Steadfast Medishield Pvt. Ltd

Description
Calcitriol is a synthetic vitamin D analog which is active in the regulation of the absorption of calcium from the gastrointestinal tract and its utilization in the body. Calcitriol is a white, crystalline compound which occurs naturally in humans. It has a calculated molecular weight of 416.65 and is soluble in organic solvents but relatively insoluble in water.
Composition
ActiveD is available as soft gelatin capsules containing 0.25 micrograms of Calcitriol.
PharmacologyPharmacodynamics
Calcitriol is the most important active metabolite of Vitamin D₃. It is normally formed in the kidney from its precursor 25-hydroxycholecalciferol (25-HCC). Physiological daily production is normally 0.5 – 1.0µg and is somewhat higher during periods of increased bone synthesis (e.g., growth or pregnancy). The natural supply of Vitamin D in humans depend mainly on exposure to ultraviolet rays of the sun for conversion of 7-dehydrocholesterol in the skin to Vitamin D₃ (cholecalciferol). Vitamin D₃ must be metabolically activated in the liver and the kidney before it is fully active as a regulator of calcium and phosphorus metabolism at target tissues. The initial transformation of Vitamin D₃ is catalysed by a Vitamin D₃-25-hydroxylase enzyme (25-OHase) present in the liver and the product of this reaction is 25-hydroxyvitamin D₃ [25-(OH) D₃]. Hydroxylation of 25-(OH) D₃ occurs in the mitochondria of kidney tissue, activated by the renal 25-hydroxyvitamin D₃-1 alpha-hydroxylase (alpha-OHase), to produce 1,25-(OH)₂ D₃ (Calcitriol), the active form of Vitamin D₃.
Calcitriol binds to an intracellular receptor, a member of the steroid receptor superfamily. The calcitriol receptor complex interacts with specific DNA sequences that regulate transcription and protein synthesis in a variety of cells including osteoblasts, mucosal cells of the intestine, renal tubular cells and parathyroid cells. The changes in protein synthesis induced in these cells by Calcitriol are responsible for its profound physiological effects. A Vitamin D-resistant state exists in uremic patients because of the failure of the kidney to convert precursors to the active compound. The uremic state may also inhibit the binding of the Calcitriol receptor to its specific DNA responsive elements. The key role of Calcitriol in the regulation of bone and calcium homeostasis, which includes stimulating effects on osteoblastic activity in the skeleton, provides a sound pharmacological basis for its therapeutic effects in osteoporosis. The treatment of established osteoporosis with Calcitriol is associated with an increase in bone density and a reduction in new vertebral fractures. Established osteoporosis is defined as the finding of bone mineral density measurements of 2 or more standard deviations below the gender specific peak bone mass; or the presence or history of osteoporotic fracture. Calcitriol also reduces bone loss associated with corticosteroid therapy.
In patients with marked renal impairment, synthesis of endogenous Calcitriol is correspondingly limited or may even cease altogether. This deficiency plays a key role in the development of renal osteodystrophy.

Description:

AddKay is a solid oral dosage form of potassium chloride and is an electrolyte replenisher. Its structural formula is KCl.

This formulation is intended to provide prolonged-release of potassium, minimise the likelihood of producing high, localised concentrations of potassium within the gastrointestinal tract. Each 750 mg of prolonged release Potassium Chloride tablet provides 10 mEq of potassium.

Composition:

Each Prolonged Release Tablet Contains Potassium Chloride I.P. 750 mg

Pharmacology:

The potassium ion is the principal intracellular cation of most body tissues. Potassium ions participate in a number of essential physiological processes including the maintenance of intracellular tonicity, the transmission of nerve impulses, the contraction of cardiac, skeletal and smooth muscle and the maintenance of normal renal function.

The normal adult plasma concentration is 3.5 to 5 mEq per litre. An active ion transport system maintains this gradient across the plasma membrane.

The usual dietary intake of potassium is 50 to 100 Eq per day. Potassium depletion will occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake. Such depletion usually develops slowly as a consequence of prolonged therapy with oral diuretics, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhoea, or inadequate replacement of potassium in patients on prolonged parenteral nutrition. Potassium depletion due to these causes is usually accompanied by a concomitant loss of chloride and is manifested by hypokalemia and metabolic alkalosis.

Potassium depletion may produce weakness, fatigue, disturbances of cardiac rhythm (primarily ectopic beats), prominent U-waves in the electrocardiogram and, in advanced cases, flaccid paralysis and/or impaired ability to concentrate urine.

If potassium depletion associated with metabolic alkalosis cannot be managed by correcting the fundamental cause of the deficiency, e.g., where the patient requires long term diuretic therapy, supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels.

Indications and Usage

1. For the therapeutic use of patients with hypokalemia, with or without metabolic alkalosis; in digitalis intoxication; and in patients with hypokalemic familial periodic paralysis. If hypokalemia is the result of diuretic therapy, consideration should be given to the use of a lower dose of diuretic, which may be sufficient without leading to hypokalemia.

2. For the prevention of Hypokalemia in patients who would be at particular risk if Hypokalemia were to develop, e.g., digitalised patients or patients with significant cardiac arrhythmias.

Contraindications:

Potassium supplements are contraindicated in patients with hyperkalemia since a further increase in serum potassium concentration in such patients can produce cardiac arrest.

All solid oral dosage forms of potassium chloride are contraindicated in any patient in whom there is structural, pathological (e.g., diabetic gastroparesis) or pharmacologic (use of anticholinergic agents or other agents with anticholinergic properties at sufficient doses to exert anticholinergic effects) cause for arrest or delay in tablet passage through the gastrointestinal tract.

Presentation:

AddKay is available as a strip of 10 tablets & each box contains 5 such strips.