6 Caring for the patient with a disorder of the endocrine system

ANATOMY AT A GLANCE

The endocrine system does not constitute a single organ. It consists of a series of glands scattered throughout the body whose function is to secrete hormones which are usually delivered by circulating blood to their target organs. Sometimes hormones act on neighbouring cells without needing to be carried in the blood stream, (paracrines) or even within the cell that secreted them (autocrines). Endocrine glands can either make up a whole organ as in the thyroid, or can be part of a larger organ such as the islets of Langerhans within the pancreas. Hormones regulate the functioning of their target organs and are therefore essential for the maintenance of a stable internal environment. Figure 6.1 shows some of the main endocrine glands in the body.

Figure 6.1 Endocrine glands in the body.

The endocrine system is closely linked to the nervous system and some chemical molecules can either act as a hormone or a neurotransmitter such as epinephrine (adrenaline). This neuro-endocrine linkage is closest in the hypothalamus gland, a small part of the brain inferior to the thalamus, which acts as the overall controller of the endocrine system. Adjacent to the hypothalamus is the pituitary gland, which is divided into an anterior and posterior lobe. Hormones released by hypothalamus generally control the hormone secretions of the anterior lobe of pituitary gland which in turn regulate many aspects of body function.

The posterior lobe of the pituitary stores the hormones oxytocin (responsible for uterine contractions and expressing breast milk) and antidiuretic hormone (ADH or vasopressin), which acts on the renal tubules to reduce urine output and so conserve fluids, as well as having a vasoconstrictor effect.

PHYSIOLOGY YOU NEED TO KNOW (P551)

A typical example of how the hypothalamus and pituitary work together is provided by the way the hypothalamus secretes thyrotrophin-releasing hormone. This stimulates the anterior pituitary to produce thyroid-stimulating hormone (TSH), which in turn stimulates the thyroid gland to secerete the thyroid hormones T3 and T4. These hormones play a large part in controlling basal metabolic rate, and are also important in growth and development. There are six other ‘releasing’ hormones produced by the hypothalalmus, which stimulate the anterior pituitary to release further hormones which act elsewhere in the body. For example, the corticotropin-releasing hormone stimulates the anterior pituitary to produce the adrenocorticotropic hormone (ACTH) which in turn stimulates the adrenal glands to produce glucocorticoids such as cortisol.

Other endocrine glands function without direct control from the hypothalamus/pituitary glands, responding to changes in the internal body environment. For example, the alpha and beta cells in the islets of Langerhans (within the pancreas) secrete the hormones glucagon and insulin, respectively, to regulate blood glucose levels:

Glucagon production increases in response to a falling blood glucose level and its main effect is on liver cells leading to a breakdown of glycogen and an increase in blood glucose levels.

Insulin production increases as blood glucose levels rise. Its main effect is on muscle and adipose (fat) tissue where it promotes the removal of glucose from the blood and into the cells for storage as glycogen (muscle cells) and triglycerides (adipose tissue). In the liver, insulin promotes the utilization of glucose for energy production and storage as glycogen.

Other examples include endocrine tissue in the kidneys, which can secrete erythropoietin in response to hypoxia, resulting in increased production of red blood cells. The adrenal cortex secretes aldosterone to regulate sodium and potassium concentrations in plasma, whilst calcium levels are regulated by the release of parathormone (from the parathyroid glands) and calcitonin (from specialized cells within the thyroid).

DIABETES MELLITUS (P557)

PATHOLOGY: Key facts

Diabetes is a group of disorders of carbohydrate, fat and protein metabolism. The consequences of this disorder are profound, typically involving chronic elevated blood sugar levels (hyperglycaemia), degenerative vascular changes and damage to the nervous system (neuropathy). The damage that occurs both to the large blood vessels and the microcirculation has many serious debilitating effects. Few systems of the body escape the long-term effects of diabetes.

There are approximately 2.5 million people in the UK with diabetes and it is estimated that some 50% of people with type 2 diabetes (see below) are undiagnosed.

