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Toxicology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What is a toxicant?

A

a compound causing toxicity (natural or man-made)

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2
Q

What is a xenobiotic?

A

foreign substance

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3
Q

What is an antidote?

A

This is a substance that prevents/relieves the effects of a toxicant.

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4
Q

How are poisons classified?

A

The lower the dose the more toxic!

toxic dose with <1mg/kg being extremely toxic and > 15 g/kg being relatively harmless

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5
Q

Dose-response curve?

A

Assumes a cause/effect relationship and that response is proportional to dose
- in general more toxin is bad!

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6
Q

What factors influence toxicity?

A

Exposure, subject (spp.) & environment

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7
Q

What’s the difference between concentration and dose?

A

Concentration: amount of chemical per volume
dose: amount given to an animal

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8
Q

What animals have genetic defects affecting metabolism?

A

o Cats are deficient in glucuronidation- affecting phase 2
o Dogs are deficient acetylation
o Pigs are deficient sulfonation

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9
Q

Metabolism can…

A

detox compound & increase elimination.

  • bioactivation
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10
Q

Bioactivation & list some examples

A

conversion of parent compound into something more toxic

Ex. ethylene glycol toxicosis, benzopyrene (petroleum), aflatoxin & acetaminophen

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11
Q

What is the process of toxicity?

A

Delivery from exposure site to target → Rxn of the ultimate toxicant with the target molecule → Cellular dysfunction & resultant toxicities → Repair (apoptosis, tissue regeneration) or disrepair (tissue necrosis, fibrosis, cancer

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12
Q

What makes an organ sensitive to toxin?

A

Receptor type and amount, amount of transporters present

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13
Q

How do toxicants cause toxicity?

A
  1. Damage cells
    - Ex. Acetaminophen, arsenic
  2. Organ system dysfunction
    - Ex. insecticides, rodenticides
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14
Q

What are 5 life-threatening problems that require immediate attention?

A

Respiratory distress, CNS, Cardiovascular, Hemorrhage, Thermoregulation

  • ID toxin is helpful nOT crucial so treat the pt not the poison!
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15
Q

When is ventilation needed?

A

hypoventilation/hypercapnia (PCO2 >45mmHg), metabolic acidosis (venous pH <7.35) hypoxia (PaO2<65mmHg)

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16
Q

How do you treat hypoxia?

A

Treat with 40% O2 (brief start w/100%): 100% O2 for a short period of time, because it will cause damage to lung epithelium

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17
Q

how do you prevent aspiration of vomitus?

A

positioning

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18
Q

How do you control CNS hyperactivity? (Seizures)

A

Diazepam, phenobarbital, methocarbamol, gabapentin

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19
Q

How do you control CNS depression?

A

analeptics & doxapram

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20
Q

How do you control tachycardia & arrhythmias?

A

lidocaine, propanolol

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21
Q

How do you control hypertension?

A

nitroprusside, hydralazine

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22
Q

What are the four major themes for completing a history?

A

health history, current clinical history, diet & environment

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23
Q

What is the goal of GI decontamination?

A

reduce absorption of toxin & facilitate transport out of GI system. Done with emesis & activated charcoal

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24
Q

What medication induces vomiting in cats?

A

xylazine; may cause hypotension & bradycardia

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25
Q

What medication induces vomiting in dogs & pigs?

A

apomorphine; may cause prolonged vomiting

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26
Q

When should you induce emesis?

A

Perform if toxic dose ingested, no vomiting has yet occurred & activated charcoal is not an option

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27
Q

When should you NOT induce emesis?

A

caustic chemicals, sharp items, volatile chemicals, risk of aspiration pneumonia

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28
Q

When should you give activated charcoal?

A

known substance, recent ingestion or undergoes enterohepatic circulation, pt. can tolerate or no need to administer oral rx immediately

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29
Q

When should you not give activated charcoal?

A

protracted vomiting, caustic/basic substance that charcoal doesn’t bind, intestinal FB (physical GI damage), obstructed airway, chronic exposures

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30
Q

What doesn’t bind activated charcoal?

A

acids/alkalis, alcohols/glycols, metals, oils, petroleum, detergents, cyanide

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31
Q

MOA for strychnine?

A

competitive antagonist to glycine receptors (spinal cord & medulla) causing

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32
Q

Strychnine clinical signs

A

stiff neck and gait, “grinning” (facial muscles tighten), tetanic seizures, sawhorse stance

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33
Q

Strychnine DX

A

CS, elevated CPK and LDH in serum, increased anion gap- lactic acidosis, hyperkalemia, leukocytosis

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34
Q

Strychnine TX

A

Decontamination, ammonium chloride (ion trapping), seizure control +/- ventilate with pentobarbital

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35
Q

Ammoniated Feed Toxicosis- MOA

A

imidazole and/ or non-protein nitrogen added to cattle feed and byproduct causes too much ammonia–> blood
* Ruminants are most susceptible*

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36
Q

Ammoniated Feed Toxicosis- CS?

