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ENDOCRINE DISEASE
Georgina Burke
Thyroid disease
The thyroid gland lies in the anterior midline of the neck below
the thyroid cartilage. It is buttery shaped, with two lobes and a
central isthmus. Its main function is to regulate metabolic rate
by production of thyroxine (T4), and triiodothyronine (T3). By
production of calcitonin it has a role in calcium homeostasis.
Over- or under-activity of the thyroid gland is the commonest
of all endocrine problems. Figure 6.1 shows the hypothalamic
pituitarythyroid feedback system.
Hypothyroidism
Under-activity of the thyroid gland may arise from disease
of the thyroid or secondary to pituitary disease (reduced
TSH drive). Causes of hypothyroidism are given in
box on next page.
Diagnosis
Diagnosis is made from thyroid function tests: free T4 level
is low; a high TSH conrms primary hypothyroidism.
Treatment
Treatment is
(thyroxine).
with
life-long
replacement
therapy
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Endocrine disease
Hypothalamus
TRH
Anterior pituitary
gland
T3
and
T4
TSH
Thyroid gland
T3 and T4 feed back on the pituitary and perhaps hypothalamus to reduce
thyroid releasing hormone (TRH) and thyroid stimulating hormone (TSH)
levels.
Fig. 6.1 The hypothalamicpituitarythyroid feedback system.
n CAUSES OF HYPOTHYROIDISM
Secondary
Hypopituitarism.
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Hyperthyroidism
Mental slowness
Deep voice
Goitre (defects of
hormone synthesis)
Cold intolerance
Anaemia
Bradycardia
Pulmonary
effusions
Weight gain
Dry skin
Constipation
Menorrhagia
Myxoedema
(accumulation of
mucopolysaccharide in
subcutaneous tissue)
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Endocrine disease
CAUSES OF HYPERTHYROIDISM
Graves disease
Solitary toxic nodule/adenoma
Toxic multinodular goitre
Rarer causes include: acute thyroiditis (viral/autoimmune/
post-irradiation) and drugs (e.g. amiodarone).
Hyperthyroidism
This is common, affecting 25% of all females with a sex ratio
of 5 : 1. Nearly all cases are caused by intrinsic thyroid
disease. Causes of hyperthyroidism are given in box
above. Figure 6.3 lists the clinical features of hyperthyroidism, while Figure 6.4 shows proptosis in Graves
disease.
Diagnosis
Diagnosis is made from thyroid function tests: serum TSH
is suppressed with a raised T3 or T4.
Treatment
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Hyperthyroidism
Exophthalmos
(Graves disease)
Heat intolerance
Palpitations
Irregularly
irregular pulse
(atrial
fibrillation)
Warm
vasodilated
peripheries
Goitre
Heart failure
Tremor
Weight loss
Proximal
myopathy
Pretibial
myxoedema
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Endocrine disease
Thyroid lumps
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Thyroid lumps
Clinical features
Most thyroid lumps are asymptomatic and detected by the
patient, dentist or doctor during a routine examination.
Rarely there may be pain, difculty in swallowing, the
feeling of a lump in the throat, stridor (difculty inhaling), symptoms of hyperthyroidism or hoarseness of the
voice. Differential diagnosis of thyroid nodules is given in
box below.
The thyroid gland develops from the foramen caecum at
the tongue base and descends to its nal position in the
neck during embryogenesis. Thus thyroid swellings may
be detected at any point along this course of descent.
The classic feature of thyroid swellings is that they move
on swallowing which should be checked for when examining any midline neck swelling.
Diffuse enlargement of the gland is most likely to be due
to thyroiditis in the UK. If there are multiple nodules this
is most likely to be a benign multinodular goitre. Single
nodules are more sinister, but the majority of these will
turn out to be benign in nature.
DIFFERENTIAL DIAGNOSIS OF
THYROID NODULES
Adenoma
Cyst
Carcinoma
Multinodular goitre
Hashimotos thyroiditis
Effect of previous operation or radioiodine therapy
Parathyroid cyst or adenoma
Thyroglossal cyst
Aneurysm
Laryngocele
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Endocrine disease
male
age <20 or >60
pain
xation to underlying muscles
hoarseness of the voice
cold nodule on scan.
Investigation
This is carried out by a combination of ne-needle aspiration cytology, ultrasound scan, thyroid function tests and
autoantibody detection.
Treatment
Asymptomatic benign nodules may just require close
observation. Toxic (thyroid hormone-producing) nodules
can be removed surgically or treated with radioiodine.
Non-toxic nodules which are symptomatic or suspected
malignant should be surgically removed. Thyroid cysts
can be aspirated. Thyroid surgery is usually carried out
through a necklace incision (see Fig. 6.5).
Figure 6.5 shows a scar resulting from thyroid surgery.
The dental relevance of thyroid nodules is shown in
the box.
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Hypoparathyroidism
Parathyroid disease
There are normally four parathyroid glands, one located at each
pole of the thyroid. They are central to calcium regulation.
Hypoparathyroidism
This condition is usually caused as a result of post-thyroid
surgery or as idiopathic/autoimmune cases although there
are rarer genetic causes (e.g. Di George syndrome). Clinical
features are related to the hypocalcaemia which causes
neuromuscular instability:
Chvostek sign: circumoral twitching secondary to
gentle tapping of the facial nerve
Trousseaus sign: carpal spasm when blood pressure
cuff is >20 mmHg higher than systolic blood pressure
Seizures
Laryngospasm and bronchospasm
Circumoral paraesthesia.
DENTAL RELEVANCE OF
HYPOPARATHYROIDISM
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Endocrine disease
Hyperparathyroidism
This condition has an incidence of 1 per 1000 and is more
common in females and in the fth decade. Eighty percent
of cases are due to a parathyroid adenoma; the majority of
the rest arise from parathyroid hyperplasia.
