Neoplasms of thyroid

1. NEOPLASMS OF THYROID&
INFLAMMATORY DISORDERS OF
THYROID
• PRESENTER: Dr B. Sneha
• Junior resident,
Department of General
urgery
MODERATOR: Dr Varundeep,
Assistant professor
Department of General surgery

2. THYROID GLAND

3. INTRODUCTION TO NEOPLASMS OF THYROID
Most common endocrine tumour
Responsible for about 6 deaths per million persons annually
It accounts roughly for about 0.5% of all cancers in men and 1.5% of all
cancers in women
5% of all thyroid nodules are all malignant
Single nodule more likely to be malignant than multiple nodules

4. BENIGN
Follicular adenoma
(or)
Thyroid adenoma
Primary
• Follicular epithelium ( differentiated) –
follicular, papillary, Hurthle cell
• Follicular epithelium (undifferentiated)-
anaplastic
• Parafollicular cells-medullary
• Lymphoid cells
Secondary
• Metastatic
• Local infiltration
MALIGNANT
CLASSIFICATION OF THYROID TUMOURS

6. ENDODERMALLY DERIVED
FOLLICULAR CELLS
• Medullary thyroid
carcinoma
NEUROENDOCRINE DERIVED
CALCITONIN PRODUCING C
CELLS
• Papillary thyoid
carcinoma
• Follicular thyroid
carcinoma
• Anaplastic thyroid
carcinoma
 Thyroid lymphomas- are derived from
lymphoid tissue
 Sarcomas –are derived from connective tissue
of thyroid gland
THYROID CANCER ARISES FROM 2 TYPES OF CELLS

7. BENIGN TUMORS
1. FOLLICULAR ADENOMA :
• Follicular adenomas clinically they present as the solitary nodules of
thyroid, besides the follicular adenoma of thyroid there are other
conditions which present as solitary thyroid nodules.
• The differentiation between follicular carcinoma and follicular adenoma
can be made only by histological examination
• In follicular adenoma there is no invasion of capsule or pericapsular
blood vessels
• FNAC provides only cytological details but not tissue architecture and
hence we cannot differentiate between benign and malignant follicular
lesions
• Diagnosis and treatment is by wide excision i.e .total lobectomy

8. Follicular adenoma of thyroid

9. PRIMARY TUMORS
• Majority of primary
malignancies are
carcinomas derived
from follicular cells
• If such tumors are well
differentiated they are
known as differentiated
tumors of thyroid and
they are again divided
as -
1. Differentiated Thyroid tumors:-
a) Papillary thyroid carcinoma
b) Follicular thyroid carcinoma
c) Hurthle cell carcinoma
2. Undifferentiated thyroid tumor:-
a) Anaplastic thyroid carcinoma
3.Parafollicular c cells:-
a) Medullary carcinoma of thyroid
4.Thyroid lymphoma
MALIGNANT TUMORS

10. SECONDARY TUMORS
1.Metastatic –lymph node and blood borne
metastasis to thyroid either from bone and
lung
2.Local infiltration- from surrounding
structures such as larynx and oesophageal
cancers

11. MALIGNANT TUMORS
ETIOLOGY
• Majority of the thyroid cancers have
unknown etiology
• Most important identifiable
etiological factor for differentiated
thyroid carcinoma is (particularly
papillary) is irradaiation of thyroid
under 5 yrs old
• In town of Gomel in Ukraine ,the
incidence of childhood thyroid
cancers increased following
Chernobyl nuclear disaster
• The incidence of follicular carcinomas
are high in endemic goitrous areas
• Malignant lymphomas sometimes
develop in autoimmune thyroiditis
and lymphocytic infiltration in the

12. CLINICAL FEATURES OF THYROID CANCERS:
• Most common presenting symptom is thyroid swelling
• Enlarged cervical lymph nodes may also be seen
• RLN paralysis is suggestive of locally advanced disease
• Pain often referred to the ear, is suggestive of nerve involvement
• A differentiated tumour is often indistinguishable from benign swelling
• Anaplastic cancers are usually hard , irregular and infiltrating

