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ANSC 460 > Module 4- Hypocalcemia & Displaced Abomasum > Flashcards

Module 4- Hypocalcemia & Displaced Abomasum Flashcards

1
Q

most abundant mineral

A

Calcium

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2
Q

calcium uses in body (2)

A

98% structural
2% ECF & soft tissue

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3
Q

5 functions of calcium

A

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

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4
Q

in cows that have milk fever, what other diseases will they develop if it is not fixed? Why?

A

1) mastitis - calcium infects immune signalling
2) ketosis- less contractility
3) displaced abomasum- no smooth muscle contractility

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5
Q

where is calcium absorbed?

A

50% rumen & 50% small intestine

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6
Q

Is vitamin D required for ruminal calcium absorption?

A

no, but it is required for absorption in small intestine

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7
Q

what drives absorption of calcium in the small intestine

A

short chain fatty acids

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8
Q

what is the normal blood calcium level?

A

10 mg/100mL

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9
Q

when is calcium the lowest?

A

calving & week after

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10
Q

why does calcium concentration start decreasing even before calving?

A

b/c colostrum is really high in calcium so it is pulled from the bland into the mammary gland to support colostrogenesis

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11
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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12
Q

2 other names for milk fever

A

hypocalemia or parturient paresis

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13
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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14
Q

what % of cows exhibit clinical vs sub-clinical milk fever

A

8-10%, 50-60%

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15
Q

what other 4 diseases can milk fever be linked to?

A

1) displaced abomasum
2) ketosis
3) retained placenta & mestritis
4) mastitis

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16
Q

mestritis vs mastitis

A

mes- infection of uterus
mas- infection of udder

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17
Q

PTH ( ) blood Ca through what 2 mechanisms

A

increases, kidney reabsorption or bone resorption

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18
Q

PTH ( ) production of vitamin D3, which stimulates ( )

A

stimulates, intestinal Ca absorption

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19
Q

calcitrol

A

vitamin D3

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20
Q

calcitonin ( ) blood Ca by what 2 mechanisms

A

lowers, raises kidney excretion & inhibits bone resorption

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21
Q

what stimulates PTH release?

A

low blood Ca

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22
Q

what does PTH do? (3)

A
  • resorption of calcium (reduces renal output)
  • bone mobilization
  • production of vit D3
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23
Q

what is calcitrol & what does it do?

A

vitamin D3, stimulates intestinal Ca absorption

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24
Q

How does the mammary gland contribute to regulation?

A

release PTHrP which has many same functions as PTH

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25
Q

PTHrP

A

parathyroid hormone released protein

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26
Q

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

A

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

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27
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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28
Q

why are jerseys more susceptible to milk fever?

A

lower intestinal vitamin D3 receptors

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29
Q

T or F: colostrum contains high concentrations of Ca

A

T

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30
Q

T or F: high Ca demand exceeds homeostatic mechanisms

A

T

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31
Q

why does incomplete milking not prevent milk fever?

A

it does not change serum Ca bc it has already been exported
-> the mammary gland supply of Ca at 1st milking is already set bc it has already been exported

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32
Q

why do cows have problems when they have low ca concentration?

A

muscle contractions & nerve functions are impaired = depressed cows

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33
Q

early symptoms of milk fever & what can they cause?

A

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

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34
Q

Why is measuring Ca in blood not done from a production standpoint?

A

expensive & not easy to do

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35
Q

advanced symptoms of milk fever (3)

A

laying down, head displaced to 1 side, paralysis

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36
Q

why is retained placenta related to Ca? (2)

A

1) uterine wall needs to contract
2) no inflammation = no release

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37
Q

first approach to prevent milk fever

A

low ca diets during dry period -> hard to do bc most feeds have high ca

38
Q

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

A

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

39
Q

Ca binding agents

A

bind to divalent cations (mg, k) & reduce Ca availability in diet = can still feed higher Ca diet

40
Q

2 examples of Ca binding agents

A

zeolite & vegetable oils

41
Q

Ca & P are ( )regulated

A

co

42
Q

ideal Ca:P ratio

A

2:1

43
Q

what does high dietary P do?

A

reduces ability to regulate Ca = reduces Ca absorption

44
Q

T or F: zeolite treated cows have lower reduction than untreated cows & they respond faster after calving

A

T

45
Q

What kind of diets should be fed to prevent milk fever?

