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ANSC 460 > Revised flashcards (pre-midterm) > Flashcards

Revised flashcards (pre-midterm)

1
Q

when is high risk period for scours/respiratory disease?

A

14-21 days
- between end of maternal antibody production & start of calf antibody production

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2
Q

3 reasons for variation in colostrum quantity

A

1) heifers vs cows
2) pre-partum diet
3) seasonality -> photoperiod / cold stress

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3
Q

5 Q’s of colostrum management

A

1) quantifying-> serum test
2) quality-> 50g/L IgG
3) quantity-> 4L
4) quickness-> within 4 hours
5) clean -> bacteria count

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4
Q

2 functions of bioactive compounds

A

1) gut development
2) immune cell programming

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5
Q

6 things beside antibodies in colostrum

A

1) insulin
2) glucagon
3) prolactin
4) growth hormone
5) insulin growth factor 1
6) insulin growth factor 2

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6
Q

what colostrum components increase glucose uptake & metabolism in the duodenum in early calf life

A

IGF-1 & insulin

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7
Q

beef vs dairy calf feeding management (3)

A

dairy:
- restricted amounts of milk
- ad libitium supply of grains & some forage
- weaning: 8-12 weeks

beef:
- ad libitum milk
- forage & little grain
- weaning: 6-9 months

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8
Q

3 benefits of calf housing pens

A

1) reduces risk of disease
2) prevent cross suckling
3) protect from drafts

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9
Q

2 disadvantages to individual housing

A

1) increased aggressiveness
2) increased fear responses

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10
Q

how is lactose, protein & fat digested?

A

lactose-> glucose + galactose, rapidly absorbed
protein-> AA & peptides, rapidly absorbed
fats -> fatty acids + glycerol, slowly absorbed

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11
Q

2 advantages & disadvantages of whole milk

A

advantages:
- broad range of nutrients
- highly palatable

disadvantages:
- might not be homogenous
- degradable
- expensive

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12
Q

4 benefits of pasteurizing whole milk for calves

A

1) less sickness
2) lower mortality rates
3) lower health costs
4) heavier weights at weaning

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13
Q

2 advantages & disadvantages of acidified milk

A

advantages:
- cheap
- easy to store

disadvantages:
- less palatable
- more separation = not homogenous

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14
Q

3 advantages & disadvantages of milk replacer

A

advantages;
- cost effective
- homogenous
- not degradable

disadvantages:
- may lack nutrients
- less palatable
- mixing problems

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15
Q

starter vs forages

A

starter- VFA, increased energy, palatable
forages: decreased energy, ruminal abrasion, rumination, gut movement

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16
Q

role of milk, starter & forage

A

milk: nutrients necessary for maintenance & slow growth

starter: rumen development & supplemental growth

forage: increase size of rumen

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17
Q

3 benefits of providing pre-choice water

A

1) increases weight gain -> helps establish ruminal micro fauna
2) eat more calf starter
3) decreased incidence of scours

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18
Q

conventional vs accelerated feeding programs

A

conventional: less milk fed, more frequently

accelerated: more milk fed, less frequently

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19
Q

2 benefits of calves fed concentrate compared to forages

A

1) match nutrient composition better
2) rapid increase in concentrate

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20
Q

functions of short chain fatty acids (2)

A

1) cellular growth / gut growth
2) alter blood flow -> more O2 to gut

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21
Q

5 factors that impact weaning

A

1) plane of nutrition
2) age
3) step down of milk
4) water
5) forage -> low quality

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22
Q

why does energy intake decrease at weaning?

A

cannot switch to where they are getting their energy fast enough

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23
Q

abrupt diet change cows would have ( ) body weights

A

lower

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24
Q

what can occur if you wean calves too early?

A

increased risk of leaky gut

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25
Q

2 advantages of enhanced growth rates

A

1) less labour & feed costs
2) faster genetic gain

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26
Q

why does DMI decrease during transition period?

A
  • hormonal changes
  • inflammation
  • calf is taking up space
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27
Q

what makes some cows more susceptible to metabolic diseases?

