Pituitary and adrenal pathology

Question 1

Parts of the anterior pituitary

Answer 1

Pars intermedia - suurounds residual Rathke’s pouch. serparates pars nervosa from pars distalis.

Pars distalis - ACTH, GH, prolactin, TSH, LH, FSH

Question 2

Parts of the posterior pituitary (neurohypophysis)

Answer 2

Pars nervosa - mainly axonal projections from hypothalamic neurons. Oxytocin and ADH.

Question 3

Canine pituitary-dependent hyperadrenocorticism

Answer 3

Pituitary neoplasms can be functionally active - secreting trophic factors, e.g. ACTH from a corticotroph adenoma.

Most common cause of pituitary dependent hyperadrenocorticism.

Question 4

Adrenal gland function

Answer 4

Situated either side of CdVC

Cortex derived from coelomic mesoderm. Medulla is derived from neuroectoderm.

Cortex under control of ACTH and produces mineralocorticoids, glucocorticoids, and some sex steroids.

Medulla produces catecholamines.

Question 5

Zones of adrenal cortex

Answer 5

Zona glomerulosa - mineralocorticoids

Zona fasciculata - glucocorticoids

Zona reticularis - glucocorticoids and small amoutns of sex steroids

Question 6

Clinical signs of canine hyperadrenocorticism (Cushing’s)

Answer 6

Alopecia
Hair coat dull
Soft skin may be wrinkled or hyerpigmented
Circular macules and papules
Mineral (calcium) deposition
Pot-bellied appearance
PU/PD

Question 7

Pathogenesis of canine hyperadrenocorticism

Answer 7

Excess cortisol from zona fasciculata cells

80-90% pituitary dependent hyperplasia.

Less commonly functional adrenal tumours or iatrogenic.

Question 8

Pathology found in canine hyperadrenocorticism

Answer 8

Osteoporosis

Metastatic calcification

Calcinosis cutis

Epidermal / dermal atrophy

Hyperkeratosis / follicular keratosis

Reduced lymphocyte and eosinophil count (cf. Addison’s)

Hyperglycaemia

Question 9

Pathogenesis of canine hypoadrenocorticism (Addisons disease)

Answer 9

Functional disorder due to insufficient adrenocortical production of mineralocorticoid and glucocorticoid hormones.

Usually autoimmmune - adrenals infiltrated by lymphocytes and macrophages.

Cortical atrophy - diffuse and severe.

Question 10

Usual signalment of canine hypoadrenocorticism

Answer 10

Young adult to middle aged, slight female predominance

Question 11

Less common causes of adrenocortical insufficiency

Answer 11

Grnulomatous inflammation

Thrombosis of adrenal vessels

Invasion and destruction by neoplasms, haemorrhage and necrosis, or amyloid deposition.

Question 12

Functional disturbances of hypoadrenocorticism

Answer 12

Acute necrosis: acute shock, vomiting, collapse

Chronic degeneration: dehydration, diarrhoea, anorexia, weakness

Hyponatraemia

Hypokalaemia

Hypoglycaemia

Increased circulating lymphocytes and eosinophils

Eosinophils prominent in lymph node sinuses

Skin pigmentation is increased

Question 13

Adrenocortical neoplasms

Answer 13

Benign adenomas or malignant carcinomas

Most functional neoplasms secrete cortisol, but can secrete aldosterone, or oestrogen

Carcinomas may be invasive, and may be bilateral

Unilateral functional neoplasms may lead to trophic atrophy of contralateral adrenal cortex

Question 14

Phaeochromocytomas

Answer 14

Adrenal medullar neoplasm

Most common in cattle and dogs

Can be benign or malignant

If functional, tend to produce norepinephrine - may cause systemic hypertension.

Usually orange/red macroscopically, with only a thin rim of cortex being visible grossly.

Question 15

Pathogenesis of proliferative lesions in ferrets

Answer 15

Pituitary independent

May be gonadectomy related

Disruption of the negative feedback mechanism of GnRH and LH release

Question 16

Pathology of proliferative lesions in ferrets

Answer 16

Adrenocortical hyperplasia - nodular, often bilateral

Adrenocortical adenoma - unilateral

Adrenocortical carcinoma - unilateral, livermetastases

Tumours often have a spindle cell component, identified using immunohistochemistry

Question 17

Clinical signs of proliferative lesions in ferrets

Answer 17

Hair loss
Loss of appetite
Lethargy
Papery thin or translucent looking skin
Excessive scratching and itchiness
Increase in musky odour
Excessive grooming
Sexual agression and mating behaviour
Swollen vulva
Difficulty urinating for males
Weakness in hind limbs
PU/PD
Weight loss

Question 18

Cutaenous manifestations of endocrine skin disease

Answer 18

Alopecia commom - may be bilaterally symmetrical, follicles in telogen

Hypotrichosis

Pigmentary disturbances

Dull, dry, brittle hair coat - fails to regrow after clipping

Seborrhoea

Non-pruritic

Secondary infection and inflammation

Question 19

General cutaneous changes due to endocrine disease

Answer 19

Hyperkeratosis
Follicular hyperkeratosis
Follicular atrophy
Telogen follicles
Epidermal atrophy
Epidermal hypermelanosis
Sebaceous atrophy

Question 20

Cutaneous manifestations of hypothyroidism

Answer 20

Epidermis normal to slightly hyperplastic

Increased dermal mucin (myxoedema)

Question 21

Cutaneous manifestations of hyperadrenocorticism

Answer 21

Calcinosis cutis - calcium deposition in the dermis, stained with Von Kossa stain

Epidermal and follicular thinning

Question 22

Cutaneous manifestations of growth hormone deficiency

Answer 22

Dermal elastin reduced
Increased numbers of telogen and kenogen follicles
Retention of puppy haircoat