ENDOCRINE

Thyroid & Parathyroid

Dr. Hiwa Omer Ahmed
Assistant Professor in grneral Surgery
Thyroid
 Embryology

• The thyroid gland

develops from the median
bud of the pharynx (the
thyroglossal duct) which
passes from the foramen
caecum at the base of the
tongue to the isthmus of
the thyroid.
• Parafollicular cells (C-cells) are
derived from the neural crest and
reach the thyroid via the
ultimobranchial body
• The ultimobranchial body which
arises from a diverticulum of the
fourth pharyngeal pouch.
 Surgical anatomy
The normal gland weighs 20—
25 g.
The functioning unit is the
lobule supplied by a single
arteriole and consisting of
24—40 follicles which are
lined by cuboidal epithelium.
The resting follicle contains
colloid in which thyroglobulin
is stored.
• Some residual thyroid
tissue along the course of
the thyrogbossal tract is
not uncommon, and may
be lingual, cervical or
intrathoracic. Very rarely
the whole gland is
ectopic.
 Lingual thyroid
• at the foramen caecum and it
may represent the only thyroid
tissue present.
• It may cause dysphagia,
impairment of speech,
respiratory obstruction or
hemorrhage.
• It is best treated by full
replacement with thyroxine
when it should get smaller,
• but excision or ablation with
radioiodine is sometimes
necessary.
 Thyroglossalcyst
The common situations, in order of frequency, are
beneath the hyoid, in the region of the thyroid
cartilage, and above the hyoid bone. Such a cyst
occupies the midline, except in the region of the
thyroid cartilage, where the thyroglossal tract is
pushed to one side, usually to the left. It is to be
remembered that the swelling moves upwards
on protrusion of the tongue as well as on
swallowing because of the attachment of the
tract to the foramen caecum. A thyroglossal cyst
should be excised because infection is inevitable
 Thyroglossal fistula
• Thyroglossal flstula is
never congenital:
Characteristically the
fistula is drawn upwards
on protrusion of the
tongue.
• discharges mucus, and is
the seat of recurrent
attacks of inflammation.
• Treatment. Surgery
 Physiology
• Steps of thyroid hormone formation:
• •trapping of inorganic iodide from the blood;
• •oxidation of iodide to iodine;
• •binding of iodine with tyrosine to form iodotyrosines;
• •coupling of mono-iodotyrosines and di-iodotyrosines to
form 13 and T4
• when hormones are required the complex is resorbed
into the cell and thyroglobulin broken down; T3 and T4
are liberated and enter the blood where they are bound
to serum proteins: albumin and thyroxine binding
globulin (TBG) and prealbumin (TBPA). A small amount
of hormone remains free in the serum
 INVESTIGATION OF THYROID
• T3
• T4
• TSH
• Thyroid autoantibodies ,
against thyroid peroxidase and thyroglobulin
are useful in determining the cause of
thyroid dysfunction and swellings.
Titres of greater than 1:100 are considered
significant
 Isotope scan
• radiolabelled iodine (123I) or technetium-99m
(99”m’Tc,
• This test is inappropriate for distinguishing
benign from malignant lesions because the
majority (80 per cent) of cold swellings is benign
and some (5 per cent) functioning or warm
swellings will be malignant. Its principal value is
in the toxic patient with a nodule or nodularity of
the thyroid
HYPOTHYROIDISM
 Cretinism (foetal or infantile
hypothyroidism)
• Hypothyroidism occurs in I in 4000 live
births
1.Sporadic is due to complete or near
complete failure of thyroid development
• the parents and other children may be
perfectly normal.
2.In endemic areas, goitrous cretinism is
common, and is due to maternal and foetal
iodine deficiency.
Immediate diagnosis
and treatment with
thyroxine within a few
days of birth are
essential if physical and
mental development are
to be normal,

Women under treatment

with antithyroid drugs
may give birth to a
hypothyroid infant.
 Adult hypothyroidism
• The term myxoedema should be reserved for severe thyroid failure
and not applied to the much commoner mild thyroid deficiency.
• The signs of thyroid deficiency are:

• bradycardia;
• cold extremities;
• dry skin and hair;
• periorbital puffiness;
• hoarse voice;
• bradykinesis —slow movements;
• delayed relaxation phase of ankle jerks
• The symptoms are:
• • tiredness;
• • mental lethargy;
• • cold intolerance;
• • weight gain;
• • constipation;
• • menstrual disturbance;
• • carpal tunnel syndrome.
• Comparison of the facial appearance with a
previous photo-graph may be helpful.
 The signs
• The facial appearance) is typical, and
there isoften
1. supraclavicular puffiness,
2. a malar flush and a yellow tinge to the
skin.

