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A smooth red tongue with diffuse papillary atrophy occurs in

iron or vitamin B12 deficiency. Tongue protrusion may be limited

by neurological disease, painful mouth or a tight frenulum.

Macroglossia (enlarged tongue) occurs in Down’s syndrome,

acromegaly (see Fig. 10.9), hypothyroidism and amyloidosis.

Wasting and fasciculation of the tongue are features of motor

neurone disease.

White plaques of candidiasis on the tongue or mucosa (Fig.

9.27A) come away easily when scraped but leukoplakia (a

keratotic precancerous condition) does not and requires excision

Fig. 9.26 Angular stomatitis.

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Fig. 9.27 Disorders of the tongue and teeth. A Oral thrush. B Leukoplakia. C Aphthous stomatitis causing a deep ulcer in a patient with

inflammatory bowel disease. D Dental caries. (B) From Bull TR. Color Atlas of ENT Diagnosis. 3rd edn. London: Mosby–Wolfe; 1995.

190 • The ear, nose and throat

swelling (p. 194), while movement on tongue protrusion

suggests a thyroglossal cyst (Fig. 9.28).

• Palpate the posterior triangle of the neck, including the

posterior border of sternocleidomastoid and anterior

border of trapezius. Palpate for occipital lymph nodes

posteriorly.

• For any mass, note the size, site, consistency, edge,

fixation to deeper structures, tethering to the skin, warmth,

fluctuance, pulsatility and transillumination (p. 32).

Investigations

Initial investigations are summarised in Box 9.11.

9.11 Mouth, throat and neck investigations

Investigation Indication/comment

Full blood count Infective causes of mouth, throat or

neck symptoms

Monospot Infectious mononucleosis

Hepatosplenomegaly can occur in

infectious mononucleosis so liver

function tests can be useful

Throat swab Acute tonsillitis and pharyngitis

Patients may carry Streptococcus

pyogenes and have a viral infection

(detected by PCR), so swab does not

always help direct management

PCR may help identify viral causes

Endoscopy and biopsy Cancer of larynx and pharynx, changes

in vocal cords

Under general anaesthetic

Ultrasound ± fine-needle

aspiration

Neck lumps, swellings

Computed tomography Cancer and metastases

Useful in staging

PCR, polymerase chain reaction.

OSCE example 1: Hoarseness

Mr Smith, 65 years old, presents with hoarseness.

Please take a history from the patient

• Introduce yourself and clean your hands.

• Invite the patient to describe the presenting symptoms, using open questioning.

• Take a detailed history of the presenting symptoms, asking specifically about onset, progression, fluctuation or constancy, provoking factors (work,

singing, shouting) and weak or croaky voice. Enquire about associated cough, shortness of breath, throat pain, ear pain, dysphagia or weight loss.

• Ask about relevant past history, including previous neck surgery, neck trauma, prolonged intubation, reflux disease and significant systemic

conditions, including neurological problems.

• Enquire about drug history: specifically, recent courses of antibiotics (laryngeal candidiasis), anticholinergics (causing dry throat) or angiotensinconverting enzyme inhibitors (causing chronic dry cough).

• Ask about social history, including profession (singer, teacher), smoking and alcohol consumption.

• Address any patient concerns.

• Thank the patient and clean your hands.

Summarise your findings

The patient is a heavy smoker and reports slowly progressive hoarseness associated with breathlessness and a dry cough.

Suggest a diagnosis

This history suggests recurrent laryngeal nerve damage from a bronchial carcinoma. The differential diagnosis would include laryngeal carcinoma.

Suggest initial investigations

Full ear, nose and throat examination, including oral cavity, throat and neck, with a chest X-ray to exclude a bronchial carcinoma at the left hilum

causing recurrent laryngeal nerve palsy. Persistent hoarseness (>3 weeks) requires referral for laryngoscopy to exclude laryngeal malignancy.

Fig. 9.28 Thyroglossal cyst.

Investigations • 191

9

OSCE example 2: Neck lump

Mrs Lewis, 55 years old, presents with a lump just under her left ear at the angle of her jaw.

