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veterinary toxicology > Gastrointestinal Toxicology, Pt. 2 > Flashcards

Gastrointestinal Toxicology, Pt. 2 Flashcards

1
Q

What is essential mineral are baby pigs born deficient in?

A

iron —> typically supplemented with an injection

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2
Q

What is the most common cause of iron toxicosis? What is a hereditary cause in humans? In what animals is toxicosis most common?

A

overdosing or ingestion of iron-containing products

hereditary hemochromatosis - mutation of high iron (HFE) gene causing excessive intestinal absorption and storage of iron leading to overload

dogs

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3
Q

What are the most common exposures to iron in dogs and cattle/horses/pigs?

A

DOGS = accidental ingestion of iron-containing vitamins, supplements, molluscicides (phosphate, EDTA), fertilizer, oxygen-absorbing sachets or hand-warming pads

CATTLE/HORSES/PIGS = administration of excess amounts of iron supplements or fertilizer

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4
Q

Where is iron absorbed? In what form is it absorbed best? How does it circulate in blood?

A

small intestine, massive overdose results in absorption in all parts of the GIT

Fe2+, by divalent metal transporter (DMT1)

bound to transferring

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5
Q

Where is iron found in the body? How is it excreted?

A
  • 70% in hemoglobin
  • 5-10% in myoglobin
  • rest in storage as ferritin and enzymes

exfoliation of intestinal epithelium (in small amounts)

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6
Q

What 4 mechanisms of toxicity does iron have on the GIT?

A
  1. direct corrosive effect
  2. redox recycling between Fe2+ and Fe3+ causes the production of ROS and oxidative damage to cells and organelles (membrane lipid peroxidation)
  3. stimulate serotonin and histamine release
  4. causes metabolic acidosis by causing hypovolemia, hypotension, anaerobic metabolism, interference with mitochondrial ETC
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7
Q

What 4 effects does iron toxicosis have on the cardiovascular system?

A
  1. fatty necrosis of myocardium
  2. vasodilation
  3. increased capillary permeability
  4. decreased cardiac output
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8
Q

How does iron toxicosis affect the clotting cascade?

A

inhibits the formation of fibrin from fibrinogen

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9
Q

What are the 5 major systems affected by iron toxicosis? What clinical signs are associated with each?

A
  1. GI - vomiting/hematemesis, melena, diarrhea, ulceration, abdominal pain
  2. CVS - hypotension, hypovolemia, increased capillary permeability, shock, cardiomyopathy due to fat necrosis
  3. HEPATIC - hypoglycemia, hyperammonemia, hepatic encephalopathy
  4. CNS - depression, cerebral edema, seizures, tremors, coma
  5. BLOOD - coagulation defects
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10
Q

What does peracute iron toxicity in pigs resemble?

A

anaphylactic shock

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11
Q

What are the 4 stages of iron toxicosis? What clincal signs occur at each?

A
  • STAGE I: 0-6 hr; GI effects and depression
  • STAGE II: 6-12 hr; latent period with apparent clinical recovery
  • STAGE III:12-96 hr; acidosis, GI, hepatic, CVS, CNS
  • STAGE IV: 2-6 weeks; GIT ulcers heal with scar tissue formation causing stricture development and GI obstruction
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12
Q

How is iron toxicosis diagnosed? What are some differential diagnoses?

A
  • measurement of serum iron levels within 4-6 hours of ingestion
  • measurement of serum iron binding capacity
  • radiography may show a mass of iron tablet (bezoar) or foreign body in the GIT

garbage toxicosis, gastric torsion, ingestion of caustic/corrosive agents, snake bites, bacterial or viral enteritis

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13
Q

How is gastric decontamination done in iron toxicosis? What is avoided?

A
  • give eggs, water, or milk and induce emesis for recent exposure
  • perform gastric lavage
  • surgical removal is radiography reveals iron tablet bezoar followed by aggressive gastric lavage

activated charcoal

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14
Q

What is used to treat iron toxicosis? What adverse effect does it have?

A

chelation therapy with deferoxamine (Desferal)

causes reddish-brown discoloration of urine

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15
Q

What supportive treatment is recommended for iron toxicosis? What is recommended for anaphylactic shock in pigs?

A
  • restore fluids, electrolytes, and acid-base status
  • GI protectants: sucralfate, cimetidine, misoprostol, gastric acid secretion inhibitors

antihistamines, epinephrine, oxygen, IV fluids

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16
Q

What rodenticide affects the GIT?

A

metallophosphide rodenticides (zinc phosphide) extensively used around farms and barns to protect grain

  • Rattoff
  • ZP Tracking Powder
  • Eraze
  • Sweeney’s Poison Peanuts
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17
Q

What happens following zinc phosphine ingestion?

