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605 Toxicology > Hepatic Toxicants > Flashcards

Hepatic Toxicants Flashcards

1
Q

Where can our pets get into too much iron?

A

vitamins, fertilizers, and slug/snail baits

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2
Q

Clinical Signs of Iron Toxicity

A

vomiting, diarrhea, stomach ulcers

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3
Q

Iron Toxicity MOA

A

not enough ferritin and transferrin, results in free iron which gets into liver, heart, brain, and more, increases free radicals

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4
Q

First Organ System Affected by Iron Toxicity?

A

gastrointestinal (GI)

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5
Q

Iron Overdose Treatment

A

emesis, then magnesium hydroxide (Maalox) to form iron hydroxides which is poorly absorbed so less gets to the liver; also Desferal to protect the liver to get rose wine urine

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6
Q

Antidote to Iron Overdose?

A

Desferal (deferoxamine)

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7
Q

Acetaminophen Clinical Signs

A

methemoglobinemia, tachycardia, tachypnea, weakness, lethargy, face/paw edema, hypothermia, vomiting, death

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8
Q

Methemoglobinemia

A

chocolate/muddy brown blood and mucous membranes

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9
Q

Acetaminophen Toxicity Treatment

A

emesis, activated charcoal and cathartic, N-acetylcysteine, fluids

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10
Q

Can you give Cimetidine to cats?

A

NO!! It inhibits cytochrome p450 which is a cat’s only way to convert

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11
Q

Antidote for acetaminophen toxicity?

A

N-acetylcysteine!

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12
Q

NAC (N-acetylcysteine)

A

precursor to glutathione, binds directly to NAPQI, decreases half-life of methemoglobin

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13
Q

Are ferrets sensitive to acetaminophen?

A

yep, just like cats! (obligate carnivores)

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14
Q

NAPQI

A

metabolite of acetaminophen that causes centrilobular liver necrosis

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15
Q

Xylitol affects what species?

A

DOGS and only dogs

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16
Q

Are all 5-carbon sugar alcohols a problem?

A

no, only xylitol (others include sorbitol, mannitol, etc)

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17
Q

Clinical Signs of Xylitol Poisoning

A

high insulin, hypoglycemia, leads to liver failure
(also vomiting, depression, weakness, ataxia, seizures/coma, diarrhea, cramping, hypokalemia, hypernatremia)

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18
Q

Can you treat xylitol with activated charcoal?

A

no, it doesn’t bind

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19
Q

Primary treatment for xylitol ingestion?

A

dextrose

also small frequent meals and liver protectants, monitor blood glucose

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20
Q

Pyrrolizidine Alkaloid Plants

A

essentially weedy, wild, yellow or blue flowers and seed pods

ragwort, groundsel, fiddleneck, rattlebox

21
Q

Pyrrolizidine Alkaloids MOA

A

hepatic P450s make toxic pyrroles, react with macromolecules, alkylation of DNA, and then hepatocytes grow but can’t divide (hepatomegaly) and body tries to repair with fibrosis

22
Q

Species most sensitive to Pyrrolizidine Alkaloids?

A

pigs (but uncommon)

23
Q

Species where we see most Pyrrolizidine Alkaloid toxicity?

A

cattle and horses (these plants grow pretty wild in the west)

24
Q

Clinical Signs of ACUTE Pyrrolizidine Alkaloid Toxicity

A

hepatic failure, anorexia, depression, icterus, ascites

25
Q

Clinical Signs of CHRONIC Pyrrolizidine Alkaloid Toxicity

A

overall unthrifty, photosensitive, icteric

Horses: Walla Walla Walking Disease, Missouri Bottoms Disease (circling, head pressing)
Cattle/Pigs: chronic liver failure and hard liver disease

26
Q

3 pathognomonic Lesions for Pyrrolizidine Alkaloid Toxicity

A
  1. Hepatocytomegaly
  2. Fibrosis
  3. Bile Duct Proliferation
27
Q

Treatment for Pyrrolizidine Alkaloid Toxicity

A

not really… give fluids, laxative, high protein/low carb diet

28
Q

Clinical Signs Cycad and Sago Palm Toxicity

A

[bloody] vomit, depression, anorexia, hyperbilirubinemia –> liver failure

29
Q

3 Toxins in the Palms

A
  1. Cycasin (GI irritation and hepatic necrosis)
  2. BMAA (neurotoxic AA)
  3. Unidentified (Parkinson’s like)
30
Q

Toxin in Palms that affects dogs?

A

cycasin

31
Q

Toxin in Palms that affects cattle?

A

BMAA

32
Q

Amatoxins

A

found in mushrooms; inhibits RNA polymerase interfering with transcription and translation, eventually breaking down cell membranes in the liver

33
Q

3 Phases of Clinical Signs in Amatoxin

A
  1. GI Signs
  2. The Honeymoon
  3. Hepatic failure, abdominal pain, seizures, encephalopathy, coma, death
34
Q

Treatment for Amatoxins

A

emesis, activated charcoal, aspirate the gallbladder, NPO, give OCTREOTIDE

35
Q

octreotide

A

main treatment for amatoxin mushrooms (blocks carrier molecule OATP1B3 so amatoxins cannot leave the gallbladder)

36
Q

2 Syndromes of Blue Green Algae

A
  1. Acute hepatotoxicosis
  2. Acute neurotoxicosis
37
Q

Blue Green Algae MOA

A

microcystin causes hyperphosphorylation of cytoskeletal proteins leading to disorganization of actin and cellular collapse, eventually causing intrahepatic hemorrhage and death

38
Q

Clinical Signs of Blue Green Algae

A

weakness, stupor, prolonged CRT, pale MM, bloody diarrhea, coma, tremors, seizures, hypovolemic shock –> hemorrhage and liver failure

39
Q

Blue Green Algae Prognosis?

A

poor

40
Q

Aflatoxins

A

aspergillus, in crops with high energy content (corn, peanuts, cottonseed, rice, sweet potaters)

41
Q

How are aflatoxins eliminated?

A

bile, urine, feces, eggs, milk

42
Q

Acute Aflatoxin Signs

A

massive liver necrosis and death

43
Q

Chronic Aflatoxin Toxicity Signs

A

reduced weight gain, rough hair coats, anemia, jaundice, anorexia, depression, ascites, elevated hepatic enzymes

44
Q

Aflatoxin Lesions

A

diffuse fatty liver, distorted liver, bile duct proliferation, granules and vacuoles in hepatocytes

45
Q

Screening for Aflatoxins

A

test, also blacklights

46
Q

Can aflatoxins lead to carcinogenesis?

A

yes

47
Q

Prevention of Aflatoxins

A

prevent crop damage
dry corn (15% moisture or less)
clays (bind and make less toxic)
ammoniation of feedstuffs

48
Q

Kojic Acid

A

metabolite of aspergillus that causes problems

605 Toxicology (9 decks)

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