sequestration as calcium oxalate causes hypocalcemia and impairment of cardiac function
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18
Q

What are the main clinical signs associated with stage II of ethylene glycol toxicosis?

A

CADIOPULMONARY/ACIDOTIC

  • PD subsides with EG metabolism, but the metabolites cause severe acidosis
  • vomiting, miosis
  • tachycardia/bradycardia, tachypnea
  • muscle fasciculation, depression
  • hypothermia
  • many animals die at this stage
19
Q

What are 3 characteristics of stage III of ethylene glycol toxicosis?

A

RENAL TOXICITY

  1. formation of calcium oxalate crystals in the kidney
  2. cytotoxicity of EG metabolites to renal tubular epithelium
  3. glycolic acid and glyoxylic acid elevate the anion and osmolar gaps, leading to renal edema, compromisation of intrarenal blood flow, and renal failure
20
Q

What is the anion gap? How is it calculated?

A

difference between serum cations and anions, laong with unmeasured anions and cations

AG = [Na + K] - [Cl + HCO3]

21
Q

What are the unmeasured anions and cations calculated in the anion gap? How is it affected by ethylene glycol toxicosis?

A
  • UA = SO4, PO4, lactate, ketones, EG metabolites
  • UC = Ca, Mg, sometimes K

increased anion gap caused by a decrease in serum HCO3- (used to buffer H+) and an increase EG metabolites that contribute to the unmeasured anions pool

22
Q

What is the normal anion gap in dogs and cats?

A

DOGS = 8-19

CATS = 9-21

23
Q

What are some differential diagnoses for an increased anion gap?

A

Carbon monoxide, cyanide
Aminoglycosides
Toulene/theophylline

Methanol/melamine-cyanuric acid
Uremia
Diabetic ketoacidosis
Propylene glycol
Infection/ischemia/iron
Lactate
Ethylene glycol/ethanol
Salicylates/starvation

24
Q

What’s the difference between osmolality and osmolarity?

A

OSMOLALITY - # of particles per kg of solvent

OSMOLARITY - # of particles per L of solvent

25
Q

What is the osmolar gap? What 6 molecules contribute most to it?

A

difference between measured and calculated serum osmolality

Na+, K+, Cl-, HCO3-, glucose, and urea*

26
Q

How does ethylene glycol toxicity affect the plasma osmolarity?

A

osmolality is usually 280-310 mOsm/kg and will increase because EG is an osmotically active small molecute

27
Q

How is plasma osmolarity calculated? What are the units for each value?

A

[1.86 (Na + K)] + (glucose/18) + (BUN/2.8) + 9

  • electrolytes = mEq/L = mmol/L for monovalent ions
  • glucose and BUN = mg/dL = mg/100 mL
  • all values are converted to millimolar units to do the math
28
Q

What is the normal osmolar gap? How is this affected by ethylene glycol intoxication?

A

10 mOsm/L

increases to >/= 60 mOsm/L because EG and its metabolites are measured by the osmometer, but are not considered in the formula used to calculate osmolarity

29
Q

What are the 4 major clinical signs of stage III of ethylene glycol toxicity?

A

RENAL TOXICITY

  1. olguric renal failure - PU, oliguria/anuria, dehydration, calcium oxalate crystalluria, decreased GFR, increased BUN and creatinine
  2. uremia - lethargy, vomiting, oral ulceration, convulsions, seizures, coma, death
  3. anterior uveitis and vitreous hemorrhage - blepharospasms, miosis, unilateral slow pupillary reflex
  4. enlarged and extremely painful kidneys
30
Q

What are the main clinical signs of stage III of ethylene glycol toxicity in cats, cattle, swine, and chickens?

A

RENAL TOXICITY

  • CATS: similar to dogs, but lack PD and depression is persistent
  • CATTLE: staggering, ataxia, paraparesis, tachypnea, dyspnea, recumbency, bradycardia that develops into tachycardia, hemoglobinuria, epistaxis
  • SWINE: depression, weakness, ataxia, knuckling of hindlimbs, muscle tremors, loss of reflexes, ascites, hydrothorax, weak heart sounds, recumbency
  • CHICKEN: ruffled feathers, listlessness, ataxia, dyspnea, watery droppings, recumbency with drooping wings, closed eyes with head resting on floor propped up by the beak, comb cyanosis
31
Q

How is ethylene glycol toxicity diagnosed? How is urine especially tested?