13. DIAGNOSIS OF THYROID NEOPLASMS :
Clinical history and examination of neck are the cornerstone for
diagnosis , history including the radiation exposure and family
history should be discussed .
Examination of central neck and regional lymphatics should be
done along with assessment of vocal cords.
Thyroid functional tests should be done .
After initial assessment the patient should be subjected to
ultrasonography of thyroid . This is anon invasive method and
most accurate .used to asses the presence , size and number of
thyroid nodules and estimates the risk of malignancy.

14.  Following USG , lesions are classified into benign
, indeterminate or malignant . Benign lesions
needs no further assessment only if surgery is
considered due to compressive symptoms .
 Indeterminant or malignant lesions are subjected
to FNAC.
 In case of thyrotoxic patient , radio iodine uptake
scan can be done . Hot nodules are very rarely
malignant , cold nodules needs further
assessment for neoplasms.

15. In patients with wide spread nodal disease or locally invasive
disease affecting the airway , contrast enhanced imaging of neck
and chest should be considered
In patients with rapidly growing thyroid mass , particularly solid
and fixed should be considered as risk of anaplastic carcinoma, in
this setting core or even open biopsy may be required to make a
confident diagnosis

16. DIFFERENTIATED THYROID
TUMORS
• It is 70-80% most common thyroid
malignancy
• Most common in females and younger age
group
• Best prognosis
• Route of spread is lymphatic spread
ETIOLOGY:
• Exposure to Radiation either externally or
radioactive iodine therapy
• Family history
• Obesity
SYNDROMES ASSOCIATED :
• Familial intestinal polypoisis
• Cowdens syndrome
• MEN 2 syndrome
• Werner syndrome
1. 1.Papillary thyroid
carcinoma (PCT)

17. GENETICS:
• The most common gene is BRAF
• Glial derived neurotrophic factor (GDNF)
• RET/PTC mutations
• RET/PTC3 –more aggressive
• RET/PTC1-less aggressive
PRESENTATION:
• Females: males 3:1
• 3rd to 5th decade of life
• Patients present with thyroid swelling

18. • GROSS :
• Papillary carcinoma may range
from microscopic foci to
nodules upto 10 cm
• Cut surface of the tumour is
greyish white , hard scar like

19. MICROSCOPY:
• Papillary pattern with fibrovascular
stalk of the tumour cells can be seen
• Tumour cells have characteristic nuclear
features due to dispersed nuclear
chromatin ground glass or optically
clear nucleus , oval nucleus, nuclear
grooves, intranuclear pseudo
inclusions(orphan Annie eye nuclei)
• Psammoma bodies, they are small
concentric calcified spherules in the
stroma

20. SPREAD
• Slowly progressive and less aggressive tumor
• Multicentric
• Spreads within the gland through intrathyroidal lymphatics , comes
out of the capsule and spreads to cervical lymphnodes
• Usually no blood spread
CLINICAL FEATURES:
• Soft or hard or firm, solid or cystic , solitary or multinodular thyroid
swelling
• Compression features
• Lymphnode enlargement in neck

21.  DIAGNOSIS:
 FNAC of thyroid nodule and lymph node
 Radio isotope scan , which shows cold nodule.
 Thyroid function tests shows elevated TSH
 Plain X ray of neck shows fine calcification whereas
nodular goitre shows coarse ring /rim calcification
 Usg of neck is also done to identify any non palpable
lymphnodes
 MRI may be useful

