1. NEOPLASMS OF THE THYROID PATHOLOGY OF PARATHYROID GLANDS
BY: Shifaa’ Qa’qa’

2. Neoplasmas of the thyroid
thyroid nodules
Neoplastic benign, malignant
Non neoplastic

3. Solitary nodules ----- neoplastic
Nodules in younger patients neoplastic
Nodules in males ---- neoplastic
history of radiation treatment to the head and neck malignancy
hot nodules benign

4. Adenomas Follicular adenomas Solitary
Nonfunctional---- M.C--- RAS, PAX8/PPARG fusion gene
toxic adenomas---- TSHR, α-subunit of Gs (GNAS)---- autonomy---- thyrotoxicosis
Carcinoma ??

5. well-defined, intact capsule
Adenoma----- no invasion
Carcinoma----- invasion
Multinodular goiter---- no capsule
Uniform follicles

7. Hürthle cell adenoma ???
endocrine atypia ??

9. cold nodules---10% of cold nodules eventually prove to be malignant.
hot nodules---- malignancy is rare---- toxic adenoma
ultrasonography
fine needle aspiration biopsy (FNA)
Because of the need for evaluating capsular integrity, the definitive diagnosis of thyroid adenoma can be made only after careful histologic examination of the resected specimen.

10. Carcinomas Papillary carcinoma (85% of cases)
Follicular carcinoma (5% to 15% of cases)
Anaplastic (undifferentiated) carcinoma (less than 5% of cases)
Medullary carcinoma (5% of cases)

11. Papillary thyroid carcinomas:
m.c
ionizing radiation
nonfunctional tumors
- Activation of the MAP kinase pathway:
Rearrangements of RET (RET/PTC)
BRAF
nuclear features ???
Papillae ????
lymphatic permeation, LN
indolent lesions, with 10-year survival rates in excess of 95%.

13. Follicular thyroid carcinomas:
older age than that typical for papillary carcinoma
iodine deficiency
Solitary cold thyroid nodules
- mutations in the PI-3K/AKT signaling pathway:
RAS and PIK3CA
PTEN
PAX8/PPARG fusion genes
widely invasive
minimally invasive
hematogenous dissemination
surgical excision, radioactive iodine

14. Anaplastic Carcinoma:
- undifferentiated
Mortality rate approaching 100% (mets, local effect)
mean age of 65 years
giant cells
Spindle cells

15. Medullary Carcinoma:
- parafollicular cells, or C cells----neuroendocrine
neoplasms
Sporadically
familial cases (30%)---- MEN syndrome 2A, 2B, familial medullary thyroid carcinoma
RET mutations
Multicentricity????
multicentric C cell hyperplasia????
Mass
peptide hormone

17. PARATHYROID GLANDS
free (ionized) calcium

18. HYPERPARATHYROIDISM
primary
Secondary
tertiary

19. Primary Hyperparathyroidism:
- Adenoma—85% to 95%
- Primary hyperplasia (diffuse or nodular)—5% to 10%
Parathyroid carcinoma—1%
Sporadic----- m.c---- Cyclin D1, MEN1
Familial MEN1, MEN2A, Familial hypocalciuric hypercalcemia
hypercalcemia

20. parathyroid adenomas:
By definition, parathyroid adenomas are almost invariably confined to single glands g.
dipose tissue is inconspicuous within adenomas
rim of compressed, non-neoplastic parathyroid tissue, generally separated by a fibrous capsule

21. Parathyroid hyperplasia: Multiglandular process weight of all glands rarely exceeds 1.0 g Parathyroid carcinomas: exceed 10 g in weight invasion of surrounding tissues and metastasis

22. Morphologic changes in other organs:
osteitis fibrosa cystica
brown tumors
Nephrolithiasis
Nephrocalcinosis
Metastatic calcification

23. The most common manifestation of primary hyperparathyroidism is an increase in serum ionized calcium
primary hyperparathyroidism is the most common cause of clinically silent hypercalcemia--- PTH is high, hypophosphatemia
The most common cause of clinically apparent hypercalcemia in adults is paraneoplastic syndromes associated with malignancy and bone metastases

25. “painful bones (fractures), renal stones, abdominal groans, and psychic moans.”
Gastrointestinal disturbances: constipation, nausea, peptic ulcers, pancreatitis, and gallstones
Central nervous system alterations: depression, lethargy, and seizures
Neuromuscular abnormalities: weakness and hypotonia
Polyuria and secondary polydipsia

26. Secondary Hyperparathyroidism
Renal failure is by far the most common cause of secondary hyperparathyroidism
RF: hyperphosphatemia, hypocalcemia----- Serum calcium remains near normal
The parathyroid glands in secondary hyperparathyroidism are hyperplastic
tertiary hyperparathyroidism

27. HYPOPARATHYROIDISM
Surgically induced hypoparathyroidism (hyroidectomy)
Congenital absence ???
Autoimmune hypoparathyroidism
Hypocalcemia:
increased neuromuscular irritability (tingling, muscle spasms, facial grimacing, and sustained carpopedal spasm or tetany),
Cardiac arrhythmias,
increased intracranial pressures and seizures