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Hyperthyroidism
ophthalmoplegia
(in Graves’ disease)
Graves’ disease)
Oligomenorrhoea
(in Graves’ disease)
General
increased appetite
Hypothyroidism
Periorbital
oedema
Husky voice
Goitre
Bradycardia
Carpal tunnel
syndrome
Menorrhagia
Constipation
General
Fig. 10.4 Features of hyper- and hypothyroidism.
pretibial myxoedema: 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). A less common extrathyroidal
manifestation of Graves’ disease is thyroid acropachy, a soft
tissue swelling and periosteal hypertrophy of the distal phalanges
which mimics finger clubbing (see Fig. 10.2C). It is almost always
associated with dermopathy and ophthalmopathy.
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 dry or coarse hair and
periorbital puffiness (see Fig. 10.5).
• Inspect the hands for vitiligo, thyroid acropachy (see
Fig. 10.2C), onycholysis and palmar erythema.
• Assess the pulse (tachycardia, atrial fibrillation, bradycardia)
and blood pressure.
Fig. 10.5 Typical facies in hypothyroidism.
• Ask the patient to extend their arms. Inspect for a fine tremor
due to sympathetic overactivity; laying a sheet of paper over
the patient’s fingers may improve detection.
• Auscultate the heart for a midsystolic flow murmur
(hyperthyroidism).
• Inspect the limbs for coarse, dry skin or pretibial myxoedema
(see Fig. 10.2D).
• Assess proximal muscle power and deep tendon (ankle) re-
flexes (p. 155).
Thyroid gland
Examination sequence (Video 21)
• 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 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.
The history • 225
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• Palpate for cervical lymphadenopathy (Fig. 3.27, the neck
examination sequence on p. 214, and the new neck video).
• Percuss the manubrium to assess for dullness due to retro-
sternal 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, but carotid bruits or murmurs transmitted from the
aorta are louder over the carotid 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 the gland diffusely enlarged; 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 10.4.
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; 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; Fig. 10.2B).
• 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 downward movement of the
eyeball and descent of the upper eyelid, exposing the sclera
above the iris.
• Assess eye movements (Fig. 8.9, p. 189). Graves’ oph-
thalmopathy is characteristically associated with restriction of
upgaze.
10.4 Investigations in thyroid disease
Investigation Indication/comment
Biochemistry
Thyroid function tests To assess thyroid status
Immunology
Antithyroid peroxidase (TPO)
antibodies
Antithyroid stimulating hormone
receptor antibodies (TRAbs)
Imaging
Ultrasound Goitre, nodule
Thyroid scintigraphy (
99m
Tc)
Computed tomography To assess goitre size and aid surgical
Invasive/other
Fine-needle aspiration cytology Thyroid nodule
Respiratory flow-volume loops To assess tracheal compression from
Lid retraction (a staring appearance due to widening of the
palpebral fissure) and lid lag (see above) are common eye signs
associated with hyperthyroidism. Both are thought to be due to
contraction of the levator palpebrae muscles as a result of
sympathetic hyperactivity. Periorbital puffiness (myxoedema) is
sometimes seen in hypothyroidism.
Graves’ ophthalmopathy is an inflammatory infiltration of the soft
tissues and extraocular muscles which affects around 20% of patients with Graves’ disease (see Fig. 10.2A and 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 from the orbit) may occur in both
active and inactive Graves’ ophthalmopathy and is often called
exophthalmos. Inflammation of the orbital soft tissues may lead to
other more severe features, including corneal ulceration, diplopia,
ophthalmoplegia and compressive optic neuropathy (Fig. 8.8D).
123
I,
Non-specific, high in autoimmune
thyroid disease
Specific for Graves’ disease
To assess areas of hyper-/hypoactivity
planning
a large goitre
10
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 symptom s
Parathyroid disease is commonly asymptomatic. In hyperparathyroidism, the most common symptoms relate to
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hypercalcaemia: polyuria, polydipsia, renal stones, peptic ulceration, tender areas of bone fracture or deformity (‘Brown
tumours’) and delirium or psychiatric symptoms. In hypoparathyroidism, hypocalcaemia may cause hyper-reflexia or tetany
(involuntary muscle contraction), most commonly in the hands
or feet. Paraesthesiae of the hands and feet, or around the
mouth, may occur. Hypoparathyroidism is most often caused
by inadvertent damage to the glands during thyroid s urgery but
may also be caused by autoimmune disease. Patients with the
rare autosomal dominant condition pseudohypopa rathyroidism
have end-organ resistance to parathyroid hormone and typically have short stature, a round face and shortening of the
fourth and fifth metacarpal bones.
