6.2.3: Ketosis

Question 1

What does subclinical ketosis lead to an increased risk of?

Answer 1

• Clinical ketosis
• RFM
• LDA
• Metritis
• Lameness
• Mastitis
• Culling
• Death

Question 2

When (and why) does Type I ketosis occur?

Answer 2

• 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

Question 3

When (and why) does Type II ketosis occur?

Answer 3

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

Question 4

What type of ketosis is shown here?

Answer 4

Type II
Yield is increasing faster than food intake

Question 5

What type of ketosis is shown here?

Answer 5

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

Question 6

This image shows the pathophysiology of which type of ketosis?

Answer 6

Type I

Question 7

This image shows the pathophysiology of which type of ketosis?

Answer 7

Type II

Question 8

Describe the pathophysiology of Type I ketosis

Answer 8

• 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

Question 9

Describe the pathophysiology of Type II ketosis

Answer 9

• 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

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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.

Question 12

How can we treat ketosis/hepatic lipidosis?

Answer 12

• 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

Question 13

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

Answer 13

• 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.

Question 14

Diagnostic testing for ketosis

Answer 14

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

Question 15

Diagnostic testing for hepatic lipidosis

Answer 15

• 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

Question 16

When are the effects of Type I ketosis typically seen?

Answer 16

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

Question 17

When are the effects of Type II ketosis typically seen?

Answer 17

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

Question 18

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

Answer 18

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

Question 19

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

Answer 19

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

Question 20

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

Answer 20

• 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

Question 21

When do we see pregnancy toxaemia?

Answer 21

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

Question 22

What is Twin Lamb Disease?

Answer 22

Twin Lamb Disease = Pregnancy toxaemia

Question 23

Clinical signs of pregnancy toxaemia

Answer 23

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

Question 24

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

Answer 24

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

Question 25

Prevention of pregnancy toxaemia

Answer 25

* 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

Question 26

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

Answer 26

* LDA * Ketosis * Metritis * Mastitis Subclinical ketosis is a risk factor for all of these!

Question 27

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?

Answer 27

* 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.

Question 28

What happens when camelids are in negative energy balance?

Answer 28

* 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

Question 29

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

Answer 29

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

Question 30

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

Answer 30

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

Question 31

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

Answer 31

Glucose is needed

Question 32

Type I ketosis occurs as a result of...

Answer 32

undersupplying energy at peak lactation.

Question 33

Type II ketosis occurs as a result of...

Answer 33

excessive fat mobilisation at calving.

Question 34

Diagnostic testing for hepatic lipidosis

Answer 34

* 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

Question 35

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

Answer 35

* 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)