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Toxicology-soph-c > Tox-2 > Flashcards

Tox-2 Flashcards

1
Q

How do you treat salt toxicity?

A

Slow rehydration and furosemide (to prevent pulmonary edema)

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2
Q

What other differentials must you consider when suspecting salt toxicity?

A

Polio, lead, pesticides, encephalitis

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3
Q

What are examples of products that contain phenoxyacetic acid herbicides?

A

2,4-D (Scott’s weed and feed), 2,4,5-T, Silvex

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4
Q

How toxic are phenoxyacetic acid herbicides?

A

Low toxicity in most animals, though Silvex is very toxic

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5
Q

What are the clinical signs of phenoxyacetic acid herbicide toxicity?

A

GI effects (vomiting, diarrhea +/- blood, ulcerations, muscle effects, renal tubular degeneration, hepatic necrosis

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6
Q

How do you treat phenoxyacetic acid herbicide toxicity?

A

GI decontamination (emesis, lavage, activated charcoal, cathartic), ion trapping with NaHCO3 if kidneys normal to enhance excretion; prognosis is good with treatment

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7
Q

What is the mechanism of toxicity of ergot alkaloids?

A

Dopamine and serotonin receptor agonists

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8
Q

What are the clinical signs of ergot alkaloid toxicity?

A

Reduced feed intake and weight gain, heat intolerance, retain winter coat, necrotizing ergotism, fat necrosis, poor reproductive performance

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9
Q

How do you diagnose ergot alkaloid toxicity?

A

Evidence of sclerotia in feed, fescue in forage matter, chemical analysis of feed and forage

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10
Q

What is the gold standard treatment for ergot alkaloid toxicity?

A

Metoclopromide and domperidone to increase prolactin secretion and normalize gestation in mares

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11
Q

Ionophores are approved for use in dairy cattle to…

A

Improve efficiency of milk production

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12
Q

What is the mechanism of action of ionophores?

A

Increase intracellular Na+ and Ca++, leading to mitochondrial swelling and cell death, especially in muscle (remember it’s target is the mitchondrial MEMBRANE)

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13
Q

What is a common sign of ionophore toxicity?

A

Anorexia

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14
Q

What clinical signs are associated with ionophore toxicity in horses?

A

Anorexia, colic, profuse sweating on flanks; may be uncoordinated and weak

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15
Q

What clinical signs are associated with ionophore toxicity in cattle?

A

Same as horses but with diarrhea and respiratory difficulty

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16
Q

At necropsy, what are the characteristics of ionophore toxicity?

A

Hemorrhage in the hear, pale heart, infiltration of macrophages in the muscle

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17
Q

How do you diagnose ionophore toxicity?

A

Evidence of muscle damage on serum biochem, decreased K and Ca, chemical analysis of feeds and liver

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18
Q

What other differentials must you consider when suspecting ionophore toxicity?

A

Colic, vitamin E and Se deficiency, white snakeroot, blister beetle, gossypol, botulism

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19
Q

How do you treat ionophore toxicity?

A

No specific treatment or antidote; change feed, offer supportive therapy, anti-oxidants

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20
Q

What is the most common cause of tetanus?

A

Spores in puncture wounds

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21
Q

What is the mechanism of action of tetanus?

A

Blocks release of GABA and glycine (inhibitory neurotransmitters) resulting in overstimulation of muscles leading to stiffness

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22
Q

What are the clinical signs of tetanus?

A

Stiffness and reluctance to move, twitching and tremors, lockjaw, unsteady gait, bloat in ruminants

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23
Q

What is the treatment for tetanus?

A

Antitoxin if very early, supportive therapy; prognosis is very poor

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24
Q

First generation anticoagulants, such as warfarin, have a short/long half-life with a low/high potency?

A

Short half-life, low potency

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25
Q

Second generation anticoagulants, such as brodifacoum, have a short/long half-life with a low/high potency?

A

Long half-life, high potency

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26
Q

What is the mechanism of action of anticoagulants?

