CHAPTER 12 The adenohypophysis consists of three portions: the pars distalis, pars tuberalis, and pars intermedia (Fig. 12-2). In many animal species, the adenohypophysis completely surrounds the pars nervosa of the neurohypophyseal system. The pars distalis is the largest and is composed of several different endocrine cell populations surrounded by abundant capillaries to facilitate secretion of their trophic hormones (Web Fig. 12-1). Fig. 12-2 Pituitary gland and brainstem, normal dog. Web Fig. 12-1 Pituitary gland, pars distalis, normal dog. A specific population of endocrine cells is present in the pars distalis (and also in the pars intermedia of dogs for ACTH secretion) that synthesizes, processes, and secretes each of the pituitary trophic hormones (Fig. 12-3). Secretory cells in the adenohypophysis are classified as acidophils, basophils, and chromophobes based on the reactions of their secretory granules with pH-dependent histochemical stains (Fig. 12-4). Based on contemporary specific immunohistochemical staining, acidophils can be further subclassified functionally into somatotrophs that secrete growth hormone (GH; somatotrophin) and lactotrophs that secrete prolactin. Basophils include gonadotrophs that secrete luteinizing hormone (LH) and follicle-stimulating hormone (FSH), thyrotrophs that secrete thyrotrophic hormone (thyroid-stimulating hormone [TSH]), and ACTH-secreting corticotrophs. Chromophobes are pituitary cells that by light microscopy lack stainable cytoplasmic secretory granules. They include the pituitary cells involved with the synthesis of ACTH and melanocyte-stimulating hormone (MSH) in some species, nonsecretory follicular (stellate) cells, degranulated chromophils (acidophils and basophils) in the actively synthesizing phase of the secretory cycle, and undifferentiated stem cells of the adenohypophysis. Fig. 12-3 Hypothalamic-pituitary-target gland axis. Fig. 12-4 Pars distalis, normal dog. Fig. 12-5 Adrenal gland, normal dog. Fig. 12-6 Aldosterone secreted by the zona glomerulosa of the adrenal cortex acts on the distal portions of the nephron to increase tubular excretion of potassium and increase resorption of sodium (and secondarily of chloride). Fig. 12-7 Dehiscence of surgical wound, skin, ventral abdomen, dog. Web Fig. 12-2 Thyroid follicular cells, thyroid gland, normal dog. The synthesis of thyroid hormones is unique among those of the endocrine glands because the final assembly of hormone occurs extracellularly within the follicular lumen. Follicular cells trap essential raw materials, such as iodide from the blood, by a sodium-iodide symporter in the basolateral plasma membrane and then transport them rapidly against a concentration gradient to the lumen, where the iodide is oxidized by thyroid peroxidase in the microvilli to iodine (I2) (Fig. 12-8). The assembly of thyroid hormones within the follicular lumen is made possible by a unique protein, thyroglobulin. Thyroglobulin is a high molecular weight (600,000 to 750,000 Da) glycoprotein synthesized in successive subunits on the ribosomes of the endoplasmic reticulum in follicular cells. The constituent amino acids (tyrosine and others) and carbohydrates (e.g., mannose, fructose, galactose) are derived from the circulation. Recently synthesized thyroglobulin (17S) leaves the Golgi apparatus and is packaged into apical vesicles that are extruded into the follicular lumen (see Fig. 12-8). The amino acid tyrosine, an essential component of thyroid hormones, is incorporated within the molecular structure of thyroglobulin. Iodine is bound to tyrosyl residues in thyroglobulin at the apical surface of follicular cells to form monoiodotyrosine (MIT) and diiodotyrosine (DIT) (see Fig. 12-8). The resulting MIT and DIT combine to form the two biologically active iodothyronines, T4 and T3, secreted by the thyroid gland. Fig. 12-8 Thyroid follicular cells illustrating two-way traffic of materials from capillaries into the follicular lumen. TSH is delivered to thyroid follicular cells where it binds to the basilar aspect of the cell, activates adenyl cyclase, and increases the rate of all biochemical reactions concerned with the biosynthesis and secretion of thyroidal hormones. If the secretion of TSH is sustained (hours or days), thyroid follicular cells become more columnar and follicular lumina become smaller as a result of increased uptake of colloid by endocytosis (Fig. 12-9). Numerous periodic acid–Schiff (PAS)-positive colloid droplets are present in the luminal aspect of the hypertrophied follicular cells. The converse occurs in the