Please examine her neck lump

• Introduce yourself and clean your hands.

• Inspect the neck for scars or swelling. If a neck lump is visible, describe its size, shape and site, as well as any skin changes. If it is in the midline,

ask the patient to swallow and stick out their tongue.

• Ask if the lump is painful and if the patient minds you examining it.

• Palpate the lump to assess consistency, edge, fixation to deeper structures, tethering to the skin, warmth, fluctuance, pulsatility and

transillumination.

• Palpate the anterior and posterior triangles of the neck, and the parotid region.

• Examine the oral cavity, throat, nose and ears (as potential primary sites of infection or malignancy that might be causing the neck mass).

• Assess facial nerve function if you suspect a parotid mass.

• Thank the patient and clean your hands.

Summarise your findings

Examination confirms a firm, non-tender, mobile lump about 1 cm in diameter behind the angle of the jaw on the left.

Suggest a diagnosis

The most likely diagnosis is a pleomorphic salivary adenoma in the tail of the parotid.

Suggest investigations

Ultrasound scan with or without fine-needle aspiration.

Integrated examination sequence for ear, nose and throat disease

• Position the patient: on an examination couch with the upper body at 45 degrees and neck fully exposed.

• Examine the ears:

• Inspect: pinna skin, shape, size, position, deformity, scars.

• Palpate: pinna, tragus, mastoid.

• Otoscopy: external auditory canal (swelling, discharge), tympanic membrane (red, perforated).

• If there is hearing loss: whispered voice test and tuning fork tests.

• If there are balance symptoms: vestibular examination, including Dix–Hallpike.

• Examine the nose:

• Inspect:

– External nose (swelling, bruising, skin changes, deformity).

– Anterior nasal septum (swelling, visible vessels, crusting ulceration, septal perforation). Exclude septal haematoma in nasal trauma.

– Inferior turbinates (hypertrophy, swelling, polyps).

• Palpate:

– Nasal bones (bony or cartilaginous deformity).

– Airway patency using metal spatula.

• Examine the mouth and throat:

• Listen to the voice (rough, breathy, wet, muffled, nasal escape).

• Remove any dentures.

• Inspect:

– Oral cavity, oropharynx.

– Mucosal discoloration, inflammation, ulceration, masses, opening of parotid and submandibular ducts.

– Hard palate for cleft, abnormal arched palate, telangiectasia.

– Soft palate for cleft, bifid uvula, swelling or lesions.

– Tonsils, noting size, symmetry, colour, pus or membrane.

• Palpate:

– Any lesion, identifying characteristics.

– Base of tongue or tonsils if asymmetrical.

– Parotid and submandibular ducts, feeling for stones.

• Examine the neck:

• Inspect:

– Scars, skin changes.

– If there is midline swelling, ask the patient to swallow and stick out their tongue.

• Palpate:

– Anterior and posterior triangles of the neck and parotid region.

– If there is a neck lump, note size, site, shape, consistency, edges, attachments, tenderness, warmth, pulsatility, transillumination.

– If there is a parotid lump, assess the facial nerve.