Ask about:
• Symptoms of hypercalcaemia:
• polyuria, polydipsia
• abdominal pain or constipation
• confusion or psychiatric symptoms
• bone pain
• Symptoms of hypocalcaemia:
• muscle cramps, perioral or peripheral paraesthesia.
Past medical, drug, family and social history
Ask about:
• recent neck surgery or irradiation
• past history of bone fractures
• past history of renal stones
• family history of hyperparathyroidism (which can be part of
the autosomal dominant multiple endocrine neoplasia
syndrome) or other endocrine disease (Addison’s disease
and type 1 diabetes can occur with hypoparathyroidism in the
autosomal recessive type 1 autoimmune polyglandular
syndrome).
Fig. 10.6 Trousseau’s sign.
The physical examination
Examination sequence
• Hands: ask the patient to make a fist and assess the
length of the metacarpals (4th and 5th are shortened in
pseudohypoparathyroidism).
• Examine the neck for scars. Parathyroid tumours are rarely
palpable.
• Measure blood pressure and assess hydration (p. 279).
Inflating the blood pressure cuff in a patient with hypocalcaemia may precipitate a typical pattern of muscle
contraction, with the thumb adducted, the proximal interphalangeal and distal interphalangeal joints extended and the
metacarpophalangeal joints flexed (‘main d’accoucheur’
(hand of the obstetrician), or Trousseau’s sign; Fig. 10.6).
• Test for muscle weakness and hyper-reflexia (p. 254).
• Look for evidence of recent fractures or bone deformity/
tenderness.
• Perform urinalysis (renal stones may cause haematuria).
THE PITUITARY
Anatomy and physiology
The pituitary gland is enclosed in the sella turcica at the base of the
skull beneath the hypothalamus. It is bridged over by a fold of dura
mater (diaphragma sellae) with the sphenoidal sinus below and the
optic chiasm above. Lateral to the pituitary fossa are the cavernous
sinuses, containing cranial nerves III, IV and VI and the internal
carotid arteries (Fig. 8.3, p. 171). The gland comprises anterior and
posterior lobes. The anterior lobe secretes adrenocorticotrophic
hormone (ACTH), prolactin, growth hormone (GH), thyroidstimulating hormone (TSH) and gonadotrophins (luteinising hormone (LH) and follicle-stimulating hormone (FSH)). The posterior
lobe is an extension of the hypothalamus and secretes vasopressin
(antidiuretic hormone) and oxytocin.
The history
Common presenting symptom s
Pituitary tumours are common and are found incidentally in around
10% of patients undergoing head computed tomography (CT) or
magnetic resonance imaging (MRI). Hypopituitarism can result
from a space-occupying lesion or from a destructive or infiltrative
The physical examination • 227
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• changes in facial features (ask to see old photographs)
• an increase in shoe, ring or glove size
• associated medical conditions: arthropathy, carpal tunnel
syndrome, hypertension, diabetes, colonic malignancy, sleep
apnoea.
Hypopituitarism
Apart from headache due to stretching of the diaphragma sellae
and visual abnormalities, clinical presentation depends on the
deficiency of the specific anterior pituitary hormones involved.
Individual or multiple hormones may be involved, so questioning
in relation to deficiencies of the thyroid, adrenocortical and
reproductive hormones is needed.
Fig. 10.7 Pituitary macroadenoma. The tumour extends into the supra-
sellar cistern and is compressing the optic chiasm. Courtesy Dr Dilip Patel.
process such as trauma, radiotherapy, sarcoidosis, tuberculosis
or metastatic disease. Pituitary infarction or haemorrhage can
result in acute hypopituitarism (pituitary apoplexy) and is a medical
emergency; it is often associated with headache, vomiting, visual
impairment and altered consciousness. Secondary adrenal
insufficiency due to pituitary apoplexy may be life-threatening and
must be identified and treated urgently (see p. 231).
