Final Exam Flashcards
What is a toxicant?
a compound causing toxicity (natural or man-made)
What is a xenobiotic?
foreign substance
What is an antidote?
This is a substance that prevents/relieves the effects of a toxicant.
How are poisons classified?
The lower the dose the more toxic!
toxic dose with <1mg/kg being extremely toxic and > 15 g/kg being relatively harmless
Dose-response curve?
Assumes a cause/effect relationship and that response is proportional to dose
- in general more toxin is bad!
What factors influence toxicity?
Exposure, subject (spp.) & environment
What’s the difference between concentration and dose?
Concentration: amount of chemical per volume
dose: amount given to an animal
What animals have genetic defects affecting metabolism?
o Cats are deficient in glucuronidation- affecting phase 2
o Dogs are deficient acetylation
o Pigs are deficient sulfonation
Metabolism can…
detox compound & increase elimination.
- bioactivation
Bioactivation & list some examples
conversion of parent compound into something more toxic
Ex. ethylene glycol toxicosis, benzopyrene (petroleum), aflatoxin & acetaminophen
What is the process of toxicity?
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
What makes an organ sensitive to toxin?
Receptor type and amount, amount of transporters present
How do toxicants cause toxicity?
- Damage cells
- Ex. Acetaminophen, arsenic - Organ system dysfunction
- Ex. insecticides, rodenticides
What are 5 life-threatening problems that require immediate attention?
Respiratory distress, CNS, Cardiovascular, Hemorrhage, Thermoregulation
- ID toxin is helpful nOT crucial so treat the pt not the poison!
When is ventilation needed?
hypoventilation/hypercapnia (PCO2 >45mmHg), metabolic acidosis (venous pH <7.35) hypoxia (PaO2<65mmHg)
How do you treat hypoxia?
Treat with 40% O2 (brief start w/100%): 100% O2 for a short period of time, because it will cause damage to lung epithelium
how do you prevent aspiration of vomitus?
positioning
How do you control CNS hyperactivity? (Seizures)
Diazepam, phenobarbital, methocarbamol, gabapentin
How do you control CNS depression?
analeptics & doxapram
How do you control tachycardia & arrhythmias?
lidocaine, propanolol
How do you control hypertension?
nitroprusside, hydralazine
What are the four major themes for completing a history?
health history, current clinical history, diet & environment
What is the goal of GI decontamination?
reduce absorption of toxin & facilitate transport out of GI system. Done with emesis & activated charcoal
What medication induces vomiting in cats?
xylazine; may cause hypotension & bradycardia
What medication induces vomiting in dogs & pigs?
apomorphine; may cause prolonged vomiting
When should you induce emesis?
Perform if toxic dose ingested, no vomiting has yet occurred & activated charcoal is not an option
When should you NOT induce emesis?
caustic chemicals, sharp items, volatile chemicals, risk of aspiration pneumonia
When should you give activated charcoal?
known substance, recent ingestion or undergoes enterohepatic circulation, pt. can tolerate or no need to administer oral rx immediately
When should you not give activated charcoal?
protracted vomiting, caustic/basic substance that charcoal doesn’t bind, intestinal FB (physical GI damage), obstructed airway, chronic exposures
What doesn’t bind activated charcoal?
acids/alkalis, alcohols/glycols, metals, oils, petroleum, detergents, cyanide
MOA for strychnine?
competitive antagonist to glycine receptors (spinal cord & medulla) causing
Strychnine clinical signs
stiff neck and gait, “grinning” (facial muscles tighten), tetanic seizures, sawhorse stance
Strychnine DX
CS, elevated CPK and LDH in serum, increased anion gap- lactic acidosis, hyperkalemia, leukocytosis
Strychnine TX
Decontamination, ammonium chloride (ion trapping), seizure control +/- ventilate with pentobarbital
Ammoniated Feed Toxicosis- MOA
imidazole and/ or non-protein nitrogen added to cattle feed and byproduct causes too much ammonia–> blood
* Ruminants are most susceptible*
Ammoniated Feed Toxicosis- CS?
Bovine Bonkers- hyperexcitability & SLUD
Ammoniated Feed Toxicosis- DX?
CS/HX, feed analysis, increased ammonia/ glucose/BUN & acidosis
Ammoniated Feed Toxicosis- TX?
Remove feed, sedation (prevent self-mutilation), milking out cows +/- cold H20 + vinegar
Salt Tox MOA
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!
