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ANSC 460 > Key points pre-midterm > Flashcards

Key points pre-midterm Flashcards

1
Q

How can there be more nitrogen leaving the rumen than coming into the rumen?

A

1) nitrogen coming in from saliva
2) nitrogen entering rumen wall from urea recycling

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2
Q

what occurs as cows reach peak lactation?

A

massive DMI for milk production = lags behind energy released through milk = cows lose body weight b/c have to mobilize own body reserves for demand of energy for milk production

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3
Q

why do cows near parturition often face an immunocompromised state

A

Plasma vitamin A, E, selenium & zinc decline

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4
Q

4 NEFA fates

A

1) peroxisomes -> beta oxidation = acetyl CoA for TCA
2) mitochondria - regulated by CPT-1, completely oxidized to provide energy for hepatocytes
3) ketone bodies
4) TG -> stored or exported as VLDLs

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5
Q

why does DMI decrease during transition period?

A
  • hormonal changes
  • inflammation
  • calf is taking up space
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6
Q

3 things that occur during the pre-partum phase

A
  • decline in DMI = neg energy & protein balance
  • increase in energy demand due to fetal growth & mammary development
  • mobilization of fat & skeletal muscle
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7
Q

why does most negative energy balance occur post-partum?

A

due to rapid increase in nutrient demand for milk production

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8
Q

why does steaming up not work in close up diets?

A

if reduce DM intake more = higher ketone bodies in blood after calving

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9
Q

how does the Goldilocks diet help? (2)

A

1) Lowers decrease in DMI pre-partum & increases DMI post partum
2) decreases risk for DA, ketosis & milk fever

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10
Q

when are cows most at risk for milk fever?

A

1st week after calving, most commonly within the first 3 days

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11
Q

how does calcitonin decrease blood Ca? (2)

A

1) increases kidney excretion
2) inhibits bone resorption

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12
Q

what does PTH do (3)

A

1) decrease renal output by increasing resorption in kidneys
2) increases bone mobilization
3) stimulates calcitrol release

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13
Q

why does incomplete milking not prevent milk fever?

A

Ca has already been exported to mammary gland for 1st milking -> cannot change serum Ca levels

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14
Q

early symptoms of milk fever & what can they cause? (2)

A

1) loss of appetite -> DA, ketosis, compromise immune system, drop in milk/colostrum production
2) unsteadiness, incoordination, sleepliness

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15
Q

first approach to prevent milk fever

A

low ca diets during dry period

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16
Q

how does a diet low in Ca help prevent milk fever?

A

low Ca =stimulates PTH = increases intestinal absorption & bone resorption of ca

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17
Q

purpose of using negative DCAD diet?

A

to induce a mild, but compensated metabolic acidosis

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18
Q

drenching at calving

A

targeting ketosis and milk fever issues with prophylactic treatment

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19
Q

how to treat milk fever? (4)

A

1) sub-q calcium
2) Ca gels
3) drenching at calving
4) IV infusion ( very severe cases)

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20
Q

how do milk fever treatments work?

A

increase Ca = causes delay = need reduction in serum Ca to occur to upregulate homeostatic mechanisms

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21
Q

3 main causative factors of why displaced abomasums occur?

A

1) calving -> everything is adjusting after calf was inside
- uterus displaces it during pregnancy
2) low DMI
3) abomasal atony

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22
Q

2 causes of abomasal atony

A

1) depleted blood Ca
- reduce #, frequency & amplitude of contractions
2) VFA passage to abomasum
- higher grain diets = less rumen fill = more opportunity for abomasum to move around

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23
Q

prevention of displaced abomasum (4)

A

1) feed high quality feeds, good quality forage & TMR over concentrates
- goldilocks diet
2) minimize changes between late dry & early lactation rations
3) maximize cow comfort to reduce stress to avoid reduction of DMI
4) prevent / promptly treat other diseases to avoid secondary ones

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24
Q

when does fatty liver occur most?

A

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

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25
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

26
Q

symptoms of FLS (2)

A

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

27
Q

FLS impacts on immune function (2)

A

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

28
Q

treatment of ketosis (3)

A

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

29
Q

treatment of FLS (2)

A

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

30
Q

prevention of ketosis & FLS (3)

A

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

31
Q

how does choline work in feed restricted cows?

A

mimics neg energy balance = increases milk yield & fat yield

32
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

33
Q

how to restrict energy intake in the dry period? (2)

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

34
Q

4 important management practices to prevent metabolic diseases

A

1) separate cows based on feeding groups
2) feed a balanced diet
3) minimize environmental stressors during transition
4) maintain BCS

35
Q

how is milk synthesis stimulated in late gestation?

