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163 Cards in this Set
- Front
- Back
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Pb Species Effected
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dogs #1, cattle #2
other = ↓ access/susceptibility |
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Pb Mechanism
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interact w/ sulfhydryl enzymes in mitochondria
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Pb Lesions
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intranuclear acid-fast inclusion bodies in kidney
usually few; lead in GIT, cerebral edema, tubular necrosis |
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Pb: CS
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GI+CNS (young + seizure)
Hematopoietic (all spp): microcytic hypochromic anemia d/t (1) impaired heme synthesis + (2) ↓RBC lifespan (membrane fragility) -> reticulocytosis, basophilic stippling, nRBCs |
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Pb: Horse CS
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chronic, laryngeal paralysis (roaring), lower lip paresis
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Pb: Dx
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Whole blood lead >0.35ppm best marker of toxicity
Lead in GIT |
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Pb: Tx
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(1) Diazepam for seizures
(2) GIT removal: MgSO4 cathartic, gastrotomy, rumen lavage (3) Livestock chelation: Ca EDTA + thiamine, consider milk w/d (4) Dog chelation: succimer > Ca EDTA > D-penicillamine; *chelation may worsen seizures* |
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Cu: Most Susceptible species
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Sheep most affected
Dogs: Bedlingtons, Skye, WHWT, female Dobermans |
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Cu Sources
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Metallic Cu
Copper sulfate (emetic, fungicide, anthelmentic) |
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Cu: Risks for hemolytic crisis
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Cattle ration fed to sheep
Transportation Lactation Over-exercise Poor nutrition Ingest hepatotoxic plants |
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Cu: Interaction w/Molibdinum
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INVERSE relationship with molybdenum:
↓Mb = ↑Cu |
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Cu: Cause of Acute Toxicity
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Overdose of Cu salts
(anthelmentic drenches, minerals, rations, neonatal Cu injection) |
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Cu: Sheep Pathophysiology with chronic ingestion
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Sheep/SR: excessive intake ->
massive release of Cu in liver -> sudden ↑ plasma [Cu] -> lipid peroxidation + IV hemolysis |
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Cu: Acute CS
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severe gastroenteritis, hemolysis/hgburia (3d), centrilobular necrosis
death 1-2d OR survive and die of renal failure |
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Cu: CS Sheep (Acute-on-Chronic)
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MetHgb, Hgburia
Low morbidity, high mortality |
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Cu: Dx
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[Cu] in blood and tissues postmortem
Classic: gun-metal blue kidneys liver failure, hemolysis |
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Cu: Tx Sheep
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(1) Penicillamine (Cu chelator): $$, pets only
(2) Calcium versenate (Cu chelator) (3) Ammonium tetrathyo-molybdenate to ↑Cu excretion (4) Zn acetate supp (↓Cu absorption) |
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Dx: Cu hepatopathy
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Liver bx (~1g) = >850ppm
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Tx: Cu Toxicity in Dogs
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slow progression of dz, can’t stop it!
(1) Genetic screening (2) Low Cu diet (3) Lifelong Cu chelation (d-Penicillamine) (4) Zn acetate supp (↓Cu absorption) (5) +/- ascorbic acid |
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Fe: Sources
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iron vitamins
(fumarate 33%, sulfate 20%, gluconate 20% elemental Fe) |
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Fe: Cause of piglet toxicity
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sporadic Fe toxicity with SQ/IM Fe overdose
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CS: 4 Stages of Fe toxicity
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1: (<6hr): local “corrosion” in gut ->
V/D, abd pain, hypotension, acidosis 2: (6-14hr): stabilization-> mvmt of free plasma iron into cells 3: multisystem organ failure-> iron toxic to liver, heart, kidney, CNS 4: 2nd wave of GI damage -> scarring, fibrosis, obstruction |
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Fe toxicity mimics this condition
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Acute sepsis
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CS: Acute form of piglet Fe toxicity
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mm damage @ inj, ↑K+, arrhythmias, tremors, resp distress
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CS: LESS Acute form of piglet Fe toxicity
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immunosuppression, death in 2-4d from bacteria/viral
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CS: Rare form of Piglet Fe Toxicity
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Ca mobilization -> hard swelling -> death, other calcification
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Dx: Fe toxicity
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Serum [Fe]: peaks 2-4hrs post-ingestion
Serum [Fe] no longer predictive in Phase 4 |
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Tx: Fe toxicity
