Anatomy of thyroid gland

 Weight : 15 – 25 gm
 Shape : Butterfly , consisting of two lobes connected by an isthmus. The
 pyramidal lobe is projection extends up wards from left border of the
 isthmus
 Extension : - Upper pole which extends to the middle of thyroid cartilage .
 - Lower pole which extends to the 5th tracheal ring.
 Capsule : The thyroid gland has two capsules :
 True capsule from condensation of its connective tissue
 False capsule from pretracheal fascia.
 Relations :
 Anteriorly : Skin , SC. fat , platysma , deep cervical fascia,
 pretracheal muscles :-
 Omo hyoid muscle .
 Sterno hyoid muscle.
 Sterno thyroid muscle.
 Its lower poles is overlapped by sterno mastoid muscle.
 Posteriorly :
 Two tubes ( trachea , esophagus)
 Two cartilages ( thyroid , cricoid )
 Two muscles (Cricothyroid , inf. Constrictor of the pharynx)
 Two nerves ( recurrent – external laryngeal )
 Blood supply : It is high vascular organ
Arterial : 5
 Superior thyroid artery from external carotid artery
 Inferior thyroid artery from thyrocervical trunk of
subclavian artery.
 Thyrodima artery from innominate

Venous : 6
 Sup. thyroid vein
 
→
Drain into internal jugular vein.
 Middle thyroid vein

→

 Inferior thyroid vein Drains into innominate vein.

Nerves related to the gland :
1- The Superior laryngeal nerves.
2- The Recurrent laryngeal nerves.

1- The Superior laryngeal nerves :

(branch. of the vagus)
 Divides into two branches :

a) Internal laryngeal nerve, which pierces (with sup.

laryngeal art.) the thyrohyoid membrane to the
larynx.
It is sensory to larynx above the level of vocal cords
b) The external laryngeal nerve, which descends with
the sup. thyroid art.
 It is motor to the cricothyroid muscle.
2- The Recurrent laryngeal nerves : ( branches of vagi )
 In the early fetus the neck is divided into 6 branchial
arches each contains an aortic arch.
 the recurrent laryngeal nerve is the nerve of the 6th
branchial arch which gives rise to the developing
larynx.
 As the neck elongates and the heart descends, the
recurrent laryngeal nerves are dragged downward by
the descending aortic arches.
 On the Rt. side the 5th & 6th arches disappear
leaving the Rt. R.L.N. to hook around the 4th arch
=Rt. subclavian artery.
 On the Lt. side R.L.N. remains hooking around the
6th arch, which doesn`t disappear but forms the
ductus arterious which later gives ligamentum.
Arteriouses which is overlapped by the aortic arch.
So
 The Lt. one hooks around the aortic then
ascends
 The Rt. one hooks around the Rt. subclavian
art. then ascends.
 Both of them ascends in the trachea-esophageal
groove to enter larynx JUST behind the
suspensory ligament of berry ( anatomical
landmark for recurrent laryngeal nerve )
 The recurrent nerves are motor to all intrinsic
muscles of larynx and sensory to the larynx
below the level of vocal cords.
 Lymphatics : Into the near by deep cervical
lymph nodes
 Surgical important points

Thyroid gland is one of sites of occult carcinoma in the body
 The thyroid gland moves up and down during deglutition because it is
enclosed in the pretracheal fascia "false capsule""surgical capsule"which is
attached to the ligament of berry " suspensory ligament" which attached to
the tracheal and thyroid cartilage.
 The middle thyroid vein must be ligated first, as it`s easily ruptures
with massive hemorrhage which may be mask the surgical field.
 The Superior Thyroid Artery must be ligated within the gland to
avoid injury of superior laryngeal nerve which leads to :
- Choking : due to loss of sensation above level of vocal cords. (I.L.N)
- Loss of high pitched voice due to paralysis of erico-thyroid M. (E.L.N)
 The Inferior Thyroid Artery must be ligated away and lateral to the
gland to avoid injury of recurrent nerve and parathyroid glands
 The infrahyoid muscles must be divided ( in thyrodectomy for big or
malignant gland) near their upper end to avoid injury of its nerves which
comes from below ( from ansacervicalis)
 In Near Total Thyroidectomy we must leave post medial part of the
gland to avoid injury of parathyroid glands and recurrent nerves.
 In thyroidectomy we have to put a drain before closure of the skin to
avoid post operative hematoma.
 In unilateral recurrent nerve injury :
vocal cord on that side becomes motionless so
the voice is weak and hoarseness is usually
improve within weeks
 In bilateral recurrent injury :
Incomplete : Leads to adduction of cords and suffocation
so, tracheostomy must be done immediately.
Complete : Leads to aphonia as the cord lie mid way
between adduction and abduction in
cadaveric position.
 Complete removal or devascularization of the four
parathyroid glands leading to Tetany
 Development of thyroid gland
 The thyroid gland develops as a median
downgrowth of a column of cells from the
pharyngeal floor between the 1st and the 2nd
pharyngeal pouch (subsequently marked by
the foramen caecum of the tongue). The
canalized column becomes the thyroglossal
duct. The thyroglossal duct forms the
pyramidal lobe, the isthmus and most of
lateral lobes of the thyroid. Its remnant may
appear in adult as :
 Thyroglossal cyst or thyroglossal fistula or
ectopic thyroid.
 Thyroglossal Cyst
 It may occur at any site along the course of the thyroglossal duct.
It is considered to be one type of tubulodermoids. It may occur
above the hyoid bone (suprahyoid) but it is more commonly
found below it (infrahyoid).
 It has the following characters :
 Exactly in the middle line (in 25% of cases it may be shifted to one
side , usually to the left) - Shape → globular .

 - Surface → smooth .

