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79 Cards in this Set

  • Front
  • Back
Caladium spp.
Caladium spp.
Caladium spp.
Castor Bean
Castor Bean
Castor Bean
Rosary Pea
Rosary Pea
Rosary Pea

a. common cause of poisoning
b. signs
c. toxicokinetic features
d. dx
e. tx
a. pennies: copper & zinc alloy
start w/in a few days of ingestion
vomiting, diarrhea, anorexia, CNS depression, ↓ milk yield, hemolysis, regenerative anemia, renal failure
pica (large animals), spherocytosis, inflammatory leukogram
rarely renal tubular changes, icterus
c. 20-30% net absorption, widely distributed (highest to liver, kidney), induces metallothionein production
d. rads, ↑ serum Zn levels, clinical signs, hx of exposure
e. sx to remove pennies (endoscopic removal preferred)
What are the 1st & 2nd generation anticoagulant rodenticides?
1st generation: warfarin, dicoumarol

2nd generation (more potent): diphacinone, brodifacoum
What is the mode of action of the anticoagulant rodenticides?
prevent blood from clotting by irreversibly inhibiting vitamin K epoxide reductase, which is needed to convert inactive vitamin K epoxide to active vitamin K

vitamin K needed for clotting factors II, VII, IX, X

clinical signs emerge once vitamin K dependent clotting factors are depleted: 8-24 hrs
What are the clinical signs of anticoagulant rodenticide toxicosis?
depend on site at which bleeding occurs

warfarin: external sites (hematuria, melena, facial swelling, etc.)
2nd generation products: internal

in order of decreasing frequency: dyspnea, lethargy, coughing/hemoptysis, pallor, epistaxis, vomiting, melena, lameness, hematochezia, SQ hemorrhage
What are some tests used to dx anticoagulant rodenticide toxicosis?
ACT, OSPT, APTT should all be prolonged (OSPT becomes prolonged 1st)
-↑ ACT (100%), ↑ OSPT (94%), ↑ APTT (93%)
-if ingestion just occurred, ACT will still be normal

PIVKA Test (Thrombotest): very sensitive, but hard to interpret, expensive

continued bleeding from venipuncture site is a clue

clin path findings (in order of ↓ frequency): anemia (PCV < 35%), hypoproteinemia, thrombocytopenia, ↑ FDPs, hyperfibrinogenemia

rads findings (in order of ↓ frequency): pleural effusion, pulmonary infiltrates, loss of abdominal detail, widened cranial mediastinum, normal, extraluminal tracheal compression
What is the tx for anticoagulant rodenticide toxicosis if > 1/16 of lethal dose is ingested?
decontaminate GI tract w/ emetics, AC
monitor for depression, anorexia, hemorrhage
What is the tx for anticoagulant rodenticide toxicosis if > 1/10 of lethal dose is ingested?
decontaminate GI tract

vitamin K1: will correct coagulopathy but may require 12-48 hrs before coag times normalize
loading dose, then BID to TID, PO preferred
warfarin: 7-10 d.
brodifacoum: 21-30 d.
reevaluate OSPT 36-48 hrs after cessation of tx
high doses (esp. if given IV) may cause Heinz body anemia
if ACT still ↑ after 1 mo. of tx, animal may not be absorbing vitamin K completely

blood or fresh plasma transfusions
-transfusion indicated if PCV < 20: need active clotting factors from fresh whole blood
IV fluids: careful w/ IV catheters: if dog chew it out  hemorrhage
supplemental O2
White Clover

a. species most affected
b. conditions of poisoning
c. toxic principles & corresponding lesions
a. sheep
b. moldy sweet clover hay
c. glycoside w/ the aglycone coumarin --> hemorrhagic syndromes; phytoestrogens --> infertility
What are the clinical signs of cholecalciferol rodenticide toxicosis?
w/in 12-36 hrs: signs d/t hypercalcemia
anorexia, depression, abdominal pain, vomiting (very common), dehydration, muscle weakness, constipation

