Disorders of energy metabolism in dairy cattle Flashcards

1
Q

Ketosis is either

A

primary disease or occurring due to other diseases causing anorexia and called secondary ketosis.

Basically, ketosis is characterized as lack of energy in the organism. Cow starts to use ketone bodies as a secondary energy source, because glucose is available only for milk production.

Hence, ketosis can be diagnosed with blood sample, where glucose level is decreased, and ketone body level is increased.

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2
Q

Clinical ketosis is treated with

A

intravenous glucose or dextrose infusion and subclinical ketosis with oral propylene glycol.

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3
Q

Primary ketosis occurs typically at what point of a cows life?

A

at early lactation (6-8 weeks after
parturition aka 50-60 days after calving)

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4
Q

Secondary ketosis occurs typically at what point?

A

Sick cow → usually anorexic → no food = no energy → secondary ketosis.

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5
Q

The main predisposing factor for development of primary ketosis is

A

poor adaption to milk production
during transition period (3 wk before parturition – 3 wk after parturition).

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6
Q

Cellulose → produces which acids?
Starch → produces which acids?

A

Cellulose → butyric and acetonic acid
Starch → propionic acid

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7
Q

Butyric and acetonic acid are used for..?
Propionic acid is used for..?

A

Butyric and acetonic acid are used as
primary energy source.

Propionic acid is used for glucose
production – most of the glucose will
be used for formation of milk lactose.

(Cellulose → butyric and acetonic acid
Starch → propionic acid)

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8
Q

what percentage of glucose produced in a cow will be used for lactation?

A

70-90 % of glucose produced

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9
Q

Why do cow have a reduced dry matter intake around calving and during the transition period to peak lactation?

A

this is an unavoidable physiological phenomenon

if dry cows get too much feed when dry, their “satiety settings” get set to “don’t eat so much” and remain at those settings after parturition because the settings can’t change overnight even though they are suddenly lactating.

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10
Q

What leads to low insulin levels?

A

hypoglycemia leads to hypoinsulinemia which in turn triggers lipolysis

NEFAs are produced during lipolysis of adipose tissue

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11
Q

NEFAs produced from body fat are used in three ways in the organism. What are these?

A
  1. They are oxidised to energy in the muscles and liver. (If this is incomplete, ketone bodies are produced)
  2. They are re-esterified to triacylglycerol in the liver.
  3. They are used in milk fat synthesis in mammary gland.
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12
Q

Molecule that causes fatty liver?

A

triacylglycerol or TAG

The cow liver cannot process, package (VLDL) and send it off fast enough.

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13
Q

What increases lipolysis?

A

decreased insulin concentrations in blood

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14
Q

Negative energy balance always causes metabolic stress which in turn predisposes to… (3)

A

inflammatory responses (oxidative stress from free radicals)

infections (e.g. mastitis)

reproduction disorders (decreased fertiltiy + metritis etc.)

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15
Q

What does insulin resistance occur in ketosis?

A

It is not known actually.

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16
Q

Describe how cows can acquire ketone bodies from external sources.

A

Exogenous source such as badly fermented silage may contain butyric acid which is a ketone body precursor.

Is silage preservation goes wrong the pH of the silage can remain too high (>4.0) and butyric acid is produced instead of lactic acid which is what we want.

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17
Q

Cow related factors to contribute to development of ketosis? (3)

A

days in milk
BCS
milk yield

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18
Q

Herd related factors to contribute to development of ketosis? (4)

A
  • Dry cow management
  • Dry cow feeding strategy
    (above are most important for herd level prevention)
  • Sick cow pen management
    (if this is poorly managed, the sicknesses won’t be caught in time)
  • Fresh cow management
    (feeding issues in recently freshened cows)
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19
Q

Cows freshening with a BCS of how much are more disposed to ketosis?

A

> 3,5

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20
Q

dextrose vs glucose

A

Glucose refers to a sugar with several chemical forms. One of the forms is dextrose (also called dextroglucose), which is found in fruit, animal tissue, and other natural substances. In use, typically dextrose refers to this sugar when found in food, while glucose refers to it when it’s in the bloodstream.

