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Animal nutrition > Animal nutrition - ketosis, fatty liver > Flashcards

Animal nutrition - ketosis, fatty liver Flashcards

1
Q

Broadly speaking, Metabolic diseases are most frequently
caused by (3)

A

– rapid change of animals nutrient factor requirements in relation to the lactation cycle

– abrupt changes in the ration

– lack of knowledge

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2
Q

Main 4 non-selective culling reasons

A

– mastitis 35%,
– fertility problems 35%,

– hoof diseases 22%,
– metabolic diseases related to energy metabolism 8%

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3
Q

Feeding-related metabolic diseases could be conditionally divided into three groups

A
  1. Energy metabolism-related diseases
  2. Diseases caused by a lack of fibre (crude / effective)
  3. mineral and vitamin deficiency or excess -diseases
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4
Q

Fat cow syndrome is

A

is an umbrella term to refer to a group of energy metabolism diseases that affect overweight cows

e.g.
– Ketosis
– Fatty liver
– Retained placenta - conditionally in this group
– Infertility - conditionally in this group

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5
Q

fat cow syndrome diseases (4)

A

– Ketosis
– Fatty liver

– Retained placenta - conditionally in this group
– Infertility - conditionally in this group

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6
Q

Examples of Diseases caused by a lack of fibre (crude / effective) (5)

A
  • Rumen acidosis
  • Laminitis
  • Liver abscesses
  • Displaced abomasum
  • Bloat (rumen tympany) - conditionally in this group
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7
Q

Examples of Diseases caused by mineral element and vitamin deficiency or excess (3)

A
  • Deals with all the vital vitamins and mineral elements deficiency diseases and poisoning
  • Milk fever and hypocalcaemia
  • Metabolic acidosis
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8
Q

Fat cow syndrome results from

A

Ration high energy content (high amount of concentrates) at the end of lactation and in the dry period causes excessive fatness of cows.

Overly fat cows lose their appetite at the beginning of
lactation and intensively use body reserves.

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9
Q

In the dry period the cows’ body weight can increase only due to

A

gestation tissues

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10
Q

At calving, a cows’ BCS must be between

A

3.25- 3.50

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11
Q

During the NEB (negative energy balance) period the cows should not lose any more than -how many points from BCS-?

A

0.5 points from their BCS

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12
Q

Cows body condition can be regulated only in the what period?

A

in the lactation period and not in the dry period

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13
Q

When the cows get too fat at the end of the lactation period, reduce what

A

reduce the ration amount of grain (energy), but add protein feed

Thus, with ration protein content we can affect the cow’s body condition, and increase or decrease milk yield.

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14
Q

When the cows lose their body weight too quickly after calving, reduce what?

A

reduce the ration protein content and add grain (energy)

Thus, with ration protein content we can affect the cow’s body condition, and increase or decrease milk yield.

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15
Q

another term for ketosis

A

acetonaemia

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16
Q

acetonaemia (or?) is a

A

or ketosis, is a disease of very productive cows.
an energy metabolism disease.
mostly occurs in cows with the subclinical form.

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17
Q

ketosis occurs in what period, typically

A

occurs in the postpartum period during NEB

– most often at 10 to 40 days after calving
– most critical is the 3rd postpartum week

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18
Q

What is a good indicator of ketosis potentially developing?

A

Refusal of fed concentrates is a good indicator of ketosis potentially developing.

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19
Q

(patho)Genesis of ketosis

A

If the demand for glucose exceeds the amount of glucose received from feeds and the cows’ capability to synthesise glucose, the organism will start to look for the other ways to synthesise glucose.

When the blood glucose content decreases the
insulin content also decreases, Low insulin content activates insulin sensitive lipase in the adipose tissue and due to this lipolysis increases in the adipose tissue in addition to gluconeogenesis process in the liver.

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20
Q

Genesis of ketosis

The easiest way to fulfil the glucose requirement is to use ?

A

glycerol – a component of body’s triglycerides and released during lipolysis.

From glycerol as a substrate, glucose is synthesised during
gluconeogenesis in the liver.

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21
Q

insulin sensitive lipase is found in

A

adipose tissue

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22
Q

nefa

A

nonesterified fatty acids or free fatty acids)

an important source of energy for the heart and for aerobically conditioned skeletal muscle.

