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Large Animal Medicine > Metabolic Disease of Ruminants > Flashcards

Metabolic Disease of Ruminants Flashcards

1
Q

You are called out to look at a down 4 y/o Holstein/Angus cross that freshened (gave birth) an hour ago. Which mineral is she most likely deficient in?

A

calcium

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2
Q

What is milk fever?

A

hypocalcemia most common in dairy cattle within hours of calving, resulting in the cow becoming sternally recumbent with an “S” curve of the neck into the flank

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3
Q

What cattle are most commonly affected by milk fever? Why?

A

mature dairy cattle > heifers

heifers have metabolically active bones able to efficiently move calcium into the serum

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4
Q

What signs are most commonly seen with milk fever?

A
  • acute downers with somnolence
  • no rumen motility or strength*
  • no PLR*
  • flaccid paralysis*
  • cold ears
  • rare tetanic spasms
  • mastitis, metritis
  • increased HR* with weak pulse
  • decreased body temperature
  • = calcium necessary for muscular contraction
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5
Q

What are some rule outs for milk fever?

A
  • broken bones (hip, legs) - downer
  • displaced abomasum - will hear a “ping” on percussion
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6
Q
A
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7
Q

What is the best test for diagnosing milk fever?

A

PLR

  • pupil will likely be dilated but cannot constrict
  • calcium required for muscle contraction
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8
Q

What kind of restraint is preferred when treating cows with milk fever?

A

tie halter with a quick release just above the hock to keep the head pulled for IV

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9
Q

What treatment is recommended for cows with milk fever? What response is expected?

A

calcium magnesium IV (500 mL) through bell catheter that attached to the bottle

  • decreased HR - slow/stop if there are CVS signs
  • burp followed with rumen motility
  • can follow up with more SQ or oral drench/gels
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10
Q

What diet manipulation is recommended for cows in a dry period to prevent milk fever?

A
  • add anionic salts to reduce metabolic alkalosis and blunt PTH responsiveness
  • acidity (negative DCAD) enhances calcium mobilization and uptake from the gut

monitor urine pH to see if diet is working (expect it to be ~6)

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11
Q

Why does milk fever occur in ruminants? What onset is associated in cows and small ruminants?

A

COWS = at calving due to sudden call for calcium to go to udder for milk production

SR = month prior parturition as a result to calcium demands for nurturing multiple feti in the last trimester

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12
Q

How does treatment for milk fever in small ruminants compare to cows?

A

treat the same with IV calcium magnesium if downer

  • can do oral or SQ if ambulatory
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13
Q

What is grass tetany? When does this most commonly occur?

A

hypomagnesemia more commonly seen in adult female cattle (both dairy and beef)

in pastures with rapidly growing green grass in the spring

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14
Q

How do cattle present with grass tetany?

A
  • acute downer with lateral recumbency
  • aggressive attitude, hyperesthesia
  • tetanic seizures = elevated temperature
  • uncoordinated, frenzied galloping
  • opisthotonos
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15
Q

How is grass tetany diagnosed? What other electrolytes are affected?

A
  • clinical signs, history, time of year
  • blood Mg levels may be normal in convulsing cows
  • low levels of Mg in CSF, but is difficult to obtain on seizing cows

low calcium

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16
Q

What are some differentials for grass tetany?

A
  • rabies
  • mad cow disease
  • nervous ketosis
  • nervous coccidiosis
  • tetanus
  • grass staggers
  • viral encephalopathies
  • heavy metal toxicants
  • heat stress
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17
Q

What treatment is used for grass tetany? How long does it take for signs to improve following treatment?

A

IV magnesium hypophosphate + calcium, leave cattle undisturbed (may need tranquilizers) +/- magnesium-rich gels or enemas

1-5 hours - takes time to reach CSF, relapses common, treatment is much more disappointing and difficult in comatose

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18
Q

How is grass tetany controlled?

A
  • provide magnesium in feed daily
  • supplement year-round in the south and a month before problem seasons (Spring!)
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19
Q

In what cattle is grass tetany most common? Why? What can decrease magnesium uptake?