Either one may be administered iv to cows suffering from ketosis. Depends on what is available in your region.

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21
Q

When evaluating cow BCS score - at the side view, what are you looking at exactly?

A

pins
hooks
thurl &
short ribs

22
Q

When evaluating cow BCS score - at the rear view, what are you looking at exactly?

A

hooks
pins
thurl

short ribs &
sacral ligament +
tailhead ligament

23
Q

When evaluating cow BCS score, where do you start?

A

Evaluate the angle between the hooks and pins from the side first.

If the angle forms a V, the cow has a BCS of 3 or lower.

If the angle forms a U, the BCS is more than 3.

If its not clear from the side, move to the rear and observe the same angle.

24
Q

Looking only at the hook and pin angle - what would you say the BCS is?

A

> 3

If its not clear from the side, move to the rear and observe the same angle.

25
Q

2nd step of BCS evaluation after hooks-and-pins angle evaluation.

A

From the rear, evaluate the shape of the hooks.

Are they angular or are they rounded?

Depending on what the hooks-and-pins angle was:
cows with a BCS of 3 or less

cows with a BCS >3

26
Q

A cow with a V- hooks-and-pins angle (BCS of 3 or less) has rounded hooks from rear view.

What is the honed BCS score now?

A

BCS = 3

27
Q

A cow with a V- hooks-and-pins angle (BCS of 3 or less) has angular hooks from rear view.

What is the honed BCS score now?

A

BCS = 2.75 or less

28
Q

3rd step of BCS evaluation after hooks-and-pins angle evaluation and hooks shape eval. ?

A

Are the pins padded or not?

This criteria is assessed in conjunction with what you’ve already assessed.

29
Q

Explain the withers pinch.

A

One common diagnostic test for traumatic reticuloperitonitis (or other abdominal pain) is the withers pinch test, in a normal cow if you pinch their withers the cow should dip and perform a shrug like action.

In a cow with hardware disease or other, they will be reluctant to perform the dip, or will grunt whilst dipping; indicating pain.

Optional: auscultate the trachea at the same time someone else does the withers pinch so you can detect a groan indicating pain.

30
Q

succussion =

A

ballottement and auscultation at the same time

31
Q

How do you a refine a BCS score of greater than 3?

A

You assess how visible the sacral and tailhead ligaments are.

32
Q

Incidence of clinical ketosis at the herd level is 2-15% → Just the tip of the iceberg.

Herd presentation of ketosis in fresh cows is due to 3 main factors:

A
  1. Managemental problems in silage preserving process → high intake of butyrate → FIX THE SILAGE PRESERVING PROCESS.
  2. Cows in very poor BCS with poor quality feeds → limited capacity for gluconeogenesis, decreased dry matter intake and rumen fermentation rates → starvation → FIX THE FEED QUALITY AND
    COW BODY CONDITION SCORE.
  3. Cows with excessive BCS with feeds high in energy (especially in the dry period) → excessive lipid mobilization → decreased
    dry matter intake → FIX THE DRY COW FEEDING MANAGEMENT.
33
Q

Optimal cow body condition score (BCS) at the calving is?

and for heifers?

A

Optimal cow BCS at the calving is 3.0

for heifers 3.25

34
Q

Obese cows have higher chances of getting problems. Why?

A

In obese cows (BCS > 3.75) lipid mobilization is increased compared to cows in optimal BCS.

Also obese cows have smaller dry matter intake (DMI) in early lactation period.

Hence, in early lactation, when cows are anyway in NEB, obese cows eat less and have greater adipose tissue usage for energy source.

This leads to greater risk of having fatty liver and ketosis.

35
Q

Main 2 Clinical signs of ketosis that are noticed first are:
Anorexia
Drop in milk yield

Other clinical signs of ketosis are..? (4)

A

Dehydration (metabolic acidosis causes this)
Dry feces (dehydration causes dry feces)
Weight loss - / +
Smell of acetone (volatile molecule excreted via lungs)

= CLINICAL KETOSIS

36
Q

Nervous form of ketosis – why do nervous signs occur?