A

Bovine Bonkers- hyperexcitability & SLUD

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37
Q

Ammoniated Feed Toxicosis- DX?

A

CS/HX, feed analysis, increased ammonia/ glucose/BUN & acidosis

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38
Q

Ammoniated Feed Toxicosis- TX?

A

Remove feed, sedation (prevent self-mutilation), milking out cows +/- cold H20 + vinegar

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39
Q

Salt Tox MOA

A

decreased water intake/lots of salt–>blood becomes hypernatremia–> fluids in the brain movie into the hypertonic cerebral circulation (brain dehydration)–>drinking water provided and blood becomes hypotonic relative to the brain–>osmotic edema and swelling if water is not returned slowly!

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40
Q

Salt tox CS

A

primarily salivation/increased thirst, progressing to circling, head pressing, seizures, blindness, partial paralysis

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41
Q

Salt tox DX

A

blood sodium levels, high sodium levels in brain diagnostic in swine & cattle (> 2000 ppm)

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42
Q

Salt tox TX

A

slow rehydration starting with hyperosmotic fluid, furosemide to prevent pulmonary edema

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43
Q

What are mycotoxins & the three subgroups?

A

Fungal secondary metabolites

i. Slaframine
ii. Fumonisin
iii. Tremorgenic Mycotoxins- produced by Penicillium, Aspergillus, Claviceps, etc.

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44
Q

Slaframine MOA

A

Acts as a muscarinic cholinergic agonist (esp. in exocrine glands) ~ “Ach mimic”

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45
Q

Slaframine CS

A 
Most common in horses & cattle 
copious salivation (slobbers), +/- bloat, diarrhea, frequent urination, feed refusal
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46
Q

Slaframine TX

A

Remove source, atropine

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47
Q

Fumonisin MOA

A

MOA: inhibits sphingosine N-acetyltransferase causing increase sphingosine level cytotoxic

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48
Q

Diseases linked to Fumonisin?

A

i. Equine leukoencephelomalacia (ELEM): affecting CNS

ii. Porcine pulmonary edema (PPE): affecting respiratory system

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49
Q

Fumonisin TX

A

isolate, can change feed +/- Ultrasorb S (mycotoxin deactivator)

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50
Q

Porcine pulmonary edema (PPE) CS?

A

inactivity/tachypnea/bradycardia (pigs); wipe out of large swine population.
& die of hypoxia, indicated by cyanosis

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51
Q

Porcine pulmonary edema (PPE) DX?

A

Increases liver enzyme and in serum/tissue sphingoid bases

- post mortem: pulmonary edema & hepatic lesions

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52
Q

ELEM CS?

A

CNS- terminal frenzy before death (mania, profuse sweating), prior to anorexia/ataxia/blindness

LIVER- HE & jaundice

Brain- liquefaction (unilat)

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53
Q

What is one toxic principle of tremorgenic mycotoxins?

A

Penitram A

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54
Q

Tremorgenic mycotoxin MOA?

A

multiple mechanisms including GABA receptor antagonist-like, acts on varied neurotransmitters to cause excitation

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55
Q

Tremorgenic mycotoxin CS?

A

muscle tremor, ataxia, tetanic seizures tremors in vertebrates

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56
Q

Alprazolam MOA

A

Benzodiazepone, that acts at limbic, thalamic, and hypothalamic level of CNS

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57
Q

Alprazolam CS

A

ataxia, depression, vomiting, tremors, tachycardia, hypothermia, diarrhea, paradoxical hyperactivity

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58
Q

Alprazolam TX

A

induce emesis, use gastric lavage with activated charcoal if toxic dose, flumazenil

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59
Q

What is flumazenil?

A

Benzodiazepine antagonist; blocks GABA receptor and can be used as an alprazolam tox “antidote”

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60
Q

Zolpidem MOA?

A

inhibits neuronal excitation by binding to benzodiazepine site oN GABA receptors (rapid absorption from GI)

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61
Q

Zolpidem CS

A

ataxia, vomiting, lethargy, disorientation, hyper-salivation, paradoxical excitement

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62
Q

What breeds are susceptible to ivermectin toxicosis?

A

Border collies, Shelties & Australian shepherds

- MDR1 gene mutation causes bioaccumulation in brain & tissues.

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63
Q

Ivermectin MOA?

A

GABA receptor agonist that decreases ability to respond to other stimuli

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64
Q

Ivermectin TX?

A

decontamination w/ activated charcoal, lipid emulsion, picrotoxin
- seizures? don’t use benzodiazepines OR use short acting like propofol & phenobarbital

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65
Q

Organophosphate Pesticides MOA

A

reversible inhibition of acetylcholinesterase activity- can become irreversible with time
continuous stimulation of neuron (muscarinic & nicotinic receptors)–> death

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66
Q

Organophosphate Pesticides CS?

