MECHANISM OF KETOSIS WAN NUR SHAMIMI BINTI WAN

MECHANISM OF KETOSIS WAN NUR SHAMIMI BINTI WAN ZAHARI D 11 B 045

�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).

�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 ◦ ketone bodies and low concentrations of glucose. �In contrast to many other species, cattle with hyperketonemia do not have concurrent

�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.

Clinical sign murshidah binti mohd asri D 11 A 20

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

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

Diagnosis, Treatment By: Muhammad Affrrin Biring D 11 A 044 Source: The Merck Veterinary Manual

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 �

Treatment � Aim : Re-establishing normoglycemia and reducing serum ketone body concentrations. Bolus IV administration , common therapy, orally – rapid recovery. � Administration of glucocorticoids, IM -more sustained response. � Glucose and glucocorticoid therapy may be repeated daily as necessary. � Propylene glycol acts as a glucose precursor - may be effective as ketosis therapy, especially in mild cases or in combination with otherapies. � This dose may be administered twice per day. �

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 glucocorticoid to prevent hypoglycemia. � Otherapies that may be of benefit in refractory ketosis cases are continuous IV glucose infusion and tube feeding. �

Prevention and Control of Ketosis in Animal By Lee Joy Yoong

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

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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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/d. L) are at increased risk of developing clinical ketosis, compared with cows with lower serum BHB concentrations.