Ross & Wilson Anatomy and Physiology in Health and Illness (105 page)

This is caused by overstimulation of normal glands by the excessively high blood levels of renin and angiotensin that result from low renal perfusion or low blood sodium.

Hyposecretion of mineralocorticoids

Hypoaldosteronism results in failure of the kidneys to regulate sodium, potassium and water excretion, leading to:

•
blood sodium deficiency (hyponatraemia) and potassium excess (hyperkalaemia)

•
dehydration, low blood volume and low blood pressure.

There is usually hyposecretion of other adrenal cortical hormones, as in Addison’s disease.

Chronic adrenocortical insufficiency (Addison’s disease)

This is due to hyposecretion of glucocorticoid and mineralocorticoid hormones. The most common causes are development of autoantibodies to cortical cells, metastatic tumours and infections. Autoimmune disease of some other glands is associated with Addison’s disease, e.g. thyrotoxicosis and hypoparathyroidism. The most important effects are:

•
muscle weakness and wasting

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gastrointestinal disturbances, e.g. vomiting, diarrhoea, anorexia

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increased pigmentation of the skin, especially of exposed areas, due to excess ACTH and the related melanin-stimulating hormone secreted by the anterior pituitary

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listlessness and tiredness

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hypoglycaemia

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mental confusion

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menstrual disturbances and loss of body hair in women

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electrolyte imbalance, including hyponatraemia, low blood chloride levels and hyperkalaemia

•
chronic dehydration, low blood volume and hypotension.

The adrenal glands have a considerable tissue reserve and Addison’s disease is not usually severely debilitating unless more than 90% of cortical tissue is destroyed, but this condition is fatal without treatment.

Acute adrenocortical insufficiency (Addisonian crisis)

This is characterised by sudden severe nausea, vomiting, diarrhoea, hypotension, electrolyte imbalance (hyponatraemia and hyperkalaemia) and, in severe cases, circulatory collapse. It is precipitated when an individual with chronic adrenocortical insufficiency is subjected to stress, e.g. an acute infection.

Disorders of the adrenal medulla

Learning outcome

After studying this section you should be able to:

explain how the features of the diseases in this section are related to excessive secretion of adrenaline (epinephrine) and noradrenaline (norepinephrine).

Tumours

Hormone-secreting tumours are the main abnormality. The effects of excess adrenaline (epinephrine) and noradrenaline (norepinephrine) include:

•
hypertension, often associated with arteriosclerosis and cerebral haemorrhage

•
weight loss

•
nervousness

•
headache

•
excessive sweating and alternate flushing and blanching of the skin

•
hyperglycaemia and glycosuria.

Phaeochromocytoma

This is usually a
benign tumour
, occurring in one or both glands. The secretion of hormones may be constantly elevated or in intermittent bursts, often precipitated by raised intra-abdominal pressure, e.g. coughing or defaecation.

Neuroblastoma

This is a rare and
malignant tumour
, occurring in infants and children under 15 years of age. Tumours that develop early tend to be highly malignant but in this condition there may be spontaneous regression.

Disorders of the pancreatic islets

Learning outcomes

After studying this section you should be able to:

compare and contrast the onset and features of types I and II diabetes mellitus

relate the signs and symptoms of diabetes mellitus to deficiency of insulin

explain how the causes and effects of the following conditions occur: diabetic ketoacidosis and hypoglycaemic coma

describe the long-term complications of diabetes mellitus.

Diabetes mellitus (DM)

This is the most common endocrine disorder and usually occurs when there is deficiency or absence of insulin or, rarely, impairment of insulin activity (insulin resistance). Varying degrees of disruption of carbohydrate and fat metabolism occur. The incidence of type I and, especially, type II diabetes is increasing worldwide.

Type I diabetes mellitus

Previously known as insulin-dependent diabetes mellitus (IDDM), this occurs mainly in children and young adults; the onset is usually sudden and can be life threatening. There is severe deficiency or absence of insulin secretion due to destruction of β-islet cells of the pancreas. Treatment with injections of insulin is required. The exact cause remains unknown, although, in most people, there is evidence of an autoimmune mechanism involving autoantibodies that destroy the β-islet cells. Genetic predisposition and environmental factors, including viral infections, are also implicated.