Myxoedema coma occurs in neglected cases

and carries a high mortality; the body
temperature is low and the
patient must be warmed slowly:1 g of
intravenous hydrocortisone (in divided
doses) should be given daily, and
intravenous tri-iodothyronine in slowly
increasing doses
 The classic symptoms
• Severe progression of disease can result in
cardiovascular symptoms, including
hypertension,
• pericardial effusion,
• bradycardia, and
• pleural effusions.
• Abdominal distention with bowel edema and
constipation is a sign of severe hypothyroidism.
• Anemia may occur in 12% of cases.
 Aetiology
• In many underdeveloped countries, lack of
sufficient iodine intake explains a large
proportion of hypothyroid conditions.
• In more developed countries, most cases
of adult hypothyroidism are caused by
• Hashimoto's thyroiditis,
• radioactive iodine therapy
• surgical removal.
• antiarrhythmic drug amiodarone.
 Other rarer causes
• of hypothyroidism include
1.inherited defects in thyroid hormone synthesis,
2.congenital aberrant thyroid development can
occur in children, including thyroid agenesis and
thyroid hypoplasia.
3.Central nervous system abnormalities resulting
in either anterior pituitary gland disease or
hypothalamic disorders
4.Finally, peripheral tissue resistance to the action
of thyroid hormone, possibly through an altered
receptor mechanism, has been described
 Dx. & Rx.
• Thyroid function tests show low T4 and T3 levels
• high TSH
• High serum titres of antithyroid antibodies
• Treatment Oral thyroxine (0.10—0.20 mg) as a
single daily dose is curative.
• Caution is required in the elderly or those with
cardiac disease and the replacement dose is
then commenced at 0.05 mg daily and
cautiously increased.
• If a rapid response is required, tri-iodothyronine
(20 mg three times a day) may be used
THYROIDITIS
 Acute Suppurative Thyroiditis
• Acute suppurative thyroiditis is extremely
rare and usually the result of a severe
pyogenic infection of the upper airway.
The process results in severe localized
pain and is generally unilateral. Abscess
drainage followed by the administration of
antibiotics is effective, and long-term
deleterious effects on thyroid function
rarely result.
 Hashimoto's Thyroiditis
This leads to alterations in thyroid cell
function that impair T3 and T4 production.
These cellular reactions ultimately result in
infiltration of lymphocytes and resultant
fibrosis, which decreases the number and
efficiency of individual follicles.
Ultimately, a clinical hypothyroid state can
occur in patients with persistent TSH-
blocking antibodies
 Subacute Thyroiditis
• Subacute thyroiditis occurs predominantly in females (2:1)
• The mean age of patients is in the 40s in most series.
• The exact cause is not known,
• Patients have diffuse swelling in the cervical area and a sudden
increase in pain.
• Approximately two thirds of patients demonstrate fever, weight loss,
and severe fatigue.
• Fine-needle aspiration (FNA) can be diagnostic if it demonstrates
giant cells of an epithelioid foreign body type, which characterizes
the lesion.
• Treatment with corticosteroids or nonsteroidal anti-inflammatory
drugs is effective in relieving symptoms.
• However, the disease process generally continues, unaffected by
these medications.
 Riedel's thyroiditis (struma)
rare
characterized by a firm thyroid secondary to a chronic inflammatory
process involving the entire gland.
Symptoms of severe discomfort can occur and are due to extension
into the trachea, esophagus, and laryngeal nerve.
As a result, patients may have impending airway obstruction or
dysphagia. Unilateral involvement of symptoms may suggest a
malignancy and lead to surgical intervention.

• Treatment with thyroid hormone replacement is effective.

