Adrenal Gland

Function 

Mineralcorticoids:

• Loss of potassium and conservation of sodium. Acts on cells of the kidney DCT and sweat gland. 

Glucocorticoids:

• Intermediate glucose metabolism.
• Acute effect- within 15-30 minutes before the compensatory effects of insulin. 
• Increased glucose production- hyperglycaemia due to:

1. Overall decreased glucose uptake.
2. Increased glucose catabolism in tissue and muscle.
3. Increased gluconeogenesis (liver).
4. Decreased lipogenesis, increased lipolysis in adipose tissue-> glycerol and ffa. 
5. Increased protein catabolism. 

Hypoadrenocorticism

• Primary (addison's disease). Idiopathic cortical atrophy. All zones affected. Non specific symptoms. 
• Secondary- due to hypopituitary. 

Hyperadrenocorticism 

Hyperaldosterone:

• Dogs and cats.
• Nodular hyperplasia, adenoma or carcinoma.
• Zona glomerulosa. 
• Metabolic acidosis and oedema are the consequences. 

Hypercortisolism:

• Generally seen in the dog.
• Adenoma/carcinoma of the zona fasiculata.
• Iatrogenic- prolonged use of glucocorticoid therapy.
• Paraneoplastic- ectopic ACTH production in non pituitary tumours e.g. bronchial carcinoma, thymoma. 

General features:

1. Increased appetite and food intake.
2. Weak and atrophic muscles- extremities and abdomen. 
3. Gradual abdominal enlargement, lordosis and muscle trembling.
4. Temporal muscle atrophy.
5. Skin alterations.

Other Adrenal Gland Disorders

• Hyperaemia/haemorrhage with intoxication or sepsis.

Regressive Changes

• Adrenal cortical insufficiency- stress induced (circulatory, infectious, toxic etc). Often with cortical necrosis. Addison's crisis.
• Adrenal cortical atrophy- prolonged glucocorticoid use. Z.fasiculata. Addison's crisis with sudden cessation of therapy. 
• Idiopathic cortical atrophy- autoimmune disorder. 

All lead to hypoadrenocorticism:

• Reduced mineralcorticoid levels lead to hyperkalaemia and reduced serum sodium and chlorine. Hyperkalaemia leads to vascular disturbances whereas there is progressive haemoconcentration and dehydration due to loss of sodium. 
• Reduced glucocorticoid levels lead to moderate hypoglycaemia due to decreased gluconeogenesis and increased insulin sensitivity. Also leads to skin hyperpigmentation due to increased MSH release. 

Neoplasia & Hyperplasia

• Bilateral cortical (secondary) due to persistent ACTH levels via the pituitary in the zona reticularis and fasiculata.
• Primary cortical hyperplasia in old dogs. Endocrine activity or silent. Atrophy of zona fasiculata in non hyerplastic areas due to negative feedback.
• Nodular hyperplasia of the zona glomerulosa- hyperaldosterone- metabolic acidosis and oedema.
• Cortical adenoma/adenocarcinoma. 
• Medulla phaeochromocytomas- cattle, dogs and horses. Endocrine activity (catecholamines). Malignant= infiltrative and metastasis. Consequences- arterial hypotonia, left cardiac hypertrophy and myocardial necrosis.