A

Inhibits vitamin K1 epoxide reductase preventing formation of vitamin K dependent clotting factors

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27
Q

What are the clinical signs of anticoagulant toxicity?

A

Delayed onset; depression, anorexia, and anemia, dyspnea, nosebleeds, bleeding gums, and bloody feces, hemorrhage and hematoma

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28
Q

What are the three most common methods of diagnosing an anticoagulant toxicity?

A

History of exposure, evidence of coagulopathy, response to vitamin K1 therapy (will also have prolonged PT)

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29
Q

How do you treat anticoagulant toxicity?

A

GI decontamination if recent; Vitamin K administration (low doses/short time for first gens, high doses/long time for second gens); transfusion if necessary

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30
Q

What are the common sources of nitrates that can cause nitrate toxicosis?

A

Fertilizers, plants, water

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31
Q

What is the mechanism of action of nitrates?

A

Nitrate -> nitrite -> vasodilation and ferrous iron+Hgb -> methemoglobin -> oxygen starvation of tissues

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32
Q

What are the hallmark clinical signs of nitrate toxicosis?

A

Cyanosis, brown blood; with serious toxicity, ataxia, seizures, coma, death

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33
Q

How do you diagnosis nitrate toxicosis?

A

Nitrate levels in feed or water; save eye for analysis after death

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34
Q

What treatment is most effective in nitrate toxicosis of ruminants?

A

IV methylene blue (urine will become dark green)

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35
Q

What treatment is most effective in nitrate toxicosis in cats and horses?

A

Ascorbic acid

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36
Q

What plants are common sources of cardiac glycosides?

A

Foxglove, oleander, lily of the valley

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37
Q

What is the mechanism of action of cardiac glycosides?

A

Inhibits Na-K ATPase through competition with K for binding sites

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38
Q

What are the clinical signs of cardiac glycoside toxicity?

A

Trembling, staggering and dyspnea in grazing animals; racing heart rate and rhythm/arrhythmia, weak pulse

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39
Q

How do you diagnose cardiac glycoside toxicity?

A

Hx, access to plants, CSs, and vomit analysis

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40
Q

What is the antidote for digoxin and similar glycosides?

A

Digoxin immune Fab fragments (i.e., digibind)

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41
Q

How do you treat cardiac glycoside toxicity?

A

GI decontamination if recent, propranolol for arrhythmias, treat hyperkalemia

42
Q

What is the mechanism of action of cyanide toxicity?

A

Inhibition of cytochrome oxidase and oxidative phosphorylation

43
Q

What is the classic symptom of cyanide toxicity?

A

Cherry red (superoxygenated) blood that is slow to clot

44
Q

How do you treat cyanide toxicity?

A

Induce methemoglobin formation with sodium nitrate to bind cyanide, then give sodium thiosulfate to increase formation of thiocyanate by rhodanese; if necessary, treat metHb with methylene blue

45
Q

What substances include methylxanthines?

A

Caffeine, theobromine, theophylline (coffee, chocolate, medications)

46
Q

What kind of chocolate is especially toxic?

A

Unsweetened baking chocolate

47
Q

What is the mechanism of action of methylxanthines?

A

Competitive antagonist of adenosine receptors (causes CNS stimulation, vasoconstriction, and tachycardia); prevents Ca++ reuptake leading to increased skeletal and cardiac muscle contractility

48
Q

What are the clinical signs of methylxanthine toxicity?

A

Vomiting, diarrhea, diuresis, hyperactivity, “bounce”, panting, tachycardia, hypertension, ataxia, tremors, seizures, death (from arrhythmias or respiratory failure)

49
Q

How do you treat methylxanthine toxicity?

A

GI decontamination (emesis, activated charcoal), monitor EKG (treat arrhythmias with lidocaine and then metoprolol if needed), diazepam for seizures, maintain respiration, fluid diuresis

50
Q

Where is the toxin gossypol found?

A

In pigment glands of cottonseed (provides insect resistance)

51
Q

What is the mechanism of action of gossypol?

A

Chelates iron and causes anemia, inhibits dehydrogenase leading to decreased energy and stress (can be cumulative as it is lipophilic)

52
Q

What are the clinical signs of gossypol toxicity?