A

adult beef cattle within 2 months of calving - 70% of magnesium is found in the bone and teeth and not readily available

high potassium in soil or plants (high K fertilizers!)

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20
Q

What are 3 other magnesium-related syndromes seen in cattle?

A
  1. WINTER TETANY - energy and magnesium deficient diets during severe weather, most common in mature animals
  2. TRANSPORT TETANY - high stress
  3. MILK TETANY - 2-4 m/o calves raised indoors and entirely on milk
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21
Q

What is seen on necropsy in cases of grass tetany? What 2 samples are specifically collected?

A

no definitive lesions - representative of convulsions, not disease

  1. vitreous humor (good for 48 hours)
  2. urine
    (check Mg levels)
22
Q

What clinical signs are associated with phosphorus deficiency? When is it most common?

A
  • ALERT downer
  • recumbency and muscular weakness
  • thin blood with icterus
  • CHRONIC: osteomalacia, post-parturient hemoglobinuria, ricketts
  • hypocalcemia associated, expect hypophosphatemia if Ca supplementation does not have an effect

late pregnancy and early lactation

23
Q

What causes pica in cattle?

A

mineral deficit they’re trying to meet

24
Q

What are 2 environmental causes of hypophosphatemia? How can this be seen in plants?

A
  1. deficient soils in dry, tropical regions
  2. heavy rainfall can leach P from the soil

purple discoloration - look around pasture!

25
Q

What is the normal Ca:P ratio in the bovine diet?

A

2:1

26
Q

What treatment is preferred for hypophosphatemia?

A

PHOSPHATES (monosodium phosphate) in fleet enemas —> PHOSPHITES in CMPK is NOT biologically active

  • hypocalcemia is most common, try this once calcium treatment fails and blood work is run
27
Q

How is hypophosphatemia controlled?

A

balance ratio —> Ca:P = 2:1

28
Q

When is hypokalemia commonly seen in cattle? What causes severe decreases?

A

milk fever cow with prolonged recumbency - excessive leakage from muscle fibrils

isoflupredone acetate (Predef) administration for ketosis (not as commonly seen with Dexamethasone)

29
Q

What are some signs of hypokalemia in cattle? How is it treated?

A
  • flaccid paralysis
  • sternal/lateral recumbency
  • cardiac arrhythmias

IV and oral KCl, most die or are euthanized

30
Q

What causes ketosis in ruminants?

A

animals unable to take in enough energy to meet their energy needs, which results in fat mobilization quicker than the liver can handle it, forming ketone bodies —> anorexia makes it worse!

  • most common in dairy cattle early in lactation
  • sheep and goats in last trimester
31
Q

How is ketosis diagnosed? Treated? What is specifically considered in small ruminants?

A

urine chemistry or ketostix +/- bedside ketone tests on milk for confirmation

glucose/dextrose +/- propylene glycol —> dextrose only elevates glucose for a couple of hours

induce parturition or abortion

32
Q

How can ketosis be prevented?

A
  • maintain optimal BCS
  • increase energy when in high-energy demands
33
Q

What 3 ketone bodies are elevated with ketosis?

A
  1. acetoacetic acid
  2. acetone
  3. beta-hydroxybutyric acid
34
Q

What are the 2 forms of ketosis?

A
  1. PRIMARY - negative energy balance during late pregnancy (SR mostly) and early lactation (dairy cattle) due to elevated BCS
  2. SECONDARY - increased negative energy balance due to other disease causing partial or complete anorexia (displaced abomasum) —> something made the cow go off feed
35
Q

How does ketosis develop?

A

milk production needs > intake = milking off her back

  • mobilizes fat to meet energy needs, causing the formation of ketone bodies by the liver
36
Q

What BCS is ideal for dairy cattle to avoid ketosis following parturition?

A

3-3.5 —> will be worse in fatter cows = more fat to mobilize to the liver!