 - Consistency → firm .
 Moves with deglutition and protrusion of the tongue.
 A fibrous band can usually be felt extending from the cyst
upwards towards the tongue.
 Attached to deep structures but not to the skin unless infection
has occurred.
 Treatment : Excision and dissection of the tract “Sistrunk’s
operation”. The thyroglossal cyst must be excised because
infection is inevitable due to fact that the wall contains nodules of
lymphatic tissue which communicate by lymphatics of lymph
nodes of the neck.
 Thyroglossal Fistula " Sinus"
 It is never congenital , always acquired due to infection or
incision of pre-existing cyst. It appears as a tiny opening in
the middle line of the neck discharging serous fluid or
purulent mucoid material. The opening moves up with
deglutition and protrusion of the tongue and becomes
inverted inward due to uneven rates of growth of the neck
as a whole and that of the thyroglossal tract. The tract can
be felt as a fibrous band extending upwards from the fistula.
It is adherent to hyoid bone and may even pass through it.
 Treatment : excision of the whole tract up to the base of the
tongue. In order to avoid the recurrence the middle portion
of hyoid bone must be excised.
 Multiple transverse incisions in the neck the first enclosing
the opening of the fistula and dissection proceeds upwards
as for as possible. Another incision may done following the
tract upwards “Sistrunk’s operation”. Unless the fistula is
completely removed recurrence is inevitable.
 Ectopic Thyroid
 Ectopic thyroid tissue may occur anywhere along the course of the
thyroglossal tact. The comment site is the point of origin of the
thyroid at the base of tongue or foramen cecum (lingual , cervical
intro thoracic)
 The lingual thyroid appears as a firm nodule dating from birth
and may increase in size during menstruation If it is big it may
interfere with swallowing , speaking and breathing. Ulceration
and bleeding may be caused by trauma
 Treatment :excision , but , before excision one must be sure of
the presence of the normal thyroid in the neck thyroid tissue
present in the body this can be achieved by :
 Radio – active iodine uptake.
 Surgical exploration of the neck.
The lateral aberrant thyroid
 Thyroid tissue to be ectopic in nature but it is now
considered to be secondaries in the lymph gland from a
small papillferous cacinoma of the thyroid.

Retrosternal Goitre
A very few retrosternal goitres arise from ectopic thyroid T. but , most arise from
the lower pole of nodular goitre. If the neck is short and pretracheal muscles are
strong as in men , intrathoracil pressure tends to draw these nodules into superior
mediastinum.
The degree of descent :
Substernal type : when nodule is palpable.
plunging type : when intrathoracic goitre is forced into the neck by increased intra
thoracic pressure.
Intra thoracic type :
Clinical Features
It may be symptomless or produce severe obstructive symptoms :
 Dyspnea particularly at night / cough "brassy cough" which is spasmodic
with stridor.
 Engorgement of neck veins : in severe cases sup. veins on chest wall.
 Dysphagia rare (Recurrent N. paralysis)
 It also may be malignant or toxic.

Investigation
 X.Ray (AP and lat. View) : soft T. shadow in the sup. mediastinum ,sometimes with
calcification, Deviation or compression of trachea.
 I3 scan : may help to distinguish a retrosternal goitre from a mediastinal tumor.
Treatment : if obstructive symptoms are present, it is unwise to treat a retrosternal
goitre with anti-thyroid drugs or radio iodine as these may enlarge the goitre so
resection must done and carried out from the neck.
 Struma ovarii
 It is not ectopic , but port of an ovarian teratoma very rarely
carcinogenic change occurs or hyperthyroidism develops.
Cretinism
 It is a congenital deficiency of thyroid function which may
be associated with aplasia of the thyroid or with a goitrous
gland cretinoid goitre.
 Clinically
The child is sluggish , constipated, puffy face, thick lips ,
flattened nose, protruding tongue , short neck and thick
short hand (spade shaped hands). He rare cries , and learn
to suck , walk, talk and control of the sphincters much later
than normal.
In adolescence , the pat is dwarfed and mentally retarded
with dry wrinkled skin , supraclavicular pads of fat delayed
epiphyseal ossification and very low B.M.R.
 Treatment :
Thyroid extract should be given for life. In continued goitre
partial thyroidectomy is indicated to reduce the size of the
swelling.
 Goiters
"" guttur = throat
 definition : Any enlargement of thyroid gland
 clinical diagnoses : mass in the anatomical site of thyroid gland
and moves up and down with deglutition.
Physiology
 - The circulating inorganic iodine is picked up to the thyroid cells and
oxidation occurs by peroxidase enzyme forming oxidized iodine
 - This oxidized iodine bind to tyrosine forming mono and
di-iodotyrosine by the iodonase enzyme.
 - Coupling of mono iodotyrosine and di-iodotyrosine occurs forming
tri-iodotyrosine T3 and two molecules of di-iodotyrosine forming
tetra-iodotyrosine T4 which stored in the thyroid follicles .
 - When T3 and T4 are required ,the protease enzyme acted on
thyroglobulin to release the free T3 and T4 into the circulation .
 - The thyroid hormones in the blood are bound to serum protein (thyroid
binding globulin) and only very small part of it are free in the serum .
This free fraction of the thyroid hormones is the biological active part .
 - T3 is more rapid and more potent in its action than T4 .
Hormones of thyroid glands:
 Hormones secreted by the thyroid :
 Tetraiodothyronine (T4) or thyroxine.
 Tri-iodothyronine (T3)
 Thyrocalcitonine, which regulates calcium metabolism .
its increase leads to hypocalcemia and vice-versa.
 Hormones acting on the thyroid :
 Thyroid stimulating hormone (T.S.H). it is secreted by the
anterior pituitary to regulate the thyroid function. Its level rises
in cases of stress and according to a feed-back mechanism
whenever thyroid hormones (T3 and T4) are diminished T.S.H.
increase the vascularity of the gland.
 Long Acting Thyroid Stimulator (L.A.T.S). This is an Lg found
in 85% of cases of thyrotoxicosis and may be cause of
exophthalmos.
 Exophthalmos Producing Substance (E.P.S). This is supposed
to to produce infiltrative changes in the orbit in cases of
exophthalmos and its level drops after hypophysectomy.
CLASSIFICATION
OF
GOITRE
 Simple Goiter
 It is due to stimulation of thyroid gland by the anterior pituitary
i.e. by increased levels of circulating T.S.H. secretion is increased
by low levels of circulating thyroid hormones. Any factor ,
therefore that maintains a persistently low level of circulating
thyroid hormones can be responsible for a simple goitre. The most
important factor is iodine deficiency but , defects in hormone
synthesis may be responsible.
1. Iodine deficiency : one mg/kg/body wt/daily - Daily requirement
of iodine is about 100 – 125 mg. In endemic areas there is very low
iodide content in the water and food. The endemic areas are rocky
mountains , the alps and the Himalayas. In England it is found in
Mendips , Chilterns and Cotswolds. Endemic goitres is also found
in low land areas where the water supply comes from far away
mountain areas e.g. great lakes of North America , the Nile Valley
and the Congo although iodides in food and water may be
adequate , failure of intestinal absorption may produce iodine
deficiency .
2. Defects in synthesis of thyroid hormones.
 Enzyme deficiency within the thyroid gland.
 Goitrogens :
 Vegetables of the brassica family (cabbage , kale and
cauliflower) contains thiocynate.
 P.A.S / Anti thyroid / cyanides / cyanates sulphur
containing drugs.
 Iodides in large quantities are goitrogenic as they
inhibit the organic binding of iodine and give and
iodide goitre which is usually seen in asthmatics who
have taken proprietary preparations containing iodides
over a prolonged period.
 Genetic enzymatic deficiencies , the condition may
be associated with congenital hypothyroidism.
 Natural History of simple Goitre:
"stages of goitre formation "
 Persistent T.S.H stimulation causes diffuse hyperplasia all
lobules are composed of active follicles and iodine uptakes is
uniform. This is a diffuse hyperplastic goitre which may
persist for along time but , is reversible if T.S.H stimulation
stop.
 Later , as result of fluctuating T.S.H levels mixed pattern
develops with in area of active lobules and areas of inactive
lobules.
 Active lobules become more vascular and hyperplastic till
hemorrhage occurs causing central necrosis and leaving only
a surrounding rind of active follicles.
 Necrotic nodules coalesce to form nodules filled either with
iodine free colloid or a mass of new but inactive follicles.
Continual repetition of this process result in a nodular
goitre.
Clinical types of S.N.G :

