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SECTION THREE
Thyroid gland
Sternomastoid muscle
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(see Fig. 19.8A) with the fingers slightly flexed, such
that the tips of the index fingers lie just below the
cricoid in order to palpate the isthmus. Now rotate
the fingers down and slightly laterally in order to
feel the lateral lobes, including the inferior border
(see Fig. 19.8B). The anterior surface of each lobe
should be no larger than the terminal phalanx of the
patient’s thumb.
The following points should be addressed:
Is the thyroid diffusely enlarged, as in thyroid-
stimulating hormone (TSH)- mediated or
autoimmune enlargement (see Fig. 19.8D)? If
A
Feeling the isthmus
so, is it soft (e.g. dyshormogenesis, diffuse goitre
of puberty) or firm/hard (e.g. autoimmune
thyroiditis). In general, the firmer the texture
of an enlarged thyroid, the more likely is the
pathology to be autoimmune.
Are there two or more identifiable nodules
(see Fig. 19.8E, Fig. 19.9)? If so, is the patient
thyrotoxic and does the gland extend downward
behind the sternum? (If the gland is partially or
completely retrosternal, the inferior border may
not be palpable or palpable only on swallowing.)
Most multinodular goitres are benign, but a history
Hyoid bone
Trachea
C
Clavicle
Manubrium of
the sternum
B
Feeling the lateral lobes
Thyroid cartilage
Cricoid cartilage
Lobe
Isthmus
Sternal notch
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Figure 19.8 Examination of the thyroid. (A)
Feeling the isthmus; (B) feeling the lateral
lobes; (C) anatomical landmarks; (D) diffuse
enlargement; (E) multinodular goitre; (F)
single nodule.
D
E
F
Figure 19.9 A large multinodular goitre. Note the asymmetrical
growth of the nodules.
of neck irradiation, enlarged cervical lymph nodes
or progressive enlargement of one of the nodules
raises the suspicion of malignancy.
Is the palpable abnormality a single focal nodule
(see Fig. 19.8F), suggesting a cyst, adenoma or
carcinoma? Rapid growth, hard texture, lack of
movement on swallowing (see above), enlarged
regional lymphadenopathy, male gender and
a history of neck irradiation all increase the
probability of malignancy.
Is the goitre firm and asymmetrical?
Are there features of local pressure effects or
local infiltration (e.g. dysphonia from recurrent
laryngeal involvement)?
Are there weight loss and debility? These suggest
anaplastic carcinoma or lymphoma.
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Is there a bruit, indicating increased blood
supply? This is frequently found in untreated
Graves’ disease, but should not be confused with
a transmitted bruit from the carotid.
The cardiovascular system
Particular attention should be paid to any postural
drop in blood pressure. This may indicate a depleted
extracellular fluid volume, for example in patients
with adrenal insufficiency, or autonomic dysfunction,
the most common cause of which is diabetes mellitus.
Additional indicators of the latter include failure of
reflex bradycardia during the Valsalva manoeuvre
and loss of beat- to- beat variation in cardiac cycle
length, as determined by electrocardiography. A
hyperdynamic circulation, sinus tachycardia or atrial
fibrillation may be found in thyrotoxicosis; this may
progress to cardiac decompensation and cardiac
failure.
The breasts and genitalia
A detailed description of growth and pubertal
development is beyond the scope of this chapter.
In brief, however, in the average adolescent female,
pubertal development usually commences between
the ages of 10 and 11 and takes 3 to 4 years to
complete. A growth spurt starts about 1 year before
breast development, peak height velocity is reached
on average 1 year later and menarche follows in an
average of 1 year. In males, pubertal development
usually commences between the ages of 11 and
12, takes approximately 3 years to complete and
has a characteristic sequence of adrenarche (onset
of adrenal androgen secretion with the appearance
of secondary sexual hair), testicular development,
beginning of pubic hair, beginning of growth spurt
and peak height velocity.
