NUTRITION N METABOLIC DISEASE IN DAIRY CATTLE Flashcards

1
Q

Fatty liver is caused by :

A
  1. cow cannot meet its energy demand
  2. less DM intake
  3. Negative energy balance
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2
Q

Factors of fatty liver :

A

not enough nutrition
poor management
genetic
cows with BCS above 4.5 has a high risk

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3
Q

fatty liver is a condition when

A

having to much fat build up in the liver.

Occur during early lactation.

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4
Q

obese cows tend to have :

A
  1. lipolysis of adipose tissue increase more than normal cow.
  2. have greater decrease in feed intake around calving.
  3. more severe -ve energy balance
    * energy balance = calories eaten equals the number of calories used
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5
Q

what happen during -ve energy balance?

A
  1. body fat is metabolized into bloodstream in the form of non-esterified FA (NEFA)
  2. NEFA r taken up and oxidize by liver (not all)
  3. NEFA accumulate (in form of triglycerides) within liver.
    * In early stage, it is reversible.
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6
Q

NEFA in blood circulation is important in

A

milk fat synthesis.

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7
Q

fatty liver is associated with

A

ketosis and displaced abomasum.

ketosis = process that happens when your body doesn’t have enough carbohydrates to burn for energy. Instead, it will burn fat to produce ketones for energy.

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8
Q

Effect of fatty liver

A

decreased in milk production and feed intake.

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9
Q

how to prevent fatty liver ?

A

improve the nutrition of cows to improve its metabolic state by :
1. supplying an extra source of blood glucose

  1. decreasing mobilization of NEFA from adipose tissue
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10
Q

Preventative used to treat fatty liver :

A

Monensin, glucagon , Ammonium propionate, Na borate

may beneficial/not : glycerol, insulin

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11
Q

Ketosis occur during early lactation. It is characterized by :

A
  1. hypoglycemia = low blood sugar// when energy demands (e.g. high milk production) exceed energy intake and result in a negative energy balance.
  2. hyperketonemia = energy demands for milk production are greater than the amount of energy cows can consume. This will cause -ve enrgy balance which leads to excessive body fat mobilization (accumulation), which triggers excessive production of ketone bodies in the liver > abnormal increase in blood levels.
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12
Q

3 main ketones body :

A

acetoacetate
beta-hydroxybutrate
acetone

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13
Q

Causes of ketosis :

A
  1. -ve energy balance:
    to support high energy demand > body mobilizes fat reserves > release NEFA in blood > excessive NEFA in liver converted into ketone.
  2. less DM intake/less feed intake
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14
Q

4 main types of ketosis

A
  1. primary ketosis (production ketosis) - 2-4 weeks of lactation
    - when glucose demand exceed gluconeogenesis capacity of liver > increase ketogenesis > high ketone bodies in blood, milk, urine
  2. 2ndary ketosis
    - results from other disease > decrease feed intake n increase body fat mobilization > increase NEFA production > more ketone bodies will be produced
  3. Butyric acid ketosis
    - silage with high [butyrate] > increased [beta-hydroxybutyrate] in blood
    - consumed this silage in lower amount than usual > butyric acid ketosis
    * b-hydroxybutyrate = provides energy when not enough carbohydrates or sugars have been eaten.
  4. underfeeding ketosis
    - occurs in cow tht r fed insufficiently.
    - underfed animals > low in glycogenic precursors > increased ketogenesis
    * glycogenic precursors = enabling the net synthesis of glucose
    - in order for the cow to obtain enough energy > fat is mobilized > high ketosis occur
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15
Q

Treatment for ketosis

A
  1. increase blood sugar lvl (500ml of 50% glucose)
  2. vet recommends intravenous injection of glucose + insulin
  3. supply corticosteroids to boost blood glucose lvls.
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16
Q

Rumen acidosis occur during? occur to?

A
  • during early to mid lactation.

- occur in high yielding cows( produces a lot of milk) with high grain ration

17
Q

2 types of rumen acidosis:

A
  1. acute rumen acidosis

- rumen

18
Q

Effect of Subacute rumen acidosis :

A
  1. low feed intake to reduce acid load in their rumen. Cow will start eating again when >ph5.
  2. reduced rumination (cud-chewing)
  3. mild diarrhoea
  4. foamy feces + appearance of undigested grain
  5. low ph cause ruminitis, metabolic acidosis, lameness, pneumonia
  6. hairless shiny skin due to chronic acid damage to skin
19
Q

Prevention of rumen acidosis :

A
  1. balancing diet for starch n effective fibre
  2. avoid sudden change of feed
  3. feed roughages with/immediately after feeding grain/molasses
20
Q

Laminitis ?

A

inflammation of sensitive layers of tissue (laminae) inside the hoof in horses and other animals.

21
Q

Causes of laminitis

A
  1. Inflammation
    inflammation > dysfunction of digital vasculatory sys (circulatory disturbance) > hypoxia (deficiency amount of o2 reaching tissue) at hoof wall > claw bone can rotate & sink inside hoof > laminitis
  2. ruminal acidosis (acute/ SARA)
    - acidosis > damage of ruminal epithelium > allows absorption of histamine n endotoxins(induce inflammation) into blood > cause vasoconstriction n inflammation of lamella of hoof > laminitis
  3. feeding of high lvl of crude protein
    - products of degradation of protein excess in rumen may be the causative agents.
22
Q

prevention/nutrition to cure laminitis :

A
  1. supplement biotin & zinc help to reduce lameness (improve claw horn quality).
    - biotin : for keratinisation, keratin protein synthesis, lipogenesis
    - zinc : formation of proteins for keratinization
  2. vit A n E maintani claw integrity
  3. mineral (iodene,Cu, Manganese)
  4. feed additional buffers n good quality roughages
  5. foot baths (2-5% CuSo4)