CV signs often not appreciated, but often have EKG abnormalities d/t hypercalcemia
ddx for hypercalcemia
cholecalciferol toxicosis, hypercalcemia of malignancy (esp. LSA), pseudohyperparathyroidism, primary hyperparathyroidism, feed mixing error (↑ vitamin D in feed)
How would one dx cholecalciferol rodenticide poisoning?
gold standard: serum vitamin D conc.
rads to look for calcification (high Ca x P): doesn’t tell you anything about px
clin path:
hypercalcemia: often > 11 mg/dl
hyperphosphatemia: develops w/in 24-48 hrs
other changes may include: azotemia, hyperproteinemia, proteinuria, glucosuria, hyposthenuria, ↑ serum vitamin D
How would one tx cholecalciferol rodenticide poisoning?
decontamination if < 4 hr. after ingestion: emetic, AC + saline cathartic

diuresis/calciuresis: normal saline & furosemide (PO BID-TID)
high dose steroids: ↓ GI Ca absorption, ↑ urine Ca elimination (Pred PO BID)
maintain furosemide & Pred PO for 2-3 wks
salmon calcitonin: ↓ Ca absorption from GI tract (SQ q 2-3 hrs): use if animal got a really high dose
pamidronate disodium (Aredia): bisphonate: inhibits bone resorption
renal: +/- peritoneal dialysis
CV: +/- tx for arrhythmias
What are some major factors concerning the:

a. absorption
b. metabolism
c. excretion

of ethylene glycol?
a. rapidly absorbed, half life of 2.5-3.5 hrs in dogs
b. occurs in liver
oxidation by alcohol dehydrogenase to glycoaldehyde: rate limiting step
glycoaldehyde --> glycolic acid --> glyoxylic acid --> oxalic acid --> oxalate --> CaOx crystals
c. excreted unchanged in urine
What are the 3 stages of clinical signs assoc. w/ EG toxicosis?
stage 1: occurs w/in 30 min. to several hours
ataxia, “drunken appearance”, +/- CNS depression, PU, anorexia, hypothermia, vomiting
if huge dose ingested: coma, death
after stage 1, become asymptomatic for 12-24 hrs

stage 2: occurs 12-24 hrs. after ingestion
CV effects (rarely seen clinically in SA): tachypnea, tachycardia, or bradycardia

stage 3: occurs 12-72 hrs. after ingestion (when animal is usually presented)
-oliguric renal failure: renal pain, enlarged kidneys on palpation, dehydration, CNS depression, vomiting, PU --> oliguria/anuria
-renal failure largely d/t crystalluria
-seizures, oral ulcers, retinal detachment, retinal edema, anterior uveitis
What are some clin path & U/A findings consistent w/ EG toxicosis?
stress leukogram, hemoconcentration, azotemia, hyperphosphatemia, hyperglycemia, hypocalcemia, hyperkalemia, metabolic acidosis, ↑ anion gap (> 25) & osmolal gap

isosthenuria, hematuria, proteinuria, glucosuria

sediment: RBCs, WBCs, renal epi cells, casts, CaOx (monohydrate or dehydrate) & hippuric acid crystals
How would one dx EG toxicosis?
CaOx crystalluria w/ ↑ AG is highly suggestive of EG toxicosis
also hx of exposure, clinical signs, metabolic acidosis, azotemia, dilute urine
analysis for EG in blood or urine: practical only in early stages (< 24 hrs)
analysis of serum for glycolic acid: possible for 3-60 hrs post ingestion
EG test kits: lots of false negatives (only detects EG, not metabolites)
What is the tx for EG toxicosis?
recent ingestion: emetics, AC, saline cathartic

ethanol or 4-methylpyrazole: inhibit alcohol dehydrogenase
-not indicated for patients already in oliguric renal failure: will make it worse
-maintain elevated blood level for up to 72 hrs

sodium bicarb to tx metabolic acidosis
fluids + dopamine
diuretics if anuric or pulmonary edema
+/- dialysis
What are some prognostic indicators for EG toxicosis?
dogs w/ very low blood pH, severe base deficit, & high venous PO2 (assoc. w/ ↑ RR & ↓ activity) less likely to respond to tx