thyroid gland in response to increases in circulating T4 and T3, which cause a corresponding decrease in TSH. Thyroid follicles become enlarged and distended with colloid as a result of decreased TSH-mediated endocytosis of colloid. Follicular cells lining the involuted follicles become low cuboidal, with only a few endocytic vacuoles at the interface between the colloid and follicular cells (Fig. 12-10). Fig. 12-9 Hyperplasia, thyroid gland, horse. Fig. 12-10 Atrophy, thyroid gland, dog. Web Fig. 12-3 Thyroid C cell, thyroid gland, normal dog. C cells store substantial amounts of calcitonin in their cytoplasm, and the hormone is discharged rapidly into interfollicular capillaries in response to hypercalcemia (Fig. 12-11). C cells respond to long-term hypercalcemia by hyperplasia. When the blood calcium concentration is reduced, the stimulus for calcitonin secretion is diminished, and numerous secretory granules accumulate in the cytoplasm of C cells (see Fig. 12-11). Calcitonin exerts its function by interacting with target cells located primarily in bone and kidneys. The actions of parathyroid hormone (PTH) and calcitonin are antagonistic on bone resorption, but synergistic in decreasing the renal tubular reabsorption of phosphorus. Fig. 12-11 Response of thyroid C cells and parathyroid chief cells to hypercalcemia and hypocalcemia. Fig. 12-12 Parathyroid gland, normal dog. Biologically active PTH secreted by chief cells is a straight-chain polypeptide consisting of 84 amino acid residues, with a molecular weight of approximately 9500 Da. Secretory cells in the parathyroid glands of most animals store relatively small amounts of preformed hormone but are capable of responding to minor fluctuations in calcium ion concentration rapidly, by altering the rate of hormonal secretion, and more slowly, by altering the rate of hormonal synthesis (Fig. 12-13). In contrast to most endocrine organs that are under complex control, the parathyroid glands have a unique feedback control system based primarily on the concentration of calcium and, to a lesser extent, of magnesium ions in blood. Calcium ion concentration controls not only the rate of biosynthesis and secretion of PTH but also other metabolic and intracellular degradative processes within chief cells. Increased calcium ion concentration in extracellular fluids rapidly inhibits the uptake of amino acids by chief cells, and consequently synthesis of proPTH, its conversion to PTH, and secretion of stored PTH (see Fig. 12-13). Fig. 12-13 Bypass secretion of parathyroid hormone (PTH) in response to increased demand signaled by decreased blood calcium ion concentration. Fig. 12-15 Pancreatic islet, normal dog. Web Fig. 12-4 Pancreatic islet, normal dog. Pathogenic Mechanisms of Endocrine Diseases Although injury of cells in endocrine glands is often attributable to processes, such as necrosis, inflammation, and autoimmunity, discussed in Chapters 1, 3, and 5, respectively, many diseases of endocrine glands are characterized by dramatic functional disturbances and characteristic clinicopathologic alterations affecting one or more body systems. The affected animal can have changes primarily involving the skin (alopecia caused by hypothyroidism), nervous system (seizures caused by hyperinsulinism), urinary system (polyuria caused by diabetes mellitus, diabetes insipidus, and hyperadrenocorticism), or skeletal system (fractures induced by hyperparathyroidism). There are several mechanisms that can disrupt normal endocrine function, with the majority of processes resulting in insufficient or excessive hormone production. Fig. 12-16 Secondary hypofunction of adrenal glands, brain, pituitary gland and left (longitudinal section) and right (cross section) adrenal glands, dog. TABLE 12-1 Primary Hyperfunction of an Endocrine Gland Fig. 12-17 Secondary hyperfunction of adrenal glands, brain, pituitary gland and left and right adrenal glands, dog. Fig. 12-18 Iatrogenic hyperadrenocorticism, left and right adrenal glands, dog. Fig. 12-19 Iatrogenic acromegaly, beagle (center) compared with unaffected littermates (left and right). Disorders known or thought to have a genetic basis and/or be inherited are listed in Web Table 12-1. WEB TABLE 12-1 Inherited Endocrine Diseases of Animals Hypopituitarism and Neoplasms of the Adenohypophysis Aplasia and Prolonged Gestation: See the section on Disorders of Ruminants for a discussion of aplasia and prolonged gestation. Pituitary Cysts and Pituitary Dwarfism: See the section on Disorders of Dogs for a discussion of pituitary cysts and pituitary