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(1) Emetic, AC + SC (AC doesn’t bind Fe; cathartic helps more)
(2) Deferoxamine: Fe chelator (3) Continue chelation as long as reddish urine (vin rose) = Fe- deferoxamine complex excretion |
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Most toxic form of Arsenic
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AsIII (trioxide) = 60x more toxic than AsV (pentoxide)
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Organic sources of Arsenic
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Organic arsenic
roxarsone, nitarsone, arsanilic acid feed additives, coccidiostats in poultry/swine chronic toxicity from mismixed diets |
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Severity:
Acute vs. Chronic As toxicity |
Acute: medical emergency
Chronic: environmental prob, rare in USA (well water in SW USA) SE Asia: skin probs (As in water), carcinogen |
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Action of As III
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binds thiol/sulfhydryl groups in tissue proteins
Sources: MSMA / DMSA |
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Action of As V
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uncouples oxidative phosphorylation
Source: Arsanilic Acid |
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As: Stored in these organs
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Kidneys, Liver
Deposition in hair, nails, bones, teeth; |
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As: Effect on GI
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GI mucosal sloughing
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Inorganic As: CS
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Death in 12-24hr
GI: vomiting, hemorrhagic gastroenteritis, abd pain, salivation MS: tremors, ataxia, weakness CV: hypotension, shock, tachyC, arrhythmias Other: nephrosis + hepatic injury |
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Organic As: CS
Monogastric/ Poultry |
Monogastrics/poultry: neurologic signs -> ataxia, blindness, hindlimb paresis, wt loss with OK mentation
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Organic As: CS
Ruminants |
break down into elemental AS -> inorganic As poisoning
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As: Dx
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Inorganic: acute HGE, liver + kidney [As], urine [As], water samples
Organic: hx; demyelination + gliosis of peripheral nn + optic tract |
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As: Ddx
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Salt poisoning, botulism, Pb, Hg, VitA, pigweed, pseudorabies
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Tx: Organic As
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No tx; remove problem feed; effects reversible w/in 2-3d of ataxia; irreversible post-paralysis
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Tx: Inorganic As
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(1) Emetic, AC + SC
(2) Sodium thiosulfate (sulfhydryl source): chelates As in GIT (3) Give IV acetylcysteine orally (4) GI protectants: kaolin-pectin, sucralfate (5) As chelators: dimercaprol/BAL IM, D-penicillamine PO, mercapto- succinic acid agents (DMPS, DMSA) (6) Fluid therapy (7) Monitor kidney/liver fxn |
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Organophosphates/ Carbamates: Sources
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Pet shampoos, Parasiticide, Garden dust, Lotions
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Organophosphates/ Carbamates: Action
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Acetylcholinesterase inhibitors
@ cholinergic synapses |
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Difference between Organophosphates & Carbamates
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Carbamate: reversible (carbamylation)
OP: initially reversible, then irreversible when aged (12-24hr = phosphorylation) |
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Organophosphates/ Carbamates:
Site of absorption |
Rapid GI/skin absorption
liver metabolism -> rapid onset |
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Organophosphates/ Carbamates: CS
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Acute neurologic syndromes
SLUDs, CNS, bronchospasm, ↑bronchial secretions, mm tremors, resp paralysis Colic, diarrhea, miosis (variable), bradyC |
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Organophosphates/ Carbamates: Dx
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Cholinesterase activity:
>50% inhibition = poison >75% = diagnostic Atropine test dose: pre-anesthetic dose should NOT ↓muscarinic signs Chem analysis: brain, liver, kidney, rumen, skin, feed/water (5-10d) |
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Organophosphates/ Carbamates: Dx problems in cats
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cross-react with pseudocholinesterase
Incubation: can reverse carbamate activity |
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Organophosphates/ Carbamates:
Tx |
#1: Atropine high-dose:
(IV, SQ, IM; half-dose for horses) reverse muscarinic effects (dose to effect): evaluate miosis, bradycardia, bronchospasm (will NOT reverse nicotinic effects) #2: AC + SC or gastric lavage NO EMETICS: many insecticides use petroleum distillate as vehicle; Bathe in mild detergent #3: 2-PAM (pralidoxamine): (IV or IM, q4-6hr, d/c if no benefit after 36hr) cleave off OP from enzyme before aged |
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This drug will not work for Carbamate toxicity
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2-PAM NOT good for carbamates
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Pyrethrins: Sources
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chrysanthemum
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Pyrethroids: Sources
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synthetic
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Pyrethrins/ Pyrethroids:
Sensitive Animals |
young, cats, fish, reptiles
