Pituitary and adrenal pathology Flashcards
Parts of the anterior pituitary
Pars intermedia - suurounds residual Rathke’s pouch. serparates pars nervosa from pars distalis.
Pars distalis - ACTH, GH, prolactin, TSH, LH, FSH
Parts of the posterior pituitary (neurohypophysis)
Pars nervosa - mainly axonal projections from hypothalamic neurons. Oxytocin and ADH.
Canine pituitary-dependent hyperadrenocorticism
Pituitary neoplasms can be functionally active - secreting trophic factors, e.g. ACTH from a corticotroph adenoma.
Most common cause of pituitary dependent hyperadrenocorticism.
Adrenal gland function
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.
Zones of adrenal cortex
Zona glomerulosa - mineralocorticoids
Zona fasciculata - glucocorticoids
Zona reticularis - glucocorticoids and small amoutns of sex steroids
Clinical signs of canine hyperadrenocorticism (Cushing’s)
Alopecia
Hair coat dull
Soft skin may be wrinkled or hyerpigmented
Circular macules and papules
Mineral (calcium) deposition
Pot-bellied appearance
PU/PD
Pathogenesis of canine hyperadrenocorticism
Excess cortisol from zona fasciculata cells
80-90% pituitary dependent hyperplasia.
Less commonly functional adrenal tumours or iatrogenic.
Pathology found in canine hyperadrenocorticism
Osteoporosis
Metastatic calcification
Calcinosis cutis
Epidermal / dermal atrophy
Hyperkeratosis / follicular keratosis
Reduced lymphocyte and eosinophil count (cf. Addison’s)
Hyperglycaemia
Pathogenesis of canine hypoadrenocorticism (Addisons disease)
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.
Usual signalment of canine hypoadrenocorticism
Young adult to middle aged, slight female predominance
Less common causes of adrenocortical insufficiency
Grnulomatous inflammation
Thrombosis of adrenal vessels
Invasion and destruction by neoplasms, haemorrhage and necrosis, or amyloid deposition.
Functional disturbances of hypoadrenocorticism
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
Adrenocortical neoplasms
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
Phaeochromocytomas
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.
Pathogenesis of proliferative lesions in ferrets
Pituitary independent
May be gonadectomy related
Disruption of the negative feedback mechanism of GnRH and LH release
Pathology of proliferative lesions in ferrets
Adrenocortical hyperplasia - nodular, often bilateral
Adrenocortical adenoma - unilateral
Adrenocortical carcinoma - unilateral, livermetastases
Tumours often have a spindle cell component, identified using immunohistochemistry
Clinical signs of proliferative lesions in ferrets
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
Cutaenous manifestations of endocrine skin disease
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
General cutaneous changes due to endocrine disease
Hyperkeratosis
Follicular hyperkeratosis
Follicular atrophy
Telogen follicles
Epidermal atrophy
Epidermal hypermelanosis
Sebaceous atrophy
Cutaneous manifestations of hypothyroidism
Epidermis normal to slightly hyperplastic
Increased dermal mucin (myxoedema)
Cutaneous manifestations of hyperadrenocorticism
Calcinosis cutis - calcium deposition in the dermis, stained with Von Kossa stain
Epidermal and follicular thinning
Cutaneous manifestations of growth hormone deficiency
Dermal elastin reduced
Increased numbers of telogen and kenogen follicles
Retention of puppy haircoat
