Metabolic Diseases and Trace Elements of Cattle Flashcards

1
Q

What is milk fever?

A

Hypocalcaemia +/- hypophosphataemia

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2
Q

How does PTH control calcium levels?
What does calcitonin do?
What does Vitamin D3 do?

A

PTH: Increases calcium absorption from the gut
Mobilises calcium from bone
Calcitonin: reduces calcium absorption
Vitamin D3: Increases calcium absorption from the gut

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3
Q

What are 4 differential diganosis for a recumbent cow after calving?

A
  1. Milk fever
  2. Acute coliform mastitis
  3. Botulism
  4. Calving injury (nerve damage, femoral head fracture/dislocation)
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4
Q

What is the treatment for milk fever?

What site is best for injection?

A

IV Calcium Borogluconate
Place in sternal recumbency
Jugular vein

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5
Q

What is the problem with using the milk vein for injections?

A

Risk of haematomas
Lack of drainage
Lying on that area can cause abscesses

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6
Q

What is the best prevention strategy for milk fever?

A

Low calcium and high magnesium diet pre-calving

Maximise DMI

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7
Q

What does Zeolite do?
What is a risk of using it?
In which cows is it contraindicated?

A

Binds calcium in ration
Improves mobility of calcium in order to prevent milk fever
Risk of hypophosphataemia
Don’t use in lactating ration!

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8
Q

What is the difference between hypocalcaemia in sheep and cattle?

A

Sheep: Pre-lambing (stress)
Cattle: At/after calving (poor mobilisation of and drained calcium reserves)

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9
Q
  1. What can cause grass staggers/hypomagnaesemia?

2. What can cause it in calves?

A
  1. High potassium (e.g. lush grass), reduces Mg absorption and STRESS
  2. Unsupplemented all milk diet (no Mg)
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10
Q

What are 5 differential diagnoses for a cow/sheep found dead in a field?

A
  1. Lightening strike
  2. Electrocution
  3. Toxaemia
  4. ANTHRAX!
  5. HypoMg
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11
Q

What are 2 differences between milk fever and grass staggers?

A

Diarrhoea in hypoMg (milk fever - no faeces)

Flaccid paralysis in milk fever, but hypoMg convulsive/paddling

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12
Q

How is glucose produced?

How is lactose synthesised?

A

Via gluconeogenesis from proprionate (in Krebs cycle)

From glucose

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13
Q

What happens if there is insufficient proprionate?

A

Insufficient oxalo-acetate

Acetyl CoA can’t enter Kreb’s cycle, metabolised to Ketones

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14
Q

Where does metabolisation of ketones and fat deposition occur?

A

Liver

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15
Q

What are NEFAs/FFAs produced from?

What are they metabolised to in the liver?

A

Lipolysis of adipose tissue

Metabolised to Ketones

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16
Q

What are ketones an energy source for?

A

Muscle (not milk production or brain)

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17
Q

Name 3 ways insulin decreases blood glucose

A
  1. Increases uptake of glucose into cells
  2. Decreases gluconeogenesis
  3. Suppresses lipolysis and ketogenesis
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18
Q

What are 3 treatments for clinical ketosis?

A
  1. Oral propylene glycol
  2. Corticosteroid (dexamethasone)
  3. B Vitamins: B12 (cobalamin), B1 (thiamine) for Kreb’s cycle
19
Q

What are 4 clinical signs of ketosis?

A
  1. Reduced milk yield
  2. Refusal of concentrates
  3. “Pear drop” smell on breath (ketone bodies)
  4. “Shiny” firm faeces
20
Q

What can propylene glycol toxicity cause?

A

Haemolysis

Release of sulphur

21
Q

What is the treatment for nervous ketosis?

What are your differential diagnosis?

A

IV glucose 40%

DDx: HypoMg, listeriosis, BSE

22
Q

How much BCS should cows lose between dry period and early lactation?

A

0.5

23
Q

What BCS should cows be:
At calving?
Early lactation?

A

2.5-3
(lose 0.5)
2-2.5

24
Q
  1. What is BHOB testing used for?

2. What is NEFA testing used for?

A
  1. Ketone body, NEB

2. Evidence of fat mobilisation

25
Q

When should metabolic testing be carried out after a diet change?

A

2 weeks after a diet change

26
Q

What does low butterfat in milk indicate?
If it is very high, what can this indicate?
What can low milk protein indicate?

A

Lack of fibre in diet
Excessive fat mobilisation
Energy deficit

27
Q

What does high blood urea indicate?

A

Excess ERFP (effective rumen degradable protein)
Or insufficient ME (microbial energy)
Basically the rumen microbial ability to digest protein is overwhelmed!

28
Q

Why do you want to reduced excretion of urea?

A
  1. Turns into ammonia, which is a greenhouse gas

2. Indicates non-absorption of protein, so protein in the ration is being wasted

29
Q

What are 3 ways during the dry period to prevent FMS/Ketosis?

A
  1. Feed a low energy diet
  2. Maximise DMI
  3. Monitor BCS, avoid fat cows!
30
Q

What are Scottish Blackface sheep susceptible to?

A

Copper deficiency

31
Q

What breeds are susceptible to copper deficiency?

A

Texel, North Ronaldsey

32
Q

Where is copper stored?

How do you diagnose copper deficiency?

A

Liver

Liver biopsy

33
Q

What causes Copper:

  1. Deficiency?
  2. Toxicity
A
  1. Molybdenum (clinical signs) or iron-induced

2. Excessive supplementation

34
Q

Which trace element is associated with teat keratin?

What is it also important in?

A

Zinc

Immune function

35
Q

How are Selenium and Vitamin E related?

A

Vitamin E maintains Selenium in body in active form (GSHPx)

Selenium allows Vitamin E absorption

36
Q

Why is Selenium crucial for thyroid function?

A

Selenium dependent enzyme (iodothyronine deiodinase)

Converts thyroxine to T3

37
Q

What causes Blind Staggers?

A

Acute Selenium toxicity

38
Q

Which trace element is MOST important for reproductive function?

A

Iodine

39
Q

What is a goitrogen?

A

Interfere with iodine uptake by the thyroid

Pituitary gland releases TSH, promoting growth of thyroid tissue (goitre)

40
Q

Give 3 examples of goitrogens

A
  1. Brassicas (kale, cabbage, turnips)
  2. Maize
  3. White clover
41
Q

How can Potassium and Fertilizer (nitrogen) cause iodine deficiency?

A

Potassium increases excretion

Fertilizer reduces iodine in forage

42
Q

What are 3 ways to diagnose iodine deficiency?

A
  1. Palpation of goitre (best?)
  2. T4 (thyroid function)
  3. Plasma inorganic I (recent intake)
43
Q

What is the best test for Cobalt deficiency?

Why is testing serum not recommended in cattle?

A

Vitamin B12 in milk or Liver B12 (biopsy)

Serum binding proteins, discrepancies and underestimations