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Y4 FA - GIT and nutrition > Metabolic disease in ruminants 1 + 2 > Flashcards

Metabolic disease in ruminants 1 + 2 Flashcards

(57 cards)

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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?

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A

Aim for a negative DCAD before calving

24
Q

When is hypocalcaemia seen in sheep?

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A

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

25
What is the cause of grass staggers?
Hypomagnesaemia
26
Describe the stores of magnesium in the body
No body stores of magnesium compared to bone for Ca
27
Describe the input and output of magnesium in the body
Output – milk Input – diet - absorbed in rumen, reticulum, omasum
28
High levels of ... reduce magnesium absorption
Potassium - lush grass, fertilisers
29
Calves on what kind of diet may develop hypomagnesaemia?
Unsupplemented all milk diet
30
Calves on what kind of diet may develop hypomagnesaemia?
Unsupplemented all milk diet
31
What are the clinical signs of acute hypomagnesamia?
- Often found dead - Twitchy and hypersensitive - Recumbent and convulsive
32
How is hypomagnesaemia treated?
- 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
Which 2 drugs can be used to control convulsions in a hypomagnesaemia cow
- Xylazine i/v (licensed) (5 – 7 ml to effect) - Pentobarbitone (Euthatal) (unlicensed) (10 -20 ml to effect)
34
How can hypomagnesaemia be prevented?
- Move off affected pasture (fertilisers) - be aware of possible stress induction - Give additional Mg
35
What is fat mobilisation syndrome
- Excessive mobilisation of fat for energy - Similarities to Diabetes Type 2 (Insulin resistance)
36
What are the 2 products of lipolysis?
Non-esterised fatty acids Glycerol
37
In the udder lactose is synthesised from?
Glucose
38
What happens to non-esterised fatty acids in the liver?
- NEFA metabolised to Ketones - NEFA re-synthesised to FAT
39
What is the energy source for muscle?
Ketone bodies
40
What are the functions of insulin
- 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
What are the clinical signs of clinical ketosis?
Reduced milk yield Selective appetite - refuses concentrates Ketone bodies in blood - smell Firm, shiny faeces
42
List the treatments for ketosis
- Propylene glycol (oral) - Dexamethazone - Glucose IV - Vitamin B12 - Vitamin B1 - Kexxtone = monensin bolus
43
Describe nervous ketosis
Clinical manifestation - Hyper-excited - Twitchy - Maniacal licking, salivation - Dangerous? Be careful, restrain
44
How can you treat nervous ketosis?
IV glucose
45
What is the main issue surrounding sub-clinical ketosis?
Gateway condition - acts as a massive risk factor for other conditions
46
What should be observed in a herd to assess nutritional status?
- BCS - DMI - Cudding - Rumen fill - Faeces - Cleanliness - Lying time
47
In the dry period what should you aim for the BCS to be?
2.5
48
In early lactation what do you want they BCS to be?
2-2.5 Ideally don't lose more than 0.5 CS, but rarely achieved
49
What is βHOB?
A ketone body
50
What do βHOB levels in the blood tell you?
Suggest a negative energy balance
51
Non-esterised fatty acids in the blood indicate?
Fat metabolism
52
List the 3 biochemical parameters of energy
- βHOB - NEFA - Glucose
53
List the 4 biochemical parameters of protein
- urea - total protein - albumin - globulin
54
How can milk quality be used to monitor nutrition?
- Milk protein: Low MP ~ energy deficit - Butter fat: low - lack of fibre, high - high fibre diet - Fat: protein
55
Crude protein is a measure of?
Feed nitrogen content
56
Digestible Crude Protein (DCP) = ERDP + UDP - What is ERDP - What is UDP
ERDP = effective rumen degradable protein -> micro-organisms UDP = undegradable dietary protein -> undegraded in rumen and passed into abomasum
57
How can you prevent fat mobilisation syndrome/ketosis?
- Low energy feeding in the dry period - Maximise DMI in cows: comfort, palatability, ab lib feeding - Monitor BCS: avoid fat cows

Y4 FA - GIT and nutrition (11 decks)

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