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IP11 - Food Animal Medicine > Metabolic and Nutritional Diseases > Flashcards

Metabolic and Nutritional Diseases Flashcards

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1
Q

Primary copper deficiency is due to:

A

Inadequate dietary copper concentration

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2
Q

Secondary copper deficiency can be due to:

A

Iron, sulfates, zinc - make copper poorly absorbed

Molybdenum in excess - binds to copper and lowers copper bioavailability

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3
Q

Risk factors to copper deficiency

A
  • All milk diets (low copper levels)
  • Young animals
  • High growth rate
  • Animals on forage diets instead of concentrate diets
    • Fescue plants impair copper absorption
  • Lack of Supplementation
  • Breed - Simmentals are overrepresented
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4
Q

Why do cows need copper?

A
  • Involved in a variety of enzyme systems (superoxide dismutase, cytochrome oxidase, lysol oxidase, ascorbic acid oxidase, ceruloplasmin)
  • Required for iron metabolism
  • Prevention of cellular oxidative damage
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5
Q

Copper Deficiency Syndromes - presents in a variety of clinical signs, what is the MC? Why does it happen?

A

Hypochromotrichia - lightening of hair coat - morphologic and functional changes in the melanocytes (reduction of tyrosinase activity)

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6
Q

Diarrhea is a sign of copper deficiency - why do we see it?

A

Mucosal and villous atrophy

Crypt elongation + goblet cell hyperplasia –> unable to absorb things appropriately

Cytochrome oxidase does not work

Mitochondrial change - cells will not function appropriately chronically

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7
Q

Why do we see spontaneous fractures in copper deficiency?

A

Irregular thickness of physis joint deformation, and bone fragility due to decreased lysyl oxydase function and decreased Cu-ATPase.

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8
Q

What kind of CNS abnormalities are seen with copper deficiency and why do they occur?

A

Sway back + enzootic ataxia and weakness in back legs

Cows born with oligodendrocyte dysfunction - NOT acquired

Decrease cytochrome oxidase and decreased superoxide disumutase in utero

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9
Q

What kind of anemia is present on blood work in an animal with copper deficiency?

A

Secondary iron deficiency anemia - macrocytic, hyperchroic anemia

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10
Q

Why do we see anemia in copper deficienct cows?

A

Decrease in ceruloplasmin and iron oxidation

Decrease in ALA dehydrase and heme syntehsis

Decrease in erthrocyte survivability

Protein cytoskeleton alterations

Increased cell viscosity via lipid loading

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11
Q

Clinical manifestations of reduced repro performance in copper defiency include:

A

Increased time to puberty

Decreased conception rates

Anestrus

Fetal resoprtion

Decreased semen quality

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12
Q

Copper deficiency can compromise the immune system. How does this represent itself in a herd?

A

When cows start becoming infected with pathogens that are unlikely to cause disease normally.

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13
Q

What is the timeline of copper deficiency in regards to where it gets depleted first, and when clinical signs start to show up

A

First copper ges depleted from tissues, then plasma, then from the enzyme systems (biochemical function effected).

When copper gets depleted from tissues and plasma, we often do not see any C/S yet. However, once there is not enough copper for all the normal enzyme systems and it effects biochemical function, we start seeing disease.

With copper - you have to really depelete body stores before animal shows C/S.

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14
Q

Where is copper stored in? What significance does this play in our diagnosis of copper deficiency?

A

Stored in the liver - if we are looking for early deficiency - liver is our best sample to detect copper deficiencies.

Once copper gets depleted from the liver, plasma levles will drop off and clinical signs start showing - so testing blood levels will diagnose copper deficiency at this point.

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15
Q

When testing cows for copper deficiency, can you test cows from just one pasture, if you have 15 differnt pastures?

A

No - each pasture is a different herd that NEEDS to be tested becuase each pasture has different micronutrients in the soil.

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16
Q

Treatment and prevention of copper deficiency

A

Copper supplementation:

dietary - test for copper, molybdenum, sulfer; adequate feed levels not always enough (remmeber inhibitors)

Injection

Copper oxide needles for sustained copper release

Copper boluses

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17
Q

Reason for selenium deficiency?

A

Inadequate intake

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18
Q

Syndromes that result from selenium deficiency

A
  • Nutritional myodegeneration
  • Decreased reproductive performance
  • Retained fetal membranes
  • Increased disease susceptibility
  • Increased gram negative mastitis
  • General ill thrift
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19
Q

During what season (drought or wet) will make selenium less available in plants?