at 30 hrs post exposure, persistence of hypothermia, hypocalcemia, hyperkalemia, & elevated BUN & creatinine indicate a poor px

if presented in coma: poor px
propylene glycol

a. sources
b. clinical signs of toxicosis in cats
c. clinical signs of toxicosis in horses
a. preservative & carb source in moist pet food; in some antifreezes
b. ↑ in Heinz body production & hemolytic anemia
c. salivation, ataxia, pain, abnormal breath odor, rapid shallow breathing, cyanosis, death

a. species most commonly affected
b. clinical signs of toxicosis
c. lesions
d. tx
a. cats
b. occur w/in hours of ingestion
-CNS depression, vomiting, oliguria, adynamic ileus
c. acute nephrotoxic tubular necrosis
d. emetic, AC, cathartic if recent ingestion
What are some plants that contain oxalates?
oxalate containing plants

a. effects
b. clinical signs
soluble more toxic than insoluble
oxalic acid absorbed & complexes w/ calcium in blood stream --> CaOx, hypocalemia --> muscle tremors, weakness, collapse, eventually death
oxalates directly toxic to mitochondria --> inhibit ATP production
chronic oxalate poisoning: insoluble CaOx --> nephrosis
Mg can also complex w/ oxalic acid to some extent --> hypomagnesemia
b. muscle tremors, tetany, weakness, reluctance to move, depression, recumbency
coma & death may result w/in 12 hrs
renal failure: severe depression, anorexia, coma, death
chronic Ca deficiency: most common in horses

a. species most commonly affected
b. toxic principles
c. clinical signs
d. dx
e. tx
f. prevention
a. pigs
oxalate (up to 30% dry weight): leaves have 3x more than stems
nitrate (< 3%)
unknown agent: perirenal edema, nephrosis
c. perirenal edema, nephrosis (unique to pigweed)
onset: 5-10 days after initial ingestion
ataxia, weakness, tremors, knuckling at pasterns, sternal recumbency, flaccid paresis of hind limbs, distended abdomen, sit like a dog
subsequently develop coma & die w/in 48 hrs of onset of signs
5-50% mortality
d. ID of plant, evidence of consumption, clinical signs, lesions
e. remove plant, avoid stress & dehydration
f. mow, then spray w/ herbicide: spraying may ↑ nitrate accumulation
remove all animals from pasture for 1 wk. following spraying

a. species most commonly affected
b. lesions
a. sheep
b. CaOx crystalluria --> renal failure

a. conditions of poisoning
b. toxic principles
c. clinical signs
affects cattle, sheep, horses, pigs
consumption of oak buds can be markedly ↑ in late spring snowstorm
as leaves mature, become less toxic
ripe acorns less toxic than when green
gallotannin (GI irritant): reacts w/ cell proteins to denature them --> cell death
most severe lesions in kidneys, liver, GI tract
acorns contain tannic acid
goats & wild ruminants better able to detoxify b/c they have a tannin binding protein in their saliva: neutralizes tannic acid
c. anorexia, depression, intestinal stasis, +/- PU/PD, black tarry diarrhea, teeth grinding & hunched back (colic), icterus, red urine, dehydration
animals may live 5-7 days after onset of clinical signs

a. toxic principles & effects
leaf blades contain oxalic acid, CaOx, KOx
oxalate interferes w/ energy metabolism --> death
also contains anthraquinone glycosides: cathartic
red maple

a. clinical signs
b. lesions
c. tx
a. develop 2-3 days post ingestion
anorexia, depression, icterus, dehydration, weakness, tachycardia, brown mm, dark brown urine, coma, death, splenomegaly (2º to anemia)
causes methemoglobinemia, methemoglobinuria, hemolytic anemia --> pigment nephropathy
b. dark brown tissues, icterus, splenomegaly, swollen dark kidneys (prox. tubular epithelial necrosis, Hg cast formation), Heinz bodies
c. if recent ingestion: give ~ 1 lb. AC
else tx methemoglobinemia w/ methylene blue: animals usually don’t do well

