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540 (cow class) > Hyperketonemia > Flashcards

Hyperketonemia Flashcards

1
Q

What is the numerical value for defining clinical ketosis?

A

BHBA ≥ 3.0 mmol/L

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2
Q

what is the numerical value for defining sub-clinical ketosis?

A

BHBA ≥ 1.2 mmol/L - ≤ 2.9 mmol/L

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3
Q

What is type 1 ketosis?

A

occurs later in lactation period - lack of feed intake to meet negative energy requirements (primary ketosis)

insufficient glucose from not eating

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4
Q

what is type 2 ketosis?

A

occurs early in lactation period - fat infiltration in liver impairs hepatic gluconeogenesis (secondary ketosis)

insufficient glucose from not eating because of another condition

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5
Q

What is the numerical value for defining hyperketonemia? And why do we use this instead of clinical/subclinicla ketosis?

A

BHBA ≥ 1.2 mmol/L

C/S not based on BHBA cut-point, so the distinction doesn’t really matter

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6
Q

What is the pathophysiology of hyperketonemia?

A
  1. hypoglycaemia
  2. decreased insulin
  3. increased glucagon
  4. activation of hormone-sensitive lipase (HSL) [prolactin also does this]
  5. acceleration of lipolysis in adipose tissue
  6. large increase in albumin-bound FFAs and NEFAs
  7. beta oxidation of FFAs accelerated
  8. coenzymes for ATP synthesis build up
  9. acetyl CoA accumulates, diverted into other reactions (esp ketone body formation) bc there is too much for TCA cycle
  10. FFAs exceeding liver’s capacity for metabolization are re-esterified to triglycerides
  11. Triglycerides exported or accumulate in liver (fatty liver)
  12. liver function compromised
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7
Q

why is there decreased insulin with hypoglycaemia with hyperketonemia?

A

the mammary doesn’t require insulin for glucose uptake. low insulin adds glucose available for lactose production, which further decreases glucose for peripheral use

it’s a vicious cycle

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8
Q

what process does increased NEFA in the blood support?

A

fat going to colostrum and milk

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9
Q

why is there lipolysis in the periparturient/parturient time frame?

A

glucose is spared for fetal development

lipolysis provides NEFAs as a source of fuel for organs (esp liver) –> euglycemia maintained by this

NEFA elevation in blood required for increased fat conc of colostrum and milk

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10
Q

What are the risk factors for hyperketonemia?

A
  • selection for increased milk production has resulted in cattle that lose greater BCS after calving
  • jersey > Holstein > ayrshire > brown Swiss
  • primiparous > multiparous
  • limitation of DMI & poor management
  • previous ketosis
  • ≥24 months at first calving
  • increased pre-calving NEFA
  • increase BCS
  • increase calving to conception interval
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11
Q

Why is hyperketonemia bad?

A

cows with hyperketonemia are at increased risk for:
- adverse health conditions (displaced abomasum, metritis, clinical ketosis)
- early culling
- decreased milk prod
- increased calving to conception intervals

these can cause huge cost increases for the producers

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12
Q

What are the prevalence and incidence ranges for hyperketonemia?

A

P: 10-20%
I: 30-40%

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13
Q

What are the clinical signs of hyperketonemia?

A

decrease in DMI (usually 1st sign)
decrease in milk prod
lethargy
dry firm faces
rapid and severe loss of BCS
nervous ketosis (rare)

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14
Q

what are the C/S of nervous ketosis?

A

Pica, abnormal licking/chewing, aggression, ataxia or gait abnormalities, excessive salivation, apparent blindness

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15
Q

How can you detect ketones in a cow you suspect has hyperketonemia?

A

Lab BHBA test on serum
sweet ketone odour (smell)
urine acetoacetate
milk BHBA
Precision xtra (blood glucose and ketone monitoring, same thing diabetic people use)

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16
Q

what is important to remember when running BHBA tests on serum?

A

BHBA can vary in blood and milk day to day, as well as during the day (lowest at night, highest few hours post feeding)

17
Q

why should you not sample from milk vein when testing ketones?

