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LA Clinical Medicine > Unit 1 - Metabolic Disease > Flashcards

Unit 1 - Metabolic Disease Flashcards

1
Q

What causes ketosis in dairy cattle?

A

There is an increase in energy requirements and inadequate DMI (dry matter intake)

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2
Q

What causes an increase in energy requirements in dairy cattle that can lead to ketosis?

A

lactogenesis

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3
Q

What is the primary cause of a negative energy balance in pregnancy toxemia cases?

A

The actual process of making the baby

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4
Q

When does ketosis typically occur in dairy cattle?

A

Typically recently post parturient

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5
Q

What will the dairy likely first recognize in a cow that has ketosis post partum?

A

That the cow is having decreased milk production when it should be increasing

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6
Q

When does pregnancy toxemia typically occur?

A

2-6 weeks prepartum

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7
Q

What clinical signs are associated with ketosis?

A

Loss of appetite, decrease in milk production, and a more profound weight lost than normal

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8
Q

What clinical signs are associated with pregnancy toxemia?

A

Loss of appetite, separation from flock/herd, limb edema, and recumbency

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9
Q

What are the possible treatments for ketosis?

A

Propylene glycol, corticosteroids, IV dextrose

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10
Q

Which ketosis treatment should not be used for pregnancy toxemia and why?

A

Corticosteroids should not be used because they can induce parturition or abortion
They should only be used if you want to induce

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11
Q

What happens if you give too much propylene glycol in ketosis treatment?

A

You can kill off the rumen microbes

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12
Q

If you choose to use a corticosteroid, which should you use to treat ketosis?

A

Dexamethasone

Note: corticosteroids are not recommended because they drive gluconeogenesis and decrease milk production

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13
Q

Why shouldn’t Predef-2X be used to treat ketosis?

A

Because it is a mineralcorticoid and not a glucocorticoid. This is bad because it can influence the K levels

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14
Q

You are on a farm call and see a market value cow that is showing signs of ketosis. How would you confirm your suspicion?

A

Check blood BHBA levels (if you can’t you cant try urine or milk)

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15
Q

You are on a farm call and see a market value cow that is showing signs of ketosis. The blood BHBA is indicative of ketosis. What would you treat this cow with?

A

Propylene glycol in a paste or via a stomach tube - 300 mL a day for 3-5 days

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16
Q

You are on a farm call and see a high genetic value cow that is showing signs of ketosis. How would you confirm your suspicion?

A

Check blood BHBA levels (if you can’t you cant try urine or milk)

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17
Q

You are on a farm call and see a market value cow that is showing signs of ketosis. The blood BHBA is indicative of ketosis. What would you treat this cow with?

A

IV dextrose CRT

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18
Q

What is the best testing method to monitor for subclinical ketosis (and just ketosis in general)?

A

Blood BHBA

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19
Q

What animals should be tested (stage of production) when using BHBA to monitor a herd for subclinical ketosis and how many?

A

Sample 12 animals that are in early lactation and less than 35 days in milk (DIM)

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20
Q

When should you test the blood BHBA levels in relation to eating when you are monitoring for subclinical ketosis?

A

4-5 hours post eating

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21
Q

What is the alarm level for subclinical ketosis (with BHBA)?

A

If 10% of the cows tested are above the threshold - reevaluation needs to occur at this point

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22
Q

How do you know a cow has subclinical ketosis (with BHBA)?

A

If the blood BHBA level is >1.2, but they are showing no clinical signs

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23
Q

What is BHBA level indicates hyperketonemia?

A

Anything greater than 1.2

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24
Q

What does BHBA stand for?

A

Beta-hydroxybutyric acid - makes up 80% of the ketones

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25
Q

What are cows with subclinical ketosis at a higher risk for?

A

3x increased risk for LDA or clinical ketosis

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26
Q

What animals should be tested (stage of production) when using NEFA to monitor a herd for subclinical ketosis and how many?

A

Sample 7-12 animals 2-14 days before calving

Make sure to remove animals that have calved within 72 hours post-sampling

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27
Q

What is the alarm level for NEFA testing when you are looking for subclinical ketosis in a herd?

A

10% of the herd is above the cutpoint

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28
Q

What is the cutpoint for NEFA for subclinical ketosis?

A

> 0.4 mEq/L

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29
Q

When should NEFA testing occur in relation to feeding?

A

just prior to feeding

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30
Q

True or False: NEFA samples should be kept warm.

A

False - they need to be kept cool or frozen

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31
Q

What is the mechanism of action of propylene glycol in treatment of ketosis?