A

Weight loss, weakness, dyspnea, moderate anemia, edema secondary to heart failure, myocardial necrosis, CHF

53
Q

How do you treat gossypol toxicity?

A

high protein diet, add vitamin A, iron, lysine; remove gossypol sources in diet, symptomatic

54
Q

What is the source of the toxin cantharidin?

A

Blister beetle or spanish fly

55
Q

What is the mechanism of action of cantharidin?

A

Inhibits protein phosphatases (dysregulates protein metabolism); mucosal irritant

56
Q

What are the clinical signs of cantharidin?

A

Colic, frequent uriniation, diaphragm contraction with heart beat, shock; severe irritation and ulceration of oral, GI, and bladder epithelia (muzzle in water); cardiac toxicity

57
Q

What can be indicative of cantharidin toxicosis in a horse on clinical pathology?

A

Hypocalcemia, increased BUN

58
Q

What is a sequelae of the cardiac necrosis caused by cantharidin toxicity?

A

Sudden death with no struggle

59
Q

What is the treatment for cantharidin toxicity?

A

GI decontamination and protection, antibiotics; symptomatic and supportive

60
Q

What is the most common site in the kidney of toxin induced injury?

A

Proximal convoluted tubule

61
Q

What is the mechanism of action of ethylene glycol?

A

Major toxic agent of ethylene glycol are metabolites produced by the action of alcohol dehydrogenase; glycolic acid causes acidosis, glyoxylic acid thought to cause CNS signs, oxalate/oxalic acid causes renal damage and hypocalcemia

62
Q

What are the clinical signs of stage I ethylene glycol toxicity?

A

“Drunkenness”, ataxia, CNS depression; nausea, vomiting, PU/PD (dogs)

63
Q

What are the clinical signs of stage II ethylene glycol toxicity?

A

Tachypnea, tachycardia, depression (cats)

64
Q

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

A

PU progressing to oliguria and anuria, lethargy, anorexia, vomiting, seizures, oral ulcers, abdominal pain, dehydration, and enlarged kidneys

65
Q

In what stage of ethylene glycol toxicity do most animals present?

A

Stage III

66
Q

What is the best method of diagnosing ethylene glycol toxicity?

A

Measuring EG concentration in blood, though might miss the opportunity

67
Q

What is indicative of ethylene glycol toxicity on clinical pathology?

A

Azotemia, low urine SG, crystalluria, hyperglycemia, hypocalcemia, high anion gap

68
Q

What are competitive inhibitors of alcohol dehydrogenase that are used to treat ethylene glycol toxicity?

A

20% ethanol and Fomepizole

69
Q

What is the goal of treatment of ethylene glycol toxicity?

A

Prevent formation of toxic metabolites

70
Q

What indicates poor prognosis for dogs and cats presenting with ethylene glycol toxicity?

A

Renal failure (azotemia)

71
Q

What is the mechanism of action of cholecalciferol/vitamin D3 toxicity?

A

Causes massive increases in serum calcium by: Increasing GI absorption, decreasing renal excretion, increasing synthesis of calcium binding protein, mobilizing bone calcium

72
Q

What are the clinical signs of cholecalciferol/vitamin D3 toxicity?

A

Anorexia, weakness, depression, thirst and polyuria, diarrhea, dark feces, vomiting, hypertension, bradycardia, ventricular arrhythmias, mineralization of tissues

73
Q

What clinical pathology findings are suggestive of cholecalciferol/vitamin D3 toxicity?

A

Rapid increase in plasma phosphorous followed by increase in plasma calcium levels, low PTH, azotemia, low USG with calciuria

74
Q

What other differentials must you consider when diagnosing cholecalciferol/vitamin D3 toxicity?

A

Ethylene glycol, paraneoplastic syndrome, juvenile hypercalcemia, and hyperparathyroidism

75
Q

How do you treat cholecalciferol/vitamin D3 toxicity?

