THE THYROID AXIS - Clinical features, Investigations

The thyroid gland secretes predominantly thyroxine (T4) and only a small amount of the biologically active hormone triiodothyronine (T3). Most circulat-ing T3 is produced by peripheral conversion of T4. lodine is an essential requirement for thyroid hormone synthesis. Over 99% of T4 and T3 circulate bound to plasma proteins, mainly thyroxine-binding globulin (TBG) but only the free hormone is available for tissue action. Thyroid hormones control the metabolic rate of many tissues. The feedback pathway that controls the secretion of TSH is discussed on page 609. Thyroid function is assessed by measurement of:

■ Serum TSH concentration

■ Serum free T4 (or T3) concentration.

Drugs and illness can alter the concentrations of binding proteins or inter-action of the binding hormones with T4 and T3. Thus free and total hormone concentrations may not be concordant. For instance, oestrogens (e.g. in pregnancy and in women taking the oral contraceptive pill) increase concen-trations of TBG and hence total T4, but the physiologically important free T4 concentrations are normal.

Assessment of thyroid function tests

Measurement of thyroid function is indicated in patients falling into the fol-lowing categories:

■ Symptoms or signs suggestive of hypo- or hyperthyroidism (Table 14.2). Thyroid function should not be assessed in patients who have co-existing acute illness such as pneumonia (unless thyroid disease is strongly suspected) since changes in binding proteins, serum thyroid hormones (low total and free T4 and T3) and TSH (normal) occur in severe non-thyroidal illness (the ‘sick euthyroid syndrome'). Most will be euthyroid on re-testing after recovery from the acute illness

■ Receiving treatment for hypo- or hyperthyroidism

■ Treatment with drugs causing thyroid disorders, e.g. amiodarone

■ Post-irradiation - radioactive iodine therapy or external neck irradiation

■ Post-surgery - subtotal thyroidectomy.

Hypothyroidism

Underactivity of the thyroid gland may be primary, from disease of the thyroid gland, or much less commonly, secondary to hypothalamic or pituitary disease (secondary hypothyroidism).

Aetiology

Hypothyroidism affects 0.1-2% of the population. It is much more common in women, and the incidence increases with age. The most common cause of primary thyroid failure in iodine-replete areas of the world is autoimmune thyroiditis.

Table 14.2 Characteristics of thyroid function tests in thyroid disease

TSH
(0.3–3.5 mU/L)

Free T4
(10–25 pmol/L)

Free T3
(3.5–7.5 pmol/L)

Thyrotoxicosis

↓(<0.05 mU/L)

Primary

hypothyroidism

↑ (>10 mU/L)

↓ or low-normal

↓ or normal

TSH deficiency

↓ or low-normal

↓ or low-normal

↓ or normal

T3 toxicosis

↓ (<0.05 mU/L)

Normal

Borderline

hypothyroidism

Slightly T (5-10 mU/L )

Normal

Normal

↑, increased; ↓, suppressed

Autoimmune thyroiditis may be associated with a goitre (Hashimoto's thyroiditis) or thyroid atrophy. There is cell- and antibody-mediated destruc-tion of thyroid tissue. Almost all patients have serum antibodies to thyroglobu-lin, thyroid peroxidase enzyme (thyroid microsomal antibodies) and antibodies that block the binding of TSH to its receptor. It is associated with other autoimmune conditions, such as pernicious anaemia and Addison's disease. A normally transient autoimmune thyroiditis can occur postpartum, causing hypo-hyperthyroidism, or both, sequentially.

latrogenic Thyroidectomy (for treatment of hyperthyroidism or goitre), radioactive iodine treatment or external neck irradiation for head and neck cancer all cause hypothyroidism.

Drug induced as a result of carbimazole, lithium, amiodarone and interferon.

lodine deticiency still exists in some areas, particularly mountainous areas (Alps, Himalayas, South America). Goitre, occasionally massive, is common. Iodine excess can also cause hypothyroidism in patients with preexisting thyroid disease.

Congenital hypothyroidism is related to thyroid aplasia or dysplasia or defective synthesis of thyroid hormones.

Clinical features

Symptoms and signs of hypothyroidism are illustrated in Figure 14.6. The term myxoedema refers to the accumulation of mucopolysaccharide in sub-cutaneous tissues. Features are often difficult to distinguish in elderly people and young women. Hypothyroidism should be excluded in all patients with oligomenorrhoea/amenorrhoea, menorrhagia, infertility and hyperprolacti-naemia. Many cases are detected on routine biochemical screening.

