Peak yield at 46 wks but high dry matter intake at 810 wks so there will be negative energy balance Low levels of glucose Mobilisation of adipose tissue Increase in NEFA amp BHBA Ketogenesis ID: 302757
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Slide1
BOVINE KETOSISSlide2Slide3
Peak yield at 4-6 wks but high dry matter intake at 8-10 wks so there will be negative energy balance.
Low levels of glucose
Mobilisation
of adipose tissue
Increase in NEFA & BHBA
Ketogenesis
&
gluconeogenesis
liverSlide4Slide5
Type I:
Gluconeogenic
pathways are maximally stimulated . Low fat accumulation in liver
More
LessSlide6
Type II:
Gluconeogenic
pathways are not maximally stimulated. “Fatty Liver condition”
More
LessSlide7Slide8
NEGATIVE ENERGYBALANCESlide9
TYPES:
1.
3.
2.Slide10
4.
5.Slide11
Epidemiology:
- Common in stall fed animal - Most common in first month
- peak prevalance in first 2 wks post calving - Low prevalance
in first lactation & high at 4th lactation.Slide12
Economic significance:
- Decreased milk yield
- Lower milk protein & Lactose
- Delayed estrus
- Increased risk of Mastitis,
metritis, cystic ovarian disease - Lowered first conception rate.Slide13
Pathogenesis:
Severity of clinical syndrome is proportional to degree of hypoglycemia.
Acetoacetic
acid may lead to coma
Changes in ruminal flora occurs leading to indigestion Respiratory burst mechanism of neutrophils fail to occur leading to
immunosupression.Slide14
Nervous signs will be due toSlide15Slide16
Wasting form:
Decreased appetite
Woody appearance
Decreased body weight Depressed & hang dog appearance
T,P,R normal Odour of ketones
in breath Slide17
Nervous form:
Symptoms appear suddenly
More of
delirum
rather than frenzyCharacteristic signs are:
walking in circles Crossing of legs Head pushing Aimless movements
Licking of skin & inanimate objects HyperesthesiaSlide18
Clinical pathology:
Hypoglycemia: decreased to 20 -40 mg/dl
ketonemia : BHBA estimation Ketonuria
: Rothera’s testElevated NEFA’s & Cholesterol levelsElevated Volatile fatty acids in rumen.
Declined hepatic glycogen levels.Slide19
DIFFERENTIAL DIAGNOSISSlide20Slide21
Treatment:
1.Replacemnt therapy:
Glucose/Dextrose 50%
soln @ 500 ml Fructose , Glucose + fructose ,
Xylitol can be used to prolong the reponse. Propylene glycol as a drench @ 225 g twice daily for 2 days followed by 110 g daily for 2 days
Slide22
Glucose precursors :
Sodium propionate @110-225 g daily.
Ammonium lactate @ 200 g for 5 days.
Hormonal therapy:
Glucocorticoids
: Produce hyperglycemia Insulin: facilitates cellular uptake of glucose , Suppress fatty acid metabolism , Stimulate hepatic glconeogenesis
. Anabolic steroids: Trenbolone acetate
Glucagon: Gluconeogenic & glycogenolytic.Slide23