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Pyrethrins/ Pyrethroids:
Action |
Enhance Na+ ion conductance Post-synaptic GABA blocker
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Pyrethrins/ Pyrethroids: Synergist
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Piperonyl butoxide
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Pyrethrins/ Pyrethroids: CS
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Hours: looks like OP/carbamates
Mm tremors, depression or excitation, salivation, vomiting, ataxia, dyspnea, hyper or hypothermia |
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Pyrethrins/ Pyrethroids: Dx
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Atropine test dose: pre-anesthetic dose will cause decrease in muscarinic signs
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Pyrethrins/ Pyrethroids: Tx
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AC + SC Bathe in mild detergent
Atropine: will reduce some signs but not real antidote Seizures: diazepam Most will resolve in 2-3d with minimal treatment |
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Citrus oil insecticides: Source
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D-limonene, others
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Citrus oil insecticides:
Sensitive Animals |
cats, hepatic disease
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Citrus oil insecticides: Action
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Mode of action unknown
GRAS (FDA) |
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Citrus oil insecticides: CS
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CNS: ataxia, weakness, mm tremors, hypothermia
Other: scrotal irritation, transient paralysis, liver failure (ingestion of melaleuca or pennyroyal) |
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Citrus oil insecticides: Tx
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Dermal: bathe in Dawn + water
Oral: AC + SC Seizures: diazepam +/- N-acetylcysteine: for pennyroyal poisoning in humans |
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Citrus oil insecticides: Site of Absorption
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Rapid GI/skin abs -> liver metab
(glucuronide and glycine conjugates) |
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Lindane
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Organochlorine
(Happy Jack) |
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Organochlorine: Source
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Persistent insecticides
Exposure: misapply SA flea control |
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Organochlorine: Action
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Na+ channel interference = CNS
Endocrine active: estrogenic, anti-androgenic, egg shell thinning (DDT) lipophilic (stored in fat) |
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Organochlorine: CS
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Acute onset (1-6hr): looks like OP/carbamates
Mm tremors, excitation, seizures, salivation, vomiting, ataxia, hyperthermia May have residual renal/liver damage |
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Organochlorine: Dx
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Hx exposure
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Organochlorine: Tx
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(1) NO emetics (seizures)
(2) AC + gastric lavage (3) Bathe (4) Seizure: barbiturates (seizures more resistant to diazepam) (5) OK if get through 12-24hr (6) To excrete more OCs: lose body fat (poor quality feed) |
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USDA monitors Meat/Milk for residues of this class of insecticide
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Organochlorine
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Fipronil: Source
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Frontline TopSpot and Spray = Low Toxicity
Technical Grade= commercial, higher concentration |
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Fipronil: Action
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N-phenylpyrazole GABA inhibition
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Fipronil: CS
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Vet products: mild self-limiting vomiting + salivation
Technical products (almost 100% fipronil): more GI irritation |
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Fipronil: Tx
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Vet Products: supportive/symptomatic
Technical: GI decontamination = gastric lavage, AC + SC; Symptomatic and supportive, seizure control |
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Bromethalin: Sensitive Animals
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Cats
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Bromethalin: Resistant Animals
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Guinea Pigs
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Bromethalin: Pathophysiology
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N-methylated pesticide
GI abs-> demethylated in liver (P450) Uncouples oxidative phosphorylation in mitochondria ->↓ATP -> myelin splitting (also lipid peroxidation) -> cerebral edema, moderate ↑ICP |
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Bromethalin: Acute high dose (rare)
CS |
rapid-onset, strychnine-like
mm tremors, seizures (sound/light induced), hyperthermia -> death -> rigor |
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Bromethalin: Low dose
CS |
Delayed (12- 72), CNS dep -> coma, anisocoria, hindlimb ataxia, paralysis,
*extensor rigidity, decerebrate posture |
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Bromethalin: Dx
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Hx exposure
White matter edema: diffuse white matter vacuolization Bromethalin or metabolites in fat, brain, liver |
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Bromethalin: Tx
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(1) Emetics, AC (repeated)
(2) Cerebral edema: Mannitol, Dexamethasone, furosemide (but difficult to mobilize edema from myelin vacuoles) (3) Ginkgo biloba? |