The breasts should be examined for mass lesions
and, if suggested by the history, for galactorrhoea.
In the adolescent female, physiological breast
enlargement provides a precise index of pubertal
status and signals the onset of the pubertal growth
spurt (Tanner stage 3 breast development). Onset
of menses (menarche) is a relatively late pubertal
event at which point pubertal breast development
is virtually complete. In males, any tendency to
gynaecomastia should be noted (Fig. 19.10). This may
range from minor degrees of subareolar glandular
enlargement to substantial breast prominence; breast
enlargement associated with generalized adiposity
should not be confused with true gynaecomastia.
Genital examination in the male should document
testicular volume. This is particularly important in
the assessment of pubertal development, for which
volume should be measured by comparison with
calibrated ovoids (Prader orchidometer; Fig. 19.11).
Prepubertal testicular volume is less than 4 ml;
increased volume implies pubertal gonadotrophin
stimulation. Onset of the pubertal growth spurt in
boys is associated with a testicular volume of 10 ml
and normal adult testicular volume is in the range
of 15 to 25 ml. In the assessment of normal puberty,
it is important to establish that growth velocity and
gonadal changes (testicular volume or breast stage)
are concordant, because a discordance of puberty
proceeding ahead of growth implies an abnormal
source of sex steroid (e.g. androgen- secreting tumours
A
Figure 19.10 Gynaecomastia. There is enlargement of both
breasts in this man.
B
Figure 19.11 Prader orchidometer. (A) Testicular volume (in
ml) may be estimated by comparison with calibrated ellipsoids.
(B) Gently grip the testis in one hand and compare its volume
(including the scrotal skin, but excluding the epididymis) with
that of the ellipsoids. The patient shown has a reduced testicular
volume of 8 ml, caused by Klinefelter’s syndrome; the normal
secondary sexual hair is owing to the provision of exogenous
testosterone.
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Figure 19.12 Corneal calcification (band keratopathy) in a
patient with long- standing hyperparathyroidism.
or congenital adrenal hyperplasia). Testicular atrophy
in the adult male indicates hypogonadism, owing
to primary testicular failure, hypothalamopituitary
dysfunction or chronic liver disease. Tumours of
Leydig cells are usually palpable and should be
sought in any patient with gynaecomastia.
Examination of the external genitalia in the
female is important when androgen hypersecretion
is suspected. Enlargement of the clitoris is a feature
of excess androgen secretion.
Ambiguity of the external genitalia is indicative of
foetal androgen excess in the karyotypic female and
of testosterone or dihydrotestosterone deficiency or
resistance in the male; these conditions are rare and
require specialized investigation.
The eyes
The hypercalcaemic patient should be carefully
examined for corneal calcification, evident as a
narrow band on the medial or lateral border of
the cornea (Fig. 19.12); this usually indicates long-
standing hypercalcaemia and a diagnosis of primary
hyperparathyroidism.
In patients with thyroid disease, the presence of
exophthalmos (proptosis) should be noted. This
may be unilateral or bilateral and may be associated
with apparent ophthalmoplegia owing to tethering
of the extraocular muscles, particularly the medial
and inferior rectus muscles, such that diplopia
occurs on upward or lateral gaze (dysthyroid eye
disease; Fig. 19.13). These ocular signs are especially
important in the diagnosis of autoimmune thyroid
disease (Graves’ disease). Remember that unilateral
proptosis may also occur with an orbital tumour. Lid
retraction, evident as a wide- eyed staring expression,
and lid lag, in which depression of the upper lid lags
behind the eye in a downward gaze, are caused by
increased activity of the sympathetic innervation
of levator palprebae superioris and are not specific
to Graves’ disease. Any degree of corneal exposure
Figure 19.13 Lid retraction and proptosis in a patient with
thyrotoxic Graves’ disease. In this patient, there had been a
6- month history of effortless weight loss, tremulousness, shortness
of breath on exertion and palpitations.
owing to the failure of complete lid apposition
should be documented.
