MECHANISM OF KETOSIS WAN NUR SHAMIMI - PowerPoint Presentation

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MECHANISM OF KETOSIS

WAN NUR SHAMIMI

BINTI

WAN ZAHARI

D11B045

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

;

I

n

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

acidemia

.

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

D11A20

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

D11A044

Source: The Merck Veterinary Manual

Diagnosis

T

ests

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.

 U

rine

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

.

Treatment

Aim

: Re-establishing

normoglycemia

and reducing serum

ketone

body concentrations

.

Bolus IV

administration ,common therapy, orally –

ra

p

id 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 other therapies

.

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

.

Other therapies 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

(prevention of acidosis)

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.

THANK YOU…

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.