Non-functioning pituitary adenomas may be asymptomatic or
may present with local effects such as compression of the optic
chiasm causing visual loss (typically bitemporal upper quadrantanopia or hemianopia; Fig. 10.7 and Fig. 8.5) or headache
due to expansion of the sella. Adenomas may produce hormones such as prolactin, GH or ACTH; the resulting symptoms
and signs will depend on the excess hormone present.
Prolactinoma
Ask about:
• galactorrhoea (breast milk secretion)
• oligomenorrhoea, amenorrhoea or infertility (in women)
• reduced libido, erectile dysfunction and reduced shaving
frequency (in men)
Acromegaly
GH excess prior to puberty presents as gigantism; after puberty,
it causes acromegaly.
Ask about:
• headache
• excessive sweating
Family history
Enquire about family history since pituitary disease can occur as
part of inherited multiple endocrine neoplasia or familial pituitary
syndromes.
The physical examination
Acromegaly
Examination sequence
• Look at the face for coarsening of features, thick, greasy skin,
prominent supraorbital ridges, enlargement of the nose,
prognathism (protrusion of the mandible) and separation of
the lower teeth (Fig. 10.8A and B).
• Examine the hands and feet for soft-tissue enlargement and
tight-fitting rings or shoes, carpal tunnel syndrome and
arthropathy (see Fig. 10.8C and D).
• Assess the visual fields (p. 183).
• Check the blood pressure and perform a urinalysis.
Hypertension and diabetes mellitus are common
associations.
Hypopituitarism
Examination sequence
Look for:
• extreme skin pallor (a combination of mild anaemia and
melanocyte-stimulating hormone deficiency)
• absent axillary hair
• reduced/absent secondary sexual hair and testicular atrophy
(caused by gonadotrophin deficiency)
• visual field defects (most often bitemporal hemianopia),
optic atrophy or cranial nerve defects (III, IV and VI), caused
by a tumour compressing the optic chiasm, optic nerve or
cavernous sinus.
10
A
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B
C
Fig. 10.8 Acromegaly. A Typical facies. B Prognathism and separation of the lower teeth. C Large, fleshy hands. D Widening of the feet.
THE ADRENALS
Anatomy and physiology
The adrenals are small, pyramidal organs lying immediately
above the kidneys on their posteromedial surface. The adrenal
medulla is part of the sympathetic nervous system and secretes
catecholamines. The adrenal cortex secretes cortisol (a glucocorticoid), mineralocorticoids and androgens.
D
The history
Common presenting symptom s
Adrenal insufficiency is due to inadequate secretion of cortisol and
can be due to intrinsic disease of the adrenal gland (primary) or
due to failure, or suppression, of ACTH signalling (secondary).
A
The history • 229
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B
Fig. 10.9 Addison’s disease. A Hyperpigmentation in a patient with coexistent vitiligo. B Buccal pigmentation.
Primary adrenal insufficiency (Addison’s disease; Fig. 10.9)is
usually secondary to autoimmune destruction of the adrenal cortex but can also be due to infections (tuberculosis, HIV, fungal
etc.), infarction, metastatic disease, or drugs (e.g. etomidate, ketoconazole, phenytoin). Secondary adrenal insufficiency is most
often due to long-term exogenous glucocorticoid use but can also
be due to pituitary disease. Symptoms are often non-specific.
Asymptomatic, non-functioning adenomas may be detected
incidentally on abdominal CT or MRI scans. Functioning adrenal
adenomas may present with refractory hypertension (Box 10.5)
or features of androgen excess (p. 231).
Cushing’s syndrome is caused by excess exogenous or
endogenous glucocorticoid exposure. Most cases are iatrogenic
and caused by side effects of glucocorticoid therapy. ‘Endogenous’ Cushing’s usually results from an ACTH-secreting pituitary
microadenoma, but other causes include a primary adrenal adenoma or ‘ectopic’ ACTH secretion by a non-pituitary tumour.