23. TREATMENT:
SURGERY :
HEMITHYROIDECTOMY – in patients with tumour size 1-4cm ,
unifocal , no lympho vascular invasion
TOTAL THYROIDECTOMY –in all patients tumour size more than
4 cm
TOTAL THYROIDECTOMY +CENTRAL NECK DISSECTION( CND) –
in patients involving level 6 lymph nodes
TOTAL THYROIDECTOMY + PROPHYLACTIC CND- in patients
with T3, T4
TOTAL THYROIDECTOMY + CND+ MODIFIED RADICAL NECK
DISSECTION (MRND)-If level 6 or more involved

24. MANAGEMENT POST SURGERY :
 WHOLE BODY IODINE SCAN done to look for residual
disease, metastatic disease,
Pre requisite : TSH > 20 IU/L
Preparation – thyroxine not given for 4 to 6 weeks after
surgery,
New method – Recombinant TSH injection
RADIOACTIVE iodine R131 delivers tumoricidal effects and Is
given for all patients with residual disease/metastatic
disease, both benign and malignant lesions.
Multiple doses can be used to treat unresectable lesions
With advancing age of patient especially If the disease is
recurrent the tumour will loose its avidity , this is called
Radio Iodine refractory disease .
In such cases external beam radiotherapy can be used

25. PROGNOSIS:
AMES SCORING
A-age less than 40 yrs better prognosis
M-distant metastasis
E-extent of primary tumor
S-size of the tumor ,less than 4 cm has better
prognosis
AGES SCORING
A-age less than 40 yrs better prognosis
G-pathologic grade of the tumor
E –extent of the tumor
S – size of the tumor , less than 4cm better

26. • It is 2nd most common thyroid tumour
• More common n females
• Most common in iodine deficient areas
GENETICS-
• PTEN gene
• BAX gene
RISK FACTORS; long standing multi nodular goitre
PRESENTATION:
Neck swelling
SPREAD :
• it is more aggressive tumour
• Spreads mainly through blood into the bones ,
lungs liver
• Bone secondaries are vascular , warm and
pulsatile , located in skull , long bones and ribs.(
Osteolytic )
2. Follicular
thyroid
carcinoma

27. CLINICAL FEATURES:
• Swelling in the neck firm or hard and nodular.
• Tracheal compression /infiltration and stridor
• Dyspnoea, hemoptysis ,chest pain when lung secondaries
• Recurrent laryngeal nerve involvement causes hoarseness of voice ,
positive BERRY’S sign (infiltration into carotid sheath and absence
of carotid pulsations ) signifies advance malignancy.

28. INVESTIGATIONS :
 Most often FNAC is inconclusive , because capsular and
angioinvasion main features of follicular carcinoma
cannot be detected
 FNAC cannot differentiate between follicular adenoma
and carcinoma
 Tru cut biopsy gives tissue diagnosis but danger of
hemorrhage and injury to vital structures like trachea,
recurrent laryngeal nerve, vessels
 USG of abdomen , chest xray , Xray of bones , CT head
may be useful.

29. • Completion of
surgery total
thyroidectomy along
with cervical
lymphnode
disssection
FOLLICULAR
CARCINOMA
• Frozen section
HEMITHROIDECTOMY
• No further surgery
FOLLICULAR
ADENOMA
TREATMENT;
 Post operative Radioactive iodine I 131 therapy with a dose of 100 mci should be
given
 Maintainence dose of L-thyroxine 0.1 mg once daily should be given life long.

30. 3.HURTHLE CELL
CARCINOMA
• Rare variant of follicular
neoplasm.
• Oxyphil (Hurthle, Askanazy)
cells predominate
histologically.( eosinophilic
cytoplasm , rich in
mitochondria)
• Occur in 6th -7th decade of
life
• More aggressive tumour
• Highest incidence of
metastasis among
differentiated cancers.

