MAKROS ADENOMA HIPOFISIS MIKROS ADENOMA HIPOFISIS MAKROS DM

MIKROS GRAVES DISEASE MAKROS GRAVES DISEASE MIKROS DM TYPE 1

MIKROS TIROIDITIS HASHIMOTO MAKROS TIROIDITIS HASHIMOTO MIKROS CUSHING SYNDROME

MAKROS NEOPLASMA TIROID MIKROS NEOPLASMA TIROID MAKROS CUSHING SYNDROME

MAKROS HIPERTIROIDISME MIKROS HIPERTIROIDISME MIKROS DM TYPE 2

PENJELASAN GAMBAR
1. ADENOMA HIPOFISIS
- Makros dan mikros ada di buku petunjuk praktikum
2. GRAVES DISEASE
- Makros: Tiroid membesar difus dan simetris, pada pemotongan berwarna daging
- Mikros: sel folikuler membesar dilapisi epitel kolumner yang tinggi yang secara aktif meresorbsi
koloid membentuk struktur scalloping dan membentuk struktur menonjol ke dalam lumen
3. TIROIDITIS HASHIMOTO
- MAKROS: Figure 15-14 Hashimoto thyroiditis, gross There is relentless destruction of thyroid
follicles over the years, with eventual atrophy, so that the thyroid is often not palpable when a patient
pres - ents with myxedema from hypothyroidism, and the serum TSH is elevated. Early in the course
of this disease, there may be transient hyperthyroid - ism from excessive release of thyroid hormones
from damaged follicles. Women are affected far more often than men. Other autoimmune diseases, such
as Addison disease or pernicious anemia, may also occur in patients with Hashi - moto thyroiditis. There
is an increased risk for subsequent development of B-cell non-Hodgkin lymphoma.
- MIKROS: ADA DI BUKU PETUNJUK PRAKTIKUM
4. NEOPLASMA TIROID
- MAKROS: Figure 19–10 Multinodular goiter. A, Gross morphologic appearance. The coarsely nodular
gland contains areas of fibrosis and cystic change.
- MIKROS: B, Photomicrograph of specimen from a hyperplastic nodule, with compressed residual
thyroid parenchyma on the periphery. The hyperplastic follicles contain abundant pink “colloid” within
their lumina. Note the absence of a prominent capsule, a feature distinguishing such lesions from
neoplasms of the thyroid.
5. CUSHING SYNDROME
- MIKROS : Figure 15-47 Adrenal adenoma, microscopic The adrenocortical adenoma on the right is
well differentiated and resembles normal adrenal fasciculata. It appears histologically nearly the same
as the compressed normal adrenal ( ) on the left, just outside the capsule of the adenoma. There may be
minimal cellular pleomorphism within these adenomas. If such an adenoma does not function, it may
not be detected except by imaging studies done for other reasons. Adenomas secreting cortisol may lead
to Cushing syndrome with central fat redistribution, hypertension, secondary diabetes, purpura, and
osteoporosis.
- MAKROS : Figure 19–36 Diffuse hyperplasia of the adrenal (bottom) contrasted with normal adrenal
gland (top). In cross-section, the adrenal cortex is yellow and thickened, and a subtle nodularity is
evident. The abnormal gland was from a patient with ACTH-dependent Cushing syndrome, in whom
both adrenals were diffusely hyperplastic. ACTH, adrenocorticotropic hormone.
6. HIPERTIROIDISME
- MAKROS : Figure 19–6 Patient with hyperthyroidism. A wide-eyed, staring gaze, caused by
overactivity of the sympathetic nervous system, is one of the classic features of this disorder. In Graves
disease, one of the most important causes of hyperthyroidism, accumulation of loose connective tissue
behind the orbits also adds to the protuberant appearance of the eyes.
- MIKROS : Figure 15-17 Graves disease, microscopic At higher magnification, the tall columnar
appearance of the hyperplastic follicular epithelial cells is evident. Small, clear vacuoles ( ) appear next
to each cell, indicating increased processing of colloid to produce increased output of thyroid hormone
leading to hyperthyroidism. The feedback on the adenohypophyseal thyrotrophs decreases the serum
TSH, whereas the serum T4 is high. Antithyroid antibodies may be present. An uncommon but serious
 complication is thyroid storm with malignant hyperthermia. Graves disease can be treated with a β-
blocker to diminish β-adrenergic effects, with antithyroid drugs such as propylthiouracil, and with
subtotal thyroidectomy
7. DM
- MIKROS DM TYPE 1 & 2 : Figure 19–26 A, Autoimmune insulitis in a rat (BB) model of
autoimmune diabetes. This disorder also is seen in type 1 human diabetes. B, Amyloidosis of a
pancreatic islet in type 2 diabetes. Amyloidosis typically is observed late in the natural history of this
form of diabetes, with islet inflammation noted at earlier observations.
- MAKROS : Figure 19–31 Nephrosclerosis in a patient with long-standing diabetes. The kidney has
been bisected to demonstrate both diffuse granular transformation of the surface (left) and marked
thinning of the cortical tissue (right). Additional features include some irregular depressions, the result
of pyelonephritis, and an incidental cortical cyst (far right).