Review/Oorsig Volume 22, Issue 03 - Page 21

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