BENIGN DISEASES OF THYROID

HYPERTHYROIDISM
• Excess of circulating thyroid hormone
• THYROTOXICOSIS:-
• INCREASED HORMONE SYNTHESIS :-
1. Graves disease
2. Toxic multinodular goiter
3. Toxic adenoma
4. Drug induced – amiodarone, iodine
5. Thyroid cancer
6. Struma ovarii
7. Hydatidiform mole
8. TSH secreting pituitary tumours
• RELEASE OF PREFORMED HORMONE
1. Thyroiditis :- acute
sub acute
 GRAVES DISEASE
• Also known as diffuse toxic goiter , primary thyrotoxicosis ,
basedow’s disease
• m/c hyperthyroidism
• Autoimmune disease :- increased levels of specific
antibodies in blood thyriod stimulating antibody,
immunoglobulin, long acting thyroid stimulators
• It is associated with diabetes , addisons , pernicious anemia
,myasthenia gravis
• Predisposing factors :- post partum
iodine excess
lithium therapy
infections
• Characterized by :- tyrotoxicosis
diffuse goiter
ophthalmopathy
dermopathy
thyroid acropachy
gynecomastia
 Symptom of Hyper thyroidism
• Gastro – Intestinal:
a) wieght loss , increased appetite
b) Diarrhoea due to increased activity at ganglion level.

• Cardio-Vascular system:
a) Palpitation
b) Shortness of breath at rest and minimal exertion
c) Angina
d) Cardiac irregularities
e) Cardiac failure in elderly ( C.C.F )
• Neuromuscular system:
a) Undue fatigue and muscle weakness
b) Tremors

• GenitoUrinary system:
a) Oligomenorrhoea or Amenorrhoea
b) Occasional urinary frequency
• Dermotological
a) Hair loss
b) Puritis

• Psychiatric
a) Irritibility
b) Nervousness
c) Insomnia
 Sympathetic over activity causes
• It causes dyspnoea, palpitation, tiredness,
heat intolerance, sweating, nervousness,
increased appetite and decrease in weight.
• Because of the increased catabolism they have
increased appetite, decreased weight and so
also increased creatinine level which signifi es
myopathy
• Fine tremor is due to diffuse irritability of grey
matter.
 Signs of Hyperthyroidism:
• Eye signs: Common in primary thyrotoxicosis

• Increase in the bulk of orbital content with a rise in retrobulbar

pressure results in exophthalmos and optic nerve compression

• A) Von GRAEFES sign:- when the patient is asked to look down,

the upper lid lags behind.

• B)DALRYMPLE’S sign:- normally the upper sclera is not visible,

but where this sign is positive the upper sclera is visible because
of retraction of upper lids.

• C) JOFFROY’S sign :- when the patient is asked to look upwards ,

when the head fixed, absence of wrinkling on the fore head.
• D) MOEBIUS Sign; lack of convergence because of lymphatic infiltration
of inferior rectus muscle in primary throtoxicosis.

• E) STELLWAG’S Sign: Absence of normal blinking ‘STARING LOOK ’ first

sign to appear.

• F) ENROTH’S Sign: Edema of eye lids and conjunctiva

• G) ROSEN BACH’S Sign: Tremors of closed eye lids.

• h) Gifford’s sign; Difficulty in everting upper eye lid in primary toxic

goitre.

• I) NAFZIGER’S Sign: Patient is sitting position

and neck fully extended, protruded eye ball can be visualized when
observed from behind.
• ORDER OF APPEARANCE OF SIGNS:
1. Stellwag’s sign – In mild cases 1st to appear
2. Von grafe’s sign – Mild cases next
3. Joffroy’s sign – Moderate cases
4. Moebius sign – In severe cases.
 EXOPHTHALMOS

Def: Proptosis of the eye, caused by infiltration

of the retrobulbar tissue with fluid and round cells with
lid spasm of upper lid.

Levator palpebra superior muscle is innervated by

sympathetic fibers. -- over activity

Sclera can be seen clearly above the limbus of the eye.

Proptosis can be measured by ophthalmometer
 Severe exophthalmos. (Malignant)
• Eye lid edema, chemosis, conjunatival injection
Diplopia, ophthalmoplegia corneal ulceration.
Papilloedema.
Loss of vision.
It is called malignant
but the word is misnomer
but it is so, depending
in the severity and
progressive condition.

