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Metabolic Disease: Hypomagnesemia
Metabolic Disease: Hypomagnesemia
Metabolic Disease
Hypomagnesemia
magnesium homeostasis
•Magnesium (Mg) homeostasis is not under direct hormonal control but is mainly
determined by absorption from the GI tract; excretion by the kidneys; and the varying
requirements of the body for pregnancy, lactation, and growth.
•Magnesium ions are by no means efficiently absorbed from the gastrointestinal tract and
only 7 to 25% is absorbed under usual dietary conditions.
•Plasma magnesium, just like calcium, is also found in ionised form, protein-bound and in
complexes, with the ionized magnesium being the most active form.
•Mg is a constituent of bones (approximately 60 to 70% of the total body magnesium is
present in the skeleton), 30-40% is distributed in the soft tissues and only about 1% can
be found in the extracellular space. Therefore, plasma Mg does not provide an indication
of intracellular or bone Mg stores.
Roles of magnesium
•The magnesium ion is essential for normal bone metabolism, normal nerve function and
muscle irritability. Magnesium also plays an essential part in the coenzyme system which
links normal carbohydrate metabolism with phosphate metabolism and the provision of
energy for muscle contraction.
•Magnesium within the cell acts as a counter ion for the energy-rich ATP and nuclear acids.
Magnesium is a cofactor in >300 enzymatic reactions.
•Thus, one should keep in mind that ATP metabolism, muscle contraction and relaxation,
normal neurological function and release of neurotransmitters are all magnesium
dependent.
•It is also important to note that magnesium contributes to the regulation of vascular tone,
heart rhythm, platelet-activated thrombosis and bone formation
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•Extracellular Mg is involved in the regulation of membrane channels as well as in
excitation-contraction coupling in skeletal muscle. Low ionic Mg concentrations
accelerate the transmission of nerve impulses
•In muscle contraction, for example, magnesium stimulates calcium re-uptake.
•Magnesium further modulates insulin signal transduction and cell proliferation and is
important for cell adhesion and transmembrane transport including transport of potassium
and calcium ions
•The normal level of magnesium in plasma for cows is in the range of 0.75-1.00 mmol/l or
1.8-2.4 mg/dl.
•Milk contains about 0.12-0.15 g magnesium /kg and a high yielding cow may lose around
3-4 g through milk per day.
•Colostrum contains about 0.4 g magnesium/kg ,Because the amount of magnesium in the
extra cellular fluid equals the amount excreted in 17 kg of milk (0.15 g/kg 4% milk; milk
production in high lactating animals can quickly deplete the extracellular pool of
magnesium, resulting in hypomagnesaemia if not rapidly replaced.
Hypomagnesemic tetany
(lactation tetany, grass tetany, grass staggers, wheat pasture poisoning)
Etiology:
*Magnesium concentrations is determined by balance between dietary intake of magnesium,
loss in feces and milk, and the modulating effect of magnesium homeostasis by the
kidney.
* Low Dietary intake of Mg.
* Renal excretion regulation.
* There are large stores of magnesium in the body, especially in bone. These are available to
the young calf but mobilization decreases with age and in the adult ruminant there is little
mobilization in response to short-term deficits of magnesium.
* Lactation: Increased requirement for magnesium is almost always associated with the loss
of magnesium in the milk during lactation.
*Low pasture Ma. The recommended minimal 'safe' concentration of magnesium in pastures
is 2 g/kg DM.
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3-Young grass fertilized with nitrogenous fertilizers has an increased crude protein which is
readily fermentable and leads to increased ammonia concentrations. A sudden rise in
ruminal concentrations of ammonia impairs magnesium absorption in the rumen.
4-magnesium absorption is depressed in ruminal acidosis.
5- hypomagnesemia can have effect on calcium homeostasis as Hypomagnesemia reduces
the production and secretion of parathyroid hormone and reduces hydroxylation of
vitamin D in the liver, therefore hypomagnesemia can increase susceptibility to milk
fever and downer cow syndrome .thus Mg, therapy must added to milk fever treatment.