A
  • history of exposure, clinical signs, clinical pathology (increased BUN and creatinine)
  • chemical analysis
  • ultrasonography showing increased renal cortical echogenicity

examined under Wood’s lamp —> fluorescin dye is added and is able to track EG leakages

32
Q

What is the goal to ethylene glycol toxicosis treatment?

A

initiate ASAP (<3 hr for cats; <5 hr for dogs) to stop EG from going down its metabolic pathway and be excreted in the urine

33
Q

When is emesis indicated in ethylene glycol toxicosis? When is gastric lavage indicated? When is activated charcoal contraindicated?

A

if exposure is within 30 min of exposure and patient does not exhibit neurological signs

within 4 hrs if scout radiograph reveals the presence of ingesta

patients being treated with ethanol orally, as it will inhibit ethanol absorption

34
Q

What are the 2 antidotes for ethylene glycol toxicosis? Can they be used together?

A
  1. ethanol - competitively inhibits alcohol dehydrogenase with a higher affinity than EG
  2. 4-methylpyrazole (Antizole-Vet, Fomepizole) - competitively inhibits alcohol dehydrogenase

NO —> ethanol (alcohol) toxicosis

35
Q

How is dehydration, metabolic acidosis, renal failure, and hypothermia due to ethylene glycol toxicity treated?

A

fluid therapy —> also promotes diuresis to excrete EG and its metabolites

sodium bicarbonate

peritoneal dialysis —> also promotes excretion of EG and its metabolites

blankets

36
Q

What are the 3 major risks associated with ethylene glycol toxicity treatment?

A
  1. EMESIS - useful early, but presents a risk of aspiration because patients are depressed
  2. FLUID THERAPY - may cause fluid overload if patient is oliguric
  3. ETHANOL - increases osmolarity and causes CNS depression
37
Q

What affects prognosis of ethylene glycol toxicity?

A

high potential for lethal outcome!

depends on dose ingested, rate of absorpton, and time interval between exposure and treatment —> timely Dx and Tx are vital —> < 3 hr in cats, < 5 hr in dogs

38
Q

What are some major sources of propylene glycol? What is it used to treat? How does it compare to ethylene glycol?

A

solvents, humectants, plasticizers, bacteriostats, cosmetic, semi-moist/canned food, coolants, de-icing solutions, antifreeze

glucose precursor for ketosis

less toxic

39
Q

What is the metabolism of propylene glycol like? How is it excreted?

A
  • metabolized in liver and kidney by alcohol dehydrogenase and aldehyde dehydrogenase to D- and L-lactic acid
  • L-lactic acid is rapidly metabolized in the Krebs cycle
  • D-lactic acid is slowly metabolized and accumulated in plasma leading to lactic acidosis

excreted in kidney un-metabolized or as a glucuronide conjugate

40
Q

What species are most susceptible to propylene glycol toxicosis? How does it cause encephalopathy? Anemia?

A

cats, dogs, cattle, horses

accumulation of lactic acid in brain

induces Heinz body anemia in cats (esp. cats with high food intake, like lactating queens and nursing kittens) by interacting with the -SH groups in Hb —> 8 -SH groups and less ability to conjugate propylene glycol with glucuronide

41
Q

What is responsible for the clinical signs of propylene glycol toxicosis? What is seen in cats/dogs, cows, and horses?

A

acidosis and narcosis

  • CATS/DOGS: PU/PD, dehydration, decreased activity, depression, ataxia, muscle twitching, drunkenness, hypotension
  • COWS: ataxia, depression, temporary recumbency
  • HORSES: pain, sweating, salivation, ataxia, depression, recumbency, rapid shallow breathing, cyanosis
42
Q

How are horses commonly inadvertently given propylene glycol resulting in toxicosis?

A

has been mistaken mineral oil and given to horses for colic treatment

43
Q

What clinical pathology is indicative of propylene glycol toxicity? What supportive treatment is used?

A

metabolic acidosis, elevated anion gap associated with high blood lactic acid

  • IV fluid containing sodium bicarbonate
  • gastric lavage
  • activated charcoal
  • Dexamethasone
  • vitamin C

Veterinary Toxicology (29 decks)

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