•
 Treatment of Exophalmos
• a) It improves with time -- but progressen of
b) sleeping propped up disease is not prevented
c) lateral tarsorrhaphy

d) massive doses of systemic steroids

e) systemic antibiotics
steroid drops
antibiotic drops
f) finally,orbital decompression
-- by injecting steroids intra orbitally
-- surgery
 Myopathy
• 1. Weakening of proximal muscle
2. Weakening will be more during
contraction.
3. Often it resembles myosthenia gravis
- once hyperthyrodism controlled
recovery is a must.
 Pretibial myxoedema
• It is a manifestation of primary thyrotoxicosis
a) symmetrical, shiny, red, thickened
skin with coarse hair,
• b) whole leg below the knee, with foot and
ankle involvement in severe cases.
•
c) It is due to deposition of myxoematous
tissue in skin and subcutanous tissues.
•
d) It may or may not regress after treatment
•
e) It is associated with exophthalmos with
high levels of thyroid stimulating antibodies.
•
f). Thyroid acropachy.
Clubbing of fingers and toes in primary thyrotoxicosis
 Thyroid Acropachy

• Thyroid acropachy is clubbing of fingers and

toes in primary
 OTHERCAUSES OF HYPERTHYRIDISM
• A) Thyrotoxicosis fictitia.
Drug induced, if more than normal requirement
of thyroxin is taken (0 -15 – 0.25 mg/day.)

• B) JOD - Basedow thyrotoxicosis

JOD – german for iodine - large doses of iodine
taken for hyperplastic endemic goitre –
hyperthyroidism
• C) Auto – Immune or dequervain thyroiditis
mild hyperthyroidism – due to liberation of
thyroid hormone from damaged tissue.

• D) Neonatal thyrotoxicosis - Thyroid

stimulating antibodies cross the placental
barrier from mother to child
– but subsides 3-4 weeks.
 Investigations
1. Thyroid profile
2. Radio isotope studies
3. ECG
4. T.C, DC, to be done before treatment as the
anti thyroid drugs produce severe
agranulocytosis.
 MANAGMENT
• Three methods of treatment:-
1. Antithyroid drugs
2. Surgical treatment
3. Radioactive iodine
 ANTITHYROID
• Carbimazole , methimazole , propylthiouracil
prevent binding of iodine to thyrosine by
interfering with TPO
• Propylthiouracil inhibits conversion of T4 to T3
100-300mg TID
• Carbimazole 10-30mg TID followed once daily
• Side effects :- skin rashes , agranulocytosis ,
aplastic anemia , vasculitis , polyarteritis
• Beta – blockers :- fast symptomatic
improvement
• Anxiety , palpitation , tremors
• Reduce conversion T4 to T3
• Propranlol 20-40mg 4times/day
• C.I : cardiac failure , asthma , diabetes
 Radio – active Isotopes
• The isotopes used are I- 131 –
B - rays half life period is 8 days
• I 131 dose is calculated after preliminary scan
generally 8-12 mci administrated orally
• Used :- older patients with moderate sized goiter
antithyroid / surgery C.I
relapsed after medical/ surgical therapy
• Contra indications : pregancy , breast feeding
young patients with thyroid nodule
ophthalmopathy
lack of acess for surgery
• Higher the intial dose of I 131 increase
incidence of hypothyroidism
 SURGICAL TREATMENT
• Goal :- complete and premenant control of graves with
minimal morbidity
• Indications:-
1. Confirmed cancer or suspicious thyroid nodule
2. Young
3. Desire to conceive
4. Have had severe reaction with antithyroid medication
5. Large goiter with compression symptoms
6. Smoker with moderate to severe ophthalmopathy
 HYPOTHYROIDISM
• Deficiency of circulating thyroid hormone
• Primary hypothyroidism – cause within
thyroid gland
• Secondary hypothyroidism – failure of TSH
production following pituitary or
hypothalamic disease
CAUSES
 CLINICAL FEATURES
• Gastrointestinal – decreased appetite
constipation
• cardiorespiratory – angina
bradycardia
hypertension
pericardial, pleural effusion
• Neuromuscular – delayed relaxation of tendon reflexes
(woltmans sign)
depression , psychosis
carpel tunnel syndrome
• Dermatological – myxoedema (non pitting
oedema ),
dry skin and hair
scanty eye brows
yellow tint to skin carotenemia
• Reproductive – menorrhagia
infertility
impotence
• Miscellaneous – tirdness
cold intolerance
weight gain
hoarseness of voice
 INVESTIGATIONS
• T4 – low and TSH – high
• Serum cholestrol and triglyceride levels –
raised
• Thyroid autoantibodies highest in hashimotos
thyroiditis ,graves , nodular goiter and thyroid
neoplasm
• ECG – flattening of Twave
TREATMENT
 THYRODITIS
• Acute thyroiditis
• Sub acute thyroiditis
• Chronic thyroiditis
 ACUTE (SUPPURATIVE) THYROIDITIS
• Due to suppurative infection of thyroid