Pathogenesis:
*Normal serum Mg. value is 1.7-3mg/dl (0.4 mmol/L) and sings start when the level of Mg.
become below1mg/dl(0.7 to 1.2 mmol/L)
*Magnesium has many influences on impulse transmission at the neuromuscular system,
including effects on the release of acetylcholine, on the sensitivity of the motor end plate,
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on the threshold of the muscle membrane and on activation of the cholinesterase system,
those were result in tetanic sings but the concurrent hypocalcemia may have a
contributory effect.
*it has also been established that magnesium concentrations in the cerebrospinal fluid (CSF)
are more predictive of clinical disease than those in serum.
Clinical findings
For convenience, lactation tetany is described in acute, subacute, and chronic forms.
Acute form
*The animal may be grazing at the time and suddenly stop grazing.
*uncomfortable twitching of the muscles and ears , severe hyperesthesia and slight
disturbances precipitate attacks of continuous bellowing, frenzied galloping, and
occasionally aggression.
* The gait becomes staggering and the animal falls with obvious tetany of the limbs, which
is rapidly followed by clonic convulsions lasting for about a minute.
*During the convulsive episodes there is:
Opisthotonos, Nystagmus, Champing of the jaws, Frothing at the mouth, Pricking of the
ears, and Retraction of the eyelids.
* The temperature rises to 40-40.5°C, after severe muscle exertion, the pulse and respiratory
rates are also high.
*Death usually occurs within 5 to 60 minutes, and the mortality rate is high because many
die before treatment can be provided.
Sub-acute :
*the onset is more gradual over a period of 3-4 days, there is slight inappetance ,and
exaggerated limb movements.
*wildness of the facial expression, and exaggerated limb movements.
* refuse to move with spasmodic urination and frequent defecation and decrease milk
production.
* Muscle tremor and mild tetany of the hind legs
* straddling gait may be accompanied by retraction of the head and trismus
*recover spontaneously within a few days or progress to a stage of recumbency.
Chronic form:
* Many animals in affected herds have low serum magnesium levels but do not show
clinical signs and There may be sudden death.
*few animals may show signs of dullness, unthriftiness, decrease appetite paresis and a milk
fever-like syndrome.
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Diagnosis:
Diagnosis is usually confirmed by response to treatment, followed by confirmation of
hypomagnesemia in samples taken prior to treatment. Clinical pathology:
*estimation of serum Mg level, risk for tetany is not present until the level falls to below 1.2
mg/ dL (0.49 mmol/L).
*Total serum calcium concentrations are often reduced to 5 to 8 mg/dL (1.25 to 2.00
mmol/L)
*In acute tetany, serum potassium concentrations are usually dangerously high and may
contribute to the high death rate.
*Estimation of Magnesium concentrations in CSF can be used as a diagnostic procedure.
*vitreous humor magnesium concentrations less than 0.55 mmol/L for cattle and less than
0.65 mmol/L for sheep up to 48 hours after death indicate the presence of
hypomagnesemia
* The occurrence of low urine magnesium levels is good evidence of hypomagnesemia.
Necropsy findings
There are no specific necropsy findings
Differential diagnosis:
Cattle
• Acute lead poisoning • Rabies • Nervous ketosis • Bovine spongiform encephalopathy
Sheep
• Hypocalcemia
Treatment:
*Slow I.V administration of preparations containing magnesium or magnesium and calcium
are used.
combined calcium-magnesium preparation 500 mL of a solution containing 25% calcium
borogluconate and 5% magnesium hypophosphite for cattle,50 mL for sheep lV followed
by a SC injection of a concentrated solution of a magnesium salt.
or magnesium sulfate 200-300 mL of a 20% solution injected half IV and half SC.
*A combination of 12% magnesium adipate and 5% calcium gluconate at a dose rate of 500
mL is also used.
Note: The rapid IV injection of magnesium may induce cardiac dysrhythmia, or medullary
depression which may be severe enough to cause respiratory failure.
*lV chloral hydrate may be administered to reduce the severity of convulsions during
treatment with magnesium.
Control
*Where possible, animals at high risk should be moved to low-risk pastures during the grass
tetany season.
*A requirement as high as 3.0 g/kg DM diet may be required for lactating cows on spring
pasture
* blocked minerals containing magnesium or foliar dressing of magnesium may be adequate
delivery systems where there is a high stocking density of cattle.
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