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LSU SVM TOXICOLOGY EXAM 1 QUESTIONS WITH CORRECT SOLUTIONS

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LSU SVM TOXICOLOGY EXAM 1 QUESTIONS WITH CORRECT SOLUTIONS Binds ligand-gated chloride channels in CNS (GABA gates - high doses) -> inhibits Cl flux and cellular hyperpolarization -> flaccid paralysis of musculature - Answer-What is the MOA of macrocyclic lactones P-glycoprotein (PGP) - ...

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  • October 28, 2024
  • 17
  • 2024/2025
  • Exam (elaborations)
  • Questions & answers

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  • lsu svm toxicology
  • lsu svm toxicology exam 1 questions

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  • LSU SVM TOXICOLOGY
  • LSU SVM TOXICOLOGY

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LSU SVM TOXICOLOGY EXAM 1
QUESTIONS WITH CORRECT
SOLUTIONS
Binds ligand-gated chloride channels in CNS (GABA gates - high doses) -> inhibits Cl
flux and cellular hyperpolarization -> flaccid paralysis of musculature - Answer-What is
the MOA of macrocyclic lactones

P-glycoprotein (PGP) - Answer-Macrocyclic lactone toxicosis in mammals occurs when
the ____ pump is overwhelmed (overdose), defective (ABCB1 mutation), or functionally
compromised (drug interactions)

CNS: depressed mentation, hyperesthesia, ataxia, bradycardia, tremors, seizure, coma,
resp depression, paralysis, death
Ocular: mydriasis > miosis, absent menace, blindness
General: vomiting, lethargy, hyper/hypothermia - Answer-What are the clinical signs of
macrocyclic lactone toxicosis (17)

Decontaminate (oral - emesis, GI lavage, topical - bath, IV lipids, repeated AC q4-8h for
2d), supportive (fluids, thermal, methocarbamol - tremors, diazepam - seizure, minimize
sensory stimuli - hyperesthesia, oxygen/ventilation - resp distress, +/- nutritional
support) - Answer-What is the treatment for macrocyclic lactone toxicosis

Lipophilic - highest concentration in brain and adipose, metabolized in liver (activation
vs detoxification pathway) - Answer-What are 2 pharmacokinetic characteristics of
OP/carbamates

Inhibition of acetylcholinesterase enzyme activity (OP - irreversible binding, carbamates
- reversible binding) - CNS excitotoxicity, additional effects on NMDA/GABA/monoamine
etc - Answer-What is the MOA of OP/carbamates

Muscarinic: vomiting, abdominal pain, salivation, lacrimation, urination, defecation,
miosis, resp secretions
Nicotinic: muscle fasciculations, tremors, seizures, excitation/agitation, paralysis, coma,
resp failure - Answer-What are the clinical signs of OP/carbamate toxicosis (15)

Atropine response test - Answer-What is a good way to diagnose OP/carbamate
toxicosis antemortem

Decontaminate (oral - emesis/AC/GI lavage/IV lipids, topical - remove source/bath),
atropine (OP/C) or pralidoxime (OP only), supportive care (fluids, thermal, diazepam -

,seizures, etc), monitor CV system and BG - Answer-What is the treatment for
OP/carbamate toxicosis

Opioids/barbiturates/benzodiazepines without the use of atropine, pralidoxime if
carbamate - Answer-What medications are contraindicated with OP/carbamate toxicosis

Species, size of snake/victim, age of snake/victim (younger snake = more potent), time
since last envenomation, number of strikes, depth of penetration, location - Answer-
What are 7 factors that influence the severity of a snake bite

Elliptical pupil, facial pit, triangular head, retractable maxillary fangs (rattlesnakes,
moccasins, copperheads) - Answer-What are characteristics of crotalidae snakes and
what are examples

Round pupils, rounded head, smaller fixed maxillary fangs (coral snake) - Answer-What
are characteristics of elapidae snakes and what is an example

