Endocrine system Flashcards
Normal thyroid seen microscopically consists of follicles lined by a cuboidal epithelium and filled with pink, homogenous colloid. The follicles vary somewhat in size. The interstitium, which may contain “C” cells, is not prominent.
This immunohistochemical stain with antibody to calcitonin identifies the “C” cells (parafollicular cells) of the thyroid interstitium between the follicles or adjacent to the epithelium of follicles. These cells secrete calcitonin.
This symmetrically small thyroid gland demonstrates atrophy. This patient was hypothyroid. This is the end result of Hashimoto’s thyroiditis.
This low power microscopic view of thyroid gland shows an early stage of Hashimoto thyroiditis with prominent lymphoid follicles containing large, active germinal centers. In this autoimmune disease, antithyroglobulin and antimicrosomal (thyroid peroxidase) autoantibodies can often be detected in serum. Other autoimmune diseases such as Addison disease or pernicious anemia may also be present. Both thyroid growth immunoglobulins (TGI) and thyroid stimulating immunoglobulins (TSI) are present, though blocking antibodies to TSI mitigate their effect so that hyperthyroidism is usually not the most prominent features.
This high power microscopic view of the thyroid with Hashimoto’s thyroiditis demonstrates the pink Hürthle cells at the center and right. The lymphoid follicle is at the left. Hashimoto’s thyroiditis initially leads to painless enlargement of the thyroid, followed by atrophy years later.
This is an example of an immunofluorescence test positive for anti-microsomal antibody, one of the autoantibodies that can be seen with autoimmune diseases of the thyroid. A major component of the antimicrosomal antigen is thyroid peroxidase (TPO) which is often measured serologically. Note the bright green fluorescence in the thyroid epithelial cells, whereas the colloid in the center of the follicles is dark.
Here is an example of immunofluorescence positivity for anti-thyroglobulin antibody. Patients with Hashimoto’s thyroiditis may also have other autoimmune conditions including Graves disease, SLE, rheumatoid arthritis, pernicious anemia, and Sjogren’s syndrome.
This is subacute granulomatous thyroiditis (DeQuervain disease), which probably follows a viral infection and leads to a painful enlarged thyroid. This disease is usually self-limited over weeks to months, with transient hyperthyroidism and/or hypothyroidism, and affected patients return to a euthyroid state. Note the presence of large foreign body giant cells with inflammatory destruction of thyroid follicles.
This thyroid gland is about normal in size, but there is a larger colloid cyst at the left lower pole and a smaller colloid cyst at the right lower pole. Such cysts could appear as “cold” nodules on a thyroid scan. They are incidental benign lesions but can appear as a mass to be distinguished from possible carcinoma.
The follicles are irregularly enlarged, with flattened epithelium, consistent with inactivity, in this microscopic appearance at low power of a multinodular goiter. The earlier phase of a diffuse (non-toxic) goiter leading up to this point may have resulted from either “endemic” goiter (seen in parts of the world where dietary deficiency of iodine may occur) or the uncommon “nonendemic” or sporadic goiter (young adult women are most often affected). Inborn errors of thyroid hormone biosynthesis leading to goiter are extremely uncommon.
A diffusely enlarged thyroid gland associated with hyperthyroidism is known as Graves disease. At low power microscopically, note the prominent infoldings of the hyperplastic follicular epithelium. In this autoimmune disease the action of thyroid stimulating immunoglobulins (TSI’s) predominates over that of thyroid growth immunoglobulins (TGI’s).
Shown at high power, the tall columnar thyroid epithelium with Graves disease lines the hyperplastic infoldings into the colloid. Note the clear vacuoles in the colloid next to the epithelium where the increased activity of the epithelium to produce increased thyroid hormone has led to scalloping out of the colloid in the follicle.
Here is another follicular neoplasm (a follicular adenoma histologically) that is surrounded by a thin white capsule. It is sometimes difficult to tell a well-differentiated follicular carcinoma from a follicular adenoma. Thus, patients with follicular neoplasms are often treated with subtotal thyroidectomy just to be on the safe side.
Fine needle aspiration (FNA) cytology can be utilized to obtain cells from a thyroid lesion for diagnosis.
