Section 2: Metabolic Diseases of Ruminants: Ketosis (Donovan) Flashcards Preview

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Flashcards in Section 2: Metabolic Diseases of Ruminants: Ketosis (Donovan) Deck (40):
1

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)

2

KET predisposing factors

cow: early lactation, high milk prod., high BCS
ewe: late gestation, low BCS
inappetence
low exercise

3

normal to have neg. energy balance during early lactation?

yes

4

KET etiology

-neg. energy balance of early lact.
-VFA prod. in rumen (acetic and butyric VFAs become ketone bodies)

5

propionate from grain usually goes to form:

glucose, lactose

6

acetate and butyrate from forage usually go to form:

activated acetate --> fat, energy in liver

7

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

8

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).

9

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.

10

wasting form of KET: clinical signs

-dec. feed intake
-dec. milk yield
-weight loss
-ketone breath
(most common form)

11

nervous form of KET: clinical signs

-staggering
-abnormal stance
-apparent blindness
-pica
-uncommon

12

clin. path. of KET

-hypoglycemia
-hyperketonemia
-fatty liver ( a primary dz problem)

13

KET tx

-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)

14

KET prevention in dry cows

-maintain BCS, exercise, energy dense feed, dec. stress

15

KET prevention in lactating cows

-feed changes, DMI, energy dense feed, fiber

16

clin. signs of preg. tox. in SR

blind, demented, off feed, head pressing, CNS signs, DEATH. Necropsy: fatty liver, emaciation, multiple feti

17

preg. tox. tx

-C-section
-glucose drip
-propylene glycol
-hand feed
POOR PROGNOSIS

18

preg. tox. prevention

-feed more
-parasite control
-weather
-BCS

19

Grass tetany =

hypomagnesemia

20

HM predisposing factors

-early lact.
+/-high milk prod.
-lush pasture
-stress

21

Energy drain: cattle vs. SR *

cattle: milk production
SR: fetus

22

Stage of prod. cycle: cattle vs. SR *

cattle: lactation
SR: gestation

23

Body condition: cattle vs. SR *

cattle: high
SR: low

24

Prognosis: cattle vs. SR *

cattle: good
SR: poor

25

lush growing pasture can have what properties:

low Mg, high K, +/- high in NH3
--> leads to decreased Mg intake and HM

26

where is Mg absorbed? Mech?

rumen, abomasum via Na linked active transport

27

Interactions resulting in decreased Mg absorption

-high dietary Ca
-low dietary Na:K ratio
-high rumen NH3
-rumen alkalosis
-stress

28

see slide 45 flowchart

:)

29

How can stress decrease Mg absorption?

excess transfer of Mg from extracellular fluid to intracellular fluid, which decreases serum Mg

30

decreased serum Mg -->?

-decreased feed intake, Mg. intake, VFA prod.
-increased pH of rumen, nonionized cations in rumen (Mg, K, Na, Ca)

31

What is Mg required for on cellular/metabolic lvl?

-maintenance of normal resting membrane potential of nervous tissue
-low Mg:Ca ratio --> Ach release!

32

HM general clinical signs

-uncontrolled firing of neuronal/muscle cells
-cardio-resp. failure
-death common w/o clinical signs

33

1ary cause of mortality in adult beef cattle

HM!

34

HM acute clinical signs (observed over a few hours). Treatment effective if these develop?

-hyperesthesia
-staggering
-vocalization
-seizure activity
-death

Good response to treatment

35

HM sub-acute signs (observed gradually). Tx effective if these develop?

-off feed
-muscle tremor
-exaggerated gait
-easily excited

Tx effective, but tendency to relapse

36

HM chronic signs. Tx effective?

-dull
-unthrifty
-down

Tx usually unsuccessful

37

HM rare or common in dairy cattle?

rare

38

cows with HM w/o concurrent HC don't exhibit tetany

:)

39

HM tx

-MgSO4, calcium products

40

HM prevention

-feed Mg salts during danger period
-provide hay/rotate off "at risk" grazing (brown grass) eod