• Immediate tracheal or esophageal obstruction may require a
surgical approach to relieve symptoms. Only the constricting portion
of the thyroid is removed.
Hyperthyroidism
 Hyperthyroidism

• increased thyroid secretion result in a predictable

hypermetabolic state.
• primary alterations within the gland (Graves' disease,
toxic nodular goiter, toxic thyroid adenoma) or central
nervous system disorders and increased TSH-produced
stimulation of the thyroid. Most hyperthyroid states occur
because of primary malfunction.
• Even more unusual hyperthyroid states can result from
mismanaged exogenous thyroid ingestion, molar
pregnancy with increased release of human chorionic
gonadotropin, and unusually, thyroid malignancy with
overproduction of thyroid hormone.
 Graves' Disease

• Grave's disease is the most common

cause of hyperthyroidism (diffuse toxic
goiter).
• Women between the ages of 20 and 40
years are most commonly affected.
• The hyperthyroidism in Grave's disease is
caused by stimulatory autoantibodies to
TSH-R.
 Clinical Features
A patient with classic Graves' disease
usually has triad
1.a visibly enlarged neck mass
consistent with a goiter that may
demonstrate an audible bruit
secondary to increased vascular
flow.
2.Clinical thyrotoxicosis
3 exophthalmos
Hair loss, myxedema, gynecomastia,
and splenomegaly can accompany
the clinical findings. Tracheal
compression
 Clinical features
The symptoms are:

• • tiredness;
• • emotional lability;
• •heat intolerance;
• • weight loss;
• • excessive appetite;
• •palpitations.
 The signs of thyrotoxicosis are:
• tachycardia;
• hot, moist palms;
• exophthalmos;
•lid lag/retraction;
•agitation;
•thyroid goitre and bruit.
 The ocular consequences
• proptosis, supraorbital and infraorbital
swelling, and conjunctival swelling and
edema, can be severe.
• The ophthalmopathy is thought to be due
to stimulation of the overexpressed TSH-R
in the retro-orbital tissues of Grave's
patients
WYNE CRITERIA
 Dx
1.Thyroid Function test
• T3
• T4
• TSH
2.US
3.CT & MRI ?
Rx
1.Medical
a.betablockers
b. antithyroid
c.iodine
2. Radioisotope I131
3. Surgery; indicated
– obstructive goiter
– have a fear of radioactivit
– are noncompliant
– have had an adverse effect with antithyroid drugs
– pregnant patients or those with a suspicious nodule.
 PO complications
• Haematoma
• RLN Paralysis i3% mostly temp for 3 monthes
• Hypothyroidism <0.5%
• HypoparathyroidismRates of postprocedure
hypocalcemia are about 5%, and it resolves in
80% of cases in about 12 months
• Thyrotoxic crisis (storm) is an acute
exacerbation of hyperthyroidism
• Superir LN palsy
• The external branch can run closely adherent to
the superior thyroid artery, and care must be
exercised during dissection in this area. Injury to
the branch causes voice changes, huskiness,
poor volume voice fatigue, and inability to sing at
higher ranges
• RLN Palsy
A wide spectrum of injuries to the voice or
swallowing mechanisms, or to both, can occur
because of the mixed fibers contained within the
nerve.Temporary or permanent voice change
can result and is extremely distressing to the
patient.
 The hypermetabolic state
• of hyperthyroidism is clinically manifested as
sweating, weight loss, heat intolerance, and
thirst. Cardiovascular stress can be
demonstrated by high-output cardiac failure,
congestive heart failure with peripheral edema,
and arrhythmias such as ventricular tachycardia
or atrial fibrillation. Gastrointestinal signs may
include diarrhea and electrolyte wasting. The
menstrual cycle can be altered to the point of
amenorrhea. Psychiatric signs may include
altered sleep patterns, emotional mood swings,
fatigue, excitability, and agitation.
LECTURE 2
SOLITARY THYROID NODULE
 WORKUP AND DIAGNOSIS OF A
SOLITARY THYROID NODULE
• Management and the ultimate decision to proceed to
surgical intervention after detection of a solitary nodule
depend on the findings of a cost-effective workup and
the prognosis .
• The majority of patients with a solitary thyroid nodule will
have a benign lesion; however, thyroid cancer is a
definite possibility in all patients. Deciding between
conservative management or surgical therapy relies on
careful analysis of the clinical findings, assessment of
images, and interventional diagnostic methods
 Clinical Features