Normal thyroid follicles appear at the lower right. The follicular adenoma is at the center to upper left. This adenoma is a well- differentiated neoplasm because it closely resemble normal tissue. The follicles of the adenoma contain colloid, but there is greater variability in size than normal.
Sectioning through a lobe of excised thyroid gland reveals a papillary carcinoma. This neoplasm can be multifocal, as seen here, because of the propensity of this neoplasm to invade lymphatics within thyroid, and lymph node metastases are also common. The larger mass shown here is cystic and contains papillary excresences. These tumors most often arise in middle-aged women.
This is the microscopic appearance of a papillary carcinoma of the thyroid. The fronds of tissue have thin fibrovascular cores. The fronds have an overal papillary pattern. There is no such thing as a papillary adenoma, and all papillary neoplasms of the thyroid should be considered malignant.
In this papillary carcinoma of thyroid note the small psammoma body in the center. The cells of this neoplasm often have nuclei with a central clear appearance from fixation. Papillary carcinomas are indolent tumors that have a long survival, even when metastases occur. The most favorite site of papillary carcicnoma metastasis is to local lymph nodes in the neck. In fact, some papillary carcinomas may first be detected as a nodal metastasis.
At the center and to the right is a medullary carcinoma of thyroid, which is much more cellular than the adjacent normal thyroid follicles at the left. At the far right is pink hyaline material with the appearance of amyloid. These neoplasms are derived from the thyroid “C” cells and, therefore, can have neuroendocrine features such as secretion of calcitonin or other hormones.
C-cell hyperplasia is a precursor lesion to MTC, and it appears as aggregates of cells with abundant pink to clear cytoplasm and granular chromatin. It is common in the 25% of MTCs that are hereditary from germline RET gene mutations, and occasionally is observed in sporadic MTCs.
This pheochromocytoma demonstrates the chromaffin reaction. This neoplasm of the adrenal medulla contains catecholamines (epinephrine and norepinephrine). The section of tumor at the bottom has been placed into a dichromate fixative which turns the tissue brown as the catecholamines are oxidized. Compare to the section of pink to yellow tumor at the top which has not been placed in dichromate fixative.
There is some residual adrenal cortical tissue at the lower center right, with the darker cells of the pheochromocytoma seen above and to the left.
Microscopically, a pheochromocytoma is composed of large cells that are pink to mauve and arranged in nests with capillaries in between. Remember 10% when you think of a pheochromocytoma: 10% are bilateral, 10% are in children, 10% are malignant.
Here is a normal pancreatic islet of Langerhans surrounded by normal exocrine pancreatic acinar tissue. The islets contain alpha cells secreting glucagon, beta cells secreting insulin, and delta cells secreting somatostatin.
A pancreatic neuroendocrine tumor, with cells resembling those in the islets of Langerhans, is seen here, separated from the pancreas by a thin collagenous capsule. A few normal islets are seen in the pancreas at the right for comparison.
The pancreatic neuroendocrine tumor at the left contrasts with the normal pancreas with islets at the right. Some of these adenomas function. Those that produce insulin may lead to hypoglycemia. Those that produce gastrin may lead to multiple gastric and duodenal ulcerations (Zollinger-Ellison syndrome).
In parathyroid hyperplasia, there is little or no adipose tissue, but any or all cell types normally found in a parathyroid gland are present. Note the pink oxyphil cells in the nodule seen here.
This case shown here is “secondary hyperparathyroidism” with all parathyroid glands enlarged as a consequence of chronic renal failure with impaired phosphate excretion. The increased serum phosphate tends to drive serum calcium down, which in turn drives the parathyroids to secrete more parathormone.
Here is a parathyroid adenoma, which is the most common cause for primary hyperparathyroidism. A rim of normal parathyroid tissue admixed with adipose tissue cells is seen compressed to the right and lower edge of the adenoma.
This is a parathyroid carcinoma seen at medium power on the left and higher power on the right. The nests of neoplastic cells that are not very pleomorphic. Note the bands of fibrous tissue between the nests. Parathyroid carcinomas infiltrate surrounding structures in the neck.
Here is a normal parathyroid gland for comparison. Adipose tissue cells are mixed with the parathyroid tissue. The amount of fat varies somewhat.
Thyroid medullary carcinoma - nests and cords defined by sharply outlined fibrous bands
