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RUSVM Toxicology > Plant Related Toxicants -Nitrate, Cyanide, Oxalate > Flashcards

Plant Related Toxicants -Nitrate, Cyanide, Oxalate Flashcards

1
Q

How do plants accumulate nitrate?

A

Nitrate is absorbed from solid
Nitrate (NO3) —> Nitrite (NO2) —> ammonia (NH3) —> amino acids and protein

Rate of conversation of nitrate to nitrite is slower than uptake from soil resulting in accumulation

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2
Q

What factors favor plant nitrate accumulation?

A

Plant species - sweet clover, alfalfa, wheat, corn
Content and form in soil - nitrate or ammonia
Soil conditions - moisture, acid, low molybdenum/sulfur/phosphorus, low temp
Decreased light reduces activity of nitrate reductase
Phenoxy acetic acid herbicides increases accumulation

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3
Q

What are the nitrate accumulating plants?

A 
Pigweed
Oat
Beet
Johnson grass
Corn
Lambs quarters 
Sweet clover 
Alfalfa 
Wheat 
Sunflower
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4
Q

What are sources of nitrite toxicity?

A

Forages/hays containing high amounts of nitrate
Accidental ingestion of contaminated feed or water
Overdose with nitrite IV (vasodilator)

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5
Q

What is the LD50 of nitrate for ruminants?

A

0.5-1g/kg

Need huge amount for toxicity

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6
Q

What species are the most susceptible to nitrate poisoning ?

A

Ruminants

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7
Q

Is nitrite or nitrate more toxic?

A

Nitrate is 10x more toxic than nitrate

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8
Q

A forage nitrate greater than _____% can cause acute toxicosis

A

1

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9
Q

T/F: young ruminants are more susceptible than adults to nitrite toxicity

A

False

Young animals are more resistant because they have not developed the rumen microflora to convert nitrate to nitrite

Monogastrics are also more resistant because they do not have the microflora

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10
Q

What types of diseases will cause increased nitrate toxicity?

A

Anemia

Methemoglobinemia

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11
Q

How is nitrate normally used in the body? When do you see accumulation

A

Nitrate —> nitirite —> ammonia —> amino acids —> protein

Accumulation occurs when the rate of conversion of nitrite to ammonia is slower than the rate of conversion of nitrate to nitrite

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12
Q

What body system does nitrite ion affect?

A

Erythrocytes

Nitrite ion enters the erythrocytes in exchange for chloride ion (can also cross placental and enter fetal erythrocytes)

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13
Q

What is the MOA of nitrite?

A

One nitrite interacts with two hemoglobin —> oxidation of ferrous iron to ferric and conversion of hemoglobin to methemoglobinemia

Lack of oxygen carrying capacity —>Anoxia

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14
Q

In chronic nitrate toxicosis, abortion occurs due to decreased ___________ but in the acute toxicosis, abortion occurs due to _______

A

Progesterone; methemoglobinemia

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15
Q

What lesions do you see in nitrate poisoning?

A

Brown-chocolate colour of the blood

Congestion of organs

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16
Q

What clinical signs are observed in nitrate toxicosis?

A

Sudden death

Rapid breathing, restlessness, apprehension, dyspnea, weakness, ataxia, sternal recumbency, cyanosis, terminal convulsions

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17
Q

What would you do to diagnose nitrate toxicity?what is the specimen for choice?

A

Chemical analysis

  • forage, hay, water
  • ocular fluid for animals that have been dead for several hours

Methemoglobinemia concentration

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18
Q

What specific test can qualitatively determine presence of nitrate?

A

Ddiphenylamine test

-positive result (dark blue colour) indicate greater than 5000ppm nitrate

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19
Q

What is the DDX for methemoglobinemia and anoxia?

A

Agents causing methemoglobinemia

  • nitrate and nitrite
  • copper
  • acetaminophen

Agents inhibit oxygen utilization of tissues

  • cyanide (bright red blood)
  • hydrogen sulfide (dark blood)

Hemolytic agents
-copper, since, naphthalene, bromate, iodate, arsine gas, onion, mustard red maple, gossypol, snake venom, other

Carbon monoxide (bright red blood)

Cardiac toxicants - digitalis, magnesium, calcium, potassium, flouroacetate

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20
Q

What is the treatment for nitrate toxicity?

A

Methylene blue IV for ruminant and monogastrics (except cat) as a reducing agent

Activated charcoal, ruminal lavage with cold water, oral antibiotics

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21
Q

Where the the cyanogenic plants?

A

Wild cherry

Sudan grass, Johnson grass and sorghums (fall grasses) -> these also accumulate selenium, nitrate and cyanide

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22
Q

What is usually the source of cyanide toxicity in small animals?

A

Hydrogen cyanide and cyanide salts

  • rodenticide
  • fertilizers
  • sodium nitroprusside used as hypotensive
  • combustion of plastic compounds
23
Q

Cyanogenic plants contain ______________ that can liberate toxic amounts of HCN

A

Cyanogenic glycosides

24
Q

What is the characteristic odor of cyanide?

A

Bitter almond or ammonical

Probably not a good way to diagnose if you want to continue living

25
Q

Thiocyanate SCN, a metabolite of cyanide, has a ___________ effect

A

Antithyroid

Only see effects in chronic toxicosis

26
Q

What species are most susceptible to cyanide poisoning?

A

Ruminants (cattle> sheep) > horse> swine

Hydrolysis by rumen microflora causes release of cyanide from cyanogenic plants

27
Q

T/F: plant damage like wilting, frost, or drought decreases cyanide toxicity

A

False

INCREASE toxicity —> cause release of B-glucosidate that causes hydrolysis of cyanogenic glycosides and release of cyanide

28
Q

What part of the plant has the highest concentration of cyanide? How does this compare to nitrate accumulation

A

Cyanide: Seed > leaves> bark > stems and fruit

Nitrate: stems> leaves > seeds

29
Q

Will young or old plants accumulate more glycoside

A

Young

Same as nitrate accumulation in plants

30
Q

HCN is absorbed from??