A

Muscarinic: salivation, lacrimation, urination, GI distress/defecation, emesis, myosis
Nicotinic: muscle fasciculations, tremors, weakness, paralysis
CNS: respiratory depression, ataxia, clonic-tonic seizures, delayed neuropathy

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67
Q

Organophosphate Pesticides DX?

A

HX/CS, reduced rbc ACHE, atropine challenge- if no response/change means OP poisoning

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68
Q

OP TX?

A

GI decontamination, atropine (corrects muscarinic receptor), glycopyrrolate, oximes (protopam/2-PAM : to reactivate anticholinesterase, diazepam/barbiturates for seizures & time!

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69
Q

organophosphate-induced delayed neurotoxicity/ neuropathy

A

OP inhibited NTE- neuropathy, will get degeneration over time of motor axons due to excessive anti-cholinesterase degeneration (occurs after 2 weeks of exposure)

Results: Hindlimb weakness, paralysis

no treatment

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70
Q

Pyrethrin MOA

A

Bind voltage-gated sodium channels and causes hyperactivity

* cats are sensitive due to inefficient glucuronidation

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71
Q

Pyrethrin CS? Cat vs. Dog

A

Cat-drooling, paresthesia, muscle tremors/seizures/hyperthermia Dog- paresthesia

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72
Q

Pyrethrin TX

A

Methocarbamol, diazepam, bathe multiple times with dishwashing liquid, lipid infusion, IV fluids to protect kidneys from myoglobin breakdown products in cats-created d/t trembling

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73
Q

Bromethalin MOA

A

block oxidative phosphorylation in CNS leading to dysregulation

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74
Q

Bromethalin CS

A

ataxia, hindlimb paralysis, hyper-excitability, severe muscle tremors, seizures

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75
Q

Bromethalin DX

A

cerebral edema and cerebellar degeneration

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76
Q

Bromethalin TX

A

Emesis, charcoal, furosemide for cerebral & pulmonary edema, treat seizures, lipid infusion

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77
Q

Acetaminophen MOA?

A

metabolized by glucuronidation, sulphonation & oxidation pathways~ bioactivated to NAPQI (N-acetyl-p-benzoquinone imine).

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78
Q

What spp. is extremely sensitive to acetominophen?

A

Cats because they cannot glucoronidate

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79
Q

Acetaminophen CS?

A

Cats: cyanosis, methemoglobinemia, depression & edema of paws/ face

Dogs- Hepatotoxicity- hepatic necrosis nausea, v/d/shock

Other- hemolysis, Heinz bodies

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80
Q

Acetaminophen TX:

A

N-acetyl cysteine OR cimetidine (cats), ascorbic acid, antioxidants, silymarin (milk thistle) & s-adenosylmethionine

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81
Q

Xylitol MOA

A

Dose dependent insulin release causing lethal liver injury & hypoglycemia (dogs)

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82
Q

Xylitol CS

A

vomiting, lethargy, ataxia, collapse & seizures, liver enzymes, BG & hypokalemia (d/t endogenous induced insulin)

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83
Q

Xylitol TX

A

activated charcoal is NOT effective or recommended (poor binding ability) & monitor BG/liver function (supplement accordingly)

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84
Q

What toxins do some cyanobacteria or blue green algae produce?

A

Microcystin- impairs phosphatase affecting cell regulation/signaling and affects the liver.

Anatoxin- affect CNA & will see ataxia/ disorientation with toxicosis

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85
Q

Cyanobacteria CS & DX

A

v/d/pale mm, ataxia, seizures

DX: blood in stool, elevated liver enzymes & hx

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86
Q

Cyanobacteria TX?

A

Atropine ( helps with anatoxins), fluid & seizure control

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87
Q

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

A

PCT

88
Q

Acute renal failure

A

transient damage to tubule/glomerulus/ vasculature causing decreased GFR & azotemia

  • CS: vomiting, GI bleed, anuria
89
Q

Chronic renal failure

A

secondary changes triggered by initial injury (not all chemicals effect one organ)

Signs: edema, hypocalcemia, reduced rbc

90
Q

Ethylene Glycol MOA

A

metabolites produced by action of alcohol dehydrogenase
- Glycolic acid–> metabolic acidosis

  • Glyoxylic acids–> CNS signs
  • Oxalate/Oxalic acids–> renal damage & hypocalcemia (crystal formation in kidney)
91
Q

Ethylene Glycol CS (3 Stages)

A
  1. Drunkenness, nausea, vomiting, PU/PD (Dogs)
92
Q

What stage of ethylene glycol toxicosis does the animal normally present?

