Dairy: energy deficiency syndromes

Question 1

who does bovine ketosis occur in?

Answer 1

well conditioned animals

Question 2

What are the products of carbohydrate metabolism

Answer 2

proprionate
butyrate
acetate

Question 3

What is the etiology of ketosis?

Answer 3

glucose requirements > inetake
hypoglycemia
ketogenesis
ketones suppress apetite
low carbohydrate absorbance

Question 4

What is primary ketosis?

Answer 4

good to excessive body condition
high lactation potential
good quality rations
predisposes cattle to abomasal displacement

Question 5

What is secondary ketosis?

Answer 5

alimentary ketosis (butyrate in silage)
nutritional deficiency (cobalt, phosphorus)

Question 6

What are the clinical signs of ketosis

Answer 6

wasting form: decrease in appetite and milk yield, preferncially eats hay, rapid body weight loss, ketones on breath

subclinical: decreased production, infertility, other diseases
nervous: circling, straddling/crossingl legs, head pressing, delirium, due to isopropyl alcohol (from acetoacetic acid) and lack of glucose in brain

Question 7

What are the lab findings of ketosis?

Answer 7

1. hypoglyccemia variable
2. blood ketone levels increased (BHBA >1.2mmol/L)
   increased urine ketons: urine test strips tend to ony detect aetoacetate
   increased milk ketones (BHBA >100mmol/L; acetone >0.70mmol/L

Question 8

What are the differentials for ketosis?

Answer 8

wasting
-displaced abmasum
-traumatic reticulitis
-primary indigestion
-cystitis/pyelopephritiss
nervous
-rabies
-hypomagnesmia
-BSE

Question 9

What is treatment for ketosis?

Answer 9

PROPYLENE GLYCOL: only evidence based treatment!!!! 300g daily for up to 5 days, drench or feed

(glucose: 500mL 50% dextrose IV, never SQ, transient response, renal excretion and abomasal dysfunction–overdose, –»second line treatment/nervous ketosis)

isofluprednone (predef) doesn’t really work, more mineralocorticoid activity–hypokalemia

dexamethsaone: not labeled, glucose repartitioning causes hyperglycemia, decent efficacy based on evidence

insulin–enhances glucose ptake and gluconeongenesis, not alone, suppresses fatty acid metabolism, may be useful if refractory to glucose and glucocorticoids

anabolic steroids=illegal

other treatments: vit B12, cobalt, niacin,

Question 10

How do you prevent ketosis

Answer 10

ensure adequate body condition at calving
less than 10% of cattle have BCS >4/5 in transition period
ionophores?

Question 11

What is small ruminant pregnancy toxemia

Answer 11

major energy drains are fetuses
decreased plane of nutrition late preg
differences in suscpetiblity may be hepatic efficiency?

Question 12

What are the primary causes of preg toxemia?

Answer 12

decreased plane of nutrition in late preg
shor tperiod of fast
cold weather/abscence of shelter
poor pasture

Question 13

Why are fat ewes more likely to get preg toxemia?

Answer 13

overconditioned in late preg–vluntary fall in feed due to intrabdominal fat

Question 14

What are risk factors for preg toxemia?

Answer 14

1. last 6 weeks preg
2. twins and triplpets
3. increased parity
4. interurrent dz
5. por plane of nutrition (hill breeds may be nore resistant)
6. case fatality 100% if don’t treat

Question 15

What are the clinical signs of preg toxemia?

Answer 15

more nervous–hypoglycemic encephalopathy

1. separate from group
2. blindness
3. tremors of head muscles
4. abnormal postures
5. recumbence in 304 days
6. dystocia
7. hypoglycemia early in dz
8. ketonemia, ketonuria
9. metabolic acidosis (as opposed to large ruminants off feed???)
10. renal failure and terminal uremia

Question 16

When is treatment of preg toxemia effective?

Answer 16

early in dz

Question 17

WHat is treatment for preg toxemia?

Answer 17

1. fluid and electrolyte replacement
2. GLUCOSE +/- insuline
3. propylene glycol if brain is ok and can swallow
4. glucocorticoids ineffective
5. REMOVAL OF FETUSES: cesarian or induce parturition

Question 18

How do you control preg toxemia?

Answer 18

BCS 2.5-3/5 at 90 days allows response to increased feeding later
last 2 months important 70% lambs weight gained in last 6 weeks
10% protein concentrate, 0.25kg/day-1kg/day
feed maiden ewes separately

Question 19

What are issues of starvation

Answer 19

look at notes

Question 20

When might you see starvation in neonatal calves?

Answer 20

poor quality milk replacers
-insufficient energy
-indigestible non-milk protein
diarrhea without extra nutritional support

Question 21

What are the effects oprotein deficiency

Answer 21

look at notes

Question 22

What are the clinical signs of starvation?

Answer 22

similar to toher nutritional deficiency or subclin dz

Question 23

What are situations where nutritional deficiency may occur?

Answer 23

1. late gestation in beef cattle
2. rare in dairy cattle
3. concurrent diarrhea
4. diagnosis based on analysis of feed
5. prevention based on providing adequate diet

Question 24

What is fatty liver also known as in cattle?