During active β-oxidation not all NEFAs can be hydrolysed, because NEFA influx into liver cells is too fast.

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23
Q

Fate of free FAs in the liver are subjected to what 2 processes

A

– β-oxidation or
– re-synthesis of triglycerides, which are then packed into the composition of lipoproteins

During active β-oxidation not all NEFAs can be hydrolysed, because NEFA influx into liver cells is too fast.

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24
Q

During active β-oxidation not all NEFAs can be hydrolysed, because NEFA influx into liver cells is too fast.

Due to this, what compounds occur?

A

Due to this, intermediates called ketone bodies occur:

– β-hydroxybutyrate (BHB or BHBA) or

– Acetoacetate (AcAc) -> Acetone (Ac)

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25
Q

Name the 2 main ketone bodies

A

– β-hydroxybutyrate
– Acetoacetate (AcAc) which in turn can become, acetone (Ac) (the 3rd ketone body)

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26
Q

In the normal situation, the body uses ketone bodies for

A

ATP energy production in the peripheral tissues.

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27
Q

The use of ketone bodies also depends on

A

milk yield

if milk yield is lower, then coping with ketone bodies is better, and vice versa

if milk yield is higher, ketone bodies are withstood more poorly

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28
Q

Excess ketone bodies are excreted how?

A

the animal excretes them actively via the urine, milk, and exhaled air (only acetoacetate & acetone)

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29
Q

Blood beta-hydroxybutyrate content in subclinical ketosis

A

> 1.4 mmol/l

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30
Q

Blood beta-hydroxybutyrate content in clinical ketosis

A

> 3.0 mmol/l

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31
Q

secondary ketosis is also called

A

alimentary ketosis

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32
Q

Secondary or alimentary ketosis is Caused by

A

feeding butyric acid-rich silage

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33
Q

During absorption, the rumen wall epithelia change a large part of the butyric acid into

A

BHB/ beta-hydroxybutyrate, which is a ketone body.
Thus, butyric acid rich silage increases ketone bodies in the blood (milk, urine).

– only a small amount of it is unchanged and used by the epithelium to produce ATP energy

34
Q

The additional maximum amount of butyric acid to a healthy cow is

A

50g per day

– not suitable for beginning and high-peak lactation cows
– +50…100g/ day would cause subclinical ketosis and +200g / day would cause clinical ketosis

35
Q

Why does feeding silage high in butyric-acid cause alimentary ketosis?

A

Because during the absorption of butyric acid by the rumen epithelia, it is converted into beta-hydroxybutyrate which is a ketone body and contributes to ketosis upon accumulation.

36
Q

What are some non feed-related reasons for development of alimetnary ketosis?

A

Occurs due to reduced feed intake and decreased absorption of nutrients.

e.g. displaced abomasum - either partial or complete or
leg problems

37
Q

Why can displaced abomasum cause alimentary ketosis?

A

displaced abomasum - either partial or complete, can be caused by a sudden change in the ration ->
e.g. from a fibre-rich ration to rumen highly fermentable concentrate-rich ration

Another correlation:
A concurrent milk fever or ketosis can make the abomasum atonic and consequently filled with gas.

The combination of these factors can result in the abomasum floating from its normal position at the base of the abdomen to the left side of the rumen.

38
Q

Why can leg problems cause alimentary ketosis?

A

when feed intake is reduced due to different diseases,
animals become thin and resort to use of body reserves

39
Q

The standard treatment for ketosis

A

consists of IV glucose solution administration (a single dose 500 ml repeated several times)

but this doesn’t treat the cause

40
Q

Prevention of ketosis (4)

A
  • Optimal body condition score at calving
  • After calving do not overdo silage feeding
  • Cow much eat sufficient quantities of starchy feeds (cereals, potatoes)
  • Do not overdo concentrates (up to 50% in DM), increase the amount of concentrates step by step
41
Q

After calving do not overdo silage feeding, favor what type of silage?

A

favor silages with restricted fermentation ->
metabolic load ->
liver ability to re-process silage acids

– add some good hay into the ration

42
Q

What are silages with restricted fermentation?

A

It means that the pH is still rather high, and not all lactic acid bacteria are able to produce the lactic acid which eventually dropsthepHdown.

Restricted fermentation is a good thing when you are trying to prevent ketosis so in the transition period you shouldfeedthat.