A

Stage 3

93
Q

Ethylene Glycol DX

A

Ethylene glycol blood concentration blood, Azotemia (stage 3), low USG & crystalluria (calcium oxalate monohydrate)

Chemistry: hyperglycemia, hypocalcemia & increased anion gap

94
Q

Ethylene Glycol TX

A

Fomepizole to block alcohol dehydrogenase (EG metablized via other pathways) or more trasitional ethanol & sodium bicarbonate (difficult to maintain/less exact)
* DO NOT USE IF PT IN RENAL FAILURE*

95
Q

Cholecalciferol MOA

A

Liver metabolizes cholecalciferol to 1,25 dihydroxycholecalciferols causing a massive increase in serum calcium!

96
Q

Cholecalciferol CS

A

Delayed!

anorexia, thirst, PU, dark diarrhea, bradycardia, ventricular arrhythmia, hypertension & mineralization of tissues

97
Q

Cholecalciferol Dx

A
  • clinical signs
  • hypercalcemia
  • Low PTH
  • Renal damage: low USG & azotemia
  • Hydroxycholecalciferols in bile & kidneys
  • Histo: mineralization in multiple organs
98
Q

How to differentiate cholecalciferol from ethylene glycol?

A

EG has higher kidney calcium compared to cholecalciferol

EG Ca: P ratio in kidney higher than cholecalciferol

99
Q

Cholecalciferol TX

A
  • Gi decontamination (emesis & activated charcoal 6-8 hr.)
  • reduce dietary calcium& phosphorous
  • Saline & furosemide (promotes excretion of calcium)
  • Prednisolone (reduces bone & kidney resorption & reduced calcium absorption)
  • Pamidronate- bisphosphonate, (blocks osteoclast from releasing calcium)
  • sucralfate for GI ulcers
100
Q

Grape & Raisin MOA?

A

Unknown

101
Q

Grape & Raisin CS?

A

Variable! vomiting, followed by acute renal failure signs

102
Q

Grape & Raisin DX?

A

hypercalcemia, hyperphosphatemia, increased Ca:PO4, elevated BUN/creatinine

103
Q

Grape & Raisin TX?

A
  • Emesis, lavage, or activated charcoal (grape remain in GI with slow absorption)
  • Fluid therapy + supportive therapy
104
Q

Ergot Alkaloids MOA?

A

dopamine & serotonin receptor agonist–> hallucinations, reproductive problems, lack of thermoreg.

  • Dopamine is inhibitory causing decreased prolactin so poor reproduction
  • alpha-2 adrenergic agonist affects smooth muscle contraction & vasocontraction at extremity- abortion and ischemia
105
Q

Ergot Alkaloids CS?

A

poor reproductive performance (abortion in horses & pigs see infertility)

  • Summer slump- reduced feed intake, weight gain, heat intolerance, retain winter coat
  • Fescue foot- lameness, gangrene of extremities, necrotic tissue on extremity (sores on ears, feet, tail d/t vasoconstriction)
106
Q

Ergot Alkaloids TX?

A

metoclopramide or domperidone (dopamine antagonists- primarily to correct reproductive issues), remove source

107
Q

What species are most sensitive to ionophore toxicosis?

A

Horses>Cow>Poultry

- usually caused by a feed-mixing error

108
Q

Ionophore MOA?

A

increase intracellular sodium/calcium leading to mitochondrial swelling and cell death

109
Q

Ionophore CS? in horses & cows

A

anorexia, colic, profuse sweating on flank, recumbent, incoordination, diarrhea (cattle), respiratory difficulty (cattle)

110
Q

Ionophore DX?

A

increased muscle enzymes (CK) myoglobinuria, elevated AST/LDH/BUN/bilirubin, hypokalemia, hypocalcemia, chemical analysis of feed

  • Necropsy: pale cardiac muscle; muscle has striation/ vacuolization
111
Q

Tetanus MOA

A

-spores in puncture wounds, produce toxins that blocks the release of GABA & glycine–> overstimulation of muscles leading to muscle stiffness & tetany (can animal die from exhaustion)

112
Q

Tetanus CS?

A

stiffness, twitching, lockjaw (all facial muscle lock up), unsteady gait, bloat (ruminant)

113
Q

Tetanus TX?

A

antitoxin (only useful at early stages), supportive therapy

114
Q

Bobtail Disease

A

Chronic Selenium Toxicosis: occurs with shampoo, forage or plants (locoweed)
- Horses are sensitive to locoweed
CS- lameness, hoof deformity, muscle wasting
-TX- none (remove from source)

115
Q

White Muscle Disease

A

Selenium deficiency, causing degeneration of muscle tissue (cardiac and skeletal) ~ mostly livestock

  • Clinical signs: Weakness, prostration (Lie down), muscle wasting
  • TX: selenium replacement and Vitamin E
116
Q

Phenoxyacetic Acid Herbicides moa?

A

unknown, however dogs are more susceptible

117
Q

Phenoxyacetic Acid Herbicides CS?