a. source
b. lesions in pigs
c. lesions in poultry
a. mycotoxin from Penicllium, Aspergillus
b. marked interstitial fibrosis, prox. tubular injury in swine (porcine nephropathy), immunosuppressive, urinary tract carcinogen
c. ascites
blister beetles

a. conditions of poisoning
b. toxic principle
c. clinical signs
a. alfalfa hay that has been contaminated w/ blister beetles
b. cantharidin: highly irritating, causes acantholysis & vesicle formation when in contact w/ skin or mm
c. mild depression or discomfort to severe pain, shock, & death
GI & urinary tract irritation, endotoxemia, hypocalcemia, myocardial dysfunction, sweating, delayed CRT, tachycardia, tachypnea, pyrexia
cantharidin heavily excreted in urine --> mm irritation of ureter, vulva, etc. (+/- blisters), stranguria, incomplete urine stream
horses that ingest a massive amt. of toxin may show signs of severe shocks & die w/in hours (rare)
blister beetles

a. dx
b. tx
c. px
a. ID of beetles
definitive: measure cantharidin conc. in blood or urine: conc. in urine becomes negligible in 3-4 days
gastric contents: insect fragments
clin path: hypocalcemia, hypomagnesemia, hyposthenuria, hematuria, hyperglycemia, mildly ↑ BUN, creatinine
b. oral administration of mineral oil: evacuation of GI tract, may have to do repeated dosing
Ca, Mg supplementation
symptomatic therapy: fluids, analgesics, diuretics, tx acid/base, electrolyte disturbances
c. most cases resolve on own
What is a general scheme for tx of GI toxicosis?
recent ingestion: emetic, AC +/- saline or osmotic cathartic
symptomatic & supportive tx: fluids, etc.
sucralfate: coats GI tract, protects from ulceration
H2 receptor antagonists (ex. cimetidine): ↓ acid production in stomach
metoclopramide: controls vomiting
What plants are oral irritants?
philodendron, caladium spp., dieffenbachia (dumb cane), Araceae family (Calla lily, Ceriman, Jack in the Pulpit)

a. toxic principles
b. clinical signs
c. tx
a. proteinaceous toxin (asparagines or protoanemoin)
histamine release --> immediate pain
contains needle like CaOx crystals (raphides): released when plant cell wall is damaged --> oral irritation
also contain resorcinols: allergic contact dermatitis
inflammation of mouth & throat, skin irritation (blistering from sap), occ. renal lesions (fron CaOx crystalluria), rarely death from choking
immediate pain limits amt. consumed
give milk following ingestion: Ca source that keeps oxalates in GI tract in insoluble form: not absorbed
antihistamines if swelling occurs, general nursing care
What are some plants that mainly cause just vomiting?
Amaryllidaceae family (Narcissus spp: narcissus, jonquil, daffodil), Amaryllis
What are some plants that cause vomiting & diarrhea?
pokeweed (saponins), Saponaria spp., Ranunculaceae family (glycosides): buttercup, baneberry, marsh marigold, Clematis spp

a. part of plant that's toxic
b. toxic principle
c. clinical signs
a. bulb
b. contain alkaloids, one of which is lycorine: emetic toxin
c. cause vomiting that often resolves w/in 24-36 hrs
also cause contact dermatitis d/t irritation from alkaloids or CaOx contained in bulbs

a. toxic principles
b. conditions of toxicity
c. clinical signs
d. tx
a. saponins: dissolve cell mems (act as detergents) --> GI tract irritation; bitter tasting
alkaloids: phytolaccine, phytolaccotoxin
lectin: inhibits protein synthesis by inactivating rRNA
b. all parts of plant are toxic
toxicity of berries ↓ as they mature
fatality has resulted from consumption of root
2-3 berries may be fatal to a child
dilution & possibly degradation in rumen may explain absence of some of toxic effects seen in ruminants
c. severe gastroenteritis: 2-3 hr. latent period followed by nausea, vomiting, hemorrhagic diarrhea
generally recover w/in 24-48 hrs
d. emetic, AC + saline cathartic if recent ingestion
control dehydration, seizures, & institute artificial respiration if necessary