Investigations

Measurement of serum TSH is the investigation of choice. A high TSH with a compatible clinical picture confirms primary hypothyroidism:

■ Serum free T4 levels are low.

■ Thyroid antibodies and other organ-specific antibodies may be present in the serum.

■ Other features include anaemia (normocytic or macrocytic), hyperlipid-aemia, hyponatraemia (due to increased antidiuretic hormone and impaired clearance of free water), and increased serum creatine kinase levels with associated myopathy.

Management

Treatment is with lifelong levothyroxine at a daily dose of 1.6 μg/kg body weight (100-150 μg for an average sized adult, p. 662). The adequacy of replacement is assessed clinically and by thyroid function tests after at least

Fig. 14.6 Hypothyroidism - symptoms and signs. Bold type indicates signs of greater discriminant value. (A history from a relative is often revealing. Symptoms of other autoimmune disease may be present).

6 weeks on a steady dose. The aim of treatment is normalization of serum TSH concentrations. Annual measurement of TSH is sufficient for patients on a stable dose unless there is a change in situation, e.g. large changes in body weight or pregnancy. In older patients (>60 years) and patients with ischae-mic heart disease the starting dose is 25 μg/day and then increased incre-mentally every 3-6 weeks until euthyroidism is achieved.

Borderline or subclinical hypothyroidism (‘compensated euthyoidism)

This is a slightly increased serum TSH and normal free T4 concentration (Table 14.2). Most cases are due to early phase chronic autoimmune

thyroiditis and about 2-4% will develop overt hypothyroidism each year. The benefits of treatment, or otherwise, are controversial. Treatment with levo-thyroxine is normally recommended where the TSH is consistently (i.e. 3 months after the initial test) above 10 mU/L, when there are high-titre thyroid antibodies, lipid abnormalities or when there are symptoms suggestive of hypothyroidism. In untreated patients serum TSH concentrations are meas-ured yearly to look for progression to overt hypothyroidism.

Myxoedema coma

Severe hypothyroidism may rarely present with confusion and coma, particu-larly in elderly people. Typical features include hypothermia (p. 659), cardiac failure, hypoventilation, hypoglycaemia and hyponatraemia. The optimal treatment is controversial and data are lacking, but a summary is given in Emergency Box 14.1. Treatment is begun on the basis of clinical suspicion without waiting for the results of laboratory tests. Clues to the possible pres-ence of myxoedema coma include a previous history of thyroid disease and a history from family members suggesting antecedent symptoms of thyroid dysfunction.

Myxoedema madness

Depression is common but occasionally, with severe hypothyroidism in elderly people, the patient may become frankly demented or psychotic, sometimes with striking delusions. This may occur shortly after starting thyroxine replacement.

Emergency Box 14.1
Management of myxoedema coma
Investigations

• Serum TSH, T4 and cortisol before thyroid hormone is given
• Full blood count, serum urea and electrolytes, blood glucose and blood cultures
• ECG monitoring for cardiac arrhythmias
Treatment
• T3 orally or intravenously 2.5–5 μg every 8 hours
• Oxygen (by mechanical ventilation if necessary)
• Gradual rewarming (Emergency Box 14.4)
• Hydrocortisone 100 mg i.v. 8-hourly (in case hypothyroidism is a manifestation of hypopituitarism)
• Glucose infusion to prevent hypoglycaemia
• Supportive management of the comatose patient (p. 738)

Hyperthyroidism

Hyperthyroidism (thyroid overactivity, thyrotoxicosis) is common, affecting 2-5% of all women at some time, mainly between the ages of 20 and 40 years. Three intrinsic thyroid disorders account for the majority of cases of hyperthyroidism: Graves' disease, toxic adenoma and toxic multinodular goitre. Rarer causes include viral thyroiditis (de Quervain's), thyroiditis factitia (surreptitious T4 consumption), drugs (amiodarone), metastatic differentiated thyroid carcinoma and TSH-secreting tumours (e.g. of the pituitary).

Graves’ disease is the most common cause of hyperthyroidism and is the result of IgG antibodies binding to the TSH receptor and stimulating thyroid hormone production. It is associated with characteristic clinical fea-tures (see below) and other autoimmune diseases, such as pernicious anaemia and myasthenia gravis.

Toxic multinodular goitre Many patients with toxic multinodular goitre have been euthyroid for several years before the development of nodular autonomy. It commonly occurs in older women, and drug therapy is rarely successful in inducing a prolonged remission.