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Zinc phosphide: Sources
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Grain, paste, or tracking powders
Restricted use |
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Zinc phosphide: Pathophysiology
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Converted to phospine gas in acid stomach -> cytotoxic to lungs
Pulmonary Edema & Neuro Effects |
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Zinc phosphide: CS
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Rapid-onset: respiratory + CNS,
vomiting, seizures, pulmonary edema, delayed liver/renal dz |
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Zinc phosphide: Dx
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Hx exposure
Chemical analysis of stomach contents (phosphine odor) |
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Zinc phosphide: Tx
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(1) No AC (small molecule)
(2) No emetic (semi-corrosive) (3) NaHCO3 lavage: ↓hydrolysis (4) Seizures: valium, pentobarbitol |
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Strychnine: Sources
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Gopher control
Restricted use |
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Strychnine: Action
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Competitive glycine receptor inhibitor = blocks inhibitory
Renshaw cells in CNS = net effect is cholinergic excitation |
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Strychnine: CS
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Rapid-onset: mm tremors, seizures, tonic extensor rigidity, “sawhorse stance,” opisthotonus, resp paralysis
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Strychnine: Dx
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Hx exposure
Chemical analysis of stomach contents, liver, kidney, urine |
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Strychnine: Tx
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(1) Gastric lavage + AC (tranquilized)
(2) NO emetic (seizures -> aspiration) (3) Seizures: valium, pentobarbital (4) Mm relaxants: methocarbamol: 1⁄2 quickly, rest slow to effect |
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Metaldehyde: Sources
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Molluscicide = snail/slug bait
*may contain arsenic or carbamates* |
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Metaldehyde: Action
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Mechanism unknown
acidosis + interference with CNS |
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Metaldehyde: CS
Dogs/Cats |
Acute onset: looks like OP/carbamates
tachyC, salivation, tremors, ataxia, nystagmus, mydriasis, salivation, V/D, cyanosis, hyperthermia; later CNS depression, blindness; death from respiratory failure (4-24hr) or liver failure |
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Metaldehyde: CS
Horses |
Acute onset: looks like OP/carbamates
colic, tremors, diarrhea, sweating, seizures, tachyC |
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Metaldehyde: Dx
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Hx exposure
Metaldehydes in baits, liver, urine, and plasma EG test kits would test positive |
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Metaldehyde: Tx
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(1) AC + gastric lavage
(2) IPPV (3) IV fluids +/- bicarb (4) Seizures: diazepam (xylzine + ace in horses) |
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Chlorphenoxy herbicides: Examples
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2,4-D, MCPP, SILVEX, 2,4,5-T, Agent Orange
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Chlorphenoxy herbicides: Action
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Mimic auxins = growth hormones in plants
Muscle membrane: ↑irritability and rigidity -> paralysis |
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Chlorphenoxy herbicides: CS
Dogs |
GI: V/D **Muscular: rigidity, ataxia, ↑insertional activity
Neuro: seizures, clonic spasms, opisthonus, coma Rare: oral ulcers, SI mucosal damage, kidney/liver damage |
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Chlorphenoxy herbicides: CS
Swine |
V/D, ataxia, depression
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Chlorphenoxy herbicides: CS
Ruminants |
bloat, diarrhea, oral ulceration, kidney/liver damage
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Chlorphenoxy herbicides: Tx
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AC+SC
Bathe with mild detergent Ion-trapping organic acid: bicarb |
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Chocolate: Toxic Principles
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Theobromine, caffeine
Milk: 1oz/1# Baking: 1oz/10# |
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Chocolate: CS
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GI: V/D
CNS (↑dose): agitation, hyperactivity, tremors, seizures CV: tachycardia, hyper/hypotension, arrhythmias |
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Chocolate: Tx
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(1) Emesis or gastric lavage
(2) AC: effective; use multiple doses (methylxanthines are delayed excretion in dogs AND enterohepatic circulation) (3) ECG, propranolol (4) IV fluids -> enhance excretion (5) Diazepam for seizures (6) Long half-life: signs can last 24-72hr |
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Thyroid hormone: Sources
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Thyroid hormone for tx hypothyroidism
Levothyroxine |
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Thyroid hormone: Toxicokinetics
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Poor GI abs; highly protein-bound; efficient biliary excretion; tissue buffer in liver/kidney
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Thyroid hormone: CS
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VERY high dose: hyperactivity, tachyC, tachypnea, dyspnea, abnormal PLR, V/D
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Thyroid hormone: Dx