43
Q

Why is it necessary to attract the cow to eat starchy feeds (cereals, potatoes) to prevent ketosis?

A

C3/propionate is glycogenic,
but C2/acetate and C4/beta-hydroxybutyrate are ketogenic compounds.

starch digestion produces mainly propionate
and glucose from propionate will correct the ketosis

44
Q

Why should concentrates not be overfed in order to prevent ketosis?

A

– metabolic load ->
liver’s ability to reprocess acids produced from starch fermentation in the rumen

if the proprionate amounts enetering the liver are too high, it’ll be subject to oxidation processes and this is bad.

C3 (proprionate) must enter gluconeogenesis not to oxidation process

45
Q

Why should we avoid high moisture grains?

A

because high moisture grains ferment in the rumen too quickly as the fermentation process has already begun in the silo

too fast = ketosis/tympany

46
Q

preventation of ketosis via feeding (3)

A
  • Use less highly fermentable carbohydrates
  • If possible add by-pass starch to the ration
  • Oral administration of liquid propylene glycol is the best possibility
47
Q

Prevention of ketosis:
Use less highly fermentable carbohydrates such as

A

crushed grains (barley, oats) or meals (all cereals)
versus high moisture grain which is more likely to induce ketosis

48
Q

2 examples of by-pass starch

A

maize meal, in maximum 4-5 kg;
potatoes

49
Q

Oral administration of liquid propylene glycol is themost efficient way to surely avoid ketosis. It can be given at what dosage and frequency?

A

– up to three consecutive days at up to 0.5 l per day

best response dosed straight into the mouth

Note: amount phenomena
▪ half effect if spread onto concentrate or fed in the composition of concentrates (energy feeds)

▪ no effect if added to TMR or presents in silage

50
Q

What is propylene glycol for?

A

Can be administered P.O. to cows at risk of ketosis. It can also be fed prophylactically (additional energy source).

The PG is quickly absorbed in the rumen an dconverted to glucose in the liver.

  • over 30 min, increases insulin content in the blood by 200-400%
  • decreases NEFA and Beta-hydroxybutyrate (ketone body) concentrations
  • reduces triglyceride content in the liver
51
Q

Why is propylene glycol less effective during distributed feeding?

A

Fed with silage, all the PG is converted to lactic and propionic acids which get consumed by microorganisms instead of a portion being absorbed as is an dreaching the liver.

  • it is not absorbed quickly from the rumen and microbes degrade it to VFAs
  • it doesn’t have a considerable effect on blood glucose level
    and insulin synthesis
52
Q

Precursors of gluconeogenesis (3)

A
  • Propionic acid 50%
  • Glycogenic amino acids 30%
  • Glycerol 20%
53
Q

Precursors of gluconeogenesis and their percentages

A

*Propionic acid 50%
*Glycogenic amino acids 30%
*Glycerol 20%

54
Q

Of all the blood glucose, what percentage originates from by-pass starch?

A

10-20%

(depends on the ration a bit)

55
Q

Changes in physiological and blood biochemical parameters in the transition period.

Describe changes in dry matter intake.

A

consistent and steady before calving with a sharp drop after calving after which it gradually rises to eventually near double to precalving intake amounts

56
Q

Changes in physiological and blood biochemical parameters in the transition period.

Describe changes in plasma glucose concentrations.

A

Dips down right before calving, rises during calcving after which goes into negative energy balance period with slow, steady return over around 3 weeks postpartum.

57
Q

Changes in physiological and blood biochemical parameters in the transition period.

Describe changes in liver glycogen concentrations.

A

Decreases around calving when focus isn’t on eating/storing glycogen, there is inappetance. Rises only a bit back during NEB period.

58
Q

Changes in physiological and blood biochemical parameters in the transition period.

Describe changes in plasma NEFA concentrations.

A

NEFA blood content begins to increase about a week before calving and then decrease again after calving. Helps to compensate the negative energy balance period.

Graph B represents a fat cow with ketosis, has fatty liver. Problematic.

59
Q

Changes in physiological and blood biochemical parameters in the transition period.

Describe changes in plasma BHB concentrations.

A

Marker for ketosis.

NEFA content first rises, then BHB can rise. during NEB period.

60
Q

Changes in physiological and blood biochemical parameters in the transition period.

Describe changes in liver triglyceride concentrations.