A

greater decrease in DMI = negative energy & protein balance

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28
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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29
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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30
Q

when is NEFA concentration the highest?

A

around calving

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31
Q

why are transition cows at risk for rumen acidosis (2)

A

1) change in diet @ calving= increase energy density
2) rapid DM intake

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32
Q

3 ways acid is removed from the rumen in order of most removed?

A

1) absorption of VFAs
2) salivary bicarbonate
3) passage

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33
Q

why is there a decrease in nutritional plane at dry off?

A

b/c do not need extra nutrients -> will get fat = more fat to mobilize = fatty liver

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34
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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35
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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36
Q

Goldilocks diet

A

increase straw & decrease grain to control required fiber in diet

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37
Q

5 functions of calcium

A

1) bone mineralization
2) coagulation
3) action potentials
4) cell messenger
5) muscle contractility

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38
Q

where is calcium absorbed?

A

50% rumen & 50% small intestine

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39
Q

what drives absorption of calcium in the small intestine

A

short chain fatty acids

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40
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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41
Q

homeostatic mechanisms that occur when blood calcium levels drop (3)

A

1) increased intestinal Ca absorption
2) increased bone ca mobilization
3) increased ca resorption in kidneys

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42
Q

how does calcitonin decrease blood Ca? (2)

A

1) increases kidney excretion
2) inhibits bone resorption

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43
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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44
Q

what does calcitrol do? (1)

A

stimulates intestinal Ca absorption

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45
Q

how does the mammary gland contribute to Ca regulation? (1)

A

it releases PTHrP in response to low blood Ca
- has same functions as PTH

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46
Q

what characteristics of cows make them more susceptible to milk fever? Why? (3)

A

1) older cows
2) cows with prior experience
3) jerseys

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47
Q

why are jerseys more susceptible to milk fever?

A

lower intestinal vitamin D3 receptors

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48
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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49
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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50
Q

why are older cows more susceptible to milk fever? (3)

A

1) higher Ca demand to support milk production
2) Ca absorption declines b/c less Ca receptors
3) less vitamin D3 production = lower ability to stimulate intestinal & bone Ca absorption

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51
Q

advanced symptoms of milk fever

A

laying down, head displaced to 1 side, paralysis, coma, death

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52
Q

first approach to prevent milk fever

A

low ca diets during dry period

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53
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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54
Q

what are Ca binding agents?

A

bind to divalent cations + reduce Ca availability in diet = allows us to feed higher Ca diets still

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55
Q

what does high dietary P do?

A

reduces ability to regulate Ca = reduces Ca absorption

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56
Q

when to use pos vs neg DCAD diets?

A

positive> lactating cows (if not = drop in DMI)
negative-> close up cows (1 month before calving)

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57
Q

purpose of using negative DCAD diet?

A

to induce a mild, but compensated metabolic acidosis

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58
Q

DCAD equation

A

DCAD = (Na + K) - (CI - SO4) Meq/kg feed

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59
Q

is there a benefit in feeding a DCAD diet to primiparous cows? Why or why not?

A

no because they almost never have milk fever, and they are also still growing so you do not want to compromise their growth

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60
Q

how can we tell if we are adequately acidifying the diet?

A

urine collections
- want pH below 7

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61
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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62
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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63
Q

drenching at calving

A

targeting ketosis and milk fever issues with prophylactic treatment

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64
Q

what cows should we not treat from a prophylactic basis? What ones should we?

A

heifers / normal cows
use for older cows, jerseys & cows with history of milk fever

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65
Q

how do milk fever treatments work?

A

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

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66
Q

reason for gas build up in abomasum?

A

VFA/ bicarbonate goes from rumen-> abomasum
- bicarbonate + acid = forms CO2 -> cannot be released from the abomasum

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67
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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68
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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69
Q

abomasal atony

A

no motility/contractions from lack of Ca

70
Q

symptoms of displaced abomasum

A

1) inappetance -> drop in milk production
2) reduced rumination-> use collars/ear tags to monitor
3) bloat (arched back or kick at abdomen)
4) diarrhea or reduced defecation
5) secondary ketosis

71
Q

why will a cow with secondary ketosis from displaced abomasum relapse after responding to glucose?