37
Q

What are 2 typical cases of ketosis?

A

heavy BCS cow in first couple weeks of lactation gradually goes off feed and then decreases in milk production —> depression, normal TPR

dairy cow of any BCS develops a displaced abomasum (or something else that causes her to go off feed) in early lactation

38
Q

What are some clinical signs of ketosis? What rare signs may also be seen?

A
  • gradual loss of appetite - grain —> silage —> hay
  • weight loss
  • decreased milk production
  • normal TPR
  • firm, dry feces
  • depression, slow rumen motility
  • ketone odor to breath

nervous signs - ammonia to the brain = acute onset of circling, proprioceptive defects, head-pressing, blindness, wandering, excessive grooming, hyperesthesia, bellowing, tremors, aggression, or ataxia (alternates with periods of normalcy)

39
Q

What are 3 signs of ketosis on clinical pathology? What is preferred on a herd basis?

A
  1. decreased BG ~20-40 mg/dL (usually 45-75)
  2. positive urine ketones
  3. elevated liver enzymes

elevated nonesterfied fatty acid levels = nutrition or BCS needs adjustment

40
Q

What are some predisposing factors for ketosis development? What is seen on necropsy?

A
  • within 6 weeks of lactation
  • high producers
  • overconditioned

fatty liver

41
Q

What treatments are recommended for primary and secondary ketosis?

A

PRIMARY - dextrose SID, check urine ketones daily and administer more as needed (fair to guarded)

SECONDARY - correct original problem that caused cow to go off feed, dextrose and/or propylene glycol as needed usually for 2-3 days (good)

42
Q

How does propylene glycol compare to dextrose in treating ketosis? Why must it be done carefully?

A

lasts longer and is preferred for primary ketosis and fatty liver cows

excessive use kills rumen flora, do NOT use longer than 3 days

43
Q

What are some additional treatments available for ketosis?

A
  • glucocorticoids - Dexamethasone decreases glucose uptake by tissues, reduces milk production
  • insulin - extreme cases
  • niacin
  • red wine
44
Q

How is ketosis controlled?

A
  • reach ideal BCS by the end of lactation and maintain it throughout dry period
  • provide a highly palatable ration (transition ration to increase carbs)
45
Q

What is pregnancy toxemia?

A

disease of pregnant (high BCS) sheep and goats that occurs in the last trimester (last month of gestation!) caused by negative energy balance when supporting multiple fetuses

  • will present off feed and depressed +/- neurologic signs (ammonia to the brain!)
46
Q

What are three predisposing factors associated with pregnancy toxemia in small ruminants?

A
  1. obesity
  2. multiple fetuses (or single large fetus)
  3. stress - shearing, other animals within herd or on pasture, extreme weather
47
Q

What is the ultimate cause of pregnancy toxemia in small ruminants?

A

anything that decreases the energy intake during late pregnancy, increases fat mobilization, and produces ketone bodies

  • off feed —> ketotic (ketostix for diagnosis - hold off breath for urination)
48
Q

How do goats uniquely store fat?

A

internally —> if fat on the outside, it’s worse on the inside

49
Q

What treatment is recommended for small ruminants with pregnancy toxemia before they become recumbent?

A
  • oral or IV glucose (dextrose)
  • oral propylene glycol q 12 hours
  • calcium, potassium, alkalinizing fluid supplementation (oral, IV, SQ)
50
Q

What treatment is recommended for small ruminants with pregnancy toxemia if they are recumbent?

A
  • glucose +/- propylene glycol +/- calcium, potassium, and alkalinizing fluids
  • continuous slow dextrose drip
  • flunixin meglumine - comfort, gets back on feed
  • abort or induce parturition within 1 week of birth date with Dexamethasone and PGF2a - saves ewe/doe
51
Q

How is pregnancy toxemia controlled in small ruminants?

A

reach ideal BCS before mid-gestation and maintain it throughout pregnancy (increase energy towards the end of gestation!) —> 2.5-3.25

Large Animal Medicine (34 decks)

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