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10

The endocrine system

Anna R Dover

Nicola Zammitt

The thyroid 194

Anatomy and physiology 194

The history 194

Common presenting symptoms 194

Past medical, drug, family and social history 196

The physical examination 197

General examination 197

Thyroid gland 197

Eyes 198

The parathyroids 198

Anatomy and physiology 198

The history 198

Common presenting symptoms 198

Past medical, drug, family and social history 199

The physical examination 199

The pituitary 200

Anatomy and physiology 200

The history 200

Common presenting symptoms 200

Family history 200

The physical examination 200

The adrenals 201

Anatomy and physiology 201

The history 201

Common presenting symptoms 201

Past medical and drug history 202

The physical examination 202

The gonads 204

Anatomy and physiology 204

The history 204

Common presenting symptoms 204

Diabetes 205

Anatomy and physiology 205

The history 205

Common presenting symptoms 205

Past medical, drug, family and social history 205

The physical examination 206

OSCE example 1: Neck swelling 209

OSCE Example 2: Diabetic feet 209

194 • The endocrine system

10.1 Common clinical features in endocrine disease

Symptom, sign or problem Differential diagnoses

Tiredness Hypothyroidism, hyperthyroidism, diabetes mellitus, hypopituitarism

Weight gain Hypothyroidism, PCOS, Cushing’s syndrome

Weight loss Hyperthyroidism, diabetes mellitus, adrenal insufficiency

Diarrhoea Hyperthyroidism, gastrin-producing tumour, carcinoid

Diffuse neck swelling Simple goitre, Graves’ disease, Hashimoto’s thyroiditis

Polyuria (excessive thirst) Diabetes mellitus, diabetes insipidus, hyperparathyroidism, Conn’s syndrome

Hirsutism Idiopathic, PCOS, congenital adrenal hyperplasia, Cushing’s syndrome

‘Funny turns’ or spells Hypoglycaemia, phaeochromocytoma, neuroendocrine tumour

Sweating Hyperthyroidism, hypogonadism, acromegaly, phaeochromocytoma

Flushing Hypogonadism (especially menopause), carcinoid syndrome

Resistant hypertension Conn’s syndrome, Cushing’s syndrome, phaeochromocytoma, acromegaly

Amenorrhoea/oligomenorrhoea PCOS, hyperprolactinaemia, thyroid dysfunction

Erectile dysfunction Primary or secondary hypogonadism, diabetes mellitus, non-endocrine systemic disease, medication-induced

(e.g. beta-blockers, opiates)

Muscle weakness Cushing’s syndrome, hyperthyroidism, hyperparathyroidism, osteomalacia

Bone fragility and fractures Hypogonadism, hyperthyroidism, Cushing’s syndrome, primary hyperparathyroidism

PCOS, polycystic ovary syndrome.

Endocrine glands synthesise hormones that are released into

the circulation and act at distant sites. Diseases may result

from excessive or inadequate hormone production, or target

organ hypersensitivity or resistance to the hormone. The main

endocrine glands are the pituitary, thyroid, adrenals, gonads

(testes and ovaries), parathyroids and the endocrine pancreas.

With the notable exception of the pancreatic islet cells (which

release insulin) and the parathyroids, most endocrine glands

are themselves controlled by hormones released from the

pituitary.

Since hormones circulate throughout the body, symptoms and

signs of endocrine disease are frequently non-specific, affecting

many body systems (Box 10.1). Often, endocrine disease is

picked up incidentally during biochemical testing or radiological

imaging. Careful history taking and examination are required to

recognise characteristic patterns of disease. Thyroid disease and

diabetes mellitus are common and frequently familial; establishing

a detailed family history is therefore important. Some less common

endocrine disorders (such as multiple endocrine neoplasia) show

an autosomal dominant pattern of inheritance.

THE THYROID

Anatomy and physiology

The thyroid is a butterfly-shaped gland that lies inferior to the

cricoid cartilage, approximately 4 cm below the superior notch

of the thyroid cartilage (Fig. 10.1A). The normal thyroid has a

volume of <20 mL and is palpable in about 50% of women and

25% of men. It is comprised of a central isthmus approximately

1.5 cm wide, covering the second to fourth tracheal rings, and

two lateral lobes that are usually no larger than the distal phalanx

of the patient’s thumb. The gland may extend into the superior

mediastinum and can be partly or entirely retrosternal. Rarely, it

can be located higher in the neck along the line of the thyroglossal

duct, an embryological remnant of the descent of the thyroid

from the base of the tongue to its final position. Thyroglossal

cysts can also arise from the thyroglossal duct; they often occur

at the level of the hyoid bone (Fig. 10.1A) and characteristically

move upwards on tongue protrusion. The thyroid is attached to

the pretracheal fascia and thus moves superiorly on swallowing

or neck extension.