A

drought/drying will make selenium less available

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20
Q

Selenium is requried in which enzyme system?

What vitamine does in funciton in concert with?

A

Glutathione peroxidase (GSX-Px) - reduces peroxides and super oxides within the cytosol

Functions in concert with vitamine E

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21
Q

Why do we tx selenium deficiencies with vitamin E right away, instead of just selenium?

A

Vitamin E spares glutathione peroxidase - meaning it becomes an antioxidant right away.

In contrast, selenium needs to be incorporated in the glutathion peroxidase enzyme in order to become an antioxidant, which takes 7-10 days.

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22
Q

Selenium deficiency can cause nutritional myodegeneration - what is this disease called?

A

White muscle disease

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23
Q

White muscle disease affects ____ and ____ muscles in neonates; and ____ muscles in yearling/juveniles.

A

cardiac; diaphgramatic

Skeletal

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24
Q

What is the diagnostic sample of choice in dx selenium deficiency?

A

Whole blood

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25
Q

When collecting whole blood samples to dx selenium deficiency, what tube do we use?

A

Royal blue top tube - plastic with plastic stopper

Some micronutrients can interact with the rubber stoppers, so you want plastic.

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26
Q

Serum chem on white muscle disease will show massive increases in ___ and ____.

A

High CK and AST

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27
Q

T/F: Liver biopsies are more useful in selenium deficiencies than copper deficiencies.

A

False - liver biopsies are more userful in copper deficiencies

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28
Q

Treatment and Prevnetion of selenium deficiency

A
  • Injectable selenium (must be incorporated into glutathione peroxidase to be metabolically active - takes 10-14 days)
  • Injectable vitamine E (more immediate results)
  • Commercial selenium products
  • Dietary supplementation
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29
Q

T/F: An injectable selenium product that is advertised to have vitamine E as well is enough to tx selenium deficiency.

A

False - not enough vitamine E to be a useful antioxidant - need to give a PURE vitamin E injectable product.

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30
Q

Vitamin A is required for:

A

Normal bone growth

Epithelialization

Regeneration of rhodopsin (required for night vision)

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31
Q

T/F: Night blindness is a common C/S in vitamin A deficiency.

A

True

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32
Q

Reasons of vitamin A defiency

A

Lack of intake

Sun cured forages (poor quality roughage, prolonged sotrage of roughage, no/little roughage)

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33
Q

Clinical signs of vitamin A deficiency:

A
  • Encephalopathy - coritcal based neurologic signs
  • Night blindness
  • Incoordination, weakness
  • Repro failure
  • Squamous metaplasia
  • Hyperkeratinization of the skin, rumen, reticulum, and preputial membrane
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34
Q

Dx vitamin A deficiency:

A

Increase in CSF pressure- not commonly checked

Decrease in plasma and liver vitamin A

Decrease in liver carotene

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35
Q

Tx of vitamin A deficiency

A

Vitamin A supplementation (injectable!)

High quality hay

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36
Q

Common name of parutrient paresis/hypocalcemia

A

Milk fever

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37
Q

Why does milk fever happen?

A

Failure of homeostatic mechanisms to control blood calcium levels.

Results from the onset of lactation in older high-producing dairy cows.

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38
Q

When blood calcium drops, what happens to PTH and what does PTH do?

A

PTH increases - which stimulates mobilization of calcium and phosphorous from the bone, and simtulates calcium resorption and phosphate excretion by the kidney.

Increased secretion of PTH also causes synthesis of 1,25 Vit D in the kidney which stimulates calcium binding protein, which increases intestinal absorption of calcium.

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39
Q

T/F: High calcium diets in dry cow ration can cause milk fever after parturition with the onset of lactation.

A

True

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40
Q

T/F: Calcitonin limits bone resorption and favors calcium deposition, and drives urine excretion of calcium.

A

True

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41
Q

Low Ca prepartm diet _____ PTH secretion.

Low magnesium diet ___ the normal response to PTH.

A

Increases

Blunts

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42
Q

Metabolic alkalosis _____ renal sensitivity to PTH.

Metabolic acidosis _____ in bone, favoring the function of PTH.

A

decreases

buffers

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43
Q

PTH works best at a slightly _____ pH.

A

acidic - around 7.3

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44
Q

A dry cow requires 10-12 g of calcium/day. A lactating cow requires approximately ___g/____kg of milk.

A

50g/40kg

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45
Q

Most milk fever cows present within the ____ week post calving.

