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Ketosis
Dr/Abd Elghany Hefnawy
before
As
Ketosis (Post-partureint dyspepsia)
Disease of Negative
Caloric Intake
Or Negative Energy
Balance (NEB)
Ketonemia
Ketonueria
Hypoglycemia
Etiology and predisposing factors
Alimentary K.
Starvation K.
Secondary K.
Production or
primary K.
Alimentary K.
-Feeding on ketogenic diet as silage due to it
is rich in butyric acid (Ketogenic fatty acid)
-This form usually appeared in sub-clinical
form and predispose to the primary ketosis
Production or primary K.
Low
carbohydrate
Ration
Excessive body
condition
Increase lipid
mobilization to the liver
and production of KB
High protein
Ration
Excessive
production of
butyric acid in
the rumen
(Ketogenic FA.)
Cobalt Def.
Secondary K.
Usually associated with the diseases that
characterized by anorexia for long period as:-
Traumatic
pericarditis
Hypophosphatemia
Metritis
Abomasal displacment
Mastitis
Persistent
diarrhea
Hypoglycemia
Secondary K.
FMD
R. Impaction
Recommendation of injection of
Dextrose in case of hypophosphatemia,
mastitis, metritis, abomasal
displacement or another anorexic
conditions ?
Starvation K.
-Lack of propionate
-Low quality ration
-Lack of gluconeogenesis
Incidence and occurrence
Most cases occurred post-parturient
( up to 60 days)
Occasionally in
pregnant animals
Obese Animal
Aged and high producing
animal are more susceptible
poor conditioned animals
Pathogenesis
Etiology and predisposing factors
Clinical findings
Carbohydrate in ration
Storage as
Glycogen
Milk
Energy
Propionic acid
Glucogenic
Acetic acidButyric acid
Rumen
Oxalacetate
Glucose
Liver
Cobalt
A
Ketogenic acids
Storage as
fat
Active acetat or Acetyle Co-A
Krebs cycle
B
Normal pathway of carbohydrate
Glucose
Vit B12
Propionic acid
5 Desoxyadenylcobalamine
Cobalt
*Cobalt is requiered for synthesis of vitamin B12
( 4 % 0f its chemical structure)
Vit. B12
Ruminal
microorganisms
DietCobalt
Blood
Propionic acid Glucose Energy
*Activation
of
propionat
producing
*Vitamin B12 is needed for building
proteins in the body, red blood
cells, and normal function of
nervous tissue.
Why cobalt is essential for ketotic cow?
Low carbohydrate in ration
Low Propionate in the rumen
Low Oxalaceetate production
(Hypoglycemia)
Lipolysis for gluconeogenesis
Excessive production of Keton bodies
Acetoacetic acid Acetone Beta-
Hydroxybutyric acid
Ketosis
Triglyceride (fat)
NEFA (Non-estratified fatty acid) Glycerol
Glucosis
Gluconeogensis
InComplete
oxidation when
ther is excess of
NEFA (lipolysis)
Ketogenesis
Ketosis
Complete
oxidation by TCA
(Kreb’s cycle)
L-Carnetine
ATP
1
Toxemia
Negativecaloric
Intake
How
does
ketosis
considered
as
a form
of
toxemia?
Clinical findings
Digestive form
(Woody cow)
Nervous form
(Typical )
-Gradual loss of appetite for few days.
-Rapid loss of body weight and subcutaneous
fat that leading to loss of body condition
and the cow appeared Woody (Woody cow).
Digestive form (Woody cow)
-Dry feces with mild constipation.
-Characteristic acetone Adour can be detected
in the urine and milk.
-Reduction in the milk yield up to
25%
-Normal (PTR) pulse,
body temperature
and respiration
-It is the most
common form
26
Frequency Location Intensity Duration
Normal ruminal movement
but with weak amplitude
Nervous form (Typical )
-Usually due to excessive production of isopropyl alcohol
Due to excessive production of KB.
-Aimless movement
-Head pressing
-Walking in circles
-Blindness
-Vigorous licking of the skin
-Hyperesthesia
Why
ketosis
associated
by nervous
signs?