A

negative DCAD

45
Q

when should DCAD diets be used?

A

during close up phase, 21-28 days prior to calving

46
Q

what is DCAD?

A

relative difference between sodium & potassium (cations) concentrations compared to chlorine & sulphur (anions)

47
Q

when would you use a positive DCAD diet? Why?

A

for lactating cows, b/c if not then DMI is reduced

48
Q

when would you use a negative DCAD diet? Why?

A

during the close up period
- to induce a mild, but compensated metabolic acidosis

49
Q

DCAD equation

A

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

50
Q

DCAD units

A

meq/Kg feed

51
Q

target DCAD value during close up period

A

0 to -150 meq/kg

52
Q

what can too severe of metabolic acidosis cause?

A

protein catabolism = not good

53
Q

primiparous cow

A

1st time calvers

54
Q

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

A

no
- they almost never have milk fever
- are still growing so you do not want to compromise their growth

55
Q

what ions are we trying to decrease in a negative DCAD diet?

A

sodium & potassium

56
Q

normal vs target pH of urine

A

normal - 7
target -5.5-6.5

57
Q

how is blood pH regulated?

A

acid excretion via urine

58
Q

T or F: see effects on blood pH with DCAD

A

F

59
Q

why is timothy valuable?

A

b/c of its mineral composition and its low DCAD

60
Q

what does it mean if it is a low DCAD diet?

A

it has less sodium & potassium relative to chlorine & sulphur

61
Q

DCAD of timothy can be decreased by what 2 factors?

A

1) selection of soil low in K
2) CI fertilization

62
Q

DCAD values close to ( ) can induce a mild acidosis

A

0, or negative

63
Q

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

A

urine collections
- want pH below 7

64
Q

what % of reduction of DMI is expected when close to calving?

A

35%

65
Q

when would we want to see a DCAD diet of 20?

A

lactation or further out in gestation

66
Q

2 ways to avoid veterinary intervention with milk fever

A

1) low DCAD diet
2) add zeolite

67
Q

how to treat milk fever

A

1) sub-q of calcium
2) IV infusion in very severe cases

68
Q

why should IV infusion of calcium source be only used in severe cases?

A

it must be infused very slowly, if too fast = cardiac arrest

69
Q

drenching at calving

A

targeting ketosis and milk fever issues with prophylactic treatment

70
Q

3 less invasive milk fever treatments

A

1) Ca gels
2) drenching at calving
3) IV calcium

71
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

72
Q

what should calcium (milk fever) products do?

A

increase serum Ca concentrations = delay when cow adapts to increased Ca = therefore need a reduction in serum Ca to occur to upregulate homeostatic mechanisms

73
Q

T or F: cows treated often relapse a day later

A

T

74
Q

most common side for displaced abdomen

A

right

75
Q

when do most displaced abdomens occur?

A

early lactation

76
Q

if looking directly at a cow, the rumen is on the ( ) side

A

right

77
Q

if looking from the back of a cow, what side is the rumen on?

A

left

78
Q

what happens with a displaced abdomasum?

A

abomasum should be on bottom, but it is now positioned to the right or left

it can also get filled with gas

79
Q

reason for gas build up in abomasum?

A

VFA or bicarbonate passes out of rumen to abomasum
- bicarbonate + acid = problem b/c it forms CO2, which cannot be released from the abomasum

80
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) abomasl atony

81
Q

abomasal atony

A

lack of motility & contractions -> lack of Ca = why milk fever & displaced abomasums are linked
- no motility = abomasum gas build up b/c less material is entering

82
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

83
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

84
Q

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

A

bc not eating

85
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

86
Q

treatment of displaced abomasum

A

1) rolling cow -> try move abomasum back into place
2) surgical treatment

87
Q

advantages & disadvantage of non-surgical rolling to treat DA?

A

A: quick & easy, not invasive
D: >50% redisplace

88
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

89
Q

advantages & disadvantages of surgical treatment of DA

A

A- effective, standing procedure
D- costly, invasive, long recovery, need antibiotics = milk withdrawal

90
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

91
Q

goldilocks diet

A

control energy supply to reduce magnitude of DMI reduction

ANSC 460 (16 decks)

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