With peripheral neuropathy, also take an alcohol history and check vitamin B12 levels to take other common causes of peripheral sensory loss into

account. Peripheral neuropathy can be confirmed on nerve conduction studies. Offer an examination for other microvascular complications, such as

retinopathy (fundoscopy) and nephropathy (test urine for microalbuminuria).

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11

The reproductive system

Oliver Young

Colin Duncan

Kirsty Dundas

Alexander Laird

Breast 212

Anatomy and physiology 212

The history 212

Common presenting symptoms 212

The physical examination 214

Investigations 216

Female reproductive system 216

Anatomy and physiology 216

The history 217

Common presenting symptoms 217

Drug history 219

Family and social history 220

Sexual history 220

The physical examination 220

Passing a speculum 220

Taking a cervical smear 222

Bimanual examination 222

Investigations 223

Obstetric history and examination: the booking visit 225

The history 225

Past medical history 225

Drug, alcohol and smoking history 225

Family history 225

Social history 225

Investigations 226

Routine antenatal check in later pregnancy 226

The history 226

Common presenting symptoms 226

The physical examination 228

Investigations 230

Male reproductive system 230

Anatomy and physiology 230

The history 230

Common presenting symptoms 231

Past medical history 233

Drug history 233

Social history 233

The physical examination 233

Skin 233

Penis 233

Scrotum 234

Prostate 235

Investigations 235

OSCE example 1: Breast examination 236

OSCE example 2: Scrotal pain history 236

212 • The reproductive system

BREAST

Anatomy and physiology

The breasts are modified sweat glands. The openings of

the lactiferous ducts are on the apex of the nipple, which is

erectile tissue. The nipple is in the fourth intercostal space in

the mid-clavicular line, but accessory breast/nipple tissue may

develop anywhere down the nipple line (axilla to groin) (Figs 11.1

and 11.2). The adult breast is divided into the nipple, the areola

and four quadrants (upper outer to lower inner), with an axillary tail

(of Spence) projecting from the upper outer quadrant (Fig. 11.3).

The size and shape of the breasts are influenced by age,

hereditary factors, sexual maturity, phase of the menstrual cycle,

parity, pregnancy, lactation and nutritional state. Fat and stroma

surrounding the glandular tissue determine the size of the breast,

except during lactation, when enlargement is mostly glandular. The

breast responds to fluctuations in oestrogen and progesterone

levels. Swelling and tenderness are common in the premenstrual

phase. The glandular tissue reduces and fat increases with age,

making the breasts softer and more pendulous. Lactating breasts

are swollen and engorged with milk, and are best examined

after breastfeeding.

The history

Benign and malignant conditions of the breast cause similar

symptoms but benign changes are much more common. The

most common presenting symptoms are a breast lump, breast

pain, and skin and nipple changes. Men may present with

gynaecomastia (breast swelling). Women are often worried that

they have breast cancer, whatever breast symptom they have,

and it is important to explore these concerns.

The history of the presenting symptoms is crucial. Find out

the nature and duration of symptoms, any changes over time

and any relationship to the menstrual cycle.

Ask about risk factors for breast cancer, in particular:

previous personal history of breast cancer

family history of breast or ovarian cancer and the age of

those affected

use of hormone replacement therapy

previous mantle radiotherapy for Hodgkin’s lymphoma.

Common presenting symptoms

Breast lump

Not all patients have symptoms. Women may present with an

abnormality on screening mammography or concerns about

their family history.

Ask:

Is it a single lump or multiple lumps?

Where is it?

Fig. 11.1 Accessory breast tissue in the axilla.

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Fig. 11.2 Cross-section of the female breast.

Tail of Spence

Upper outer

Lower inner

Upper inner

Lower outer

Fig. 11.3 Adult right breast.



Fig. 10.10 Hypopituitarism. A Hypopituitarism caused by a pituitary adenoma (note the fine, pale skin). B Absent axillary hair.

The physical examination • 203

10

A B

C

D

Fig. 10.11 Cushing’s syndrome. A Cushingoid facies. B After curative pituitary surgery. C Typical features: facial rounding and plethora, central

obesity, proximal muscle wasting and violaceous skin striae. D Skin thinning: purpura caused by wristwatch pressure.

10.4 Adrenal causes of endocrine hypertension

Condition Hormone produced in excess Associated features

Conn’s syndrome Aldosterone Hypokalaemia

Cushing’s syndrome Cortisol Central obesity, proximal myopathy, fragility fractures, spontaneous bruising,

skin thinning, violaceous striae, hypokalaemia

Phaeochromocytoma Noradrenaline (norepinephrine),

adrenaline (epinephrine)

Paroxysmal symptoms, including hypertension, palpitations, sweating

204 • The endocrine system

insufficiency, the pituitary increases ACTH secretion in

response to low cortisol levels. High levels of ACTH increase

melanocyte-stimulating hormone, leading to increased skin

pigmentation (most striking in white Caucasians). Vitiligo

(depigmentation of areas of skin) occurs in 10–20% of

Addison’s disease cases (Fig. 10.12A).

