Flashcards in Section 2: Metabolic Diseases of Ruminants: Ketosis (Donovan) Deck (40):
Types of ketosis
1) starvation (uncommon in cattle)
2) primary (healthy high producing dairy cattle, or ewes carrying multiple feces)
3) secondary (to some other malady)
KET predisposing factors
cow: early lactation, high milk prod., high BCS
ewe: late gestation, low BCS
normal to have neg. energy balance during early lactation?
-neg. energy balance of early lact.
-VFA prod. in rumen (acetic and butyric VFAs become ketone bodies)
propionate from grain usually goes to form:
acetate and butyrate from forage usually go to form:
activated acetate --> fat, energy in liver
if cow ingests CHO deficient in energy, what happens?
propionate goes down, so all of the propionate is utilized in milk and none goes to fat/energy. Cow wastes. Excess acetate and butyrate --> excess activated acetate --> converted to aceto-acetate and beta-hydroxybutyrate, which effect feed intake and neutrophil function
primary ketosis explained
high demand for energy depletes the body's supply of free and stored glucose, dietary intake can't keep pace with demand, and the body begins to use fatty acids and ketone bodies as its fuel source. Lipolysis depletes the body's fat stores and results in rapid loss of body condition, particularly in cattle. Further, mobilization of lipids leads to accumulation and metabolism of free fatty acids in the liver, often resulting in excessive retention of lipid by the hepatocytes (fatty degeneration).
wasting vs. nervous form of ketosis explained
The wasting form involves mobilization of fat stores and loss of body condition. The nervous form involves the effects of ketones on the central nervous system. The presence of high levels of ketones leads to trembling, ataxia, and erratic behavior.
wasting form of KET: clinical signs
-dec. feed intake
-dec. milk yield
(most common form)
nervous form of KET: clinical signs
clin. path. of KET
-fatty liver ( a primary dz problem)
-glucose solution IV
-propylene glycol oral
-Ca or Na-propionate oral
*act to speed up Krebs cycle*
last resort: glucocorticoids (facilitate breakdown of protein-->glucose)
KET prevention in dry cows
-maintain BCS, exercise, energy dense feed, dec. stress
KET prevention in lactating cows
-feed changes, DMI, energy dense feed, fiber
clin. signs of preg. tox. in SR
blind, demented, off feed, head pressing, CNS signs, DEATH. Necropsy: fatty liver, emaciation, multiple feti
preg. tox. tx
preg. tox. prevention
Grass tetany =
HM predisposing factors
+/-high milk prod.
Energy drain: cattle vs. SR *
cattle: milk production
Stage of prod. cycle: cattle vs. SR *
Body condition: cattle vs. SR *
Prognosis: cattle vs. SR *
lush growing pasture can have what properties:
low Mg, high K, +/- high in NH3
--> leads to decreased Mg intake and HM
where is Mg absorbed? Mech?
rumen, abomasum via Na linked active transport
Interactions resulting in decreased Mg absorption
-high dietary Ca
-low dietary Na:K ratio
-high rumen NH3
see slide 45 flowchart
How can stress decrease Mg absorption?
excess transfer of Mg from extracellular fluid to intracellular fluid, which decreases serum Mg
decreased serum Mg -->?
-decreased feed intake, Mg. intake, VFA prod.
-increased pH of rumen, nonionized cations in rumen (Mg, K, Na, Ca)
What is Mg required for on cellular/metabolic lvl?
-maintenance of normal resting membrane potential of nervous tissue
-low Mg:Ca ratio --> Ach release!
HM general clinical signs
-uncontrolled firing of neuronal/muscle cells
-death common w/o clinical signs
1ary cause of mortality in adult beef cattle
HM acute clinical signs (observed over a few hours). Treatment effective if these develop?
Good response to treatment
HM sub-acute signs (observed gradually). Tx effective if these develop?
Tx effective, but tendency to relapse
HM chronic signs. Tx effective?
Tx usually unsuccessful
HM rare or common in dairy cattle?
cows with HM w/o concurrent HC don't exhibit tetany
-MgSO4, calcium products