FIGURE 17.1

Section of anterior pituitary gland stained by the immunoperoxidase technique with an antibody to ACTH. Corticotrophs (ACTH-producing cells) are scattered among immunonegative cells, producing other hormones.

FIGURE 17.2

FIGURE 17.2 Sections from a pituitary tumour in a patient with hyperprolactinaemia. (A) Immunostaining for prolactin is negative, because the tumour cells are not storing the hormone. (B) In-situ hybridization for prolactin mRNA gives a positive signal, confirming that the tumour is producing the hormone.

FIGURE 17.5

Enhanced MRI scan showing the pituitary tumour (arrow).

FIGURE 17.6

Section of pituitary adenoma immunostained for growth hormone, confirming it as the source of secretion.

FIGURE 17.7

A large non-functional adenoma of anterior pituitary gland that has grown up out of the sella turcica, and has compressed the optic chiasma.

FIGURE 17.8

The synthetic pathway and secretion of thyroid hormones.Inorganic iodide is trapped (1) and is oxidized within the follicular cells by the action of thyroid peroxidase (2). It is then secreted into the colloid and undergoes organification close to the cell membrane by the iodination of tyrosyl residues on thyroglobulin (Tg), also secreted by the follicular cells (3). First, mono-iodotyrosine (MIT) and di-iodotyrosine (DIT) are produced. Thyroxine (T₄) is then formed by the coupling of two molecules of DIT, and tri-iodothyronine (T₃) by coupling of MIT and DIT. When hormone is required, thyroglobulin is reabsorbed (4) and undergoes proteolysis (5), releasing T₃ and T₄ (6) which diffuse into the circulation (7). The excess, along with MIT and DIT, undergoes deiodination (8).

FIGURE 17.9 

(A) A cut section through a multinodular goitre showing gross asymmetrical enlargement. (B) Nodularity is clear on histological assessment.

FIGURE 17.10

Hashimoto’s thyroiditis. The thyroid is enlarged, and the cut surface is pale in contrast to the normal brown appearance.

FIGURE 17.11

Hashimoto’s thyroiditis showing the diffuse lymphoid infiltrate with destruction of the thyroid epithelium.

FIGURE 17.12

Follicular carcinoma. Tongues of tumour are seen breaching the capsule and invading the surrounding gland in this minimally invasive follicular carcinoma of the thyroid.

FIGURE 17.13

This autopsy specimen shows invasion of the trachea and oesophagus by a follicular carcinoma of thyroid.

FIGURE 17.14

The clinical appearance of the thyroid nodule is shown on the right, with the radio-iodine scan on the left.

FIGURE 17.15

The fine needle aspiration cytology specimen showed a microfollicular pattern, consistent with a follicular neoplasm. (Leishman).

FIGURE 17.16

The follicular carcinoma shows capsular invasion.

FIGURE 17.17

Vascular invasion is also seen.

FIGURE 17.18

Papillary carcinoma of thyroid showing papillae with fibrovascular cores and classical optically clear nuclei.

FIGURE 17.19

Medullary carcinoma of thyroid showing immunopositivity for calcitonin (brown).

FIGURE 17.20

Pathways of adrenal steroidogenesis. The enzymes involved are: 20–22 = 20,22 desmolase (CYP 11A); 3 = 3β-hydroxysteroid dehydrogenase; 21 = 21 hydroxylase (CYP 21); 11 = 11β-hydroxylase (CYP 11B1); aldo = aldosterone synthase (CYB 11B2). DHEA = dehydroepiandrosterone.

FIGURE 17.21

A patient with Cushing’s syndrome. Note the characteristic obesity of the neck and trunk and the relative wasting of the limbs. (Figure courtesy of Professor JMC Connell, University of Glasgow.)

FIGURE 17.22

Computed tomography scan of the abdomen in a patient with Conn’s syndrome. An adenoma (CA) is seen in the left adrenal, continuous with normal adrenal tissue (A). The kidney (K) and spleen (S) are also shown. (Figure courtesy of Professor JMC Connell, University of Glasgow.)

FIGURE 17.23

Adrenocortical carcinoma, showing necrosis and haemorrhage. This tumour was causing Cushing’s syndrome.

FIGURE 17.24

Phaeochromocytoma removed from a patient with hypertension. The normal adrenal can be seen to the bottom right.

FIGURE 17.25

Nodular parathyroid removed from a patient with multiple endocrine neoplasia, type I (MEN1) who had hypercalcaemia. The other glands were also nodular, but much smaller.

FIGURE 17.26

Insulitis. Lymphocytes infiltrating and destroying an islet.

FIGURE 17.27

Immune events in the pancreas in type 1 diabetes.

FIGURE 17.28

Amyloid (pink indicated by arrows) largely replacing two islets.