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↑↑↑T4/T3 levels
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Thyroid hormone: Tx
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(1) Gastric decontamination: emetics, AC +SC
(2) Propranolol (3) Diazepam |
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Amphetamine: Sources
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Prescription drug
Popular recreation drug |
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Amphetamine: Action
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Sympathomimetic
↑ catecholamine release, ↓catecholamine reuptake, ↑serotonin release |
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Amphetamine: CS
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CNS: agitation, hyperthermia, tremors, seizures, coma
CV: tachyC, hypertension, arrhythmias Signs for 12-18 hours |
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Amphetamine: Tx
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(1) Gastric decontamination
(2) Tranquilization (chlorpromazine/ace) *caution, may lower seizure threshold, induce severe hypotension (3) Cyproheptadine: serotonin antagonist (4) Propranolol (5) Acidify urine: NH4Cl or ascorbic acid = ion-trap amine to promote elimination (contraindication: rhabdomyolysis) |
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Amphetamine: Potential contaminations with...
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phenylpropanolamine, caffeine, PCP
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Phenol: Sources
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Household disinfectants, coal tar, clay pigeons, solvents
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Phenol: Pathophysiology
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Oral or dermal -> glucuronide conjugation -> excretion
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Phenol: Sensitive Animals
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Cats most sensitive
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Phenol: CS
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Dermal: white discoloration Respiratory: stim -> alkalosis
CNS: mm tremors, seizure, coma, death GIT: corrosive injury Liver: icterus +/- metHgb Renal: tubular nephrosis Sudden death |
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Phenol: Dx
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Ferric Chloride Urine Test (purple)
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Phenol: Tx
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(1) Emetics (unless conc) +/- lavage
(2) AC + SC (3) Demulcents (milk, egg) (4) Bathe (5) Resp support: IPPV (6) Shock/acidosis support (7) Manage MetHgb |
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Acetaminophen: Sensitve Animals
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Cats most sensitive
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Acetaminophen: Pathophysiology
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metabolized by cytochrome P450 to quinines = hepatotoxic -> glutathione detox
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Acetaminophen: CS in Dogs
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hallmark = centrilobular necrosis
Initial (2-24hr); anorexia, vomiting Then asymptomatic: ↑liver enzymes 3-5d: hepatic necrosis 7-8d: recovery |
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Acetaminophen: CS in Cats
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Die of MetHbg before liver phase
Early: HBHA, facial/paw edema, MetHgb, icterus Days later: CNS dep, vomiting, dyspnea, hepatic necrosis |
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Acetaminophen: Tx
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(1) <2hr: emetic, AC + SC
(2) O2 therapy (3) N-acetylcysteine within 16hr, QID (alternate conjugation pathway) (4) Ascorbic acid QID |
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Factors necessary for Photosensitization
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Adequate concentration of phototoxicant in peripheral circulation
Ultraviolet light of appropriate wavelength (UVA - 270-380 nm) Susceptible skinned animal Molecular oxygen |
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Action of Photosensitizing Agents
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DNA interaction - photoadducts and cross-linking
Cell membrane alterations Protein interactions = inactivation of enzymes |
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Early CS: Photosensitization
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Erythema
Puritis Shaking of head & ears Pain around coronary bands - hoofs and horns **Seeks shade** |
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Progressive CS: Photosensitization
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Swelling and edema of ears and other exposed skin surfaces
Cracking of skin with exuding serum Secondary infections Corneal opacity - 1o PS - sheep , cattle & deer |
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Photosensitization: Tx
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Eliminate direct exposure to sunlight
Remove green plant material from diet if indicated Switch pastures Supportive care |
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Bishop’s Weed: Toxic Principle
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Primary Photosensitization
Xanthotoxin Bergapten These are furocoumarins |
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Rain Lily: Toxic Principle
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Primary Photosensitization
Unknown |
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Bishop’s Weed: Species Affected
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Cattle
Sheep Geese & ducks |
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Rain Lily: Species Affected
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Cattle
Deer “Sand Burn” in Horses |
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Bermuda grass: Toxic Principle
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Hepatogenous Photosensitization
Unknown |