1. Diffuse hyperplastic goitre.

2. Nodular goitre.
3. Solitary nodule.
4. Retrosternal goitre.
 1. Diffuse hyperplastic goitre
(physiological and colloid goitre)
The diffuse hyperplastic goiter corresponds to the first
stages of the natural history of simple goitre.
Physiological goitre :
It occurs usually in female during puberty, menstruation
and lactation where the metabolic demands are high. If
T.S.H stimulation stop , the goitre may regress but , tends
to recur later at times of stress such as pregnancy, the
gland is symmetrically enlarged soft , smooth surface , not
associated with general or local manifestation.
Cut section the gland is fleshy and pale , the cells lining
the acini are columnar with minimal colloid.
Treatment :
 Prophylactic : Iodized table salt
 Curative : - Reassurance of the patient and her parents
- L. thyroxin
 Colloid goitre :
Frequently seen between 15 – 30 years , marked
enlargement of gland with smooth surface , soft
consistency , rarely produces local pressure effects
by its size.
Microscopically :the acini are distended with
abundant colloid and lined with squamous cells.
Colloid goitre is a late stage of diffuse hyper plastic
type of goitre when T.S.H stimulation has fallen off
and when many follicles are inactive and full of
colloid.
Treatment :
- Early: L thyroxin
- Late : Subtotal thyroidectomy for huge goiter
 Nodular Goiter. 2
As regards to natural history of S.N.G , persist
fluctuating T.S.H stimulation results inevitably in
progressive nodule formation nodules are usually
multiple forming a multinodular goitre nodules may
be colloid or cellular and cystic degeneration and
hemorrhage are common , as is subsequent
calcification when epithelial hyperplasia is marked ,
it may be associated with hyperthyroidism and
condition is then referred to as 2ry toxic goitre. All
types of S.G are more common in the female than in
male.
Clinically : the gland is variable in its enlargement not
symmetrical , nodular surface , its consistency may
be firm , soft or cystic.
 Diagnosis of S.N.G : diagnosis of nodular
goiture is usually straightforward the pat is
euthyroid , nodules are palpable and often
visible , they are usually smooth , firm , not
hard painless moves with swallowing.
Investigation of S.N.G:
 Thyroid function test to exclude mild hyper
thyroidism.
 Estimation of titres of thyroid antibodies to
differentiate from lymphadenoid goitre.
 Plain X-Ray : may show calcification,
tracheal deviation or compression ,
pulmonary metastases, retrosternol goitre.
Complication of nodular goitre :
1. Toxic change : In long standing cases in about 30%.
2. Hage into cyst : This cause rapid distension of the cyst.
3. Malig. Change : In about 4 – 8 % cases commoner with
solitary type.
4. Calcification : Hard nodule.
5. Pressure effect : Dyspnea / dysphagia/ hoarseness of
voice.
6. Disfigurement : when it is big .
7. Tracheomalacia : Rare due to long standing goitre
pressing on trachea for long time ending into soft
trachea so after operation , collapsing occurs leading
to suffocation.
Indication for surgical removal of nodular goiter :
1. Suspicion of malignancy
2. Symptoms of pressure
3. Hyper thyrodism
4. Substernal extension
5. Cosmetic deformity
6. Solitary nodule that are cold on radio – iodine
scan and solid by ultrasound should be removed.
Non operative treatment is indicated in
Hashimoto’s disease
Prevention and treatment of simple goitre :
 All table salt should be iodised.
 In endemic areas , the incidence has been reduced by
this prophylaxis.
 In early stages a hyper plastic goitre is reversible if 1
thyroxine is given in maximum doses 0.3 mg daily for
several months and then very slowly reduction to 0.1
mg daily for many years. If regression does not occur .
 Thyroidectomy may be indicated for cosmetic reasons
or pressure symptoms.
 Nodular stage of S.G is irreversible so subtotal
thyroidectomy is indicated. The rule is to leave a
portion equal to one normal thyroid lobe , on each
side.
The problem of clinically solitary nodule and
its evaluation :
Clinically only one macroscopic nodule is
found , but microscopic changes will be
present throughout the gland. This is one form
of clinically solitary nodule which is referred
to as cystadenoma of the thyroid and its
commonest site is at junction of the isthmus
with one lobe , and although it appears
solitary multiple small adenomata are
scattered around it. When there is a solitary
nodule of thyroid it is must be differentiated
from true adenoma.
Causes of solitary nodule in thyroid:
1. solitary nodular goiter.
2. Toxic nodular goiter.
3. Malignant nodule (medullary adenoma)
4. True adenoma of thyroid.
Adenoma of thyroid may be :
 Embryonal adenoma
 Fetal or micro-follicular adenoma
 Colloid or macro-follicular adenoma
 Hurthle-cell adenoma with acidophilic cytoplasm
 Papillary cystadenoma highly suspicious of being malignant.
Diagnoses of solitary nodule in thyroid
1. Clinically
 Many cases are asymptomatic
 The solitary nodule in thyroid is more likely be malignant than
multi nodular goitre.
 A thyroid nodule is more likely to be cancer in man than in
woman.
 Patient with thyroid nodules who received X-Ray treatment to the
head and neck in infancy and childhood have 35 – 50 % chance of
having thyroid cancer.
 cystic lesions less than 10 Cm in diameter are almost never cancer.
 Toxic manifestation in toxic nodule
 Malignant features in malignant nodule
2. Investigations
A. Thyroid scan : is helpful in determining whether the lesion is single
or multiple and whether it is functioning (hot) or non functioning
(cold).
 Hot nodule = overactive nodule
Takes up isotope , while the surrounding tissue does not , here , the
surrounding. T. is inactive because the nodule is producing such high
levels of thyroid hormones that T.S.H is suppressed.
 Worm nodule = active nodule
Takes up isotope and so does normal surrounding tissue about it.
 Cold nodule = inactive nodule Takes up no isotope

D.D of cold nodule : degenerative cyst, calcification, haemorrhage,

abscess or hydatid cyst.
N.B.
The fluorescent scanning using a collimated source of radiation
is now used to differentiate benign from malignant thyroid
nodules. This procedure has advantage that no radio – active
materials are introduced into the body.
B. Ultrasound (echography)
• It is helpful to differentiate solitary from multiple
nodules
• It is also used for differentiating solid from cystic
lesions .
C. Biopsy
• FNAC or Trucut or Excisional biopsy.