For this reason, diabetes is now being recognized as a major epidemic posing a serious threat to public health.

Two types of diabetes mellitus are recognized:

Type 1 is caused by the destruction of the beta cells in the islets of Langerhans. It is thought that this is an autoimmune response associated with genetic and environmental factors. It typically develops early in life and although the onset of symptoms can be very rapid, the destructive process may have been active for several years prior to clinical signs emerging.

Type 2 develops as the islets gradually reduce their output of insulin or there is increased resistance in the peripheral tissues to the action of insulin. Onset is slow and this condition is associated with obesity and lack of exercise. Although the typical age of onset is 50–70 years, the growing problem of obesity in western society is now resulting in the development of Type 2 diabetes amongst children and young adults who are seriously overweight. There is also a strong genetic influence with Type 2 diabetes being far more common in some families and in certain ethnic groups. For example, in the UK, Pakistanis and Bangladeshis are five times more likely than the general population to develop Type 2 diabetes, whilst Indians are three times more likely.

Effects on the Patient

Long-term effects are many and varied. The following list notes only the more common:

• Microvascular degenerative changes affecting the skin, kidneys and retinas.

• Retinopathy or minute aneurysms in the retinal blood vessels which are prone to rupture. This ultimately leads to blindness.

• Cataract formation.

• Renal failure caused by changes in the glomerular capillaries and larger blood vessels.

• Macrovascular degenerative changes associated with the deposition of cholesterol in the arteries, narrowing their lumen and reducing blood supply to the distal organ. This can lead to angina or myocardial infarction if the coronary arteries are involved or if the vessels supplying blood to the legs are affected, this leads to peripheral vascular disease, gangrene and potentially amputation of the limb.

• Diabetic neuropathy affecting the peripheral nervous system and typically leading to abnormal burning feelings or loss of sensation in the lower limbs.

Acute metabolic emergencies:

• Diabetic ketoacidosis. This life-threatening complication develops insidiously over a few days and is associated with inadequate insulin levels and rising blood glucose concentrations. Ketones accumulate in the blood making the patient acidotic, dehydration develops because of the kidney’s increased urine output caused by the elevated glucose levels; the patient also loses sodium and potassium. The severity of this condition is not related to the blood glucose levels, and the patient may be awake and conscious although feeling unwell. The classic ‘diabetic coma’ is a rare event. The pulse tends to be rapid with a low blood pressure. In severe cases, where the patient’s level of consciousness is seriously affected, breathing is often of a deep sighing nature as the person attempts to correct for the acidosis by excreting as much carbon dioxide as possible.

• Hyperglycaemic hyperosmolar non-ketotic diabetic coma. This situation develops if blood glucose levels climb but the person’s metabolism does not produce excess ketone bodies. The person is therefore not severely acidotic. It often happens in older people with Type 2 diabetes and blood glucose levels can be extremely high with profound dehydration and hypovolaemia (shock) eventually leading to confusion and coma as fluid shifts from the intracellular into the extracellular spaces. This condition has a high mortality rate.

• Hypoglycaemia. In this situation, the patient’s blood glucose levels fall dangerously low usually owing to inappropriate self medication and nutrition or excess exercise. Early signs are of confusion, drowsiness, unsteadiness. The person may appear drunk – an easy mistake to make for a lay person who does not know the patient.

WHAT TO LOOK OUT FOR

Type 1 and Type 2 diabetes tend to have different presentations and these are summarized in Table 6.1.

Table 6.1 Classification of diabetes mellitus

	Type 1	Type 2
Synonyms	Juvenile onset	Maturity onset
Age of onset	Usually before 30 years	Usually after 40 years
Type of onset	Frequently sudden	Usually gradual
Presentation	Polydipsia, polyuria	Often asymptomatic
Bodyweight	Thin	Usually (80%) obese
Ketoacidosis	Ketosis-prone	Ketosis-resistant
Control of diabetes	Difficulty; brittle	Generally easy
Control by diet alone	Not possible	Frequently possible
Control by oral agents	Not possible	Frequently possible
Long-term complications	Frequent	Frequent