Volume 22 • Issue 03 • 2018
output (Normal serum Ca levels are 2.0
mmol/l).
2.9
The amount of Calcium (Ca++) freely available
in the blood is very small relative to the amount
required for milk production (see figure). Most
of the body’s Ca++ is stored in bone, and there
has to be an active metabolism of Ca++ to ensure
rapid availability of stored Ca++ at the onset of
lactation. Osteoblasts are active bone cells that
deposit Ca++ in bone while osteoclasts are similar
cells that break down stored Calcium structures
in bone and deposit Ca++ in the blood. Ca++
metabolism is regulated mostly by two prominent
hormones: parathyroid hormone (PTH) and
calcitonin. PTH responds to low blood Ca++
levels and is responsible to increase levels back to
normal, while calcitonin is secreted in response to
high blood Ca++ levels having the opposite effect
to PTH. Vitamin D3 also plays a role by increasing
intestinal uptake of Ca++, and the manufacturing
of this vitamin from cholecalciferol in the kidney
is stimulated by PTH and inhibited by calcitonin.
Apart from its effect on Vitamin D3, calcitonin
also has a direct inhibitory effect on intestinal
Ca++ uptake, a stimulatory effect on urinary
loss of Ca++, an inhibitory effect on osteoclasts
and a stimulatory effect on osteoblasts. PTH on
the other hand stimulates osteoclastic activity
and stimulates kidney reabsorption of Ca++ in
exchange for phosphorus. It is important to note
that the loss of Ca++ in milk is not hormonally
regulated, leading to ongoing loss despite
critical deficiencies.
In hypocalcaemia in cattle, paralysis occurs as a
result of inadequate calcium availability at the
neuromuscular junction, where it is required for
the release of the neurotransmitter acetylcholine.
Impulse conduction through peripheral nerves
(above the level of the neuromuscular junction)
and through muscle fibres (below the level of the
neuromuscular junction) is also modulated by
calcium through its membrane stabilizing effect
and hypocalcaemia will also have an effect at
these locations.
Calcium input is determined by intestinal uptake
and skeletal mobilisation. Calcium output is
determined by levels in colostrum and milk,
foetal tissue and calcium loss in faeces and urine.
Pathophysiology of Milk Fever
The diagramme below is a simplified
representation of the mechanisms involved in
maintaining blood Ca levels. Make sur e that you
revise and understand these mechanisms and
interactions: a sound knowledge of this is needed
to understand and interpret this disease at farm
level.
CALCITONIN
_
PARATHYROID
HORMONE
INTESTINAL
UPTAKE OF
CALCIUM
(34 g/d)
_
Vit. D
+
OS
A V A IL A B L E
C A L C IU M
R E S E R V O IR
(3 g ra m s )
+
U R IN E
AND
FAEC AL
LOSS
(8 g /d )
+
_
TE
OS
L
OC
+
TE
O
AS
C A L C IU M
S T O R E D IN
BONE
TS
A
BL
ST
(6 0 0 0 g ra m s )
S
M A G N E S IU M
_
C A L C IU M L O S T
THROUGH
M IL K
C O R T IS O L
(2 6 g /d )
Diagramme illustrating the metabolic pathways of Calcium homeostasis
21