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ACVIM General copy > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What is the MOA of acetaminophen toxicity?

A
  1. Reactive oxygen metabolites → oxidative damage to hemoglobin → causes Fe3+ methemoglobinemia and Heinz bodies → hemolysis
  2. Hepatotoxicity
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2
Q

What diagnostic results would be supportive of acetaminophen toxicity?

A
  1. Heinz body anemia

2. Elevated liver enzymes

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3
Q

How is acetaminophen toxicity treated?

A
  1. N-acetylcystein
  2. Cimetidine
  3. Ascorbic Acid
  4. SAMe
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4
Q

What are clinical signs associated with acetaminophen toxicity?

A
  1. Muddy mucous membranes

2. Anemia

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5
Q

What is the MOA of anticoagulant rodenticide (warfarin, brodifacoum, bromadiolone, etc)?

A
  1. Inhibit recycling of Vit K by inhibiting vitamin K epoxide reductase
    - Will cause a reduction in factors II, VII, IX, and X
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6
Q

What clinical signs are associated with anticoagulant rodenticide toxicity?

A
  1. Prolonged bleeding
  2. Hemorrhage into body cavities
  3. Hematomas
  4. Anemia
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7
Q

What diagnostic findings would be supportive of anticoagulant rodenticide toxicity?

A
  1. Prolonged PT then ACT/PTT
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8
Q

How is anticoagulant rodenticide toxicity treated?

A
  1. Vitamin K supplementation

- Bioavailability is best by mouth!

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9
Q

What is the MOA of ethylene glycol toxicity?

A

FIRST PHASE: Causes neuro signs/depression within one hour
- Ethylene glycol → alcohol dehydrogenase (rate limiting step) → Glycoaldehyde

SECOND PHASE: Causes acidosis/cardiopulmonary signs (within 8-24 hours)
- Glycoaldehyde → aldehyde dehydrogenase → glycolic acid

THIRD PHASE: Stone formation (calcium oxalate monohydrate) in 3hrs (cat) and 5hrs (dog); also renal failure (1-3 days)
- Glycolic acid → lactic dehydrogenase/glycolic acid oxidase → glycoxylic acid → glycine, oxalic acid, CO2

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10
Q

What are the main causes of acidoses in ethylene glycol toxicity? What is the most important final metabolite of ethylene glycol?

A
  1. Glycolic acid and lactic acid

2. Oxalic acid → cytotoxic to renal tubule and causes Ca precipitation

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11
Q

What are the diagnostic findings associated with ethylene glycol toxicity?

A
  1. “Halo” effect on AUS → decreased echogenicity of corticomedullary junction
  2. Isosthenuria
  3. AG acidosis
  4. Hypocalcemia
  5. Hyperosmolarity
  6. Crystalluria
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12
Q

What are the clinical signs associated with ethylene glycol toxicity?

A
  1. Gastric irritant

2. CNS depression

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13
Q

When should the ethylene glycol test be performed?

A
  1. Within 1-12 hours of exposure
    - Will not work after 24-48 hours-
    - Wont detect <50 mg/dl so it wont work well in cats
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14
Q

What are causes of false positives on the ethylene glycol test?

A
  1. Glycerol
  2. Metaldehyde
  3. Propylene glycol
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15
Q

How is ethylene glycol treated?

A
  1. Ethanol → competitive inhibitor of alcohol dehydrogenase
  2. 4-MP → competitive inhibitor of alcohol dehydrogenase but doesn’t cause CNS signs like ethanol
  3. Treatment for acute renal failure
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16
Q

What is the MOA of bromethalin rodenticide?

A
  1. Uncouples oxidative phosphorylation → leads to hyper excitability acutely, and then depression chronically
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17
Q

What is the MOA of strychnine?

A
  1. Inhibits glycine on motor neurons and interneurons → it inhibits the buffering effect of glycine on post-synaptic motor/interneurons
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18
Q

What clinical signs are seen with strychnine toxicity?

A
  1. Extensor rigidity (esp after stimuli) → spastic paralysis also noted
  2. Respiratory muscle paralysis
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19
Q

How is strychnine toxicity treated?

A
  1. Pentobarbital
  2. Methocarbamol
  3. Sedation to prevent seizures
  4. Urinary acidification → with ammonium chloride to help with urine trapping (ionizes the strychnine)
20
Q

What is the MOA of zinc phosphide? How is it treated?

A
  1. Acid stomach contents cause the release of phosphine gas

2. Increase the pH of the stomach (milk of magnesia or 5% orogastric bicarb)

21
Q

What is the MOA of organophosphates and carbamates?

A
  1. Organophosphates: IRREVERSIBLY INHIBIT acetylcholinesterase
  2. Carbamates: REVERSIBLY INHIBIT acetylcholinesterase
22
Q

What are the clinical signs seen with organophosphate and carbamate toxicity?

A

MUSCARINIC EFFECTS:

  1. Salivation
  2. Lacrimation
  3. Bronchial secretion
  4. Vomiting
  5. Diarrhea

NICOTINIC EFFECTS:

  1. Muscle tremors
  2. Respiratory paralysis
23
Q

How are organophosphate and carbamate toxicities treated?

A
  1. Atropine → anti-muscarinic effects → alleviate severe bradycardia and excessive bronchiolar secretion/constrction → WILL NOT ALLEVIATE NICOTINIC SIGNS
  2. 2-PAM → act on the OP-Acetylcholinesterase complex to free the enzyme and restore normal function → WILL ALLEVIATE NICOTINIC SIGNS as well as muscarinic → DOES NOT WORK IF ACE IS CARBAMYLATED
24
Q

What is the MOA of lead toxicity?