A

It is a precursor for proprionate which is an important volatile fatty acid that is metabolized to glucose in the liver

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32
Q

What is the mechanism of action of IV dextrose in treatment of ketosis?

A

It bypasses the need for the liver to convert proprionate into glucose, and instead the glucose is in the blood stream

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33
Q

What risk is associated with using IV dextrose to treat ketosis?

A

You run the risk of inducing other electrolyte abnormalities in order to make the ketosis better

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34
Q

What is the mechanism of action of corticosteroids in the treatment of ketosis?

A

They can increase glucose levels by reducing the action of insulin

35
Q

What is the mechanism of action of niacin in the treatment of ketosis?

A

It plays an important role in the transfer of propionate into the TCA cycle (this reduces the amount of fat in the liver)

36
Q

Why is an increase in glucose so important in the treatment of ketosis?

A

When there are NEFA in the liver they can take two pathways, one results in the formation of ketones via oxidation and the other results in the formation of triglycerides via esterification. If there isn’t enough glucose, the oxidation pathway is preferred and we get more ketones. SO when we are treating for ketosis we need the NEFAs to be converted into triglycerides and not ketones, therefore we need more glucose

37
Q

You have a cow that is non-responsive to treatment, obese, and post-partum. What is your top differential?

A

Hepatic lipidosis

38
Q

What confirmatory tests can be done in ruminants for hepatic lipidosis?

A

Diagnostic ultrasound and percutaneous liver biopsy

39
Q

How is hepatic lipidosis treated?

A

Oral propylene glycol or IV glucose if possible

Insulin can be used in some cases

40
Q

Why are ruminants at a higher risk of developing hepatic lipidosis than other species (like small animals)/?

A

Because they do not readily move fats out of the liver like other species do

41
Q

How are ruminants and small animals different in regards to their risk/predisposing factors in developing hepatic lipidosis?

A

Emaciated small animals are at a higher risk of hepatic lipidosis
Well-conditioned or over conditioned ruminants are at a higher risk of developing hepatic lipidosis

skinny cat, fat cow

42
Q

What role does preparturient fatty infiltration of the liver play in the development of ketosis?

A

A negative energy balance has started prior to calving and resulted in the fatty infiltration into the liver. This results in decreased liver function making the negative energy balance even worse

43
Q

Why is glucose availability important in the treatment of hepatic lipidosis in ruminants?

A

It can provide continuing energy and induce an insulin/glucagon ratio that will decrease hormone-sensitive lipase mobilization of fatty acids and stimulate production of VLDLs (lipoproteins). Lipoproteins are what carry triglycerides, cholesterol, and other fats around the body (thus out of the liver)

44
Q

How can insulin treat hepatic lipidosis?

A

It can induce the insulin/glucagon ratio that will decrease hormone-sensitive lipase mobilization of fatty acids and stimulate production of VLDLs

45
Q

How can proprionate salts treat hepatic lipidosis?

A

They can change the volatile fatty acid profile and increase proprionate which is needed for gluconeogenesis

46
Q

How do other periparturient disease processes such as metritis, LDA, and mastitis play a role in the development of metabolic disease?

A

These disease processes can cause a negative energy balance and thus fat mobilization and ketone production in the cow which will result in the development of a metabolic disease

47
Q

How does metabolic disease predispose animals to other disease processes?

A

They leave the animal’s defenses and immune system weak which ultimately makes them vulnerable to disease processes

48
Q

What causes hypocalcemia?

A

metabolic alkalosis

49
Q

What is the pathophysiology of hypocalcemia?

A

If we have a high potassium diet we will have a decreased presence of hydrogen ions which results in metabolic alkalosis. The PTH receptor protein is then altered and its ability to bind to PTH is weakened. PTH is needed for calcium to be mobilized out of the bones, into the blood, and then integrated into the milk.
The PTH receptor has a magnesium cofactor as well so if we are low on magnesium the receptor will not recognize the PTH

50
Q

When does hypocalcemia manifest in dairy cattle?

A

after parturition

51
Q

When does hypocalcemia manifest in beef cattle and small ruminants?

A

Prior to or after parturition

52
Q

What clinical signs are associated with hypocalcemia?

A 
Reduced smooth muscle contraction 
Reduced feed intake
Impaired immune cell function
Recumbency with a bent neck
Fine muscle fasciculation 
Muffled heart beat due to poor contraction
Tachycardia
Ambient temperature
53
Q

How/Where does reduced smooth muscle contraction manifest in cases of hypocalcemia?