Solitary toxic nodule/adenoma is responsible for about 5% of cases of hyperthyroidism. Prolonged remission is again rarely induced by drug therapy.

de Quervain’s thyroiditis Transient hyperthyroidism sometimes results from acute inflammation of the gland, probably as a result of viral infection. It is usually accompanied by fever, malaise and pain in the neck. Treatment is with aspirin, reserving prednisolone for severely symptomatic cases. Postpartum thyroiditis (p. 620).

Clinical features

Typical symptoms and signs are shown in Figure 14.7. Clinical features vary with age and the underlying aetiology. Ophthalmopathy (see below), pretibial myxoedema (raised, purple-red symmetrical skin lesions over anterolateral aspects of the shins) and thyroid acropachy (clubbing, swollen fingers and periosteal new bone formation) occur only in Graves' disease. Elderly patients may present with atrial fibrillation and/or heart failure, or with a clinical picture resembling hypothyroidism (‘apathetic thyrotoxicosis').

Investigations

■ Serum TSH is suppressed (<0.05 mU/L).

■ Serum free T4 and T3 are elevated. Occasionally T3 alone is elevated (T3 toxicosis).

■ Serum microsomal and thyroglobulin antibodies are present in most cases of Graves' disease. TSH receptor antibodies are not measured routinely.

■ Thyroid ultrasound will help differentiate Graves' disease from a toxic adenoma.

Management

Three approaches are used to decrease thyroid hormone synthesis: drugs, radioiodine ablation and surgery. Radioiodine is the first-line treatment of choice in the USA and medical treatment in the UK.

Antithyroid drugs Carbimazole (20-40 mg daily, p. 663) is most often used in the UK and its metabolite, thiamazole (methimazole) is used in the USA. They block thyroid hormone biosynthesis and also have immunosup-pressive effects which will affect the Graves' disease process. As clinical benefit is not apparent for 10-20 days, p-blockers (usually propranolol) are used to provide rapid symptomatic control because many manifestations are mediated via the sympathetic system. After 4-6 weeks at full dose, carbimazole is gradually reduced over 6-24 months to 5 mg daily and dis-continued when the patient is euthyroid. The aim of treatment during this time is to maintain normal free T4 and TSH levels. Fifty per cent of patients with Graves' disease relapse on discontinuation of drug treatment, mostly within the following 2 years and then need further treatment (long-term anti-thyroid drugs, radioactive iodine or surgery). The most severe side-effect of carbimazole is agranulocytosis. All patients starting treatment must be warned to stop carbimazole and seek an urgent blood count if they develop a sore throat or unexplained fever. If toxicity occurs propylthiouracil is used instead.

Radioactive iodine (oral sodium 131I) is widely used for the treatment of hyperthyroidism but is contraindicated in pregnancy and while breast feeding. It accumulates in the gland and results in local irradiation and tissue damage with return to normal thyroid function over 4-12 weeks. If hyperthyroidism persists, a further dose of 131I can be given, although this increases the rate of subsequent hypothyroidism.

Surgery Subtotal thyroidectomy should only be performed in patients who have been rendered euthyroid. Antithyroid drugs are stopped 10-14 days before the operation and replaced with oral potassium iodide, which inhibits thyroid hormone release and reduces the vascularity of the gland. Complications of surgery include bleeding, hypocalcaemia, hypothyroidism, hypoparathyroidism, recurrent laryngeal nerve palsy and recurrent hyper-thyroidism.

The choice of therapy for hyperthyroidism depends on patient preference and local expertise. Surgery is particularly indicated in patients who have a large goitre, in patients who have drug side-effects or poor compliance with drug therapy but do not want radioiodine, or if there is a suspicion of malig-nancy in a nodule. Lifelong measurement of TSH to look for hypothyroidism is indicated after surgery or radioiodine treatment.

Thyroid crisis or ‘thyroid storm’

This is a rare life-threatening condition in which there is a rapid deterioration of thyrotoxicosis with hyperpyrexia, tachycardia, extreme restlessness and eventually delirium, coma and death. It is usually precipitated by infection, stress, and surgery or radioactive iodine therapy in an unprepared patient. With careful management it should no longer occur and most cases referred to as ‘crisis' are simply severe but uncomplicated thyrotoxicosis. Treatment of thyroid storm is with large doses of carbimazole (20 mg 8-hourly orally), propranolol (80 mg 12-hourly orally), potassium iodide (15 mg 6-hourly orally, to block acutely the release of thyroid hormone from the gland) and hydrocortisone (100 mg i.v. 6-hourly, to inhibit peripheral conversion of T4 to T3 ).