A

GI decontamination within 6-8 hours, reduce dietary calcium and phosphorus, normal saline and furosemide, prednisolone (to reduce bone and kidney resorption and reduce intestinal calcium absorption), pamidronate (drug that acts like calcitonin), sucralfate or milk of magnesia

76
Q

What is the mechanism of action of grape and raisin toxicity?

A

Unknown

77
Q

What are the clinical signs of grape and raisin toxicity?

A

Vomiting followed by symptoms of acute renal failure

78
Q

What clinical pathology findings are indicative of grape and raisin toxicity?

A

Renal damage: hypercalcemia, hyperphosphatemia, azotemia

79
Q

What is the recommended treatment for ingestion of any quantity of grapes or grape products in dogs?

A

GI decontamination (emesis, lavage, or activated charcoal), fluid therapy (for 72 hours at least), supportive therapy (furosemide, dopamine, mannitol, hemodialysis, or peritoneal dialysis)

80
Q

The oxidation pathway of acetaminophen results in what highly reactive metabolite?

A

NAPQI (N-acetyl-p-benzoquinoneimene)

81
Q

What species is extremely sensitive to acetaminophen due to the lack of glucuronidation?

A

Cats

82
Q

What is the mechanism of action of acetaminophen?

A

Formation of NAPQI causes liver tissue necrosis and increased methemoglobin, oxidative damage of erythrocytes in cats (methemoglobin and heinz body production)

83
Q

What are the clinical signs of acetaminophen toxicity?

A

Methemoglobinemia and hepatotoxicity = tachycardia, hyperpnea, weakness, and lethargy; centrilobular hepatocyte degeneration and necrosis in dogs (nausea, vomiting, anorexia, abdominal pain, shock, tachypnea, tachycardia); hemolysis

84
Q

What is the goal of treatment of acetaminophen toxicity?

A

Replenish glutathione stores!

85
Q

How do you treat acetaminophen toxicity?

A

Early decontamination, give the glutathione precursor N-acetylcysteine (NAC), ascorbic acid for methemoglobin, antioxidants, supportive care

86
Q

Which NSAID in particular are dogs sensitive to?

A

Ibuprofen

87
Q

Which NSAID in particular are cats sensitive to?

A

Aspirin

88
Q

What is the mechanism of action of NSAIDs?

A

Uncoupled oxidative phosphorylation at high doses, blocks COX-1 and COX-2 decreasing prostaglandins

89
Q

What two organ systems are affected in NSAID toxicity?

A

Stomach and Kidneys (Gastric ulceration and renal toxicity)

90
Q

What is the acid-base balance observed in Aspirin toxicosis?

A

Acidosis with anion gap

91
Q

What clinical signs are seen in an acute Aspirin toxicosis?

A

Nausea, vomiting, anorexia, fever and respiratory stimulation, depression, lethargy, seizure, coma

92
Q

What is the most common problem in a chronic Aspirin toxicosis?

A

Gastric irritation and ulceration

93
Q

What clinical signs are seen in a chronic Aspirin toxicosis?

A

Anemia, Heinz bodies, thrombocytopenia

94
Q

What is the toxic dose of Aspirin in the dog?

A

50 mg/kg/day

95
Q

What is the toxic dose of Aspirin in the cat?

A

25 mg/kg/day

96
Q

What are the clinical signs of a Naproxen toxicosis?

A

Bloody vomiting and black-tarry stool, diarrhea, anorexia, weakness, lethargy, painful abdomen, pale gums

97
Q

How do you diagnose an NSAID toxicity?

A

Hx and CSs, increased anion gap, increased liver enzymes & jaundice, prolonged clotting time, acute renal failure

98
Q

How do you treat NSAID toxicity?

A

Induce emesis and activated charcoal, treat GI ulceration and AKI (ranitidine or sucralfate/misoprostol), supportive care, transfusion if needed

99
Q

How long do you treat for GI ulceration after an NSAID toxicity?

A

Sucralfate and misoprostol for a few weeks

100
Q

What is the #1 priority pollutant affecting up to 1 billion people and countless animals?

A

Arsenic

Toxicology-soph-c (4 decks)

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