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Bermuda grass: CS
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Typical photosensitization
Often with reddish-brown urine |
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White Snakeroot: CS
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Liver dysfunction
Photosensitization occurs if the affected animals survive for more than one to two days |
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White Snakeroot: Toxic Principle
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Tremetol - alcohol form
Tremetone -ketone May be excreted from milk of lactating animals (affects animals & humans) |
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Bees, Wasps, Hornets
Stinger Properties |
Bees: stinger is eviscerated - kills bee, stinger and venom sack remain in victim
–scrape out stinger - don’t squeeze Wasps don’t leave stinger in victim - can sting multiple times |
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Bee & Wasp venom
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Phospholipase A1 and A2
Hyaluronidase Acid phosphatase Antigen-5 Melittin, Apamin Various kinins ~ bradykinin |
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Ant envenomation process
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Bites with jaws, then stings with ovipositor apparatus
circular pattern of stings with two centralized punctate holes Stings can result in scars or 2° infection |
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Blister beetles: toxic principle
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Cantharadin
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Blister beetles: CS
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Acute, severe colic, shock, death in 2- 3 days
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Black Widow Spider: Toxic Principle
(Latrodectus mactans) |
α-Latrotoxin, neurotoxin
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Black Widow Spider: general CS
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Severe cramping of large muscle masses
abdominal cramping may interfere with respiration intense pain |
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Black Widow Spider: Dog CS
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Some regional numbness
Muscular fasiculations Seldom fatal |
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Black Widow Spider: Cat CS
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Paralytic signs develop rapidly
Severe pain Salivation Tremors, ataxia Death - respiratory collapse |
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Black Widow Spider: Tx
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muscle relaxants (methocarbamol)
atropine to reduce salivation shock therapy (corticosteroids, fluids) control seizures - diazepam Specific antivenin available for humans and has been used in small animals |
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Brown Recluse Spider: Toxic Principles
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hyaluronidase, proteases
spreading factors, hemolysins |
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Brown Recluse Spider: CS
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Bite not painful initially
2-6 hours, pain erythema 12 hours, blister - bulls-eye lesion Focal ulceration and necrosis Fever, arthralgia, lethargy, vomiting, seizures Wound slow to heal - often requires open wound management and debridement |
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Brown Recluse Spider: Tx
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Specific antidotes not available
Dapsone - leukocyte inhibitor Corticosteroids if systemic effects Fluids and bicarbonate if hemolysis/hemoglobinuria Surgical excision may be necessary |
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Pit Vipers (Crotalidae)
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rattlesnakes, cottonmouth, moccasin, copperhead
long, hinged, hollow fangs; they strike, inject venom (a voluntary action), and withdraw |
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Venomous Snake Characteristics
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Elliptical Eyes
Pit Viper have triangular head Pit Vipers have a “pit” underneath each eye used as a heat sensor. Some have unique characteristic marks |
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Pit Viper: Dx
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Characterized by severe local tissue damage that spreads from the bite site
The tissue becomes markedly discolored within a few minutes Dark, bloody fluid may ooze from the fang wounds if not prevented by swelling • Skin sloughing Fang marks: One fang mark/ Multiple punctures |
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Pit Viper: CS
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Pain and edema around the bite site
• Swelling • Dyspnea • Nausea, vomiting, or diarrhea Coagulopathy: – Thrombocytopenia – Hematemesis, hematochezia Neurologic symptoms: – Weakness – Paresthesias – CNS depression • Hypotension/hypertension • Tachycardia • Muscle fasciculations |
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Pit Viper: Late CS (>24h)
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Active and alert after 24 hours, death due to the direct effects of the venom is unlikely
Infection (possibly anaerobic) may be of concern Tissue necrosis may occur |
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Pit Viper: Tx
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IV fluids to combat hypotension
Preventing or controlling DIC Preventing secondary infection Corticosteroids Maintain patent airway Tetanus antitoxin |
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Elapidae Snakes
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Cobra, mamba, kraits, coral snakes
|
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Eastern Coral Snake: Tx
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Definitive therapy for coral snake venom poisoning is antivenom administration
Tetanus toxoid Antibiotic prophylaxis is not indicated for coral snake bites |