Hyperparathyroidism is usually asymptomatic but a
few patients have the classic bones, stones, groans and
abdominal moans symptoms related to hypercalcaemia.
Causes of hypercalcaemia are listed in box below, and the
clinical features of hyperparathyroidism are given in
Figure 6.6.
CAUSES OF HYPERCALCAEMIA
Primary hyperparathyroidism
Carcinoma
Abnormal vitamin D metabolism
Immobilisation
Other endocrine disorders
Drugs: e.g. thiazide diuretics
Renal disease.
DENTAL RELEVANCE OF
HYPERPARATHYROIDISM
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Hyperparathyroidism
Groans: malaise,
weakness and depression
Bones: salt-and-pepper
skull, bone cysts,
subperiosteal resorption
of the distal phalanges
Abdominal moans:
peptic ulceration
Renal stones
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Endocrine disease
Pituitary disease
Pituitary tumours are the commonest cause of pituitary
disease. As with most endocrine disease, problems may
arise due to excess hormone secretion, by local effects of
the tumour, or by inadequate hormone production by the
remaining normal pituitary (hypopituitarism). See box
below for size and frequency of pituitary tumours.
Level
Features
Gonadotrophin (LH
and FSH)
Prolactin
Growth hormone
TSH
ACTH
Large:
non-secreting (50%)
prolactinomas (25%)
Medium:
acromegaly (12%)
Small:
Acromegaly
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Hypopituitarism
Hypopituitarism
Deciency of hypothalamic releasing hormones or of pituitary trophic hormones can either be selective or multiple.
Panhypopituitarism refers to deciency of all anterior
pituitary hormones (see Table 6.1); it is most commonly
caused by pituitary tumours, surgery or radiotherapy.
Clinical features depend on the extent of deciency.
Rather than prolactin deciency, hyperprolactinaemia
occurs due to the loss of the normal inhibitory control by
dopamine.
Steroid and thyroid hormones are essential for life and
must be given as oral replacement drugs. Other hormones are replaced for symptomatic control.
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Endocrine disease
Adrenal disease
The adrenal gland produces steroid hormones (from the
cortex) and secretes catecholamines (from the medulla).
Three classes of steroid hormones are produced:
glucocorticoids (wide ranging effects on metabolism,
uid balance and the immune response)
mineralocorticoids (affect sodium and potassium
balance)
androgens.
Addisons disease
Primary hypoadrenalism due to destruction of the adrenal
cortex is rare. It usually occurs in females and is most often
caused by autoimmune disease (80%). Clinical features are
shown in Figure 6.8.
Diagnosis
Diagnosis is made by measuring plasma cortisol and/or
an ACTH stimulation test can be performed.
Treatment
Treatment is with long-term glucocorticoid and mineralocorticoid replacement.
Cushings syndrome
This condition arises from sustained over-production of
glucocorticoid (cortisol). It occurs most often following
therapeutic administration of exogenous steroids (e.g.
prednisolone). For clinical features see Figure 6.9.
Diagnosis
Diagnosis is made by conrming hypercortisolism (loss of
diurnal variation in cortisol or dexamethasone suppression test) and then localising the cause. For causes of this
syndrome see box below.
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Cushings syndrome
Buccal pigmentation
Dehydration
Postural hypotension
(dizziness on standing
up). Anorexia and
malaise
Weight loss
Pigmentation,
especially of
new scars
Pigmented
palmar
creases
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Endocrine disease
Depression/psychosis
Moon face
Plethora
Acne
Buffalo hump
Thin skin
Hypertension
Weight gain/
fluid retention
Bruising
Diabetes
Striae
Osteoporosis
Proximal myopathy
(muscle weakness)
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Phaeochromocytomas
Phaeochromocytomas
These are rare tumours of the adrenal medulla. Clinical
features are due to hypersecretion of catecholamines and
include hypertension (particularly episodic), headache,
sweating, cardiomyopathy and weight loss.
90% are benign tumours
90% arise in the adrenal medulla
90% are unilateral.
Diabetes mellitus
Diabetes mellitus is a syndrome characterised by high blood
glucose levels (hyperglycaemia) and deranged metabolism resulting from defects in insulin secretion and/or insulin action.
Epidemiology
Diabetes is a common problem and affects 1.8 million
people in the UK. Although the condition can affect
all ages, it is rare in infants and becomes more common
with age. For classication of diabetes mellitus see
box below.
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Endocrine disease
Aetiology
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Clinical features
The main features of diabetes are a direct consequence of
hyperglycaemia. The excess glucose in the blood is excreted
via the kidneys (glycosuria) which causes an osmotic
diuresis (polyuria) leading to dehydration and thirst (polydipsia) with subsequent weight loss.
Hypoglycaemia
Autonomic symptoms (sweating, palpitations,
shaking)
Neurological symptoms (confusion, seizures, coma)
Diabetic ketoacidosis (seen mainly in type 1 DM)
Hyperosmolar non-ketotic coma (seen mainly in type
2 DM).
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Endocrine disease
Diet control
Exercise
Frequent self-monitoring of blood glucose levels
Insulin and/or oral hypoglycaemic medications
Diagnosis and aggressive treatment of complications.
Treatment
Treatment involves a multidisciplinary approach. The
objective is to maintain blood glucose levels as close to
normal as possible in order to delay the onset or progression of complications. Management: box top of next page.
Type 1 diabetes is treated by injections of insulin; formulations of different durations are available.
Type 2 diabetes is usually treated with oral hypoglycaemic
drugs including sulphonylureas (stimulate insulin
secretion and increase insulin sensitivity) and biguanides
(increase insulin sensitivity only).
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