Salt tox CS
primarily salivation/increased thirst, progressing to circling, head pressing, seizures, blindness, partial paralysis
Salt tox DX
blood sodium levels, high sodium levels in brain diagnostic in swine & cattle (> 2000 ppm)
Salt tox TX
slow rehydration starting with hyperosmotic fluid, furosemide to prevent pulmonary edema
What are mycotoxins & the three subgroups?
Fungal secondary metabolites
i. Slaframine
ii. Fumonisin
iii. Tremorgenic Mycotoxins- produced by Penicillium, Aspergillus, Claviceps, etc.
Slaframine MOA
Acts as a muscarinic cholinergic agonist (esp. in exocrine glands) ~ “Ach mimic”
Slaframine CS
Most common in horses & cattle copious salivation (slobbers), +/- bloat, diarrhea, frequent urination, feed refusal
Slaframine TX
Remove source, atropine
Fumonisin MOA
MOA: inhibits sphingosine N-acetyltransferase causing increase sphingosine level cytotoxic
Diseases linked to Fumonisin?
i. Equine leukoencephelomalacia (ELEM): affecting CNS
ii. Porcine pulmonary edema (PPE): affecting respiratory system
Fumonisin TX
isolate, can change feed +/- Ultrasorb S (mycotoxin deactivator)
Porcine pulmonary edema (PPE) CS?
inactivity/tachypnea/bradycardia (pigs); wipe out of large swine population.
& die of hypoxia, indicated by cyanosis
Porcine pulmonary edema (PPE) DX?
Increases liver enzyme and in serum/tissue sphingoid bases
- post mortem: pulmonary edema & hepatic lesions
ELEM CS?
CNS- terminal frenzy before death (mania, profuse sweating), prior to anorexia/ataxia/blindness
LIVER- HE & jaundice
Brain- liquefaction (unilat)
What is one toxic principle of tremorgenic mycotoxins?
Penitram A
Tremorgenic mycotoxin MOA?
multiple mechanisms including GABA receptor antagonist-like, acts on varied neurotransmitters to cause excitation
Tremorgenic mycotoxin CS?
muscle tremor, ataxia, tetanic seizures tremors in vertebrates
Alprazolam MOA
Benzodiazepone, that acts at limbic, thalamic, and hypothalamic level of CNS
Alprazolam CS
ataxia, depression, vomiting, tremors, tachycardia, hypothermia, diarrhea, paradoxical hyperactivity
Alprazolam TX
induce emesis, use gastric lavage with activated charcoal if toxic dose, flumazenil
What is flumazenil?
Benzodiazepine antagonist; blocks GABA receptor and can be used as an alprazolam tox “antidote”
Zolpidem MOA?
inhibits neuronal excitation by binding to benzodiazepine site oN GABA receptors (rapid absorption from GI)
Zolpidem CS
ataxia, vomiting, lethargy, disorientation, hyper-salivation, paradoxical excitement
What breeds are susceptible to ivermectin toxicosis?
Border collies, Shelties & Australian shepherds
- MDR1 gene mutation causes bioaccumulation in brain & tissues.
Ivermectin MOA?
GABA receptor agonist that decreases ability to respond to other stimuli
Ivermectin TX?
decontamination w/ activated charcoal, lipid emulsion, picrotoxin
- seizures? don’t use benzodiazepines OR use short acting like propofol & phenobarbital
Organophosphate Pesticides MOA
reversible inhibition of acetylcholinesterase activity- can become irreversible with time
continuous stimulation of neuron (muscarinic & nicotinic receptors)–> death
Organophosphate Pesticides CS?
Muscarinic: salivation, lacrimation, urination, GI distress/defecation, emesis, myosis
Nicotinic: muscle fasciculations, tremors, weakness, paralysis
CNS: respiratory depression, ataxia, clonic-tonic seizures, delayed neuropathy
Organophosphate Pesticides DX?
HX/CS, reduced rbc ACHE, atropine challenge- if no response/change means OP poisoning
OP TX?
