MECHANISM OF KETOSIS

1. MECHANISM OF KETOSIS WAN NUR SHAMIMI BINTI WAN ZAHARI D11B045

2. Ketosis results from the accumulation in the blood of ketone bodies • formed during the oxidation of fatty acids to produce energy. • During fasting ketosis is due to insufficient ingestion of carbohydrates; • In diabetes, to insufficient carbohydrate metabolism arising from lack of insulin. • The serum ketone bodies are • acetone, • acetoacetate, and • β-hydroxybutyrate (BHB).

3. It requires the combination of intense adipose mobilization and a high glucose demand. • Both of these conditions are present in early lactation, • time negative energy balance leads to adipose mobilization • milk synthesis creates a high glucose demand. • Adipose mobilization is accompanied by high blood serum concentrations of nonesterified fatty acids (NEFA). • During periods of intense gluconeogenesis, • a large portion of serum NEFA is directed to ketone body synthesis in the liver. • the clinicopathologic characterization of ketosis includes high serum concentrations of NEFA • ketonebodies and low concentrations of glucose. • In contrast to many other species, cattle with hyperketonemia do not have concurrent acidemia.

4. Immediate postpartum period is slightly different than that of cases occurring closer to the time of peak milk production. • Cases of ketosis in very early lactation are usually associated with fatty liver. • Both fatty liver and ketosis are probably part of a spectrum of conditions associated with intense fat mobilization in cattle. • Ketosis cases occurring closer to peak milk production, • usually occurs at 4-6 wk postpartum, • may be more closely associated with underfed cattle experiencing a metabolic shortage of gluconeogenic precursors than with excessive fat mobilization. • They do not appear to be associated directly with serum concentrations of either glucose or ketone bodies.

5. Clinical signmurshidahbintimohdasri D11A20

6. In cows • Reduced feed intake • Reduced milk production • Afebrile and slightly dehydrated • Hyperactive and hypoactive • CNS disturbance • It can lead to hypoglycemia

7. In cats • Usually sign of diabetes mellitus • Dehydration and vomiting • Ketoacidosis is fatal • Diabetic ketoacidosis • Sudden weight loss • Increase thirst • Constant hunger • Excessive urination • Prone to infection

8. Diagnosis, Treatment By: Muhammad AffrrinBiring D11A044 Source: The Merck Veterinary Manual

9. Diagnosis • Tests for the presence of ketone bodies in urine or milk  •  The majority of commercial test kits detect the presence of acetoacetate or acetone in milk or urine. •  Dipstick tests - to detect acetoacetate or acetone in urine but not suitable for milk testing. • All of these tests are read by observation for a particular colour change. •  Urine ketone body concentrations are always higher than milk ketone body concentrations. • Trace to mildly positive results for the presence of ketone bodies in urine do not signify clinical ketosis. • Without clinical signs, such as partial anorexia, these results indicate subclinical ketosis. • Milk tests for acetone and acetoacetate are more specific than urine tests. • Positive milk tests for acetoacetate and/or acetone usually indicate clinical ketosis.

10. Treatment • Aim : Re-establishing normoglycemia and reducing serum ketone body concentrations. • Bolus IV administration ,common therapy, orally – rapid recovery. • Administration ofglucocorticoids, IM -more sustained response. • Glucose andglucocorticoidtherapy may be repeated daily as necessary. • Propylene glycolacts as a glucose precursor -may be effective as ketosis therapy, especially in mild cases or in combination with other therapies. • This dose may be administered twice per day.

11. Treatment • Ketosis cases occurring within the first 1-2 wk after calving frequently are more refractory to therapy than those cases occurring nearer to peak lactation. • In these cases, a long-acting insulin preparation, IM, may be beneficial. • Insulin suppresses both adipose mobilization and ketogenesis, but should be given in combination with glucose or a glucocorticoidto prevent hypoglycemia. • Other therapies that may be of benefit in refractory ketosis cases are continuous IV glucose infusion and tube feeding.

12. Prevention and Control of Ketosis in Animal By Lee Joy Yoong

13. Prevention, Control and Treatments • Administration of dextrose (d-glucose of high glycemic index) solution (50%) (allows rapid recovery, for severe ketosis) • Administration of glucocorticoids intramuscularly (may be repeated daily) • Oral medication of propylene glycol (glucose precursor) (for mild ketosis) • Non ruminants can be given a new diet of higher carbohydrate and lower fats ; ruminants can be given a diet of lower fats but the carbohydrate content should not exceed the maintenance and production requirement (prevention of acidosis)

14. Difference in treatment compare to human • In animals, insulin administration is not common (considering economics, especially in production animals) • Prevention, through diet, is more emphasised compared to treatments (as a higher cost is required for drug administration) • Animal’s DMI should be constantly inspected to ensure it’s energy requirement meets it’s supply.

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16. Epidemiology: • All dairy cows in early lactation (first 6 wk) are at risk of ketosis. • The incidence in lactation is estimated at 5-16%, but incidence in individual herds varies substantially. • Ketosis occurs in all parities (although it appears to be less commin in primiparous animals) and does not appear to have a genetic predisposition, other than being associated with dairy breeds. • Cows with excessive adipose stores (body condition score ≥3.75 out of 5.0) at calving are at increased risk of ketosis, compared with those with lower body condition scores. • Lactating cows with hyperketonemia (subclinical ketosis—serum BHB concentrations >12 mg/dL) are at increased risk of developing clinical ketosis, compared with cows with lower serum BHB concentrations.