Soluble oxalate (FINAL) Flashcards

1
Q

What are some of the plants that contain large amounts of soluble oxalates?

A
  • Halogeton (Halogeton glomeratus)
  • Greasewood (Sarcobatus vermiculatus)
  • Pigweed (Amaranthus spp)
  • Lamb’s quarters (Chenopodium album)
  • Sorrel, sour sob (Oxalis spp)
  • Sorrel, dock (Rumex spp)
  • Rhubarb (Rheum rhaponticum)
  • Beet, mangold (Beta vulgaris)
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2
Q

What are other sources of soluble oxalate toxicity (besides all the plants)?

A
  • Potassium and sodium oxalates are found in household and industrial products such as rust removers, bleaches, and tanning compounds
  • Fungi (Aspergillus, Penicillium)
  • Ethylene glycol in small animals and poultry
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3
Q

What is this?

A

Halogeton (Halogeton glomeratus)

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4
Q

What plant is this?

A

Greasewood (Sarcobatus vermiclatus)

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5
Q

What plants are these?

A

Curly dock, Dock (Rumex spp)

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6
Q

What is this?

A

Rhubarb (Rheum rhaponticum)

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7
Q

What plant is this?

A

Beet (Beta vulgaris)

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8
Q

Toxic doses in sheep?

A
  • Sheep may be poisoned by 0.55% of body weight
  • Starved or water-deprived sheep can be killed by only 0.1% body weight
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9
Q

What is the nonfatal toxic dose for adult horses?

A

200 g/day for 8 days

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10
Q

Which species are most susceptible to toxicosis?

A

Cattle and sheep are most susceptible (although the rumen microflora can detoxify oxalates to carbonates and bicarbonates)

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11
Q

How does rumen microflora accomodate to soluble oxalates?

A

Ruminants allowed to graze small amounts of oxalate containing plants gradually results in detoxification of up to 70% soluble oxalates than normal

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12
Q

Which part of the plant contains the highest concentration of oxalates?

A

Oxalate is highest in the leaves, followed by the seeds, then the stem

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13
Q

T/F: A large amount of oxalate over a short period is more toxic

A

TRUE

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14
Q

T/F: Presence of food in the rumen reduces the rate of oxalate absorption

A

TRUE

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15
Q

Does calcium affect oxalate toxicity?

A

Yes–Ca or Ca-rich diets decreases toxicity by forming insoluble calcium oxalate which is not absorbed

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16
Q

T/F: Oxalate-producing fungi may increase the oxalate content of some moldy forages

A

TRUE

17
Q

Where/what are soluble oxalates metabolized to?

Where are they absorbed to?

A
  • Can be metabolized to a certain extent in the rumen to carbonate and bicarbonate
  • Absorbed to the blood and may affect serum and tissue calcium
18
Q

What happens to soluble oxalates after absorption? What does this lead to?

A
  • After absorption, soluble oxalates combine w/ Ca ion to form insoluble Ca oxalate
  • This leads to hypocalcemia and tetany in acute cases or affects bone and milk production in lower levels
19
Q

Where does precipitation of Ca oxalate crystals take place and what is the result?

A

In the kidney tubules –> kidney damage and necrosis

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

20
Q

When do clinical signs appear?

A

Onset of clinical signs is in a few hours from ingestion of a toxic dose

21
Q

Clinical signs?

A
  • Colic, dullness, depression, muscle twitching and weakness, head and neck pulled to one side in sheep (as in milk fever in cattle) then prostration, coma, and death
  • Rapid breathing and blood-tinged froth around the mouth
  • Convulsions in some cases
22
Q

What might animals develop if they don’t die from acute toxicosis?

A

Chronic tubular nephrosis and polyuria

23
Q

5 lesions that can be seen from soluble oxalate toxicosis?

A
  • Plant in the rumen
  • Excess fluid in abdominal and thoracic cavities, petechial hemorrhages in GI mucosa
  • Emphysema in the lungs which may contain inspired ingesta
  • Mouth and esophagus may be filled w/ blood-tinged froth
  • Kidneys show dark red cortex and medulla separated by a gray line from accumulation of oxalate crystals in the renal tubules
24
Q

Laboratory diagnosis (3)?

A
  • Presence of Ca oxalate crystals (polarizing rosette-shaped) in the kidney tubules
  • Hypocalcemia
  • High BUN
25
Q

Diagnosis?

A

History, clinical signs, lesions, and presence of Ca oxalate crystals in kidneys and blood vessels

26
Q

DDx and how to differentiate?

A
  • Rumen acidosis (carbohydrate engorgement)
    • pH is rumen in oxalate toxicity is alkaline
  • Milk fever
    • Doesn’t have such prominent lesions like oxalate toxicosis
  • Hypocalcemia
27
Q

T/F: Treatment is usually of little value once clinical signs appear

A

TRUE

28
Q

Treatment?

A
  • Activated charcoal or limewater to prevent absorption
  • Calcium gluconate IV slowly may cause transient improvement, but is not curative
  • Saline-glucose to treat alkalosis and cause diuresis
29
Q

Prevention?

A
  • Supplementation of Ca salts (dicalcium phosphate) or Ca-rich diet is protective
  • Supportive therapy for nephrosis