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FARM ANIMAL > 6.2.3: Ketosis > Flashcards

6.2.3: Ketosis Flashcards

1
Q

What does subclinical ketosis lead to an increased risk of?

A
  • Clinical ketosis
  • RFM
  • LDA
  • Metritis
  • Lameness
  • Mastitis
  • Culling
  • Death
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2
Q

When (and why) does Type I ketosis occur?

A
  • Slightly later in lactation (e.g. 30 days post calving onwards)
  • This is at peak lactation
  • In the high yielding cow, it is difficult to provide enough energy for peak lactation
  • Rarer nowadays as we have improved our rations for these cows
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3
Q

When (and why) does Type II ketosis occur?

A
  • Around calving/early lactation
  • Energy requirements increase faster than appetite can keep up
  • Most common form of ketosis seen today
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4
Q

What type of ketosis is shown here?

A

Type II
Yield is increasing faster than food intake

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5
Q

What type of ketosis is shown here?

A

Type I
This cow is high-yielding and at peak lactation it is difficult to provide her with sufficient energy

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6
Q

This image shows the pathophysiology of which type of ketosis?

A

Type I

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7
Q

This image shows the pathophysiology of which type of ketosis?

A

Type II

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8
Q

Describe the pathophysiology of Type I ketosis

A
  • Occurs due to underfeeding, seen at peak lactation
  • There is a reduced supply of propionate (source material for gluconeogenesis) and therefore glucose
  • There is incomplete oxidation of NEFAs in liver (due to low glucose) that leads to ketone body production
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9
Q

Describe the pathophysiology of Type II ketosis

A
  • Occurs in hepatic lipidosis, early lactation (close to calving, NOT peak lactation)
  • Excessive mobilisation of fat -> increased NEFAs
  • Incomplete oxidation of NEFA (ketones) and excessive fat accumulation in the liver. There are now so many NEFAs that no matter how much glucose we have, the liver is overwhelmed and can’t keep up.
  • Reduced gluconeogenesis (liver inefficient) and liver function
  • Metabolic effect of all these NEFAs causes insulin resistance
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10
Q

Type II ketosis is more common in which kind of cows around calving?

A

Over-conditioned cows! This means there are more fat reserves to mobilise and overwhelm the liver

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11
Q

True/false: there is higher BHB in Type II compared to Type I ketosis.

A

True - higher in Type II, but probably not used that much clinically to distinguish between the two.
This may be due to the fact that the liver is less efficient.

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12
Q

How can we treat ketosis/hepatic lipidosis?

A
  • Glucose precursor: oral propylene glycol
  • Glucocorticoids are sometimes given in practice
  • IV glucose can be given to resolve nervous ketosis signs, making the cow stable enough to tolerate a propylene glycol drench
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13
Q

Why can’t we give oral glucose to treat ketosis?

A
  • Oral glucose will be utilised by rumen bacteria and so will not effectively reach the cow and address her NEB.
  • Propylene glycol is a glucose precursor that is able to reach the liver and enter the TCA cycle, so the cow can thus obtain glucose.
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14
Q

Diagnostic testing for ketosis

A
  • Blood -> cow-side ketone meter (BHB) or lab
  • Urine -> ketone dipstick
  • Milk -> Rothera’s reagent (turns purple if positive)
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15
Q

Diagnostic testing for hepatic lipidosis

A
  • Look for ketones (as with ketosis)
  • Blood NEFA
  • Look for evidence of liver damage e.g. AST, GGT
  • Assess fat in liver e.g. biopsy, necropsy
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16
Q

When are the effects of Type I ketosis typically seen?

A

20-60 days in milk (causes occur around this time too)

17
Q

When are the effects of Type II ketosis typically seen?

A
  • Effects normally seen at <20 DIM (Days in milk)
18
Q

____ _ ketosis occurs as a result of undersupplying energy at peak lactation.

A

Type I ketosis occurs as a result of undersupplying energy at peak lactation.