A

decrease in progesterone & increase in prolactin = colostrum production

36
Q

what does light do for milk production

A

inhibits metatonin release = increases prolactin = increases activity of milk secreting cells = increases milk production

37
Q

3 factors that limit persistency

A

1) pregnancy -> progesterone & estrogen = drop in milk
2) mastitis/metabolic disease = hinders production
3) stressors-> incomplete milking = more apoptosis

38
Q

3 phases of mammary involution

A

1) active involution
2) steady-state involution
3) redevelopment & colostrogenesis

39
Q

4 ways to control heat in a barn

A

1) ventilation systems
2) shade
3) clean water
4) misting in low/moderate humidity

40
Q

indirect evaporative cooling

A

water is spraying on incoming air to cool air before coming into barn

41
Q

direct evaporative cooling

A

misters/sprayers coupled with fans blowing over top

42
Q

why are we starting to see more soakers used over misters? Where would be a good place to use these

A

1) lesser effect on increasing environmental humidity
2) greater water effect on reducing heat transfer

use these in holding pens

43
Q

6 impacts of heat stress

A

1) reduced DMI
2) reduced milk production
3) reduced pregnancy rates
4) increased lameness, disease & mortality
5) shorter gestation, lower birth weights, impaired immune function
6) calves from heat stressed dams make less milk
-> change show DNA is read/expressed

44
Q

5 physiological coping mechanisms to heat stress

A

1) elevated body temp
2) panting = loss of saliva = loss of potassium & sodium
- need high DCAD
3) increased blood flow to skin
4) increased time standing = increased risk for lameness
5) reduced rumen health
- less eating = less rumination = less saliva = less buffering = higher rumen pH

45
Q

3 nutritional strategies to mitigate heat stress during summer only

A

1) reduce fiber & increase fat bc we know they will eat less-> this is hard to do

2) positive DCAD diet = more Na & K = stimulate water intake

3) feed additives to buffer
- sodium bicarbonate

46
Q

how many carbons do glucose, pyruvate, acetate & butyrate have?

A

6, 3, 2, 4

47
Q

main difference between NSC & NFC

A

NFC is predicted, NSC is measured

48
Q

why is NFC fed if we want to feed as little as possible?

A

b/c it increases energy for higher milk production

49
Q

3 issues with particle size under 4mm

A

1) less chewing = less ruminanting = less saliva = reduced rumen pH
2) reduced milk fat
3) increases diet NDF

50
Q

how are RDPs digested?

A

cleaved by microbes into smaller units to synthesize microbial proteins or deaminate the amino acid to create ammonia
- ammonia is absorbed across rumen wall into blood & excreted as urine or is recycled back to GI across rumen wall or saliva

51
Q

why do we not use CP anymore? (3)

A

1) expensive
2) poor efficiency
3) negative environmental impact

52
Q

what occurs from a too low CP % in the ration? (2)

A

reduction in DMI & reduction in milk yield

53
Q

what is the relationship between milk yield & dietary CP%?

A

increasing CP will not drive a more positive response on milk output
- will increase and then decrease

54
Q

how to implement a lower CP ration on farm (4)

A

1) conduct in depth analysis of operation - collect feed samples
2) use modern feeding programs
3) ensure management is good to handle this
4) high MUN & low CP

55
Q

what cows should not be considered for low CP diet? Why?

A

transition cows b/c DMI is decreased already from neg energy balance

56
Q

constraints of using a low CP diet

A

1) require use of bypass AA -> hard to meet AA supply with feed we have available
2) need to think about cost & composition of additives

57
Q

what is the response of cows that are experiencing heat stress? (3)

A

1) decreased DMI intake -> b/c lot of heat produced from fermentation so they reduce DMI to reduce upcoming heat load
2) stand more -> try to alter convective heat loss
3) hopefully increased water intake -> effective form of heat transfer

58
Q

why do we not see a lot of fat mobilization during heat stress despite higher insulin? What do they mobilize instead?

A

increased respiration = lose Na & K = divert blood flow to peripheral tissues = reduces nutrient absorption = low grade systemic inflammation = become insulin resistant = no fat mobilization

59
Q

how is MUN used as a tool for milk testing?

A

excess N in form of urea is excreted in urine and milk
- over feeding CP = spike plasma urea = increase urinary & milk excretion of urea

60
Q

Why would ketosis be a secondary response to a cow that went off feed?

A

less glucose consumed = acetyl CoA cannot enter TCA = instead lots of ketone bodies will be produced

61
Q

what is another factor that contributes to pH change in rumen?

A

NSC = decrease rumen pH

62
Q

primary ketosis

A

lack of sufficient glucose to support milk production

ANSC 460 (16 decks)

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