Thyrotoxicosis is a clinical state of increased metabolism caused

by elevated circulating levels of thyroid hormones. Graves’ disease

is the most common cause (Fig. 10.2 and Box 10.2). It is an

autoimmune disease with a familial component and is 5–10

times more common in women, usually presenting between 30

and 50 years of age. Other causes include toxic multinodular

goitre, solitary toxic nodule, thyroiditis and excessive thyroid

hormone ingestion.

Hypothyroidism is caused by reduced levels of thyroid

hormones, usually due to autoimmune Hashimoto’s thyroiditis,

and affects women approximately six times more commonly

than men. Most other causes are iatrogenic and include previous

radioiodine therapy or surgery for Graves’ disease.

The history

Common presenting symptoms

Neck swelling

Goitre is enlargement of the thyroid gland (Fig. 10.3). It is not

necessarily associated with thyroid dysfunction and most patients

The history • 195

10

occult nodules; thus many are found incidentally on neck or

chest imaging.

Neck pain

Neck pain is uncommon in thyroid disease and, if sudden in

onset and associated with thyroid enlargement, may represent

with goitre are euthyroid. Large or retrosternal goitres may cause

compressive symptoms, including stridor, breathlessness or

dysphagia.

Thyroid nodules may be solitary (Fig. 10.3C) or may present as

a dominant nodule within a multinodular gland. Palpable nodules

(usually >2 cm in diameter) occur in up to 5% of women and

less commonly in men, although up to 50% of patients have

A B

Hyoid bone

Sternocleidomastoid

muscle

Thyroid cartilage

Cricothyroid membrane

Cricoid cartilage

Parathyroid

Lobe of thyroid gland

Isthmus of thyroid gland

Trachea

Manubrium of the sternum

Fig. 10.1 The thyroid gland. A Anatomy of the gland and surrounding structures. B Palpating the thyroid gland from behind.

A

B

C

D

Fig. 10.2 Graves’ hyperthyroidism. A Typical facies. B Severe inflammatory thyroid eye disease. C Thyroid acropachy. D Pretibial myxoedema.

196 • The endocrine system

Past medical, drug, family and social history

Ask about:

prior neck irradiation (risk factor for thyroid malignancy)

recent pregnancy (postpartum thyroiditis usually occurs in

the first 12 months)

drug therapy: antithyroid drugs or radioiodine therapy;

amiodarone and lithium can cause thyroid dysfunction

family history of thyroid or other autoimmune disease

residence in an area of iodine deficiency, such as the

Andes, Himalayas, Central Africa: can cause goitre and,

rarely, hypothyroidism

smoking (increases the risk of Graves’ ophthalmopathy).

bleeding into an existing thyroid nodule. Pain can also occur in

viral subacute (de Quervain’s) thyroiditis.

History suggesting hyperthyroidism

Ask about:

fatigue, poor sleep

tremor, heat intolerance, excessive sweating (hyperhidrosis)

pruritus (itch), onycholysis (loosening of the nails from the

nail bed), hair loss

irritability, anxiety, emotional lability

dyspnoea, palpitations, ankle swelling

weight loss, hyperphagia, faecal frequency, diarrhoea

proximal muscle weakness (difficulty rising from sitting or

bathing)

oligomenorrhoea or amenorrhoea (infrequent or ceased

menses, respectively)

eye symptoms: ‘grittiness’, excessive tearing, retro-orbital

pain, eyelid swelling or erythema, blurred vision or diplopia

(these symptoms of ophthalmopathy occur in the setting

of autoimmune thyroid disease).

History suggesting hypothyroidism

Ask about:

fatigue, mental slowing, depression

cold intolerance

weight gain, constipation

symptoms of carpal tunnel syndrome

dry skin or hair.

A

B

C D

Fig. 10.3 Thyroid enlargement. A 99mTechnetium radionuclide scan demonstrating diffuse goitre due to Graves’ disease. B Diffuse goitre due to

Graves’ disease. C Solitary toxic nodule. D 99mTechnetium radionuclide scan confirming multinodular goitre. (A and D) Courtesy of Dr Dilip Patel.