GI decontamination, atropine (corrects muscarinic receptor), glycopyrrolate, oximes (protopam/2-PAM : to reactivate anticholinesterase, diazepam/barbiturates for seizures & time!
organophosphate-induced delayed neurotoxicity/ neuropathy
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
Pyrethrin MOA
Bind voltage-gated sodium channels and causes hyperactivity
* cats are sensitive due to inefficient glucuronidation
Pyrethrin CS? Cat vs. Dog
Cat-drooling, paresthesia, muscle tremors/seizures/hyperthermia Dog- paresthesia
Pyrethrin TX
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
Bromethalin MOA
block oxidative phosphorylation in CNS leading to dysregulation
Bromethalin CS
ataxia, hindlimb paralysis, hyper-excitability, severe muscle tremors, seizures
Bromethalin DX
cerebral edema and cerebellar degeneration
Bromethalin TX
Emesis, charcoal, furosemide for cerebral & pulmonary edema, treat seizures, lipid infusion
Acetaminophen MOA?
metabolized by glucuronidation, sulphonation & oxidation pathways~ bioactivated to NAPQI (N-acetyl-p-benzoquinone imine).
What spp. is extremely sensitive to acetominophen?
Cats because they cannot glucoronidate
Acetaminophen CS?
Cats: cyanosis, methemoglobinemia, depression & edema of paws/ face
Dogs- Hepatotoxicity- hepatic necrosis nausea, v/d/shock
Other- hemolysis, Heinz bodies
Acetaminophen TX:
N-acetyl cysteine OR cimetidine (cats), ascorbic acid, antioxidants, silymarin (milk thistle) & s-adenosylmethionine
Xylitol MOA
Dose dependent insulin release causing lethal liver injury & hypoglycemia (dogs)
Xylitol CS
vomiting, lethargy, ataxia, collapse & seizures, liver enzymes, BG & hypokalemia (d/t endogenous induced insulin)
Xylitol TX
activated charcoal is NOT effective or recommended (poor binding ability) & monitor BG/liver function (supplement accordingly)
What toxins do some cyanobacteria or blue green algae produce?
Microcystin- impairs phosphatase affecting cell regulation/signaling and affects the liver.
Anatoxin- affect CNA & will see ataxia/ disorientation with toxicosis
Cyanobacteria CS & DX
v/d/pale mm, ataxia, seizures
DX: blood in stool, elevated liver enzymes & hx
Cyanobacteria TX?
Atropine ( helps with anatoxins), fluid & seizure control
Where in the kidney is the most common site of toxin-induced injury?
PCT
Acute renal failure
transient damage to tubule/glomerulus/ vasculature causing decreased GFR & azotemia
- CS: vomiting, GI bleed, anuria
Chronic renal failure
secondary changes triggered by initial injury (not all chemicals effect one organ)
Signs: edema, hypocalcemia, reduced rbc
Ethylene Glycol MOA
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)
Ethylene Glycol CS (3 Stages)
- Drunkenness, nausea, vomiting, PU/PD (Dogs)
What stage of ethylene glycol toxicosis does the animal normally present?
Stage 3
Ethylene Glycol DX
Ethylene glycol blood concentration blood, Azotemia (stage 3), low USG & crystalluria (calcium oxalate monohydrate)
Chemistry: hyperglycemia, hypocalcemia & increased anion gap
Ethylene Glycol TX
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*
Cholecalciferol MOA
Liver metabolizes cholecalciferol to 1,25 dihydroxycholecalciferols causing a massive increase in serum calcium!
Cholecalciferol CS
Delayed!
anorexia, thirst, PU, dark diarrhea, bradycardia, ventricular arrhythmia, hypertension & mineralization of tissues
Cholecalciferol Dx
- clinical signs
- hypercalcemia
- Low PTH
- Renal damage: low USG & azotemia
- Hydroxycholecalciferols in bile & kidneys
- Histo: mineralization in multiple organs
How to differentiate cholecalciferol from ethylene glycol?
EG has higher kidney calcium compared to cholecalciferol
EG Ca: P ratio in kidney higher than cholecalciferol
Cholecalciferol TX
- 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
Grape & Raisin MOA?
Unknown
Grape & Raisin CS?
Variable! vomiting, followed by acute renal failure signs
Grape & Raisin DX?
hypercalcemia, hyperphosphatemia, increased Ca:PO4, elevated BUN/creatinine
Grape & Raisin TX?
- Emesis, lavage, or activated charcoal (grape remain in GI with slow absorption)
- Fluid therapy + supportive therapy
Ergot Alkaloids MOA?
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
Ergot Alkaloids CS?
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)
Ergot Alkaloids TX?
metoclopramide or domperidone (dopamine antagonists- primarily to correct reproductive issues), remove source
What species are most sensitive to ionophore toxicosis?