A

When the hypoglycemia is severe enough that there isn’t enough glucose for the brain.

The brain can’t manage with only ketone bodies for long.

37
Q

Signs of nervous ketosis. (7)

A

◦ Pica
◦ Salivation

◦ Ataxia
◦ Head pressing

◦ Blindness
◦ Tetany
◦ Aggression

38
Q

Golden standard for diagnosis of ketosis is

A

blood BHB measurement with enzymatic laboratory test.

Prefered sample type is whole blood or
plasma.

Normal blood ketone body level is <1
mmol/l for lactating dairy cows (max 1.2).

(Some tests measure acetoacetate but its not as stable as BHB in blood.)

39
Q

When should you use a cow-side ketosis test since blood analysis is gold standard but…?

A

When a single cow is considered ketotic or when you’re rechecking a cow.

NB Specificity is low, false-positive results are not uncommon.

Use especially when you need to confirm a cow to be negative - ruling diagnoses out.
Re-check any positives cows with another type of ketosis test.

40
Q

3 main principles in ketosis treatment:

A
  1. Provide glucose → 500 ml of 50% dextrose or 30-40% glucose IV which causes transient hyperglycemia
  2. 300 g (200-500 g) propylene glycol PO per day for 5 days.
  3. Stimulate gluconeogenesis using corticosteroids → 0.04 mg/kg dexamethasone IM one time.

Decrease lipolysis in general.

41
Q

How do steroids help in ketosis treatment? (4)

A

They stimulate gluconeogenesis.

They decrease milk yield which will help decrease energy requirements.

They increase appetite.

They cause insulin resistance which will cause the hyperglycemia to last for longer which will aid in stopping lipolysis.

42
Q

Dose and route for dexamethasone in ketosis treatment.

A

0.04 mg/kg dexamethasone IM one single time

e.g. 600 kg cow would get 24 mg

43
Q

Dexamethasone is NOT used in cows with what type of ketosis?
Why?

A

secondary ketosis

In case the animal needs an operation e.g. in L/RDA which causes secondary ketosis.

Side effects of steroids:
lower immunity
longer wound healing times

44
Q

Treatment of subclinical ketosis?

A

usually propylene glycol PO 300g / day for 5 days is sufficient
(but produces sulfuric acids so not for longer than 5 days!)

Glycerol may be used in place of propylene glycol but its not quite as effective so its double-dose and longer course.

45
Q

Why is Vit B12 / cobalamin sometimes used in ketosis treatment?

A

because its needed in rumen microbe function and thus believed to aid in glucose production

However, this is not evidence based medicine.

46
Q

Incidence of fatty liver in the early lactation period.

A

All dairy cows

47
Q

How to diagnose fatty liver disease?

A

Diagnosis for verifying fatty liver disease is difficult in practice.

◦ Liver biopsy and histologic/chemical diagnosis confirm the diagnosis – but may not be of value in practice.

In reality - we rely on clinical signs and existence of negative energy balance.

Blood sample is an indirect diagnosis tool.
◦ NEFAs > 600 μmol/l for prolonged period → TAG starts to accumulate in the liver.

48
Q

Treatment of fatty liver disease?

A
  1. Decrease lipolysis – propylene glycol PO
  2. Provide nutrients – feed with the rumen content of another cow 5-10 l (this “wakes up” the rumen and transplants healthy microbes)
  3. Fluid therapy
  4. Decrease usage of nutrients – decrease
    milking.
49
Q

Fatty liver leads to (3)

A

poor immunity (eg. noticed when treatment of mastitis/metritis is not effective)

poor milk yield

liver cannot modify toxins

These are indirect clinical signs of fatty liver.

50
Q

Mild vs severe cases of fatty liver.

A

MILD CASE:
Decreased body condition + increased ketone body levels

SEVERE CASE:
Anorexic, increased ketone body levels
Downer cow
Hepatic encephalopathy -> liver coma

51
Q

Prevention of fatty liver disease. (4)

A
  1. Optimal body condition score
  2. NO STRESS
  3. Treat other diseases during transition period effectively.
  4. Propylene glycol/glycerol
52
Q

This info will be on the exam.

A