Pituitary Gland - Pathology

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Anatomy and Physiology

Anatomy and Physiology of the pituitary gland can be found here.

General Pathological Principles

Two major changes can occur in an endocrine gland:

• Failure of hormone production:
  • Destruction or lack of cells.
  • Lack of trophic drive.
• Overproduction of hormone:
  • Hyperplasia or neoplasia.
  • Excessive trophic drive.

Pituitary Hypofunction

Congenital Panhypopituitarism

Also known as Pituitary Dwarfism, Congenital Panhypopituitarism is defined by failure of differentiation of oesophageal ectoderm from which the pituitary is derived. The pituitary is replaced by a cystic dilatation of Rathke's Cleft which replaces normal tissue with multilocular cysts- lined with non-secretory cuboidal epithelium.

Cystic Rathke's Pouch. Courtesy of A. Jefferies

Incidence:

• Seen in German Shepherd Dog. Inherited as a simple autosomal recessive trait in affected dogs.
• Congenital hypoplasia of the pituitary in the cat has also been reported.

Clinical signs:

Variable with degree of involvement of the pituitary. Most obvious signs are due to the lack of GH during the growing phase of the puppy's life:

• Pups appear normal at birth as the placenta supplies the foetus' need for GH.
• Retarded growth and proportionate dwarfism.
• Delayed growth plate closure; long bone physes normally close at 7-12 months but those of a pituitary dwarf will remain open until 3-4 years.
• Delayed dental eruption.
• Prognathism; undershot lower jaw as GH needed for mandible length.
• Pups are quieter, more nervous and perhaps slower to learn.
• Retention of puppy coat; wooly. Adult coat does not develop and a bilaterally symmetric, non-pruritic alopecia occurs over areas of friction E.g. neck and trunk.
• Hyperpigmentation with comedomes.
• Reproductive signs E.g. failure to cycle, testicular atrophy.

May also see signs of

• Secondary hypothyroidism
• Secondary hypoadrenocorticism

Diagnosis:

• Presumptive diagnosis based on signalment and clinical signs.
• Radiography to detect growth plate closure.
• GH stimulation test; Use alpha-2 agonist E.g. Xylazine which inhibit somatostatin and so induce GH production and release. Normal dogs will have 2-4X increased GH after 20 mins while a pituitary dwarf will show little change in GH upon stimulation.
• Somatomedin Assay; Also called insulin-like growth factors. GH mediates its effects by stimulating the production of IGFs which can be more easily measured. Low levels will be found in pituitary dwarfs.
• May also need to consider TSH and ACTH stimulation tests.

Treatment:

Need to treat early or will remain dwarfs.

• Sub-cut bovine/human GH can induce the growth of an adult haircoat.
  Nb. GH is diabetogenic so overdose will induce Diabetes Mellitus.
• Progestagens may induce GH production from the mammary gland.
• May need to replace thyroid hormones and/or glucocorticoids.

Pituitary cysts

Pituitry cyst. Courtesy of A. Jefferies

Act as space-occupying lesions producing a pathology of the pituitary. May arise from two developmental structures:

• The cranio-pharyngeal ducts which are the route by which the developing anterior pituitary ascends from the pharynx. The craniopharyngeal ducts are the neck of Rathke's pouch which, during development, narrows, closes and separates the vesicle of Rathke's pouch from the oral cavity. These cysts have columnar ciliated epithelial cells lining the cyst and contain mucin.
  The craniopharyngeal ducts may also become neoplastic; Craniopharyngioma. These tumours contain single or multiple cysts.
• Rathke's Pouch which may fail to differentiate and becomes cystic.

Pituitary Neoplasia

Tumours within the pituitary fossa may be functional and sectrete trophic factors. However, more commonly they are non-functional and are space-occupying lesions. Pressure on neighbouring structures causes clinical signs, for example:

• Pressure on the optic chiasma produces ocular signs.
• Pressure on the hypothalamus may lead to Frohlich's adiposogenital syndrome.
• Pressure on the neurohyposphysis may lead to failure of ADH secretion. This will allow large volumes of water to be lost form the kidney; diabetes insipidus.

Pituitary neoplasia. Courtesy of A. Jefferies

Neoplasia may be derived from:

• Pituitary itself.
• Surrounding brain tissue.
• Ependyma.

Pituitary neoplasia in the horse

Neoplasia usually occurs in the pars intermedia of the anterior pituitary and compresses the hypothalamus.

Clinical signs:

• Polyuria and polydipsia.
• Increased appetite reulting in increased food intake and downregulation of insulin receptors. This leads to a hyperglycaemia.
• Somnolence.
• Muscle wekaness.
• Hirsutism.
• Hyperhidrosis.

Pituitary Hyperfunction

• In the foetus results in Gigantism. Oppostie of pituitary dwarfism, not documented in animals.
• In the adult results in Acromegaly.

Acromegaly

Due to excess levels of GH after closure of the physeal plates. As the bones cannot increase in length they respond by appositional growth.

Clinical signs:

General increase in tissue mass throughout the body. Skin is thickened and forms folds. Also:

• Large paws.
• Prognathism with an overshot lower jaw.
• Dyspnoea due to overgrowth of tissues around the larynx.
• Neurological signs due to overgrowth of the bony parts of the skull.

Most often iatrogenic due to progestagen therapy in dogs. Progestagens stimulate the release of GH from mammary tissue in dogs and bitches. In the cat, aetiology is often neoplasia.