a. toxic principles
b. clinical signs
c. tx
a. ranunculin (nontoxic glycoside): found in all parts of plant: forms protoanemonin: irritant volatile oil
+/- anemonol (alcohol)
drying destroys toxicity
b. ingestion: gastroenteritis, vomiting, bloody diarrhea, +/- hematuria, rarely convulsions & death
c. symptomatic, supportive (emetic, AC)
What are some plants that cause gastroenteritis that can be fatal?
cochicine: crocus, meadow saffron
solanine: nightshades (incl. bittersweet), jessamines, ground cherries
toxalbumins: castor bean, rosary pea, European mistletoe
Bittersweet (Nightshades)

a. toxic principles
b. clinical signs
a. solanine (an alkaloid), plus several other alkaloids
highest concentration in green berries, but varies w/ soil, climate, & season
nitrate accumulators: can produce nitrate toxicity in LA
b. alkaloid causes fairly severe GI irritation --> bloating, anorexia, vomiting, abdominal pain, diarrhea
pyrexia, headache
Castor Bean

a. species most commonly affected
b. toxic principle
c. clinical signs if inhaled
d. clinical signs if ingested
e. dx
f. tx
a. cattle, horses
b. ricin: blocks protein synthesis
c. severe pulmonary edema, fibropurulent pneumonia, tracheitis, death w/in 36-48 hrs
d. severe GI irritation, vomiting, diarrhea, nausea, GI ulceration, & hemorrhage (w/in 1-2 hrs), necrosis of liver, spleen, & kidneys, leukocytosis, death w/in 1-3 days
e. generally based on hx of exposure
-ELISA of airway swabs (inhalation) or blood: circulating Abs develop w/in 1-2 weeks of exposure
f. symptomatic, supportive (emetic, AC if known exposure)
Rosary Pea

a. toxic principle
b. clinical signs
a. contains toxalbumin: abrum
b. same as for castor beans: acute onset gastroenteritis, multiple organ failure
inorganic arsenic

a. stable oxidation states
b. sources
c. conditions of poisoning
d. distribution in body
a. As (III) ~ 60x more toxic than As (V)
b. smelters, pesticides, herbicides (rare), vintners, most soil has trace amts
c. accidental exposure to pesticides, contaminated water: SW US, burning of wood treated w/ arsenical preservatives
d. stored mainly in liver, kidneys, heart, & lungs, w/ smaller amts in muscle & nervous tissue
deposited in hair & nails & remains fixed to keratin for years
deposited in bones & teeth
inorganic arsenic

a. mode of action
b. clinical signs
c. dx
a. inactivates up to 200 enzymes: cellular energy pathways, DNA replication & repair, etc.
substituted for phosphate in high energy compounds such as ATP
trivalent: binds thiol & sulfhydryl groups in tissue proteins --> protein inactivation
pentavalent: uncouple oxidative phosphorylation
most common presentation: sudden death
vomiting (w/in 30 min. of ingestion), abdominal pain, profuse watery diarrhea (+/- blood), excessive salivation, tremors, ataxia, weakness, hypotension, shock, tachycardia, prolongation of QT, V fib
severe vomiting & diarrhea --> shock --> multi-organ failure --> death, usually w/in 12-24 hrs
c. HGE, liver & kidney arsenic concentrations, ↑ urine arsenic conc.
suspect As toxicosis in animal w/ ACUTE severe hemorrhagic diarrhea
drinking water containing > 0.25% arsenic potentially toxic, esp. for large animals
What is the tx for inorganic arsenic poisoning?
generally don’t give emetic: animal almost always already vomiting from As
activated charcoal
sodium thiosulfate: chelates arsenic in GI tract (PO): rarely found at pharmacy
other arsenic chelators: given for 2-4 days
dimercaprol (BAL): given IV or IM; GI effects of arsenic continue
D-penicillamine, DMPS, DMSA: given PO; ↓ GI absorption (preferred); less toxic & more effective than BAL
GI protectants: kaolin-pectin
supportive therapy: fluids
monitor liver & kidney function during tx
organic arsenic

