Feed and water related toxicants--NPN Flashcards

1
Q

3 main feed/water-related toxicants?

A
  • Non-protein nitrogen (NPN)
  • Ionophore
  • Water deprivation–sodium salt
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2
Q

Sources of NPN toxicosis?

A
  • Urea is most commonly used
  • Excess urea in feed as an additive
  • Inadequate concentrates
  • Contamination of feed by urea fertilizer
  • Ammonium salts and ammoniated feed products
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3
Q

NPN toxicosis causes liberation of what?

A

Ammonia

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4
Q

One part urea produces what?

A

About 3 parts protein

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5
Q

What does urea by urease (rumen microflora) change to?

A

Ammonia (NH3) and CO2

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6
Q

What does ammonia aminate?

A

Ammonia aminates ketoacids (from soluble carbohydrates) to amino acids

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7
Q

In NPN toxicosis, what do amino acids form? What does that then converted to?

A

Amino acids form bacterial protein, which is then converted to animal protein

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8
Q

What enhances hydrolysis of urea by urease?

A

Alkaline pH (urea is basic)

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9
Q

Most susceptible species to urea toxicity?

A

Ruminants (horses also susceptible)

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10
Q

Which is the most toxic of all NPN compounds?

A

Urea

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11
Q

What is the usual urea concentration of the grain and total ration?

A
  • 3% of the grain ration
  • 1% of total ration
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12
Q

Which animals are more tolerant to NPN?

A

Animals that are adapted or preconditioned to NPN

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13
Q

What are the toxic doses of NPN?

A
  • Toxic dose in not preconditioned/adapted = 0.45g/kg
  • Lethal dose in adapted animals = 1-1.5g/kg
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14
Q

How do age, fasting, and hydration status affect NPN toxicity?

A
  • Age
    • Animals <1 yr are more sensitive
    • Very young animals (3-6wks) are tolerant
  • Fasting
    • Increases toxicity
  • Dehydration or low water intake
    • Increases toxicity
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15
Q

What are 3 other things that increase NPN toxicity?

A
  • Feeds rich in urease (soybeans)
  • Hepatic insufficiency
  • Diet low in energy and protein but high in fiber
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16
Q

Is all ammonia produced in the rumen toxic?

A

No–ammonia produced in the rumen at normal pH (5-6.5) is in the ionized form (NH4+) which is not absorbed

17
Q

What does too much urea and ammonia in the rumen result in?

A
  • Results in elevation of the rumen pH (8-9) and ammonia is in the non-ionized form
  • Non-ionized ammonia is absorbed and is converted by the liver to urea which is excreted in the urine
  • Too much ammonia (more than the capacity of the liver) will produce hyperammonemia
  • Non-ionized ammonia crosses cell membranes, the blood brain barrier, and the placenta
18
Q

Mechanism of action

Toxicity of urea is due to what?

A

Ammonia

19
Q

Mechanism of action

What does ammonia inhibit?

A

Ammonia inhibits the citric acid cycle–> lack of energy and decreased cellular respiration and tissue damage

20
Q

Mechanism of action

What all does NPN toxicity increase?

A
  • Blood ammonia
  • Anaerobic glycolysis
  • Blood lactate and systemic acidosis
  • Blood glucose
  • BUN
  • Serum potassium and phosphorus
  • Transaminases and PCV
21
Q

Mechanism of action

What might be the cause of death with NPN toxicosis?

A

Cardiac or respiratory failure

22
Q

Clinical signs of NPN toxicosis?

A
  • Rapid onset (0.5-3hrs)
  • Restlessness, aggression, muscle tremors, salivation, teeth grinding, colic, bloat, rumen stasis, sternal recumbency while standing on the hind limbs, convulsions, and death w/in 1-2 hours
  • Usually no diarrhea
23
Q

Lesions of NPN toxicosis?

A
  • No characteristic lesions
  • Main lesions due to vascular damage
  • Congestion and degeneration in liver and kidney
  • Ammonia odor
  • Usually dead animals are extremely bloated
24
Q

Laboratory diagnosis?

A
  • Analysis of feed for urea content
  • Analysis of ammonia in whole blood, rumen fluid, and vitreous fluid (depends on the lab)
  • The specimens (except blood) should be frozen immediately
  • Elevated rumen pH (7.5 or more)
  • Blood chemistry
25
Q

Diagnosis?

A
  • History of exposure
  • Clinical signs
  • Ammonia odor
  • Lab diagnosis
26
Q

DDx?

A
  • Agents which cause colic such as caustics or inorganic arsenic
  • Lead
  • Metaldehyde
  • Chlorinated hydrocarbon pesticides
  • Organophosphates
  • Grain engorgement, nitrate poisoning, enterotoxemia and cyanide poisoning
27
Q

How can you differentiate NPN toxicosis from agents that cause colic such as caustics or inorganic arsenic?

A

Caustics/inorganic arsenic generally cause diarrhea (often bloody) and no nervous signs

28
Q

Difference between NPN toxicosis signs and signs of lead, metaldehyde, or chlorinated hydrocarbon pesticide poisonings?

A

No abnormal posturing, jumping over objects and maniacle behavior in urea poisoning as in chlorinated hydrocarbon poisoning

29
Q

How can you differentiate between NPN toxicosis and organophosphate toxicosis?

A

Organophosphates cause parasympathomimetic signs and respond to atropine therapy

30
Q

What is done to distinguish NPN toxicosis from grain engorgement, nitrate poisoning, enterotoxemia, or cyanide poisoning?

A

Differentiated by necropsy and lab tests

31
Q

NPN toxicosis treatment?

A
  • Bloat should be relieved first
  • Acetic acid 5% or vinegar to cattle (2-6L) or sheep and goats (0.5-1.0L) followed by a large volume of water
  • Treatment should be repeated every 4-5hrs for 48hrs
  • Normal saline for dehydration
  • Sodium bicarbonate IV for acidosis
  • Rumenotomy