• Increasing numbers of thyroid nodules are being found

incidentally, possibly because of the increasing
availability and sophistication of imaging techniques. The
frequency of palpable and nonpalpable thyroid nodules
rises with age. Solitary palpable nodules are about four
times more prevalent in women than in men. Several
different disorders can cause a thyroid nodule. It is
important to exclude thyroid cancer in any clinical
setting. Rapid growth and signs of possible invasion,
such as pain or hoarseness, are most suggestive, but
not conclusive of malignancy
 On physical examination
• it is important to include thorough
palpation of the thyroid, as well as the
anterior and posterior cervical triangles.
Determining the size and consistency of
the nodule is important. Multiple nodules
or diffuse nodularity is associated with a
more benign diagnosis. A firm solitary
nodule, particularly in older men, is
suggestive of a malignant diagnosis.
 Diagnosis

• The workup of a patient with a solitary nodule begins

with a careful history and physical examination. Clinical
groups with the highest risk for malignancy in a thyroid
nodule are children, males, adults younger than 30 or
older than 60 years, and those exposed to radiation
therapy, especially during childhood. A careful history
includes any exposure to radiation, either through
occupational sources or through irradiation of the head
or neck, particularly in childhood. Additionally, a
thorough history of specific endocrine disorders,
including medullary carcinoma, MEN 2, or papillary
thyroid cancer (PTC), or a history of familial polyposis,
including Gardner's syndrome, is warranted.
 Radioisotope Scanning

• Whereas ultrasound allows anatomic evaluation, radionuclide scans

allow assessment of thyroid function.
• Technetium pertechnetate (99mTc) is taken up rapidly by the normal
activity of follicular cells. It is trapped by follicular cells, but not
organified. 99mTc has a short half-life and low radiation dose. Its
rapid absorption allows quick evaluation of increased uptake (so-
called hot) or hypofunctioning (so-called cold) areas of the thyroid.
Because screening with 99mTc shows uptake in the salivary glands
and major vascular structures, interpretation of thyroid pathology
requires a higher level of expertise.
• Malignancy has been shown to occur in 15% to 20% of cold nodules
and, additionally, in 5% to 9% of nodules with uptake that is warm or
hot, thus mandating a continued aggressive approach to clinically
suspicious nodules, even if they are not cold.
Tumors & MALIGNANCY
 Benign tumours

• Follicular adenomas present as clinically solitary nodules

and the distinction between a follicular carcinoma and an
adenoma can only be made by histological examination:
in the adenoma there is no invasion of the capsule or of
pericapsular blood vessels. Treatment is, therefore, by
wide excision —preferably a lobectomy. The remaining
thyroid tissue is normal so that prolonged follow up is
unnecessary. It is doubtful whether there is such an
entity as a papillaryadenoma and all papillary tumours
should be considered asmalignant even if encapsulated
 Malignant
• The vast majority of primary
growths is carcinomas .
Dunhill classified them
histologically as
differentiated and
undifferentiated: and the
differentiated carcinomas are
now subdivided into follicular
and papillary. Secondary
growths are rare but blood-
borne metastases occur
Blood borne metastases
more usually occur from
primary carcinomas of
breast, colon and kidney and
from melanomas.
 Aetiology

• Differentiated thyroid carcinoma, particularly

papillary, frequently follows accidental irradiation
of the thyroid in childhood7. The incidence of
follicular carcinoma is high in endemic goitrous
areas, possibly owing to TSH stimulation.
Malignant lymphomas can present in a patient
known to have autoimmune thyroiditis, so that
the lymphocytic infiltration in the autoimmune
process may be an aetiological factor. Indeed,
itis likely that all lymphomas of the thyroid arise
in glands affected by such thyroiditis
 Clinical features

• The annual incidence is about 3.7 per 100 000 of the popu-lation
and the sex ratio is three females to one male. The mortality should
only be of the order of 2—3 per cent. The commonest
presentingsymptom is a thyroid swelling (Fig. 44.36) and a 5-year
history is far from uncommon indifferentiated growths. Enlarged
cervical lymph nodes may be the presentation of papillary
carcinoma. Recurrent laryngeal nerve paralysis may be a presenting
feature of locally advanced disease.
• Anaplastic growths are usually hard, irregular and infiltrating. A
differentiated carcinoma may be suspiciously firm and irregular, but
is often indistinguishable from a benign swelling. Smallpapillary
tumours may be impalpable (occult carcinoma) — even when
lymphatic metastases are present (so-called lateral aberrant
thyroid). Pain, often referred to the ear, is frequent in infiltrating
growths.
 Diagnosis of thyroid neoplasms