dwarfism. Endocrinologically Inactive Chromophobe Adenomas: Nonfunctional pituitary neoplasms occur in dogs and cats but are uncommon in other species. Although chromophobe adenomas seem endocrinologically inactive, they can cause significant functional disturbances and clinical signs by compressing and causing atrophy of adjacent portions of the pituitary gland, as well as dorsal extension into the overlying brain (Fig. 12-20). The clinical disturbances result either from the lack of secreted pituitary trophic hormones and subsequent diminished target organ function (e.g., adrenal cortex; see Fig. 12-16) or from dysfunction of the CNS. Affected animals often have decreased spontaneous activity, incoordination, and disturbances of balance; are weak; and sometimes collapse after exercise. Chronically affected animals are blind and have dilated and fixed pupils because of compression and disruption of the optic nerves by dorsal extension of the pituitary neoplasms (see Fig. 12-20). Endocrinologically inactive pituitary adenomas often become large before they cause clinical signs or kill the animal (see Figs. 12-16 and 12-20). Fig. 12-20 Adenoma, pituitary gland, dog. Pituitary Gland Carcinomas: Pituitary gland carcinomas are uncommon neoplasms compared with adenomas but have been seen in older dogs and cattle. They usually are endocrinologically inactive but can cause significant functional disturbances by destroying the pars distalis and neurohypophyseal system, leading to panhypopituitarism and diabetes insipidus. Carcinomas are large and invade extensively into the overlying brain, along the ventral aspect of the cranial cavity, and into the basisphenoid bone where they cause osteolysis. Metastases occur infrequently to cervical lymph nodes or distant sites such as the spleen or liver. Carcinomas are highly cellular and often have large areas of hemorrhage and necrosis. Giant cells, nuclear pleomorphism, and mitotic figures are encountered more frequently than in adenomas. Craniopharyngiomas (Intracranial Germ Cell Tumors): Craniopharyngiomas are benign neoplasms derived from epithelial remnants of the oropharyngeal ectoderm of the craniopharyngeal duct (Rathke’s pouch). They often occur in animals younger than those with other types of pituitary neoplasms and are present in either suprasellar or infrasellar locations. Craniopharyngioma is associated with dwarfism in young dogs because it causes subnormal secretion of somatotrophin and other trophic hormones at an early age, before closure of the growth plates. Fig. 12-21 Craniopharyngioma (C), pituitary area, left and right adrenal glands, left and right thyroid glands, dog. • A lack of secretion of pituitary trophic hormones resulting in trophic atrophy and subnormal function of the adrenal cortex and thyroid gland, atrophy of the gonads, and failure to attain somatic maturation because of a lack of secretion of growth hormone • Disturbances in water metabolism (polyuria, polydipsia, low urine specific gravity, and osmolality) resulting from an interference in the synthesis and release of ADH by the large neoplasm • Deficits in cranial nerve function • CNS dysfunction caused by extension into the overlying brain Pars Intermedia Adenomas: Adenomas derived from cells of the pars intermedia are the most common type of pituitary gland neoplasm in horses and the second most common type in dogs, but they are rare in other species. Adenomas develop in older horses, more frequently in females. Nonbrachycephalic breeds of dogs have adenomas of the pars intermedia more often than brachycephalic breeds. Fig. 12-22 Hirsutism, skin, horse. In horses, adenomas of the pars intermedia often are large neoplasms that extend out of the fossa hypophysialis and severely compress the overlying hypothalamus (Fig. 12-23). The adenomas are yellow to white and multinodular and enclose the pars nervosa. When the neoplasm is incised, the pars distalis usually can be identified as a compressed subcapsular rim of tissue on the anterior margin. A sharp line of demarcation remains between the neoplasm and the compressed pars distalis. The neoplastic cells are arranged in cords and nests along the capillaries and connective tissue septae and are large, cylindrical, spindle-shaped, or polyhedral with oval hyperchromatic nuclei (Fig. 12-24). The pattern is often reminiscent of that of the prominent pars intermedia of normal horses. Ribbons of more cuboidal to columnar neoplastic cells occasionally form follicular structures that have dense eosinophilic colloid. Fig. 12-23 Adenoma, brain, pituitary gland, horse.