• m/c children  URTI or otitis media

• Thyroid gland resistant to infection due to extensive blood

and lymphatic supply , high iodide , and fibrous capsule

• Spread :- hematogenous or lymphatic route

direct spread from persistent pyriform sinus
fistulae or thyroglossal duct cyst
penetrating injury
immunosuppression
• Streptococcus and anaerobes- 70%

• Clinical feature :-
-thyroid pain referred to throat or ear (small and tender
goiter)

- Fever , dysphagia and erythema over goiter

- Febrile illness and lymphadenopathy

• Complications : systemic sepsis , tracheal and esophageal

rupture , jugular venous thrombosis , laryngeal chondritis ,
perichondritis
• Investigations :
-thyroid function test normal
- ESR , WBC count raised
- FNA biopsy – infiltration by
polymorphonuclear leukocytes
- Culture
- Persistent pyriform sinus fistula suspected in
children with recurrent acute thyroiditis
• TREATMENT :-
- Parenteral antibiotics and drainage of abscess
- Pyriform sinus fistulae – complete resection
 SUBACUTE THYROIDITIS
• De quervain’s /granulomatous / viral
thyroiditis
• 30- 50 yrs , women >men
• Follows URTI
• Strong association with HLA – B35 haplotype
• 4 stages :
- Intial hyperthyroid phase – release of
preformed thyroid hormone
- Euthyroid phase
- Hypothyroid phase
- Resolution and return to euthyroid state >90%
patients
• Clinical features:-
-painful enlarged thyroid
-features of thyrotoxicosis or hypothyroidism
-URTI symptoms may precede thyroid related
features
-pain referred to jaw or ear
-complete resolution is usual outcome
• INVESTIGATIONS:-
-ESR elevated >100mm/h
-RAIU is decreased even in euthyroid stage , due to
release of thyroid hormones from destruction of
follicles
-FNAC – characteristic gaint multinucleated cells
-T4 , T3 and TSH depend on stage of disease
-
• TREATMENT:-
-symptomatic – as disease is self limited
- Aspirin or other NSAIDS sufficient to control
symptoms inmost cases
- Severe cases – glucocorticoids
- Hypothyriod phase – thyroid replacement
- Thyroidectomy – not responsive to medical
measure
 HASHIMOTO’S THYROIDITIS
• Struma lymphomatosa – transformation of
thyroid tissue to lymphoid tissue
• MC inflammatory disorder of thyroid ,leading
cause of hypothyroidism
• Genetic association – HLA B8 ,DR3 , DR5
• More common women (M:F 1:10), near
menopause (30-50 yrs)
• ETHIOPATHOGENESIS:-
-autoimmune disease
-initiated by activation of T –helper cells which
recruit cytotoxic T cells
-thyroid tissue destroyed by cytotoxic T cells and
autoantibodies
- Autoantibodies :- thyroglobulin , TPO , TSH-R
- Associated with increased intake of iodine, drugs
such as interferon alpha , lithium , amiodarone
• Microscopic examination:-
-diffusely infiltrated with small lymphocytes and
plasma cells
-small follicles with reduced colloid
-follicles lined by hurthle or askanazy cells
• CLINICAL FEATURES:-
-min to moderately enlarged firm gland
-mild hyperthyroidism may present initially
-hypothyroidism-permanent
• INVESTIGATIONS :-
-elevated TSH and reduced T3 , T4
-presence of thyroid autoantibodies confirm the
diagnosis(particularly TPO antibody)
-FNA biopsy –solitary suspicious nodule or rapidly
enlarging goiter
• MANAGEMENT:-
-thyroid hormone replacment
-surgery indicated :- suspicion malignancy , goiter
causing compression symptoms
 RIEDELS THYROIDITIS
• Invasive fibrous thyroiditis
• Replacement of all or part of thyroid parenchyma
by fibrous tissue
• Invades into adjacent tissue
• Etiology : primary autoimmune
• Associated with : mediastinal and retroperitoneal
fibrosis
-periorbital or retro orbital fibrosis
-sclerosing cholangitis
• CLINICAL FEATURES:
-women , 30- 60 ys
-painless , hard anterior neck mass
- Progress to produce compression symptoms –
dysphagia , dyspnea , choking and hoarsness
- May present with symptoms of hypothyroidism
