This document discusses diseases of the parathyroid gland, including its structure and functions in regulating blood calcium levels. The diseases are classified into hyperparathyroidism, hypothyroidism, and pseudohypoparathyroidism. Primary hyperparathyroidism is caused by autonomous overproduction of PTH, often due to a tumor. It can result in kidney stones, bone abnormalities, and other clinical issues. Hypothyroidism is a deficiency of PTH secretion and causes low calcium levels and tetany. Pseudohypoparathyroidism occurs when there is end-organ resistance to PTH despite normal levels.

1. DISEASES OF THE
PARATHYROID
GLAND
By: HERMAN NDJAMEN
GROUP: 305

2. STRUCTURE OF GLAND
FUNCTION & REGULATION OF GLAND
DISEASE CLASSIFICATION
EXPLANATION
CONCLUSION

3. STRUCTURE

4. STRUCTURE CONTINUES
This gland contains 3 groups
of cells:
The chief cells which are
the main cells with
endocrine
functioncontaining lots of
secretary granules.
The Oxyphil and
transitional oxyphil cells are
the larger cells that contain
lots of mitochondria and
glycogen lakes.

5. FUNCTION
• DIRECT REGULATION OF BLOOD CALCIUM
ION LEVEL
• PARTICIPATES INDIRECTLY IN REGULATION
OF PHOSPHATE

6. REGULATION

8. HYPERPARATHYROIDISM
HYPOPARATHYROIDISM
PSEUDOHYPOPARATHYROIDISM

9. • It is classified into:
- PRIMARY HYPERPARATHYROIDISM: an
autonomous, spontaneous overproduction of PTH.
Example: Tumor
- SECONDARY HYPERPARATHYROIDISM: any
condition that gives rise to chronic hypocalcemia,
which in turn leads to compensatory overactivity
of the parathyroid glands. Example Chronic Renal
insufficiency
NB: Hypercalcemia occuring in these cases is
unable to downregulate production of PTH.

10. RESULT
• Two major sites of complication of primary
hyperparathyroidism are Kidneys and bones.
• The kidneys may have renal stones (nephrolithiasis)
or diffuse deposition of calcium-phosphate
complexes in the parenchyma (nephrocalcinosis).
• In skeleton a condition called “osteitis fibrosa
cystica” could occur characterized by subperiosteal
resorption of the distal phalanges, distal tappering
of the clavicles, a “salt and pepper” appearance of
the skull as well as bone cysts and brown tumors of
the long bones.

12. Other clinical manifestations
• cardiac arrhythmias, tremors (Ca++ necessary for
normal muscle contraction
• Anorexia, vomiting, constipation
• Weakness
• Polyuria, polydipsia, hypercalcuria
• peptic ulcer disease, acute pancreatitis,
hypertension, gout and pseudo gout, and anaemia

14. HYPOPARATHYROIDISM
• Deficient secretion of PTH
CAUSES
- Surgically induced hypoparathyroidism
- Autoimmune hypoparathyroidism: associated with
autoimmune polyendocrine syndrome type 1.
- Autosomal-dominant hypoparathyroidism is caused
by gain-of-function mutations in the calcium-sensing
receptor (CASR) gene.
- Familial isolated hypoparathyroidism (FIH)
- Congenital absence of parathyroid glands
• Functional hypoparathyroidism: due to low level
of magnesium which is required for PTH release
from the glands

15. Clinical manifestations
• The hallmark of hypocalcemia is tetany, which is
characterized by neuromuscular irritability. Symptoms
range from circumoral numbness or paresthesias
(tingling) of the distal extremities and carpopedal
spasm, to life-threatening laryngospasm and generalized
seizures.
• Mental status changes include emotional instability,
anxiety and depression, confusional states,
hallucinations, and frank psychosis.
• Intracranial manifestations include calcifications of the
basal ganglia, parkinsonian-like movement disorders,
and increased intracranial pressure with resultant
papilledema.
The major clinical manifestations of hypoparathyroidism are
related to the severity and chronicity of the hypocalcemia.

16. • Ocular disease takes the form of calcification of
the lens and cataract formation.
• Cardiovascular manifestations include a
conduction defect that produces a characteristic
prolongation of the QT interval in the
electrocardiogram.
• Dental abnormalities occur when hypocalcemia is
present during early development. These findings
include: dental hypoplasia, failure of eruption,
defective enamel and root formation, and
abraded carious teeth.

17. • Hypoparathyroidism occuring as a result of
end-organ resistance to the actions of PTH.
• PTH like TSH, FSH & LH signal via G-protein–
triggered second messengers, and the
disorder results from genetic defects in this
pathway.
• Thus level of PTH may be normal but all the
symptoms of hypocalcemia are present.