13. Toxicity: Liver & GI Tract II

What can develop within 30 minutes of ingesting xylitol?

hypoglycemia

What are other symptoms associated with xylitol toxicity?

V
W
A
D
H
S
C

• vomiting

• weakness

• ataxia

• depression

• hypokalemia

• seizures

• coma

When might liver injury occur with ingestion of xylitol? What other symptoms might occur at this time?

until over 24-48 hours after ingestion; depression, vomiting, icterus, and coagulopathy

Xylitol toxicity only occurs in what species? What other species could it possibly occur in?

canids; ferrets

What is the toxic principle in dieffenbachia (dumbcane) toxicity?

calcium oxalate crystal produce physical damage to skin and mucous membranes in which they contact

Systemically, what else can oxalate produce?

hypocalcemia and crystallize in renal tubules resulting in kidney damage

What can occur within seconds or minutes with oxalate toxicity? If systemic effects occur, when can they develop?

crystal penetration of soft tissues of the GI tract; several days

What is the mechanism of toxicity for oxalate toxicity?

chewing the leaves and stems causes sharp crystals, called raphides, to be forcibly ejected from idioblast cells in the plant

What does the stomatitis associated with oxalate toxicity depend on?

the amount of plant tissue chewed and the degree of maceration

What amount of oxalate can be fatal in a cat?

less than 100 mg/kg

What are immediate clinical signs associated with oxalate toxicity?

evidence of pain in the mouth, head-shaking, intense salivation, and unusual vocalization

What are other clinical signs associated with oxalate toxicity?

N
V
D
S

• nausea

• vomiting

• diarrhea

• swelling of the mucous membranes of the pharynx and tongue that may result in severe dyspnea, pharyngeal spasm, obstruction, and death

What is the toxic principle in pokeweed phytolacca americana?

saponins, oxalates, and phytolaccotoxin

Where is the highest amount of toxin found in pokeweed?

roots and seeds

What is the mechanism of toxicity of pokeweed?

irritation of the mucosal surface

What species are susceptible to the toxic effects of pokeweed?

sheep, cattle, goats, horses, pigs, and poultry

What are signs of pokeweed intoxication?

O
E
V
C
B
D
P
D

• oral irritation

• excessive salivation

• vomiting

• colic

• bloody diarrhea

• depression

• prostration

• death

What is a common finding with pokeweed ingestion on postmortem examination?

mild to severe gastroenteritis with ulceration of the gastric mucosa

What is castor seed the source of? What does this contain?

40-60% castor oil; triglycerides and ricinolein

What is the toxic principle of castor beans, ricinus communis?

ricin

Where is the highest concentration of toxin found with castor beans?

in the seeds

Ricin and all lectins are ________ soluble and _______ well absorbed from the GI tract. In spite of this, signs of intoxication appear within ____ ________ in dogs.

water; not; 6 hours

What is the mechanism of toxicity of the castor bean?

ricin is transported into cells by endocytosis and once in the cytoplasm can migrate into the endoplasmic reticulum where it depurinates the 28S ribosomes in rRNA, causing protein synthesis to cease and the cell dies and also interferes with Ca transport

Where are the primary effects of castor bean toxicity seen?

GI tract, particularly the intestinal mucosa

What are clinical signs associated with caster bean toxicity?

D
V
D
I
H

• diarrhea

• vomiting

• decreased nutritional absorption

• increased bacterial infections

• hemorrhagic gastroenteritis

What is the toxic principle in buttercups ranunculus spp?

ranunculin converted to proroanemonin by the action of plant enzymes released when the plant is chewed

What form of buttercup appears to be non-toxic?

dried form

What is the mechanism of toxicity of buttercups?

protoanemonin is a potent vesicant that irritates mucous membranes of the GI system

With severe buttercup intoxication, effects to what organ have been reported?

kidney

What clinical signs are associated with buttercup intoxication?
I
S
D
V
C

• irritation to the mouth and upper GI tract

• swelling of the muzzle and lips

• diarrhea

• vomiting

• colic

What is the toxic principle of the autumn crocus?

colchicine

Where is the autumn crocus metabolized? Then what happens?

in the liver; secreted in the bile and mostly excreted by the kidney

What is the mechanism of toxicity of the autumn crocus?

interferes with spindle formation in normally dividing cells

What type of cells are most affected by autumn crocus?

rapidly dividing cell such as epithelium are most affected

True or false: In autumn crocus toxicity, a few seeds are considered potentially lethal. The leaves are toxic at about 0.1% of an animal’s weight.

true

What are the clinical signs associated with autumn crocus toxicity?

V
D
G

• vomiting

• diarrhea

• GI hemorrhaging

What might be seen in animals that survive autumn crocus toxicity?

myelosuppression

What does the fungus rhizoctonia leguminicola produce? What is this a common fungal pathogen of? What does it cause in plants?

slaframine and swainsonine; red clover; black patch disease

What are the symptoms of slaframine toxicity?

salivation (slobbers)

What is the treatment for NSAID toxicity?

often multimodal (steroids + NSAIDS)

What effects do analgesic NSAID toxicities have? What else may they involve?

CNS and peripheral effects; non-PG related effects

What effects do antipyretic NSAID toxicities have?

CNS effect

What effects do anti-inflammatory (except acetaminophen) show? What is it due to?

activation, aggregation, adhesion of neutrophils, and release of lysosomal enzymes; PG inhibition

While NSAIDs are a diverse group of chemicals, what do they all inhibit?

cyclooxygenase

With NSAIDs, what is largely responsible for their therapeutic effects? What about inhibition of PG synthase in the gastric mucosa?

inhibition of PG synthesis; GIT damage

Where does cyclooxygenase exist? In what form?

in the tissue; constitutive isoform (COX-1)

What occurs at the site of inflammation?

cytokines stimulate the induction of the 2nd isoform (COX-2)

Most currently used NSAIDa are somewhat selective for what?

COX-1

Sudden death in cattle that presented with hemorrhagic gastroenteritis, watery diarrhea, cramping, and bloating pre-mortem is usually associated with what?

arsenic