A

First

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46
Q

__% of cattle relapse with milk fever. How can we prevent relapse?

A

20%; give calcium via IV and sunQ

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47
Q

Predisposing factors to milk fever

A
  • Older cows
    • Fewer active bone cells
    • PTH receptors decrease with age
  • High milk producers
  • Prepartum diets (high phosphorus and calcium)
  • Anion cation balance
    • Na/K alkalinizing - bad
    • (Cl/sulfur acidifying - promote bone resorption - good)
  • Jersey breed
    • Decrease in intestinal 1,25 vit D receptors
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48
Q

During midlactation, a cow depends almost entirely on _____ calcium abosprtion to replenish blood calcium content.

A

Intestinal

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49
Q

Hypomagensemia can precipitate midlactation hypocalcemia. What seasons is this most common?

A

Spring and fall in pasture based dairies

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50
Q

Estrogen ___ bone resorption.

A

Inhibits

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51
Q

Describe the three stages of milk fever

A
  • Stage 1
    • Cow is standing
    • Mild signs often missed
    • Nervousness, agitation, excitement, tetany
    • Muscle tremors, anorexia, stiff gait
  • Stage 2
    • Sternal recumbency
    • “classic signs” - head to side, elevated HR, cold extremities
  • Stage 3
    • Lateral recumbency
    • Comatose, faccid, heart hard to auscult, severe bloat, death
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52
Q

General clinical presentaiton of milk fever

A
  • Anorexia
  • Rumenal atony
  • Generalized weakness
  • Circulatory collpase - decreased CO by 60%
    • Tachycardic, weak heart sounds
  • Dry muzzle (sweat glands not working)
  • Mental depression
  • Hypothermia - cannot regulate body temp b/c not circulating
    • May be hypothermic if sitting in the sun
  • Dilated sluggish pupils
  • Scant feces (GI not moving)
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53
Q

Hypocalcemia in ewes is most often seen when? Why?

A

Late gestation - stress induced, often concurrent with preg tox

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54
Q

Hypocalcemia can occur both in the ____ and _____ period in goats.

A

Prepartum and postpartum

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55
Q

Dx milk fever in small ruminants:

A

Recumbency with typical history is very suggestive.

Can check serum calcium - diagnostic test of choice - however we do not often run blood calcium levels

Magnesium should be elevated

Phosphorus typically low

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56
Q

T/F: Ionize calcium levels are a much better dictator of the cows status than total calcium.

A

True

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57
Q

Alkalosis increases albumin/Ca binding and reduces ionized calcium concentrations. What effect does this have on the cow in terms of clinical signs?

A

Alkalotic cow may have clinical signs in face of a normal serum calcium.

58
Q

Treating milk fever with oral Ca-chloride or Ca-proprionate gels work very well, but need to be careful becuase they are _____ to damaged mucous membranes, and only work if the rumen is _____.

A

Caustic; moving

59
Q

The cornerstone of milk fever tx is?

A

Calcium borogluconate/gluconate IV or subQ

60
Q

How can you reudce milk fever relapse?

A

Give 2nd bottle of calcium SQ

61
Q

T/F: High calcium diets prevent milk fever

A

False - do NOT work - increase in calcitonin - slower response

62
Q

Best way to prevent milk fever?

A
  • Mobilize Ca prepartum
    • Low calcium transition diet
    • Anionic salts - to create mild metabolic acidosis
      • Needs to be in a total mixed ration - b/c bitter and tastes horrible
63
Q

What is required when giving anionic salts to prevent milk fever?

A

It is important to have multiple dry cow groups (different stages of dry cow diets) - cannot let cows eat anionic salts throughout the whole dry period

64
Q

What is our target DCAD when feeding anionic salts as a preventative for milk fever?

A

-50 mEq/kg

65
Q

We can acidify diet with DCAD diet in cows to prevent milk fever how many weeks prepartum?

A

3-5 weeks, but no sooner - cannot be on this diet for entire dry period

66
Q

We can restrict dietary calcium at least ___ days prepartum to prevent milk fever.

A

10 days

67
Q

How is phosphorous lost in the body?

A

Through urine, saliva, and feces

68
Q

Effects of PTH on phosphorous

A

Increased renal and salivary P loss (with hypocalcemia often see hyposphatemia)

Increased efficiency of intestinal P abosprtion (stimualtes kindey to make 1,25 vit D

69
Q

T/F: Hypoposphatemia stimulates PTH secretion

A

FALSE - only hypocalcemia stimulates PTH - calcium is the driver for PTH, phosphorous just comes along for the ride

70
Q

Signs of chronic hypophosphatemia

A
  • Failure to grow
  • Inappetance
  • Unthriftiness
  • Poor reproductive performance
  • Pica (animals go out and eat tings they typically do not - like bones from carcasses)
71
Q

What infectious disease can pica lead to?

