1. Glucose Ketone bodies

2. Early Lactation Increased milk yield Negative energy balance

3.  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 liver

4. KetosisType IType II

5.  Type I: Gluconeogenic pathways are maximally stimulated. Low fat accumulation in liver gluconeogene sis NEFA’S Trigl yceri des More Less

6.  Type II: Gluconeogenic pathways are not maximally stimulated. “Fatty Liver condition” glucon eogen esis NEFA’S Triglycerides MoreLess

7. In Case of early lactation there will be low Insulin:glucagon ratio & this will stimulate Lipolysis in adipose tissue & ketogenesis in liver. Ketone bodies will be produced from butyrate in rumen and by mobilization of fat which will yield aceto acetate in absence of oxaloacetic acid

8. Etiology: NEGATIVE ENERGYBALANCE

9. TYPES: “Estate Acetonemia” In cows with high lactation yield and good quality ration but in negative energy balance PRIMARY ketosis Secondary to other disease with decreased feed intake Eg., Abomasal displacement, TRP etc. Secondary ketosis Feeding of silage with high butyric acid Feeding spoiled silage Alimentary ketosis 1. 3. 2.

10. Feeding with poor quality feed & animals with poor condition Can be corrected with proper feeding Starvation ketosis Cobalt is needed for metabolizing propionic acid into TCA cycle Def. of phosphorus & Diet low in TDN. Ketosis due to defeciencies 4. 5.

11.  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 4 th lactation.

12.  Economic significance: - Decreased milk yield - Lower milk protein & Lactose - Delayed estrus - Increased risk of Mastitis, metritis, cystic ovarian disease - Lowered first conception rate.

13. 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.

14. Production of ISOPROPYL ALCOHOL a break down product of aceto acetic acid in rumen Defeciency of glucose which is needed for normal function of nervous tissue Nervous signs will be due to

15. Clinical signs Wasting form Nervous form

16. Wasting form : Decreased appetite Woody appearance Decreased body weight Depressed & hang dog appearance T,P,R normal Odour of ketones in breath

17. Nervous form: Symptoms appear suddenly More of delirum rather than frenzy Characteristic signs are: walking in circles Crossing of legs Head pushing Aimless movements Licking of skin & inanimate objects Hyperesthesia

18.  Clinical pathology: Hypoglycemia: decreased to 20 -40 mg/dl ketonemia : BHBA estimation Ketonuria : Rothera’s test  Elevated NEFA’s & Cholesterol levels  Elevated Volatile fatty acids in rumen.  Declined hepatic glycogen levels.

19. Cystitis & Nephritis TRP Diabetes mellitus Indigestion Wasting form Abomasal displacement DIFFERENTIAL DIAGNOSIS

20. Nervous form RabiesHypomagnesemia Bovine spongiform encephalopathy

21.  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

22.  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.