L14: Ketosis Of Dairy Cows (Risco) Flashcards

1
Q

3 ketone bodies

A

BHBA
Acetoacetate
Acetone

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2
Q

Energy balance =

A

(NE dmi - NE m - NE I) + NE bwt

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3
Q

Peak milk yield occurs when

A

4 weeks PP

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4
Q

Peak DMI occurs when?

A

8 weeks PP, and is about 3.5% of BW

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5
Q

Why does cow go into negative energy balance PP?

A

Milk yield peaks before DMI peaks, so fat is mobilized to make up deficit

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6
Q

Propionate is converted to what via the TCA cycle?

A

Oxaloacetate, then glucose

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7
Q

Ketone body precursors

A

NEFAs from adipose tissue stores –> FFA –> acetate –> Acetyl CoA –> acetoacetyl CoA –> acetoacetate –> acetone and BHBA

-acetyl CoA should normally go into TCA cycle to make glucose, but if oxaloacetate is low, it instead goes to form ketone bodies**

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8
Q

Ketosis occurs when:

A
  • absorption/production of ketone bodies is greater than their use for energy source
  • NEFAs are high
  • ketone bodies are high
  • blood glucose is low
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9
Q

Most common ketone body used to diagnose SUBCLINICAL ketosis and concentration cutoffs***

A

BHBA

Lower threshold concentration of BHBA for SCK is 1.2 mmol/L, so SCK = 1.2-2.8 mmol/L***

Clinical signs develop when >3.0 mmol/L***

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10
Q

Sequelae of SCK

A
  • inappetance w/ wt. loss
  • reduced fertility and milk production
  • increased risk for LDA and herd removal
  • immunosuppression (predisposing to metritis and mastitis)
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11
Q

Clinical ketosis manifests as:

A
Acute onset of bizarre neuro signs:
-excessive grooming, licking
-head-pressing, ataxia, wandering, leaning
-apparent blindness
-hyperesthesia, bellowing, aggression
BHBA > 3.0 mmol/L
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12
Q

Clinical/nervous ketosis Ddx

A

Hypermagnesemia
Rabies
Acute lead poisoning
Listeriosis

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13
Q

Median time for resolution of SCK

A

5 days

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14
Q

Average SCK incidence rate (in NY)

A

43%

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15
Q

Incidence of SCK =

A

(# new cases of SCK during the risk period)/(# cows that completed the risk period)

  • must measure BHBA conc. Twice
  • approximately 2.2 x the prevalence
  • better than prevalence at estimating the impact of SCK in a dairy herd*
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16
Q

Prevalence of SCK =

A

The proportion of cows with BHBA concentration between 1.2-2.9 mmol/L at a given point in time (7-14 days PP)

  • doesn’t require repeat measurements
  • not as good as incidence at estimating impact over time
17
Q

Risk factors for ketosis

A
  • age: older cows
  • BCS 4 or higher
  • BCS loss of >1 during first 60 DIM**
  • lower DMI due to dz, temp change, inadequate housing, dietary factors
18
Q

Clin path of ketosis

A
  • BHBA >1.2 mmol/L
  • hypoglycemia (20-40 mg/dl)
  • liver enzymes may be elevated w/ lipidosis
  • mild electrolyte abn. If off feed
  • stress leukogram
  • increased NEFAs
19
Q

Dx of ketosis

A
  • hepatic lipidosis at necropsy

- elevated ketone bodies in plasma, urine, and/or milk

20
Q

Which ketone bodies detected in urine?***

A

Acetoacetate

Acetone

21
Q

Most common ketone body found in urine

A

Acetoacetate

22
Q

Which ketone body can be detected in milk?***

A

BHBA

23
Q

Which ketone bodies detected in blood?***

A

BHBA
Acetone
Acetoacetate

24
Q

Which ketone body used to determine if ketosis is clinical?***

A

BHBA

25
Q

Precision Xtra blood test has highest sensitivity and specificity in detecting subclinical ketosis (better than Ketolac and Ketostix)

A

:)

26
Q

Treatment goals for ketosis

A
  • restore normal DMI to resolve hypoglycemia, hyperketonemia and break the cycle that leads to excess ketogenesis
  • ID and tx underlying conditions
27
Q

Glucose precursors

A
IV dextrose (an isomer of glucose)
-causes a transient increase in glucose (most lost in urine)
Propylene glycol
Propionate
Glucocorticoids
Insulin
28
Q

Oral propylene glycol as tx for hypoglycemia

A
  • use 8-14 oz. drench SID-BID 3-5 days
  • rumen motility required for absorption
  • metabolized in liver to glucose
  • toxicity can –> appetite suppression, diarrhea
29
Q

Glucocorticoids as tx for hypoglycemia

A
  • shifts glucose distribution and utilization by increasing blood glucose and decreasing milk production by less uptake
  • stims. Appetite
  • don’t use in pregnant cows or cows w/ concurrent infectious dz
  • may not be good to use if hepatic lipidosis present (controversial) - may increase lipolysis and NEFAs
  • dexamethasone or isoflupredone acetate used
  • must administer dextrose in conjunction
30
Q

Caution with isoflupredone acetate for ketosis tx

A

May increase hypokalemia due to mineralocorticoid activity

-if used, only use once

31
Q

Rank txs for ketosis

A

Best: propylene glycol
Ok: dextrose
Worst: steroids

32
Q

Prevention of ketosis

A
  • maximize DMI in transition cows
  • avoid over-conditioning late lactation cows
  • niacin fed in transition rations to decrease blood ketone lvls
  • propylene glycol administered prophylactically to high-risk animals
  • monensin increases production of propionate in the rumen (can decrease SCK in early lactation by 50% if given during late dry period)
  • monitor incidence of SCK 3-16 days PP
  • adequate bunk space
33
Q

Ketosis

A

Abnormally elevated concentrations of circulating ketone bodies

  • can be clinical or subclinical (most subclinical**)
  • during early lactation most common