N.B.
Percutaneous needle biopsy is helpful if good
endocrine cytologists are available , needle biopsy
should not performed in patients with history of
irradiation to the neck, because radiation – induced
tumors are often multi focal and –ve biopsy may
therefore be unreliable.
3. Treatment :
A. Enucleation : Removal of the nodule from its capsule.
But it is not recommended because recurrence
is the rule as the nodule is never solitary.
B. Resection Enucleation : Excision of the nodule with the
surrounding thyroid tissue.
It is the recommended operation as
we remove the scattered small nodules
around the clinical solitary nodule.
C. Hemithyroidectomy : Removal of the affected lobe together
with the isthmus and pyramidal lobe.
The specimen must be sent for biopsy.
It is the operation of choice.
N.B.
 The term thyrotoxicosis is retained because hyperthyroidism i.e.
symptoms due to a raised level of circulating thyroid hormones
are not responsible for all manifestations of the disease.
 Toxic Goitre
Clinical Types :
1. primary toxic goitre (Grave’s disease)
2. Toxic nodular goitre (2ry toxic)
3. Toxic nodule
4. Hyper thyrodism due to rare cases.

1. Primary Toxic Goitre : (Greave’s disease)

 It is a diffuse vascular goitre appearing at the same time as the hyper
thyroidism usually in the younger woman than man (8 times), and
frequently associated with eye signs.
 The onset is usually insidious with insomnia , irritability and wt loss.
Sometimes the onset is acute and the course may be progressive or
intermittent.
 The whole of the functioning thyroid tissue is
involved and the hypertrophy and hyperplasia are due to abnormal
thyroid stimulators such as L.A.T.S which is an immunoglobulin ,
found in 85% of cases of thyrotoxicosis.
 Grave`s disease is considered now an auto immune disease in which
antibodies binding to T.S.H receptors leading to release of thyroxine.
I. Pathology :
A. Gross appearance :
 The gland : is moderately enlarged , brick red in
colour and highly vascular, fleshy in consistency
with an opaque meaty appearance. In some cases no
enlargement is detected clinically and even at
operation the gland may not enlarged at all. The
enlargement is characteristically diffuse although
one lobe may be more affected than the other.
B. Microscopically :
 Marked hyperplasia of the cells , which become
arranged in several layers.
 Marked diminution of the lumen of the acini.
 Disappearance of the colloid from the lumen.
 Marked lymphocytic infiltration
II. Clinical Features :
 Thyrotoxicosis affects all the systems of the body starting
with excitation and ending with failure or depression
 Wayne’s clinical diagnostic index gives all the important
symptoms and signs of thyrotoxicosis and indicates by their score
the relative importance of each.
Cardinal signs of thyrotoxicasis are : E + 3T
1. Eye manifestation.
2. Tremors
3. Tachycardia.
4. Tumors
Cardinal symptoms of thyrotoxicasis are : HLP
1. Heat intolerance.
2. Loss of weight in-spite of good appetite.
3. Palpitation.
A) General Features
1. C.V.S
a) Dyspnea on exertion , palpitation , tachycardia are early features
b) Slight elevation of systolic pressure. with decrease of
diastolic pressure so that , the pulse pressure is increased. The
pulse is easily felt at the wrist (water hammer pulse).
c) Auricular fibrillation and heart failure may occur but , this is
more usual in 2ry toxic goitre.
2. C.N.S
a) Insomnia, occurs early in the course of the disease.
b) Irritability , anxiety and tremors of out stetted hands and
protruding tongue are common features.
c) In severe cases , mania may be present.
3. Metabolic disturbances :
a) Loss of weight in-spite of good appetite.
b) Sweating especially of the palms of hands , which feel worm.
c) Intolerance to heat the patient can tolerate cold weather well.
d) Flushing and feeling of hotness.
4. Gastro – intestinal :
 Polyphagia i.e. increased appetite, later there may be loss of appetite.
 Abdominal pains.
 Looseness of stools or even diarrhea.
5. Sexual system.
a) Menorrhagia, dysmenorrhea or amenorrhea.
b) In male , at first there is increase sexual desire, later the patient may
become impotent.
6. Muscle – skeletal system
a) Bone pains due to osteoporosis
b) Muscle weakness (thyrotoxic myopathy or myasthenia)
7. Urinary system
a) Polyuria
b) Glycosuria
8. Skin
a) Flushing
b) Abdominal pigmentation
c) Pretibial myxedema
 It is thickening of skin by a mucin – like deposit. It is
rare sign of thyrotoxicosis but may occur at any stage of
the disease it is usually follows thyroidectomy , Iodin
therapy or prolonged antithyroid treatment .
 It is usually associated with progressive exophthalmos.
 It starts as bilateral symmetrical pitting edema with red and
then deep purple colour.
 In severe cases , whole leg below its knee is involved
“thyroid acropachy”. Although it is resistant to treatment .
it tends to subside spontaneously.
B) Thyroid manifestation
 Moderately, symmetrical enlargement of thyroid gland
with smooth surface and firm or rubbery in consistency
associated with increased vascularity.
Evidence of increased vascularity :
1. Dilated vein on the skin
2. Hot sensation
3. Bruit may be felt
4. Murmur may be heard.
 Sometimes the enlargement is very small or no
enlargement at all, this type occurs in old patients
who present with weight loss and myasthenia over
a long period, the eye manifestation in that cases is
absent and the heart is mainly affected so it may be
pass into heart failure while the original causes are
over locked .
C) Eye Manifestation
Exopthalmos is commonly classified into 4 grades :
1. Mild : consists of widening of the palpepral fissure due to
retraction of the upper eyelids without any bulging of
the eyes.
Stellwag’s sign and Von Graefe’s sign are positive.
2. Moderate : due to actual bulging of eyeballs from increased
compositions of retrobulbar fat.
Darlymple and Joffroy’s signs are positive.
3. Severe : due to intra – orbital oedema and congestion ,
marked protrusion of the eye balls is associated with watering
of the eyes , dilatation of conjunctival vessels and muscle
paresis.
 Limitation of movement in an upwards and outwards
directions, also downwards and inwards directions must be
tested.
Moebius signs is positive
4. Malignant exophthalmos :
It is a progressive form , which may increased after
otherwise successful treatment of thyrotoxicosis
particularly by thyrodectomy increasing exophthalmos is
associated with chemosis of conjunctiva impairment of
corneal sensibility and paralysis of the eye muscles with
grave risks of corneal ulceration, panophthalmitis and loss
of vision.
Exophthalmos of graves disease is probably due to
infiltration of retrobulbar tissues with fluid and round
cells with varying degree of retraction or spasm of upper
eyelid the cause is unknown but it is not due to an increase
of T.S.H as it is not found in mxyedema where TSH is at
its highest level.
L.A.T.S or E.P.S may be responsible.
The condition is usually bilateral but unilateral may
occur in rare cases.
 Stellwag’s sign : infrequency of blinking with a
staring look.
 Von graefe’s sign : upper lid lays behind the eye
ball as the patient looks down without moving
the head.
 Dalrymple‘s sign : a rim of white sclera between
the upper eye lid and upper edge of cornea due to
retraction of upper lid and protrusion of the eye
ball.
 Joffroy’s sign : lack of wrinkling of the forehead
on looking upwards without moving the head.
 Moebius sign : imperfect convergence on looking
at a near object due to muscular paresis (medial
recti muscles)
 N.B.
Other causes of exophthalmos :
1. A space – occupying lesion in orbit.
2. Cavernous sinus thrombosis.
Treatment of exophthalmos :
I. Mild cases ( most common ) :
It is usually self limiting and may even regress
treatment of thyrotoxicosis will improve the eye signs.
lid retraction disappears in 2/3 of cases.
II. Severe cases ( rare ):
The proptosis can be measured with an exophthalmometer.
1. Protection of eye (wind – dust – sun)
2. Sleep sitting to decrease venous pressure.
3. Lateral tarsorrhaphy may be needed.
4. Prednisone with massive doses + metronidazole (flagyl)
5. Irradiation of retro orbital Tissue may be necessary.
• Pituitary :
irradiation
stalk section
cryo surgery
• Orbital decompression (trans-frontal and trans-antral)
 2. Secondary toxic goiter
 Here a simple nodular goitre is present for long time before the hyperthyroidism.
 In many cases of toxic nodular goitre ,the nodules are inactive and it is the
internodular thyroid tissue that is over active , here the hyperthyroidism is due to
abnormal thyroid stimulators such as L.A.T.S.
 In some toxic nodular goitre one or more nodules are overactive and here the