31. UNDIFFERENTIATED
THYROID TUMOURS
• Most aggressive and rare
tumour
• This disease is characterised by
rapid growth, visceral invasion
and distant metastasis
• 5-7th decades
• Due to p53 mutations
CLINICAL FEATURES :
• Hoarseness of voice,
• Dysponea, stridor, very hard
swelling
Anaplastic carcinoma

32. DIAGNOSIS:
• FNAC , if FNAC inconclusive – TRUCUT/ CORE NEEDLE
BIOPSY
MANAGEMENT:
• If tumour is restricted to thyroid / localised disease- total
thyroidectomy + central neck dissection + modified radical
neck dissection
• If tumour is beyond thyroid / advanced – palliative
management, chemotherapy , tumour debulking (
isthmusectomy)

33. PARAFOLLICULAR CELLS
• Accounts for 5% of all the thyroid
tumours
• These are the tumours arising from the
parafollicular C cells of the thyroid
derived from neural crest cells
• High levels of serum calcitonin and
carcinoembryogenic antigen are
produced
• Calcitonin levels fall after resection of
tumour and rise again with recurrence,
making it a valuable tumour marker.
• TYPES:
a) Sporadiac form
b) Familial form
Medullary carcinoma of
thyroid

34. SPORADIAC FORM
• They occur at any
age with no sex
predominance
mostly age >45 yrs
• Most common
• They are mostly
unilateral solitary
cold thyroid mass
• The disease frequently affects children and
younger age group
• 2-3rd decade of life
• They are multiple and usually bilateral
• They are associated with MEN 2A & MEN 2B
syndrome
• In MEN2A, medullary carcinoma occurs in
combination with adrenal pheochromocytoma ,
and hyperparathyroidism
• In MEN2B , it is associated with neuromas of lip ,
tongue and inner aspect of eyelid, with
marfanoid habitus
• Associated with RET protooncogene mutation
FAMILIAL FORM

35. FEATURES:
• Thyroid swelling is the most common presentation,
• Atypical symptoms include: Diarrhoea , due to 5 hydroxy tryptamine or prostaglandin
produced by tumour cells,
• flushing and cushing disease may be seen
 Involvement of lymphnodes accurs in almost 55-60% of the cases along with blood borne
metastasis( lymphatic & hematogenous spread)
 Tumours are not TSH dependant and do not take up radioactive iodine
 DIAGNOSIS:- FNAC, which shows characteristic “ cell balls’ and ‘amyloid’

36. MANAGEMENT
SURGERY
• If restricted to thyroid ; Total Thyroidectomy and elective dissection of
Cervical nodal dissection ( CND)
• If thyroid + level 6 lymphnodes or other lymphnodes -: Total thyroidectomy
+ CND + MRND
• Prophylactic thyroidectomy recommended in familial cases of medullary
carcinoma after genetic screening
• High risk mutations are associated with early onset disease and hence total
thyroidectomy recommended during infancy
• PROGNOSIS
• Serum calcitonin should be monitored along with CEA

37. MALIGNANT LYMPHOMA
• Very rare tumour
• May occur in 5-7th decade of life
• In past malignant lymphomas were
diagnosed as small round cell anaplastic
carcinomas
• Risk factors: long standing hashimotos
thyroiditis
• Presentation; thyroid swelling ,fever
night sweats and weight loss

38. DIAGNOSIS:
• Diagnosis is established by Biopsy
MANAGEMENT:
• In patients with tracheal compression ISTHUMUSECTOMY is most appropriate
• Chemotherapy and radiotherapy
• PROGNOSIS:
• Prognosis is good particularly if there is no involvement of cervical
lymphnodes
• if the tumour is wide spread malignant lymphoma disease and the prognosis
is worse.

