anatomi dan histologi kelenjar paratiroid.pptx

paratiroid

1. Parathyroid Glands

2. Four small ovoid masses Size 3x6 mm, each. Total weight 0,4 gram. Location: On the back of thyroid gland  embedded in the larger gland’s capsule. The microvasculature of each arises from the inferior thyroid arteries. Each parathyroid gland is contained within a thin capsule from which septa extend into the gland. A Mescher AL. Junqueira’s basic histology: text and atlas . 15th ed. New York: McGraw-Hill Education; 2018.

3. The endocrine cells of the parathyroid glands Principal (chief) cells , are small polygonal cells with round nuclei and pale-staining, slightly acidophilic cytoplasm oxyphil cells , are sometimes also present in parathyroid glands, more commonly in older individuals Irregularly shaped cytoplasmic granules contain the polypeptide parathyroid hormone (PTH) , an important regulator of blood calcium levels. The function of the parathyroid glands  regulate calcium homeostasis. Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

4. Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

5. Parathyroid disorder Hyperparathyroidism Hypoparathyroidsm Primary Hyperparathyroidism Secondary Hyperparathyroidism Pseudohypoparathyroidism Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

6. Primary Hyperparathyroidism Primary hyperparathyroidism is one of the most common endocrine disorders, and it is an important cause of hypercalcemia. The frequency of the various parathyroid lesions underlying hyperfunction is as follows: Adenoma: 85% to 95% Primary hyperplasia (diffuse or nodular): 5% to 10% Parathyroid carcinoma: ~1% M ore common in women than in men by ratio of nearly 4 : 1 The most common cause of primary hyperparathyroidism is a solitary sporadic parathyroid adenoma Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

7. There are three molecular defects that have an established role in the development of sporadic adenomas: Cyclin D1 (CCDN1) gene inversions leading to overexpression of cyclin D1 protein, a major regulator of the cell cycle. MEN1 mutations: Approximately 30% to 35% of sporadic parathyroid tumors have somatic mutations of the MEN1 gene, a tumor suppressor gene on chromosome 11q13, with loss of heterozygosity (LOH) of the second allele. CDC73, which encodes a protein known as parafibromin , is mutated in ~70% of sporadic parathyroid carcinomas, but rarely in adenomas. Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

8. Primary hyperplasia M ay occur sporadically or as a component of MEN syndrome. T here is frequently asymmetry with apparent sparing of one or two glands, making the distinction between hyperplasia and adenoma difficult. The combined weight of all glands rarely exceeds 1 g and is often less. Microscopically: C hief cell hyperplasia, which may involve the glands in a diffuse or multinodular pattern. T he constituent cells contain abundant glycogen, giving them a clear appearance in histologic sections (“water-clear cell hyperplasia”). T here are islands of oxyphils, and poorly developed, delicate fibrous strands may envelop the nodules. As in the case of adenomas, stromal fat is inconspicuous within hyperplastic glands. hypercellular - usu. chief cell predominant, decreased adipose tissue, +/-"water-clear" cells (cells with abundant granular/foamy cytoplasm, mild nuclear pleomorphism) Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

9. Parathyroid carcinomas Parathyroid carcinomas may be circumscribed lesions that are difficult to distinguish from adenomas. These tumors enlarge one parathyroid gland and consist of gray-white I rregular masses that sometimes exceed 10 g in weight. The cells are usually uniform and resemble normal parathyroid cells, and are arrayed in nodular or trabecular patterns. The mass is usually enclosed by a dense, fibrous capsule Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

10. Clinical Features Asymptomatic hyperparathyroidism M ost patients with primary hyperparathyroidism are diagnosed incidentally. P rimary hyperparathyroidism is the most common cause of asymptomatic hypercalcemia. M alignancy stands out as the most frequent cause of symptomatic hypercalcemia in adults, and must be excluded by appropriate clinical and laboratory investigations. Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

11. B. Symptomatic primary hyperparathyroidism. The constellation of symptoms includes the following: • Bone disease and bone pain secondary to fractures of bones weakened by osteoporosis. • Nephrolithiasis (renal stones)  attendant pain and obstructive uropathy. Chronic renal insufficiency and abnormalities in renal function lead to polyuria and secondary polydipsia. • Gastrointestinal  constipation, nausea, peptic ulcers, pancreatitis, and gallstones • Central nervous system alterations  depression , lethargy, and eventually seizures • Neuromuscular abnormalities  weakness and fatigue • Cardiac manifestations  aortic or mitral valve calcifications (or both) Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

12. Secondary Hyperparathyroidism C aused by any condition that gives rise to chronic hypocalcemia  leads to compensatory overactivity of the parathyroid glands. Example: Renal failure inadequate dietary intake of calcium Steatorrhea vitamin D deficiency Clinical Features The clinical features of secondary hyperparathyroidism are usually dominated by the inciting chronic renal failure. Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

13. HYPOPARATHYROIDSM Hypoparathyroidism is far less common than is hyperparathyroidism. Acquired hypoparathyroidism is almost always an inadvertent consequence of surgery There are several genetic causes of hypoparathyroidism: Surgically induced hypoparathyroidism Autoimmune hypoparathyroidism Autosomal-dominant hypoparathyroidism Familial isolated hypoparathyroidism (FIH) Congenital absence Clinical Features neuromuscular irritability Intracranial manifestations Ocular disease Cardiovascular manifestations Dental abnormalities Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.

14. Pseudohypoparathyroidism PTH resistance is the most obvious clinical manifestation. It presents as hypocalcemia, hyperphosphatemia, and elevated circulating PTH. TSH resistance is generally mild, while LH/FSH resistance manifests as hypergonadotropic hypogonadism in females. Kumar V, Abbas AK, Aster JC. Robbins & Cotran pathologic basis of disease . 10th ed. Philadelphia: Elsevier; 2020. p. 1093-1097.