Endocrine System*
Structure and Function
Pituitary Gland (Hypophysis)
Longitudinal section of the pituitary region illustrating the close relationship to the optic chiasm (O), hypothalamus (H), and overlying brain. The pars distalis (D) forms a major part of the adenohypophysis and completely surrounds the pars nervosa (N). The residual lumen of Rathke’s pouch (arrow) separates the pars distalis and pars nervosa and is lined by the pars intermedia. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Follicular cells (NF) in the pars distalis form a framework and extend cytoplasmic processes (arrows) around extracellular accumulations of colloid (C). Adjacent follicular cells are joined by prominent terminal bars (T). Acidophils in the storage phase of the secretory cycle contain numerous large, uniformly electron-dense secretory granules (S), scattered lipofuscin (L) bodies, a small amount of endoplasmic reticulum (ER), and a small Golgi apparatus. Hypertrophied acidophils (NA) have few mature secretory granules but many distended profiles of endoplasmic reticulum and large Golgi apparatuses (GA) associated with prosecretory granules in the process of formation. TEM. Uranyl acetate and lead citrate stain. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Releasing hormones produced by the hypothalamus act on anterior or posterior portions of the pituitary gland to release trophic hormones. Trophic hormones act on specific endocrine glands, stimulating them to produce hormones that exert ultimate actions on downstream tissues. CRH, Corticotropin-releasing hormone; FSH, follicle-stimulating hormone; GHIH, growth hormone–inhibiting hormone; GHRH, growth hormone–releasing hormone; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone; PRH, prolactin-releasing hormone; PRIF, prolactin release–inhibiting factor; TRH, thyrotropin-releasing hormone. (Modified from Huether SE, McCance KL: Understanding pathophysiology, ed 2, St Louis, 2000, Mosby; and Squire L, Bloom F, McConnell S: Fundamental neuroscience, ed 2, San Diego, 2003, Academic Press.)
The pars distalis is composed of acidophils (arrows), basophils (none shown here) and chromophobes (arrowheads). H&E stain. (Courtesy Dr. J.F. Zachary, College of Veterinary Medicine, University of Illinois.)
Adrenal Gland
Interface between the finely vacuolated (lipid droplets) cells of the adrenocortical zona reticularis (left) and chromaffin cells of the adrenal medulla (right). H&E stain. (Courtesy Dr. J.F. Zachary, College of Veterinary Medicine, University of Illinois.)