Visual acuity should be measured, both with and
without a pinhole, to correct for any refractive error.
Reduced acuity may be a feature of optic nerve
compression in severe dysthyroid eye disease or of
asymmetrical pressure on the optic chiasm owing
to hypothalamopituitary space- occupying lesions. In
the latter, assessment of the visual fields may reveal a
bitemporal hemianopia; this is frequently incomplete
and incongruous, reflecting the asymmetrical growth
of the tumour. A detailed description of the visual
pathways and examination of the visual fields is
given in Chapter 16. In the context of suspected
pituitary/peripituitary disease, use of a red object
(e.g. a hat pin) is preferable to finger movements
because this provides a more sensitive marker of
early visual pathway compression. Examination of
the optic discs with the ophthalmoscope may show
papilloedema, indicating recent onset of optic nerve
compression, or pallor, indicating neural atrophy
resulting from long- standing pressure. In the context
of a pituitary mass lesion, pallor of the optic discs
suggests that full visual recovery is improbable.
The nervous system
In thyrotoxicosis, examination of the nervous system
reveals a rapid fine tremor. Proximal weakness, with
or without wasting of the shoulder and hip girdle
musculature (proximal myopathy), is a typical
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feature of thyrotoxicosis, glucocorticoid excess and
vitamin D deficiency. Osteomalacic myopathy is
often associated with myalgia.
Hypocalcaemia is associated with increased neural
excitability, which may be demonstrated by gentle
percussion over the proximal part of the facial
nerve (as it exits from the parotid gland). The test is
positive if this manoeuvre evokes involuntary facial
muscular twitching (Chvostek’s sign).
Tendon reflexes will be abnormally brisk in patients
who are thyrotoxic and may show a slow relaxation
phase in hypothyroidism. Both hypothyroidism
and acromegaly may give rise to nerve entrapment
syndromes, particularly of the median nerve at the
wrist (carpal tunnel syndrome).
Investigation
The investigation of endocrine and metabolic
disorders usually involves (a) the measurement of
electrolytes, minerals, metabolites or hormones
in plasma and (b) isotopic, ultrasonographic,
radiological or magnetic resonance (MR) imaging of
specific endocrine glands. In investigating endocrine
disease, one is usually interested in whether a
specific gland is overactive or underactive. An
important principle of endocrine testing is that if
underactivity of a gland is suspected then blood
samples taken at a time of day when the hormone
level, in health, is maximum are most informative;
a good example of this is the measurement of
an early morning cortisol to assess adequacy of
the hypothalmo- pitiutary- adrenal axis given the
circadian rhythm of cortisol secretion. Conversely,
if overactivity of a gland is suspected, sampling at
a time of day when the relevant hormone levels
should be minimal provides useful diagnostic
information; this explains the common practice of
measuring cortisol in blood or saliva at midnight
in patients with suspected Cushing’s syndrome.
For many patients the relevant clinical questions
may be answered by basal hormone measurements;
for example, serum free thyroxine and TSH in
thyrotoxicosis and hypothyroidism. In many
instances, however, the lack of a clear distinction
between basal hyposecretion, normal secretion and
hypersecretion necessitates the use of stimulation
and suppression tests. If underperformance of an
endocrine gland is suspected and basal testing has
not provided sufficient clarity, then a stimulation
test may be necessary. If hormonal overproduction
is suspected, a suppression test may be needed.
Insulin tolerance testing, in which carefully
controlled insulin- induced hypoglycaemia
stimulates hypothalamopituitary secretion
measured by serum growth hormone, cortisol and
prolactin
Tetracosactrin testing, in which an injection
of a synthetic ACTH analogue is used to assess
adrenocortical reserve
Oral glucose tolerance test, which is an indirect
test of insulin secretion and action as determined
by the rise and subsequent fall in the plasma
glucose level following an oral glucose load
Endocrine suppression tests
Endocrine suppression tests indicate whether a
physiological feedback mechanism is intact or if
secretion of the hormone in question has become
at least partly autonomous. For example, the
suppression of plasma cortisol by the synthetic
glucocorticoid dexamethasone is incomplete in
Cushing’s syndrome, and suppression of serum
growth hormone by an oral glucose load fails to
occur in acromegaly. These tests are needed because
of the huge variation in serum levels of cortisol and
growth hormone in health, making isolated, random
measurements of both almost valueless in diagnosis.