Horses>Cow>Poultry
- usually caused by a feed-mixing error
Ionophore MOA?
increase intracellular sodium/calcium leading to mitochondrial swelling and cell death
Ionophore CS? in horses & cows
anorexia, colic, profuse sweating on flank, recumbent, incoordination, diarrhea (cattle), respiratory difficulty (cattle)
Ionophore DX?
increased muscle enzymes (CK) myoglobinuria, elevated AST/LDH/BUN/bilirubin, hypokalemia, hypocalcemia, chemical analysis of feed
- Necropsy: pale cardiac muscle; muscle has striation/ vacuolization
Tetanus MOA
-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)
Tetanus CS?
stiffness, twitching, lockjaw (all facial muscle lock up), unsteady gait, bloat (ruminant)
Tetanus TX?
antitoxin (only useful at early stages), supportive therapy
Bobtail Disease
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)
White Muscle Disease
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
Phenoxyacetic Acid Herbicides moa?
unknown, however dogs are more susceptible
Phenoxyacetic Acid Herbicides CS?
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)
Phenoxyacetic Acid Herbicides TX?
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)
What are three common respiratory toxins?
- ventilatory muscle paralysis- botulism, tetanus, OP, strychnine, venom
- Respiratory center depression- barbiturates, opiates, hypnotics, sedatives & antidepressants
- Aspiration pneumonia: ethylene glycol, petroleum & bleach
Paraquat MOA?
non-selective herbicide that induces oxidative damage
- lungs are sensitive and will absorb at a higher affinity than O2)
Paraquat CS?
lung damage, renal failure, pulmonary fibrosis, vomiting, burning skin, acute pulmonary edema
Paraquat tx?
no oxygen unless hypoxic (b/c can worsen lung issues), emesis, charcoal, lavage
Polytetrafluoroethylene (PTFE
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
What species is mostly effected by PTFE?
birds
First generation anticoagulant- Warfarin
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)
Second Generation - Brodifacoum
oLong half-life (20 days), high potency, kills in single feeding
Anticoagulant MOA
- inhibits Vitamin K epoxide reductase
- when it is blocked vitamin K cannot be used to make clotting factors.
Anticoagulant CS
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
Anticoagulant DX
history of exposure, evidence of coagulopathy, response to Vitamin K therapy
o Testing: increased PT/PTT
Anticoagulant TX?
emetic (recent exposure) adsorbent, cathartic therapy & Vitamin K
- low dose treat for 2 wk for first generation & 1 month for second generation
Gossypol toxicosis MOA?
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
Gossypol toxicosis CS?
- 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)
Gossypol toxicosis DX
HX of cotton ingestion, cardiac necrosis, edema, vacuolization, chemical analysis
Gossypol toxicosis TX
feed high protein diet with Vitamin A/iron/lysine supplementation, remove sources from diet & symptomatic treatment
Cantharidin (Blister beetle or Spanish fly) toxicosis
inhibits protein phosphates and mucosal irritant
** usually affects horses**
Cantharidin toxicosis CS?
colic, frequent urination, diaphragm contraction with heartbeat, shock, irritation/ ulceration of epithelia (muzzle in water- irritated in mouth so constantly drinking water) & cardiac toxicity
Cantharidin toxicosis DX?
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
Cantharidin toxicosis TX?
GI decontamination and protection with sucralfate, antibiotics
Methylxanthines MOA?
antagonist of adenosine receptors –> CNS stimulation (overstimulation), vasoconstriction, tachycardia
oPrevents calcium reuptake –> increased skeletal/cardiac muscle contractility
oInhibits phosphodiesterase–> increase cAMP and cGMP
Methylxanthines CS?
vomiting, diarrhea, diuresis, hyperactivity (bounce), panting, tachycardia, hypertension, ataxia, tremors, seizures, coma, death from arrhythmia or respiratory failure
Methylxanthines DX?
history, stomach content analysis, plasma/serum/urine/liver analysis
Methylxanthines TX?
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
Nitrate toxicosis MOA?
Nitrate converted to nitrite, which causes vasodilation & oxidized ferrous iron in hemoglobin to ferric state–> methemoglobinemia (O2 starved tissues)
What spp. is most susceptible to nitrate toxicosis?
