• thirst: due to the resulting loss of fluid

• weight loss: due to fluid depletion and breakdown of fat

and muscle secondary to insulin deficiency.

Other common symptoms are tiredness, mood changes and

blurred vision (due to glucose-induced changes in lens refraction).

Bacterial and fungal skin infections are common because of the

combination of hyperglycaemia, impaired immune resistance

and tissue ischaemia. Itching of the genitalia (pruritus vulvae in

women, balanitis in men) is due to Candida yeast infection (thrush).

Past medical, drug, family and

social history

Ask about:

• Previous glucose intolerance or gestational diabetes, which

are risk factors for progression to type 2 diabetes.

• Other autoimmune conditions such as thyroid disease

(increased incidence of type 1 diabetes).

• Drug therapy: glucocorticoids can cause steroid-induced

diabetes.

• Family history of diabetes or autoimmune disease.

Monogenic diabetes is usually inherited in an autosomal

dominant manner. Patients are often slim (unlike those with

type 2 diabetes) but do not require insulin at diagnosis (unlike

those with type 1 diabetes). Monogenic diabetes should be

considered in people presenting with diabetes under the age

of 30 who have an affected parent or a family history of

early-onset diabetes in around 50% of first-degree relatives.

• Smoking habit: combines with diabetes to increase the

risk of vascular complications.

• Alcohol: raises the possibility of pancreatic diabetes.

DIABETES

Fig. 10.13 Klinefelter’s syndrome. Tall stature, gynaecomastia, reduced

pubic hair and small testes.

Fig. 10.14 Facial hirsutism.

Anatomy and physiology

The pancreas lies behind the stomach on the posterior abdominal

wall. Its endocrine functions include production of insulin (from beta

cells), glucagon, gastrin and somatostatin. Its exocrine function

is to produce alkaline secretions containing digestive enzymes.

Diabetes mellitus is characterised by hyperglycaemia caused

by absolute or relative insulin deficiency.

Diabetes may be primary or secondary. Primary diabetes is

divided into:

• type 1: severe insulin deficiency due to autoimmune

destruction of the pancreatic islets. These patients are

susceptible to acute decompensation due to hypoglycaemia

or ketoacidosis, both of which require prompt treatment.

• type 2: commonly affects people who are obese and

insulin-resistant, although impaired beta-cell function is

also important. These patients may decompensate by

developing a hyperosmolar hyperglycaemic state.

Secondary causes of diabetes and the associated history and

examination features are described in Box 10.5.

The history

Common presenting symptoms

Diabetes mellitus commonly presents with a classical triad of

symptoms:

• polyuria (and nocturia): due to osmotic diuresis caused by

glycosuria

206 • The endocrine system

Assessment of a patient with newly

diagnosed diabetes

Examination sequence

• Look for evidence of weight loss and dehydration.

Unintentional weight loss is suggestive of insulin deficiency.

• Check for clinical features of acromegaly or Cushing’s

syndrome.

• Look for Kussmaul respiration (hyperventilation with a

deep, sighing respiratory pattern) or the sweet smell of

ketones, both of which suggest insulin deficiency and

diabetic ketoacidosis.

• Skin: look for signs of infection such as cellulitis, boils,

abscesses and fungal infections, paying particular attention

to the feet (see later). Look for signs of insulin resistance

such as acanthosis nigricans (Fig. 10.15A). Necrobiosis

lipoidica, a yellow, indurated or ulcerated area surrounded

by a red margin indicating collagen degeneration (Fig.

10.15B), may occur on the shins in type 1 diabetes and

often causes chronic ulceration.

• Look for xanthelasmata and xanthomata (Fig. 10.15C; see

Fig. 4.6); these are suggestive of dyslipidaemia, which may

occur in type 2 diabetes.

• Measure the pulse and blood pressure, and examine the

cardiovascular and peripheral vascular systems, with a

particular emphasis on arterial pulses in the feet (p. 69).

• Examine the central nervous system, with a particular

focus on sensation in the lower limbs (p. 143).

• Test visual acuity and perform fundoscopy (p. 164; see

Fig. 8.16).

• Perform urinalysis for glycosuria.

Microvascular, neuropathic and macrovascular complications

of hyperglycaemia can occur in patients with any type of diabetes

mellitus, and may be present at diagnosis in patients with

slow-onset type 2 disease.

Glycosuria is in keeping with diabetes; the presence of urinary

(or blood) ketones suggests insulin deficiency and the possibility

of diabetic ketoacidosis. Other investigations to consider are

summarised in Box 10.7.

In established diabetes, vital aspects of the history (Box

10.6) and examination should be reviewed at least once

a year.

The physical examination

The physical examination will differ, depending on whether this

is a new presentation of diabetes or a patient with established

diabetes attending for their annual review.

10.6 Routine history taking as part of the annual

review in diabetes

Glycaemic control

• Ask about frequency of blood glucose testing and frequency and

awareness of symptoms of hypoglycaemia

• When relevant, give guidance on driving and/or pre-pregnancy

preparation

Injection sites

• Enquire about any lumpiness (lipohypertrophy), bruising or

discomfort

Symptoms of macrovascular disease

• Ask whether there has been any angina, myocardial infarction,

claudication, stroke or transient ischaemic attack since the last

clinic review

Symptoms of microvascular disease

• Ask whether there has been any change in vision or any numbness

or altered sensation in the feet

Feet

• Ask about neuropathy and peripheral vascular symptoms as above

• Enquire about any breaks in the skin, infections or ulcers

Autonomic neuropathy