hyperthyroidism is due to autonomous thyroid tissue as in toxic nodule.

The 2ry toxic goitre differs from Grave’s diseases in the following :
 The thyroid gland is nodular either prior to toxic manifestation or nodularity and
toxicity started together.
 C.V. manifestations are prominent and nervous manifestation are less marked than
in Grave’s disease.
 Proptosis is usually absent.
 Medical treatment is less effective and has to be given for long periods to obtain a
response.
 Recurrence of symptoms after thyroidectomy : for 2ry toxic goitre is rare (1% or
less) where as in grave’s disease the incidence of recurrence is from 10 to 20
percent.
 Post operative myxedema is extremely rare in 2ry toxic goitre but it is frequent in
graves’s disease.
 2ry toxic goitre occurs in an older age group it is better treated surgically because
the other lines of treatment usually fail to control it.
 More ever the cardiac affection which is commonly associated with it responds to
surgical removal of the goitre.
 3. Toxic Nodule
It is solitary over active nodule (hot nodule)
4. Thyrotoxicosis due to other causes
1. Thyrotoxicosis fastitia
Patients whose given thyroxine as tonic.
2. Jod-basedow thyrotoxicosis
when large doses of iodide were given for an endemic goitre.
3. Neonatal thyrotoxicosis
It occurs in babies who were born from hyperthyroid mothers.
L.A.T.S titres in both mother and child will be high.
Hyperthyroidism manifestation will be gradually subsides in
3 or 4 weeks
 Investigations for thyrotoxicosis
1. Clinical diagnosis by Wayne Diagnostic Index.
2. Sleeping pulse.
3. Thyroid function tests
Sleeping pulse
It is very important in grading the severity of
thyrotoxicosis
80 – 90 Mild case
90 – 110 Moderate case
Above 110 Severe case
 Thyroid function tests
1. Measurements of thyroid hormone in serum
A. Serum protein bound iodine ( P.B.I. )
B. Total serum thyroxine ( T4 )
C. Total serum T3
D. Free serum T4
E. Thyroid index
2. Measurements of free binding sites for thyroid hormones
3. Uptake and discharge of radio active iodine
A. Radio active iodine uptake.
B. T3 resin uptake test .
C. T3 suppression test “ werner “.
D. Thyroid scanning.
E. Iodine clearance test.
4. Miscellaneous tests
A. B.M.R N. -10% to +15% of the standard
( 40 cal. / square meter / surface area / hour )
False results in : neurosis / pregnancy / fever.
B. Serum cholesterol : normal 150 – 250 mg%
It is decreased in thyrotoxicosis & Increased in
myxedema.
False result in : hypercholesteremia.
C. Serum creatinine : normal 0.6 mg/100 ml
It increased in thyrotoxicosis
False increase in renal failure.
D. E.C.G.
 Protein bound iodine P.B.I
 iodine containing hormones T3 and T4 are transported in the
plasma mainly by specific binding proteins (thyroxine
binding globulin) (T.B.G). As only a very small amount of T3
and T4 are free in the blood, The P.B.I effectively represents
total circulation Thyroid hormones.
 The euthyroid rang 4 – 8 Mg/100ml
False low results in :
 hereditary decrease of T.B.G
 Nephrotic syndrome.
False high results in:
 X-ray contrast media containing Iodine biligrafin
 Expectorants containing Iodine, Lugol’s Iodine
 Pregnancy
 Oral contraceptives
 Estrogen administration
 Early hepatitis
 Total serum T3 - free Serum T4
 Both measured by Radio - Immuno assay, and
are available in special laboratories, but, they will
eventually become routine tests, for the two
reasons
1- Some cases of hyper thyroidism are due to
excessive production of T3 without any
accompanying rise in level of serum P.B.I or total
serum T4
2- Free serum T4 ( which not protein bound) is far
more representative of the level of hormone
available to the individual thyroid cell than is the
total serum T4.
2- Measurement of free binding sites for thyroid hormones
in the blood :
 Radio active T3 is incubated with patient’s serum so that it
becomes fixed to any thyroid binding protein not already
carrying T3 or T4.
 The amount so fixed can be measured and from this can be
estimated the number of binding sites in the serum which are
un occupied.
 In the hyperthyroidism, the number of free binding sites is
low because a few are not already carrying hormone
 In hypothyroidism and myxedema, the number of free sites
are high.
 This is not accurate test in itself , but in conjunction with the
total serum T4 or serum P.B.I
 the free thyroxin index can be calculated from the formula:
 FTI = serum T4 or (B.P.I) × T3 uptake percent
 euthyroid range of FTI 2.5 – 7.0
3. Uptake and discharge of radio active iodine :
A. Radio active iodine uptake.
normal thyroid uptake is 15 – 55 % of the given dose in
thyrotoxicosis the uptake increase above 55% in
hypothyrodism it decrease below 10% technique.
1- No drugs or materials containing iodine are allowed for
the previous 3 weeks.
2- 5 Micro curies of radio active iodine are given by mouth
in a small amount of water or milk it is rapidly
absorbed from the small bowel into blood and the
thyroid and kidneys compete for it in hyper thyroidism
the thyroid uptake is rapid and little is excreted in the
urine.
3- After 24h the uptake is measured over the thyroid by
Geiger Muller Counter.
B- T3 Resin uptake test :
 By incubating iodine T3 (Radioactive T3) with
patient’s serum. Part of T3 is fixed by plasma
protein and the part which is not fixed is
precipitated by resin and estimated.
In the hyperthyroidism , the proteins are already
saturated with thyroxine and the resin uptake is
high
in the hypothyroidism the resin uptake is low.
This is another vitro test through which hazards
of irradiation are thus avoided.
C- T3 suppression test “Werner”.
 Goitre due to iodine deficiency in endemic areas
has a rapid radio active iodine uptake , but
simple goitre is under T.S.H control so that
uptake can be diminished by suppressing T.S.H
that is done by giving 40 Mg every 8 hourly for
7 days.
 In a toxic goitre 10 – 20 % reduction in uptake
by suppression whole in simple goitre 50 – 80%
reduction.
D- Thyroid scanning
scanning of thyroid after a tracer dose of radio
active iodine shows which parts of the gland are
functioning or functionless (Hot or Cold) : whilst
scanning is sometimes helpful in cases of thyroid
carcinoma its principle value is in the diagnosis of
toxic nodule either as solitary or as a part of toxic
multinodular goitre.
E- Iondine clearance test :
in thyrotoxicosis most of isotope is taken by
thyroid and there fore there is less excretion of
radio active iodine by the kidney. The normal
range of excretion in 48h is 30 – 70% of given dose
lower values are suggestive of thyrotoxicosis.
 D.D of thyrotoxicosis
 Anxiety.