-Nervous manifestations
occurred in episodes
-In-coordination with moderate
tetany
-Coma and death
-Acetone Adour of the breath
Diagnosis
-Case history of occurrence, incidence
and predisposing factors
Clinical
findings
Lab. Findings
1-Hypoglycemia the glucose level is below 25mg% (Normal = 40 – 60 mg%)
2-Ketonaemia 10-1000mg% (Normal = up to 10 mg%)
3-Ketonuria 80-1300mg% (Normal = up to 50-70 mg%)
4-Milk ketone 40mg% (Normal = 3 – 10 mg%)
5-High level of plasma non-protein nitrogen in the terminal stage due to
decomposition of fetuse – level of BUN and creatinine.
6-High level of cortisone.
7-Iron, magnesium, potassium  low level.
-Lymphocytosis
-Neutropenia
-Esinophilia
-High GOT
Rapid cow side test
Differential diagnosis
Hypomagnesemia Rabies
HypocalcemiaAbomasal displacment
Listeriosis (Nervous
manifestations are
prolonged not in
episodes)
-Traumatic
-Vagal indigestion
‫ماكان‬ ‫زي‬ ‫بيتنا‬ ‫عنوان‬
‫العنوان‬ ‫نسيت‬ ‫انت‬ ‫بس‬
‫بالش‬ ‫و‬ ‫اسأل‬ ‫و‬ ‫ابعت‬
‫ناااخد‬ ‫احسن‬ ‫تتاءل‬
‫عالنسيان‬
Treatment
Correction of hypoglycemia
Correction of dehydration
Stimulation of depressed appetite
Precursors of glucose
Good management
Correction of hypoglycemia
IV of glucose 40-50% Precursors of glucose
-Glycerol 120 ml 50%
-Sodium propionat or lactate
-Propylene glycol 125-250g twice
daily
-Dexamethason
(Gluconeogenesis)
Correction of dehydration
IV of fluid therapy Stimulation of
depressed appetite
Stomachic
Injection
of insulin
40-50 IU
X
Adipose
Tissue
Free fatty
acids
Liver
Ketone BodiesInsulin
Pancreas
Mechanism for prevention of ketosis due to
excess ketone body production that can lead to ketoacidosis
KETOSIS
Excessive build-up of ketone bodies results in ketosis eventually
leading to a fall in blood pH due to the acidic ketone bodies.
Prevention and control
-Providing of food rich in glucose as
ground maize which rich in glucose
(alpha polymerized glucose these
substances not fermented in the rumen
and pass to the intestine and absorbed
there)
Good calculated feeding system
(4 weeks prior to calving).
(A)- At calving (1kg concentrate/ day and
this amount is increased gradually to 5 kg
concentrate/ day at the time of calving).
(B)-At lactation 3 kg hay / 100 kg body
weight + 1kg grain /3 kg milk produced.
NB. 1kg hay = 3 kg silage.
* Prophylactic feeding of sodium
propionate 110 gm daily for 6
weeks before calving
Monensin (anti–coccidial drugs) as growth
promoter leading to increase the ratio of
propionate to acetate
*Propylene glycol 350 ml daily for
10 days after calving
1.When you feed more grain, the transition cow eats more
2. Increased grain encourages the rumen to produce more propionate A
volatile fatty acid
3. Propionate is converted to glucose in liver.
4. Increased levels of propionate and glucose stimulate insulin production in
the pancreas.
5. Insulin helps reduce fat release from body fat stores. Therefore, less fat
reaches the liver, reducing fatty liver and ketosis.
Increase grain intake
How
Increased
Grain
Reduces
Ketosis?
Definition
It’s one of most important metabolic disease of
cow due to disturbance in the carbohydrate and fatty
acids metabolism which leading to hypoglycemia,
ketonuria and ketoneamia and decrease in the level
of the liver glycogen. And characterized clinically by
digestive and nervous signs.
‫كفااااااااايه‬
QUESTIONS
The reference
‫التواصل‬ ‫وسائل‬
Email: abdelghany_hefnawy@yahoo.com
Abdelghany.hefnawy@bu.edu.eg
Facebook abdelghany hefnawy
‫د‬.‫حفناوي‬ ‫الغني‬ ‫عبد‬
Web site to download lectures
www.bu.edu.eg/staff/abdelghanyhefnawy
(Courses)
Tel 01001609986 - 01011676482

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