A

vomiting, diarrhea, oral/GI ulceration, ataxia, weakness, seizures at high doses, myotonia with serious toxicosis, rumen acidosis, renal tubular degeneration, hepatic necrosis
• GI effects (often only sign in dogs)

118
Q

Phenoxyacetic Acid Herbicides TX?

A

emesis, lavage, bathe, activated charcoal, cathartic, ion trapping using basic compound (since this is a weak acid- making urine more basic, traps compound in urine, so it is excreted with sodium bicarbonate)

119
Q

What are three common respiratory toxins?

A
  1. ventilatory muscle paralysis- botulism, tetanus, OP, strychnine, venom
  2. Respiratory center depression- barbiturates, opiates, hypnotics, sedatives & antidepressants
  3. Aspiration pneumonia: ethylene glycol, petroleum & bleach
120
Q

Paraquat MOA?

A

non-selective herbicide that induces oxidative damage

  • lungs are sensitive and will absorb at a higher affinity than O2)
121
Q

Paraquat CS?

A

lung damage, renal failure, pulmonary fibrosis, vomiting, burning skin, acute pulmonary edema

122
Q

Paraquat tx?

A

no oxygen unless hypoxic (b/c can worsen lung issues), emesis, charcoal, lavage

123
Q

Polytetrafluoroethylene (PTFE

A

oBurning of Teflon from cooking pans,
o MOA - respiratory tract irritant
oClinical signs - choking, dyspnea, ataxia, edema, hemorrhage, rapid death
oTreatment - fresh air, oxygen, diuretics

124
Q

What species is mostly effected by PTFE?

A

birds

125
Q

First generation anticoagulant- Warfarin

A

o Short half-life (15 hours), low potency, requires multiple feedings
o Can be used in human medication (blood thinning), found in sweet clover (affecting LA) & with rodenticides (less common)

126
Q

Second Generation - Brodifacoum

A

oLong half-life (20 days), high potency, kills in single feeding

127
Q

Anticoagulant MOA

A
  • inhibits Vitamin K epoxide reductase

- when it is blocked vitamin K cannot be used to make clotting factors.

128
Q

Anticoagulant CS

A

Initially okay w/ delayed onset (3-5 days) due to native anticoagulants. depression, anorexia, anemia, dyspnea, nosebleeds, bleeding gums, bloody feces, hemorrhage (chest/abdomen), hematoma, prolonged bleeding from injection

129
Q

Anticoagulant DX

A

history of exposure, evidence of coagulopathy, response to Vitamin K therapy
o Testing: increased PT/PTT

130
Q

Anticoagulant TX?

A

emetic (recent exposure) adsorbent, cathartic therapy & Vitamin K

  • low dose treat for 2 wk for first generation & 1 month for second generation
131
Q

Gossypol toxicosis MOA?

A

increases with time & accumulates b/c lipophilic.

  • iron chelation causing anemia & reducing protein availability, binds to dehydrogenase leading to increased oxidative damage and decreased energy
132
Q

Gossypol toxicosis CS?

A
  • Low concentration: weight loss, weakness, dyspnea
  • Other levels: moderate anemia, edema secondary to heart failure, myocardial necrosis, congestive heart failure, sudden death (dairy cows/lamb)
133
Q

Gossypol toxicosis DX

A

HX of cotton ingestion, cardiac necrosis, edema, vacuolization, chemical analysis

134
Q

Gossypol toxicosis TX

A

feed high protein diet with Vitamin A/iron/lysine supplementation, remove sources from diet & symptomatic treatment

135
Q

Cantharidin (Blister beetle or Spanish fly) toxicosis

A

inhibits protein phosphates and mucosal irritant

** usually affects horses**

136
Q

Cantharidin toxicosis CS?

A

colic, frequent urination, diaphragm contraction with heartbeat, shock, irritation/ ulceration of epithelia (muzzle in water- irritated in mouth so constantly drinking water) & cardiac toxicity

137
Q

Cantharidin toxicosis DX?

A

alfalfa hay consumed, beetles in hay or stomach, hypocalcemia, increased BUN, ulceration of mucous membranes, cardiac necrosis & sudden death “with no struggle”
o Necropsy: hemorrhage & ulceration of the bladder.
o Can perform mass spectrometer

138
Q

Cantharidin toxicosis TX?

A

GI decontamination and protection with sucralfate, antibiotics

139
Q

Methylxanthines MOA?

A

antagonist of adenosine receptors –> CNS stimulation (overstimulation), vasoconstriction, tachycardia
oPrevents calcium reuptake –> increased skeletal/cardiac muscle contractility
oInhibits phosphodiesterase–> increase cAMP and cGMP

140
Q

Methylxanthines CS?

A

vomiting, diarrhea, diuresis, hyperactivity (bounce), panting, tachycardia, hypertension, ataxia, tremors, seizures, coma, death from arrhythmia or respiratory failure

141
Q

Methylxanthines DX?

