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FAMS > Transition Cow (Ketosis, Fatty Liver, DA) > Flashcards

Transition Cow (Ketosis, Fatty Liver, DA) Flashcards

1
Q

In a FED state, what is the path of glucose after intake?

A

ruminal microbes break glucose down into VFA (proprionate). Proprionate is used in the liver to be taken up into muscle, go into the udder for milk (lactose), or for fat synthesis (when in excess)

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1
Q

T/F: more glucose = more milk production

A

true

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2
Q

Can an early lactation cow eat enough food to meet her glucose demand?

A

no
she is in negative energy balance

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3
Q

When in a negative energy balance, a cows body will release NEFAs. How are NEFAs used?

A

they travel to the liver and either:
1. make it into the mitochondria, get converted into ketones, and ketones get exported and used as a fuel source for the tissues
OR
2. liver repackaged the NEFAs as triglycerides

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4
Q

T/F: in a negative energy balance, the liver can convert fat to ketone bodies and provide fuel to muscles and brain

A

true

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5
Q

In a negative energy balance, the liver can convert fat to ketone bodies for an energy source. It spares limited glucose for cells that ONLY utilize glucose. What 5 cells/things are these?

A
  1. fetus
  2. mammary glands
  3. inflammatory cells
  4. follicles
  5. tumors
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6
Q

Many cows make the transition without any problems, so what goes wrong?

A

We have altered adipose sensitivity of cows.
We increased their sensitivity to fatty acid release and decreased their sensitivity to insulin. Resulting in excessive release of NEFAs.

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7
Q

In normal cows, how much daily energy do ketones provide?

A

10%+

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8
Q

Ketosis is a metabolic disorder that occurs in cattle when ____________ exceeds _____________ by the cow.

A

ketone production exceeds ketone utilization

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9
Q

what are the clinical signs of ketosis?

A
  1. dull
  2. lack of appetite
  3. hard feces
  4. dull hair coat
  5. decrease in milk production
  6. +/- nervous ketosis (ataxia, hyperesthetic, aggressive, wandering, head pressing)
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10
Q

You are called to a farm to investigate a cow that is normally a high-producing cow on this farm. the farmer states she was normal yesterday but is dull, anorexic, and her milk production is decreased today. She is 5 weeks into lactation. You take her blood glucose and its low. What is the diagnosis?

A

spontaneous ketosis

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11
Q

You are called back to a farm that you visited 5 days ago. You treated a cow who had retained placenta. She is now dull, anorexic, and her milk production is down. What is most likely the diagnosis?

A

secondary ketosis from retained placenta

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12
Q

what pathologies can lead to secondary ketosis (usually due to being off-feed) within the first 30 days of lactation?

A
  1. retained placenta
  2. metritis
  3. mastitis
  4. hypocalcemia
  5. displaced abomasum
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13
Q

T/F: all cows have elevated ketones during the periparturient period

A

true
its when concentrations exceed a limit that she is officially considered ketotic. this limit is diagreed upon by many.

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14
Q

when is peak incidence of ketosis in dairy cows?

A

between wks 3-5 into lactation

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15
Q

T/F: ketosis is occurs more frequently in heifers

A

false – more frequent in older cows even though heifers have a larger NEB. This is likely due to the older cows not being able to adapt as well.

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16
Q

Describe the values below of normal FRESH cows (first 2 weeks of lactation) in comparison to close up (3 weeks prior to parturition) or mid-lactation cows:
A. glucose:
B. BHBA:
C: NEFA:

A

A. glucose: LOWER
B. BHBA: HIGHER
C: NEFA: HIGHER

17
Q

How do we measure ketones? (what samples)

A

blood, urine, or milk

18
Q

T/F: ketones are LOWEST 3-4 hours after feeding, so you should sample right before they eat

A

TRUE

19
Q

T/F: blood ketone concentration is lowest in mammary vein

A

false – higher

20
Q

are the concentrations of ketones the SAME between blood, milk, and urine?

A

no
highest in urine.
Blood and milk are about the same.

21
Q

What are the 7 cowside tests for subclinical ketosis?

A
  1. ketostix for measuring urine AcAc (low sensitivity, high specificity)
  2. KetoTest strip for measure milk BHBA (moderate sensitivity and specificity)
  3. KetoCheck for measuring milk AcAc (really low sensitivity but high specificity)
  4. precision Xtra for measuring BHBA (high sensitivity, low specificty)
  5. TailDoc (high sensitivity, low specificity)
  6. NovaMax (low sensitivity, high specificity)
  7. NovaVet (mod-high sensitivity and specificity)
22
Q

What is the ONLY treatment for ketosis that is supported by evidence/clinical trials?

A

propylene glycol (300 mL once daily for 3-5 days)

23
Q

what treatment is used for nervous ketosis but is NOT supported by clinical trials?

A

500 mL 50% glucose

24
Q

Propylene glycol administration _____ plasma insulin and ______ NEFAs.

A

increases plasma insulin
reduces NEFA

25
Q

T/F: drenching propylene glycol is MORE effective than adding it to the ration

A

true

26
Q

T/F: giving excess propylene glycol to treat ketosis will decrease appetite

A

true

27
Q

What are other traditional treatments for ketosis that are not necessarily supported by clinical trials?

A
  1. steroids – dexamethasone
  2. insulin
  3. BST
  4. rumen support (fresh cow drenches – Ca, proprionate, yeast, K)
28
Q

what is the “poster child” for fatty liver?

A

cow BCS >4.0
eating free choice corn silage diet in late gestation

29
Q

what are other names for hepatic lipodosis?

A

liver steatosis
fat cow syndrome

30
Q

what is the gross and microscopic appearance of fatty liver?

A

gross – pale liver which non-distinct edges

microscopic – lots of fat deposits

31
Q

T/F: fat infiltration of the liver occurs in the liver of all dairy cows in periparturient period

A

true

in terms of research the levels can be defined as:
moderate – 30-50 mg triglycerides
severe – >50mg triglycerides

32
Q

T/F: fatty liver is also referred to as type I diabetes

A

false type 2
the glucose is LOW but the insulin is HIGH.

33
Q

What is the limiting factor of fatty liver?

A

mitochondrial uptake of NEFAs

triglycerides accumulate in the liver (synthesis > export –> fatty liver)

34
Q

what is the biggest clinical sign of fatty liver?

A

anorectic, fat cow eating less pre-calving
(but she does NOT have to be fat in order to diagnose this)

35
Q

what is the treatment for fatty liver?

A
  • empirical: treat it like ketosis, give rumen suport, IV lfuids

she is entering hepatic failure, so impt functions of the liver (albumin, clotting factors, acute phase proteins, and energy metabolism) are impaired and this is usually what causes death.

36
Q

T/F: one disorder occuring in the fresh cow can increase the risk of other disorders developing

A

true

37
Q

T/F: ketone bodies are immune suppressing

A

true
they reduce chemotaxis, oxidative burst, and lymphocyte blastogenesis

38
Q

what 3 conditions are more severe in fresh cows as compared to mid-lactation cows due to immune suppression associated with parturition?

A
  1. metritis
  2. mastitis
  3. pneumonia
39
Q

What does the cortisol surge at calving lead to?

A

stimulates anti-inflammatory cytokines, inhibits pro-inflammatory cytokines, and reduces L-selectin and CD18

in general, cortisol surge is IMMUNE SUPPRESSION

FAMS (36 decks)

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