Endocrine imaging
Plain X- ray imaging is of limited value in the
investigation of endocrine disorders. However, lateral
and anteroposterior views of the pituitary fossa can
be useful in demonstrating abnormal calcification
in the fossa or gross expansion and erosion of
the fossa owing to large intrasellar or suprasellar
tumours. Plain abdominal radiology may show
renal calcification (nephrocalcinosis; Fig. 19.14) in
patients with long-standing hypercalcaemia or renal
tubular acidosis.
Endocrine stimulation tests
Endocrine stimulation tests are designed to
demonstrate how much hormone a gland can secrete
in response to a near- maximal stimulus. Examples
include the following:
Figure 19.14 Widespread renal calcification typical
of nephrocalcinosis in a patient with long- standing
hyperparathyroidism.
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Figure 19.15 Axial CT scan of the abdomen in a patient with a
right adrenal medullary phaeochromocytoma. Note the extensive
tumour mass, with areas of hypodensity indicating episodes of
partial tumour infarction.
Figure 19.17 Technetium- labelled isotope scan of the thyroid in
a patient with a focal thyroid nodule. Note the focal area of uptake
corresponding to the palpable lesion, with surrounding inactivity
indicating autonomous function within the nodule.
Diabetes mellitus
Figure 19.16 Magnetic resonance imaging (sagittal view) of the
pituitary, demonstrating a large pituitary adenoma with suprasellar
extension.
Computed tomography (CT) imaging is useful in
assessing the pituitary, adrenal glands (Fig. 19.15) and
thorax. However, MR imaging of the pituitary (Fig.
19.16) offers definite advantages over CT in terms
of improved precision in detecting small intrasellar
tumours and better definition of the lateral border
of the pituitary and the cavernous sinus.
Isotopic imaging is particularly useful for
demonstrating autonomous function within
endocrine tumours. This technique is applicable
to the thyroid gland (radiolabelled pertechnetate;
Fig. 19.17), the adrenal medulla (radiolabelled
metaiodobenzylguanidine) and parathyroids
(combined radiolabelled sesta- methoxy- isobutylisonitrile (MIBI) and pertechnetate differential
scanning).
Diabetes is a Greek word meaning ‘a passer
through; a siphon’, and mellitus derives from the
Greek word for ‘sweet’. The Greeks named it thus
because of the excessive amounts of urine produced
by sufferers that attracted insects because of its
glucose content. The ancient Chinese tested for
diabetes by observing whether ants were attracted
to a person’s urine.
Diabetes mellitus is the most common metabolic
disorder encountered in clinical practice. It is
strongly linked to obesity. Diabetes mellitus is
characterized by abnormal carbohydrate and lipid
homoeostasis, leading to elevation in plasma glucose,
or hyperglycaemia, and abnormality of serum
lipids, or dyslipidaemia. Glucose homoeostasis is
modulated mainly by the release of insulin from
the islet cells (β cells) of the pancreas. Diabetes
develops as a result of a variable combination of
absolute insulin deficiency caused by pancreatic
islet cell dysfunction and tissue insulin resistance
owing to reduced cellular responsiveness to insulin.
The World Health Organization (WHO) has
developed a classification of diabetes mellitus
based on its pathogenesis (Box 19.8). Type 1 is
characterized by absolute insulin deficiency owing
to autoimmune- mediated pancreatic islet cell
destruction. In contrast, type 2 diabetes is associated
with a variable degree of tissue insulin resistance,
leading—at least in the early stages—to high plasma
insulin levels, then subsequently to relative insulin
deficiency as pancreatic islet cell function fails to
overcome this resistance. The diagnostic criteria for
disorders of glucose metabolism are shown in Box
19.9. Note that glycosuria itself (glucose in the urine)
is not a reliable diagnostic test for diabetes mellitus.