39. INFLAMMATORY THYROID
DISORDERS
1. GRANULOMATOUS
THYROIDITIS/ HASHIMOTOS
THYROIDITIS
2. RIEDEL’S THYROIDITIS
3. CHRONIC LYMPHOCYTIC
THYROIDITIS / HASHIMOTOS
DISEASE

40. CHRONIC LYMPHOCYTIC(AUTOIMMUNE)
THYROIDITIS
• Also known as Hashimoto’s disease/ Hashimotos thyroiditis
• It is the most common cause for thyroiditis and most common cause for
hypothyroidism in females > males
• Associated with HLA DR 3/B8, Down’s and Turners syndromes
• It is associated with raised titres of thyroid antibodies. They are against
THYROID PEROXIDASE ( TPO ENZYME) , THYROGLOBULIN, THYROID
RECEPTORS ( ( TSH receptors)
• It commonly presents as a goitre, which may be diffuse or nodular with a
characteristic bosselated feel or with established or subclinical thyroid failure.
• Autoantibodies include: thyroglobulin antibody, thyroid peroxidase antibody,
TSH receptor blocking antibody.
• Primary myxoedema without detectable thyroid enlargement represents the end
stage of the pathological process.

41. •Autoantibodies
•Stimulate the lymphocytes to infiltrate the gland
• Destruction of follicles
• Stored thyroid hormones are released in the circulation (
phase of hyperthyroidism / HASHITOXICOSIS)
• Follicles cannot regenerate due to repeated attacks from
lymphocytes
• Leads to prolonged hypothyroidism
CLINICAL COURSE

42. CLINICAL FEATURES:
• Diffuse goiter
• Features of
hypothyroidism
• DIAGNOSIS :
Autoantibody levels
Usg ; pseudo nodular
appearance
Histopathologically –
lymphocytic infiltration
, reduced colloid ,
hurthle cells

43. MANAGEMENT
• Thyroxine replacement – usually started with 25
micrograms and gradually titrated the dose by
monitoring the TSH levels
• If goiter present – surgery either subtotal / near
total/ total thyroidectomy depending on extension

44. GRANULOMATOUS THYROIDITIS
(SUBACUTE THYROIDITIS)
• Also known as De Quervain's thyroiditis
• Most common cause of thyroid pain and tenderness
• Acute inflammatory disease most likely due to viral infection
• Seen in patients with URTI , post partum or pregnant females
• In a typical Subacute presentation , there is pain in the neck,
fever, malaise, and a firm , irregular enlargement of one or both
the lobes of thyroid
• Patient may present with symptoms of hyperthyroidism in 10%
cases when onset is acute , the goitre is very painful and tender.
• The condition is usually self limiting , and in few months later the
patient may be in period of hypothyroidism before eventual
recovery.

45. Viral infection • 4-6 weeks
later
Lymphocytes infiltrate the
gland ( painful neck
enlargement)
• Destruction of
follicles
A brief phase of
hyperthyroidism
• Followed by
hypothyroidism
• Euthyroid state in
3-4 months(self
limiting)
CLINICAL COURSE

46. MANAGEMENT
• Symptomatic management
• The specific treatment for the acute patient with severe
pain is to give PREDNISONE 10-20mg daily for 7 days
and the dose is then gradually reduced over the next
month.
• If thyroid failure is prominent , treatment with thyroxine
DIAGNOSIS:
• Raised inflammatory markers ( ESR , CRP),absent thyroid antibodies
serum T4 is high normal or slightly raised
• Radioactive uptake of the gland is low
• If diagnosis is doubt it can be confirmed by FNAC

47. REIDEL’S THYROIDITIS
• It is a very rare , accounting for 0.5% of goitres
• Thyroid tissue is replaced by cellular fibrous tissue , which
infiltrates through capsule into adjacent structures , including
parathyroids , recurrent nerves and carotid sheath.
• It may occur in association with retroperitoneal and mediastinal
fibrosis and is most probably a collagen disease .
• The goitre may be unilateral or bilateral and is very hard and
fixed
• It can be differentiated from anaplastic carcinoma only by biopsy
• If unilateral the other lobe is usually involved later and leads to

48. MANAGEMENT
• Treatment with high dose steroids , TAMOXIFEN and
thyroxine replacement is done .
• Reduction in the size of the goitre and long term
improvement in symptoms are expected if treatment
commenced early

49. THANK YOU