A
  • Carried primarily on RBCs*
    1. Interferes and competes with Ca ions → also substitutes for Ca in bone matrix
    2. Binds to cellular and enzymatic sulfhydryl (thiol) groups
    3. Alters vitamin D metabolism
    4. Inhibits membrane associated enzymes
    5. Inhibit of ferrochelatase and gaba-aminolevulinic acid dehydrates → inhibits heme synthesis
    6. GI signs due to alteration of smooth muscle contractility due to interference with Ca dependent mechanisms
25
Q

What clinical signs are associated with lead toxicity?

A
  1. Cats can get lead induced seizures
  2. GI signs
  3. Ataxia
  4. Tremors
  5. Blindness
  6. Dementia
  7. Agression
  8. Picca
  9. Vestibular signs
  10. Megaesophagus (cat)
26
Q

What are diagnostic findings associated with lead toxicity?

A
  1. Anemic (usually not hemolysis though)
  2. Nucleated RBCs!!!
  3. “Lead lines” → linear opacities on the physes of long bones
27
Q

How is lead toxicity treated?

A
  1. Must decontaminate before chelation
  2. CaEDTA! → NOT NaEDTA → NaEDTA will bind CA and cause hypocalcemia
  3. Succimer → British anti-Lewisite (BAL) analog) → often used in combination with CaEDTA especially when CNS signs present
28
Q

What is the MOA of xylitol toxicity?

A
  1. Causes a rapid dose dependent INCREASE in blood insulin concentration → concurrent DECREASE in blood clues
  2. Hepatic necrosis can also be seen → secondary to interference with hepatocellular ATP production
29
Q

How is xylitol toxicity treated?

A
  1. First with dextrose supplementation
  2. Hepatic protectants
  3. Charcoal is debatable
  4. Emesis if possible
30
Q

What parts of lilies are toxic?

A
  1. All parts but the flowers are most toxic
31
Q

What diagnostic findings are associated with lily toxicity in cats?

A
  1. Increased BUN
  2. Increased Creatinine
  3. Increased Potassium
  4. Increased Phosphorus
    * Creatinine will be disproportionately elevated compared to the increased BUN
32
Q

What clinical signs are found with marijuana toxicity?

A
  1. Depression
  2. Bradycardia
  3. Ataxia
  4. Lethargy
  5. Vomiting
  6. Urine dribbling
33
Q

(Older/Younger) animals are more affected by lead toxicity?

A
  1. Younger → more lead absorption following ingestion
34
Q

What is the MOA of aflatoxicosis?

A
  1. Metabolized in the liver by P450 enzymes → reactive intermediates then conjugate with glutathione
  2. Reactive intermediates result in hepatic necrosis
35
Q

What are the clinical signs associated with aflatoxicosis?

A
  1. Anorexia
  2. Weakness
  3. Obtundation
  4. Vomiting/Diarrhea
  5. Icterus
  6. Coagulopathy
36
Q

What diagnostic findings are associated with aflatoxicosis?

A
  1. Increased t. bili
  2. Liver enzyme elevation
  3. Decreased albumin
  4. Decreased protein C
  5. Decreased cholesterol
37
Q

What is the MOA of caster bean toxicity?

A
  • Contains the toxalbumin RICIN*
    1. Ricin → has a neutral A chain and acidic B chain
    2. B-subunit binds to glycoproteins on the surface of epithelial cells and allows the A subunit to enter via receptor mediated endocytosis
    3. A subunit then inactivates ribosomal RNA → inhibits protein synthesis → leads to cell death
38
Q

Which part of the caster bean plant is toxic?

A

All parts

*seeds have a tough coating that requires mastication but even a very small dose can be lethal

39
Q

What clinical signs are associated with caster bean toxicity?

A
  1. Most commonly there is a 12-24 hours quiescent period from exposure
  2. Then development of severe hemorrhagic gasteroenteritis
  3. Other clinical signs may include:
    - Hyperthermia
    - Vomiting
    - Dehydration
    - Leukopenia
    - Hemolysis
    - Hemoglobinuria
    - Kidney failure
    - Terminal seizures progressing to death
40
Q

How is caster bean toxicity treated?

A
  1. Emesis followed by gastric lavage or charcoal in the asymptomatic patient
  2. Shock doses of IVF and additional digestive support can be used as indicated by patient condition
41
Q

What is the MOA of mushroom toxicity?

A
  • Amanita Mushrooms*
    1. Contain amatoxins → inhibit RNA polymerases → leads to decreased mRNA generation → arrested protein synthesis → necrosis of metabolically active cells (includes intestinal crypt cells, hepatocytes, and renal tubular cells)
42
Q

What are clinical signs associated with mushroom toxicity?

A

6-24 hours after ingestion

  1. Vomiting
  2. Bloody diarrhea
  3. Abdominal pain

24-48 hours after ingestion
1. Severe hypoglycemia caused by insulin release stimulated by alpha-amantin

36-84 hours after ingestion
1. Massive hepatic necrosis and renal tubular necrosis

43
Q

How is mushroom toxicity treated?

A
  1. Silybin → inhibits amatoxin uptake by hepatocytes
44
Q

What is the MOA of blue green algae toxicity?

A
  1. Cyanotoxins microcystin and nodular inhibit serine/threonine protein phoshpatases in the liver → subsequent hyperphosphorylation and disruption of cytoskeletal proteins → leads to hepatic dissociation, hepatic necrosis, and glutathione depletion
45
Q

How is blue green algae toxicity treated?

A
  1. Intensive supportive therapy

2. Cholestyramine can bind cyanotoxins in the gut

46
Q

What is the MOA of sago palm toxicity?

A
  1. The toxin cycasin is activated to methylazoxymethanol by gut bacteria → causes gastrointestinal and hepatic toxicosis

ACVIM General copy (15 decks)

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