Makindo Medical Notes

Related Subjects: |PTH Physiology |Calcium Physiology |Magnesium Physiology |Calcitonin |Hypocalcaemia |Hypercalcaemia |Hypomagnesaemia |Hypermagnesaemia |Primary Hyperparathyroidism |Familial hypocalciuric hypercalcaemia (FHH) |Sarcoidosis

🔎 Overview of Parathyroid Physiology

🟢 The parathyroid glands are four tiny endocrine glands on the posterior thyroid that regulate calcium and phosphate balance via secretion of parathyroid hormone (PTH). Calcium is crucial for nerve conduction, muscle contraction, and coagulation — so tight regulation is vital. ⚡

📍 Anatomy of the Parathyroid Glands

• Usually four glands: two superior + two inferior, each ~3–5 mm (grain of rice size 🍚).
• Embryologically: superior glands arise from the 4th pharyngeal pouch, inferior from the 3rd (which explains ectopic locations, e.g. mediastinum).

⚙️ Synthesis and Secretion of PTH

• Synthesis 🧪:
  • Produced by chief cells as prepro-PTH → pro-PTH → active PTH.
• Secretion 🔄:
  • Regulated by serum calcium via a negative feedback loop.
  • ⬇️ Low Ca²⁺ → ↑ PTH secretion. ⬆️ High Ca²⁺ → ↓ PTH secretion.

🧩 Actions of PTH

• Bone 🦴:
  • ↑ Osteoclast activity indirectly: PTH stimulates osteoblasts → ↑ RANKL → osteoclast activation → bone resorption.
  • Releases Ca²⁺ and phosphate into blood.
• Kidneys 🩸:
  • ↑ Ca²⁺ reabsorption in distal tubules.
  • ↓ Phosphate reabsorption in proximal tubules → prevents Ca²⁺–phosphate precipitation.
  • Stimulates 1-α hydroxylase → ↑ 1,25-dihydroxyvitamin D (calcitriol).
• Intestines 🍽️:
  • Indirect effect: calcitriol ↑ absorption of Ca²⁺ and phosphate from diet.

🛠️ Regulation of PTH Secretion

• Calcium-sensing receptor (CaSR) 🧭:
  • High Ca²⁺ activates CaSR → inhibits PTH release.
  • Low Ca²⁺ → less CaSR activation → more PTH released.
• Vitamin D ☀️: Active vitamin D suppresses PTH gene expression (negative feedback).
• Phosphate 🧂: High phosphate indirectly stimulates PTH by lowering free Ca²⁺ (binding). Chronic hyperphosphataemia (e.g. CKD) → secondary hyperparathyroidism.

⚠️ Clinical Relevance

• Hyperparathyroidism 📈:
  • Primary: parathyroid adenoma → hypercalcaemia (“stones, bones, groans, psychiatric overtones”).
  • Secondary: CKD → low calcitriol + high phosphate → compensatory ↑ PTH.
  • Tertiary: autonomous gland hyperplasia after long-standing secondary disease.
• Hypoparathyroidism 📉:
  • Causes: post-thyroid/parathyroid surgery, autoimmune, DiGeorge syndrome (22q11 deletion).
  • Features: hypocalcaemia → tetany, seizures, Chvostek’s & Trousseau’s signs, arrhythmias.

🧪 Diagnosis & Management

• Labs: Serum Ca²⁺, phosphate, PTH, vitamin D.
• Imaging: Neck ultrasound, sestamibi scans (localising adenomas).
• Treatment:
  • Hyperparathyroidism → surgery (parathyroidectomy) if symptomatic or Ca²⁺ >0.25 mmol/L above normal.
  • Hypoparathyroidism → calcium + activated vitamin D (alfacalcidol/calcitriol).
  • Calcimimetics (e.g. cinacalcet) for some refractory hypercalcaemia cases.

📝 Summary

The parathyroid glands are calcium guardians ⚖️. PTH raises serum calcium by acting on bone, kidneys, and indirectly the gut. Disorders include hyperparathyroidism (too much PTH → hypercalcaemia, kidney stones, bone resorption) and hypoparathyroidism (too little PTH → hypocalcaemia, tetany). Diagnosis = labs + imaging. Treatment targets the underlying cause and correcting mineral imbalance.