A

Botulism (from eating rotten carcasses)

72
Q

Acute hypophosphatemia occurs in late gestation due to ____ fetal phosphorous demands and at the start of lacation becuase P goes into _____.

A

increased; colstrum

73
Q

C/S of acute hypophosphatemia

A

Recumbent, unable to ruse, but will still eat!

74
Q

Acute hypophosphatemia can cause postparturient hemoglobinuria (although uncommon) within the first ___ weeks of lactation.

A

6

75
Q

Postparturient hemoglobinuria is the result of _____ hemolysis.

A

Intravascular

76
Q

Why does acute hypophosphatemia cuase intravascular hemolysis?

A

Inorganic phosphorous is essential for erythrocyte glycolytic activity and ATP production. Low ATP levels result in increased RBC fragility.

77
Q

Cows with hypophosphatemia often have concurrent _______ and ______.

A

Hypocalcemia and hypomagnesemia

78
Q

One way to dx hypophosphatemia is to detect serum P in a blood chem. However it is important to separate the serum from your clot quickly, otherwise, hemolysis of the sample can falsely ____ P levels.

A

elevate

79
Q

T/F: Postparturient hemoglobinuria/hyposphatemia present with a slow onset of anemia.

A

False - RAPID

80
Q

Tx of acute hypophosphatemia

A

Oral: monosodium phosphate drench

IV: P supplied via monosodium phosphate dissolved in saline (usually need more than one single IV tx)

81
Q

You can also give a diluted fleet enema IV to tx hypophosphatemia. It is important to not give within ___ hours of IV calcium administration, and can be followed by oral _____ supplementation.

A

2 hours; phosphorous

82
Q

Enemas are VERY ______, therefore, they must be diluted with at least __ mL of water for ever 1 mL of enema solution.

A

hyperosmotic; 4 mL

83
Q

Hypomagnesemic tetany common names

A

Lactation tetany, grass tetany, wheat pasture poisoning, milk tetany

84
Q

Hypomagnesemic tetany is most common in foudn in what two seasons? Why?

A

Spring and fall (more common in fall in Missouri, spring in other states)

As grass grows quickly, no magnesium availabel in soil to support growth

85
Q

What are the four main types of hypomagnesemic tetany:

A
  • Grass tetany (late spring/early fall)
  • What/oat/barley pasture poisoning (young cereal grain pastures)
  • Winter tetany (poor plane of nutrition, poor quality roughage)
  • Milk tetany (calves 2-6 months of age on all milk diets with no access to pasture or milk replacer)
86
Q

Function of magnesium in the body

A
  • ATPases, kinases, phosphatases
  • RNA, DNA, and protein synthesis
  • Regulates membrane channels
  • Modulates synaptic transmission
87
Q

Vast majority of mangesium is found in the _____ (60-70%), then 2nd most in ____ _____ (30-40%), and the _____ at 1%.

A

Bone; soft tissues; ECF

88
Q

______ magnesium concentration is what dictates if animal gets sick from hypomagnesemia.

A

Extracullar fluid - due to ECF homeostasis

89
Q

ECF homeostasis is maintained when ____ meets or exceeds ____. There is no reserve mechanism.

A

Inflow; ouflow

90
Q

How is excess magnesium removed?

A

Excretion via kidneys

91
Q

What is the major absorption site of magnesium in preruminating (and monogastric) animals? In ruminating animals?

A

Large and small intestine in preruminating

Forestomach in adults

92
Q

Cattle will not absorb magnesium unless you have at least ____ g/day.

A

5.6

93
Q

How can low or normal intake of magnesium while grazing lush early pasture lead to hypomagnesmic tetany?

A
  • Excess cations (K+)
    • Decrease the absorption of Mg and Ca from diet
    • Decreases reabsorption of Mg and Ca from bone
  • Low sodium - secretion of aldosterone
    • Decrease of Na+ and increase of K+ in the saliva and hence the rumen
    • Increased K+ in the rumen decreases absorption of Mg+ from the diet
  • High protein - increases rumen ammonia (NH4)
    • Increased NH4 decreases Mg+ absorption from the diet
94
Q

Hypomagnesemic tetany can occur late in ____ and early in ____ due to the increased demand for magensium an calcium.

A

gestation; lactation

(decreased caclium will exacerbate condition)

95
Q

How can catechoalmines lead to hypomagnesemic tetany?

A

Cause shift of Mg from ECF to ICF

May be precipitated by stress of transport or severe cold weather

96
Q

T/F: Magnesium labile rerserves are decreased in older animals.

A

True

97
Q

Hypomagensemic tetany is more common in which breeds of cattle?

A

Angus; shorthorn (dairy)

98
Q

_____ breed of cows have higher absorption and retnetion of magnesium.

A

Brahman

99
Q

Hypomagnesemic tetany is most common just prior to and up to ____ days post calving during lactation.

A

30

100
Q

A ____ factor is often involved prior to the onset of clinical disease of hypomagnesemic tetany.

A

trigger

101
Q

Clinical signs of hypomagnesemic tetany are more closely associated with ___ Mg concentrations than serum Mg concentrations.

A

CSF

102
Q

C/S of acute hypomagnesemic tetany

A

Anorexia, decreased production, separation from the herd

Unusual state of alertness, aggressiveness, hyperasthesia

103
Q

C/S of acute hypomagensemic eventually progress to:

A

Stiff gait, stagger, wobbly nystagmus

Tiatnic spasms, thrashing,opisthotonus (severe hyperextension)

104
Q

T/F: Gross pathologic lesions are diagnostic of hypomagnesemic tetany.

A

False - not sepcific - nondiagnostic

105
Q

Best antemortem samples in diagnosiing hypomagnesemic tetanus

A

Serum Mg

CSF Mg

Urine Mg

106
Q

What postmortem samples can you take to dx hypomagnesemic tetany:

A

Heart blood

CSF tap up to 12 hours

Eyeball up to 24-48 hours on ice

107
Q

Tx of hypomagnesemic tetany

A

IV Ca-Mg preparations (hypercalcemia provides some protections form toxic effects of Mg)

Often follow with SQ or oral

Can give magnesium chloride enema diluted in water

108
Q

Prevention of hypomagnesmeic tetany

A

Daily supplementation of Mg salt

Transition feed changes

Legume hays

Avoid high Na+ and K+ fertilized pastures

Avoid stressors

109
Q

Ketosis is a disease of ____ energy balance.

A

Negative

110
Q

Cattle are particularly at risk of ketosis becuase little dietary ______ is absorbed yet a substantial requirement for ____ is present.

A

Carbohydrate; glucose

111
Q

In early lactation, milk production does not fall proportionally to _____ availability.

A

glucose

112
Q

Why is ketosis more common in early lactation than late lactation?

A

In early lactation - we will start to use fat stores if glucose is low. In late lactation - lactation/milk production will simply fall if glucose is low.

113
Q

Another word for ketosis

A

Acetonemia

114
Q

Primary vs seconary ketosis

A
  • Primary
    • cattle are in good body condition
    • High lactation potential
    • Can’t eat enough to supply demand
  • Secondary
    • Decreased intake due to other diseases (LDA, metritis, mastitis, hypocalcemia)
    • Intake must be proportionately more than production in order for animal to not become ketotic
115
Q

60% cases of ketosis occur within ___ days of calving, most in the first ____.

A

60; month

116
Q

Risk factors for ketosis

A
  • LDA, metritis, mastitis, hypocalcemia
  • Long dry period (fatter/higher condition score)
  • Excessive condition at calving
  • Twins
117
Q

Ketosis is common in high producing dairy cattle. Why?

A

The need more energy for milk production, but can only eat so much - not enough to maintain that high milk production, so they start mobilizng fat.

118
Q

Out of the three volative fatty acids (acetate, proprionate, and butyrate) that are absorbed through the rumen, which one is the most efficient in making glucose by directly entering the TCA cycle right away?

A

Proprionate - 3 carbon backbone - can go straight into the TCA cycle

119
Q

Three pathways free fatty acids can go in:

A
  1. Complete oxidation - goes into TCA to generate glucose - good!
  2. Incomplete oxidation - formation of ketone bodies
  3. Esterification - triglyceride deposition (fat deposition)
120
Q

Why are ketone bodies not an ideal source of energy?

A

Not all tissues can utilize them - mammary gland and brain cannot use ketone bodies

121
Q

VFAs vs Ketones

A
  • VFAs
    • Absorbed form the rumen; biproducts of microbe metabolism
    • Acetate, proprionate, butyrate
  • Ketones
    • Produced in the liver, alternate energy source, product of fat metabolism
    • Acetoacetate, acetone, betahydroxybutyrate
122
Q

Subclinical ketosis often occurs within the first ___ months post partum

A

2

123
Q

Subclinical ketosis often has no apperent clinical signs, but may decrease _______ and increase ______.

A

Decrease milk production

Increase disease susceptibility

124
Q

C/S of ketosis

A
  • Anorexia
  • Decreased milk production
  • Dramatic weight loss
  • Dry feces
  • Depressed
  • Smell ketones on breath and milk (acetone or garlic-like)
125
Q

Nervous system signs of ketosis

A

Intermittent!!

Head pressing, blindness, aimless wandering, licking and chewing at objects, bellowing, belligerent

126
Q

Best diagnosis of ketosis

A

Measuring in the serum!

127
Q

Why are urine dipsticks not the best diagnostic method for ketosis? Why are milk ketones not hte best diagnostic method?

A

Becuase urine dipsticks only detct acetone or acetoacetate, but the most common ketone in ketosis is betahydroxybutyrate.

Milk ketones are only detectable if cow is severely ketotic.

128
Q

Serum chem for ketotic cow

A

Ketones (beta-hydroxybutyrate MC) + NEFAs (non-esterified fatty acids)

Low blood glucose

Liver parameters - elevated AST, GGT, bilirubin due to depositing fat in the liver

129
Q

Fatty liver starts prepartum, and is the result of lipid accumulation triggered by increases ____ due to reduced ____.

A

NEFAs; DMI

130
Q

Fat cows have a greater drop in ____ at calving and more health problems.

A

DMI

131
Q

Insulin resistance results in suppression of ____ and more fat _______, inreasing risk for fatty liver.

A

Lipolysis

mobilized

132
Q

Clinical presentation of fat cow syndrome

A
  • Overconditioned in dry period (BCS of 4 or 5 out of 5)
  • Depression
  • Anorexia
  • Decreased milk production
  • Loss of condition
  • Enlarged liver - pale, often friable, with round borders
  • Concurrent disease (b/c liver cannot detox, making animal susceptible to variety of inflammatory and infectious diseases)
  • Lack of response to tx for other pathology
133
Q

Dx of fat cow syndrome

A
  • Changes in liver enzymes, ketones and triglycerides
  • Liver biopsy - diagnostic of choice for definifive diagnosis
134
Q

Tx of ketosis

A
  • Correct underlying disease
  • Get cow eating again!!!
  • IV dextrose
  • Oral propylene glycol - source of glucogenic precursors, rumen MUST be functioning!
  • Transfaunation (transfer of microbes from healthy cow to sick cow)
  • Glucocorticoides (increase plasma gluconeogenesis, decrease glucose uptake by mammary gland)
  • Insulin
  • Rumensin (monensin) - ionophore
135
Q

Why do farmers often prefer isoflupredone acetate over dexamethasone when tx ketosis in a cow?

A

Isoflupredone acetate is labelled for adjunct tx of ketosis, it has a lot of mineralocorticoid activity which bottoms out pogassium levels, however has less glucocroticoid activity than dex, so it will not drop milk production as much.

136
Q

Why is insuline used to tx ketosis? What must be monitored when giving insulin?

A

Insulin decreases FFA mobilizaiton and facilitates cellular uptake of glcoses.

However, MUST monitor blood glucose to make sur eyou have not pushed htem in the opposite direction.

137
Q

Why do we use rumensin as a tx of ketosis

A

Rumensin is an ionophore - it pushes microbe population towards making proprionate VFAs

138
Q

Tx of fat cow syndrome

A
  • Similar to ketosis
  • Regain positive energy balance
    • Dextrose CRI
    • Insulin
    • Propylene glycol
  • Increased feed intake - palatable, force feeding
  • Antibiotics to keep off secondary infectious inflammatory events
139
Q

prevention of ketosis

A

Fix dry period problems:

Correct length (45 days), maintain body condition score of 3.5, adequate diet

Monensin - to drive proprionate formation

140
Q

Prevention of fat cow syndrome

A
  • Dry cow:
    • Increase ration energy content
    • Avoid condition loss
    • Avoid condition gain
  • Early lactation
    • Optimize energy intake
    • Maximize intake of high quality roughage
    • Well balanced energy and protein
    • Ionophores

IP11 - Food Animal Medicine (10 decks)

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