Metabolic disease in ruminants 1 + 2 Flashcards

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1
Q

List some causes of ‘post natal depression’ in the dairy cow

A

Milk fever
RFM / Metritis / Endometritis
Mastitis
Displaced abomasum
Ketosis
Fertility
Lameness

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2
Q

What is milk fever?

A

Hypocalcaemia ± hypophosphatemia

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3
Q

Which animals are most affected by milk fever?

A

Dairy cows at/after calving
Increased risk with increasing parity

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4
Q

Why do calcium levels decrease at/after calving?

A

Due to colostrum/milk demands

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5
Q

Failure to respond to milk fever promptly will lead to the body mobilising what resource?

A

Calcium from bone

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6
Q

Describe the role of parathyroid hormone in homeostatic calcium control

A
  • Mobilisation of Ca2+ from bone “stores”
  • Increased absorption from gut - Requires Mg2+ to function
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7
Q

Describe the role of calcitonin in homeostatic calcium control

A

Reduces Ca2+ absorption and availability

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8
Q

Describe the role of vitamin D3 in homeostatic calcium control

A

Increased absorption from gut

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9
Q

Describe the different forms of calcium in the blood

A

Bound (chiefly to albumin)
Ionised - Ca2+ - active

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10
Q

The ratio of bound and ionised calcium in the blood is dependant on?

A

pH dependant – reduced binding with reduced blood pH

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11
Q

List the 3 main functions of calcium in the body

A

Muscle function
Nerve impulses
Immune response

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12
Q

What are the signs of acute milk fever

A
  • Seen at/after calving
  • Initial hyper-excitement: tremor, etc
  • Recumbent as muscles have stopped working
  • Guts/glands stopped working: no faeces, no urination, dry noses, postural bloat
  • Slow pulse/HR
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13
Q

List the DDx of a recumbent cow after calving

A
  • Milk fever
  • Acute coliform mastitis
  • Botulism
  • Injury at calving
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14
Q

How does acute coliform mastitis present?

A

High pulse rate/heart rate
Temp – high/normal/low!
Endotoxaemic – mucous membranes injected
± Diarrhoea

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15
Q

If a cow has milk fever which single treatment should they respond to?

A

Ca alone

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16
Q

Describe how to treat hypocalcaemia

A
  • I/V Ca Borogluconate 40% (11.9g/400ml) calcium
  • HypoCa often complicated by HypoPhos (will do no harm if not hypoP)
  • S/C administration of little use as its absorbed too slowly
  • Place in sternal recumbency
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17
Q

When administering IV Ca borogluconate what must be considered

A

Care with rapid infusion - Heart

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18
Q

Hypophosphatemia is most commonly seen with which other deficiency?

A

Hypocalcaemia

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19
Q

How is hypophosphataemia treated?

A
  • Vigophos solution for injection for cattle (Forte) contains organic phosphorous source, with Vitamin B12 supplementation
  • Calciject 40 CM for treating milk fever has 5% magnesium hypophosphite hexahydrate
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20
Q

Sub-clinical hypocalcaemia acts as a risk factor for which other diseases?

A
  • Immunosuppression
  • Coliform mastitis
  • Metritis/endometritis
  • “post-partum depression”
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21
Q

List the prevention strategies for hypocalcaemia at/after calving

A

“Aim to tone up the parathyroids prior to calving”
- Feed low Ca diet pre-calving
- Feed high Magnesium pre-calving
- Boluses/drench/stomach tube at calving
- Maximise DMI pre-calving
- Forage mineral analysis to determine extent of challenge

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22
Q

What does DCAD stand for?

A

Dietary cation/anion difference

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23
Q

What is the aim of DCAD before calving?

A

Aim for a negative DCAD before calving

24
Q

When is hypocalcaemia seen in sheep?

A

Not after lambing
Associated with a fall in DMI
Pre-lambing stress

25
Q

What is the cause of grass staggers?

A

Hypomagnesaemia

26
Q

Describe the stores of magnesium in the body

A

No body stores of magnesium compared to bone for Ca

27
Q

Describe the input and output of magnesium in the body

A

Output – milk
Input – diet - absorbed in rumen, reticulum, omasum

28
Q

High levels of … reduce magnesium absorption

A

Potassium - lush grass, fertilisers

29
Q

Calves on what kind of diet may develop hypomagnesaemia?

