Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Veterinary Toxicology > Gastrointestinal Toxicology > Flashcards

Gastrointestinal Toxicology Flashcards

1
Q

Why is it difficult to determine the cause of GI injury?

A
  • many conditions that cause GI signs are not toxic in nature
  • a wide array of poisons affect the GI system
  • animals exhibit GI signs secondary to other diseases/toxicoses (liver, kidney, neurologic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the main 6 mechanisms of direct GI injury?

A
  1. irritation
  2. corrosion
  3. impaired mucosal blood supply
  4. impaired nutrient or water absorption
  5. epithelial cell necrosis
  6. altered motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the main clinical signs associated with GI toxicosis?

A
  • anorexia, salivation, diarrhea in all species
  • colic, cramps, abdominal pain
  • vomiting in cats and dogs
  • regurgitation in ruminants and birds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What lectins cause GI toxicosis? What is the most common sources? What produces the most potent ones?

A

hemaglutinins, toxalbumins

mostly beans and other plants, like Jahtropha, Robina, Momordica, Hura, and Sophora

Ricinus communis (castor bean) —> ricin (white powder) and abrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is toxicity to lectins associated with? What species are affected?

A

ingestion and chewing of seeds, destroying the seed coat and releasing lectins —> poorly absorbed in the GIT

MANY: dogs, poultry, wild fowl, pigs, horses, sheep, goats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 4 toxic principles of lectin? Which ones are cytotoxic? Why?

A
  1. ricin*
  2. abrin*
  3. ricine
  4. ricinus communs agglutinin

contain A and B chains linked by a sulfide bond

  • A inactivates eukaryotic ribosomes and impairs peptide elongation —> inhibits protein, DNA, and RNA synthesis
  • B binds to galactose-containing glycoproteins and glycolipids on the surface of cells facilitating the entry of ricin into cytosol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 3 specific actions of ricin on the GIT? How can it affect the CVS?

A
  1. irritates GIT mucosa
  2. impairs nutrient absorption and cell viability
  3. inhibits protein synthesis in GI epithelial cells

disturbs calcium homeostasis by decreasing calcium uptake by the sarcoplasmic reticulum and increases Na/Ca exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What effect do ricinine and ricinus communis agglutinin found in lectin have?

A

RICININE = inhibits GABA receptors and increases glutamate release, causing seizures

RCA = causes RBC agglutination leading to hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the most common clinical signs seen in lectin toxicity?

A
  • severe watery/bloody diarrhea
  • vomiting
  • salivation
  • abdominal pain
  • decreased BP, weakness, trembling, anorexia
  • severe reddening, edema and necrosis of GIT mucosa
  • decreased nutrient absorption and growth rate
  • increased incidence of bacterial infections
  • seizures, coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When should emesis be induced during lectin toxicosis? What treatment is recommended?

A

animals that vomit

  • GI protectants: kaolin-pectin, sucralfate
  • fluid and electrolyte therapy
  • bland diet
  • seizures: Diazepam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 2 major toxic principles of cycad palms? What parts are the most toxic? What species are affected?

A
  1. glycosides: cycasin and macrozamin
  2. β-ethylamino-L-alanine (BMAA)

nuts produced by females (especially Zamiaceae)

cattle, sheep, dogs, cats, horses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the mechanism of toxicity of cycad palms?

A

glycosides are hydrolyzed by β-glycosidases in the GIT into the toxic aglycone, methylazoxy-methanol (MAM) and sugars that are toxic themselves and alkylate DNA and RNA to cause carcinogenesis, mutagenesis, and teratogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the effects of the specific toxic principles of cycad palms? What additional effect has an unknown cause?

A
  • cycasin - irritates GIT
  • BMAA - neurotoxic by stimulating NMDA receptor leading to excitotoxicity

axonal degeneration in the CNS causes hind limb paralysis in cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the specific clinical signs of cycad palm toxicity in dogs, sheep, and cattle?

