Lecture 2 Flashcards

(26 cards)

1
Q

What are the 3 most important toxins

A
  1. Nitrate-nitrite
  2. Cyanogenic glycosdeis
  3. Soluble oxalates
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2
Q

List some plants that cause nitrate-nitrite toxicity

A
  1. Sorghum
  2. Rye grass
  3. Button grass
  4. Oats
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3
Q

Where are nitrates concentrated

A
  1. Stem and stalks
  2. Toxic amounts can also persist in hay
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4
Q

Describe the mechanism of action of nirtates

A

Nitrates are converted to nitrites by rumen bacteria. High levels of nitrites in the digestive tract will be absorbed into the blood stream. In the blood stream, nitrite oxidises haemoglobin to methamoglobin which means cells are unable to transport oxygen

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5
Q

What % of KNO3 is toxic

A

Greater than 1.5%

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6
Q

Explain how nitrates are toxic to monogastrics

A

They are unable to convert nitrate to nitrite in their digestive tract, however they are suseptible after microbial conversion of nitrate to nitrite in swill or wet hay

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7
Q

10 factors affecting the risk of nitrate-nitrite poisoning

A
  1. decreased sunlight
  2. Termperature
  3. Increased herbicides
  4. Increased insect damamge
  5. Increaed virus infection
  6. Previous exposure
  7. Carbohydrate supply increased
  8. Decresed Mo
  9. Decreased Fe
  10. Decreased Ionophores
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8
Q

5 Clincial Signs of nitrate-nitrie poisoning

A
  1. Salivation
  2. Abdominal pain
  3. Diarrhoea and vomiting
  4. Cyanosis
  5. Bloat
  6. Termors
  7. Staggers
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9
Q

What is the pathology of nitrate-nitirte poisoning

A

Chocolate-brown blood

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10
Q

Nitrate-nitrite is also a vasodialator: what is the problem with this

A

Reduced peripheral perfusion and circulation to the uterus

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11
Q

How to diagnose nitrate-nitrite poisoning

A

Phenylamine test is applied to plants or the aqueous humour of the eye

Merck test and urine analysis test are also avaliable for live animals

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12
Q

How to treat nitrate-nitrite toxicity

A

IV injection of methyl blue - converts methaemoglobin back to haemoglobin

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13
Q

How to prevent nitrate-nitrite poisoning

A
  1. Analysing feed
  2. Not grazing stock on dangerous pastures
  3. Frequent observation if on risky feed
  4. Not over stocking on risky pastures
  5. Disallowing grazing on high nitrate pastures
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14
Q

What is another name for a source of cyanide

A

Prussic acid

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15
Q

Plant species involved in cyanogenic glycoside poisoning

A
  1. Sorghum
  2. Native couch
  3. Reed sweet grass
  4. Cyodon
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16
Q

Why are runimants more suseptible to cyanogenic glycoside poisoning than monogastrics

A
  1. Ruminal microbial beta-glucoside releases HCN rapidly
  2. Low stomach pH of monogastrics inhibits beta glucosidase
17
Q

Mechanism of action of cyanide poisoning

A

Plants store cyanide as cyanogenic glycosides in vacules and the activating agent in the cytosol. When animals chew the plant they mix producing HCN (prussic acid). HCN is rapidly absorbed into the animals blood and spreads into its cells

HCN blocks mitochondria cytochrome oxidase > no ATP is made > body goes into energy starvation

18
Q

What is the HCN potential of plants influenced by

A
  1. Age
  2. Genotype
  3. Nutrition
  4. Stress
19
Q

The poisoning occurance is influenced by (HCN)

A
  1. Feed intake
  2. Time since last feed
  3. Rumen pH
  4. Sulphur nutrition status
  5. Exposure history
20
Q

Clinical signs of acute cyanide poisoning in cattle

A
  1. Rapid deep breaths
  2. Mucous membranes appear bright pink
  3. Irregular weak pulse
  4. Birgnt red blood
  5. Muscle spasms
  6. Coma
21
Q

Rapid field test that can be used to test for free HCN in plants, rumen contents, liver and skeletal muscles

A

Prcric acid spot test

22
Q

A compound that treats cyanide poisoning

A

Sodium thiosulphate IV and PO

23
Q

How to prevent and control HCN poisoning

A
  1. Avoid feeding hungry ruminants stressed or exposed plants
  2. Reduce intake by feeding hay before hand
  3. Provide sulfur supplements
  4. Avoid sorghum crops under 45cm tall or those with regrowth
  5. Avoid hay made from cyanogenic plants
24
Q

Soluble oxalates affect homeostasis of which ion in the body

25
Main clinical effects of soluble oxalates
1. Rumenitis 2. Hypocalcaemia 3. Nephrosis, crystals 4. Oedema 5. Stiff gait, staggers, collapse, coma
26
How to treat soluble oxalates
Admininister calcium borogluconate IV and SC