A

history, stomach content analysis, plasma/serum/urine/liver analysis

142
Q

Methylxanthines TX?

A

o GI decontamination: induce emesis, repeated administration of activated charcoal (every 3 hr)
o EKG: arrhythmias with lidocaine (not in cats) or metoprolol (cats)
o maintain respiration, fluid diuresis

143
Q

Nitrate toxicosis MOA?

A

Nitrate converted to nitrite, which causes vasodilation & oxidized ferrous iron in hemoglobin to ferric state–> methemoglobinemia (O2 starved tissues)

144
Q

What spp. is most susceptible to nitrate toxicosis?

A

Pig>cattle>sheep>horses

145
Q

What are plants that cause nitrate toxicosis?

A

lambsquarters, black nightshade, pigweed

146
Q

Nitrate toxicosis CS?

A

depending on level of methg: cyanosis (15%)
ataxia, seizures, coma (50%)
death (>70%)

147
Q

Nitrate toxicosis DX?

A

methemoglobinemia, nitrate in feed/water, necropsy (eyes)

148
Q

Nitrate toxicosis TX?

A

1-2% methylene blue IV (urine will turn green), ascorbic acid (cats, horses), feed cattle corn to increase nitrite reduction by rumen flora

149
Q

Examples of cardiac glycosides?

A

Digitalis, digoxin

Plant examples: Foxglove, oleander (SE region), lily of the valley

150
Q

Cardiac glycosides MOA

A

inhibit sodium/potassium ATPase through competition (found on cardiomyocytes)- leading to increased intracellular calcium

151
Q

Cardiac glycosides CS

A

staggering, trembling, dyspnea, increased intracellular sodium and calcium, hyperkalemia, tachycardia, arrhythmia
- over time can become bradycardia & weak pulse

152
Q

Cardiac glycosides TX

A

GI decontamination, propranolol (for arrhythmias), insulin w/ glucose (treat hyperkalemia), Digoxin fragment antibodies- designed from toxin in foxglove (antidote) “digibind”

153
Q

What is digibind?

A

Digoxin fragment antibodies- designed from toxin in foxglove (antidote for digoxin and similar cardiac glycosides)

154
Q

Cyanide toxicity MOA

A

inhibition of cytochrome C oxidase (no ATP production)- shuts down oxidative respiration

155
Q

Cyanide toxicity CS

A

super oxygenated (cherry red) blood that is slow to clot, bitter almond smell, sudden death, dyspnea, weakness, tremors

  • Rapid onset of toxicosis (20 min)
156
Q

Cyanide toxicity TX

A 
Find a cyanide recipient: 
1. give sodium nitrate to bind cyanide (inducing methemoglobinemia)
2. Then, sodium thiosulfate to increase formation of nontoxic thiocyanate by rhodanese --> eliminated in urine
OR
One step approach:
Cyanokit: 
- Vit B12 (higher affinity for cyanide)
- sulfanegan sodium (bind cyanide)
- cobalt-EDTA
157
Q

What spp are sensitive to NSAIDs?

A

Dog- ibuprofen

Cat- Aspirin d/t lack of glucoronidation

158
Q

NSAIDs MOA

A
  • inhibit cyclooxygenase (COX1&2) and damage GI and liver

- Uncouples oxidative phosphorylation at high doses-increased lactic acid, metabolic acidosis

159
Q

NSAIDs CS

A

Acute- vomiting, anorexia, fluid imbalances, seizures, acidosis with anion gap, renal failure

Chronic- gastric irritation, ulceration
- Cats: Heinz body (oxidative damage), anemia (cats), thrombocytopenia (cats)

160
Q

NSAIDs DX

A

HX/CS, increased anion gap due to acidosis (specific to salicylates such as aspirin), increased liver enzymes, jaundice, prolonged clotting time, acute renal failure (see renal tubular cell cast)

161
Q

NSAIDs TX

A

induce emesis, activated charcoal (multiple doses), ranitidine (H2 blocker), sucralfate & misoprostol (prostaglandins analog), supportive care +/- transfusion with hemorrhage

162
Q

What is the #1 priority pollutant?

A

Arsenic

163
Q

Arsenic MOA?

A

o pentavalent reduced and metabolized in rumen to reduce metabolic energy & CNS problems
o trivalent inhibits oxidative phosphorylation and causes blood/mucosal issues

164
Q

Arsenic CS?

