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Toxicology > Renal & Hepatic > Flashcards

Renal & Hepatic Flashcards

1
Q

Why kidneys are susceptible to effects of toxicity

A

High blood flow
High concentration of toxins
Critical for excretion of xenobiotics

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2
Q

Most common site of kidney for toxin-induced injury

A

Proximal tubule

Because:
Cytochrome p450 and cysteine conjugates can bioactivate toxins
Loose epithelium allow compounds to enter cells
Increased transport of anion, cations, and heavy metals causes accumulation and can cause ischemic injury to epithelial cells

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3
Q

Characteristics of ethylene glycol

A

Antifreeze
2nd most common of fatal poisonings in animals
Most frequently used for malicious poisonings
Exposure most common in spring and fall when people change their antifreeze
Very high rate of lethality (80%) due to delays in presentation
Tastes “sweet”

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4
Q

Lethal dose of ethylene glycol in cats

A

1.5 ml/kg of undiluted antifreeze

About 1 tbsp of 50% antifreeze

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5
Q

Lethal dose of of ethylene glycol in dogs

A

7 ml/kg of undiluted antifreeze

4.5oz of 50% antifreeze

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6
Q

Mechanism of action in ethylene glycol toxicity

A
  1. Glycolic acid causes acidosis
  2. Glyoxylic acid causes CNS signs
  3. Oxalate/oxalic acid causes renal damage and hypocalcemia
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7
Q

Stage 1 of ethylene glycol toxicity

A

30 min - 3 hours after ingestion

“Drunkenness”, ataxia, CNS depression
Nausea, vomiting
PU/PD (dogs)
Usually missed with unobserved ingestions

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8
Q

Stage 2 of ethylene glycol toxicity

A

12-24 hours post ingestion
Tachypnea, tachycardia (or bradycardia)
Often not severe and not recognized by owner
Cats typically remain depressed

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9
Q

Stage 3 ethylene glycol toxicity

A

12-72 hours post ingestion
Most animals present in this stage!
Polyuria progression to oliguria and anuria
Lethargy, anorexia, vomiting, seizures
Oral ulcers, abdominal pain, dehydration, enlarged kidneys

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10
Q

Diagnosis of ethylene glycol toxicity

A

Best method is measuring EG concentration in blood (peak concentrations at 1-6 hours, undetectable by 24 hours)
Chem panel: elevated BUN and creatinine in Stage 3, hyperglycemia, hypocalcemia, increased anion gap
Urinalysis: low SG, crystalluria
Calcium oxalate crystals in kidney

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11
Q

Treatment of ethylene glycol toxicity

A

Goal: prevent formation of toxic metabolite

Give 20% ethanol + sodium bicarbonate, or fomepizole

No benefit if E.G. Has already been metabolized

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12
Q

Prognosis of EG toxicity (cats and dogs)

A

Cats: prognosis best if treated in first 3-4 hours, 90% mortality rate

Dogs: prognosis best if treated in the first 6-8 hours

Renal failure indicates poor prognosis for both

For the survivors: therapy may be needed every 72 hours, treatment may take 3-5 days

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13
Q

Why is sodium bicarbonate given with ethanol in treatment of ethylene glycol toxicity?

A

Correct metabolic acidosis

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14
Q

Why would you not use decontamination as a treatment for ethylene glycol toxicity?

A

It is rapidly absorbed in stomach so these treatments would be ineffective unless the ingestion was observed/could treat within 1 hour of ingestion

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15
Q

Sources of cholecalciferol (Vit D3) that may cause toxicity

A

Vitamin supplements

Some rodenticides

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16
Q

Mechanism of action of cholecalciferol (Vit D3)

A

Is metabolized to 1,2 dihydroxycholecalciferol

Causes massive increases in serum calcium by:
Increasing GI absorption
Decreasing renal excretion
Increased synthesis of Ca binding protein
Mobilizing bone calcium

17
Q

Clinical signs of cholecalciferol (Vit D3) toxicity

A

Signs usually appear 36-48 hours after ingestion
Anorexia, weakness, depression
Thirst and polyuria
Diarrhea, dark feces due to intestinal bleeding
Vomiting
Hypertension
Bradycardia, ventricular arrhythmia
Mineralization of tissues when Ca * P >70 mg/l

18
Q

Diagnosis of cholecalciferol (Vit D3) toxicity

A

Based on history of ingestion, clinical signs, and hypercalcemia
Rapid increased in P followed by increase in plasma Ca
Low PTH
Increased BUN, creatinine
Low urine SG with calciuria
High hydroxycholecalciferol levels in bile and kidney

19
Q

Differential diagnoses for cholecalciferol (Vit D3) toxicity

A

Mineralization in multiple organs

Ethylene glycol
Paraneoplastic syndrome
Juvenile hypercalceimia
Hyperparathyroidism

20
Q

Treating cholecalciferol (Vit D3) toxicity

A 
GI decontamination within 6-8 hours
Monitor and reduce dietary Ca and P
Saline, furosemide
Prednisolone
Pamidronate
Sucralfate or milk of magnesia for ulceration
21
Q

Mechanism of action of grape/raisin toxicity

A

UNKNOWN

22
Q

Major result of grape/raisin toxicity

A

Renal failure

23
Q

Clinical signs/diagnosis of grape/raisin toxicity

A

Vomiting followed by symptoms of acute renal failure

Hypercalcemia
Hyperphosphatemia
Increased CaPO4
Elevated BUN and serum creatinine

24
Q

Treatment of grape/raisin toxicity

A

Recommended following ingestion of ANY quantity
Emesis, lavage, activated charcoal
Fluid therapy for a min 72 hours
Furosemide
Other supportive therapies: Dopamine, mannitol, hemodialysis, peritoneal dialysis

25
Q

Mechanism of action of acetaminophen toxicity

A

Metabolized bin liver by glucuronidation, sulphonation, and oxidative pathways that result in the formation of NAPQI (causes most of the damage)

NAPQI binds macromolecules and proteins to cause liver tissue necrosis and causes erythrocytes injury (MetHb and Heinz bodies)

Cats especially susceptible!

26
Q

Clinical signs of acetaminophen toxicity

A

MetHB, Heinz bodies
Hepatotoxicity, Liver necrosis
Tachycardiaa, hyperpnea, weakness, lethargy

27
Q

Diagnosis of acetaminophen toxicity

A

Cats: cyanosis, MetHb, dyspnea, weakness, depression, edema of face/paws, anemia

Dogs: centrilobular hepatic necrosis, nausea, vomiting, anorexia, abdominal pain, tachypnea, tachycardia

28
Q

Treatment of acetaminophen toxicity

A

REPLENISH GLUTATHIONE STORES! Give NAC (N-acetylcysteine)

Early decontamination if possible

Decreased MetHb by giving ascorbic acid (Vit C)

Cimetidine

Antioxidants

Supportive care

Toxicology (7 decks)

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