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ANSC 460 > Module 4- Ketosis & Fatty Liver > Flashcards

Module 4- Ketosis & Fatty Liver Flashcards

1
Q

fatty liver syndrome (FLS)

A

ability of liver to mobilize fats is altered via consumption of too much fat

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2
Q

when does fatty liver occur most?

A

last week of gestation & first 5-7 weeks of lactation

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3
Q

what cows are more prone to fatty liver?

A

over-conditioned cows = more fat = more fat to mobilize & lower DMI

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4
Q

ideal BCS

A

3.25

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5
Q

ketone body function

A

provide energy for muscle, brain & mammary gland for de novo milk synthesis

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6
Q

how does the storage of triglycerides contribute to FLS?

A

TGs are repackaged as VLDLs = limited capacity = build up of fat

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7
Q

what is the outcome for complete oxidation of NEFAs?

A

ATP

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8
Q

what is the outcome for incomplete oxidation of NEFAs?

A

ketone bodies are produced which can be used by other tissues for energy

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9
Q

how are fatty acids broken down?

A

triglycerides are cleaved into NEFAs (free fatty acids)

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10
Q

what is the outcome for impaired metabolism of NEFAs?

A

FLS & ketosis

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11
Q

why do cows mobilize body reserves?

A

during neg energy balance -> not consuming enough feed to support lactation = mobilizes body reserves for energy

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12
Q

why can acetyl CoA not enter TCA cycle?

A

b/c not enough glucose coming in

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13
Q

where does propionate enter TCA cycle?

A

at succinyl to allow circulation of TCA cycle so acetyl CoA can enter

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14
Q

acetyl CoA can be converted to

A

ketone bodies
- b-hydroxybutyrate, acetoacetate & acetone
- these are released from liver into blood, milk & urine

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15
Q

ureagenesis

A

ammonia -> urea

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16
Q

threshold accumulation of VLDLs in liver

A

10%

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17
Q

symptoms of ketosis

A

1) inappetance = low milk yield & BW loss
2) nervousness
3) high levels of ketone bodies in blood & urine
4) sweetish odour of breath

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18
Q

when does ketosis become a problem?

A

when cows are not eating
-> if they are eating & have a higher ketone level = not problematic bc need ketones to support lactation

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19
Q

threshold for ketone body concetration

A

1.2mmols/L = hyperketonemia

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20
Q

symptoms of FLS

A

similar to ketosis
- high ketone levels in blood & urine
- impaired liver function -> low blood glucose & high blood ammonia bc ureagenesis is altered

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21
Q

what testing can be done to confirm FLS?

A

liver biopsies & post-mortem

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22
Q

what % of early lactation cows develop at least moderate FLS?

A

50

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23
Q

moderate FLS

A

recover after positive energy balance

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24
Q

consequences of FLS on immune function (2)

A

1) impaired immune function -> inflammation & no energy to mount immune response
2) immunosuppression = mastitis, metritis, pneumonia

25
Q

mortality of FLS is as high as (%)

A

50

26
Q

how to prevent FLS & ketosis

A

boost glucose supply in propionate

27
Q

treatment of ketosis (3)

A

1) dextrose orally or IV (only lasts 2 hours)
2) propylene glycol orally
3) boost glucose supply

28
Q

why is propylene glycol used to treat ketosis?

A

is metabolized in rumen to form propionate = makes TCA function
- converted into lactate -> acetate to enter TCA

29
Q

what is dextrose

A

sugar water

30
Q

treatment of FLS (2)

A

1) 2 week glucagon infusion
2) boost glucose to stimulate liver to start producing glucose

31
Q

Should you cull a cow that has FLS? Why or why not?

A

yes b/c high relapse rate

32
Q

prevention of ketosis & FLS

A

1) goldilocks diet -> prevents overconsumption of energy
2) monensin ->increases propionate = allows TCA to function = less ketone body production = less oxidation of FA

33
Q

outer coating of VLDL

A

phosphatidyl choline -> is a phospholipid

34
Q

what is required for phosphatidyl choline synthesis?

A

choline

35
Q

2 different pathways to create phosphatidyl choline

A

1) de novo-> from choline
2) salvage pathway

36
Q

when should choline be supplemented? Why?

A

transition period -> has carry over effect on entire lactation

37
Q

why are hydrophillic tails on outside of phospholipid?

A

allows triglycerides to be transported in blood

38
Q

choline is considered a ( ) vitamin

A

B

39
Q

when is phosphatidylcholine the lowest?

A

around calving

40
Q

how does choline work?

A

increases ability to export TG out of liver inside VLDLs is increased

41
Q

increased intake of choline = ( ) TG in liver storage

A

lower

42
Q

energy corrected milk yield increased by ( ) with choline

A

2.18kg

43
Q

choline has a regularly ( ) effect, but a ( ) effect on milk fat yield

A

quadratic, linear = increased fat in milk

44
Q

when is it recommended to supplement choline? Why?

A

transition period, has carry over effect on entire lactation

45
Q

1 supplier of choline

A

Reashure

46
Q

how does choline work in feed restricted cows?

A

mimics neg energy balance = increases milk yield & fat yield

47
Q

what is the optimal amount of supplemental choline per day?

A

12.9g

48
Q

T or F: choline has many functions

A

T

49
Q

why can niacin (vitamin B3) supplementation be used to prevent ketosis & FLS?

A

it is a coenzyme for NADH production = provides energy
- increases glucose & TCA
- reduces ketone bodies -> b-hydroxybutyrate in specific

microbes can normally provide B vitamins to cows but production is not adequate during transition period

50
Q

why can niacin (vitamin B3) supplementation be used to prevent ketosis & FLS?

A

it is a coenzyme for NADH production = provides energy
- increases glucose & TCA
- reduces ketone bodies -> b-hydroxybutyrate in specific

microbes can normally provide B vitamins to cows but production is not adequate during transition period

51
Q

monensin supplementation function

A

stimulates propionate production to boost supply of glucose

52
Q

how much monensin should be supplemented?

A

17-22mg/kg diet of DMI

53
Q

why do not want to feed high energy diets pre-partum?

A

overconsumption of energy = low DMI = put on more body fat = greater BSC loss

54
Q

how to restrict energy intake in the dry period

A

1) dilute with straw, fed ab libidium to minimize how much body condition put on during dry period
2) lower decrease in DMI pre-partum & greater DMI post-partum

55
Q

main cause of metabolic disorders

A

improper feeding
- diet formulated vs diet delivered

56
Q

important management practices to prevent metabolic diseases

A

1) separate cows based on feeding groups
- to meet nutrient requirements
2) feed a balanced diet
3) minimize environmental stressors during transition
4) monitor forage quality nutrient of feed ingredients
5) maintain BCS
6) maintain monitoring programs
- measure urine ph (milk fever)
- record clinical diseases

57
Q

T of F: good quality forage stimulates DMI intake

A

T

58
Q

1st & 2nd steps to addressing metabolic disorders

A

1) body condition
2) feed additives

ANSC 460 (16 decks)

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