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Mineral Deposits:
Calcium:
Pathologic calcification implies the abnormal deposition
of calcium salts, together with smaller amounts of iron, magnesium and
other mineral salts. It is a common process occurring in a variety of
pathologic conditions. There are two forms of pathologic calcification
. When the process occurs locally in nonviable or dying tissues, it is
known as dystrophic calcification; it occurs despite normal serum levels
of calcium and in the absence of derangements in calcium metabolism. In
contrast, the deposition of calcium salts in vital tissues is known as
metastatic calcification, and it almost always reflects some disturbance
in calcium metabolism, leading to hypercalcaemia.
Dystrophic calcification:
Dystrophic calcification is seen at sites of tissue
damage, especially at sites of scarring, haemorrhage, and necrosis. Lesions
of chronic disease such as tuberculosis, trichinosis, histoplasmosis,
and caseous lymphadenitis are frequently mineralised.
Calcium salts develop within foci of damaged interstitial ground substance
that contain altered glycosaminoglycans.
Calcinosis circumscripta is a variant of dystrophic calcification in which
tissues are converted into masses of calcium salts surrounded by foreign
body giant cells. These hard, circumscribed deposits occur in the skin
over bony prominences and in the tongue of dogs.
Metastatic Calcification:
Persistent hypercalcaemina leads to deposition of calcium
salts in tissue. The most common causes of metastatic calcification are:
Vitamin D toxicity
Parathyroid hormone hypersecretion
Renal failure (uraemia)
Bone Destruction
Paraneoplastic syndrome
The calcium salts may be deposited in many sites but
are commonly seen in the gastric and intestinal mucosa, the interstitium
of blood vessel walls, the lung and the kidney. Very often they are deposited
along basement membranes. Why these sites are more susceptible than others
to metastatic calcification is poorly understood.
Copper:
In ruminants, excessive dietary intake of copper leads
to accumulation of copper in hepatocytes where it may be seen as a blue
brown pigment. Copper pigmentation is often difficult to see but the presence
of copper can be confirmed using special staining techniques such as rubeanic
acid.
Copper can cause disease in animals in 3 main ways:
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Chronic copper poisoning (long term accumulation
of copper in liver from grazing high copper content pastures as
in this case)
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Acute copper poisoning (rapid intake of high
doses of copper in processed feed eg when sheep are fed pig grain
rations by mistake, causes liver necrosis)
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Copper storage disease.
Chronic copper poisoning is most commonly the result
of long term exposure to excess dietary copper with a concurrent disease
imparing hepatocyte mitosis. Eventually large numbers of hepatocytes with
accumulated copper undergo lysis releasing large amounts of copper in
to the blood. This sudden increase in blood copper levels leads to lipid
peroxidation and intravscular haemolysis.
 
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