The resulting osmotic gradient facilitates movement of water from the glomerular filtrate into the extracellular fluid (ECF). (Redrawn with permission from Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Wounds heal slowly in dogs with cortisol excess because of an inhibition of fibroblastic proliferation. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Thyroid Gland
Thyroid follicular cells with long microvilli (V) that extend into the colloid (C) within the follicular lumen. Numerous lysosomes (L) and colloid droplets (CD) are present in the apical portion of the follicular cells. An interfollicular capillary (arrow) is present at the base of the follicle. TEM. Uranyl acetate and lead citrate stain. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Raw materials, such as iodide, are concentrated by follicular cells and rapidly transported into the lumen (left side of drawing). Amino acids (tyrosine and others) and sugars are assembled by follicular cells into thyroglobulin (Thg), packaged into apical vesicles (AV) and released into the lumen. The iodination of tyrosyl residues with the thyroglobulin molecule to form thyroid hormones occurs within the follicular lumen. Elongation of microvilli (MV) and endocytosis of colloid (Co) by follicular cells occur in response to thyroid-stimulating hormone (TSH) stimulation (right side of drawing). The intracellular colloid droplets (CD) fuse with lysosomal bodies (Ly), active thyroid hormone is enzymatically cleaved from thyroglobulin, and free T4 and T3 are released into the circulation. ATP, Adenosine triphosphate; cAMP, cyclic adenosine monophosphate; CHO, carbohydrates; ECF, extracellular fluid; GA, Golgi apparatus; M, mitochondrion; Mf, microfilaments; Mt, microtubules; PL, phagolysosome; TBG, thyroid-binding globulin; TPO, thyroid peroxidase; TSH-R, thyroid-stimulating hormone receptor; TTR, transthyretin. (From Capen CC: Pathophysiology of the thyroid gland. In Dunlop RH, Malbert C-H, editors: Veterinary pathophysiology, Ames, IA, 2004, Blackwell Publishing.)
Follicular epithelial cells following prolonged thyroid-stimulating hormone stimulation are columnar. Note the many collapsed follicles. The lumens of remaining follicles contain pale pink colloid and have numerous endocytic vacuoles at the epithelial cell-follicular lumen interface. H&E stain. (Courtesy Dr. B. Harmon, College of Veterinary Medicine, The University of Georgia; and Noah’s Arkive, College of Veterinary Medicine, The University of Georgia.)
Thyroid follicular epithelial cells (arrow) after long-term administration of exogenous thyroxine are cuboidal and follicular lumens are distended with dense colloid. Periodic acid–Schiff reaction. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Thyroid C (Parafollicular) Cells
Thyroid C (parafollicular) cell with numerous secretory granules (S) and moderate development of Golgi apparatus and rough endoplasmic reticulum. Microvilli from follicular cells (arrow) extend into the colloid of the follicular lumen (C). The secretory polarity of the C cell is directed toward an interfollicular capillary (arrowhead) with fenestrae. TEM. Uranyl acetate and lead citrate stain. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
C cells accumulate secretory granules in response to hypocalcemia, whereas chief cells are nearly degranulated but have an increased development of synthetic and secretory organelles. In response to hypercalcemia, C cells are degranulated and parathyroid chief cells are predominantly in the inactive stage of the secretory cycle. (Redrawn with permission from Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Parathyroid Glands
Numerous chief cells are separated and supported by a fine fibrovascular stroma. H&E stain. (Courtesy Dr. J.F. Zachary, College of Veterinary Medicine, University of Illinois.)
Recently synthesized and processed active PTH can be released directly without entering the storage pool of mature (“old”) secretory granules in the cytoplasm of chief cells. PTH from the storage pool can be mobilized by cyclic adenosine monophosphate (cAMP) and β-agonists, such as epinephrine, norepinephrine, and isoproterenol, and by lowered blood calcium ion, whereas secretion from the pool of recently synthesized PTH can be stimulated only by a decreased calcium ion concentration. RER, Rough endoplasmic reticulum; GA, Golgi apparatus. (Redrawn with permission from Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Pancreatic Islets
The islet is surrounded by the exocrine pancreas. H&E stain. (Courtesy Dr. J.F. Zachary, College of Veterinary Medicine, University of Illinois.)