Swelling begins unilateral and is progressive and painful +/- evident puncture wounds -
Answer-How can you differentiate facial swelling from anaphylaxis from facial swelling
from a snake bite

Painful swelling, bruising, puncture wounds, +/- tachycardia, weak pulses, +/-
depressed mentation, +/- V/D (may have blood) - Answer-What are common exam
findings indicative of snake enovenomation

CBC (thrombocytopenia), coag panel (incr PT, PTT), +/- ECG, +/- chem, +/- UA
(pigmenturia), blood smear (echinocytosis) - Answer-What diagnostics should be used
in suspected snake envenomation cases and what findings would you see

False, only reverses coagulopathy and limits progression of swelling but does not
reverse local tissue injury/necrosis - Answer-T/F: antivenins reverse venom-induced
coagulopathy and local tissue injury

Antivenin (crotalidae) polyvalent (ACP) - Answer-Type of antivenin that contains
complete IgG immunoglobulins (horse) and contaminates (albumin, alpha and beta
globulins, IgM)

Crotalinae polyvalent immune fab (crofab) - Answer-Type of antivenin that contains IgG
antibody fragments (ovine) - 2 fab fragments

Fab2 antibody fragment (antivipmyn, venomvet) - Answer-Type of antivenin that
contains IgG antibody fragments - 2 fab segments + small portion of Fc segment
(equine)

ACP > Crofab > Fab2 - Answer-List the 3 types of antivenin in order from most likely to
cause a hypersensitivity reaction to least likely to

, Fluids (avoid colloids), plasma (coag support - need antivenin too), pain management
(opioids ideal - full mu), antibiotics (open wounds, significant tissue necrosis,
abscessation) - Answer-What treatment besides antivenin should be given to snake
envenomation patients

Multiple bites, antivenin reaction, thoracic strike, smaller patients - Answer-What are
negative prognostic factors for snake bite patients

Cytotoxins, hemotoxins, neurotoxins - Answer-What are the 3 types of biotoxins

Alpha latrotoxin - mass release and subsequent depletion of neurotransmitters -
Answer-What is the principle toxin released by widow spiders and what effect does that
toxin have on the body

Localized pain at site of bite, generalized muscle spasm/pain, tachycardia,
hypertension, hypersalivation, restlessness, V/D, ataxia, progresses to atonic paralysis -
death by resp failure - Answer-What are the clinical signs of a widow spider bite

Cats (up to 91% mortality) - Answer-Are dogs or cats more sensitive to widow spider
bites

Lactrodectus antivenin, opioids, methocarbamol and benzodiazepines for muscle
spasms - Answer-What is the treatment for widow spider bites

Sphingomyelinase D (and other necrotizing enzymes) - causes neutrophil recruitment,
intravascular coagulation, platelet activation, subsequent capillary occlusion/factor
depletion -> local tissue necrosis, thrombocytopenia, petechiation/ecchymoses, possible
hemolysis - Answer-What is the principle toxin released by brown recluses and what
effects does it have on the body

Targetoid lesion within 8 hours -> sloughing and non healing ulcer, hemolysis, anemia,
hemoglobinuria, pyrexia, myalgia, vomiting, DIC, coma - Answer-What are clinical signs
of brown recluse bites

Wound care (chemical debridement, chronic wound management), supportive
(diphenhydramine - pruritus, NSAIDs/opioids - pain, +/- antibiotics) - Answer-What is the
treatment or brown recluse bites

Beta scorpion toxin - blockage of voltage gated Na and K channels in nerves -> pain,
edema, erythema, pruritus, numbness, myalgia, Brady/tachycardia, resp depression,
seizures, hypersensitivity rxn - Answer-What is the principle toxin released by bark
scorpions and what effects does it have on the body

Analgesics (NSAIDs/opioids), general wound care, diphenhydramine - allergic reaction -
Answer-What is the treatment for bark scorpion stings

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