• Diagnosis is obvious on clinical examination in most

cases of anaplastic carcinoma, although Riedel’s
thyroiditis (see later) is indistinguishable. The localised
forms of granulomatous thyroiditis and lymphadenoid
goitre may simulate carcinoma. It is not always easy to
exclude a carcinoma in a multinodular goitre, and solitary
nodules, particularly in the young male, are always
suspect. Failure to take up radio-iodine is characteristic
of almost all thyroid carcinomas [only very rarely will
differentiated carcinoma (primary or secondary) take up
1231in the presence of normal thyroid tissue], but occurs
also in degenerating nodules and all forms of thyroiditis.
Thyroid antibody titres are often raised in carcinoma.
 The role of FNAC
• in preoperative diagnosis has already been
discussed. No diagnostic test is absolutely
certain, and exploration with excision in the form
of lobec-tomy is essential when indoubt.
Incisional biopsy may cause seeding of cells and
local recurrence, and is most inadvisable ina
resectable carcinoma. In an anaplastic and
obviously irremovable carcinoma, however,
incisional or needle biopsy is justified.
• papillary
• follicular carcinoma
• Hurthle cell tumours
• Undifferentiated (ana plastic) carcinoma
• Lymphoma

• 2ndaries
 Surgical treatment

• There is continuing disagreement on the most

appropriate operation for differentiated thyroid
carcinoma. The con-servative approach
advocates lobectomy with isthmusectomy in
most patients with total thyroidectomy reserved
for specific indications (viz, those with bilateral
disease or judged to be in a high-risk category).
The more radical approach advocates routine
total thyroidectomy often as a staged procedure
depending on the pathological findings of the
initial lobectomy
 Additional measures

• Thyroxine. It is standard practice to prescribe

thyroxine in a dose of 0.1—0.2 mg daily, to
suppress endogenous TSH production, for all
patients after operation for differentiated thyroid
carcinoma on the basis that some tumours are
TSH dependent. Suppression of the TSH level
should be con-firmed by measurement. Failure
of suppression to a level of <0.1 i.t/litre may
indicate an inadequate dose of thyroxine or
more usually that the patient is noncompliant.
 Radioiodine
• If metastases take up radioiodine they
may be detected by scanning and may be
treated with large doses of radioiodine. For
effective scanning, all thyroid tissue must
have been ablated by either surgery or
preliminary radioiodine and the patient
must be hypothyroid to improve uptake
 Medullary Carcinoma

• MCT accounts for 5% to 10% of thyroid cancers. The

malignancy involves the parafollicular cell, or C cell,
derived from the neural crest. MCT is associated with the
secretion of a biologic marker, calcitonin. Excess
secretion of calcitonin has been demonstrated to be an
effective marker for the presence of MCT. Calcitonin
excess is not associated with hypocalcemia.
• Medullary carcinoma can occur in a sporadic form or as
part of MEN 2A or 2B. The MEN syndromes are covered
in more detail in Chapter 40 . MEN 2A usually has a
more favorable long-term outcome than MEN 2B or
sporadic MCT does
 Clinical Features

• A patient with a sporadic medullary carcinoma may have either of

two manifestations: a palpable mass for which a diagnosis can be
made with FNA or the finding of an elevated calcitonin level. In
sporadic MCT, the tumors are usually single and have no familial
predisposition. The presence of both a mass and an elevated
calcitonin level is virtually diagnostic of MCT, whereas the finding of
an elevated basal calcitonin level in the absence of a thyroid mass
might require further workup, including repeat basal calcitonin
measurement and a calcium-stimulated or gastrin-stimulated test.
Family members of patients with MEN 2 ideally are screened for the
RET proto-oncogene. The workup of these patients includes a
detailed and in-depth family history to inquire about the
characteristics of MEN 2 in the patient and family members ( Fig.
36-19 ). If MCT is suspected, serum calcium and urinary
catecholamines must be determined to evaluate for
hyperparathyroidism and possible pheochromocytoma
 Treatment
•
• The surgical approach to sporadic medullary carcinoma
involves at least total thyroidectomy with or without
central lymph node dissection. Total thyroidectomy
allows complete removal of the gland and a search for
multicentricity. In sporadic MCT, the lesion is generally
contained within one lobe, whereas in MEN 2, the
malignancy involves the upper halves of both lobes.
Dissection of the central lymph node compartment
allows appropriate staging of this process. Any palpable
lymph nodes in lateral areas require a modified radical
neck dissection.
Parathyroid
 Parathyroid glands