• Measure the blood pressure and test for postural

hypotension (p. 51), resulting from salt and water loss due

to inadequate mineralocorticoid.

Addison’s disease

Examination sequence

• Look for signs of weight loss.

• Examine the skin for abnormal or excessive pigmentation.

This is most prominent in sun-exposed areas or epithelia

subject to trauma or pressure: skin creases, buccal mucosa

(Fig. 10.12B) and recent scars. In primary adrenal

B

A

Fig. 10.12 Addison’s disease. A Hyperpigmentation in a patient with coexistent vitiligo. B Buccal pigmentation.

THE GONADS

Anatomy and physiology

The gonads (testes and ovaries) secrete sex hormones

(testosterone and oestrogen) in response to gonadotrophin

(FSH and LH) release by the pituitary. The reproductive system

is covered in Chapter 11.

The history

Common presenting symptoms

Most commonly, men present with androgen deficiency, whereas

women present with hyperandrogenism.

Hypogonadism can be primary (failure of the gonad itself) or

secondary (where reduced gonadotrophin levels cause gonadal

failure). Klinefelter’s syndrome (47XXY) is the most common cause

of primary hypogonadism in men (1:600 live male births; Fig.

10.13). Secondary hypogonadism may be caused by pituitary

disease, extremes of weight, or drugs that suppress hypothalamic

gonadotrophin releasing hormone release (such as anabolic

steroids or opiates). Presenting symptoms in men include loss

of libido, erectile dysfunction, loss of secondary sexual hair,

reduction in testicular size and gynaecomastia (p. 214).

Hyperandrogenism in women usually presents with hirsutism

(excessive male-pattern hair growth; Fig. 10.14), acne and/or

oligomenorrhoea, and is commonly due to polycystic ovarian

syndrome (PCOS; usually also associated with obesity).

Other less common causes should be considered (such as

congenital adrenal hyperplasia). Virilisation is suggested by

male-pattern baldness, deepening of the voice, increased

muscle bulk and clitoromegaly; if present in women with a short

history of severe hirsutism, consider a testosterone-secreting

tumour.

The history • 205

10

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

• Enquire about erectile dysfunction in men

• Ask about postural hypotension, sweating, diarrhoea and vomiting in

all patients

10.5 Causes of secondary diabetesa

Cause of diabetes Examples Clinical features

Pancreatic disease Pancreatitis Abdominal pain

Trauma/pancreatectomy Surgical scar

Neoplasia Weight loss

Cystic fibrosis Chronic cough, purulent sputum

Haemochromatosis Skin pigmentation (‘bronze diabetes’)

Endocrinopathies Acromegaly, Cushing’s syndrome p. 202

Drugs Glucocorticoids (e.g. prednisolone)

Antipsychotics (e.g. olanzapine)

Features of Cushing’s syndrome (see Fig. 10.11)

Immunosuppressants (e.g. ciclosporin, tacrolimus) Gum hypertrophy may be seen with ciclosporin use

Pregnancy Gestational diabetes may develop in the third trimester Gravid uterus

Monogenic defects in

beta-cell function

Glucokinase deficiency Glucokinase deficiency is present from birth with

stable mild hyperglycaemia

Genetic syndromes associated

with diabetes

Down’s syndrome p. 36

Turner’s syndrome p. 36

a

Based on classification by the American Diabetes Association.

The physical examination • 207

10

The diabetic foot

Up to 40% of people with diabetes have peripheral neuropathy and

40% have peripheral vascular disease, both of which contribute

to a 15% lifetime risk of foot ulcers (Fig. 10.16).

Early recognition of the ‘at-risk’ foot is essential. There are

two main presentations:

Neuropathic: neuropathy predominates but the major

arterial supply is intact.

Neuroischaemic: reduced arterial supply produces

ischaemia and exacerbates neuropathy.

Infection may complicate both presentations.

Examination sequence

• Look for hair loss and nail dystrophy.

• Examine the skin (including the interdigital clefts) for

excessive callus, skin breaks, infections and ulcers. Look

for any discoloration. Distal pallor can suggest early

ischaemia, while purple/black discoloration suggests

gangrene.

• Ask the patient to stand so that you can assess the foot

arch; look for deformation of the joints of the feet.

• Feel the temperature of the feet.

• Examine the dorsalis pedis and posterior tibial pulses. If

absent, arrange Doppler studies and evaluate the

ankle:brachial pressure index (p. 69).

• Test for peripheral neuropathy: use a 10-g monofilament

to apply a standard, reproducible stimulus. The technique

Routine review of a patient with diabetes

Examination sequence

• Weigh the patient: weight gain in type 2 diabetes is likely

to be associated with worsening insulin resistance while

weight loss in type 1 diabetes often suggests poor

glycaemic control and inadequate insulin dosage.

• For patients on insulin, examine insulin injection sites for

evidence of lipohypertrophy (which may cause

unpredictable insulin release), lipoatrophy (rare) or signs of

infection (very rare).

• Measure the pulse and blood pressure.

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

Fig. 8.16).

• Examine the feet (see the next section).

• Perform routine biochemical screening (Box 10.7).

A

B

C

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