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Box 19.8
The World Health Organization classification of diabetes mellitus
Type Common subtypes/pathogenesis Treatment
Type 1 Destruction of pancreatic islet cells leading to insulin deficiency Insulin
Type 2 Ranges from predominantly insulin resistance with
relative insulin deficiency (often associated with obesity)
to predominantly insulin deficiency
Other types
Genetic defects of β- cell
function
Genetic defects of insulin
action
Diseases of the exocrine
pancreas
Endocrinopathies Cushing’s syndrome, acromegaly, phaeochromocytoma,
Drug- or chemical- induced Glucocorticoids, α- adrenergic agonists, β- adrenergic agonists,
Uncommon forms of
immune- mediated diabetes
Other genetic syndromes
associated with diabetes
Gestational diabetes Diet/insulin
Hybrid forms of diabetes Slowly evolving immune- mediated diabetes of adults
Diabetes associated with glucokinase, hepatic nuclear
factor (HNF) 1α, HNF1β, HNF4α, Neurod1 and insulin promotor
factor mutations (all previously grouped under maturity- onset
diabetes of the young (MODY))
Mitochondrial diabetes
Insulin- resistance syndromes (type A insulin resistance,
leprechaunism, Rabson- Mendenhall syndrome lipoatrophic
diabetes)
Fibrocalculous pancreatic diabetes, pancreatitis, trauma/
pancreatectomy, neoplasia, cystic fibrosis, haemochromatosis,
others
glucagonoma, hyperthyroidism, somatostatinoma, others
thiazides, interferon- α therapy
Insulin autoimmune syndrome (antibodies to insulin), anti-
insulin receptor antibodies, ‘stiff man’ syndrome
Down’s syndrome, Friedreich’s ataxia, Huntington’s chorea,
Klinefelter’s syndrome, Lawrence- Moon- Biedl syndrome,
myotonic dystrophy, porphyria, Prader- Willi syndrome, Turner’s
syndrome, Wolfram’s syndrome
Ketosis prone type 2
Diet/oral hypoglycaemic agents/
insulin
Tablets or insulin, depending on
genetic defect
Insulin- sensitizing agents and
insulin
Frequently insulin required
Treatment of underlying cause
Avoid
Variable
Variable
Box 19.9
Diabetes mellitus ≥7.0 or ≥11.1 ≥11.1 >48 [6.5] (if asymptomatic
Impaired glucose
tolerance (IGT)
Impaired fasting
glucose (IFG)
Presenting symptoms of diabetes
Many people with type 2 diabetes may be
asymptomatic at diagnosis, for example by routine
screening of blood or urine, when there may be
only mildly increased levels of hyperglycaemia.
Once diagnosed, however, many patients do admit
to some long- standing, often mild symptoms. Acute
metabolic decompensation, leading to marked
hyperglycaemia, occurs infrequently.
In contrast, type 1 diabetes is often abrupt in onset,
and characterized by severe hyperglycaemia with
World Health Organization criteria for diagnosis of diabetes mellitus
Fasting plasma
glucose (mmol/l)
<7.0 and Between 7.8 and
Between 6.1 and
6.9
and <7.8 –
2- hour plasma
glucose (mmol/l)
11.0
acute life- threatening decompensation (diabetic
ketoacidosis).
The cardinal symptoms of diabetes mellitus are
unintentional (effortless) weight loss, polyuria and
polydipsia, and their presence should always result
in an immediate test for blood glucose and urine for
ketones.