A

DOGS = (bloody) vomiting, depressing, diarrhea, anorexia, and seizures secondary to hepatic injury

SHEEP = lethargy, anorexia, weight loss, (hemorrhagic) gastroenteritis, death

CATTLE = weight loss, weakness, ataxia, paresis (zamia staggers), hepatic damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When is decontamination no longer useful with cycad palm toxicity? What 4 treatments are recommended in small animals? What supportive treatment is used?

A

> 2-4 hours after ingestion

  1. GI protectants - Sucralfate
  2. H2 blockers - Cimetidine
  3. Misoprostol
  4. hepatoprotectants - acetylcysteine, silymarin, SAMe

IV fluids/electrolytes and blood transfusions for severe GI hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are common sources of acids? What are they referred to as? What molecules do they commonly contain?

A

toilet cleaners, drain openers, antirust compounds, automobile battery fluid, pool sanitizers

corrosives

HCl, HNO3, H2SO4, H3PO4, C2H2O4, NaHSO3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are common sources of alkalis? What are they referred to as? What molecules do they commonly contain?

A

drain openers, oven cleaners, bleaches, industrial cleaners, denture cleaners, bathroom and household cleaners, hair relaxers, alkaline batteries, detergents, cement

caustics

potash, NaOH, KOH, Ca(OH)2, Cac2, NaHCO3

18
Q

What are the mechanisms of toxicity of acids and alkalis? What happens when they are diluted?

A

ACIDS - corrosive and cause severe burns on contact with tissue —> coagulative necrosis with resulting scabs limiting penetration

ALKALIS - form hydroxyl ions on contact with water and cause liquefactive necrosis, depending on concentration, pH, viscosity, amount ingested, and duration of contact (more penetrating than acids)

DILUTE = irritants

19
Q

What are common clinical signs of acid and alkali toxicosis?

A
  • dysphagia
  • excessive salivation
  • vocalization
  • bloody vomiting
  • abdominal pain
  • PD
  • pawing at the mouth
  • laryngeal irritation —> laryngospasms, edema —> airway obstruction —> dyspnea, asphyxia
20
Q

What lesion is associated with acid and alkali toxicosis?

A

lesions on lipids, tongue, gums, or esophagus

  • ACIDS = gray-black
  • HNO3 = yellow
21
Q

What causes renal, CNS, and CVS signs of acid toxicosis? What dermal, respiratory, and ocular signs are observed?

A

oxalic acid causes systemic binding of calcium, resulting in hypocalcemia

  • DERMAL: severe burns, cellulitis, infection, contractures, shock
  • RESP: pneumonitis, bronchitis, dyspnea, pleuritic chest pain, pulmonary edema, hypoxemia, bronchospasms
  • OCULAR: corneal ulceration, pain, blepharospasms
22
Q

What specific clinical sign is associated with alkali toxicosis? What ocular and dermal signs are observed?

A

stridor, vomiting, drooling, and gastric burns due to esophageal ulceration, esophagitis, and stricture formation

  • OCULAR: conjunctival irritation and chemosis, corneal defects, perforation, vision loss
  • DERMAL: pain, irritation, redness, full thickness burns
23
Q

What routes of decontamination are recommended for oral, ocular, and dermal exposure to acids and alkalis?

A

ORAL - milk, water; emesis, gastric lavage, and activated charcoal are contraindicated

OCULAR - irrigate eyes with tepid water or physiologic saline, monitor for ulceration

DERMAL - bathe with water and mild hand dishwashing detergent or non-insecticidal pet shampoo, analgesics, anti-inflammatories, antibiotics

24
Q

What supportive treatment is recommended for animals with severe upper GI injury in acid/alkali toxicosis? What other supportive therapy is recommended?