Anatomy
• The parathyroid glands, four in number, are small, oval in shape,
commonly about 0.5 cm in size, soft, mobile, yellowish brown in
colour and arranged in pairs — most often closely applied to the
thyroid gland, either within or closely applied to its capsule. The
upper pair is more constant in position than the lower: 80 per cent
are found on the posterolateral aspect of the thyroid, immediately
above the termination of the inferior thyroid artery, close to the
cricothyroid articulation. Most of the remaining 20 per cent are
posterolateral to the upper pole of the thyroid lobe. The lower pair is
more variable in position: 40 per cent are found at the lower pole of
the thyroid and 40 per cent are within the thymic tongue (Fig. 45.1).
The remaining 20 per cent are variable in site, most often some
distance lateral to the thyroid, and less often in the mediastinal
thymus a few centimeters below the sternal notch or, very
occasionally, ectopicallv situated near the carotid sheath, sometimes
as high as the carotid bifurcation.
 Physiology
• The chief cells of the parathyroids produce parathormone, the hormone being
released directly into the bloodstream. The circulating level of parathormone can be
measured by radioimmuno-assay, which is sufficiently reliable to distinguish between
high and low levels. Facilities for obtaining the estimation are widely available.
• Parathormone:
• •stimulates osteoclastic activity, thereby increasing bone resorption by mobilizing
calcium and phosphate;
• •increases the reabsorption of calcium by the renal tubules, thus reducing the urinary
excretion of calcium;
• •augments the absorption of calcium from the gut;
• •reduces the renal tubular reabsorption of phosphate, thus promoting phosphaturia.
• Parathyroid hormone is an 84 amino acid peptide which has a short half-life before
degradation into amino-terminal and carboxy-terminal fragments, with the amino-
terminal fragment having biological activity. The amino-terminal fragment retains
biological activity with a half-life of minutes and the carboxy-terminal fragment a half-
life of hours. Available assays measure either the intact hormone, the amino- or
carboxy-terminal or ‘mid-portion’ fragments.
• Calcitonin(Copp) is secreted by the parafollicular cells of the thyroid (thyrocalcitonin).
It lowers the serum calcium and affects calcium storage in bones; quite the opposite
action of parathormone.
 Parathyroid hormone-related protein
(PTH-rP)
• is a hypercalcaemic factor with similar
bioactivity to that of parathyroid hormone.
Since its isolation from cancer cell lines
and carcinoma of the breast, strong
evidence has emerged that it is an
important hormonal mediator of cancer-
associated hypercalcaemia in patients with
solid tumours. Plasma PTH-rP 1—86
concentrations may be measured by a
two-site immunoradiometric assay.
 Hypoparathyroidism

• Parathyroid tetany, due to hypocalcaemia, is a rare com-plication of

subtotal thyroidectomy (less than 1 per cent) but a more common
complication of total thyroidectomy. At these operations, some of the
parathyroid glands may be removed or have their blood supply
temporarily embar-rassed. It may also occur after surgery to the
parathyroids themselves. Symptoms usually appear on the second
or third postoperative day, and are temporary. Milder forms of
hypoparathyroidism have been described in the follow-up of
thyroidectomised patients. Permanent hypoparathyroidism, most
commonly encountered following radical thyroidectomy for cancer,
requires constant supervision and treatment. Tetany in the newborn
may occur within the first few days of life in the child born of a
mother with undiagnosed hypoparathyroidism.
• Spontaneous hypoparathyroidism is an unusual form of autoimmune
disease.
 Clinical features

• The first symptoms are tingling and numbness in the face, fingers
and toes. In extreme cases, cramps in the hands and feet are very
painful; the extended fingers are flexed at their
metacarpophalangeal joints, with the thumb strongly adducted (Fig.
45.3); the toes are plantar-flexed and the ankle joints extended —
the so-called carpopedal spasm. Spasm of the muscles of
respiration results in not only pain and stridor, but also dread of
suffocation. In infancy, the symptoms of tetany may be mistaken for
epilepsy, although there is no loss of consciousness.
• Latent tetany may be demonstrated by the following.
• • Chvostek’s sign. Tapping over the branches of the facial nerve at
the angle of the jaw will produce twitching at the corner of the
mouth, the ala of the nose and the eyelids.
• • Trousseau’s sign. A sphygmomanometer cuff applied to the arm
and inflated above the systolic blood pressure for not more than 2
minutes will produce carpal spasm.
 Treatment

