Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

ACVIM General Exam > 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What diagnostic results would be supportive of acetaminophen toxicity?

A
  1. Heinz body anemia

2. Elevated liver enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is acetaminophen toxicity treated?

A
  1. N-acetylcystein
  2. Cimetidine
  3. Ascorbic Acid
  4. SAMe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are clinical signs associated with acetaminophen toxicity?

A
  1. Muddy mucous membranes

2. Anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What clinical signs are associated with anticoagulant rodenticide toxicity?

A
  1. Prolonged bleeding
  2. Hemorrhage into body cavities
  3. Hematomas
  4. Anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What diagnostic findings would be supportive of anticoagulant rodenticide toxicity?

A
  1. Prolonged PT then ACT/PTT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is anticoagulant rodenticide toxicity treated?

A
  1. Vitamin K supplementation

- Bioavailability is best by mouth!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the clinical signs associated with ethylene glycol toxicity?

A
  1. Gastric irritant

2. CNS depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A
  1. Glycerol
  2. Metaldehyde
  3. Propylene glycol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the MOA of bromethalin rodenticide?

A
  1. Uncouples oxidative phosphorylation → leads to hyper excitability acutely, and then depression chronically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
What clinical signs are associated with lead toxicity?
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
What are diagnostic findings associated with lead toxicity?
1. Anemic (usually not hemolysis though) 2. Nucleated RBCs!!! 3. "Lead lines" → linear opacities on the physes of long bones
27
How is lead toxicity treated?
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
What is the MOA of xylitol toxicity?
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
How is xylitol toxicity treated?
1. First with dextrose supplementation 2. Hepatic protectants 3. Charcoal is debatable 4. Emesis if possible
30
What parts of lilies are toxic?
1. All parts but the flowers are most toxic
31
What diagnostic findings are associated with lily toxicity in cats?
1. Increased BUN 2. Increased Creatinine 3. Increased Potassium 4. Increased Phosphorus * Creatinine will be disproportionately elevated compared to the increased BUN
32
What clinical signs are found with marijuana toxicity?
1. Depression 2. Bradycardia 3. Ataxia 4. Lethargy 5. Vomiting 6. Urine dribbling
33
(Older/Younger) animals are more affected by lead toxicity?
1. Younger → more lead absorption following ingestion
34
What is the MOA of aflatoxicosis?
1. Metabolized in the liver by P450 enzymes → reactive intermediates then conjugate with glutathione 2. Reactive intermediates result in hepatic necrosis
35
What are the clinical signs associated with aflatoxicosis?
1. Anorexia 2. Weakness 3. Obtundation 4. Vomiting/Diarrhea 5. Icterus 6. Coagulopathy
36
What diagnostic findings are associated with aflatoxicosis?
1. Increased t. bili 2. Liver enzyme elevation 3. Decreased albumin 4. Decreased protein C 5. Decreased cholesterol
37
What is the MOA of caster bean toxicity?
* 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
Which part of the caster bean plant is toxic?
All parts | *seeds have a tough coating that requires mastication but even a very small dose can be lethal
39
What clinical signs are associated with caster bean toxicity?
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
How is caster bean toxicity treated?
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
What is the MOA of mushroom toxicity?
* 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
What are clinical signs associated with mushroom toxicity?
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
How is mushroom toxicity treated?
1. Silybin → inhibits amatoxin uptake by hepatocytes
44
What is the MOA of blue green algae toxicity?
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
How is blue green algae toxicity treated?
1. Intensive supportive therapy | 2. Cholestyramine can bind cyanotoxins in the gut
46
What is the MOA of sago palm toxicity?
1. The toxin cycasin is activated to methylazoxymethanol by gut bacteria → causes gastrointestinal and hepatic toxicosis

ACVIM General Exam (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions