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NUTRITION - 2.3 Pregnancy Toxaemia

Terms in this set (35)

metabolism of glucose in starved periparturient ewe
resynthesized and incorporated into in very low density lipoproteins (VLDL) in liver

are only available to those tissues with an active lipoprotein lipase in the capillary bed
Triglycerides
are released into blood only by adipose tissue

Always being released from adipose, but their concentration in plasma increases substantially in response to starvation,
stress and high metabolic load (e.g., pregnancy and lactation)

Transport proteins that transport ____ into cells and into mitochondria are always active
Non-esterified free fatty acids (NEFA) and glycerol mobilized from adipose tissue
Produced in liver from E-oxidation of NEFA to acetyl-CoA which is then converted to _____ ____

(beta-OH-butyrate, acetoacetate and acetone) are soluble and circulate in plasma

beta-OH-butyrate and acetoacetate used to provide energy by supplying acetyl-CoA into the TCA cycle in peripheral tissues

Acetone is mostly lost in expired air, but a small amount does get converted into glucose
Ketone bodies mobilized from liver
Synthesis, repackaging and transport of lipids as VLDL in liver supplies those tissues with active lipoprotein lipase with
free fatty acids and it is an important source of cholesterol
hyperketonaemia
clinical ketosis
severe negative energy balance and hypoglycaemia
hyperketonaemia results from what?
paritary and age of cow
BCS
proximity to parturition [early lac - particularly first 7 wks, elevated risk to 14 wks]
risk of ketosis increases with what?
compromised energy intake - pasture cP, Me and or heigh and mass too low, poor sups

limited capacity to ingest and metabolise large amounts of feed in early lac [rumen and liver not adapted]
ketosis is a response to what?
wasting form of ketosis [typical]

nervous form of ketosis [less common]
types of ketosis
gradual onset
- decline appetite 2-5 days
- lack interest in cereal grain-based sups but still consume forage
- elevated b-OH-butyrate in blood
- elevated ketones in urine
- rapid reduction in BCS
- unsteady stance and gait
- head low
- rapid red milk yield
- ketone smell on breath
- disinclined to move
wasting form of ketosis
sudden onset of CNS dysfunction
- incessant tongue movements
- licking of skin
- aimless wandering
- walking in circles
- bellowing for no reason
- apparent blindness
nervous form of ketosis
glucose replacement therapy
- IV admin dextrose solution = glucose [short acting]
- drench with propylene glycol/glycerine [long acting]
- isolate and feed high qual forage 2-4 days
- treatment continued for 2-4 days
- reintroduction of cereal grain-based supps

hormone therapy
- admin of long-acting corticosteroids with glucose to avoid excessive muscle catabolism
treatment of clinical ketosis in dairy cattle
BCS 5-5.5. out of 8 @ calving
cereal grain-based sups for transition period in wks leading to calving
identify cows at risk early and dose with propylene glycose or glycerine at calving
offer sufficient high qual pasture after calving or supp with high qual conserved forages
feed cereal grain-based supps in bale at milking
prevention of ketosis in dairy cattle
milk solids yield and suppresses milk yield
even sub-clinical ketosis greatly suppresses what?

making ketosis in dairy herd very costly with respect to marginal returns and welfare concerns.
hypoglycaemia
Pregnancy toxaemia in ewes (less often does) is a consequence of what?
• Poorly fed because of inadequate pasture quality/quantity
• In late pregnancy
• Twin or triplet bearing (or single large foetus)
• Undersized (maiden ewes)
• In poor health (teeth, parasites)
• Too thin (BCSd2.5 out of 5) or too fat (BCSt4 out of 5) in late pregnancy
pregnancy tox in ewes occurs typically in what circumstances?
• compromised energy intake, and/or,
• acute stress from poor husbandry or environmental issues (storm, cold, heat, wild dogs)
preg tox in ewes primarily is a response to what 2 factors?
ketoacidosis
anorexia
ketonuria
dehydration
fatty liver

staggering
stargazing
drowsiness
convulsions
death
consequences of preg tox in ewes
• Signs of CNS dysfunction and muscle weakness (e.g., ataxia, recumbency) in response to hypoglycaemia and ketoacidosis
• Elevated plasma NEFA in response to mobilisation of triglycerides from adipose as a result of severe negative energy balance
• Elevated plasma E-OH-butyrate indicating hyperketonaemia as a result of severe negative energy balance
• Ketonuria in response to hyperketonaemia
• Acetone smell on breath or urine (or on necropsy) in response to hyperketonaemia
Clinical signs of pregnancy toxaemia in ewes
> 3.0
b-OH-butrate [mM] levels in normal ewes is around 0.7.
in ewes with preg toxaemia it is at what level?
>5-10+
acetone [mM] levels in normal ewes is around 0.

in ewes with preg toxaemia it is at what level?
plasma glucose
normal _______ _____ concentrations may be observed in sick animals in field bc _____ ____ conc can return to normal in response to release of cortisol, the development of insulin resistance in tissues to protect foetal glucose supply and or if foetuses die
• Good energy intake available from pasture
• Ewes in good health
• Actively manage at risk ewes as a separate group
• BCS around 3 in late pregnancy
• Supplement to support energy intake if necessary
• Good husbandry to avoid stress in late pregnancy
prevention of pregnancy toxaemia in ewes
• Early, support with glucose and electrolytes can resolve signs and prevent progression of disease
• Later, ewes CNS and hyperketonaemia become unresponsive to glucose
• Chemical induction of parturition or delivery by surgical intervention (C-section) may restore normal metabolism in the ewe
treatment of pregnancy tox in ewes
hypoglycaemic
Animals in negative energy balance (NEB) become _____ and mobilise glycerolaand non-esterified fA from triglycerides in adipose to meet energy reqs
acetyl-CoA
NEFA is converted to what by b-oxidation in liver and cardiac/skeletal m
ketone bodies

(acetoacetate, b-hydroxybutyrate, acetone)
build up of acetyl-CoA in liver results in formation of what?
acetyl-CoA
Ketone bodies enter circulation and become available to cells in peripheral tissues where acetoacetate and b-hydroxybutyrate
are converted back into __________ to enter the TCA cycle
Acetoacetate
_____ can convert to acetone with release of CO2 in resp to acetoacetate decarboxylase or spontaneously
hyperketonaemia
excess ketones in blood leads to _____ and systemic acidosis
hypoglycaemia and mobilisation of NEFA and production of ketone bodies
Positive feedback from ketosis typically suppresses appetite leading to a continuing cycle of ...?
suppression of circulating ketones through supplementation with glucose, gluconeogenic
compounds and, often, glucocorticoids
Reversal of ketosis requires?
• Clinical ketosis and fatty liver common in dairy cows in severe NEB in early lactation
• Pregnancy toxaemia common in ewes in NEB carrying multiple fetuses in late pregnancy
Hyperketonaemia and hypoglycaemia are important problems in two key animal production industries:
die
Pregnancy toxaemia in ewes is difficult to treat and the ewe and foetuses/lambs routinely
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