Polyuria, polydipsia and nocturia
Acute hyperglycaemia causes polyuria and
polydipsia. These presenting symptoms of diabetes
Random plasma
glucose (mmol/l)
– 42–47 [6.1–6.4]
Glycated haemoglobin
(mmol/mol (%))
should be repeated)
– pre- diabetes
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mellitus are also termed ‘osmotic symptoms’.
Raised plasma glucose leads to increased renal
tubular delivery of glucose, which then exceeds
the resorptive capacity of the renal tubule, leading
to glycosuria. Therefore, despite hyperglycaemia,
people with an increased renal threshold for glucose
may have no osmotic symptoms. Conversely,
people with a low renal threshold for glucose may
have glycosuria despite being normoglycaemic.
For this reason, glycosuria is an unreliable feature
in the diagnosis of diabetes mellitus. Nocturia is
also common in patients presenting with osmotic
symptoms of diabetes, and enquiry regarding the
frequency of passing urine at night can be helpful in
evaluating symptoms.
Weight loss and lethargy
Loss of more than 5% of total body weight should
be considered clinically important in a person not
deliberately attempting to lose weight. Weight loss
is a common presenting symptom in people with
type 1 diabetes and occasionally in type 2 diabetes
with marked hyperglycaemia. Loss of weight in
diabetes is predominantly caused by renal glucose
loss as a result of lack of insulin to enable cellular
uptake of glucose. The weight loss usually occurs
despite a normal appetite and dietary intake. This is
in contrast to the weight loss of malignant disease,
which is usually associated with reduced appetite
and oral intake.
Lethargy and fatigue are also common presenting
symptoms of diabetes mellitus, particularly type 2,
where the symptoms may have been present for
some time.
Skin problems
Dermatological manifestations of diabetes are
common at diagnosis, especially in patients with
poor glycaemic control. Skin infections, such as
staphylococcal infection leading to boils, carbuncles
or abscesses, which are often recurrent, may occur.
Severe infection itself can lead to hyperglycaemia,
and a new diagnosis of diabetes should be
reconsidered once the acute infection has cleared.
Oral and genital candidiasis can also be presenting
features of diabetes mellitus. The presence of the
characteristic white plaques on the tongue and
oropharynx in a previously healthy person not
on antibiotic therapy should alert the physician
to the possibility of diabetes mellitus, although
other conditions leading to immune paresis, such
as HIV infection or haematological malignancy,
can also lead to candidiasis. Genital candidiasis in
women leads to a thick white discharge and vaginal
soreness. Similarly, in men it can lead to a severe
balanitis (inflammation of the glans penis). Always
check the blood glucose in people with recurrent
candidiasis.
Visual disturbance
Hyperglycaemia can lead to blurred vision, owing to
osmotic changes within the aqueous humour of the
lens of the eye. This can also occur when chronic
hyperglycaemia is treated, causing further osmotic
shifts in the lens. The symptom usually settles once
normoglycaemia is achieved.
Other important aspects of a diabetic
history
Family history
A history of diabetes in first- degree relatives is a
potent risk factor for diabetes. Type 2 diabetes
appears to have a stronger genetic component than
type 1, with around a third of patients having a
positive family history compared with around 10%
of type 1 diabetic patients.
A family history of premature cardiovascular
disease is also important. Patients with diabetes
are at risk of cardiovascular disease, and this risk is
increased when there is a family history of vascular
disease in fathers or brothers aged less than 55 years,
or mothers or sisters aged less than 65.
Diet and lifestyle history
The cornerstone of management of diabetes is
lifestyle; accordingly, periodic reassessment is
important. Regularity of meals, the quality and
quantity of foods eaten and the frequency of snacks
should be known. Enquire about the following:
Regularity of meals: three meals a day is ideal.
Content of fatty/greasy foods: particularly
discourage saturated (animal) fats, as this type of
fat is linked to heart disease.
Content of fruit and vegetables: at least five
portions a day are recommended.
Content of sugar and sugary foods: avoid
carbonated drinks, cakes, sweets and biscuits.