Pig>cattle>sheep>horses
What are plants that cause nitrate toxicosis?
lambsquarters, black nightshade, pigweed
Nitrate toxicosis CS?
depending on level of methg: cyanosis (15%)
ataxia, seizures, coma (50%)
death (>70%)
Nitrate toxicosis DX?
methemoglobinemia, nitrate in feed/water, necropsy (eyes)
Nitrate toxicosis TX?
1-2% methylene blue IV (urine will turn green), ascorbic acid (cats, horses), feed cattle corn to increase nitrite reduction by rumen flora
Examples of cardiac glycosides?
Digitalis, digoxin
Plant examples: Foxglove, oleander (SE region), lily of the valley
Cardiac glycosides MOA
inhibit sodium/potassium ATPase through competition (found on cardiomyocytes)- leading to increased intracellular calcium
Cardiac glycosides CS
staggering, trembling, dyspnea, increased intracellular sodium and calcium, hyperkalemia, tachycardia, arrhythmia
- over time can become bradycardia & weak pulse
Cardiac glycosides TX
GI decontamination, propranolol (for arrhythmias), insulin w/ glucose (treat hyperkalemia), Digoxin fragment antibodies- designed from toxin in foxglove (antidote) “digibind”
What is digibind?
Digoxin fragment antibodies- designed from toxin in foxglove (antidote for digoxin and similar cardiac glycosides)
Cyanide toxicity MOA
inhibition of cytochrome C oxidase (no ATP production)- shuts down oxidative respiration
Cyanide toxicity CS
super oxygenated (cherry red) blood that is slow to clot, bitter almond smell, sudden death, dyspnea, weakness, tremors
- Rapid onset of toxicosis (20 min)
Cyanide toxicity TX
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
What spp are sensitive to NSAIDs?
Dog- ibuprofen
Cat- Aspirin d/t lack of glucoronidation
NSAIDs MOA
- inhibit cyclooxygenase (COX1&2) and damage GI and liver
- Uncouples oxidative phosphorylation at high doses-increased lactic acid, metabolic acidosis
NSAIDs CS
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)
NSAIDs DX
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)
NSAIDs TX
induce emesis, activated charcoal (multiple doses), ranitidine (H2 blocker), sucralfate & misoprostol (prostaglandins analog), supportive care +/- transfusion with hemorrhage
What is the #1 priority pollutant?
Arsenic
Arsenic MOA?
o pentavalent reduced and metabolized in rumen to reduce metabolic energy & CNS problems
o trivalent inhibits oxidative phosphorylation and causes blood/mucosal issues
Arsenic CS?
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
Arsenic DX:
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)
Arsenic TX:
o GI contamination: if acute~ emesis, activated charcoal/ cathartic
o chelation therapy- dimercaprol, sodium thiosulfate (binds arsenic) prior to clinical signs
o supportive therapy
Zinc MOA?
zinc enters the stomach- acid eats & releases zinc–> free zinc damages GI mucosa (corrosive effect & oxidative damage causing hemolysis)
Zinc CS?
v/d/ PU/PD, hemoglobinuria, hemolytic anemia, jaundice, pancreatitis & lesions along GI, liver/kidney/pancreas
Zinc DX:
serum & liver zinc values, decreased PCV, regenerative anemia, thrombocytopenia, oxidative damage, elevated liver/kidney/pancreatic enzymes, hemoglobinuria, radiographs for hardware, formation of Heinz body
Zinc TX:
remove foreign body, emesis (if possible), omeprazole (proton pump inhibitor) or H2 blockers +/- GI protectants
Soap/Shampoo
o Clinical signs: GI distress, vomiting, diarrhea
o Treatment: simple dilution with milk or water, fluid treatment
o Rarely lethal
Scouring Powder/ Bleach
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)*
Disinfectant CS
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
Disinfectant TX
dilute with gastro-protectants, activated charcoal or cathartic, 1% methylene blue for methemoglobinemia
No emesis/lavage because of aspiration pneumonia
Automatic Dishwasher Detergents:
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
Toilet Bowl Cleaner:
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
What spp. is primarily affected by zearalenone?
Pigs>livestock
* chickens are resistant*
Zearalenone MOA?
Estrogen receptor agonist (higher affinity)
Zearalenone CS?
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!