 Neurosis.

 HT disease.

 Myasthenia.

 T.B.

 Pheochromocytoma.

 Menopausal syndrome

 Other causes of exophthalmos.

 How do you differentiate between psychoneurosis and
thyrotoxicosis ?
 Anorexia is an invariable presentation in
psychoneurosis while polyphagia is always present
in thyrotoxicosis taking notice ,
in both , there is loss of weight.
 Sleeping pulse normal in psychoneurosis.

 Although the hands show tremors and sweating in

both conditions , but the hand is hot in
thyrotoxicosis and cold in psychoneurosis.
 Thyroid function tests are normal in
psychoneurosis.
Treatment of Toxic Goitre
 1. Medical treatment
Indications :
 Mild cases.
 Thyrotoxicosis occuring during periods of
stress. As puberty , pregnancy and lactation.
Anti thyroid drugs are given in accurate does
and it is better to be on under dose side. They
are stopped one month before delivery and
lugol’s iodine given instead.
 Recurrent cases after operation specially 2nd
recurrence for fear of injuring the recurrent
laryngeal nerves. (Patient under 45y).
 Bad general conditions as HT failure.
 Progressive exophthalmos.
Aim of treatment :
Inhibit the function of the gland without destroying
it.
Advantages :
 No surgery.
 No use of radio active materials.

Disadvantages :
 The treatment is prolonged and the failure rate
after course of 1.5 or 2 years is at least 50 %
 It is impossible to predict which patient is
likely to go into a remission.
 Some goitres enlarge and become very vascular
during treatment leading to pressure symptoms
and making the surgery is difficult .
 Very rarely , there is a dangerous drug reaction
e.g. a granulocytosis (0.1 – 0,4%). The drug is
stopped if sore throat develops or white count
drops and the patient is given penicillin and
streptomycin as a guard against infection.
 Allergic manifestation as itching – vomiting
and rashes.
 Persistent tachycardia due to marked
vascularity this may mislead the physician to
increase the dose of anti thyroids to degree of
producing myxoedema. Thickening of vocal
cords and aedema of the glottis may occur and
may necessitate tracheostomy.
 Myxoedema.
Drugs used :

Thiouracil.
Methyl thiouracil 300 – 600 mg /day.
Propyl thiouracil 200 – 300 mg/day
Neomercazol 5 – 15 mg/T.D.S
Potassium Perchlorate 200 – 800
mg/day
 Scheme of treatment :
 The patient is given for one month if there is
improvement it is continued for up 3 months then the
dose is halved for another 3 months. After 6 months one
fourth of the original dose is given for another one year
on the whole the course takes about 1.5 year.
 It is most important to maintain high concentration of
the drug through out 24 h by spacing the doses at three
times daily.
 If there is no improvement after the first month , it is
better to shift to surgical treatment because further
medical treatment will be ineffective and will increase the
vascularity of the gland markedly so that the operation
will be very difficult.
The results of medical treatment :
50% of cases are cured completely.
50% of cases will go into relapse , these are
treated either by surgery or radio active iodine.
With anti-thyroid drugs, the following is
essential :
1. Rest physically and mentally
2. Sedation by luminal
3. Diet and fluids 3000 cal/daily
4. Inderal.
This measures make your mild cases without
any anti-thyroid drugs
 Radio active iodine. 2
Indications : recurrent cases after surgery (over
45y) bad risky cases due to age or disease.
 Aim of treatment its modification : radio iodine
destroys thyroid cell and as in thyroidectomy ,
reduces the mass of functioning thyroid tissue to
below a critical level.
Advantages :
 Safe , simple

 Less expensive than operation

 No prolonged drug therapy.

Disadvantages :
1. No reliable method of estimating the exact dose
2. Complication of irradiation to the working physicians.
3. Delayed action :
As its effect appears after 2 – 3 months , therefore if the
symptoms are severe anti thyroid drugs are given during
this period
4. Incidence of thyroid insufficiency may reach 75% after 10
years.
Contraindication :
 Patient below 40y because of its potential carcinogenic
effect (20y or more later).
 Pregnancy as it may lead to cretinism
 Lactation as it is excreted in milk.
Dose of radio iodine for treatment :
 4 – 8 millicuries according to the size of the
gland given in a small amount of water or
milk. The dose can be repeated once after
3 months.