The catabolic effects of glucocorticoids cause widespread tissue
breakdown (leading to proximal myopathy, fragility fractures,
spontaneous bruising and skin thinning) and a central accumulation of body fat (Fig. 10.10). Patients may develop hypertension
or diabetes and are susceptible to infection.
10.5 Adrenal causes of endocrine hypertension
Hormone
produced in
Condition
Conn’s syndrome Aldosterone Hypokalaemia
Cushing’s syndrome Cortisol Central obesity, proximal
Phaeochromocytoma Noradrenaline
• nausea, vomiting, diarrhoea, constipation, abdominal pain
and weight loss
• muscle cramps
• altered skin pigmentation (vitiligo or hyperpigmentation).
excess Associated features
(norepinephrine),
adrenaline
(epinephrine)
10
myopathy, fragility
fractures, spontaneous
bruising, skin thinning,
violaceous striae,
hypokalaemia
Paroxysmal symptoms,
including hypertension,
palpitations, sweating
Adrenal insufficiency
Ask about:
• weakness
• postural light-headedness
Cushing’s syndrome
Ask about:
• increase in weight, particularly if the weight is centrally
distributed
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A
C
B
D
Fig. 10.10 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.
Anatomy and physiology • 231
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• bruising, violaceous striae and skin thinning
• difficulty rising from a chair/bath (may indicate proximal
myopathy).
Past medical and drug history
Enquire about recent or past exogenous glucocorticoid
usage (route, dose, duration) as this may contribute to either
iatrogenic Cushing’s syndrome or suppression of the hypothalamic–pituitary–adrenal axis and resultant glucocorticoid
insufficiency.
The physical examination
Adrenal insufficiency
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: s kin creases, buccal mucosa
(see Fig. 10.9B) and recent scars. In primary adrenal in-
sufficiency, 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 Caucasians). Vitiligo
(depigmentation of areas of skin) occurs in 10– 20% of
autoimmune Addison’s disease cases (see Fig. 10.9A).
• Measure the blood pressure and test for postural hypoten-
sion (p. 48), resulting from salt and water loss due to inadequate mineralocorticoid.
• Patients on long-term glucocorticoids may have features
of Cushing’ s syndrome (see below). Patients with an
existing diagnosis of primary or secondary adrenal insufficiency may be carrying a steroid emergency alert card
(Fig. 10.11).
Cushing’s syndrome
Examination sequence
• Look at the face and general appearance for central obesity;
there may be a round, plethoric ‘moon’ face (see Fig. 10.10A)
or dorsocervical fat pad ( ‘buffalo hump’).
• Examine the skin for thinning and bruising (see Fig. 10.10D),
striae (especially abdominal; Fig. 10.10C), acne, hirsutism,
signs of infection or poor wound healing.
• Measure the blood pressure.
• Perform ophthalmoscopy for cataracts and hypertensive
retinal changes (Fig. 8.18, p. 189), and assess the visual fields
(p. 162).
• Examine the spine for kyphosis and/or tenderness due to
vertebral compression fractures (p. 297).
• Examine the legs for proximal muscle weakness and oedema.
• Perform urinalysis for glycosuria.
10
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.
Common presenting symptom s and signs
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).
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.
Hyperandrogenism in women usually presents with hirsutism (excessive male-patte rn hair growth), acne and/or oligomenorrhoea and is commonl y due to polycystic ovary
syndrome (PCOS; usually also associated with obesity). Other
less common causes, such as congenital adrenal hyperplasia,
should also be considered. Virilisation is suggested by malepattern baldness, deepening o f the voice, increased muscle
bulk and clitoromegaly; if present in women with a short history of severe hirsutism, consider a testosterone-secreting
tumour.
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Steroid Emergency Card
(Adult)
IMPORTANT MEDICAL INFORMATION FOR HEALTHCARE STAFF
THIS PATIENT IS PHYSICALLY DEPENDENT ON DAILY STEROID THERAPY
as a critical medicine. It must be given/taken as prescribed and never
omitted or discontinued. Missed doses, illness or surgery can cause
adrenal crisis requiring emergency treatment
Patients not on daily steroid therapy or with a history of steroid usage
may also require emergency treatment.
Name
Date of Birth
Why steroid prescribed
Emergency Contact
NHS Number
When calling 999 or 111, emphasise this is a likely adrenal
insufficiency/Addison’s/Addisonian crisis or emergency
symptoms (vomiting, diarrhoea, dehydration, injury/shock).
