metabolic disease in cattle Flashcards
Type 1 vs type 2 ketosis
Type 1: around peak lactation i.e 6-8 weeks post-calving
Type 2: much earlier; within 2 weeks of calving
Basic pathophysiology of ketosis
Negative energy balance leads to intense adipose mobilisation + high glucose demand
- Liver produces ketones as it breaks down fat
Consequences of negative energy balance ketosis
Adipose mobilisation –> excess NEFAs (toxic) –> incomplete oxidation due to insufficient hepatic metabolism –> ketone bodies mainly BHB
Increased fat storage in the liver
When is the critical period in risk of ketosis
End of dry period i.e just before calving
BECAUSE DMI decreases by 20% due to fetus squashing rumen
+ change in energy metabolism as birth/lactation approaches
What does increased fat storage in liver (from -ve energy balance lead to)
Impaired gluconeogenic capacity
- Subclinical ketosis
- Chronic fat modbilisatio = fat fatty liver syndrome
- Massive accumulation of lipid in obese cows = fat cow syndrome
Fat infiltration of liver reduced hepatic macrophage (Kupffer cell) function so predisposition to sepsis
Signs of primary ketosis (i.e not due to other condition stopping them eating
Reduction in rumen fill
Smell of ketones on breath, urine, milk
Drier manure
Dry coat and piloerection
Neurological signs = nervous ketosis
Recumbency
ataxia
Which primary diseases are commonly responsible for secondary ketosis
LDA; get slow GI transit
Metritis: toxaemia puts animal off food
Signs of subclinical ketosis
Elevated BHB levels, reduced production, decreased appetite
What is fat cow syndrome
Severe hepatic lipidosis
From cows too fat before parturition; eat less so quickly swing into -ve energy balance
- More quickly get hepatic lipidosis because more fat available to be mobilised
What life threatening condition do we usually see alongside fat cow syndrome
Hypocalcaemia
What is pregnancy toxaemia
When cows in late pregnancy develop ketosis; often relates to multiple fetuses, inappropriate diet or restriction of intake, other illnesses
What does a urine dipstick for ketosis measure
Acetoacetate as proxy for BHB (BHB not excreted in urine)
What is Rothera’s reagent a crude test for
Ketosis
What level of BHB concentration give subclinical and clinical ketosis
Subclinical = >1.4mmol/l
Clinical = >3mmol/l
How can we diagnose hepatic lipidosis
Biochemistry can show hepatic damage/dysfunction: high AST, GGT, SHD
Liver biopsy shows fat levels; normal liver is <13%; clinical disease is >25%
Treating pregnancy toxaemia
= EMERGENCY to prevent irreversible hepatic lipidosis and organ failure
- Intensive support; glucose therapy, force feeding
- May need to induce parturition or C section to get fetus energy drain out
Treating ketosis
Give IV glucose (50% - 400ml)
ALso corticosteroids to reduce milk yield (demand for energy) + stimulate appetite and gluconeogenesis
Propylene glycol –> converted to oxaloacetate as precursor for gluconeogenesis (BUT need functioning liver for this to work)
Proprionate = direct gluconeogenesis precursor
What might vague sick cows in early lactation have
Hepatic lipidosis
How do ionophore boluses e.g monensin help prevent ketosis
Alter ruminal microflora to decrease acetate production and increase proprinoate production
What NEFA level do we want (when taken 10 days post calving) so be unlikely to get ketosis
<0.5mmol/l
When do we consider a herd to have. problem with ketosis
When >20% have a BHB concentration of >1.4 mmol/l ie subclinical ketosis
How much Ca2+ is needed per day in a cow; and how much at full term pregnant; and how much at lactation
25g normally
39g full term
100g lactation (max)
What does hypocalcaemia cause to muscles
Flaccid paralysis
is hypocalcaemia an issue of hormones or dietary intake
Hormones; failure to respond to PTH