10.2 Features suggestive of Graves’ hyperthyroidism

History

• Female sex

• Prior episode of hyperthyroidism requiring treatment

• Family history of thyroid or other autoimmune disease

• Ocular symptoms (‘grittiness’, redness, pain, periorbital swelling)

Physical examination

• Vitiligo

• Thyroid acropachy

• Diffuse thyroid enlargement (can be nodular)

• Thyroid bruit

• Pretibial myxoedema

• Signs of Graves’ ophthalmopathy (proptosis, redness, oedema)

The physical examination • 197

10

Many clinical features of hypothyroidism are produced by

myxoedema (non-pitting oedema caused by tissue infiltration

by mucopolysaccharides, chondroitin and hyaluronic acid; Figs

10.4 and 10.5). Other common findings in hypothyroidism include

goitre, cool, dry or coarse skin, bradycardia, delayed ankle reflexes

and a slowing of movement.

Examination sequence

• Observe the facial appearance, noting signs of dry or

coarse hair and periorbital puffiness (Fig. 10.5).

• Inspect the hands for vitiligo, thyroid acropachy,

onycholysis and palmar erythema.

• Assess the pulse (tachycardia, atrial fibrillation,

bradycardia) and blood pressure.

• Auscultate the heart for a midsystolic flow murmur

(hyperthyroidism).

• Inspect the limbs for coarse, dry skin and pretibial

myxoedema.

• Assess proximal muscle power and deep tendon (ankle)

reflexes (p. 139).

Thyroid gland

Examination sequence

• Inspect the neck from the front, noting any asymmetry or

scars. Inspect the thyroid from the side with the patient’s

neck slightly extended. Extending the neck will cause the

thyroid (and trachea) to rise by a few centimetres and may

make the gland more apparent. Give the patient a glass of

water and ask them to take a sip and then swallow. The

thyroid rises (with the trachea) on swallowing.

• Palpate the thyroid by placing your hands gently on the

front of the neck with your index fingers just touching,

while standing behind the patient (see Fig. 10.1B). The

patient’s neck should be slightly flexed to relax the

Hyperthyroidism Hypothyroidism

Periorbital

oedema

Husky voice

Goitre

Bradycardia

Carpal tunnel

syndrome

Menorrhagia

Constipation

General

General

 increased appetite

ophthalmoplegia

(in Graves’ disease)

Graves’ disease)

Oligomenorrhoea

(in Graves’ disease)

Fig. 10.4 Features of hyper- and hypothyroidism. Fig. 10.5 Typical facies in hypothyroidism.

The physical examination

General examination

Look for signs of weight loss or gain (calculate the body mass

index), and assess the patient’s behaviour for signs of agitation,

restlessness, apathy or slowed movements. Patients may have

abnormal speech (pressure of speech suggests hyperthyroidism,

while speech is often slow and deep in hypothyroidism).

Hoarseness is suggestive of vocal cord paralysis and should

raise suspicion of thyroid malignancy.

Features of hyperthyroidism and hypothyroidism on examination

are summarised in Fig. 10.4.

Features of thyrotoxicosis include warm, moist skin, proximal

muscle weakness (due to a catabolic energy state), tremor

and brisk deep tendon reflexes. Hyperthyroidism may also be

associated with tachycardia or atrial fibrillation, and a midsystolic

cardiac flow murmur due to increased cardiac output.

Thyroid acropachy is an extrathyroidal manifestation of

autoimmune thyroid disease. It is characterised by soft-tissue

swelling and periosteal hypertrophy of the distal phalanges, and

mimics finger clubbing (see Fig. 10.2C). It is often associated with

dermopathy and ophthalmopathy. Pretibial myxoedema is a raised,

discoloured (usually pink or brown), indurated appearance over

the anterior shins; despite its name, it is specifically associated

with Graves’ disease and not hypothyroidism (see Fig. 10.2D).

198 • The endocrine system

• Assess eye movements (see Fig. 8.11). Graves’

ophthalmopathy is characteristically associated with

restriction of upgaze.