• In acute cases the symptoms may be relieved speedily

by the slow intravenous injection of 10—20 ml of a 10
per cent solution of calcium gluconate. This may be
repeated until the patient’s circulating calcium level has
been stabilised. For longer-term management, the
absorption of calcium is enhanced by oral administration
of the most active metabolite of vitamin D — 1,25-
dihydroxycholecalciferol [1,25(OH)2D3]. Its major action
is on the gut, promoting active absorption of calcium and
phosphorus, raising calcium levels to normal within a
week. Magnesium supplements may occasionally be
needed. Serum calcium levels must be estimated daily
and the dosage adjusted as appropriate.
•
 Hyperparathyroidism

• Hyperparathyroidism is a more common

condition than had been previously believed
• •The symptomatic presentation may vary but the
increased use of auto analysers has resulted in
‘asymptomatic’ hypercalcaemic patients being
the largest group.
• A corrected serum calcium concentration above
the upper limit of normal and a simultaneous
elevation of serum parathyroid hormone level
are mandatory for the diagnosis.
• •
• Surgery should only be performed by an
experienced parathyroid surgeon.
• Long-term follow-up is essential as there is a
significant increase in risk of death from
cardiovascular disease. Hyperparathyroidism is
associated with an increased secretion of
parathyroid hormone. This occurs in:
• •Primary hyperparathyroidism, which is an un
stimulated and inappropriately high parathyroid
hormone secretion for the concentration of
plasma ionised calcium, and is due to adenoma
or hyperplasia, and very rarely carcinoma.
• A single adenoma is the commonest finding
(multiple in 6 per cent). The whole gland is
usually considerably enlarged, darker in colour,
firmer and more vascular than normal; in some a
rim of normal parathyroid tissue may be seen
surrounding the adenoma. The histological
appearances are the same as in hyperplasia,
with a predominance of chief and water-clear
cells. Carcinoma of the parathyroids is extremely
rare, less than 1 per cent. It tends to invade
locally and recur after operation. Blood-borne
metastases have been described.
 others
• Secondary hyperparathyroidism is associated
with chronic renal failure or malabsorption
syndromes. The stimulus for the hyperplasia is
chronic hypocalcaemia. All four glands are
involved.
• •Tertiary hyperparathyroidism is a further stage
in the development of reactive hyperplasia
where autonomy occurs as the parathyroids no
longer respond to physiological stimuli
 Cinical features

• Hyperparathyroidism, rarely found in the first decade of life, is

commoner in women than men, and most commonly found between
the ages of 20 and 60 years. The clinical features vary enormously,
even when the biochemical changes are similar.
• Asymptomatic cases
• The most common presentation is the detection of unsuspected and
asymptomatic hypercalcaemia by routine biochemical screening.
• Bones, stones, abdominal groans and psychic moans’
• Only 50 per cent of patients suffer from any of these.
• Nonspecific symptoms
• Nonspecific symptoms include muscle weakness, thirst, polyuria,
anorexia and weight loss — a challenge to the astute clinician!
 Bones Stones
Moans & Groans
Bone disease
• There may be generalised decalcification of the
skeleton, as in osteitis fibrosa cystica (von
Recklinghausen’s disease), single or multiple
cysts, or pseudotumours of any bone. The latter
are particularly common in the jaw bones. Early
radiological changes first appear in the skull and
in the phalanges (Fig. 45.4),with loss of density
and subperiosteal erosions. Many patients
presenting with vague pains in the bones and
joints are mistakenly diagnosed as rheumatic
 Renal stones
• Hyperparathyroidism must be considered
in every patient presenting with renal tract
stone or nephrocalcinosis (Fig. 45.5),and
even in those cases of renal colic where
no stone can be demonstrated
 Dyspeptic cases
• Patients with nausea, vomiting and
anorexia are relatively common. Peptic
ulcer and pancreatitis are not infrequently
found in association with
hyperparathyroidism, but the relationship
is not as yet fully understood.
 Psychiatric cases
• Psychiatric cases are not uncommon;
women, complaining of tiredness,
listlessness and with obvious personality
changes, are often wrongly labelled
‘neurotic’ or ‘menopausal’. Patients have
been admitted to mental institutions
because of irrational behaviour.
 Acute hyperparathyroidism