N.B.
Microcurie = 1/1000,000 of curie
Millicurie = 1/1000 of curie
 3. Surgical treatment
Indications :
moderate and severe cases
 pressure symptoms
 2ry toxic goitre
 suspicion of malignancy
 failure of medical treatment or relapse after it
 retrosternal as medical treatment will increase the
size of gland and cause more pressure symptoms.
Advantage : rapid cure , low incidence of recurrence
Disadvantage :
 Recurrence of thyrotoxicosis in about 5% of cases.
 Complication of the operation.
Preoperative investigation :
1. Indirect laryngoscope
2. Thyroid anti body titres
3. x-ray chest ( retrosternal extension –
calcification deviation of trachea ).
4. Scanning
5. Complete rest physically and mentally
6. Sedation by luminal
7. Anti thyroid drug till B.M.R falls to normal
8. 15 days before operation anti thyroid
are stopped instead we give lugol’s iodine
10 drops T.D.S to vascularity and make the
gland tough.
Lugol`s Iodine = 5% iodine in 10% KIsolution
9. Inderal may be used as B. adrenergic
blockers for severe tachycardia .
 Subtotal Thyroidectomy
 Anaesthesia : general endo – tracheal
 Position : supine with sand bag behind the shoulders
to extent the neck
 Incision : kocher’s (collar) incision in one of the
lower creases of the neck it extends from the
posterior border of one sternomastoid to the post.
Border of the other.
 Incision divides the skin and superficial fascia
containing the platysma some prefer to divide the
platysma at a slightly higher level than the skin to
obtain a good scar
 mobilization of the skin flaps: The upper to the level
of upper border of thyroid cartilage and the lower to
level of manubrium.
 Anterior jugular veins are divided between
ligatures
 Opening the investing layer of deep fascia in
midline vertically.
 Incising the sheath of pretracheal fascia in the
midline
 As a rule the larger lobe is dealt with first.
 Separation or division of infrahyoid Ms.

In order to expose the thyroid the muscles are

divided in cases of :
A. Big nodular goitre.
B. Toxic goitre to minimize manipulation.
C. Malignant goitre.
 They are divided near their upper end as their
nerve supply comes from below (from
ansacervicalis)
Devascularization :
 Ligation of middle thyroid vein (easily rupture
with more bleeding) its division makes
mobilization of the gland easier.
 Ligation of sup. Thyroid artery and vein as near to
the gland as possible to avoid sup. Laryngeal n.
 Ligation of inf. Thyroid artery as far from the
gland as possible (away and laterally) to avoid the
recurrent laryngeal n.
 Legation of inf. Thyroid vein in front of trachea.
 Removal of required portion of gland leaving post
medial part to protect parathyroid and recurrent
nerves.
 In case of simple goitre , it is advisable to leave
about equal to normal lobe on each side but , in
toxic goitre there are general tendency to leave
very little thyroid tissue since the risk of recurrent
thyrotoxicosis is greater than that of myxaedema
the amount suggested is that which equals one
third of normal lobe.
 Closure leaving a drain on each side
reaching the depth of wound behind the
infrahyoid muscles.
 The platysma is closed with plain cat gut as
a separate layer in order to allow removal of
the stitches of skin early. Skin is closed with
interrupted silk suture or with metal clips.
 The stitches or clips are removed after 3 – 4
days.
What are indications of tracheastomy after
thyroidectomy ?
1. Post operative oedema of glottis.
2. Post operative deep haemorrhage beneath
pre-tracheal M and not relieved by re-
opening of the wound.
3. Bilateral injury of recurrent.
4. Tracheomalacia .
 Complications of thyroidectomy
Local complications :
1. Hemorrhage
2. Liquefying hematoma
3. Wound infection (uncommon)
4. Tracheitis
5. Phemothorax and mediastinal emphysema
6. Air embolism
7. Unsightly scar
8. Glottic oedema
9. Tracheal collapse
10. N. injuries :
 R. laryngeal n.
 Sup. Laryngeal n.
 Cervical sympathetics ( Horner’s syndrome).
Endocrine :
1. Tetany
2. Thyrotoxic crisis
3. Recurrent thyrotoxicosis
4. Progressive exophthalmos
5. Myxaedema
1. Tetany
- It is due to removal of all parathyroids
- It is rare but permanent.
- It is frequently due to scheme resulting from
ligation of all vessels of the thyroid and is
temporary because the parathyroids regain new
blood supply from the neighboring vessels
Treatment :
- Calcium gluconate 10 cc 10% daily until
improvement occurs.
- In permanent cases oral long therapy is given .
2. Thyroxic crisis
- It is due to flooding of the circulation with
thyroxin after operation.
- Usually in adequate preoperative preparation and
excessive manipulation during the operation are
the cause of this crisis
It is characterized by :
1. Marked irritability
2. Marked sweating.
3. Severe tachycardia.
4. Hyperthermia
5. Heart failure in neglected cases
Treatment :
1. Sedation : morphia
2. anti-pyretic : cold compresses and largactil
3. Glucose 5% I.V for increased metabolic rate
4. 5 c.c. Lugol`s iodine in one bottle of glucose I.V
5. A.C.T.H and cortisone may needed in severe
cases.
6. Anti thyroid drugs should be given in big doses
7. Inderal is given to control tachycardia
 Cancer thyroid
1. Precancerous conditions
2. Pathological types
3. Clinical features.
4. Investigations
5. Treatment
1. Precancerous conditions
1. Adenoma of the thyroid
2. Nodular goitre specially in endemic areas (solitary nodular is
more liable to undergo malig.) usually gives follicular type.
3. Previous irradiation of the neck in children (never in adult) of
enlarged thymus or T.B lymphadenitis usually gives papillary
type.
4. Genetic factors : sometimes medullary carcinoma run in
families.
5. Carcinoma of thyroid is extremely rare with toxic goitre.
 2. Pathological Types
Papillary adenocarcinoma 85%
- Occult.
- Intra-thyroidal.
- Extra-thyroidal.
 It is commonest type , met with any age , common
in children specially with previous irradiation of the
neck. It is usually has good prognosis. It is formed
of delicate branching C.T covered by one or several
layers of cuboidal cells small calcified areas , called
“Psammoma bodies” are seen and may help in
differentiation from benign.
It is characterized by :
1. Low grade malignancy.
2. Slow growth it may remain stationary with or
without metastases for many years.
3. Early lymphatic spread to deep cervical L.N.
4. The affected L.N reach a big size while the
primary is small “lat aberrant thyroid T.”
5. The papillary T. has a small or no radio-iodine
uptake.
Treatment :
 Total thyroidectomy with unilateral or
bilateral block dissection of Lymph Nodes.
 Thyroid extract is given post operatively in
big doses as replacement therapy to
suppress the T.S.H in trial to inhibit further
of the gland.
2. Follicular adenocarcinoma 10 %
 It is usually common in endemic nodular goitres met with any
age usually between 40 – 60 years. It forms grey , non
encapsulated mass with varying degree of differentiation. The
well differentiated type is usually referred as “malignant
adenoma” , and may remain without metastases for many years.
While , the undifferentiated tumors grow more rapidly in size ,
spread mainly by BI. But lymphatic is also common.
 The follicular tumors in which invasion is minimal are termed
“non-invasive” and those in which invasion is moderate or
marked are termed “invasive”.
 The follicular T. has a large radio-iodine uptake.

