Parathyroid Gland

One of my favourite glands because a) they are so small and b) they cause a wide range of pathological conditions (although in hindsight this makes my exams harder to revise for...)

The normal function of this gland is to regulate calcium and phorphorus homeostasis by the production of parathyroid hormone (easy to remember right). 

It does this by:

• Mobilisation of calcium from bone. Stimulates a cell called an osteoclast to reabsorb bone material which liberates calcium into the blood. 
• Enhances calcium reabsorption in the small intestine via vitamin D. It stimulates the active form of vitamin D in the kidney which induces a synthesis of calcium binding protein in the enterocytes that facilitates the efficient absorption of calcium into the blood.
• Suppresses calcium loss in urine. Stimulates tubular reabsorption of calcium and loss of phosphate ions. Therefore parathyroid hormones acts to counteract hypocalcaemia and hyperpohosphataemia. 

Hypoparathyroidism

• Reduced parathyroid hormone release. 
• Leads to hypocalcaemia-> neuromuscular excitability-> spasms, temors and muscle tetany. Chronically osteomalacia/rickets.

Causes:

• Parathyroid agenesis.
• Inflammation- autoimmune parathyroiditis.
• Surgical excision.
• Tumour.
• Vitamin D intoxication- leads to functional hypoparathyroid due to high calcium levels.

Postnatal Hypocalcaemia in Cattle

• Milk fever.
• Dietary imbalance between parathyroid hormone and calcitonin.
• Paresis.
• Severe hypocalcaemia and hypophosphataemia near parturition. 
• Caused by excessive calcium in the diet- low rate of bone reabsorption and an inactive parathyroid with anorexia and GI stasis near parturition. When there is the switch to lactation the cow cannot cope and bows under the pressure as the net calcium outflow exceeds the inflow. 

Hyperparathyroidism 

Calcium mobilisation from bone results in hypercalcaemia. 

• Primary- hyperplasia, adenoma or carcinoma of  parathyroid gland.
• Secondary- chronic renal insufficiency or Ca/P imbalance. 
• Tertiary- end stage of secondary- non-responsive autonomous hyperplasia. 
• Pseudohyperparathyroidism- humoral malignant hypercalcaemia or dogs with adenocarcinoma of the anal sac which releases PTH-like hormone. 

Secondary hyperparathyroidism and chronic renal insufficiency:

Leads to:

• Fibrous osteodystrophy.
• Metastatic calcification.

This is due to a reduced calcium reabsorption and phosphate secretion, and a reduced vitamin D activation. Hyperphosphataemia and hypocalcaemia in the blood. Due to the reduced intestinal calcium reabsorption the calcium precipitates mineral in the tissues leading to metastatic mineralisation. Reduced blood calcium leads to parathyroid hyperplasia and fibrous osteodystrophy with overlapping osteomalacia. 

Fibrous osteodystrophy:

• Bone pain, loss of teeth, and deformity of the maxilla and mandible. Grossly= soft demineralised bone. 
• Enhanced osteoclast reabsorption of mineralised bone with substitution of normal bone by insufficiently mineralised osteoid and collagenous connective tissue. 

Other Parathyroid Changes

• Regression/inflammation- atrophy due to thyroid goitre/cysts. Diffuse lymphocytic parathyroiditis in old dogs which is rare. 
• Hyperplasia and neoplasia- primary hyperplasia (rare), secondary hyperplasia (consequence of hypocalcaemia), and primary tumours- rare (chief cell adenoma/adenocarcinoma which can be hormonally active).