Content of salt: a high salt intake can lead to
hypertension.
Alcohol intake: a maximum of two units of
alcohol per day is recommended.
The smoking history is of paramount importance;
smoking with diabetes is strongly linked to
cardiovascular disease. Occupational history may
be important, because if insulin therapy is required,
this may have an impact on legal requirements for
driving. Assess physical activity to ascertain whether
increased activity may improve glycaemia and
weight. At least 30 minutes of moderate exercise per
day, for example brisk walking, is recommended.
Assessment of other cardiovascular risk factors
Cardiovascular risk is greatly increased in people
with diabetes, and additional cardiovascular risk
factors multiply the risk. Thus, any history of
hypertension, hyperlipidaemia or previous vascular
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disease (cerebro- , cardio- or peripheral vascular)
should be noted. Take a full medication history,
including the use of antiplatelet, antihypertensive
and lipid- lowering drugs.
Home glucose testing
In a patient previously diagnosed with diabetes,
assess his self- monitoring of glucose. This will enable
a reasonable judgement of glycaemic control. Selfmonitoring can be done by home capillary blood
testing or by urine testing for glycosuria.
Insulin injections
In patients taking insulin, it is important to ascertain
whether the patient self- injects, the delivery device
used (disposable pen, cartridge pen or syringe/vial),
the sites chosen and whether they experience any
problems.
Symptoms of complications of diabetes
Chronic complications of diabetes mellitus can
be subdivided usefully into large blood vessels
(macrovascular), small blood vessels (microvascular)
and others (Box 19.10).
Symptoms of macrovascular disease
The features of ischaemic heart disease are described
elsewhere (see Chapter 13). People with diabetes have
fewer, less severe symptomatic chest pains, possibly
owing to autonomic neuropathy leading to reduced
deep pain sensation—so- called ‘silent ischaemia’.
Thus, the only symptom of ischaemic heart disease
in a diabetic patient may be breathlessness.
Peripheral vascular disease presents with
claudication. In addition, in patients with diabetes,
a combination of peripheral neuropathy and
peripheral vascular disease can lead to foot ulceration,
particularly at sites of pressure (Fig. 19.18).
Cerebrovascular disease in diabetic patients can
present with any stroke syndrome (see Chapter 16).
Transient ischaemic attacks are common.
Box 19.10
Macrovascular Coronary artery
Microvascular Retinopathy Non- proliferative
Other Dermatological Diabetic dermopathy
Chronic complications of diabetes
disease
Peripheral vascular
disease
Cerebrovascular
disease
(mild, moderate and
severe)
Proliferative
Maculopathy
Neuropathy Peripheral sensory
neuropathy
Autonomic
neuropathy
Mononeuropathy
Proximal motor
neuropathy
Nephropathy
Necrobiosis lipoidica
diabeticorum
Bullosis
diabeticorum
Granuloma annulare
Acanthosis nigricans
Rheumatological Diabetic
cheiroarthropathy
Flexor tendinopathy
Adhesive capsulitis
Diabetic
osteoarthropathy
Charcot
neuroarthropathy
Diffuse idiopathic
skeletal hyperostosis
Hepatic Non- alcoholic
steatohepatitis
Symptoms of microvascular disease
Diabetic retinopathy is frequently asymptomatic
until it causes significant visual loss, which may
be acute in onset (e.g. because of a sudden retinal
haemorrhage) or insidious (e.g. because of cataract
or maculopathy). Diabetic nephropathy is similarly
asymptomatic until renal dysfunction becomes
so severe that uraemia ensues (see Chapter 17).
Uraemic symptoms include fatigue, breathlessness
and tachypnoea, pleuritic chest pain owing to
pericarditis and pruritus. Heavy proteinuria may
lead to the development of a nephrotic syndrome.
In contrast, diabetic neuropathy can manifest
in a number of ways. Chronic peripheral sensory
Figure 19.18 Diabetic neuropathic ulcer in a patient with Charcot
neuroarthropathy.