19
Q

____ _ ketosis occurs as a result of excessive fat mobilisation around calving.

A

Type II ketosis occurs as a result of excessive fat mobilisation around calving.

20
Q

What is pregnancy toxaemia? Which species is it seen in?

A
  • Pregnancy toxaemia (a.k.a. pregnancy ketosis)
  • Same idea as Type I ketosis = animal in negative energy balance
  • Seen in sheep and occasionally in beef cattle
21
Q

When do we see pregnancy toxaemia?

A
  • Before lambing/calving as this is when peak energy demand occurs (rather than during lactation as for dairy cattle)
22
Q

What is Twin Lamb Disease?

A

Twin Lamb Disease = Pregnancy toxaemia

23
Q

Clinical signs of pregnancy toxaemia

A
  • Often similar to hypoCa
  • Off-feed
  • Dull
  • Depressed
  • Nervous signs e.g. blindness
  • Death
24
Q

True/false: sporadic cases of pregnancy toxaemia may be caused by underlying disease e.g. poor teeth, lameness.

A

True
e.g. dental disease -> eating less -> negative energy balance

25
Q

Prevention of pregnancy toxaemia

A
  • Avoid management changes prior to lambing/calving especially in diet
  • New diet can put sheep off their food -> reduced DMI -> Negative energy balance and pregnancy toxaemia
  • Stay on top of prevention of other diseases e.g. conjunctivitis spread by flies could send sheep off food
26
Q

What are some differential diagnoses for the recently calved cow who is off-food?

A
  • LDA
  • Ketosis
  • Metritis
  • Mastitis

Subclinical ketosis is a risk factor for all of these!

27
Q

You diagnose a cow with ketosis. After careful clinical exam, she has no other concerning findings (e.g. no ping on either left or right side). What might you warn the client about?

A
  • Possibility of the cow developing an LDA secondary to ketosis
  • This doesn’t mean you missed it on today’s clinical exam! But it is wise to warn the client that this is a possibility.
28
Q

What happens when camelids are in negative energy balance?

A
  • Camelids get ketosis like a cow and hyperlipidaemia like a horse
  • They don’t store fat well in the liver, so shove it into their blood and get hyperlipidaemia
  • Hepatic lipidosis can occur in extreme cases and it is usually fatal
  • They are almost always hyperglycaemic when tested but this is normal for camelids
  • Camelids can also get pregnancy toxaemia like a sheep
29
Q

You suspect a camelid to be in negative energy balance. What do you measure?
a) blood NEFAs
b) blood triglycerides
c) blood BHB

A

b) blood triglycerides not NEFAs; camelids don’t store fat in the liver
You can also check for ketones

30
Q

True/false: in the normal cow, glucose arrives in the liver from the rumen.

A

False
Any glucose in the rumen will be taken up by rume bacteria.
Glucose must be produced in the liver by gluconeogenesis

31
Q

When body fat is mobilised, NEFAs are produced. What is needed in order for complete oxidation of NEFAs in the liver?

A

Glucose is needed

32
Q

Type I ketosis occurs as a result of…

A

undersupplying energy at peak lactation.

33
Q

Type II ketosis occurs as a result of…

A

excessive fat mobilisation at calving.

34
Q

Diagnostic testing for hepatic lipidosis

A
  • Look for ketones as with ketosis (blood, urine, milk)
  • Blood NEFA
  • Look for evidence of liver damage (AST, GGT; liver enzymes)
  • Assess fat in liver e.g. biopsy, necropsy
35
Q

When might we measure NEFAs rather than BHB to assess NEB/ketosis?

A
  • BHB - tells us about current energy supply/demand - useful in fresh calved cows
  • NEFAs - transport form of fat, indicates fat mobilisation - especially useful for transition cows (late dry period)

FARM ANIMAL (56 decks)

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