Small Ruminant Periparturient Dzs Flashcards

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1
Q

Pregnancy toxemia is caused by abnormal metabolism of carbohydrates and fats in the last trimester in sheep and goats, a lot of things contribute to that cause, what are those things?

A

(Rapid fetal growth, increased metabolic demand (kinda associated with the rapid fetal growth, stress, decreased rumen capacity, and individual animal susceptibility (genetics))

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2
Q

What are the types of pregnancy toxemia?

A

(Primary pregnancy toxemia which occurs in animals with a normal BCS who have larger litters, fat ewe/doe pregnancy toxemia, starvation pregnancy toxemia, and secondary pregnancy toxemia which results from a concurrent dz)

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3
Q

Propionate is the most important glucose precursor and is derived from ruminal fermentation of what type of feed?

A

(High carbohydrate content feed so grain)

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4
Q

What is tissue fat broken down into when lipase activation occurs in animals with a negative energy balance?

A

(Glycerol (which goes to the liver to be converted into glucose) and NEFAs (which can be used for energy production or converted into ketone bodies)

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5
Q

What are some of the clinical signs of hypoglycemia encephalopathy, which is a more advanced presentation of pregnancy toxemia?

A

(Head pressing, circling, muscle tremors, blindness, star-gazing, and ataxia; these signs could also be related to a secondary thiamine deficiency)

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6
Q

What ketone value or greater found on blood work is considered clinical pregnancy toxemia in sheep/goats?

A

(> 2.4 mmol/L)

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7
Q

Listed below are blood work changes you might see in advanced cases of pregnancy toxemia, pair them to their cause:

Hyperglycemia - fetal death

A - Hepatic/renal failure
B - Dehydration/renal failure
C - Fetal death
D - Anorexia

A

Hyperglycemia - fetal death

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8
Q

Listed below are blood work changes you might see in advanced cases of pregnancy toxemia, pair them to their cause:

Hypokalemia/hypocalcemia - anorexia

A - Hepatic/renal failure
B - Dehydration/renal failure
C - Fetal death
D - Anorexia

A

Hypokalemia/hypocalcemia - anorexia

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9
Q

Listed below are blood work changes you might see in advanced cases of pregnancy toxemia, pair them to their cause:

Azotemia - dehydration/renal failure

A - Hepatic/renal failure
B - Dehydration/renal failure
C - Fetal death
D - Anorexia

A

Azotemia - dehydration/renal failure

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10
Q

Listed below are blood work changes you might see in advanced cases of pregnancy toxemia, pair them to their cause:

Hypoproteinemia - hepatic/renal failure

A - Hepatic/renal failure
B - Dehydration/renal failure
C - Fetal death
D - Anorexia

A

Hypoproteinemia - hepatic/renal failure

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11
Q

What is the mainstay treatment for mild cases of ketosis in sheep/goats?

A

(Oral glucogenic precursors → propylene glycol (60-200 ml PO q6-12h up to 6 days) or glycerol (60 ml PO q12 for 3-6 days), some alternatives are calcium propionate, sodium propionate, liquid molasses, sodium lactate, ammonium lactate but these are not metabolized as quickly as propylene glycol)

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12
Q

What is the treatment for moderate to severe cases of ketosis in sheep/goats?

A

(Oral/IV fluids and IV dextrose optimally in a hospital setting so dextrose can be given as a CRI, follow up with daily propylene glycol and fluids, and can give hypertonic bicarbonate if acidotic but need to give oral fluids if you do this; can also give insulin but these cases definitely need to be hospitalized for BG monitoring and dextrose CRI)

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13
Q

What gestational ages are safe minimums for induction in sheep and goats?

A

(Sheep 140 days, goats 143 days)

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14
Q

What two drugs are given for induction in sheep and goats?

A

(Prostaglandins (1-15mg dinoprost) and steroids (10-20 mg dex))

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15
Q

What is the difference in when hypocalcemia may be experienced in non-dairy versus dairy small ruminants?

A

(Non-dairy → greatest calcium demand is 3-4 weeks before parturition; dairy → usually post-partum)

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16
Q

What early clinical signs result from lack of membrane stabilization in cases of hypocalcemia?

A

(Stiff gait, tremors +/- hyperesthesia, and ataxia)

17
Q

What later clinical signs result from the inability to release acetylcholine at the neuromuscular junctions in cases of hypocalcemia?

A

(Hyposensitivity, weakness, recumbency)

18
Q

What clinical signs related to hypocalcemia result from inability of muscle to contract?

A

(Constipation and decreased rumen motility → bloat, absence of PLR, increased heart and respiratory rate)

19
Q

What is the treatment for uncomplicated hypocalcemia? Be specific.

A

(30-60 ml IV calcium borogluconate heated to 35-40 C and slowly administered while monitoring heart rate; alternatively can give CMPK and dextrose IV)

20
Q

Why should you avoid IV administration of calcium in hypocalcemia ewes/does that have concurrent pregnancy toxemia?

A

(Calcium solutions are fatal in animals with impaired liver function)

21
Q

What dietary compound should be avoided because they precipitate formation of nonabsorbent compounds with calcium, therefore making it inaccessible to the animal?

A

(Oxalate)

22
Q

What are the two main risk factors for hypomagnesemia in sheep/goats?

A

(Increased potassium and/or reduced sodium with an increased milk yield → reduced Mg absorption from the GI tract)

23
Q

What clinical signs are caused by the spontaneous activation of neurons in the CNS in cases of hypomagnesemia?

A

(Excitability, paddling convulsions, tonic-clonic muscle spasms, and increased respiratory rate)

24
Q

When does hypomagnesemia typically occur postpartum in small ruminants?

A

(2-4 weeks)

25
Q

What are the suggestive and diagnostic levels of magnesium in the blood in cases of hypomagnesemia?

A

(Suggestive is <1.5 mg/dL, diagnostic is <1/0 mg/dL)

26
Q

What is the treatment for hypomagnesemia?

A

(IV adm of 4-5% magnesium chloride and 50 mls of 20-25% CMPK solution with additional SQ or oral adm 12-24 hours later to prevent relapse)

27
Q

If there is an outbreak of hypomagnesemia on a farm, what can you suggest to the owner?

A

(To give 7 g/animal magnesium oxide PO to clinically healthy animals and in the future prevention can be achieved by appropriate mineral supplementation and properly balanced fertilizers)