Flashcards in Farm animal endocrinopathies Deck (32):
What are potential risks as a consueqence of subclinical ketosis in a cow?
- Clinical ketosis
- Retained foetal membranes
What are the potential outcomes of a negative energy balance in a cow?
- If mild: subclinical ketosis, and increased fat infiltration in the liver
- If severe: clinical ketosis and fatty liver syndrome
Compare ketosis in farm animals and diabetic ketoacidosis in small animals
- Ketosis is not consequence of diabetes cf. ketoacidosis
- Also different from acidosis/SARA/acute acidosis in cattle
What are risk factors for a cow developing ketosis?
- Long lactation
- Higher milk production
- Increased weight before drying off
When are cattle most at risk of ketosis?
During early lactation where milk yield increases rapidly, faster than required increase in food intake and be accomodated for
What is ketosis in early lactation called?
Type II ketosis
What is ketosis in peak lactation called?
Type I ketosis
Which cows are most at risk of type I ketosis?
High yielding cows - unable to eat enough to maintain energy
Compare the energy requirement of a normal cow and a lactating cow
- Normal: BWT/10 = MJ of metabolisable energy/day
- Lactating needs an extra 5MJ ME/litre
Describe the normal physiology of fat mobilisation in lactation
- Mobilise fat as normal
- Lipolysis puts fat into blood as NEFAs
- In gut, absorbed propionate, moves into liver and provide source of glucose via gluconeogenesis
- Glucose produced used to oxidise fatty acids
- Glucose enters tissues, insulin into tissues and milk to drive metabolism and lactose production
- NEFAs oxidised in liver using glucose from propionate and gluconeogenesis
Describe the pathophysiology of type I ketosis
- Low propionate, less glucose prod, less oxidation of FAs
- Incomplete oxidation of FFAs = ketones, enter blood stream
What is the most common ketone produced in ketosis?
Describe the pathophysiology of type II ketosis
- Fat cow, more adipose tissue stores, mobilisation of lots of fat at drying off - cannot eat much
- Excessive mobilisation of fat, increased NEFAs
- Elevated fat in blood, insufficient glucose to oxidise, accumulation of FFAs in liver = hepatic lipidosis and ketones
- Further ketones produced due to impaired hepatic function
- More ketones, more fat mobilised as less energy produced from liver, continues in a cycle
Why are fat cows more at risk of type II ketosis?
- More fat stores to mobilise
- Insulin resistance so less metabolism and less uptake of glucose into milk
How does the blood insulin in a type I ketotic cow differ from that in a type II ketotic cow?
- High in type II
- Low in type I
What are the key interventions for type I and type II ketosis?
- Type I: post-fresh feeding
- Type II: pre-fresh feeding
What are the clinical signs of ketosis in the cow?
- Off food
- Milk drog
- Smell of ketones
- Nervous ketosis possible
What is meant by nervous ketosis? What are the signs? Prognosis?
- Rare presentation of ketosis
- May be due to hypoglycaemia, ketones, other circulating chemicals
- Can become aggressive, non-stop forward movement, furious licking
- Very good prognosis and can recover quickly
What are the clinical signs of hepatic lipidosis in the cow?
- Off food
- Milk drop
- Liver failure
What is pregnancy toxaemia in sheep and when does it occur?
- Twin lamb disease
- Usually before lambing
Explain the pathophysiology of pregnancy toxaemia in sheep
Twins not split from singles, not fed enough, energy demads too high = ketosis
How does pregnancy toxaemia relate to hypocalcaemia
- Clinical signs indistinguishable
- Often one will precipitate the other
What are the clinical signs of pregnancy toxaemia?
- Off feed
- Dull, depressed
- Nervous sings e.g blindness
What conditions may cause pregnancy toxemia?
- Tooth disease/lameness may pregent eating enough
- Conjunctivitis (Mycoplasma conjunctivi), often relapse, poor immunity
- Sporadic cases
What often triggers outbreaks of pregnancy toxaemia?
- Change in management esp. diet
- May lead to reduced DMI
What diagnostic tests should be used in suspected cases of ketosis?
- Blood test for ketones
- Urine ketone dipstick (small animal/human dipstick)
- Milk Rotheras's reagent, turns purple if ketones present, rare
What diagnostic tests should be used in suspected cases of hepatic lipidosis?
- Ketones as with ketosis (blood, urine, milk)
- Blood NEFAs
- Evidence of liver damage i..e elevated liver enzymes AST, GGT
- Assess fat in liver (biopsy, necropsy)
What treatments are available for an individual with hepatic lipidosis, ketosis or pregnancytoxaemia?
- Glucose precursor
Describe the use of glucose precursors in the treatment of hepatic lipidosis/ketosis/pregnancy toxaemia
- E.g. propylene glycol
- Enters TCA cycles and creates insulin peak
- Is the base of ketosis treatment
- 300g once daily
- Use precursor so rumen flora cannot use it up before it enters blood as would occur with glucose
Describe the use of glucocorticoids in the treatment of hepatic lipidosis/ketosis/pregnancy toxaemia
- Promote gluconeogenesis
- HOWEVER evidence equivocal but still commonly used
Describe the use of glucose in the treatment of hepatic lipidosis/ketosis/pregnancy toxaemia
- Can only be given IV
- Rapid peak and decline
- No clear evidence
- Good for use in nervous ketosis to resolve signs quickly