Section 2: Metabolic Diseases of Ruminants: Hypocalcemia (Donovan) Flashcards
metabolic disease
derangement of metabolic process
milk fever =
hypocalcemia
predisposing factors for hypocalcemia in cows
> 4 yrs old
high milk production
inappetence
low exercise
high stress (i.e. calving, hormonal changes)
Jersey breed
prepartum diet high in Calcium or has a positive DCAD
When does HC usually occur?
at parturition. Ca requirement surges just prior to parturition, and more Ca is taken up from blood pool for lactational demand. Results in loss from bone, urine, fetus
During HC, there is decreased Ca input from:
- Bone (older cows and/or +DCAD)
- Diet (decreased intake or absorption)
3 hormones/vitamins involved in Ca metabolism*******
1) PTH (+)
2) Vit. D (+)
3) Thyrocalcitonin (-)
What happens if pre-partum diet is high in Ca? ***
thyrocalcitonin is upregulated, which inhibits bone mobilization of Ca. Also inhibits PTH, so bone mobilization and intestinal absorption of Ca cannot be activated. Activation of active form of vit. D in kidney is inhibited.
How is vit. D from sun transformed in the body?
turned into inactive form in liver, then active form is produced in the kidney under influence of PTH
fx of active vit D
increases absorption of Ca and bone mobilization
clinical signs of early stage milk fever
- off feed
- staggering
- protrusion of tongue
- normal temp
- fast HR
excitement stage of milk fever
- severe ataxia
- muscle tremors
- dilated pupils
- faster HR
- dry/scant feces
- rumen stasis
- body temp variable
recumbent stage of milk fever
- sternal recumb.
- loss of reflexes
- S neck (unique to milk fever!)
- fast HR
- temp variable
unconscious stage of milk fever
- lat. recumb.
- groaning
- bloat!
- no reflexes
- HR 100-120, weak
Ddx of milk fever
- no test
- good PE
- response to tx: calcium salt IV (preferred) or oral calcium gel
HC prevention
Dietary manipulation during last 3 wks of gestation:
1) Ca restriction (trad. method) or
2) negative DCAD
result of Ca restriction physiologically ***
No calcitonin produced, so PTH not inhibited. PTH stimulates bone mobilization of Ca and stimulates kidney to make active vit. D which also promotes bone mobilization and intestinal absorption of Ca
DCAD =
(Na+ + K+) - (Cl- + S-)
normal cow diets are neg/pos. charged
pos
how does neg. DCAD prevent milk fever? ***
- induces mild metabolic acidosis
- decreased pH upregulates of PTH receptors in kidney, so it takes less PTH to induce reaction to transform inactive vit. D to active vit. D
- cow also releases bone buffer, which helps maintain Ca lvls in the blood by drawing out Ca with it
anionic salts you can add to diet to make neg. DCAD
MgSO4, CaSO4, CaCl2, MgCl2, NH4Cl
HC is a major risk factor for all of the following cattle diseases:
- prolapsed uterus
- retained placenta
- early metritis
- rumen stasis
- ketosis
- DA
- peripartum immune dysfunction
- down cow syndrome
REVIEW SLIDE 35 FLOWCHART
:)
insufficient dietary effective fiber can cause:
rumen acidosis, lameness, DA
decreased DMI around calving can cause:
neg. energy/protein balance –> ketosis/fatty liver
stages of HC in order
1) early stage
2) excitement stage
3) recumbent stage
4) unconscious stage