A
  • ZP ins hydrolyzed in the acidic pH in the stomach into toxic phosphine gas
  • gas is readily absorbed by passive diffusion
  • any intact ZP is also absorbed in the GIT
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18
Q

How is zinc phosphine excreted?

A
  • intact and gas ZP = lungs
  • phosphorus oxide, phosphite, hypophosphite metabolites = renal
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19
Q

What is the GIT mechanism of toxicity of zinc phosphine? What are 4 systematic effects?

A

ZP = corrosive action leading to acute hemorrhagic emetic effect on GIT

  1. phosphine gas impairs oxidative phosphorylation by inhibiting cytochrome c oxidase
  2. phosphine gas induces ROS formation leading to oxidative damage to lipids, proteins, DNA, and cell death
  3. phosphine gas denatures hemoglobin causing methemoglobinemia
  4. phosphine gas causes cellular hypoxia
20
Q

What can increase toxicity of zinc phosphine? Decrease?

A

food in stomach increases HCl and phosphine gas production (onset is rapid with a full stomach)

ZP induces vomiting, which decreases phosphine has production

21
Q

What does zinc phosphine toxicity resemble? What is seen in dogs?

A

strychnine or fluoroacetate

  • depression, agitation, apprehension
  • dyspnea, pacing, ataxia, weakness, anorexia
  • bloody vomiting, salivation
  • tremors, convulsions, howling, aimless running
  • teeth barring or grinding
22
Q

What clinical signs are observed in zinc phosphine toxicity in ruminants and horses?

A

RUMINANTS = abdominal pain, bloating

HORSES = colic

23
Q

What unique clinical signs is caused by zinc phosphine toxicosis? What causes death?

A

acetylene (garlicky/rotten fish) odor in the breath, vomitus, and stomach contents

respiratory arrest

24
Q

How are stomach contents or vomitus analyzed for zinc phosphine?

A
  • samples are packed in airtight containers and freezed to prevent phosphine gas loss
  • PREFERABLE: freeze entire carcass, vomitus, and suspected bait and send to diagnostic lab
25
Q

What rapid screening tool is used to diagnose zinc phosphine toxicity?

A

silver nitrate paper

  • diluted gastric content heated in a flask up to 50 C for 1-5 minutes keeping the paper on the mouth of the flask
  • if it turns black, phosphine is present due to the formation of silver phosphate
26
Q

What is recommended to cause emesis in the case of zinc phosphine toxicity? What is recommended for animals that do not vomit? What treatment is able to slow the hydrolysis of ZP into its gas form?

A

centrally acting emetics - Apomorphine, Xylazine, activated charcoal

activated charcoal mixed with antacid (aluminum or magnesium hydroxide)

oral aluminum or magnesium hydroxide antacid

27
Q

What treatments are recommended for acidosis, respiratory difficulties, and shock associated with zinc phosphine toxicosis?

A

increase pH with liquid antacid gels containing Mg(OH)2, Al(OH)3, and CaCO3

oxygen administration and assisted breathing

corticosteroids

28
Q

What 5 treatments are recommended for liver failure associated with zinc phosphine toxicosis?

A
  1. sodium thiosulfate
  2. lipotropic agents
  3. B vitamins
  4. dextrose
  5. low protein diets
29
Q

How are seizures, excessive muscle activity, GI ulcers, muscarinic signs, and gastric distension associated with zinc phosphine toxicosis?

A

Propofol, Barbiturates, gas anesthetics

Methocarbamol

GI protectants - Sucralfate, H2 blockers, PPIs

Atropine

nasogastric or orogastric tubes

30
Q

What is cantharidin?

A

bicyclic terpenoid vesicant found in the hemolymph and genitalia of male blister beetles (Epicauta spp.) and is able to be transferred to females during copulation

  • aphrodisiac (Spanish Fly)
  • diuretic
  • abortifacient
  • wart medications
31
Q

What is cantharidin toxicosis associated with?

A

eating alfalfa hay in semiarid areas, like TX and OK

  • cutting and crimping increases chances of incorporating beetles in the hay (beetles are gregarious and tend to swarm)
32
Q

What is the most toxic blister beetle?

A

Striped blister beetle

33
Q

What is the mechanism of action of cantharidin? In what 4 ways does it cause this?

A

irritation of the GIT leads to acantholysis and vesicle formation with ulcers and erosions

  1. promotes mitosis in epithelial cells
  2. interferes with oxidative enzyme systems in the mitochondria causing permeability changes
  3. disrupts cell membranes
  4. inhibits protein phosphatase 2A, which modulates phosphatases and protein kinases leading to alterations of cellular processes including proliferation, apoptosis, and membrane channels/receptors activity
34
Q

What species are most susceptible to cantharidin toxicosis? How does dosage affect clinical signs?

