Page 566 - Concise Pathology for Exam Preparation ( PDFDrive )

20 Endocrinology 551

• Neuromuscular abnormalities, like weakness and fatigue
• Cardiac manifestations, like aortic or mitral valve calcification
2. Secondary hyperparathyroidism
It may be caused by any condition which is associated with chronic hypocalcaemia.
Causes:
• Renal failure
• Inadequate dietary intake of calcium
• Steatorrhea
• Vitamin D deficiency
Chronic renal insufficiency

↓Phosphate excretion

Hyperphosphataemia

↓Serum calcium levels

Stimulation of PTH activity
In addition:
Loss of renal substance
Decreased availability of α-1-hydroxylase
Decreased active form of vitamin D

Decreased intestinal absorption of calcium
FLOWCHART 20.10. Mechanism of development of secondary hyperparathyroidism.

Mechanism is complex, not fully understood (Flowchart 20.10):
Clinical features:
• Manifestations of chronic renal failure
• Bone abnormality (renal osteodystrophy) is seen but is less severe than primary hyper-
parathyroidism.
• Vascular calcification leads to ischaemia (calciphylaxis).
3. Tertiary hyperparathyroidism.
In a minor population, parathyroid activity may become autonomous and excessive, a
process sometimes referred to as tertiary hyperparathyroidism.

Q. Describe the causes and clinicopathological features of the
various types of hypoparathyroidism.
Ans. Hypoparathyroidism is far less common than hyperparathyroidism.
Causes
• Congenital absence
• Surgical ablation
• Familial hypoparathyroidism (autoimmune polyendocrine syndrome, Type I):
• Mutation in the autoimmune regulator (AIRE) gene
• Associated with mucocutaneous candidiasis and primary adrenal insufficiency
• Idiopathic hypoparathyroidism
• Autoimmune disease with isolated atrophy of the parathyroid
• Sixty percent of these patients have antibodies against CASR (calcium-sensing
receptors)

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