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PMVPH 4th Year > NEB > Flashcards

NEB Flashcards

1
Q

What 2 syndromes must be considered wrt NEB?

A
  • ketosis
  • fat mobilisation syndrome
    > 1* v 2*
  • eg. LDA -> 2* ketosis (but also ketosis PDF LDA!)
  • eg. Metritis -> 2* ketosis (and vice versa)
  • eg. 1* ketosis d/t insufficient nutrient supply
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2
Q

What substances are important wrt NEB?

A
  • glucose (C6)
  • C3 molecules (building Blocks)
  • kerbs citric acid cycle
  • gluconeiogensis
  • vitamins and coenzymes for gluconeiogensis
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3
Q

When will glucose levels be insufficient?

A

Early lactation

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4
Q

What initiates gluconeiogensis and lipolysis?

A

Hypoglycaemia

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5
Q

What is glucose necessary for?

A

Vital for brain and milk yield (milk yield insulin independent)
- other organs insulin dependent

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6
Q

Krebs cycle - how do ketone bodies form?

A
  • B oxidation of fatty acids releases Acetyl CoA molecules
  • these enter the Krebs cycle to join with C4 making C6.
  • if shortage of C4 ketone bodies produced to use up excess CoA
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7
Q

Consequences of

A
  • glucose deficient -> mobilisation of reserves -> BOTH fat and protein
  • fat cow skinny cow pendulum (overconditioned -> NEB -> skinny-> poor fertility -> long dry period -> overconditioned) INIEFFICIENT
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8
Q

Do cows get ketoacidosis?

A

No rare cf, cats etc.

- ketosis complex

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9
Q

What is ketosis complex?

A
  • excessive build up of ketone bodies in blood d/t accumulation of acetyl-coA
  • ketones elevation v appetite (vicious cycle)
  • also called acetonaemia.. NOT THE SAME AS ACIDOSIS
  • cows don’t develop ketoacidosis (cats do)
    > change in volatile fatty acid composition d/t high carbs etc. causes acidosis NOT ketones!!! OPPOSITE THIGNS
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10
Q

How common is ketosis complex?

A
  • post partum 2-10w after calving
  • lactation incidence 3-7%
  • sub clinical ketosis much higher esp if poorly managed
  • hypocalceamia, hypomagnesaemia, RFM, lameness, twin carrying cows
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11
Q

How can ketosis be divided?

A
  • 1* v 2*

- neurological v wasting form

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12
Q

What is 1* ketosis

A

= starvation ketosis

  • voluntary feed intake not meeting energy demands
  • excessive catabolism
  • sometime d/t specific deficient (choline, biotin, Vit B12)
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13
Q

Causes of 2* ketosis

A
  • any condition causing loss of appetite
  • LDA/RDA
  • endometriosis
  • lameness
  • mastitis (usually picked up)
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14
Q

What is the wasting form of ketosis

A
  • gradual reduction in appetite (esp refusing to eat concentrates)
  • marked loss of body weight
  • firm, dry feaces
  • occasional transient bouts of staggering (can dip in and out of NEURO form)
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15
Q

How is the neurological form of ketosis complex identified?

A
  • sudden onset abnormal behaviour
  • walk in circles, aimless wandering, head pushing, apparent blindness
  • develop depraved appetite, lick things, chewing
  • hyoeraesthesia
  • uncoordinated gait
    +- 10% if ketosis cows get this
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16
Q

Diagnosis of ketosis

A
  • clinical signs
  • blood glucose low
  • blood beta-hydroxybutyrate (BHBA)
    >1.4mmol/l subclin
    > 2.5mmol/l Clin
  • milk and urine ketone levels
  • serum NEFAs elevated
17
Q

Why do cows not get ketoacidosis ?

