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Food animal production > Dairy: energy deficiency syndromes > Flashcards

Dairy: energy deficiency syndromes Flashcards

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1
Q

who does bovine ketosis occur in?

A

well conditioned animals

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2
Q

What are the products of carbohydrate metabolism

A

proprionate
butyrate
acetate

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3
Q

What is the etiology of ketosis?

A 
glucose requirements > inetake
hypoglycemia
ketogenesis
ketones suppress apetite
low carbohydrate absorbance
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4
Q

What is primary ketosis?

A

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

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5
Q

What is secondary ketosis?

A 
alimentary ketosis (butyrate in silage)
nutritional deficiency (cobalt, phosphorus)
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6
Q

What are the clinical signs of ketosis

A

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

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7
Q

What are the lab findings of ketosis?

A
  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
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8
Q

What are the differentials for ketosis?

A 
wasting
-displaced abmasum
-traumatic reticulitis
-primary indigestion
-cystitis/pyelopephritiss
nervous
-rabies
-hypomagnesmia
-BSE
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9
Q

What is treatment for ketosis?

A

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,

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10
Q

How do you prevent ketosis

A

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

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11
Q

What is small ruminant pregnancy toxemia

A

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

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12
Q

What are the primary causes of preg toxemia?

A

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

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13
Q

Why are fat ewes more likely to get preg toxemia?

A

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

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14
Q

What are risk factors for preg toxemia?

A
  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
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15
Q

What are the clinical signs of preg toxemia?

A

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
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16
Q

When is treatment of preg toxemia effective?

A

early in dz

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17
Q

WHat is treatment for preg toxemia?

A
  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
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18
Q

How do you control preg toxemia?

A

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

19
Q

What are issues of starvation

A

look at notes

20
Q

When might you see starvation in neonatal calves?

A

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

21
Q

What are the effects oprotein deficiency

A

look at notes

22
Q

What are the clinical signs of starvation?

A

similar to toher nutritional deficiency or subclin dz

23
Q

What are situations where nutritional deficiency may occur?

A
  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
24
Q

What is fatty liver also known as in cattle?

A

pregnancy toxemia?

25
Q

Why does fatty live roccur?

A

excessivve fat mobilization from body reserves to liver

26
Q

When does fatty liver ocur?

A

around time of parturition

27
Q

Who does fatty liver occur in?

A

sudden increases inenergy demand or decreases in intake

28
Q

Why do cattle get fatty liver?

A

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

29
Q

What happens when liver triglyceride is high with VLDL?

A

VLDL secretion further reduced due to hepatic insufficiency

30
Q

What is the epidemiology of fatty liver?

A
  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
31
Q

How do you diagnose fatty liver?

A

liver biopsy

mild 40% lipid

32
Q

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

A

> 35%

33
Q

How high can case fatality rate be with fatty liver?

A

as high as 90%

34
Q

Wht are the clinical signs of fatty liver?

A 
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
35
Q

what are lab findings with fatty liver

A
  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.
36
Q

Why are ketones unreliable for fatty liver diagnosis?

A

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

37
Q

What is treatment for fatty liver

A

> 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)

38
Q

How do you control fatty liver?

A

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

39
Q

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

A

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

40
Q

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

A

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
41
Q

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

A
  1. reduce fat mobilization
  2. increase VLDL secretion from liver
  3. increase FA oxidation
42
Q

What are feed additives used to decrease fat mobilization

A
  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
43
Q

What are feed additives used to increase liver VLDL secretion

A
  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
44
Q

What are feed additives used to increase FA oxidation?

A

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?

Food animal production (21 decks)

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