and hypoparathyroidism
- Examination – hard “woody” thyroid gland with
fixation to surrounding tissue
• Diagnosis confirmed by open thyroid biopsy
• Treatment :-
-surgery is the mainstay treatment
- Some show improvement with tamoxifen and
corticosteroid
 GOITER
• Goiter – enlarged thyroid gland
• Etiology :-
-endemic : iodine deficiency , dietary goitrogens
-medication : iodide , amiodarone , lithium
-thyroiditis : subacute , chronic
-familial :impaired hormone synthesis from
enzymatic defects
-neoplasm : adenoma , carcinoma
• TSH stimulation secondary to inadequate
thyroid hormone synthesis
• Elevated TSH induce diffuse thyroid
hyperplasia ,followed focal hyperplasia,
resulting in nodules
• TSH dependent nodule progress to become
autonomus
• CLINICAL FEATURE :
-non toxic – asymptomatic
-large goiters pressure symptoms
- Dysphonia  RLN injury (malignancy)
- Pembertons sign
- Sudden enlarged nodule due to hemorrhage may
cause acute pain
- Examination : diffusely enlarged goiter (simple
goiter) , nodules of various size (multinodular
goiter)
• INVESTIGATIONS:-
-Thyroid profile
- RAIU patchy uptake with areas of hot and cold
nodule
- FNAB : dominant nodule or one that is painful
or enlarging
- CT scan : evaluate extent of retrosternal
extension and airway compression
• TREATMENT :
• Euthyroid with small , diffuse goiter do not
require treatment
• Exogenous thyroid hormone  reduce TSH
stimulation of gland growth  decrease /
stabilization of goiter size (most effective for
small diffuse goiter)
• Endemic  iodine administration
• Surgery :
- continue increase despite T4 suppression
- Cause obstructive symptoms
- Sub sternal extension
- Malignancy suspected or proven by FNAB
- Cosmetically unacceptable
 SOLITARY THYROID NODULE
• MC solitary thyroid nodule is benign collid nodule
(60%)
• 2nd mc is folliclar adenoma
• History :-
- Regarding nodule time of onset , change in size ,
associated symptoms such as pain(heamorrhage ,
thyroiditis , malignancy) , hoarseness of voice
- Risk factors for malignancy :- exposure to ionizing
radiation and family history of thyroid malignancy
• EXTERNAL BEAM RADIATION :
- Low dose therapeutic radiation – tinea capitis
, thymic enlargment , enlarged tonsils and
adenoids etc…,
- h/o exposure to low dose ionizing radiation to
thyroid gland increase risk for papillary thyroid
cancer
- Risk is maximum 20- 30 yrs after exposure
• Physical examination :
-thyroid gland is best palpated from behind the
patient and with neck in mild extension
- Nodules that are hard , gritty , or fixed to
surrounding structures such as trachea or
strap muscle are more likely to be malignant
• INVESTIGATION:-
FNAC:-
- Single most important test in evaluation of
thyroid masses
- Ultrasound recommended for nodule – difficult
to palpate , cystic or solid –cystic nodules that
recur after initial aspiration
- Benign lesions  cystic and colloid nodules (risk
of malignancy <3%)
-
• Laboratory studies :-
- Most patients – euthyroid
- Determine blood TSH levels
- Hyperthyroid nodule risk of malinancy 1%
• Imaging :-
• ultrasound scan evaluation features that
increase risk of malignancy –fine stippled
calcification , enlarged regional lymph nodes
• Us elastography
• CT / MRI – Substernal lesions
• Thyroid scanning I123 or Tc99 – follicular
nodule of thyroid on FNAC and suppressed
TSH
• SIMPLE THYROID CYST :
- Resolves with aspiration in 75% cases
- Lobectomy :- cyst persist after three attempts
of aspiration
cyst >4 cm in diameter
complex cyst
• Colloid nodule:-
- Observation by serial USG and Tg measurement
- L –thyroxine (TSH level 0.1 – 1 u/ml)
- 50% reduces size TSH suppression
- HEMITHYROIDECTOMY – nodule enlarges on TSH
suppression, compression sympyoms
- Total thyroidectomy – previous irradiation , family
history of thyroid cancer , high incidence of
thyroid cancer