A

bc not eating

72
Q

2 clinical signs of a displaced abomasum

A

1) pinging noise = echoing from gas filling gut (primary, can confirm)
2) blood test for ketosis

73
Q

2 treatments of displaced abomasum

A

1) rolling cow -> try move abomasum back
3 min duration
2) surgical treatment

74
Q

surgical treatment of a DA

A

20cm incision on right side, deflate abomasum, bring arm under rumen & pull abomasum into ventral state, suture back in place

75
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

76
Q

when does fatty liver occur most?

A

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

77
Q

what cows are more prone to fatty liver?

A

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

78
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

79
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

80
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

81
Q

FLS impacts on immune function (2)

A

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

82
Q

how to prevent FLS & ketosis

A

boost glucose supply in propionate

83
Q

treatment of ketosis (3)

A

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

84
Q

treatment of FLS (2)

A

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

85
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

86
Q

how does choline work?

A

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

87
Q

when do we supplement choline?

A

3 weeks before & 3 weeks after calving

88
Q

how does choline work in feed restricted cows?

A

mimics neg energy balance = increases milk yield & fat yield

89
Q

what is the optimal amount of supplemental choline per day?

A

12.9g

90
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

91
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

92
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

93
Q

pathway of milk secretion

A

alveolous -> lobule -> secondary duct -> primary duct -> gland cistern -> teat cistern -> streak canal

94
Q

how is milk synthesis stimulated in late gestation?

A

decrease in progesterone & increase in prolactin = colostrum production

95
Q

5 management factors that improve milk yield

A

1) nutrition
2) genetic selection
3) milking frequency / hormonal manipulation
4) environment factors
5) cow comfort & health

96
Q

what does light do for milk production

A

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

97
Q

photoperiod in dry vs lactating cows

A

dry: 16 dark : 8 light
lactating: 16-18 dark : 6-8 light

98
Q

prolactin responses are regulated by

A

milking frequency
-> greater concentration with longer intervals in between milking

99
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

100
Q

what does prolactin do?

A

initiates & maintains lactation

101
Q

how does a dry period work

A

reduce energy density of diet so they do not have enough nutrients to support milk production = increases mammary pressure = FIL accumulate = apoptosis relative to proliferation

102
Q

3 phases of mammary involution

A

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

103
Q

1st lactation cows calve at (%) of mature body weight

A

85

104
Q

tunnel ventilation

A

mechanical + natural ventilation combined
- fans at one end of barn create negative air pressure & draw outside air into barn
- baffles re-direct air & increase air velocity

105
Q

where is air flow in tunnel ventilation

A

perpendicular to cows at feed bunk

106
Q

advantage of tunnel ventilation

A
  • can put barns closer together b/c not relying on only natural air flow
  • can get fresh air in winter
107
Q

cross ventilation advantages & disadvantages

A

advantages: reduced heat stress, barns can be placed anyway, misting potential

disadvantages: energy dependent, bedding choice limitations, minimal air flow in cold temps

108
Q

cross ventilation

A

combining air inlets with tunnel ventilation to allow for natural & forced ventilation

109
Q

3 factors that are impacted when we design barn?

A

1) surface area
2) space for cows
3) ability to mitigate heat stress

110
Q

3 ways to regulate core body temp

A

1) convective: movement of air
2) conductive: transfer of heat from molecule to molecule
3) evaporative: moisture related temp release -> panting

111
Q

4 ways to control heat in a barn

A

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

112
Q

indirect evaporative cooling

A

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

113
Q

direct evaporative cooling

A

misters/sprayers coupled with fans blowing over top

114
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

115
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

116
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

117
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) increase DCAD = more Na & K = stimulate water intake

3) feed additives to buffer
- sodium bicarbonate

118
Q

what happens to BSC in early lactation

A

cows lose weight via neg energy balance from reduced DMI = mobilize fat reserves

119
Q

NEL

A

energy contained in milk produced

120
Q

NEL=

A

(0.0929 x fat%) + (0.0571 x protein %) + (0.0395 x lactose %)

