Transition Cow Flashcards
When is the transition period?
3 weeks before and after calving
What is going on in the body during the transition period?
-Insulin decreased responsiveness
-Reduced Immunity 1-2weeks prepartum and after
-Hypocalcemia
-Hyperketonemia
-Negative Energy Balance (eating less and producing more)
Why is management so important for transition cows?
Such great energy requirements and nutrient requirements are needed to support the calf (colostrum)
What is homeostatic?
Physiologic reactions that maintain most of the steady states in living organisms
Where does glucose come from?
Butyrate and propionate from rumen and liver and diet
Goes into muscle and adipose tissue and milk
What is lactose made up of?
Glucose and galactose
What is homeorhesis?
Fasted state: coordination of metabolism to ensure uniform flow of nutrients to support a physiologic state
When the cow is fasted where do the NEFA and glucose come from for the milk?
Adipose tissue
Muscle (fuled by NEFA and Ketones)
Liver
What are the 3 ketones made?
Acetoacetate
B-OH Butyrate
Acetone
So if making ketones is an adaptive process, why to some cows still get sick?
Excess fatty acids turn into Ketone Bodies = NEFA build up in liver as fat = fatty liver low VLDL)
What have we dont to cows to make them too lipolytic?
Altered adipose sensitivity, high genetic merit, late gestation, increased fat cows, decreased sensitivity to insulin = Increase release of NEFAs
-Dry at high BCS
When looking at clinical pathology what is a common trend for fresh cows?
Lower glucose, higher BHBA and NEFA than close up to mid lactation
What is the BHB level for clinical ketosis?
> 3.0mmol/L
Subclinical >1.2mm/L
Does hyperketonemia mean ketosis?
NO (50% of fresh cows are hyperketonemia during the first 2 months of lactation)
When is the high-risk period for true ketosis?
1st 15 days in milk, (3-7 greatest increase)
What are some risks that come from subclinical ketosis?
DA
Metritis
Clinical Ketosis
What are signs of clinical ketosis?
Lethargic
Lack of appetite
Hard Feces
Reduced rumen fill
Decreased Milk Production
Nervous Ketosis (Ataxia, hyper aesthetic, aggressive, wandering, head pressing
What is spontaneous ketosis and who does it effect?
Type 1:
3-6 weeks of lactation, normal yesterday and ketotic today, low blood glucose and insulin, (like type 1 diabetes)
What is a critical management practice to help reduce the incidence of ketosis?
BCS
-Too fat = clinical diseases
What are other risk factors for ketosis?
BCS - too fat
length of dry period (>55d)
Calvin intervals 13-15 months
Age at first calving >25months
Are the concentrations of ketones the same between blood, milk and urine?
Most are similar
How do we evaluate ketones bodies in the field?
Milk - Keto test
Urine - ketostix (acteoacetate)
Blood - Precision Xtra (freestyle Neo) (BHB)
How does treating with propylene glycol work?
Absorbed by digestive tract and converted to glucose in liver - small amount degraded in rumen to propionic acid
-Drench
-May decrease intake
-Expensive
What is the dose for propylene glycol?
300mls once daily for 3-5 days
What is the dose of Glucose for nervous ketosis?
500ml 50% glucose
What are some other more traditional treatment options?
Steroids- dexamethasone
Insulin
Bovine Somatostatin - increase milk production
Rumen support - fresh cow drench
Butaphosphan
PG, Niacin and Flunixin Meglumine
Who is the poster child for fatty liver disease?
BCS >4.0
Eating free choice corn silage diet late in gestaion
get sick and die regardless of therapy
When palpating a cow, what can you feel in the cranial portion of the abdomen that may indicate fatty liver disease?
Liver with rounded margins
What are clinical signs for fatty liver disease?
Anorectic but fat cow
How do you treat fatty liver disease?
Treat like ketosis - PG, Niacin and flunixin, rumen support, IV fluids, cow entering hepatic failure (Albumin, clotting factors, acute phase protein, energy metabolism