A

If the liver TG percentage rises too high, its problematic, fatty liver. Liver function will weaken with increased fatty infiltration.

61
Q

Fatty liver or

A

hepatic lipidosis

62
Q

Fatty liver or hepatic lipidosis is a

A

is a energy metabolism-related disease, which etiology is similar to ketosis.

As a rule fatty liver precedes ketosis.

All high yielding dairy cows suffer to some extent from fatty liver disease.

63
Q

Liver begins to become fatty at what point in relation to calving?

A

Liver begins to become fatty at approximately one week prior to calving.

Feed intake begins to decrease in cows already before calving, which leads to use of depot fats as an energy source.

All high yielding dairy cows suffer to some extent from fatty liver disease.

64
Q

As a result of the hydrolysis of body fats, the free FAs in the blood are subjected to:

A

– β-oxidation (about 50% of FAs), and

– about 50% of FAs are re-synthesized and packaged into the composition of lipoproteins to be sent out from the liver

65
Q

If the blood NEFA concentration rises, free FAs will be packed into the composition of

A

VLDL

very low density lipoproteins

66
Q

Unlike pigs, cows are not able to produce the necessary amount of

A

apoprotein called B100 and re-synthesized triglycerides then accumulate in the liver.

That apoprotein is needed to transport resynthesized TGs out of the liver to other parts of the body.

67
Q

High yielding dairy cows’ livers can accumulate up to

A

500 g of fat per day

68
Q

Lipoproteins are

A

specific high molecular weight compounds,
which contain proteins and lipids,

and their task is to transport fats via blood into the tissues.

69
Q

Lipoproteins are divided into 5 types:

A

– chylomicrons (synthesized in intestinal epithelium)

Below are synthesized in liver:
– very low density lipoproteins (VLDL)
– low density lipoproteins (LDL)

– intermediate density lipoproteins (IDL)
– high density lipoproteins (HDL)

70
Q

Very low density lipoproteins (VLDL) and chylomicrons are rich in what and low in what?
their task?

A

Very low density lipoproteins (VLDL) and chylomicrons are rich in triglycerides and poor in proteins.

– they transport the triglycerides into the tissues

71
Q

High density lipoproteins (HDL) are poor and high in?
thier task?

A

High density lipoproteins (HDL) are poor in triglycerides and rich in protein.

– their main task is to empty the cholesterol from peripheral tissues

72
Q

Low (LDL) and intermediate density (IDL) lipoproteins tasks are to

A

transport the cholesterol into the tissues

73
Q

Feeding strategies, which reduce fatty liver (4)

A

are the same as those for ketosis, because the diseases etiologies are the same

  • Optimal body condition score at calving.
  • In dry period, the cows body weight can increase only because of foetal growth.
  • Maintain an adequate feed intake during transition period.
  • Oral administration of liquid propylene glycol.
74
Q

Fatty liver is negatively correlated with all…?

A

liver functions, for example

  • ureagenesis
  • gluconeogenesis
  • detoxification
  • ATP production
  • production of liver- specific proteins
    *FA oxidation
  • synthesis of lipoproteins
  • etc.
75
Q

Which additional amount of butyric acid fed with silage per day brings out the signs of subclinical ketosis?

A. 50 g
B. 100 g
C. 200g

A

B. 100 g

76
Q

What is the adequate body condition of dairy cows at calving?

A. 2.75-3.00
B. 3.00-3.25
C. 3.25-3.50
D. 3.50-3.75

A

C. 3.25-3.50

77
Q

How many points can cows lose from their body condition without negative impact on their health during the NEB period?

A. 0.25
B. 0.50
C. 0.75
D. 1.00

A

B. 0.50

78
Q

If the cows lose their body condition too fast at the beginning of the lactation we should …

A. increase ration energy and decrease protein content

B. decrease ration energy and increase protein content

A

A. increase ration energy and decrease protein content

79
Q

Which appears first?

A. Fatty liver and then ketosis
B. Ketosis and then fatty liver

A

A. Fatty liver and then ketosis

80
Q

What is the most important to do to avoid fatty liver and/or ketosis?

A. Attract cows to eat starchy feeds
B. Do not overdo with concentrates
C. Maintain cows optimal body condition at calving
D. Use silages with restricted fermentation

A

C. Maintain cows optimal body condition at calving

Animal nutrition (19 decks)

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