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Medicine Notes Endocrinology Notes

Parathyroid Gland And Calcium Metabolism Notes

Updated Parathyroid Gland And Calcium Metabolism Notes

Endocrinology Notes

Endocrinology

Approximately 28 pages

Complete set of notes on endocrinology. Covering the most common endocrine problems, with the basic science and anatomy along with investigations and management of both chronic disease and acute presentation and crises. Colour-coded per topic and using flow diagrams and images for visual learners. Ideal for clinical finals...

The following is a more accessible plain text extract of the PDF sample above, taken from our Endocrinology Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:

Parathyroid Gland and Calcium Metabolism

Parathyroid gland

Located on the posterior aspect of the thyroid. Number of glands can range between 4 and 150 in adults (usually 4-6).

Produces parathyroid hormone.

Parathyroid hormone

  • Made as a pro-hormone and cleaved twice (in liver and kidney)

  • Has no serum binding protein

  • Half life is 4 minutes (short acting)

Actions

  • Raises serum calcium levels

  • Changes in calcium concentration stimulate PTH release

  • Acts on osteoblasts in bone = release of Ca2+ and PO4-

  • Acts on tubular cells in kidney = increased absorption of Ca2+ and decreased absorption (increased excretion) of PO4-

  • Stimulates absorption of bone and release of calcium into extracellular fluid

Also stimulates conversion of vitamin D to its active form and increases calcium uptake from the intestine = increased synthesis of active vit D

Skin UV Light

Liver

PTH (+) Kidney (+) Low PO4

Calcitrol (1,25 Vit D)

Intestine – increase Ca + PO4 absorption Bone – mobilize Ca stores

Hyperparathyroidism

Aetiology

  • Primary hyperparathyroidism due to;

    • Adenoma

    • Hyperplasia

    • (Rarely) functioning carcinoma

      • Ectopic PTH secretion

    • Calcium high

Clinical features

  • Slow onset, usually asymptomatic or incidental finding (see hypercalcaemia notes)

Investigations

  • Biochemistry

    • U+E (raised ca, low po in primary. High Cl due to high renal clearance of phosphate and mild renal tubular acidosis)

    • LFT (raised alk. Phos indicates increased bone activity

    • Serum PTH raised

    • Secondary hyperparathyroidism = high phosphate, low calcium

  • Radiology

    • Small subperiosteal bone reabsorption cysts in phalanges

    • Reduced spinal bone density

Management

  • Surgery

    • Resection of diseased parathyroid glands if serum calcium persistently over 3.0mmol/L (after correction for albumin level)

  • Biopsy

    • Determine whether glands are hyperplastic

  • Mild symptoms may not require surgery

    • Increase fluid intake to prevent stones

    • Avoid thiazide diuretics

    • Avoid high Ca2+ and vit D intake

Secondary hyperparathyroidism

  • Physiological response to hypocalcemia

    • E.g chronic renal failure or dietary vit D deficiency

  • Calcium normal

Tertiary

  • Chronic secondary hyperparathyroidism results in gland acting autonomously

  • Calcium high

  • PTH inappropriately high (unlimited by feedback control)

  • Seen in chronic renal failure

Malignant hyperparathyroidism

  • Some cancers e.g squamous cell carcinoma of lung, breast and renal cell carcinomas produce parathyroid-related protein (PTHrP)

  • PTHrP mimics PTH = increased serum calcium

  • Reduced PTH seen on assay as PTHrP not detected

Hypoparathyroidism (hypocalcaemia)

Aetiology

  • Secondary to thyroid surgery

  • Primary idiopathic

    • Organ-specific immune disease

    • Associated with Addisons, pernicious anaemia and malabsorption

  • Di George syndrome

  • Pseudohypoparathyroidism

    • End organ disease in kidneys or liver where PTH is therefore in excess amounts

Clinical features

  • Acute

    • Paraesthesia (mouth, hands – bigger homunculous...

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