A

Flaccid uterus, decreased rumination, bloating of the abomasum, relaxed teat sphincter, recumbency, decreased fecal output, and bloat

54
Q

What can cause hypomagnesemia?

A

lactation demands and lush pasture

55
Q

When does hypomagnesemia manifest?

A

When on pasture or in early lactation

56
Q

What can exacerbate hypomagnesemia?

A

stressors

57
Q

What clinical signs are associated with hypomagnesemia in cows?

A

hyperexcitability, tetany, convulsions, sudden death, reduced feed intake, muscle twitching, chomping of the jaws, frothy salivation, head arched, rapid loud heartbeat, hyperthermia from muscle activity, nystagmus

58
Q

What clinical signs are associated with hypomagnesemia in small ruminants?

A

depression, standing on their own, reluctant to move, progress to tetany and convulsions

59
Q

What causes hypophosphatemia?

A

Elevated PTH associated with hypocalcemia increases renal and salivary secretion of phosphorus

60
Q

When does hypophosphatemia occur in beef cattle and small ruminants?

A

late gestation

61
Q

When does hypophosphatemia occur in dairy cattle?

A

milking due to increased pull

62
Q

What clinical signs do beef cattle and small ruminants show when they have hypophosphatemia?

A

recumbent but alert and eating

63
Q

What clinical signs do dairy cattle show when they have hypophosphatemia>

A

unresponsive downer cattle

64
Q

What causes hypokalemia?

A

Anorexia and GI stasis

65
Q

What drug is hypokalemia associated with?

A

Isoflupredone acetate

66
Q

When is the onset of hypokalemia?

A

typically less than 60 days in milk

67
Q

What clinical signs are associated with hypokalemia?

A

flaccid paralysis, recumbency, and abnormal neck position

68
Q

Why does feeding low calcium diets in the dry period not always work well for prevention?

A

Long story short - the method is only effective if you can get Ca low enough and it is difficult to do with routine feed sources. You may just be giving them hypocalcemia without activating their osteoclasts

69
Q

How do you manage a herd’s diet in order to minimize hypocalcemia in dairy cattle?

A

i. Set dietary Na, Ca, Mg, S, and P concentrations at fixed levels. Formulate the ration to have as low a K as possible and then add Cl at a rate 0.5% lower than the K inclusion

70
Q

When should you check the urine pH in regards to feed change to an anion diet?

A

48 hours or more after the feed change - use mid stream urine

71
Q

What is the goal urine pH of holsteins? Jerseys?

A

Holsteins - 6.2-6.8

Jerseys - 5.8-6.3

72
Q

When are anion diets fed?

A

during the last 3 weeks or so prior to calving

73
Q

Which electrolyte abnormalities do you need to make sure to treat rapidly?

A

hypocalcemia and hypomagnesemia cases

74
Q

What can result if you do not treat hypocalcemia quick enough?

A

compartmental disease or crush disease

75
Q

How is hypocalcemia treated?

A

IV injection of Ca SLOWLY

Can do SQ it just takes longer

76
Q

What happens if you give IV Ca too quickly?

A

you can give the cow a fatal arrhythmia

77
Q

Why shouldn’t you use Caldex as a SQ calcium treatment?

A

It can cause an abscess

78
Q

How do you treat hypomagnesemia?

A

IV 1.5-2.25 g of Mg or rectal Mg, or Oral Mg sulfate (200-400 mL)

79
Q

How is hypophosphatemia treated?

A

Oral 50 g P supplied as 200 g monosodium phosphate drench
OR
IV 6g of P supplied as a 23 g monosodium phosphate dissolved in 1 L

80
Q

How is hypokalemia treated?

A

KCI orally at 50g/100 kg BW or IV (don’t exceed 0.5 mEq of K/kg/hr)

81
Q

What supportive care should be done when treating hypokalemia?

A

Nursing care - rolling from side to side to prevent myonecrosis, float tank, and/or treat the dehydration

82
Q

What complications are associated with downer cattle?

A

Secondary muscle and nerve damage leading to decreased blood flow and myonecrosis
Sciatic and peroneal nerve deficits
Trauma during attempts to rise - adductor rupture

83
Q

How do you treat downer cattle?

A

Correct the primary cause

84
Q

What supportive care is done for downer cattle?

A

Frequent rolling from side to side (q2-4 h), deep bedding or padding
IV fluid and maintain cardiovascular support
NSAIDs
Assistance standing or getting weight off

LA Clinical Medicine (33 decks)

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