Adrenal Gland Pathology

The adrenal gland is split into the cortex and medulla. The cortex is further split into three layers which are shown above. The cortex should appear 1mm thick.

• Outer Capsule- fibrous and dips into the cortex.
• Zona Glomerulosa- First layer beneath the outer capsule. Appears like small glomeruli. Functions to release mineralcorticoids such as aldosterone. 
• Zona Fasiculata- Middle layer. Appears like linear cord streaks. This is the main cortex component. It releases glucocorticoids such as cortisol. Cortisol gives the cytoplasm a foamy appearance.
• Zona Reticularis- Last layer before the medulla. Appears reticulated and releases sex steroid (precursor androgens). 
• Medulla are derived from sympathetic ganglia. They appear redder and very vascular. They are ganglion looking cells and the medulla can possess very large central veins. 

Mineralcorticoids- Function is the loss of potassium, and the conservation of sodium. Aldosterone is the most potent and has effects on enzyme controlled electrolyte pumps in the DCT of the kidney tubules and sweat glands. 

Glucocorticoids- Acute effects. 15-30 minutes before insulin they provide a compensatory affect. Increase glucose production and cause hyperglycaemia. Increase protein catabolism, lipolysis etc... 

Noradrenaline is released by the medulla of the adrenal glands. 

It acts to:

• Increase the rate and force of the heart muscle contraction via beta receptors.
• It causes blood vessel constriction and so increases arterial blood pressure.
• It causes bronchiolar dilation and assists in pulmonary ventilation.
• It stimulates lipolysis and aids in conserving glucose.
• It increases the metabolic rate which increases oxygen consumption and heat production. 
• It breaks down skeletal muscle glycogen.
• It also causes pupil dilation.

Adrenal Gland Pathology

Hypoadrenocorticism

Causes:

• Primary causes is known as addison's disease. These are seen in the dog, cat and horse. It is due to idiopathic cortical atrophy which occurs in all the cortical zones. It presents with non-specific symptoms.
• Secondary causes are seen in dogs. This is due to hypopituitarism which decreases ACTH which acts on the adrenal gland to release the cortical hormones. 

A decrease in the amount of mineralcorticoids released causes:

• Hyperkalaemia (increased potassium levels as potassium is no longer excreted).
• Decreased Sodium and Chlorine as these two are normally paired in travel and are no longer conserved.
• Cardiovascular disturbances due to the K+ conservation (see nerve resting potentials for information). 
• Dehydration and haemoconcentration (due to the loss of sodium). 

A decrease in the amount of glucocorticoids released causes:

• Moderate hypoglycaemia (due to decreases gluconeogensis and increased insulin sensitivity as insulin acts to lower the levels of glucose in the blood).
• Skin hyperpigmentation (due to increased melanocyte stimulating hormone release which increases melanin pigementation in the skin).

Hyperadrenocorticism 

A) Hyperaldosterone which is seen in cats and dogs. Due to the zonal release of hormones it makes sense that this is either a nodular hyperplasia (increase in the number of cells), adenoma (benign epithelial tumour of hormone secreting tissue) or adenocarcinoma (carcinoma meaning malignant tumour of epithelial tissue) of the zona glomerulosa. This leads to metabolic acidosis and oedema. 

B) Hypercortisolism is seen in dogs, cats and horses. It causes polyuria, polydypsia, polyphagia, trunk obesity, skeletal muscle atrophy, alopecia, epidermal atrophy, osteopenia and secondary diabetes mellitus. 

Cushings Disease (exposure to prolonged cortisol levels & associated symptoms) is due to:

• An ACTH producing tumour/pituitary hyperplasia.
• Primary Adrenal-> zona fasciculata tumour. 
• Paraneoplastic-> Ectopic ACTH production in non-pituitary tumours e.g. bronchial carcinoma.
• Iatrogenic (caused by damage from the vet) seen in dogs due to prolonged glucocorticoid therapy. 

Clinical Signs of Hyperadrencorticism:

• Appetite and food intake.
• Weak and atrophic muscles at extremities & on the abdomen.
• Abdominal enlargement, lordosis (kinked in spine) and muscle trembling.
• Atropy of the temporal muscles.
• Hepatomegaly.
• Bilateral, symmetric alopecia, hyperpigmentation and mineralisation. 

Skin Appearance Microscopically:

• Adnexae and dermal atrophy.
• Loss of elastin and collagen.
• Inactive follicles, infundibular dilation and hyperkeratosis.
• Diffuse orthokeratotic hyperkeratosis.
• Calcinosis Cutis. 

Circulatory Disorders

• Hyperaemia due to Sepsis.
• Haemorrhage due to stress/sepsis. 

Regressive Changes

• Adrenal Cortical Insufficiency (addison's crisis)- stress induced cortical necrosis ( how this differs from hypoadrenocorticism in the fact that necrosis is one step more extreme than atrophy). 
• Cortex Atrophy- glucocorticoid therapy which targets the zona fasiculata. Cessation of therapy results in an addison's crisis. 
• Idiopathic Cortical Atrophy- Autoimmune. 

Regeneration, Hyperplasia and Neoplasms

• Bilateral cortex hyperplasia (secondary)- dogs have persistently elevated ACTH levels. This affects the zona fasiculata and reticularis. 
• Primary cortex hyperplasia- In the old dog where the endocrine activity is silent. Atrophy of the zona fasiculata in non hyperplastic areas. This presents as nodular in pattern.
• Cortical Adenoma.
• Adenocarcinoma of the cortex (rare).
• Nodular Medullary Hyperplasia (rare).
• Phalochromocytoma of the medulla. Endocrine activity in cattle, dogs and horses. Can be malignant. Results in arterial hypertonia, left cardiac hypertrophy and myocardial necrosis.