Small Ruminant Periparturient Dzs Flashcards
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?
(Rapid fetal growth, increased metabolic demand (kinda associated with the rapid fetal growth, stress, decreased rumen capacity, and individual animal susceptibility (genetics))
What are the types of pregnancy toxemia?
(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)
Propionate is the most important glucose precursor and is derived from ruminal fermentation of what type of feed?
(High carbohydrate content feed so grain)
What is tissue fat broken down into when lipase activation occurs in animals with a negative energy balance?
(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)
What are some of the clinical signs of hypoglycemia encephalopathy, which is a more advanced presentation of pregnancy toxemia?
(Head pressing, circling, muscle tremors, blindness, star-gazing, and ataxia; these signs could also be related to a secondary thiamine deficiency)
What ketone value or greater found on blood work is considered clinical pregnancy toxemia in sheep/goats?
(> 2.4 mmol/L)
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
Hyperglycemia - fetal death
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
Hypokalemia/hypocalcemia - anorexia
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
Azotemia - dehydration/renal failure
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
Hypoproteinemia - hepatic/renal failure
What is the mainstay treatment for mild cases of ketosis in sheep/goats?
(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)
What is the treatment for moderate to severe cases of ketosis in sheep/goats?
(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)
What gestational ages are safe minimums for induction in sheep and goats?
(Sheep 140 days, goats 143 days)
What two drugs are given for induction in sheep and goats?
(Prostaglandins (1-15mg dinoprost) and steroids (10-20 mg dex))
What is the difference in when hypocalcemia may be experienced in non-dairy versus dairy small ruminants?
(Non-dairy → greatest calcium demand is 3-4 weeks before parturition; dairy → usually post-partum)