A

50% levels cf. cats so not high enough to cause acidosis

18
Q

Tx ketosis

A
  • IV dextrose (glucose) 100g quick
  • IV dextrose (glucose) 200d slow drip
  • steroids (NB: -> v milk yield, abortion though these cows empty so less of a problem)
  • appetite stimulants eg. transfaunation
  • propylene glycol 250ml BID unti the cow fights you off!
19
Q

Other names for fatty liver syndrome

A
  • fat cow syndrome

- fat mobilisation syndrome

20
Q

Causes of fatty liver syndrome

A
  • excessive weight loss
  • fat mobilised as NEFAs (lipase) deposited
  • can also become ketones, ATP, VLDLs but accumulates in liver
21
Q

Common presentation of fatty liver syndrome

A
  • fat cow (>4 BCS)
  • or very quickly losing weight cow
  • inappetence or anorexia
  • recumbent, NEURO signs and death
  • typically have concurrent condition (RFM, endometrittis,, although low grade in severity, no response to Tx)
22
Q

When will a fat cow get skinny if pregnant?

A

Last few weeks of gestation - periparturient

- should not be fat when calving down!!!

23
Q

How is FLS related to pregnancy toxaemia?

A
  • start last weeks gestation
  • most prevalent around parturition
  • twins
  • v feed intake
  • fat
  • cattle and sheep
24
Q

Which cattle are PDF pregnancy toxaemia?

A

Beef or dairy crossed to beef

  • esp Autumn calving herds
  • internal parasitism ^ risk
25
Q

Clinical signs pregnancy toxaemia

A 
> if shortly before calving 
- agitated 
- incoordinated
- difficulty rising 
- scant feaces 
> if -+ 6 weeks around calving tend to be depressed
- otherwise the same
26
Q

Which sheep do not commonly get pregnancy toxaemia?

A
  • maiden ewes rare
27
Q

PDF for pregnancy toxaemia in sheep

A
  • breed and age variation related to fecundity
  • case fatality can be 100% if clinical (cattle more subclincial)
  • outbreaks in flock higher mortality in lambs
  • may be assoc hypomagnesaemia, hypocalceamia
28
Q

Clinical signs pregnancy toxaemia sheep

A
  • separate from flock appearing blind
  • constipation and bruxism
  • drowsiness and abnormal posture (stargazing) in coordination
  • ewes become recumbent
  • depression and coma
  • recovered ewes : WOOLBREAK
29
Q

Diagnosing FLS and pregnancy toxaemia

A 
> Bloods
- NEFA >0.7mmol/l 
- glucose   Milk 
- fat >5%
- protein 1.6
> liver biopsy >15% fat
30
Q

Tx FLS and pregnancy toxaemia

A
  • as for ketosis + IVFT
  • consider insulin, steroids, choline, biotin, cobalt amine, BST [illegal uk growth hormone ]
  • high quality feed, glucose precursor rich
31
Q

Px FLS and pregnancy toxaemia?

A

Usually poor response to Tx

32
Q

Tx sheep FLS / pregnancy toxaemia

A
  • emergency ceaser
  • Tx uraemia
  • drench q4-8hrs rehydration fluids as for scouring calves
  • immediately placed on supplementary feeding/better silage/concentrates
  • early cases Tx propylene glycol (C3 molecules)
33
Q

Control and prevention of FLS and pregnancy toxaemia

A
  • Prevent fat and thin animals at calving
  • transition cow ration to reduce concurrent disease
  • early lactation cows fed balanced, high energy dense (glucose) ration *NB: balance risk of rumen acidosis these things will ^ risk**
  • good quality forage and maize silage
  • BCS recording
  • force fat cows to walk between housing and food
  • consider use of sodium propionate, niacin, biotin, cobalt
  • high risk cows : monensin bolus (KEXXSTONE) elanco $$$ not blanket Tx
34
Q

Control and prevention in sheep

A
  • as with cattle for BCS Recoring
  • ID twins and triplets and feed accordingly towards end of gestation
  • provision of shelter and supplementary hay/silage
  • minimise stress at high risk periods
35
Q

When are animals shifted into NEB?

A
  • periparturient cows and other mammals
36
Q

What is considered a high yielding farm? Range?

A

5,000 average - 10,000L/cow/year high yield

PMVPH 4th Year (34 decks)

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