Treatment :
 Total thyroidectomy with block dissection.

In case of 2ryies scanning for it with radio active iodine.

 If active : radio active iodine ablation
 If inactive deep x-ray therapy.
3. Anaplastic Carcinoma 3%
 It usually occurs in old age group.
 It grows very rapidly to infiltrate the thyroid and the
surrounding T.
 two types are recognised : the small cell and giant cell
types.
 The small cell type may be mistaken for a
lymphosarcema , while the giant cell type simulate on
anaplastic fibrosarcoma.
 The tumor spreads rapidly by the blood and lymph and
kills the patient in a short time.
 It is of bad prognoses
90% of patient are dead within 1 year.
10 % of patient are dead within 3 years
Treatment
 Surgery has little or no place , but deep x-ray therapy
chemotherapy, tracheostomy may be needed.
4. Medullary Carcinoma 2 - 4%
 It is rare tumors , a rise from para-follicular cells “C”
cells which secrete calcitonin.
 The malignant cells contains amyloid.
 The tumors are solid , hard , not hormone dependent
and do not take up radio-iodine
 High level of serum calcitonin are produced by many
medullary carcinoma.
 Diarrhea is a feature of 30% of cases , this is may due to
5 HT produced by malignant cells.
 The tumors present usually in 50 – 70 age group but
there is younger group which presents in childhood or
before 30 years with family history and is associated
with hyperparathyroidism and pheochromocytoma , a
combination known as Sipple’s Syndrome.
 The prognosis depends upon the absence or presence
of L.N. metastases.
N.B.
 Multinodular goitre is a benign lesion it
causes post. Displacement of carotid
pulsation but , malignant goitre will lead to
compression and obliteration of it without
carotid displacement.
 3. Clinical features
1. Features Suspicious of malignancy : a solitary
nodule in the thyroid gland.
2. Features Suggestive of malignancy :
 Rapid growth in size.

 Hard consistency.

 Fixity.

 Pressure manifestations :

On recurrent : hoarseness of voice

Or trachea : dyspnea.
On esophagus: dysphagia
On carotid : absence of carotid pulsation ( Berry`s
sign )
  Pain indicate infiltration of nerves , especially
which referred to the ear which passes along
auricular branch of the vagus (Arnold’s nerve).
 Increased vascularity.

 Cold adenoma.

3. Features indicating Sure malignancy :

A. presence of 2ry metastases
B. positive biopsy and paraffin section. Open biopsy is not
recommended in anaplastic type for fear of fungation ,
needle biopsy here is better.
C. Absent carotid pulsation
D. Recent hoarseness of voice
 4. Investigations
 Plain x-ray of neck and chest
 Scanning
 Laryngoscopy
 Biopsy and paraffin section .
 X-ray of skull, chest, vertebra for 2ry which is
ostohytics.
 Ultrasonography.
 Aspiration biopsy cytology ( ABC)
now it is becoming more widely applied
 DNA content to distinguish between follicular
adenoma and follicular carcinoma.
 Thyroiditis
1. Acute thyroiditis (Rare) : it is rare , it may arise in
the course of infectious fevers e.g. scarlet fever and
typhoid and is commoner in goitrous than normal
glands. The gland becomes enlarged , hot and tender
with deep diffuse pain in the neck , often referred to
the ear , occiput or jaw.
 Treatment : antibiotics , local foments and drainage of
pus if suppuration occurs. (rare)
2. Subacute thyroiditis (De Quervain’s disease) :
it is a rare condition which as supposed to be caused by the
virus of mumps. Onset : acute with pain , fever , malaise and
sweating. The gland : slightly enlarged firm , tender.
Diagnosis depend upon :
 increased S.R

 normal leucocytic count

 absent thyroid antibodies.

 Not radio-iodine uptake by gland.

 increased serum gamma globulin.

 The disease is self limited and resolution occurs in few

months.
3. Lymphadenoid goitre “Hashimoto’s disease”
 It is auto immune disease , the patient is sensitized to
her own thyroglobulin. The result is destruction of
thyroid tissue and its replacement with lymphoid
tissue.
 It usually affects females at menopause

 The gland :
 Moderate enlargement.
 Rubbery in consistency.

 Lobulated not nodular.

 More defined border than nodular.

 Hypothyroidism is common and may end in

myxaedema.
Diagnosis depends on clinically and laboratory lest :
 increased serum gamma globulin fractions.
 increased titre of thyroid antibodies.

 +ve precipitation tests on the patient’s serum.

Treatment
 Full replacement therapy of T4 for life as
hypothyroidism is inevitable
 Excision is not advised due to high possibilities of
post operative myxoedema which is common.
 If there are pressure symptoms division of thyroid
isthmus is indicated.
 Subtotal is done for cosmetic disease rarely.

 Irradiation is contraindicated of it is sensitive.

 4. Reidel’s thyroiditis “Woddy thyroid”
 It is very rare condition of unknown etiology.
 The thyroid tissue is replaced by cellular fibrous tissue which
infiltrates through the capsule into adjacent muscles ,
para tracheal C.T and carotid sheath.
 Gland : enlarges with progressive induration , till it become
stony hard in consistency and fixed.
 Adhesion are extensive and pressure symptoms are frequent.
 It affects young adult of both sexes.
 Thyroid function remains normal.
 Serum P.B.I , radio – iodine uptake are normal.
 The D.D from anaplastic carcinoma can only be made by
biopsy.
Treatment :
1. division of isthmus is usually needed to relieve
the pressure on the trachea.
2. thyroidectomy is not possible as the gland is
marked adherent to neighboring structures.
3. radio therapy is ineffective.
What are the causes of diffuse enlargement of
thyroid ?
 Physiological goitre little enlargement and soft.

 Colloid goitre may huge , always elastic

 Primary thyrotoxicosis may be minimal and soft.

 Hashimoto’s disease very firm.

 Riedel’s diseases woody thyroid.

What are the causes of painful thyroid swellings ?
1. Subacute thyroiditis.
2. Hemorrhage in a cystadenoma.
3. Infiltrated malignant thyroid.