Differences in secretion granules between β cells (B) and α cells (A); the internal cores of secretion granules in insulin-secreting β cells (arrowheads) are bar- or Y-shaped, with a prominent space between the limiting membrane and internal core. Secretion granules of the glucagon-secreting α cells have an electron-dense, circular, internal core with a narrow submembranous space (arrow). TEM. Uranyl acetate and lead citrate stain. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Responses to Injury
Secondary Hypofunction of an Endocrine Gland
A large nonfunctional chromophobe adenoma (A) has invaded and completely destroyed the adenohypophysis and hypothalamus, and infiltrated into the thalamus. Destruction of the adenohypophysis has resulted in a lack of secretion of thyrotropin, adrenocorticotropin, and other pituitary trophic hormones, resulting in severe bilateral (symmetrical) trophic atrophy of the adrenal cortex (arrowheads), especially the adrenocorticotropic hormone–dependent zona fasciculata and zona reticularis, and consequently, in a relatively more prominent medulla (M). (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Primary Hyperfunction of an Endocrine Gland
Neoplasia
Hormone
Lesion/Sign
Acidophil adenoma (pituitary gland)
Growth hormone
Acromegaly
Adrenal cortical adenoma/carcinoma
Estrogen
Feminization
Pheochromocytoma (adrenal medulla)
Norepinephrine
Hypertension
Thyroid follicular cell adenoma
T4, T3
↑Basal metabolic rate
C-cell adenoma/carcinoma (thyroid gland)
Calcitonin
Osteosclerosis
Parathyroid gland chief cell adenoma
Parathyroid hormone
Fibrous osteodystrophy
Pancreatic β-cell adenoma/carcinoma
Insulin
Hypoglycemia
Secondary Hyperfunction of an Endocrine Gland
Corticotroph (adrenocorticotropic hormone [ACTH]-secreting) chromophobe adenoma (A) in the pituitary gland and bilateral (symmetrical) enlargement of the adrenal glands. The chronic secretion of ACTH has resulted in bilateral (symmetrical) hypertrophy and hyperplasia of secretory cells of the zona fasciculata and zona reticularis in the adrenal cortex (arrows) and excessive secretion of cortisol. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Iatrogenic Syndromes of Hormone Excess
Hyperadrenocorticism, caused by long-term administration of exogenous corticosteroids, has resulted in notable trophic atrophy of the adrenocorticotropic hormone–dependent zona fasciculata and zona reticularis of the adrenal cortex (C). The adrenal medulla (M) comprises a relatively greater percentage of the atrophic adrenal gland than of a normal adrenal gland. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Note the coarseness of the facial features and the markedly thick folds of the skin of the face. These characteristic changes are the result of the protein anabolic effects of somatotropin (produced by hyperplastic mammary ductular epithelial cells), which have been stimulated by the administration of exogenous medroxyprogesterone acetate. (Courtesy Dr. P. Concannon, College of Veterinary Medicine, Cornell University.)
Disorders of Domestic Animals
Condition
Species/Breed
Pattern of Inheritance
Adenohypophyseal aplasia
Jersey and Guernsey cattle
Unknown
Pituitary dwarfism
German shepherds
Autosomal recessive
Hypoadrenocorticism
Bearded collies, Nova Scotia duck tolling retriever, Portuguese water dogs, standard poodles
Unknown or
autosomal recessive
Adrenal hyperplasia-like syndrome
Chow Chows, Pomeranians, poodles, Samoyeds
Unknown
Dyshormonogenetic goiter
Abyssinian cats, Afrikaner cattle, rat and toy fox terriers, Saanen dwarf goats, sheep
Autosomal recessive
Disorders of the Adenohypophysis
A large pituitary adenoma (A) has extended dorsally and compresses the overlying brain. The optic chiasm (arrow) is also severely compressed. The adenohypophysis, neurohypophysis, and hypothalamus have been destroyed by the neoplasm. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
The neoplasm has extended dorsally through the hypothalamus and compressed the thalamus (black arrows). The neoplasm has also destroyed the adenohypophysis and neurohypophysis, resulting in severe bilateral (symmetrical) trophic atrophy of the adrenal cortices (white arrows). The adrenal glands consist predominantly of medulla (M) surrounded by a thin rim of cortex (capsule plus zona glomerulosa). Although the thyroid follicular cells are atrophic, the overall gland (T) size is within normal limits because of colloid involution of the follicles. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
Hyperpituitarism and Neoplasms of the Adenohypophysis
The hirsutism is the result of a failure to shed hair because of hypothalamic compression by an adenoma of the pars intermedia. (Courtesy Dr. C. Capen, College of Veterinary Medicine, The Ohio State University.)
The pituitary gland is notably enlarged because of an adenoma (A) of the pars intermedia. (Courtesy College of Veterinary Medicine, University of Illinois.)You may also need
Endocrine System
Only gold members can continue reading. Log In or Register to continue
WordPress theme by UFO themes