A

GI tract
Inhalation
Intact skin

31
Q

Where is HCN metabolized and then excreted?

A

Liver and serum met: CN-in presence of thiosulfate —> thiocynate (excreted in urine)

Excreted in urine or expired air

32
Q

What is the MOA of cyanide?

A

Excess CN- binds with ferric iron and cupric copper to mitochondrial cytochrome oxidase. —> block electron transport chain —> unable to use oxygen resulting in histotoxic anoxia (brain and neuronal damage)

Metabolic acidosis due to anaerobic glycolysis
Vasoconstrictor effect
Irritant to mucus membranes

33
Q

What are the clinical signs of acute cyanide poisoning?

A

Rapid onset
Tachypnea, apparent anxiety, severe panting, gasping, and behavioural alarm

Salivation, muscle tremor,s lacrimation, urination, deviation, colic, vomiting, bright red mucous membranes, clonic convulsions,

34
Q

What are the clinical signs of chronic cyanide poisoning?

A

Posterior paralysis, urinary incontinence, and cystitis/constipation due to lower spinal cord degeneration

Goiterogenic effect (due to thiocyanide )

35
Q

What are the specimens of choice for determining cyanide poisoning??

A

Forage, rumen content, liver, muscle, brain and heart

All should be frozen immediately and kept frozen

36
Q

Elevated levels of thiocyanate can be found in ____________

A

Urine

37
Q

What commercial test can help detect toxic levels of cyanide in rumen contents of plant?

A

Sodium picrate paper test

Yellow colour changes to brick red for positive test

38
Q

What lesions do you see due to cyanide poisoning?

A

Mucus membranes are bright red and blood is cherry red and may not clot

GI tract and lung may be congested with petechial hemorrhage

Smell of cyanide may be present but leaves the rumen contents quickly

39
Q

What is the DDX for cyanide poisoning?

A 
Carbon monoxide (bright red blood) 
Hydrogen sulfide (rapid tissue death due to anoxia but tissues are dark green-purple) 
Nitrate (blood is brown-chocolate colour) 
Urea - causes few lesions but causes colic and nervous behaviour and odor of ammonia
40
Q

How do you treat cyanide toxicity?

A

Sodium nitirite IV -> causes methemoglobinemia which can bind the CN- and reactivate cytochrome oxidase

Sodium thiosulfate -> convert CN- to thiocyanate which is less toxic

Oxygen therapy
Vinegar and cold water to slow microbial hydrolysis
Mineral oil as laxative

41
Q

What plants contain large amounts of soluble oxalates?

A 
Pigweed
Beat
Lamb quarter
Halogenton 
Sorrel 
Rhubarb 
Sorrel 
Greasewood
42
Q

What are the sources of soluble oxalates poisoning?

A

Plants
Potassium and sodium oxalate in household cleaners
Fungi
Ethylene glycol

43
Q

What species are most susceptible to soluble oxalate toxcity?

A

Sheep and cattle

44
Q

What is accommodation of the rumen microflora for oxalates?

A

Ruminants allowed to graze on small quantities of oxalate contains plants gradually results in detoxification of up to 70% more soluble oxalates than normal

45
Q

What part of the plant contains highest amounts of soluble oxalates?

A

Leaves > seeds > stems

46
Q

A diet rich in __________ decreases oxalate toxicity by making insoluble oxalates which cannot be absorbed

A

Calcium

Binds to make calcium oxalate

47
Q

How are soluble oxalates metabolized in the rumen??

A

To carbonates and bicarbonate

What is not metabolized is absorbed to the blood and may affect serum tissue calcium

48
Q

What is the MOA of soluble oxalates?

A

Soluble oxalates combine with Ca to form insoluble Ca oxalate

—> hypocalcemia and tentative in acute cases
—> affect bone and milk production in lower levels
—> precipitation of crystals in kidney —> kidney damage and necrosis

49
Q

What are the clinical signs associated with soluble oxalate ??

A

Colic, dullness, depression, muscle twitching//weakness
Head and neck pulled to one side in sheep (seen in milk fever in cattle)
Prostration, coma, death

Rapid breathing and blood tinged froth at mouth
Convulsions

50
Q

Animals that do not die from acute form of soluble oxalate poisoning develop what signs??

A

Fatal renal tubular toxicosis and signs of oligura, depression, hyperkalemia, and cardiac failure

Chronic tubular necrosis and polyuria

51
Q

What lesions are present due to soluble oxalate poisoning>?

A

Plant in rumen
Excess fluid in abdominal and thoracic cavities, petechial hemorrhage in GI mucosa
Emphysema of lungs with aspirated ingesta
Esophagus and mouth with blood tinged froth
Kidney with dark cortex and medulla separated by gray line from accumulation of oxalate crystals in tubules

52
Q

How can you make a laboratory diagnosis of soluble oxalate poisoning?

A

Presence of Ca oxalate crystals in kidney tubules
Hypocalcemia
High BUN

53
Q

What is the DDX for soluble oxalate toxicosis?

A

Rumen acidosis -but pH of rumen with oxalate is alkaline
Milk fever - lacks oxalate lesions
Hypocalcemia

54
Q

What is the treatment for soluble oxalate toxicosis ?

A

Activated charcoal or limewater

Calcium gluconate IV slowly may cause transient improvement

Saline glucose to treat alkalosis and cause diuretics

Supplement of calcium salts or Ca rich diet
Supportive therapy for nephrosis

RUSVM Toxicology (23 decks)

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