Ophthalmic Graves’ disease

Lid retraction (white of sclera visible above the cornea as the patient looks forwards) and lid lag (delay in moving the upper eyelid as the eye moves downwards) are a result of increased catecholamine sensitivity of the levator palpebrae superioris and occur in any form of hyperthyroidism. Exophthalmos (proptosis, protruding eyeballs) and ophthalmoplegia (limitation of eye move-ments) only occur in patients with Graves' disease (ophthalmic Graves' disease).

Aetiology

T lymphocytes react with one or more antigens (likely to be the TSH receptor) shared by the thyroid and orbit and trigger a cascade of events leading to retro-orbital inflammation. There is swelling and oedema of the extraocular muscles leading to limitation of movement and proptosis. Ultimately increased pressure on the optic nerve may cause optic atrophy. Ophthalmopathy is more common and more severe in smokers.

Clinical features

Eye involvement is usually bilateral. Symptoms are pressure or pain in the eye, a gritty sensation, decreased vision and photophobia. Exophthalmos and ophthalmoplegia are direct effects of retro-orbital inflammation, whereas conjunctival oedema (chemosis), lid lag and corneal scarring are secondary to the proptosis and lack of eye cover (Fig. 14.8). Eye manifestations do not parallel the clinical course of Graves' disease and may appear before or after the onset of hyperthyroidism.

Investigations

The diagnosis is usually made clinically by finding typical clinical features on a background of Graves' disease. MRI of the orbits will exclude other causes of

Fig. 14.8 The eye signs of Graves’ disease.

proptosis, e.g. retro-orbital tumour, and show enlarged muscles and oedema. Visual acuity and visual fields should be formally assessed in all patients.

Management

Thyroid dysfunction should be corrected and hypothyroidism avoided because this may exacerbate the eye problem. Smoking should be stopped. Specific treatment includes artificial tears and for severe symptoms, high-dose sys-temic steroids (e.g. prednisolone 30-120 mg daily) to reduce inflammation. Surgical treatment may be necessary to sew the eyelids partially together to protect the cornea, to perform corrective eye muscle surgery to improve diplopia or to decompress the orbit particularly if sight is threatened. Occasion-ally irradiation of the orbits or surgical decompression of the orbit(s) is required.

Goitre (thyroid enlargement)

Goitre is more common in women than in men and may be physiological or pathological in origin (Table 14.3). The presence of a goitre gives no indication about the thyroid status of the patient.

Clinical features

A goitre is usually noticed as a cosmetic defect, although discomfort and pain in the neck can occur, and occasionally tracheal or oesophageal compression produces difficulty in breathing or dysphagia. The gland may be diffusely enlarged, multinodular or possess a solitary nodule. A bruit may be present and associated lymphadenopathy suggests that the goitre may be malignant.

Table 14.3 Goitre – causes and types
Diffuse
Physiological:* puberty, pregnancy
Autoimmune: Graves’ disease, Hashimoto’s disease
Acute viral thyroiditis (de Quervain’s thyroiditis)*
Iodine deficiency (endemic goitre)
Dyshormonogenesis
Goitrogens, e.g. sulphonylureas
Nodular
Multinodular goitre
Solitary nodule
Fibrotic (Riedel’s thyroiditis)
Cysts
Tumours
Adenoma
Carcinoma
Lymphoma
Miscellaneous
Sarcoidosis
Tuberculosis
*Goitre usually resolves spontaneously

Investigations

The purpose of investigations, together with the history and physical exami-nation, is to determine the patient's thyroid status and the pathological nature of the goitre:

■ Blood tests: thyroid function tests (Table 14.2) and thyroid antibodies

■ Imaging: high-resolution thyroid ultrasound can delineate nodules and determine whether they are cystic or solid. Both types of nodule are usually benign, but can be malignant, and thus require fine needle aspira-tion (see below) under ultrasound control. Chest and thoracic inlet X-rays to detect tracheal compression and large retrosternal extensions, are performed in patients with very large goitre or clinical symptoms (diffi-culty in breathing)

■ Fine-needle aspiration for cytology should be performed for solitary nodules or a dominant nodule in a multinodular goitre because there is a 5% chance of malignancy

■ Thyroid scan (125I or 131I) distinguishes between a functioning (rarely malignant) or non-functioning (10% malignant) nodule. However, FNA has largely replaced isotope scans.