a. conditions of poisonings
b. clinical signs
c. dx
d. tx
e. px
a. organic less toxic than inorganic
b. misformulated feed: used as feed additives to improve production in swine & poultry rations & to tx dysentery in pigs
b. pigs: ↓ wt. gain, incoordination, blindness, posterior paralysis, quadriplegia; animal remains alert w/ good appetite
c. hx of arsenicals added to feed in improper dosage
d. no specific tx
e. neurotoxic effects usually reversible if feed is withdrawn w/in 2-3 days of onset of ataxia
once paralysis occurs, nerve damage is irreversible
blindness is irreversible
What are ddx for neurological signs in pigs?
organic arsenic poisoning, salt poisoning, botulism, lead or mercury toxicosis, vitamin A def., pseudorabies
iron toxicosis: SA

a. conditions of poisoning in SA
b. absorption
a. human multivitamins
b. well regulated: 2-15% net absorption
absorption of ferrous ions into mucosal cells
transfer to plasma: facilitated by binding to transferrin
ferrous iron in plasma oxidized by ferroxidase I (ceruloplasmin)
O2 free radicals produced by conversion of Fe (II) --> Fe (III)
iron toxicosis: SA

a. dx
b. tx in SA
a. serum iron conc.
normal: 50-150 mg/dl
peak levels occur 2-4 hrs post ingestion, although generally remains elevated thru stage 3
>350 mg/dl correlates w/ systemic toxicity
b. o gastric decontamination: AC generally doesn’t work well since Fe is a small molecule, but give anyway
deferoxamine: iron chelating agent of choice
available at most pharmacies
iron-deferoxamine complex excreted in urine & gives urine characteristic ‘vin rose’ (reddish) appearance
continue administration until urine returns to normal
must differentiate from hematuria
What are the 4 stages of clinical signs seen in iron toxicosis in small animals?
stage 1: w/in 6 hrs of ingestion
local corrosive effects in gut lumen --> vomiting, diarrhea (often bloody), abdominal pain
GI ulceration, perforation can occur w/in 4-6 hrs
hypotension, acidosis 2º to GI losses of fluid & blood
many animals die at this stage

stage 2: 6-14 hrs
signs typically stabilize or improve as free plasma iron moves into cells

stage 3: 16-24 hrs
multiple organ failure: iron directly toxic to liver, myocardium, kidney, CNS

stage 4: marked local GI corrosion & scarring, w/ subsequent luminal obstruction
iron toxicosis in newborn pigs

a. conditions of poisoning
b. possible manifestations of toxicosis
a. SQ or IM injection of iron preparations
b. joint swelling/pain, damage to muscle at injection site, tremors, convulsions, resp. distress, immunosuppression --> E. coli enteritis (assoc. w/ vit E or selenium def.), hard swellings at injection site, sudden death
NSAID toxicosis in SA

a. clinical signs
b. dx
a. vomiting, diarrhea, gastric ulceration +/- hemorrhage +/- perforation
ARF: renal blood flow highly dependent on PGs
seizure, death may occur w/in hours if massive amt. ingested
b. hx of exposure, may be able to appreciate concretions of pills on rads if huge dose ingested
What is the tx for NSAID toxicosis in SA?
recent ingestion (< 2 hrs)
emetic, AC +/- saline or osmotic cathartic: often not very effective w/ low doses d/t rapid absorption of NSAIDs from GI tract
-repeated AC may be needed since some undergo enterohepatic recirculation
gastric lavage if concretions form

symptomatic & supportive tx
assisted ventilation +/- O2
control seizures
control hypotension & hemorrhage: fluids +/- dopamine or dobutamine (to maintain renal blood flow)
peritoneal dialysis

sucralfate PO q 8-12 hrs: coats GI tract, protects from ulceration

H2 receptor antagonists (ex. cimetidine): IM, IV, or PO TID
-some NSAIDs may cause ↑ acid production in stomach

metoclopramide PO or SQ q 6-8 hrs: controls vomiting

misoprostol: synthetic PGE1 analog
-used to prevent aspirin induced gastric ulcers
-not recommended after ulcer formation: doesn’t work as well