Emergency treatment of adrenal crisis
1) Immediate 100mg Hydrocortisone i.v. or i.m. injection.
Followed by 24 hr continuous i.v. infusion of 200mg
Hydrocortisone in Glucose 5% OR 50mg Hydrocortisone i.v. or
i.m. qds (100mg if severely obese).
2) Rapid rehydration with Sodium Chloride 0.9%.
3) Liaise with endocrinology team.
Scan here for further information or search
https://www.endocrinology.org/adrenal-crisis
Fig. 10.11 Example of a steroid emergency alert card. Courtesy Society for Endocrinology.
DIABETES
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 can be classified into the following categories:
• Type 1: severe insulin deficiency due to autoimmune
destruction of the pancreatic islets. These patients are
susceptible to acute decompensation due to ketoacidosis or
insulin-induced hypoglycaemia, both of which require prompt
treatment.
• Type 2: commonly affects people who are obese and insulinresistant, although impaired beta-cell function is also important. These patients may decompensate by developing a
hyperosmolar hyperglycaemic state.
• Gestational diabetes: diabetes first diagnosed in the second
or third trimester of pregnancy that is not clearly pre-existing
type 1 or type 2 diabetes.
• Specific types of diabetes due to other causes. Examples
with associated history and examination features are
described in Box 10.6.
AND describe
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10.6 Causes of secondary diabetes
a
Cause of diabetes Examples Clinical features
Pancreatic disease Pancreatitis Abdominal pain
Endocrinopathies Acromegaly, Cushing’s syndrome p. 226
Drugs Glucocorticoids (e.g. prednisolone)
Pregnancy Gestational diabetes may develop in the third
Monogenic defects in beta-cell
function
Genetic syndromes associated with
diabetes
a
Based on classification by the American Diabetes Association.
The history
Trauma/pancreatectomy Surgical scar
Neoplasia Weight loss
Cystic fibrosis Chronic cough, purulent sputum
Haemochromatosis Skin pigmentation (‘bronze diabetes’)
Antipsychotics (e.g. olanzapine)
Immunosuppressants (e.g. ciclosporin,
tacrolimus)
trimester
Glucokinase deficiency Glucokinase deficiency is present from birth with stable mild
Down’s syndrome p. 39
Turner’s syndrome p. 39
women, balanitis in men) suggests Candida yeast infection
(thrush).
Features of Cushing’s syndrome (see Fig. 10.10)
Gum hypertrophy may be seen with ciclosporin use
Gravid uterus
hyperglycaemia
10
Diabetes is a long-term condition where self-management is
key, and the language we use when speaking with people l iving
with diabetes matters. Always use non-judgemental, respectful
and empathic language, and avoid labelling people as ‘ diabetic’; most people prefer to be described as a ‘person with
diabetes’.
Common presenting symptom s
Newly diagnosed diabetes mellitus
Diabetes mellitus commonly presents with a classical triad of
symptoms:
• polyuria (and nocturia): due to osmotic diuresis caused by
glycosuria
• 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
Diabetic ketoacidosis
Diabetic ketoacidosis (DKA) is an acute complication of insulin
deficiency resulting in the production of ketone bodies and a
consequent metabolic acidosis and osmotic diuresis. It may occur
as the first presentation of diabetes or can develop in people with
existing diabetes. It commonly presents with symptoms of
hyperglycaemia (polyuria, thirst) alongside abdominal pain, vomiting and shortness of breath resulting from the underlying metabolic acidosis. Many people with type 1 diabetes have capillary
blood glucose meters, which can also check capillary blood ketones. A blood ketone level of 3mmol/LsuggestsDKA.The
history should cover possible triggers, such as omission of insulin
or symptoms of intercurrent illness or infection.
Hypoglycaemia
Hypoglycaemia may result from treatment with insulin or sulfonylureas. Symptoms of hypoglycaemia can be categorised as
follows:
• Autonomic: e.g. hunger, sweating, tremor, palpitations
• Neuroglycopenic: e.g. confusion, irritability
• General malaise: e.g. tiredness, nausea
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