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Ketosis and Fatty Liver - Coggle Diagram
Ketosis and Fatty Liver
main VFAs
proprionate (15-30%)
from sugar and starch digestion
glucose prodcuction in liver
cow E + lactose production in mammary gland
acetate (55070)
from cell wall/fiber digestion
synthesis of milk fat in mammary gland
butyrate (5-15%)
from cell wall and starch digestion
synthesis of milk fat and some E production
provide 60-80% of cow's E
transition period
from dry to lactating
305d lactation
first 3-4w lactation: fresh
rapid increase in milk
huge demand for nutrients
metabolic stress
dry matter intake decreases
60d dry period
3-4w early dry: maintenance of body reserves
3-4w prefresh: increased fetal demand
rumen organisms change for lactation diet
need to increase nutrient density of diet
avoid abrupt changes in diet
rapid fetal growth
calving
re-starting mammary secretion
colostrum production
rapid increase in milk production
group/social change
+/- housing change
successful transition/prevention program
goal to freshen at 3.0-3.5 BCS
maximize dry matter intake
increase E density
maximize microbial protein production
contorl periparturient health disorders
minimize stressors
increase grain feeding 3-4w prepartum
feed additives
niacin
rumen protected choline
Monensin :forbidden::flag-us::
parturient disease complex
milk fever/hypoCa
dystocia
retained placenta
metritis
ketosis
hepatic lipidosis
displace abomasum
interrelated diseases caused by negative E balance
ketosis
elevated [ketone bodies] in tissues and fluids
acetone
beta-hydroxybutyrate
acetoacidic acid
clinical
accumulation of ketones in tissue
appetite suppression/ off feed
weak rumen motility
sudden drop in milk
body mobilizes even more body fat
subclinical
normal for many cows in early lactation
35% early lactation cows
diagnosis
signalment
early lactation
well-conditioned
PE
ketone tests
can sometimes smell on breath
Clin path
:arrow_up:
ketones
NEFAs
bilirubin
AST
GGT
SDH
:arrow_down:
triglycerides
cholesterol
glucose
albumin
Mg
globulins
insulin
liver biopsy
sulfobromophthalein dye excretion test
good prognosis if caught and treated early
hepatic lipidosis
excssice triglyceride formation and deposition in liver
severe impairment of liver fxn
hepatocyte function impaired, worsening the condition
for dairy cows "fat cow syndrome"
for beef cows, "pregnancy toxemia"
for ewes and does, "ovine ketosis" "pregnancy disease"
risk factors
overconditioning
eat less at calving
mobilize more fat
highest producing
older
restricted nutrient intake
concurrent periparturient disease
milk fever
metritis
DA
ketosis
if recumbency and not responding to therapy, prognosis grave
decreased blood glucose and decrease insulin:glucagon ration mobilizes lipases
NEFAs released into bloodstream and processed in liver
usually occurs 0-6w postpartum
CS
excessiv weight loss
scant, dry feces (rumen stasis)
weakness
+/- recumbency
acute CNS signs (rare)
depression, anorexia
isolation
tachycardia/ypnea
treatment
treat primary disease
provide free choice palatable feed
propylene glycol
300mL posid 3-5d
shuts down lipolysis signal
IV glucose replacement therapy
500mL 50% dextrose IV 205hr
given once at diagnosis
+/- drench with 5-8gal of water water
ancillary
glucocorticoids
dexamethasone
mobilize glucose precuroses
stimulate appetite
B vitamines
long acting insulin
monitoring herd
monitor BCS throughout dry period
monitor dry matter intakes
record incidence of clinical metabolic diseae in fresh cows
monitor blood BHBA level sin fresh cows