Rumi Endocrine 1

sihirlifil's version from 2018-02-23 11:10


Question Answer
What is ketosis?Abnormally high ketone bodies in body tissues & fluids
T/F You always have to treat ketosisF! Certain degree is a natural state in rumis (subclinical vs clinical)
Ketosis common in who?Lactating dairy cattle
Affects 40% of lactations in N.A., incidence on some farms high as 80%
Consequences of ketosisEconomic losses! treatment, decreased milk production, decreased repro efficiency, incr risk of concurrent dz
Etiology of ketosisDrastic increase in energy demand --> Decrease DMI (fetus taking up rumen space) (peak DMI 7-8 weeks postpartum) --> peripheral insulin resistance --> Decreased gluconeogenesis --> NEGATIVE ENERGY BALANCE
Ingested CHOs are rapidly fermented into...Acetate, Butyrate, Propionate
These are VFAs
After CHOs fermented into VFAs, they are presented to...The liver
What happens to acetate?Converted to Acetyl-CoA --> Enter TCA cycle --> Ketogenic
What happens to butyrate?Converted to Acetate --> Enter TCA cycle --> Ketogenic
What happens to proprionate?Converted to Glucose (glucogenic)
What happens to VFAs (pic)
Certain body systems require glucose for energy:Brain, RBC, kidneys
Other big draws: Lactation, fetus
How much of blood glucose goes to the mammary gland for milk production?60-85%! May require 200g/h
Lactose =Galactose + glucose
If cow gets sick and the VFA system stops working...?Can't eat enough --> (TCA blocked) insulin decreases --> Glucagon increases --> negative energy balance
What else can be used to form glucose? (sufficient for MILD neg engy bal)Glycerol (fat mobilizations)
Amino acids (muscle catabolism)
Glycogen (from liver)
If sick cow (more than mild) & needs even more energy, what happens?Body mobilizes fat (lipolysis) stimulated by hormone-sensitve lipase --> releases 3 non-esterified fatty acids (NEFAs or free fatty acids) & 1 glycerol
NEFAs then metabolized by the beta-oxidation pathway --> cleaved into Acetyl-CoA --> TCA cycle!!! ...hopefully
If a cow is REALLY sick and not eating, what happens?Lots of NEFAs mobilized (esp if fat & stressed) --> Lots of beta-oxidation --> Oxaloacetate supplies run out b/c demand is too high --> Acetyl-CoA accumulates --> gets converted to ketone bodies
3 types of ketone bodiesAcetoacetate
Acetone (from spontaneous breakdown)
Fxn of ketone bodies? Important for?Serve to spare precious glucose for other needs. Important alt energy source for SOME tissues (heart, kidney, skeletal muscle)
Should an animal ever have any ketones?Small amount is normal in lactating cows & pregnant ewes/does
In high concentrations, ketonesSuppress appetite
ALter CNS fxn
Cause metabolic acidosis
Can the liver use ketones?Nope!
PRIMARY ketosis =Ration is chronically deficient in carbs
SECONDARY ketosis =Diet is fine, ketosis occurs 2ry to disease-induced inappetance
Is 1ry or 2ry ketosis more common?SECONDARY
Risk factors for ketosisPost-partum dairy cattle: High milk production, within 6 weeks of calving (peak incidence 3-4w), increased risk with parity/overconditioning, breed/genetic tendencies, repeat offenders
CS of ketosis(Often vague & nonspecific)
Inappetance, drop in milk production, poor rumen motility, mild dehydration, dullness (CS may be referable to underlying disease!)
Fun way to +/- detect ketonesSmell them! Acetone may change odor on affected cow's breath. Not everyone can smell them! (subjective & unreliable finding)
CS of NERVOUS ketosisPersistent licking, pica
Aggressive behavior
Circling, head-pressing
Pathophys of NERVOUS ketosisBrain not getting enough glucose b/c it's all going to milk!
Where can ketones be detected?Urine, milk, plasma
Dx of ketosisUrine dipstick analysis
Animals often hypoglycemic
Why use urine for dx?Ketones are concentrated in urine! Usually higher than blood (>84 in urine, >30 in blood)
Setback of urine dipstick?Only detect acetone & acetoacetate! Not beta-HB!
Dx: if you cant get the cow to urinate?Blood Beta-HB = MOST SENSITIVE INDICATOR of SUBCLINICAL ketosis (>1.4 mmol/L)
Check milk ketones: need special dipsticks, >10mg/dL
Tx of ketosisAddress underlying cause (if appetite decreased, find & fix the dz)
Increase CHO if diet not dense enough in nutrients
Proposed treatments to establish a positive energy balanceDextrose supplementation, propylene glycol, insulin, glucocorticoids, force-feeding, rumen transfaunation, B-vitamins
Dextrose supplement: does what?(500mL 50% IV)
Rapid increase in blood glucose
Increased excretion of electrolytes
Decreases Beta-HB <24h effect
Propylene glycol: when can you use?Requires functional liver & rumen
Propylene glycol: what happens?(250-400g PO q12h for 3-4d) Converted to proprionate in rumen, helps increase OXALOACETATE
OVERUSE --> rumen microbe death, decreased rumen motility
Insulin supplementation: how does it work?Antagonizes hormone-sensitive lipase --> minimizes fat mobilization
Increases tissue uptake of glucose
Stimulates hepatic glycolysis
Insulin supplementation: caveatNEVER use as sole treatment! Use with glucose/glucocorticoids
Glucocorticoid therapy: what can you use?Dexamethasone, isoflupredrone
Glucocorticoid therapy: how does it work?Mobilization of glucose, decreases milk production, stimulates appetite
Glucocorticoid therapy: be careful ofHypokalemia, immunosuppression
How does enteral feeding work?Encourage voluntary intake, consider forced if inappetance >3d
Transfaunation of rumen fluid if available
Vitamin B12 =(cyanocobalamin) Essential for gluconeogenesis
Butaphosphan =organic phosphorus source
Choline, L-methionine =Decrease fat mobilization?
Nicotinic acid, nicotinamide =(Niacin/Vit B3) used for formation of pyridine nucleotide coenzymes NAD/NADP
NAD=nicotinamide adenine dinucleotide
Signs the cow is recovering from ketosis?Increased appetite
Increased milk production
Increased glucose conc
Complications from ketosisDeath ((unlikely)
Hepatic lipidosis
Rumen acidosis
Prevention of ketosisDon't let cows get overconditioned in dry period
Minimize stress in transition period
Monitor closely for concurrent dz & subclinical ketosis