A

strictly NPO —> gastrostomy tube

  • IV fluids for hydration, urine output, and BP maintenance
  • sucralfate for ulceration
  • analgesics: Butorphanol, Buprenorphine, Morphine
  • corticosteroid usage for inflammation is controversial
  • broad-spectrum antibiotics for mucosal damage, secondary infection, or prophylaxis when corticosteroids are used
25
Q

What is the most common source of essential oils?

A

volatile fragrant organic constituents of plants found i fragrances, shampoos, dips, ointments, and oil diffusers

(AVOID using essential oil diffusers with birds in the house)

26
Q

How are essential oils absorbed? Metabolized? Excreted?

A

readily absorbed orally and dermally

metabolized in the liver to glucuronide and glycine conjugates

90% urine, 10% feces

27
Q

What does repeated exposure to essential oils cause? what species are especially affected by toxicity?

A

induces CYP450 and UDP-glucuronosyltransferase

cats and birds

28
Q

What clinical signs are associated with oral, respiratory, and dermal exposure to essential oils?

A

ORAL - vomiting, diarrhea, CNS depression, seizures at high doses

RESP - aspiration pneumonia

DERMAL - ataxia, weakness, muscle tremors, depression, transient parlysis, behavior change, collapse, hypothermia, scrotal dermatitis, liver failure

29
Q

What is the most common cause of death in essential oil toxicity?

A

grooming behavior causes concurrent dermal and oral exposure to the oils

30
Q

What are the charges of metals and non-metals?

A

metals = cations +

non-metals = anions -

31
Q

What kind of metal is arsenic? What are the most common sources?

A

metalloid - properties of metals and non-metals, making it form compounds in which it behaves as cations or anions

  • pesticides (ant and roach baits)
  • heartworm adulticide - Melarsomine
  • feed additives - Na-arsanilate, arsanilic acid, 3-nitro
  • environmental: mining/smeling sites, water contamination
32
Q

What form of arsenic is most toxic? What species is the most sensitive?

A

trivalent form —> kidneys may reduce a small proportion of an oral dose into this form

cats

33
Q

How does the form of arsenic affect absorption? Where do they tend to accumulate? What is the major detoxification mechanism? How is it exreted?

A

pentavalent organic arsenicals are more easily absorbed by the GIT (and intact skin to a smaller extent)

liver, kidney, lungs, GIT

methylation

40-70% urine, bile, and feces

34
Q

What are the 2 mechanisms of action of trivalent arsenic?

A
  1. binds to -SH group in cells, making it able. to inhibit -SH containing enzymes needed for the TCA cycle, decreasing cellular respiration
  2. damage to vascular system - capillary dilation = transudation of plasma, edema, and shock (GIT most affected)
35
Q

What is the mechanism of action of pentavalent arsenic? What clinical sign is not seen?

A

uncouples oxidative phosphorylation leading to a cellular energy deficit

fever

36
Q

What are the most common clinical signs associated with arsenic poisoning?

A
  • vomiting, salivation
  • intense abdominal pain
  • watery diarrhea, dehydration
  • ruminal or GI atony
  • weak pulse, subnormal temp
  • renal damage: oliguria, proteinuria, dehydration, acidosis, uremia
37
Q

What does dermal exposure to arsenic cause? In what animals are nervous signs most common?

A
  • blistering
  • edema
  • cracking
  • bleeding
  • secondary infection

swine exposed to organic pentavalent arsenic in feed - ataxia, blindness, dog-sitting, incoordination, paralysis

38
Q

What are the most common differential diagnoses of arsenic poisoning?

A
  • viral or bacterial gastroenteritis
  • pancreatitis
  • zinc phosphide
  • caustic or irritating agents
  • other metals
39
Q

Why are cathartics no indicated with arsenic toxicity?

A

poisoning already causes diarrhea

40
Q

What chelation therapy is preferred for arsenic toxicosis? What else is used?

A

dimercaptosuccinic acid (DMSA)/succimer

dimercaprol (BAL)

Veterinary Toxicology (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions