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LA DX & TX II > Exam 2 - Food Animal Metabolic Disorders > Flashcards

Exam 2 - Food Animal Metabolic Disorders Flashcards

1
Q

what is another name for milk fever?

A

bovine parturient paresis, hypocalcemia

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2
Q

what production animals are most commonly affected by milk fever?

A

dairy cattle, sheep, & goats

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3
Q

what is milk fever?

A

hypocalcemia - failure of calcium homeostasis to maintain normal blood calcium concentration at or near parturition & the onset of lactation due to the high demand for Ca for sudden milk production

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4
Q

what is the main clinical sign associated with milk fever in production animals that is different than dogs?

A

FLACCID PARALYSIS

dogs - more tetany/rigid

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5
Q

what is a subclinical level seen on labwork that indicates milk fever?

A

plasma calcium concentration <8.59 mg/dL

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6
Q

what is the clinical level seen on labwork that indicates milk fever where you will see clinical signs?

A

<6 mg/dL

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7
Q

when do we see the onset of milk fever?

A

usually occurs with in 48 hours of calving

twin syndrome - happens prior to calving

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8
Q

T/F: a heifer won’t produce as much milk when compared to a 3rd time lactating cow

A

true

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9
Q

what animals are most susceptible to milk fever?

A

DAIRY CATTLE!!!! rare in beef

high producing cattle - cows in 3rd or greater lactation because younger animals have more Ca/P stores available for reserve

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10
Q

why are older cows susceptible to developing milk fever?

A

the amount of labile bone calcium decreases with age

number of vitamin D receptors decrease with age

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11
Q

what breed is predisposed to milk fever? why?

A

jersey cows

they have fewer vitamin D receptors than holstein cows

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12
Q

what are calciotropic hormones?

A

hormones that are involved in the regulation of calcium

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13
Q

what are the 2 main hormones involved in calcium regulation?

A

PTH & calcitonin - both act together to regulate blood calcium

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14
Q

what effect does the release of PTH have on calcium in the body? when do we see the release of PTH?

A

increases blood calcium levels

if calcium falls below a certain set point - PTH is released

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15
Q

T/F: PTH responds to LOW blood calcium concentrations

A

true

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16
Q

what effect does the release of calcitonin have on calcium in the body? when do we see the release of calcitonin?

A

decreases blood calcium

calcium in the blood becomes higher than set point - calcitonin released

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17
Q

how does PTH work to increase calcium in the body? what organs does it act on?

A

stimulates osteoclasts to break down bone reabsorption of stored calcium - releases both calcium & phosphorus from the bone

acts on the kidney & activates vitamin D3 which stimulates the rumen to absorb more calcium

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18
Q

how does calcitonin work to decrease calcium in the body? what organs does it act on?

A

bone - calcitonin suppress resorption of bone by inhibiting the activity of osteoclasts causing less bone resorption of calcium & causes increased osteoblast activity leading to more bone deposition of calcium

kidney - calcitonin inhibits tubular reabsorption of calcium leading to the increased rate of loss in the urine

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19
Q

what are some examples of factors that may alter the body’s response to PTH or calcitonin in cows?

A

hypomagnesemia

hypophosphatemia

sufficient vitamin D

dietary cation - anion difference

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20
Q

how does hypomagnesemia alter the effects of PTH in a cow with milk fever?

A

reduces PTH secretion in response to hypocalcemia - blunts the response because magnesium is needed for PTH to bind to its targeted tissues

low magnesium = less sites for PTH to bind to

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21
Q

how can we reduce the risk of hypocalcemia due to hypomagnesemia in a cow with milk fever?

A

provide adequate magnesium in pre-fresh diets to reduce the risk for hypocalcemia

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22
Q

how does hypomagnesemia alter the effects of calcitonin in a cow with milk fever?

A

interferes with the activation of vitamin D by inhibiting activity of renal 1 hydroxylase enzyme

so without proper vitamin D, the body can’t properly absorb Ca from the diet

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23
Q

how does the dietary cation-anion difference affect cows with milk fever?

A

influences the blood acid-base status which in turn affects calcium homeostasis in the body

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24
Q

how does feeding cationic rations affect calcium homeostasis?

A

feeding a pre-partum diet higher in cations (+ charged elements: Na & K) in relation to anions (- charged elements: S, Cl, P)

results in a METABOLIC ALKALOSIS & depresses tissue response to PTH - low calcium, & PTH can’t effectively work to raise calcium levels in the blood

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25
Q

how does feeding anionic salt rations affect calcium homeostasis?

A

feeding a diet that is higher in anions than cations

RESULTS IN A METABOLIC ACIDOSIS - allows calcium carbonate to be released to correct the acidosis & increases calcium levels in the blood!!!!!!!

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26
Q

why would you want to feed an anionic ration to get a cow with milk fever into a metabolic acidosis?

A

if you get them into a metabolic acidosis, calcium carbonate is released to correct the acidosis & simultaneously raises calcium levels in the blood

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27
Q

if you are using a dietary cation-anion difference, what should you monitor for?

A

watch the amount of feed intakes

monitor the cow to ensure they are acidotic - check urine pH

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28
Q

T/F: dietary acidity/alkalinity is more important in controlling hypocalcemia than actual calcium intake

A

true

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29
Q

diets high in what increase the risk for hypocalcemia? diets high in what reduce the risk?

A

diets high in sodium or potassium - cationic rations

diets relatively high in sulfur or chlorine

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30
Q

what is stage 1 of milk fever?

A

wobbly animal that is still on their feet

will see muscle tremors, firm manure, anorexia, & slowed rumen contractions, may have cool ears, heart rate that is quiet/muffled & slightly higher, & temp usually subnormal to normal

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31
Q

what is the normal TPR of a cow?

A

temp - 100-102.5
HR - 50-80
RR - 10-30

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32
Q

what is stage 2 of milk fever?

A

EMERGENCY - down cow that is unable to rise with very cold ears

look for an animal in sternal recumbency, ‘s’ shaped neck, bladder atony (full bladder), low temp <100, increased HR >80, & trouble swallowing/eructating

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33
Q

what is stage 3 of milk fever?

A

EMERGENCY - cow is ‘out flat’

bloated (hypomotility/ileus), HR >100, temp <98, poor circulation so ears are ice cold (feel difference between neck & ears), can’t swallow (can lead to aspiration pneumonia & death)

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34
Q

what would bloodwork look like on a cow in stage 3 of milk fever?

A

decreased calcium (<6mg/dL), decreased phos, & increased magnesium

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35
Q

what stage of milk fever is seen in this photo?

A

stage 2

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36
Q

what stage of milk fever is seen in this photo?

A

stage 3 - flat out bloated cow

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37
Q

T/F: subclinical hypocalcemia at calving (serum Ca <8.59 mg/dL) is associated with impaired neutrophil function & increased risk of metritis/mastitis

A

true

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38
Q

what signs of dystocia may be seen in a cow with milk fever?

A

uterine inertia, flaccid uterus with no contractures/tone

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39
Q

T/F: milk fever can cause a retained fetal membrane or retained placenta

A

true

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40
Q

what animals with milk fever do we see uterine prolapse in?

A

beef cattle with low grade hypocalcemia

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41
Q

is milk fever associated with causing breeding issues in cows?

A

yes - high % of cows not getting bred back/multiple breedings, etc

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42
Q

what treatment is used for stage 1 milk fever?

A

oral calcium preperations - drenches, place a tube, boluses, or IV

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43
Q

why is calcium propionate often picked over calcium chloride for a cow with milk fever? what are the disadvantages of using it?

A

it is less irritating!!!! safer for a producer to do

doesn’t induce the metabolic acidosis & may not be as effective & has a slower absorption

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44
Q

what are the advantages of using calcium chloride for a cow in stage 1 of milk fever? what are the disadvantages?

A

can induce a metabolic acidosis, has a fast absorption, & provides the greatest ability to support blood calcium concentrations

compound is corrosive & a tube needs to be placed into the rumen - will cause tissue necrosis in the esophagus

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45
Q

what is the #1 direction you should give a producer with a stage 2 milk fever cow while you’re on your way there? why?

A

DON’T GIVE ANY ORAL MEDICATIONS TO A DOWN COW - risk of aspiration pneumonia

give oral treatment if the cow is standing or sternal & swallowing/ruminating normally

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46
Q

why should calcium borogluconate be administered slowly IV?

A

can cause bradycardia & hypovolemia & death - monitor the heart while giving it

hold it at head height

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47
Q

what is the dose used for IV calcium borogluconate?

A

1gm/100 lb (1-500 ml btl 23% where Ca = 115g)

most give 1 bottle per cow

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48
Q

how is IV calcium given to a stage 2 milk fever cow?

A

given slowly at head height

follow with oral products (bolus, drench, gel, paste) when sternal/up & able to swallow

monitor for hypophosphatemia, hypokalemia, & hypomagnesemia

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49
Q

how is a stage 3 milk fever cow treated?

A

cow that is out flat needs to be propped sternal if possible

treat bloat with orogastric tube or trochar to relieve gas, bloat drench

reduced milking of these animals can cause mastitis

continue calcium supplementation until cow is completely normal

educate client on subtle signs of hypocalcemia (trembling, weakness, ataxia)

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50
Q

how should a stage 3 out flat milk fever cow be handled/moved?

A

sling/mat to move or hip lifters (caution with hip lifters, don’t pick up & hold in the air) if they don’t get up, put them back down

provide good footing to prevent slipping & injuries

provide shelter, accessible food/water, & hobbies to keep them from splitting themselves

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51
Q

what is the prognosis for pursuing treatment in a stage 1 milk fever cow?

A

excellent prognosis

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52
Q

what is the prognosis for pursuing treatment in a stage 2 milk fever cow?

A

good to guarded depending on the time the animal has been down & their will to live

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53
Q

what is the prognosis for pursuing treatment in a stage 3 milk fever cow?

A

guarded to grave

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54
Q

T/F: the longer a cow is down with milk fever, the more damage to muscle & nerves & increased risk for other issues

A

true

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55
Q

how is milk fever prevented using nutrition in pasture dairy operations?

A

pre-partum diets low in Ca (20gr/cow/day) - very low & not practical in a typical dairy but may work on a pasture

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56
Q

what is the most practical prevention method for nutrition used for milk fever in cows?

A

nutrition management during the dry period using the dietary cation-anion difference adding anionic salts to create a metabolic acidosis in order to increase ionized calcium & resorption

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57
Q

if >10% of a dairy herd are affected annually by milk fever, what are you thinking?

A

herd problem!!!! likely nutrition problem

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58
Q

what are some examples of prevention used for milk fever?

A

ensure the cow has a good appetite at calving

increase Ca in diet within 48 hours of calving

management to decrease stress - look at how the cows are being managed from dry off to close up to lactation groups

calcium supplement administered at calving & 24 hours after (boluses, electrolytes in water, tube them)

producers & veterinarians should discuss with nutritionist

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59
Q

when is milk fever seen in small ruminants? why does it occur?

A

hypocalcemia in pregnant & lactating ewes & does

same as dairy cattle - calcium demand increases rapidly & reserves aren’t present in our dairy breeds

meat goats/dairy goats - later stages of pregnancy with multiple fetuses requiring calcium

abrupt decrease in calcium intake & high calcium demand where they body requires 24-72 hours to activate the metabolic machinery necessary to mobilize stored calcium

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60
Q

what is the major difference in timing seen when comparing milk fever in dairy cattle to milk fever in small ruminants?

A

milk fever usually occurs in ewes & does before parturition & less commonly after parturition

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61
Q

T/F: milk fever in small ruminants is seen a lot with pregnancy toxemia/animal is off feed

A

true

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62
Q

why do we see milk fever occur in late gestation in small ruminants?

A

the greatest demand for calcium in the body is because of the mineralization of the fetal skeleton occurs 1-3 weeks pre-partum particularly when multiple fetuses are present

can occur at any time from 6 weeks to 10 weeks after parturition

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63
Q

what clinical signs of hypocalcemia are seen in small ruminants?

A

very acute onset - stiff gait, salivation, constipation, sternal frog leg position with hind legs extended behind, tachycardia

muscle tremors more commonly seen in goats than sheep, but goats will also do the frog leg position

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64
Q

what is the treatment for milk fever in small ruminants?

A

very similar if not identical to dairy cows - calcium borogluconate IV (50-150mL bolus) - monitor the heart for arrhythmias/bradycardia

oral administration

65
Q

what is the active form of vitamin D? what does it do?

A

1, 25 DHCC - active form

stimulates the rumen to absorb more calcium/phosphorus, reduced excretion of Ca/PO4 from the kidneys

66
Q

what produces PTH in the body?

A

parathyroid gland

67
Q

what is the major source of calcitonin in the body?

A

c cells in the thyroid gland - also synthesized in lungs & intestines

68
Q

how does calcitonin work?

A

responds to high blood calcium levels to decrease calcium absorption

69
Q

what is another name of cholecalciferol?

A

vitamin D3

70
Q

___ serum phosphorus levels stimulate calcitriol synthesis, whereas _____ serum phosphorus levels inhibit it

A

low

high

71
Q

how is milk fever prevented in small ruminants?

A

dietary modifications to increase the calcium:phosphorus ratio (> 1.5:1)

ensure total calcium in the diet meets the NRC along with vitamin D

avoid sudden dietary changes/stressors during late gestation & risk factors for pregnancy toxemia investigated

watch for severe weather changes

72
Q

why do we see post-parturient hypophosphatemia in cattle?

A

occurs due to high P demands during late gestation & early lactation or can occur due to long term P deficiency

73
Q

when do we see peri-parturient hypophosphatemia in cattle?

A

occurs at the onset of lactation - widely believed to be associated with peri-parturient recumbency & downer cow syndrome, but not commonly understood

74
Q

what are the initial signs seen in peri-parturient hypophosphatemia in cattle?

A

initial decrease in milk production, muscle weakness, staggering gait, anorexia, & bone pain

75
Q

what clinical signs are seen in peri-parturient hypophosphatemia in cattle that help you differentiate it from milk fever?

A

rhabdomyolysis, increased fragility of RBC causing intravascular hemolysis, hemoglobinuria, & anemia

76
Q

how can you differentiate between hematuria & hemoglobinuria?

A

spin it down

hematuria - blood spot in the bottom

hemoglobinuria - stays the same color

77
Q

how is hypophosphatemia diagnosed?

A

rule out other causes of intravascular hemolysis & response to treatment

downer cows that don’t respond well to Ca may have low P

measure blood phosphorus - concentration in serum can be misleading (many things can mess up results)

78
Q

T/F: in animals with milk fever, their heart rate is increased but their heart sounds are difficult to hear/muffled

A

true

79
Q

how is hypophosphatemia treated in cattle?

A

NaH2PO4 & Na2HPO4 are suitable to rapidly correct hypophosphatemia - tube the cow

dose is 60 grams in water or bolus capsules SID or BID

80
Q

T/F: oral sodium phosphate salts increase the plasma phosphorus concentration within 1-4 hours & last 12-14 hours

A

true

81
Q

what clinical signs are associated with hypokalemia in cattle?

A

serum potassium concentration <2.5 mEq

muscle fasciculations, flaccid paralysis, & eventual recumbency

pay attention to the animal’s history

82
Q

T/F: occurrence of hypokalemia in cattle is rare & has 2 main causes

A

true

83
Q

what are the 2 main causes of hypokalemia in cattle?

A
  1. isoflupredone ‘predef’ - iatrogenic cause, steroid commonly given to stimulate gluconeogenesis to treat ketosis in cattle & it causes low potassium (aldosterone like effects)
  2. dairy cows not eating >2 days, losing potassium in milk & intake is low
84
Q

why does isoflupredone cause hypokalemia in cattle? what drug can you give instead?

A

mineralcorticoid with aldosterone like effects causing potassium wasting

dexamethasone - glucocorticoid that doesn’t have mineralocorticoid effects

85
Q

what is the treatment of choice for hypokalemia? how is it given?

A

oral potassium administration!!!!

inappetent lactating dairy cattle should be treated with 60-120 g of feed grade KCl every 12 hours - can be placed in gelatin boluses or given by ororuminal intubation

86
Q

how is hypokalemia prevented in large animals?

A

oral administration of potassium to inappetent cattle, sheep, & goats

ensure adequate dry matter intake - best method to prevent hypokalemia in adult cattle

use dexamethasone instead of predef for ketosis

87
Q

what is another common name for hypomagnesemia?

A

grass tetany

88
Q

what large animals are most commonly affected by grass tetany?

A

beef cattle

89
Q

what is grass tetany?

A

high fatal disease that is most common in beef cattle - hypomagnesemia

90
Q

what animals are most susceptible to getting grass tetany? why?

A

adult lactating animals

they are losing magnesium in milk

91
Q

when do we see grass tetany occur?

A

mainly when animals are grazed on a lush green pasture or green cereal crops

can also occur when lactating beef cattle are fed silage - rare in non-lactating cattle but has occurred when malnourished cattle where introduced to green cereal crops

92
Q

what are the roles of magnesium in the body?

A

help with nerve conduction, muscle function, & role in the immune system

93
Q

why do we see grass tetany occur?

A

occurs when plasma Mg concentration drops while the absorption of dietary Mg is unable to meet the maintenance requirements

94
Q

what is the maintenance Mg requirement in a cow? what about in lactating beef cattle?

A

3mg/kg/day

20 grams/day

95
Q

why are magnesium blood levels dependent upon daily intake?

A

magnesium is not stored in the tissues - it is present in the bone, ICF, & ECF

96
Q

the only significant magnesium for the ECF comes from what?

A

intake from the diet

97
Q

what is normal for magnesium levels in the body?

A

1.7-3 mg/dL

98
Q

what level of magnesium in the body will show clinical signs?

A

<1.5 mg/dL

99
Q

T/F: grass tetany is often accompanied by hypocalcemia & hypophosphatemia

A

true

100
Q

what is the epidemiology of grass tetany?

A

cows in early lactation that are grazing on LUSH GREEN PASTURES high in K, N, & Na & low Mg, <0.2% Mg on a dry matter bases

typically winter grazing (planted fields) spring pastures - fast re-growing pastures (oats, rye, or after rains)

101
Q

what are some other risk factors for hypomagnesemia?

A

high ammonia in the diet/rumen reduces Mg absorption

diarrhea reduces the absorption of Mg & increases loss of Mg

102
Q

how do other ions in the body affect Mg?

A

high potassium decreases Mg & Ca absorption from the gi tract

high sodium lowers Mg in the ECF via increased urine excretion (heavy fertilizer)

high crude protein & lipid content diet can decrease Mg

103
Q

what clinical signs are seen in animals with grass tetany?

A

hyperexcitability/aggression, opisthotonus, muscle spasms/convulsions, ataxia in the rear legs, down cow that starts off sternal with early attempts to rise & progresses to lateral recumbency where the animal flops on their side

death - high mortality rate

104
Q

what is the typical signalment of a cow with grass tetany?

A

downer lactating beef cow on lush green pasture that is more alert/excitable than an animal with milk fever with muscle spasms

105
Q

which cow do you think has milk fever? what about grass tetany? why?

A

milk fever - left, calm cow with s-shaped neck

right - grass tetany, muscle spasms

106
Q

what is the treatment recommended for a cow with grass tetany?

A

magnesium IV - 500mL solution with calcium, magnesium, & phosphorus, 6 grams

NO ORAL MEDS TO DOWNER COW - start with IV & then can do oral if the cow becomes sternal or stands

correct other electrolyte abnormalities, supportive care, supply food/water/shelter if down, & use slings/hip lifters/float tanks - never drag any down cow by any body part

107
Q

why does grass tetany in a downer cow become an animal welfare issue?

A

can’t drag them - bring them food, water, & shelter!!!!

if you can’t give proper care - euthanasia

108
Q

what treatments can be used for any downer cow?

A

float tank can be used for any downer cow once treated appropriately & can stay alert/conscious - labor intensive & expensive

move them properly - have a protocol in place with trained personnel

109
Q

lactating beef cattle require how much magnesium a day?

A

20 grams a day!!!!

110
Q

what is the prognosis of grass tetany in cattle?

A

good to guarded in standing animals & poor to grave in down cows (high mortality)

111
Q

how is grass tetany prevented in cattle?

A

provide adequate amount of magnesium daily

feed Mg salts to animals grazing in risky conditions - begin feeding prior to lush grazing

Mg mineral free choice prior to grazing winter planted fields

avoid potassium fertilization in problem areas

112
Q

is hypomagnesemia common in small ruminants?

A

no - uncommon in sheep & even more uncommon in goats

113
Q

T/F: hypomagnesemia in small ruminants has the same clinical signs as grass tetany in cattle

A

true

114
Q

when do we see hypomagnesemia occur in small ruminants?

A

may be seen during a period of temporary starvation in late pregnancy or early lactation

movement of lactating ewes to lush spring growth pasture (especially green cereal crops) - exactly like cattle with grass tetany

115
Q

what is ketosis?

A

characterized by an abnormally elevated concentration of ketone bodies in tissues & body fluids that is a common disease in adult cattle

116
Q

what are some rare occurrences of bovine ketosis?

A

cattle in late gestation & resembles pregnancy toxemia of ewes

117
Q

what is the general cause of bovine ketosis?

A

cow is in a negative energy balance - early lactation requires a high energy demand in milk (glucose) & if the animal is not meeting those demands through nutrition/feed, a state of negative energy balance occurs

increase in energy output through milk production & decrease in energy input through low blood glucose & fat mobilization for energy

118
Q

what does a cow use for energy if they don’t have enough glucose?

A

fat & protein are mobilized to produce energy for maintenance & milk production, but the breakdown by product of fat & protein are ketones

adipose mobilization is accompanied by a high blood serum concentrations of non-esterified fatty acids

119
Q

what is the pathogenesis of bovine ketosis?

A

negative energy balance -> body breaks down fat & muscle for energy -> fat mobilization causes increased NEFA’s & ketone production

during periods of intense gluconeogenesis (muscle/protein breakdown), a large portion of serum NEFA are directed to ketone body synthesis in the liver - so characterization of ketosis includes high serum concentrations of NEFAs, ketone bodies, & low concentrations of glucose

120
Q

what are normal serum levels of glucose in cattle?

A

45-95 mg/dL

121
Q

what are the 3 types of ketones? where are the broken down in the body?

A

acetone, acetoacetate, & b-hydroxybutyrate

broken down by the liver

122
Q

when do we see negative effects from ketones?

A

when hepatic production & absorption of ketone bodies exceeds their use as an energy source & the liver can no longer keep up with processing ketones

123
Q

what animals are at risk for bovine ketosis?

A

fat cows - increased risk for fatty liver which interferes with liver function & can slow ketone processing by the liver

124
Q

when is type I primary ketosis seen?

A

occurs during peak lactation (3-8 weeks) as a result of negative energy balance - cows have a production curve that increases over time & decreases over time

125
Q

when is type II primary ketosis seen?

A

occurs early in lactation (1-10 days) & is usually accompanied with hepatic lipidosis (fat cow syndrome/fatty liver)

126
Q

what is secondary ketosis? what are some examples of things that may cause it?

A

results from reduced appetite associated with other problems that occur during the peri-parturient period

retained placenta, displaced abomasum, hardware disease, mastitis, & metritis

127
Q

what are some clinical signs associated with bovine ketosis?

A

dull/depressed animal - occasionally cow becomes hyper with staggerring, aggression, neuro signs, pica (nervous ketosis)

anorexia, sunken in rumen, stops eating grain 1st, then silage, then hay

normal to mildly low temp (may be elevated in secondary ketosis)

stiff manure, decreased output, rumen contractions are variable

ketone odor

total blood ketones are >15 mg/dL, urine ketones are >84 mg/dL, milk ketones are >10 mg/dL, blood glucose is 20-40 mg/dL

128
Q

how is bovine ketosis diagnosed?

A

blood total blood ketones blood meter is the most accurate on farm test - producer must be comfortable with drawing blood - used for clinically affected cows

full exam to look for secondary causes

129
Q

how do you make a cow urinate?

A

use the back of the hand & rub up and down just under the vulva

130
Q

what do trace ketone results indicate in a cow?

A

subclinical ketosis - not clinical because no systemic signs

131
Q

how is urine/milk ketone testing used by herdsmen for diagnosing bovine ketosis?

A

easier for them to do - done 7-10 days after freshening

catching primary type II ketosis 1-10 days post freshening with secondary cows with post-partum issues (retained placenta, mastitis, metritis)

132
Q

what is the major objective in ketosis therapy for cattle?

A

re-establishing normal feed intake & correcting the negative energy balance!!!

treat underlying causes if secondary ketosis - metritis, mastitis, retained placenta

133
Q

what is the mainstay therapy used for bovine ketosis?

A

providing glucose sources to correct the hypoglycemia

IV 50% dextrose - 1 bottle given IV, never SQ, can repeat once daily (constant drip isn’t practical)

134
Q

how is propylene glycol used for treating bovine ketosis?

A

8-12 ounces are given ever 12-24 hours no more than 5 days - will cause rumen microbes to die off & overdose causes CNS depression

135
Q

how are steroids used for treating bovine ketosis?

A

predef at 10-20mg/dose every 12-24 hours or dexamethasone 5-20mg IM/IV every 24 hours

helps to mobilize glycogen stores from the liver, decreases milk production which helps decrease the output & helps correct the negative energy balance

136
Q

what other treatments apart from glucose supplementation/steroids is used for treating bovine ketosis?