A

mammary uses BHBA’s so you’ll get an artificially low #

also never poke into the milk vein in general

18
Q

When should you test for subclinical ketosis?

A

3-5 days in milk (DIM)

19
Q

Tell me the treatments options for hyperketonemia

A
  • dextrose
  • glucocorticoids
  • insulin
  • vitamin B12 ± phosphorus
  • propylene glycol
20
Q

what is the theory behind treating hyperketonemia with dextrose?

A

cows with hyperketonemia have hypoglycaemia –> tx hypoglycaemia to tx hyperketonemia

21
Q

what are the concerns with tx hyperketonemia with dextrose?

A

spike in blood glucose –> renal excretion of excess glucose wastes electrolytes

22
Q

when should you tx hyperketonemia with dextrose?

A

first line only in severe cases (ex. nervous ketosis)

23
Q

if you tx hyperketonemia with dextrose, what should you do?

A

follow up with other treatments for long term
limit tx to 250mL of 50% dextrose
ALWAYS follow up with oral propylene glycol

24
Q

what is the theory behind treating hyperketonemia with glucocorticoids?

A

they promote insulin resistance, hyperglycaemia, & hyperlipidemia, favour protein catabolism, decrease milk yield (=decrease need for E), increase appetite

25
Q

what are the concerns with tx hyperketonemia with glucocorticoids?

A

short term effects are good, but long term (past 1 week) impairs cow’s metabolic state and ability to control hyperketonemia

26
Q

when should you tx hyperketonemia with glucocorticoids?

A

NEVER!

27
Q

when should you use insulin to treat hyperketonemia?

A

never (more research is needed, currently not recommended)

28
Q

what is the theory surrounding using B12 and phosphorus for the treatment of hyperketonemia?

A

B12 supports activity of enzymes in TCA cycle = increase TCA cycle efficiency = increase gluconeogenesis

P acts similarly

29
Q

what is the recommendation for using vitamin B12 and P to tx hyperketonemia?

A

perhaps useful, but insufficient evidence to support routine use. don’t use alone, but could be helpful if used with another tx

30
Q

what is the theory behind using propylene glycol to treat hyperketonemia?

A

converted to propionate in the rumen, which stimulates insulin release and gluconeogenesis, or absorbed directly and used in the TCA cycle where it increases oxidation of Acetyl CoA and stimulates gluconeogenesis

31
Q

according to Dr. Stover, what is “the shit” for treating hyperketonemia?

A

propylene glycol

32
Q

what is the recommendation for using propylene glycol to tx hyperketonemia?

A

must be oral bolus to get insulin release
300 g = base tx, 5 days, q 24 h

33
Q

what is the recommendation for using combo tx of dextrose and propylene glycol for treating hyperketonemia?

A

not recommended, unless super severe (and only use dextrose once)

34
Q

true or false: hyperketonemia is an individual cow disease

A

false. it is usually a herd issue (more than 1 cow experiencing hyperketonemia, maybe not all clinical) - because it has lots to do with management

35
Q

true or false: negative energy balances are always abnormal for cows and should be treated as such.

A

false. NEBs are a normal physiologic condition in cattle during the periparturient period

36
Q

how important is early detection for hyperketonemia?

A

very important
early ID with appropriate tx and prevention measures can help increase favourable outcomes and limit dz events

37
Q

What are the ways you can prevent hyperketonemia?

A
  • efficient breeding programs
  • BCS management (ideal is 3-3.5 @ parturition)
  • dry off/transition diets balanced
  • Monensin supplementation
  • pre-calving monitoring
38
Q

how do you perform pre-calving monitoring?

A

gold standard: NEFA b/t 2-14 days pre-partum

can use precision xtra BHBA monitoring for cheaper option

39
Q

compare/contrast using NEFA vs BHBA for pre-calving monitoring for hyperketonemia.

A
  • BHBA quick + cowside, inexpensive - should be used as primary monitoring tool
  • NEFA gold standard, but expensive and logistically more difficult - use if herd issues suspected but without BHBA elevations

540 (cow class) (32 decks)

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