Negative energy balance Flashcards
What factors need considering in NEB?
- glucose
- C3 molecules (more important in ruminants than glucose)
- krebs (citric acid) cycle
- gluconeogenesis
- vitamins
- co-enzymes
Describe glucose levels in early lactation
Insufficient in early lactation –> gluconeogenesis and lipolysis d/t drop in insulin. Lack of glucose –> cascade of problems
Consequences of NEB
- glucose deficit
- reserve mobilisation (fat and protein)
- ketosis complex
- fat mobilisation syndrome
Describe ketosis complex
- excessive build up of ketone bodies in blood d/t accumulation of acetyl-CoA (as precursors are turned into glucose?)
- increased ketones –> reduces appetite –> vicious cycle
- aka acetonaemia which is not same as acidosis
T/F; cows don’t develop ketoacidosis
True
When does ketosis complex occur?
- post-partum (2-10 weeks after calving)
- lactation incidence 3-7%, some farms higher
- subclinical ketosis higher, esp poorly managed farms
- RISK FACTORS: hypoCa, hypoMg, RFM, lame, twins
How does hypoCa lead to ketosis complex?
HypoCa –> gut stasis –> fat mobilisation –> ketosis complex
Categorisation - ketosis complex
- primary vs secondary
- wasting form vs neurological form
Describe primary ketosis
- VFI cannot meet energy demands
- excessive breakdown of body fat and mm
- sometimes d/t specific nutritional deficiencies affecting energy metabolism (choline, biotin, vit B12)
= ‘starvation ketosis’
Describe secondary ketosis
- any condition causing cow’s appetite to decrease:
- LDA/RDA
- (endo)metritis
- lameness
- (mastitis)
Describe ‘wasting form’ of ketosis
- gradual reduction in appetite, cows refuse to eat concentrates
- marked loss of body weight
- firm, dry faeces
- occasional bouts of staggering
Describe ‘neurological form’ of ketosis
- sudden onset ‘abnormal’ behaviour
- walk in circles, aimless wandering, head pushing, apparent blindness
- develop depraved appetite, lick skin and objects, chewing
- hyperaesthesia, uncoordinated gait
+/- 10% of ketosis cows
Dx - ketosis
- CS
- blood glucose (low end)
- Beta hydroxybutyric acid (BHBA): >1.4 mmol/l subclinical, >2.5mmol/l clinical
- milk and urine ketone levels
- serum NEFAs can be elevated
Tx - ketosis
- IV dextrose 100g, quick
- ** IV dextrose, 200g, slow drip (5 hours) ***
- corticosteroids sometimes
- appetite stimulants (transfaunation)
- propylene glycol 250ml, BID, until cow fights you off!
Describe fatty liver syndrome
= fat cow syndrome = fat mobilisation syndrome
- excessive wt loss
- fat mobilised as NEFA (lipase) is deposited in liver (fat can also be turned into KB, ATP and VLDL but these are less preferable pathways)