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Figure 19.19 Diabetic amyotrophy. Note the marked wasting
of the thigh muscles (Source: Charles D. Forbes and William F.
Jackson. Color Atlas and Text of Clinical Medicine. 3 ed. Mosby Ltd.
2003.)
neuropathy is the most common form, affecting
around 5% of patients with diabetes. This can present
with symptoms varying from numbness, a feeling of
‘walking on cotton wool’ and paraesthesiae (pins and
needles) to burning, sharp and shooting pains. The
latter is a feature of selective involvement of small
pain fibres. Typically, the symptoms start distally
and spread up in a stocking distribution and are
characteristically worse at night, frequently leading
to insomnia.
Proximal motor neuropathy (diabetic amyotrophy
or femoral neuropathy) is uncommon, but is seen
predominantly in middle- aged men with type 2
diabetes. The condition is characterized by severe,
deep pain and paraesthesiae in the upper anterior
thigh, followed by weakness and wasting of the
quadriceps muscle (Fig. 19.19). The condition
is often unilateral, generally short- lived (around
3 months) and usually resolves spontaneously.
Associated weight loss and cachexia are common.
Mononeuropathies, particularly affecting the
median nerve of the hand (carpal tunnel syndrome;
see Chapter 16), are common in patients with
diabetes. This frequently presents with paraesthesiae
and numbness in the median nerve distribution of the
hand (lateral two- and- half digits) and is again worse
at night. Similar symptoms may occur in the foot
(tarsal tunnel syndrome). Cranial mononeuropathies
are rare, but palsies of cranial nerves III, VI and
VII are seen in patients with diabetes, leading to
blurred or double vision owing to ophthalmoplegia
or a lower motor neuron facial palsy (see Chapter
16). The pupillomotor fibres are usually spared in
diabetic third- nerve palsy.
Diabetes can cause autonomic neuropathy, the
symptoms of which can be very troublesome. They
include impotence, gustatory sweating (severe
facial sweating on tasting food), urinary retention
or incontinence, dizziness or syncope owing to
postural hypotension, constipation or diarrhoea (socalled diabetic diarrhoea) and recurrent nausea and
vomiting owing to diabetic gastroparesis.
Hypoglycaemia
Treatment of diabetes is aimed at reducing symptoms
and also the risk of diabetic complications. In
attempting to reduce hyperglycaemia using oral
hypoglycaemic tablets or insulin therapy, the patient
with diabetes is at risk of hypoglycaemia.
Physiological responses to hypoglycaemia start
at a plasma glucose of around 3.8 mmol/l, with
the release of counter- regulatory hormones such as
glucagon or adrenaline (epinephrine). Symptoms
of hypoglycaemia normally occur at around this
level because of sympathetic overactivation. Such
symptoms include sweating, palpitations, hunger,
agitation or blurred vision, and most patients
recognize them as hypoglycaemia and are able to
treat themselves rapidly. A further drop in plasma
glucose leads to neuroglycopenic symptoms, in
which cerebral glucose is low, leading to impaired
intellectual activity or diminished psychomotor
skills. Further drops in glucose levels can lead to
severe agitation, confusion, coma and epileptiform
seizures. The symptoms of hypoglycaemia can
be distressing and have a significant adverse
impact on quality of life. Loss of awareness of
hypoglycaemia is sometimes a problem in diabetic
patients with autonomic neuropathy; in insulintreated diabetes this can lead to unexpected
hypoglycaemia. Patients at risk should be warned
against driving motor vehicles and taught the early
symptoms of hypoglycaemia in order to raise their
awareness of this potentially serious complication of
therapy.
Examination of the diabetic patient
General assessment
Patients with diabetes can present with acute
metabolic decompensation, leading to diabetic
ketoacidosis (DKA), hyperosmolar hyperglycaemic
syndrome (HHS) or, in treated patients,
hypoglycaemia. Thus, it is mandatory for all patients
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