Pregnancy Toxemia

Question Answer
Disease of who?SR/Beef cattle
What IS preg tox?Ketosis associated with late preg
Incr energy demand from fetuses --> decreased ruminal fill
Risks factors of preg toxOverconditioned early pregnancy
Multiple fetuses (ewes >2, does >3)
CS of preg toxLate gestation
Anorexia, depression, separated from herd
Tremors, star-gazing, ataxia, recumbency
+/- odor of ketones
Dx of preg toxKetonuria, proteinuria
Ketonemia (Beta-HB)
Metabolic acidosis
Hypocalcemia, hypokalemia, hypoglycemia
Azotemia, incr liver enzymes
Treatment of preg tox: IMPORTANT FIRST THINGDecide if dam or fetus is more important!
Preg tox tx: if want to save DAM?Immediate C-section
Preg tox tx: if want to save FETI?Induce labor
Time for surfactant production
Preg tox tx: is it possible to medically manage?Risky for everyone but can med manage dam until end of pregnancy
Preg tox tx: How to restore energy balance?Energy-dense feed
Propylene glycol
IV glucose, insulin (correct Ca, K)
Preg tox tx: how to remove fetuses?Induction w/ dexamethasone in ewes, PG & dex in goats
Prevention of preg toxFeed based on # of fetuses, ionophores (feed efficiency), decrease stress, shear sheep in last trimester, monitor serum beta-HB
Prognosis: how does it compare to cattle?Can be fatal in ewes & does!

Hepatic lipidosis

Question Answer
Incr FFA mobilization --> TG produxn overwhelms ability to package into VLDLs --> TG deposited into liver
What perpetuates hep lip?Insulin resistance (insulin should decr fat mobilization)
Dx of hep lip(Liver enzymes unreliable. AST >100 IU/L)
NEFAs: >1000 uEq/L lactating, >350 uEq/L peripartum
Liver biopsy: float in distilled water. >10% 3glyc, >15% total fat

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