A

Dog- intense abdominal pain, gastroenteritis, vomiting

weakness, staggering gait, PU/PD, oliguria, anuria, dehydration

  • Blood related: cold extremities
    “black foot disease” d/t tissue necrosis
  • CNS related: salivation, trembling, depression, posterior paresis
165
Q

Arsenic DX:

A

Neocropsy: brick red abomasum, fluid GI contents, soft yellow liver, red congested lungs & kidney damage

analysis- liver or kidney has arsenic > 5 ppm, HX, stomach contents or vomitus with arsenic (must take samples early because rapidly absorbed/excreted)

166
Q

Arsenic TX:

A

o GI contamination: if acute~ emesis, activated charcoal/ cathartic
o chelation therapy- dimercaprol, sodium thiosulfate (binds arsenic) prior to clinical signs
o supportive therapy

167
Q

Zinc MOA?

A

zinc enters the stomach- acid eats & releases zinc–> free zinc damages GI mucosa (corrosive effect & oxidative damage causing hemolysis)

168
Q

Zinc CS?

A

v/d/ PU/PD, hemoglobinuria, hemolytic anemia, jaundice, pancreatitis & lesions along GI, liver/kidney/pancreas

169
Q

Zinc DX:

A

serum & liver zinc values, decreased PCV, regenerative anemia, thrombocytopenia, oxidative damage, elevated liver/kidney/pancreatic enzymes, hemoglobinuria, radiographs for hardware, formation of Heinz body

170
Q

Zinc TX:

A

remove foreign body, emesis (if possible), omeprazole (proton pump inhibitor) or H2 blockers +/- GI protectants

171
Q

Soap/Shampoo

A

o Clinical signs: GI distress, vomiting, diarrhea
o Treatment: simple dilution with milk or water, fluid treatment
o Rarely lethal

172
Q

Scouring Powder/ Bleach

A

Alkaline- corrosive effect on skin/mm, that can cause liquefactive necrosis

  • Clinical signs: vomiting, drooling & abdominal pain
  • TX: milk, water & gastro protectant
  • Avoid emesis or lavage because caustic & poor binding effect (have risk of aspiration pneumonia)*
173
Q

Disinfectant CS

A

Acute: corrosive burns, vomiting, nausea, abdominal pain, hyper-salivation, panting, respiratory depression, hypotension, ataxia, depression

Severe: shock, cardiac arrhythmia, methemoglobinemia, hepatic/renal damage, acute renal failure, pulmonary edema

174
Q

Disinfectant TX

A

dilute with gastro-protectants, activated charcoal or cathartic, 1% methylene blue for methemoglobinemia

No emesis/lavage because of aspiration pneumonia

175
Q

Automatic Dishwasher Detergents:

A

o High alkalinity & extremely causative ~ most concerning b/c of pH
o Clinical signs: vomiting, diarrhea, salivation, GI pain, oral/GI erosions
o Treatment: dilute with milk or water, analgesics +/- steroids

176
Q

Toilet Bowl Cleaner:

A

oAcidic
o CS: vomiting, salivation, dysphagia, abdominal pain, GI ulceration, dyspnea
o TX: dilution with milk/water, metoclopramide, steroids

No emesis, lavage, activated charcoal–>contraindicated

177
Q

What spp. is primarily affected by zearalenone?

A

Pigs>livestock

* chickens are resistant*

178
Q

Zearalenone MOA?

A

Estrogen receptor agonist (higher affinity)

179
Q

Zearalenone CS?

A

Symptoms depend on sex & maturity
- decreased male libido, infertility (decreased litter size), enlarged/swollen uteri, shrunken/cystic ovaries
vulva swelling/reddening vaginal/rectal prolapse, regressed testes (feminization), abortions, pseudopregnancy
o Vulva swelling can be reversed once removed from the contaminated feed source!

180
Q

Zearalenone TX?

A

change feed, activated charcoal (d/t enterohepatic recirculation) or high fiber to reduce elimination times

181
Q

Venom

A

actively injected toxin, used for hunting and defense - “If it bites you, you die”

  • LMW substance–> Cause pain, inflammation, hypotension
  • Peptides–> Direct toxic effects and allergy
  • Enzymes
182
Q

Poison

A

passive secretion as passive defense mechanism

183
Q

Bee venom MOA

A
  • melittin acts as detergent and hemolytic causing pain

* phospholipase A2 destroys membranes

184
Q

Wasp venom MOA

A

use alarm pheromones & kinins produce pain

185
Q

Ant venom MOA

A

piperidine causes dermal necrosis, formic acid causes burning sensation and pain
(also has antibacterial properties)

186
Q

Hymenoptera Venom CS

A

local swelling, red plaques, edema, regional allergy or anaphylaxis (rare), shock, hemolysis, renal/hepatic injury
- delayed hypersensitivity is possible

187
Q

Hymenoptera Venom TX

A

removal of stinger by scraping, cold compress, antihistamines, corticosteroids, epinephrine for shock/systemic toxicosis

188
Q

What is the gold standard for anaphylactic shock?

A

epinephrine

189
Q

What toxin do ticks produce?

A

Holocyclotoxin impairs acetylcholine release, causing paralysis/muscle weakness
- dermacentor may act on sodium channels.

