Exam 2 Negative Energy Balance Flashcards

1
Q

what cows are more likely to get ketosis due to hypoglycemia

A

those in the free stalls or dry lot
postpartum, multiparis > heifers, immature or old cows

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2
Q

do not exceed ___ capacity in dairy-free stall barn

A

90%

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3
Q

main substrate for gluconeogenesis in ruminants

A

proprionate

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4
Q

how can propionate be constantly supplied in ruminants with a high demand for energy (lactation/gestation)

A

high grain/concentrates
ionophores

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5
Q

normal [BG] in cattle

A

65

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6
Q

3 most common ketones

A

Acetoacetate, BHBA, & Acetone

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7
Q

normal [BHBA]

A

< 1.2 mmol/L

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8
Q

what causes the production of ketones/ketosis

A

insufficient oxaloacetate to allow ACoA to enter the TCA cycle

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9
Q

ketosis treatment

A

dextrose IV
propylene glycol
B-vitamin shot

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10
Q

primary ketosis

A

ration is deficient in carbohydrates

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11
Q

secondary ketosis

A

diet is fine but has another disease making it anorexic or younger/older animals less likely to eat compared to adults/mature animals

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12
Q

which type of ketosis is more common

A

secondary ketosis

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13
Q

why is oxaloacetate limited?

A

it is mobilized out of mitochondria to support gluconeogenesis

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14
Q

what is fatty liver/fat cow syndrome “hepatic lipidosis”

A

prolonged negative energy balance
immediately after calving or 3.5+ BCS (overconiditioned cows)

sudden, rapid loss of body condition is abnormal; normal loss is expected around time of calving

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15
Q

how hormone helps mobilize body fat in cows

A

hormone sensitive lipase (HSL)

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16
Q

how is diabetes in dogs similar to ketosis in dairy cattle

A

both are states of intracellular oxaloacetate deprivation

17
Q

how does pregnancy toxicity in ruminants occur

A

negative energy balance due to fetus draining energy

18
Q

Describe the expected hepatic and serum biochemical responses to chronic negative energy balance in horses.

A

occurs in overweight dams in late pregnancy or early lactation

horses = ACoA convert into lipoproteins resulting in hyperlipidemia (no ketosis) & hepatic fat deposition

19
Q

Describe the expected hepatic and serum biochemical responses to chronic negative energy balance in camelids.

A

Mobilized FFA go to liver → ketogenesis (like ruminants), hepatic fat deposition (ruminants & horses), hyperlipidemia (like horses)

hyperglycemic due to elevated gluconeogenesis & not heavy milk producers