A

Unsupplemented all milk diet

30
Q

Calves on what kind of diet may develop hypomagnesaemia?

A

Unsupplemented all milk diet

31
Q

What are the clinical signs of acute hypomagnesamia?

A
  • Often found dead
  • Twitchy and hypersensitive
  • Recumbent and convulsive
32
Q

How is hypomagnesaemia treated?

A
  • EMERGENCY
  • BE QUIET – risk of setting off convulsions
  • Control convulsions
  • Give Ca 40% i/v then slowly give up to 200 ml MgSO4 i/v
  • If not recumbent – bottle of MgSO4 s/c (multiple sites for quick absorption)
33
Q

Which 2 drugs can be used to control convulsions in a hypomagnesaemia cow

A
  • Xylazine i/v (licensed) (5 – 7 ml to effect)
  • Pentobarbitone (Euthatal) (unlicensed) (10 -20 ml to effect)
34
Q

How can hypomagnesaemia be prevented?

A
  • Move off affected pasture (fertilisers) - be aware of possible stress induction
  • Give additional Mg
35
Q

What is fat mobilisation syndrome

A
  • Excessive mobilisation of fat for energy
  • Similarities to Diabetes Type 2 (Insulin resistance)
36
Q

What are the 2 products of lipolysis?

A

Non-esterised fatty acids
Glycerol

37
Q

In the udder lactose is synthesised from?

A

Glucose

38
Q

What happens to non-esterised fatty acids in the liver?

A
  • NEFA metabolised to Ketones
  • NEFA re-synthesised to FAT
39
Q

What is the energy source for muscle?

A

Ketone bodies

40
Q

What are the functions of insulin

A
  • Allows glucose entry into cells
  • Decreases liver gluconeogenesis
  • Suppressed non-esterised fatty acid entry into mitochondria & ketogenesis
  • Stimulates lipogenesis in adipose tissue & in liver
41
Q

What are the clinical signs of clinical ketosis?

A

Reduced milk yield
Selective appetite - refuses concentrates
Ketone bodies in blood - smell
Firm, shiny faeces

42
Q

List the treatments for ketosis

A
  • Propylene glycol (oral)
  • Dexamethazone
  • Glucose IV
  • Vitamin B12
  • Vitamin B1
  • Kexxtone = monensin bolus
43
Q

Describe nervous ketosis

A

Clinical manifestation
- Hyper-excited
- Twitchy
- Maniacal licking, salivation
- Dangerous? Be careful, restrain

44
Q

How can you treat nervous ketosis?

A

IV glucose

45
Q

What is the main issue surrounding sub-clinical ketosis?

A

Gateway condition - acts as a massive risk factor for other conditions

46
Q

What should be observed in a herd to assess nutritional status?

A
  • BCS
  • DMI
  • Cudding
  • Rumen fill
  • Faeces
  • Cleanliness
  • Lying time
47
Q

In the dry period what should you aim for the BCS to be?

A

2.5

48
Q

In early lactation what do you want they BCS to be?

A

2-2.5
Ideally don’t lose more than 0.5 CS, but rarely achieved

49
Q

What is βHOB?

A

A ketone body

50
Q

What do βHOB levels in the blood tell you?

A

Suggest a negative energy balance

51
Q

Non-esterised fatty acids in the blood indicate?

A

Fat metabolism

52
Q

List the 3 biochemical parameters of energy

A
  • βHOB
  • NEFA
  • Glucose
53
Q

List the 4 biochemical parameters of protein

A
  • urea
  • total protein
  • albumin
  • globulin
54
Q

How can milk quality be used to monitor nutrition?

A
  • Milk protein: Low MP ~ energy deficit
  • Butter fat: low - lack of fibre, high - high fibre diet
  • Fat: protein
55
Q

Crude protein is a measure of?

A

Feed nitrogen content

56
Q

Digestible Crude Protein (DCP) = ERDP + UDP
- What is ERDP
- What is UDP

A

ERDP = effective rumen degradable protein -> micro-organisms
UDP = undegradable dietary protein -> undegraded in rumen and passed into abomasum

57
Q

How can you prevent fat mobilisation syndrome/ketosis?

A
  • Low energy feeding in the dry period
  • Maximise DMI in cows: comfort, palatability, ab lib feeding
  • Monitor BCS: avoid fat cows