121
Q

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

A

6, 3, 2, 4

122
Q

what VFA is most efficient? What is the disadvantage

A

propionate, dissociation of a proton

123
Q

Pka

A

pH at which 1/2 of the molecule will be in its base form & 1/2 in its acid form

124
Q

Pka of short chain FA

A

4.8

125
Q

pH

A

negative log of hydrogen ion concentration

126
Q

main difference between NSC & NFC

A

NFC is predicted, NSC is measured

127
Q

popcorn characteristics

A

harvest at high moisture, far bit of sugar, hard pericarp

128
Q

prolamin

A

main protein in corn that interferes with starch granules

129
Q

1kg increase in NFC intake = ( )kg increase in MY

A

2.4

130
Q

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

A

b/c it increases energy for higher milk production

131
Q

how to measure NDF? What is included?

A

measures what remains after digestion in a neutral detergent solution
-> ash & small amount of protein
- lignin, celllose

132
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

133
Q

peNDF =

A

NDF content x proportions contained on 19, 8 & 4MM screens

134
Q

peNDF

A

physically effective NDF
- fraction of fiber that stimulates chewing & contributes to rumen mat = rumen function = milk fat content

135
Q

what can you suggest if fecal starch is too high?

A

1) change NDF
2) change particle size
3) change processing

136
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

137
Q

why do we not use CP anymore? (3)

A

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

138
Q

MNE

A

milk nitrogen efficiency

139
Q

MNE =

A

milk N / feed N intake

140
Q

why do we want a lower CP?

A

1) generate greater income over feed costs
2) protect surface & ground water sources
3) better air quality b/c less ammonia
4) takes lots of energy to convert excess ammonia from N or CP to convert it into urea

141
Q

how to increase MNE? (2)

A
  • increase milk yield
  • fine tune feeding management
142
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

143
Q

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

A

reduction in DMI & reduction in milk yield

144
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

145
Q

when would you want to decrease fNDF concentration? (2)

A

1) high DMI
2) using supplemental buffers

146
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

147
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

148
Q

why do we care about milk composition & milk sampling?

A
  • it is how we get paid
  • if protein is higher than fat = milk fat depression
149
Q

normal fat vs protein %

A

fat - 4.2%
protein- 3.1-3.3%

150
Q

total solids vs water content % in milk

A

solids- 12.5-13%
water: 87-88%

151
Q

feed efficiency in relation to the dairy industry

A

feed intake relative to milk production

152
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

153
Q

what happens to lactating dairy cows that chose to not eat much feed?

A

decrease milk production

154
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

155
Q

what does insulin drive in normal cows

A

fat mobilization of NEFAs to support milk fat

156
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

157
Q

when would you decide if a calf is ready to be weaned?

A

functional microbes & adapted rumen
- 680g/day

158
Q

stimulatory & inhibitory factors that promote NEFA release

A

S: insulin, stimulates adipose tissue deposition
I: stress hormones & HSL stimulate NEFA release

159
Q

3 strengths of a free flow system

A

1) less gates = cheaper
2) not restricted = better welfare
3) less labour

160
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

161
Q

what are we trying to limit the release of with milk secretion?

A

catecholymines

162
Q

NDF =

A

ADF + hemicellulose

163
Q

ADF =

A

lignin + cellulose

164
Q

NSC =

A

starch + sugar content

165
Q

NFC=

A

pectin + NSC + organic acids

166
Q

peNDF=

A

proportion of particles x dietary NDF

167
Q

how does peNDF alter rumen pH?

A

peNDF stimulates more chewing = more buffers from saliva = changes how much acid is produced & how much are absorbed

168
Q

peDNF

A

fiber that stimulates chewing & contributes to rumen mat, rumen function & milk fat

169
Q

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

A

NSC = decrease rumen pH

170
Q

primary ketosis

A

lack of sufficient glucose to support milk production

ANSC 460 (16 decks)

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