Answer 24

pregnancy toxemia?

Question 25

Why does fatty live roccur?

Answer 25

excessivve fat mobilization from body reserves to liver

Question 26

When does fatty liver ocur?

Answer 26

around time of parturition

Question 27

Who does fatty liver occur in?

Answer 27

sudden increases inenergy demand or decreases in intake

Question 28

Why do cattle get fatty liver?

Answer 28

pre-partum: FFA mobilized pre-partum; live, muscle, kidneys; mobilization influenced by hormonal anhd energy

Question 29

What happens when liver triglyceride is high with VLDL?

Answer 29

VLDL secretion further reduced due to hepatic insufficiency

Question 30

What is the epidemiology of fatty liver?

Answer 30

1. over conditioned animals (housed in poor conditions, excessively long dry periods, attempts to decrease body condition in late preg) 2. exessive energy in late preg 3. late gestation beef cattle carrying twins

Question 31

How do you diagnose fatty liver?

Answer 31

liver biopsy | mild 40% lipid

Question 32

When would you expect to see clinical signs of fatty liver?

Answer 32

>35%

Question 33

How high can case fatality rate be with fatty liver?

Answer 33

as high as 90%

Question 34

Wht are the clinical signs of fatty liver?

Answer 34

``` precipitated by conditions that decrease appetite -milk fever -displaced abomasum -indigestion -retained fetal membranes -dystocia animals usually overfat TPR normal weak ruminantion scant feces recumbency KETOSIS NOT RESPONDING TO TREATMENT!!!!! nervous signs: aggressive, restless, excitable, uncoordinated diarrhea terminally ```

Question 35

what are lab findings with fatty liver

Answer 35

1. increased NEFAs, beta-hydroxybutyrate, liver enzymes 2. liver enzymes in cattle SDH gold standard 3. decreased cholesterol, albummin, magnesium, insulin 4. leukopenia, neutropenia and lympohpenia in severe cases 5. liver biopsy--line from ilial wing to elbow, 11th intercostal space, copper sulfate flotation, histopathology 6. ultrasonography: digital analysis to determine lipid infiltration, subjective analysis.

Question 36

Why are ketones unreliable for fatty liver diagnosis?

Answer 36

diurnal variations--some animals with hepatic lipidosis may not be ketotic when get to them

Question 37

What is treatment for fatty liver

Answer 37

>3 days anorexia--likely to die animals eating increasing daily amounts recover correct effects of fatty liver and ketosis glucose and electrolytes IV continuously corticosteroids (e.g. dex) every second day (dex corticosteroid effect better than isofluprednone)

Question 38

How do you control fatty liver?

Answer 38

in beef: maintain appropriate BCS more difficult in dairy animals because dairy animals have a huge energy requirement when start lactating -reduce blood NEFAs by reducing fat mobilization but that is an energy source during lactation! -increase COMPLETE hepatic NEFA oxidation, which yields ATP but get excess heat generated -increase VLDL export from liver--data on achieving this is sparse

Question 39

HOw do you nutritionally manage dairy cattle such that control fatty liver? do they work???

Answer 39

energy requirements only slightly increase in late gestation but negative energy balance in early lactation (vs beef tht get dz in late gestation) 1. increase grain feeding (steaming up)--but doesn't increase milk production or feed intake 2. high grain diets post-partum--already feed it, if any more run into rumen acidosis 3. pre-partum fat in intestine, intestinally synthesized lipoproteins--use by extrahepatic tissue--increased NEFA

Question 40

What are management strategies to reduce fatty liver in dairy cattle?

Answer 40

feed intake decline correlates with degree of fatty liver so decrease decline: 1. minimize group moves in small herds 2. no observed effect in larger herds 3. shorter dry period? decreased fatty liver, decreased milk production though

Question 41

What are 3 goals of feed additives to decrease fatty liver?

Answer 41

1. reduce fat mobilization 2. increase VLDL secretion from liver 3. increase FA oxidation

Question 42

What are feed additives used to decrease fat mobilization

Answer 42

1. monensin--no effet on liver TG 2. propylene glycol--in concentrate, not effective in TMR 3. niacin--no effect--degraded in rumen 4. chromium--no effet on hepatic TG 5. conjugated linoleic acid--suppresses milk fat synthesis...not good, doesn't decrease hepatic TG

Question 43

What are feed additives used to increase liver VLDL secretion

Answer 43

1. choline and methionine 2. choline deficiency in rats causes hepatic lipidosis 3. choline and methionine required for VLDL production 4. supplemental choline decreases plasma NEFA liver TG when fed prepartum, also if fed post partum it decreases fatty liver CHOLINE CHOLINE CHOLINE methionine and lysine post partum may decrease liver TG--evidence not that solid

Question 44

What are feed additives used to increase FA oxidation?

Answer 44

omega 3 fatty acids decrease ketogenesis and increase fatty acid oxidation in rodents C18:3 fatty acid isomer: decreased hepatic TG during fatty liver induction; effects seem to ocur directly on liver supplemental carnitine?