• This diagnosis is difficult and only too often made after

death. Nausea and abdominal pain is followed by severe
vomiting, dehydration, oliguria and finally coma. The
serum calcium is very high.
• Treatment is urgent after rehydration, which is vital.
Biphosphonates (disodium etidronate and pamidronate)
are specific inhibitors of bone resorption.
• They are highly effective given parenterally and may also
be used in the preoperative, short-term medical
management of severe hypercalcaemia in primary
hyperparathyroidism.
 Finding
• Corneal calcification
• Less common is band keratopathy in which a
transverse band of calcification forms across the
front of the cornea, and conjunctival
• Hypertension may be present in up to 50 per
cent of cases.
• There may be electrocardiographic changes with
a shortened QT interval, primarily by an effect on
the length of the S—T segment.
• A parathyroid adenoma is very seldom palpable in the neck.
• The diagnosis is confirmed with the following biochemical findings:
• •elevation of serum calcium (upper limit of normal 2.6 mmol/litre).
• corrected serum calcium (mmol/litre) = measured serum Ca
(mmol/litre) + (40 —A) x 0.02, where A = serum albumin (g/litre);
• •diminution of serum phosphorus (lower limit of normal 0.8
mmol/litre);
• •increased excretion of calcium in the urine (upper limit of normal 62
mmol per 24 hours for females, 75 mmol for males);
• •elevation of the serum alkaline phosphatase in cases with bone
disease;
• •elevation of serum parathormone concentration.
 The simplest localisation test
• is an ultrasonic scan but results vary according to the skill and
experience of the investigator.
• • Computerised tomography is of most value in localising a lesion
in the mediastinum rather than the neck.
• •Thallium—technetium isotope subtraction imaging may locate up to
90 per cent of parathyroid adenomas before surgery (Fig. 45.6).Like
ultrasonography, subtraction scintigraphy is more accurate the
larger the adenoma, and is inaccurate in parathyroid hyperplasia.
• •MRI is improving rapidly with some centres reporting up to 64 per
cent detection prospectively. A low signal is obtained from the
parathyroid glands on a T1-weighted image while a T2-weighted
image appears in early studies to produce good contrast resolution
from the surrounding tissues.
• •Invasive techniques such as selective angiography and selective
venous sampling may be helpful in locating an abnormally situated
gland after a failed initial exploration.
 Differential diagnosis
• Other causes of hypercalcaemia must be remembered and
excluded. They are:
• •secondary cancer in bone (breast, prostate, bronchus, kidney and
thyroid);
• •carcinoma with endocrine secretion (bronchus, kidney and ovary);
• •multiple myeloma;
• •vitamin D intoxication;
• •sarcoidosis;
• •thyrotoxicosis;
• •immobilisation;
• •medication: thiazide diuretics, lithium.
• The differential diagnosis presents no problem if the parathormone
level is estimated. In none of the above-mentioned conditions will
parathormone be detectable in the blood.
 Treatment

• The only corrective treatment is surgical removal

of the overactive gland or glands. In
symptomatic patients, the indications for
operation are clearcut
• Preoperative treatment is not usually necessary
except in acute cases, when rapid correction of
dehydration and electrolyte imbalance is
necessary, with a careful daily check on the
serum calcium
 auto transplantation
• Parathyroid tissue can be successfully auto
transplanted into the arm, a useful technique to
avoid repeated potentially difficult explorations of
the neck. The indications are tertiary
hyperparathyroidism in patients undergoing
chronic renal dialysis, and recurrent
hyperparathyroidism. The technique is to excise
all of the parathyroid tissue from the neck and to
implant eight 1-mm3 fragments into a pocket in
the forearm muscle mass, marking the site with
nonabsorbable sutures.
 Parathyroid carcinoma

• Parathyroid carcinoma is a rare condition to be

considered when a high serum calcium is associated
with a palpable lump in the neck. At operation it has a
characteristic grey—white colour and is adherent
because of local invasion of adjacent soft tissue. The
best results are obtained by early recognition, avoiding
rupture of the tumour capsule, and aggressive surgical
management including ipsilateral thyroid lobectomy.
Surgical clips should be used to outline the tumour bed
for postoperative radiotherapy.
• Multiple endocrine neoplasia syndrome — APUD cells
• Always consider that a patient with hyperparathyroidism
may also have multiple endocrine adenomas.