Metabolic Diseases of Ruminants: Energy Flashcards

1
Q

What is gluconeogenesis?

A

Creation of glucose in the liver to meet the body’s needs for this form of sugar

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2
Q

What is the main substrate for gluconeogenesis?

A

Propionate

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3
Q

What is the function of the liver cell (hepatocyte)?

A

The control center for regulation of energy metabolism

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4
Q

What happens when energy demand exceeds dietary intake?

A
  • Insulin concentration decreases
  • Glucagon concetration increases
  • The animal mobilizes its stores
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5
Q

What stores of energy are available?

A

Glycogen
* In the liver and muscle
* Polymer of glycose
Muscle amino acids
* Can be converted to glucose
Lactate
* Can be converted to glucose
Fat
* In the body, 3 fatty acids are linked to one glycerol to fore triglyceride
* Abundant hydrocarbons for oxidation as fuel!

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6
Q

What happens after prolonged energy deficit?

A
  • Insufficient propionate supply from rumen
  • Glycogen stores eventually depleted
  • Only a finite amount of muscels amino acids and lactate can be mobilized
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7
Q

What is left after a prolonged energy deficit?

A

Ketones

Ketones: Acetoacetate, butyrate, acetone

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8
Q

What are ketones a result of?

A

The result of incomplete oxidation of fatty acids

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9
Q

Why are ketones good?

A
  • Important alternate energy source for some tissues
  • Oxidized in heart, kidney, skeletal muscle, mammary gland
    ** Ketones serve to spare precious glucose for other needs**
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10
Q

Why are ketones bad?

A
  • In high concentrations, ketones can suppress appetite and cause altered CNS function
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11
Q

What are the steps of ketosis?

A
  1. Energy gap (negative energy balance)
  2. Fat mobilization
  3. If the rate of fat mobilization exceeds the liver’s ability to oxidize it into energy
  4. Production of ketones
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12
Q

What is primary ketosis?

A

Ration is chronically deficient in carbs

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13
Q

What is secondary ketosis?

A

Diet is fine, but animal has another disease that makes it anorexic

Ketosis occurs seondary to disease-induced anorexia

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14
Q

What are clinical signs of ketosis?

A
  • Gradual reduction in appetite
  • Lethargy, glassy-eyed stare
  • Decreased milk production
  • Poor rumen motility
  • Acetone odor to breath
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15
Q

What is nervous ketosis?

A

A type of ketosis in which CNS signs predominate.
* Apparent blindness
* Stupor
* Ocassionally agressive

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16
Q

How do you diagnose ketosis?

A
  • Measure ketones in blood, milk, or urine
  • Hypoglycemia
  • Incomplete oxidation of fatty acids = increased concentration of ketones
17
Q

What does treatment of ketosis include?

A
  • Find the underlying cause (what is reducing appetite)
  • Jump start gluconeogenesis: Oral propylene glycol, IV glucose, cortisol-based drugs (promote appetite), offer multiple feeds, tube feed, offer molasses in water
18
Q

Why is it important to identify ketosis?

A
  • Predisposition to other post partum diseases: 70% metritis; 80% displaced abomasum
  • Milk production: Reproductive performance, increased risk of culling
  • Costly disease: 4% direct (related to ketosis); 96% indirect (other diseases)
19
Q

What could a cow having a history of “not being normal since calving” signify?

A

Fatty liver/ fat cow syndrome

20
Q

What are some signs of fatty liver?

A
  • Depression
  • Anorexia
  • Weight loss (usually overnight before calving)
  • Decreased rumen motility
  • Decreased miilk production
  • Ketosis
21
Q

How do you treat fatty liver?

A

Treatment is difficult
* Treat concurrent diseases
* Treat like ketosis, only more aggressive and intensive care

22
Q

Prevention for fatty liver includes?

A
  • Prevention of obesity in late lactation
  • Match energy fed to milk production
23
Q

What is pregnancy toxemia also know as?

A

Twin lamb disease

24
Q

What is another disease of chronic negative energy balance?

A

Pregnancy toxemia

25
Q

When does pregnancy toxemia occur?

A

When late pregnant ewe or doe cannot or does not want to eat enough to meet energy demand

26
Q

What are clinical signs of pregnancy toxemia?

A
  • Separated from the flock
  • Star gazing
  • Glassy-eyed
  • Weak
  • Recumbent
  • Poor/ no appetite
  • Any ill doe or ewe in last 6 weeks of gestation is a possible pregnancy toxemia case
27
Q

What makes pregnancy toxemia unique?

Important i think

A
  • Glucose demand is unrelenting
  • Dam will continue to provide fetuses with glucose at her own expense
  • Severe hypoglycemia
  • Fat mobilization under conditions of carbohydrate deficiency = severe ketosis and fatty liver
  • Ketoacidosis can occur
28
Q

What happens pregnancy toxemia remains untreated?

A

The fetuses will die and the ewe or doe will soon follow

29
Q

What is the most successful treatment of pregnancy toxemia?

A

To terminate the pregnancy

30
Q

What does treatment of pregnancy toxemia include?

A
  • Remove fetuses (induce parturition, C0 section)
  • IV dextrose, propylene glycol, etc. –> like ketosis and fatty liver
31
Q

How can you prevent pregnancy toxemia?

A

Provide palatable, high energy feeds in late gestation