Lid retraction (a staring appearance due to widening of the

palpebral fissure) and lid lag (see earlier) are common eye signs

associated with hyperthyroidism. Both are thought to be due

to contraction of the levator muscles as a result of sympathetic

hyperactivity. Periorbital puffiness (myxoedema) is sometimes

seen in hypothyroidism.

Graves’ ophthalmopathy occurs in around 20% of patients

and is caused by an inflammatory infiltration of the soft tissues

and extraocular muscles (see Fig. 10.2A,B). Features suggestive

of active inflammation include spontaneous or gaze-evoked

eye pain, and redness or swelling of the lids or conjunctiva.

Proptosis (protrusion of the globe with respect to the orbit) may

occur in both active and inactive Graves’ ophthalmopathy and

is often referred to as exophthalmos. Inflammation of the orbital

soft tissues may lead to other more severe features, including

corneal ulceration, diplopia, ophthalmoplegia and compressive

optic neuropathy (see Fig. 8.8D).

sternocleidomastoid muscles. Ask the patient to swallow

again and feel the gland as it moves upwards.

• Note the size, shape and consistency of any goitre and

feel for any thrill.

• Palpate for cervical lymphadenopathy (see Fig. 3.27).

• Percuss the manubrium to assess for dullness due to

retrosternal extension of goitre.

• Auscultate with your stethoscope for a thyroid bruit. A

thyroid bruit (sometimes associated with a palpable thrill)

indicates abnormally high blood flow and is most

commonly associated with Graves’ disease. It may be

confused with other sounds: bruits from the carotid artery

or those transmitted from the aorta are louder along the

line of the artery.

Early simple goitres are relatively symmetrical but may become

nodular with time. In Graves’ disease the surface of the thyroid is

usually smooth and diffuse; in uninodular or multinodular goitre

it is irregular (see Fig. 10.3). Diffuse tenderness is typical of

viral thyroiditis. Localised tenderness may follow bleeding into a

thyroid cyst. Fixation of the thyroid to surrounding structures (such

that it does not move on swallowing) and associated cervical

lymphadenopathy increase the likelihood of thyroid malignancy.

Further investigation of thyroid disorders is summarised in

Box 10.3.

Eyes

Examination sequence

• Look for periorbital puffiness or oedema, and lid

retraction (this is present if the white sclera is visible

above the iris in the primary position of gaze; see

Fig. 10.2A).

• Examine for features of Graves’ ophthalmopathy, including

exophthalmos (look down from above and behind the

patient), lid swelling or erythema, and conjunctival redness

or swelling (chemosis).

• Assess for lid lag: ask the patient to follow your index

finger as you move it from the upper to the lower part of

the visual field. Lid lag means delay between the

movement of the eyeball and descent of the upper eyelid,

exposing the sclera above the iris.

10.3 Investigations in thyroid disease

Investigation Indication/comment

Biochemistry

Thyroid function tests To assess thyroid status

Immunology

Antithyroid peroxidase antibodies Non-specific, high in autoimmune

thyroid disease

Antithyroid stimulating hormone

receptor antibodies

Specific for Graves’ disease

Imaging

Ultrasound Goitre, nodule

Thyroid scintigraphy (123I, 99mTc) To assess areas of hyper-/

hypoactivity

Computed tomography To assess goitre size and aid

surgical planning

Invasive/other

Fine-needle aspiration cytology Thyroid nodule

Respiratory flow-volume loops To assess tracheal compression

from a large goitre

THE PARATHYROIDS

Anatomy and physiology

There are usually four parathyroid glands situated posterior to

the thyroid (see Fig. 10.1A). Each is about the size of a pea

and produces parathyroid hormone, a peptide that increases

circulating calcium levels.

The history

Common presenting symptoms

Parathyroid disease is commonly asymptomatic. In hyperparathyroidism the most common symptoms relate to hypercalcaemia:

polyuria, polydipsia, renal stones, peptic ulceration, tender areas

of bone fracture or deformity (‘Brown tumours’: Fig. 10.6A),

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