A

horses*, cattle, sheep, goats, dogs, rabbits, alpacas, emus

  • MASSIVE = shock and death within 4 hr
  • SMALLER = gastroenteritis, nephrosis, cystitis, urethritis
35
Q

What clinical signs are associated with cantharidin toxicosis in horses?

A
  • submerging muzzles without drinking, playing in the water
  • colic, diarrhea, ulceration of oral mucous membranes, salivation
  • anorexia, mucoid or bloody feces
  • dysuria, hematuria
36
Q

What general clinical signs are associated with cantharidin toxicosis?

A
  • restlessness, depression, weakness
  • collapse, prostration
  • dehydration, sweating
  • fever, muscle rigidity and fasciculations, stiff gait
  • myocarditis causes CVS signs
  • dyspnea with rales due to pulmonary edema
  • mortality in ~50% of horses
37
Q

What are 4 major clinical pathology signs associated with cantharidin toxicosis?

A
  1. hypocalcemia and hypomagnesemia
  2. elevated BUN
  3. increased PCV and protein due to dehydration and shock
  4. reduced USG
38
Q

What are the 6 major lesions associated with cantharidin toxicosis?

A
  1. erosion and ulceration of the oral cavity and GIT
  2. acantholysis or epithelium of the urinary tract and renal tubular nephrosis
  3. renal cortical hemorrhage
  4. urethra and bladder mucosa hemorrhage
  5. ventricular myocarditis
  6. pulmonary edema
39
Q

What can be used to enhance urinary and fecal elimination of cantharidin? How are hypocalcemia and hypomagnesemia treated? Pain?

A

mineral oil hastens movement through GIT and activated charcoal binds to it

supplement IV fluids with Ca and Mg, but no bicarb

α-adrenergic agonists (common analgesics may not provide adequate relief)

40
Q

What are the 3 major causes of garbage toxicosis? When is toxicosis especially common?

A
  1. waste food or dead animals contaminated with bacteria and/or toxins
  2. feeding animals food considered unfit for human consumption
  3. high moisture dog food left at warm temperatures

warm seasons/regions with poor hygiene and roaming animals

41
Q

What 4 bacteria commonly cause garbage toxicosis? What are the 2 mechanisms of toxicity?

A

Streptococcus, Salmonella, Clostridium, Bacillus

  1. sorption to and irritation of GI epithelium causes vomiting
  2. increases the permeability of GI epithelial cells, leaking fluid and electrolytes into the lumen which interferes with absorptive mechanisms
42
Q

What endotoxin causes garbage toxicosis? What results from toxicity?

A

LPS produced by Gram-negative bacterial released upon bacterial cell lysis

AFFECTS THE WHOLE BODY - circulatory shock, DIC, acute respiratory distress syndrome, systemic inflammatory response syndrome, multiple organ dysfunction syndrome, collapse, death

43
Q

What are 8 mechanisms of toxicity caused by endotoxins causing garbage toxicosis?

A
  1. activation of inflammatory mediators
  2. cardiovascular insult
  3. alteration of GIT permeability
  4. interference with gut function including endocrine regulation of gastric emptying
  5. activates pancreatic zymogens
  6. competes with insulin for the same receptor
  7. activates complement and clotting cascades
  8. uncouples oxidative phosphorylation
44
Q

What are the clinical signs associated with enterotoxicosis caused by garbage toxicosis?

A

vomiting and retching
- bloody diarrhea
- abdominal pain, stasis and dilation of gut (gas accumulation)
- dehydration, electrolyte imbalance

45
Q

What are the clinical signs associated with enterotoxemia caused by garbage toxicosis? What are signs of endotoxic shock?

A
  • fever, shivering
  • vomiting, abdominal pain, tenderness, and distension
  • muddy mucous membrane
  • watery/bloody diarrhea
  • EXCEEDINGLY foul-smelling feces

depression, collapse, hypotension, hypo/hyperthermia

46
Q

What must be ruled out when diagnosing garbage toxicosis?

A
  • foreign body and intestinal displacement (volvulus, torsion, intussusception)
  • pancreatitis
  • acute hepatic and renal failure
47
Q

What 5 supportive and systematic treatments for garbage toxicosis is suggested?

A
  1. fluid and electrolyte therapy with bicarbonate
  2. Heparin for DIC
  3. Corticosteroids for shock
  4. IV Chloramphenicol to control bacterial proliferation
  5. bland diet

veterinary toxicology (29 decks)

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