Small Ruminant Periparturient Dzs

Question 1

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?

Answer 1

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

Question 2

What are the types of pregnancy toxemia?

Answer 2

(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)

Question 3

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

Answer 3

(High carbohydrate content feed so grain)

Question 4

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

Answer 4

(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)

Question 5

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

Answer 5

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

Question 6

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

Answer 6

(> 2.4 mmol/L)

Question 7

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

Answer 7

Hyperglycemia - fetal death

Question 8

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

Answer 8

Hypokalemia/hypocalcemia - anorexia

Question 9

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

Answer 9

Azotemia - dehydration/renal failure

Question 10

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

Answer 10

Hypoproteinemia - hepatic/renal failure

Question 11

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

Answer 11

(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)

Question 12

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

Answer 12

(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)

Question 13

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

Answer 13

(Sheep 140 days, goats 143 days)

Question 14

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

Answer 14

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

Question 15

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

Answer 15

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

Question 16

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

Answer 16

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

Question 17

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

Answer 17

(Hyposensitivity, weakness, recumbency)

Question 18

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

Answer 18

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

Question 19

What is the treatment for uncomplicated hypocalcemia? Be specific.

Answer 19

(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)

Question 20

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

Answer 20

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

Question 21

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

Answer 21

(Oxalate)

Question 22

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

Answer 22

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

Question 23

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

Answer 23

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

Question 24

When does hypomagnesemia typically occur postpartum in small ruminants?

Answer 24

(2-4 weeks)

Question 25

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

Answer 25

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

Question 26

What is the treatment for hypomagnesemia?

Answer 26

(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)

Question 27

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

Answer 27

(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)