A

tube feeding/rumen fluid/probiotics/vitamin b complex

monitor ketones in blood/urine/milk for several days only stopping treatment 24-48 hours after ketones are NEGATIVE

continue to monitor feed intake & ketones in cows so they don’t relapse

137
Q

why use insulin for a cow with bovine ketosis that also has fatty liver disease?

A

suppresses both adipose mobilization & ketogenesis - need to give dextrose/glucose concurrently & monitor (long-acting insulin 150-200 IU/day)

138
Q

what is the prognosis for cattle with secondary ketosis?

A

it is dependent on the primary inciting cause

139
Q

what is the prognosis for bovine ketosis?

A

following treatment for subclinical cases - excellent

moderate to severe hepatic lipidosis in conjunction with ketosis - guarded

140
Q

how is bovine ketosis prevented?

A

avoid over conditioning cows in late lactation/early dry period (BCS of 3.5/5 higher risk for fatty liver & ketosis)

fresh cow program - monitoring ketones in blood/milk/urine on every fresh cow for 7-14 days

watch for post-partum issues

dry & up close management - transition ration, to prevent ketosis, maximize DMI & provide adequate energy density

silage ration - TMR & DMI after calving, manage to increase DMI

141
Q

what is the major difference between pregnancy toxemia in pregnant does/ewes & bovine ketosis?

A

similar pathogenesis but in does/ewes, happens prior to parturition!!!!!

142
Q

when is pregnancy toxemia seen in dairy goats?

A

last 4 weeks of gestation

143
Q

what ewes/does are typically affected by pregnancy toxemia?

A

multiple fetus pregnancy

144
Q

why does pregnancy toxemia occur?

A

insufficient intake of feed to meet the energy needs of the animal during gestation (each fetus requires 30-40 g of glucose/day in late gestation)

in order to meet energy needs, animal will break down fat stores which releases ketones

145
Q

T/F: sheep & goat fetuses add 70% of their final birth weight in the last 6-8 weeks of gestation

A

true

146
Q

how does fetus number affect the mother’s nutritional requirements during gestation?

A

singleton - 1.5-2x maintenance

twins - 1.75-2.5x

triplets - 3x maintenance

147
Q

what is the pathophysiology of pregnancy toxemia?

A

physical capacity of feed intake is reduced by the rapid abdominal expansion of the uterus & without management changes, dam can’t ingest enough to support herself or fetus which puts them into a negative energy balance

low blood glucose causes fat & protein mobilization leads to ketone production causing lethargy & loss of appetite

more fat mobilization & ketone production = negative cycle

148
Q

what is primary pregnancy toxemia?

A

thin or overweight animals with multiple fetuses that are not getting enough calories

149
Q

what is secondary pregnancy toxemia?

A

other condition causing them to go off of feed

150
Q

what are the clinical signs of pregnancy toxemia in does/ewes?

A

weakness/not wanting to rise, laying a lot more than other animals in the herd, initial signs are subtle

as it progresses - star gazing, tremors, circling, blindness, etc (looks neuro)

secondary pneumonia, muscle, & nerve problems in animals that are down for a long time

151
Q

how is pregnancy toxemia diagnosed in does/ewes?

A

blood glucose (low or can be normal), ketones in urine/milk/blood

non-esterified fatty acids can be increased above 0.4 mmol/L indicating hepatic lipidosis causing impaired liver function

152
Q

what differentials should be considered for a doe/ewe with suspected pregnancy toxemia?

A

hypocalcemia - in recumbent late gestational sheep & goats

hypomagnesemia - common in pregnancy toxemia but should be considered as a ddx

other CNS disease - polioencephalomalacia, rabies, scrapie, listeriosis

153
Q

how is pregnancy toxemia treated in does/ewes?

A

c-section if possible!!!!!!! lambs/kids may already be dead - if producer wants to save ewe/doe, use a proximal or distal paravertebral block, lay the animal in right lateral, & do the c-section on the left flank

viability of fetuses may be compromised if parturition is induced before day 144

154
Q

what is the normal gestation period in sheep & goats?

A

150 days

155
Q

successful induction of a doe/ewe with pregnancy toxemia relies on what?

A

intact fetal hypothalamic-pituitary-adrenal axis

156
Q

T/F: in goats alone, progesterone is made by the CL, so lutalyse alone will induce the animal

A

true

157
Q

*pregnancy toxemia treatment

A
158
Q

*didn’t get to fatty cow

A

LA DX & TX II (44 decks)

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