Zearalenone TX?
change feed, activated charcoal (d/t enterohepatic recirculation) or high fiber to reduce elimination times
Venom
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
Poison
passive secretion as passive defense mechanism
Bee venom MOA
- melittin acts as detergent and hemolytic causing pain
* phospholipase A2 destroys membranes
Wasp venom MOA
use alarm pheromones & kinins produce pain
Ant venom MOA
piperidine causes dermal necrosis, formic acid causes burning sensation and pain
(also has antibacterial properties)
Hymenoptera Venom CS
local swelling, red plaques, edema, regional allergy or anaphylaxis (rare), shock, hemolysis, renal/hepatic injury
- delayed hypersensitivity is possible
Hymenoptera Venom TX
removal of stinger by scraping, cold compress, antihistamines, corticosteroids, epinephrine for shock/systemic toxicosis
What is the gold standard for anaphylactic shock?
epinephrine
What toxin do ticks produce?
Holocyclotoxin impairs acetylcholine release, causing paralysis/muscle weakness
- dermacentor may act on sodium channels.
Tick CS
may appear 6-14 days after attachment.
loss of appetite *voice * incoordination, ascending flaccid paralysis, respiratory distress or death (b/c respiratory paralysis)
Tick TX:
supportive treatment, anti-emetics, oxygen therapy
atropine sulfate contraindicated!
What toad produce cardiotoxins?
Bufo marinus (cane toad) affecting dogs
Toad MOA:
biogenic amines cause vasoconstriction, hypotension, hallucination, gastrointestinal effects
bufogenins inhibit sodium/potassium ATPase activity (similar activity as digitalis)
Toad CS:
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-
Toad TX:
water lavage, activated charcoal if no seizures, diazepam/barbiturates if seizures, propranolol/lidocaine/esmolol for arrhythmia, fluid replacement therapy, digoxin-specific antigen binding fragments
What spp. is most susceptible to toad toxicosis?
Dogs
What spp. is most susceptible to black widow toxicosis? What spp. is most susceptible to brown recluse?
cats; dog
What does the black widow venom contain?
Alpha-latrotoxin
Black widow venom MOA
alpha-latroxin creates pores in membranes to allow calcium entry and massive amounts of neurotransmitter release leading to sustained muscle spasms
Black widow venom CS
muscle cramping/spasms (Latrodectism), rapid weight loss, abdominal rigidity, restlessness, writhing, vocalization, hypertension, tachycardia, respiratory collapse
Black widow venom TX
control muscle spasms and pain, calcium gluconate (controversial), anti-venom
Brown recluse venom composition & MOA?
Sphingomyelinase D- cleaves heads of phospholipids bilayers causing tissue necrosis
Brown recluse CS?
blister-like bulls eye where bitten (non healing ulcer), hemolytic anemia, fever, weakness, leukocytosis
Brown recluse TX
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
Eastern Coral Snake Venom & MOA?
Bungarotoxin prevents binding of acetylcholine leading to paralysis and local tissue necrosis
Eastern coral snake CS?
myoglobinemia (cats), hemolysis (dogs), salivation, inability to swallow, dyspnea, weakness, hyporeflexia, CNS depression, paralysis
Eastern coral snake TX?
Antivenom (expensive), broad-spectrum antibiotics and symptomatic wound care, supportive care
Pit Viper Characteristics
Characterized by heat sensing pit and hinged (retractable) fangs, head wider than body (triangle), elliptical/vertical pupil
Snake bite CS
immediate distinct fang marks, immediate swelling/pain/bruising of bite, hypotension, shock, tachycardia, tachypnea, anticoagulation, tissue necrosis
Snake bite TX
anti-venom, antihistamines, fluids, corticosteroids, glucocorticosteroids
do not cut, ice, or tourniquet
Enterotoxins MOA
enterotoxins bind to intestinal epithelium to increase permeability and cause fluid loss (diarrhea) and decreased absorption of nutrients
- Bad case of food poisoning
Endotoxin MOA
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
Endotoxin TX:
emesis, support cardiovascular function, correct fluid/electrolyte imbalance, prevent bacteria
Botulism in horses
“Forage poisoning in adult horses
“shaker foal syndrome” in foals
Botulism MOA
prevents release of acetylcholine at neuromuscular junction leading to flaccid paralysis
Botulism CS
decreased tongue and tail tone, dropping food from mouth, salivation, weakness, weak vocalization, progressive paresis, bradycardia, constipation, urinary retention
Botulism TX
supportive therapy, oxygen therapy, warm water enemas, bladder expression, antibiotics, antitoxin (will not neutralize toxin already in neurons)