Table 14.4 Characteristics of thyroid cancer

Cell type

Behaviour

Spread

Prognosis

Papillary (70%)

Young people

Local

Good

Follicular (20%)

Middle age

Lung/bone

Usually good

Anaplastic (<5%)

Aggressive

Local

Very poor

Lymphoma (2%)

Variable

Usually poor

Medullary cell (5%) Often tamilial Local and metastases Poor

Frequency of tumour type is given as a percentage in brackets. Medullary cell carcinoma (see multiple endocrine neoplasia, p. 658)

Management

Treatment is usually not required, apart from inducing euthyroidism if neces-sary. Surgical intervention is required for the cosmetic effects of large goitres, pressure effects on the trachea or oesophagus, or confirmed (positive FNA) or possible malignancy (negative FNA but rapid growth, cervical lymphadenopathy).

Thyroid malignancy

Thyroid cancer is uncommon and most present as asymptomatic thyroid nodules. The first sign of disease is occasionally lymph-node metastases or, in rare cases, lung or bone metastases. Features that suggest carcinoma in a patient presenting with a thyroid nodule are a history of progressive increase in size, a hard and irregular nodule, and the presence of enlarged lymph nodes on examination. Characteristics are listed in Table 14.4. Fine-needle aspiration cytology is the best test for distinguishing between benign and malignant thyroid nodules. Treatment of follicular and papillary cancers is total thyroidectomy with neck dissection for local nodal spread. Ablative radioactive iodine is subsequently given which will be taken up by remaining thyroid tissue or metastatic lesions. External radiotherapy may produce brief respite for anaplastic carcinoma and lymphoma but otherwise treatment is largely palliative.

Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

2. Infectious diseases

Infectious diseases

3. Gastroenterology and nutrition

Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
JAUNDICE
HEPATITIS
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
CIRRHOSIS
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
LIVER TRANSPLANTATION
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER ABSCESS
LIVER DISEASE IN PREGNANCY
LIVER TUMOURS
GALLSTONES
THE PANCREAS
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS

5. Haematological disease

Haematological disease
ANAEMIA
Assessment and treatment of suspected neutropenic sepsis
HAEMOLYTIC ANAEMIA
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
MYELOPROLIFERATIVE DISORDERS
THE SPLEEN
BLOOD TRANSFUSION
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
THROMBOSIS
THERAPEUTICS

6. Malignant disease

Malignant disease
MYELOABLATIVE THERAPY AND HAEMOPOIETIC STEM CELL TRANSPLANTATION
THE LYMPHOMAS
THE PARAPROTEINAEMIAS
PALLIATIVE MEDICINE AND SYMPTOM CONTROL

7. Rheumatology

Rheumatology
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
BACK PAIN
OSTEOARTHRITIS
INFLAMMATORY ARTHRITIS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
THERAPEUTICS

8. Water, electrolytes and acid–base balance

WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
THERAPEUTICS

9. Renal disease

Renal disease
INVESTIGATION OF RENAL DISEASE
GLOMERULAR DISEASES
NEPHROTIC SYNDROME
URINARY TRACT INFECTION
TUBULOINTERSTITIAL NEPHRITIS
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
TESTICULAR TUMOUR
URINARY INCONTINENCE

10. Cardiovascular disease

COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
CARDIAC ARRHYTHMIAS
HEART FAILURE
ISCHAEMIC HEART DISEASE
RHEUMATIC FEVER
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
MYOCARDIAL DISEASE
CARDIOMYOPATHY
PERICARDIAL DISEASE
SYSTEMIC HYPERTENSION
ARTERIAL AND VENOUS DISEASE
ELECTRICAL CARDIOVERSION
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS

11. Respiratory disease


Respiratory disease
TUBERCULOSISnd
DIFFUSE DISEASES OF THE LUNG PARENCHYMA
OCCUPATIONAL LUNG DISEASE
CARCINOMA OF THE LUNG
DISEASES OF THE CHEST WALL AND PLEURA
DISORDERS OF THE DIAPHRAGM

12. Intensive care medicine

Intensive care medicine

13. Drug therapy, poisoning, and alcohol misuse

Drug therapy, poisoning, and alcohol misuse

14. Endocrine disease

Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
THERAPEUTICS

15. Diabetes mellitus and other disorders of metabolism

DIABETES MELLITUS
DIABETIC METABOLIC EMERGENCIES
COMPLICATIONS OF DIABETES
SPECIAL SITUATIONS
HYPOGLYCAEMIA IN THE NON - DIABETIC
DISORDERS OF LIPID METABOLISM
THE PORPHYRIAS

16. The special senses

THE EAR
THE NOSE AND NASAL CAVITY
THE THROAT
THE EYE

17. Neurology

COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HYDROCEPHALUS
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES
MUSCLE DISEASES
MYOTONIAS
DELIRIUM
THERAPEUTICS

18. Dermatology

Dermatology



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