190
Q

Tick CS

A

may appear 6-14 days after attachment.

loss of appetite *voice * incoordination, ascending flaccid paralysis, respiratory distress or death (b/c respiratory paralysis)

191
Q

Tick TX:

A

supportive treatment, anti-emetics, oxygen therapy

atropine sulfate contraindicated!

192
Q

What toad produce cardiotoxins?

A

Bufo marinus (cane toad) affecting dogs

193
Q

Toad MOA:

A

biogenic amines cause vasoconstriction, hypotension, hallucination, gastrointestinal effects
bufogenins inhibit sodium/potassium ATPase activity (similar activity as digitalis)

194
Q

Toad CS:

A

immediate hyper salivation or foaming at the mouth, head shaking, vomiting, hyperemic gums, arrhythmia, neurological signs, convulsions/seizures, ataxia, hallucinations, rapid death
- can observe hyperkalemia-

195
Q

Toad TX:

A

water lavage, activated charcoal if no seizures, diazepam/barbiturates if seizures, propranolol/lidocaine/esmolol for arrhythmia, fluid replacement therapy, digoxin-specific antigen binding fragments

196
Q

What spp. is most susceptible to toad toxicosis?

A

Dogs

197
Q

What spp. is most susceptible to black widow toxicosis? What spp. is most susceptible to brown recluse?

A

cats; dog

198
Q

What does the black widow venom contain?

A

Alpha-latrotoxin

199
Q

Black widow venom MOA

A

alpha-latroxin creates pores in membranes to allow calcium entry and massive amounts of neurotransmitter release leading to sustained muscle spasms

200
Q

Black widow venom CS

A

muscle cramping/spasms (Latrodectism), rapid weight loss, abdominal rigidity, restlessness, writhing, vocalization, hypertension, tachycardia, respiratory collapse

201
Q

Black widow venom TX

A

control muscle spasms and pain, calcium gluconate (controversial), anti-venom

202
Q

Brown recluse venom composition & MOA?

A

Sphingomyelinase D- cleaves heads of phospholipids bilayers causing tissue necrosis

203
Q

Brown recluse CS?

A

blister-like bulls eye where bitten (non healing ulcer), hemolytic anemia, fever, weakness, leukocytosis

204
Q

Brown recluse TX

A

dapsone (dermal lesion), fluids and anti inflammatory glucocorticoids, antibiotics to prevent secondary infection, analgesic, aluminum acetate (Burrow’s solution) or hydrogen peroxide to clean lesion, debridement of necrotic tissue or surgical removal (questionable), bandage

205
Q

Eastern Coral Snake Venom & MOA?

A

Bungarotoxin prevents binding of acetylcholine leading to paralysis and local tissue necrosis

206
Q

Eastern coral snake CS?

A

myoglobinemia (cats), hemolysis (dogs), salivation, inability to swallow, dyspnea, weakness, hyporeflexia, CNS depression, paralysis

207
Q

Eastern coral snake TX?

A

Antivenom (expensive), broad-spectrum antibiotics and symptomatic wound care, supportive care

208
Q

Pit Viper Characteristics

A

Characterized by heat sensing pit and hinged (retractable) fangs, head wider than body (triangle), elliptical/vertical pupil

209
Q

Snake bite CS

A

immediate distinct fang marks, immediate swelling/pain/bruising of bite, hypotension, shock, tachycardia, tachypnea, anticoagulation, tissue necrosis

210
Q

Snake bite TX

A

anti-venom, antihistamines, fluids, corticosteroids, glucocorticosteroids

do not cut, ice, or tourniquet

211
Q

Enterotoxins MOA

A

enterotoxins bind to intestinal epithelium to increase permeability and cause fluid loss (diarrhea) and decreased absorption of nutrients
- Bad case of food poisoning

212
Q

Endotoxin MOA

A

lipopolysaccharide from gram negative cell walls that activates inflammatory processes & causes release of prostaglandins and histamine -> circulatory collapse, pancreatitis, activation of clotting cascade, uncoupling of oxidative phosphorylation in heart -> lethargy, fever, hypothermia, diarrhea, abdominal pain, shock, foul feces

213
Q

Endotoxin TX:

A

emesis, support cardiovascular function, correct fluid/electrolyte imbalance, prevent bacteria

214
Q

Botulism in horses

A

“Forage poisoning in adult horses

“shaker foal syndrome” in foals

215
Q

Botulism MOA

A

prevents release of acetylcholine at neuromuscular junction leading to flaccid paralysis

216
Q

Botulism CS

A

decreased tongue and tail tone, dropping food from mouth, salivation, weakness, weak vocalization, progressive paresis, bradycardia, constipation, urinary retention

217
Q

Botulism TX

A

supportive therapy, oxygen therapy, warm water enemas, bladder expression, antibiotics, antitoxin (will not neutralize toxin already in neurons)

Toxicology (1 decks)

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