5. • This is the normal
appearance of the
thyroid gland on
the anterior trachea
of the neck..
6.
7. Normal thyroid seen microscopically consists of follicles
lined
by a cuboidal epithelium and filled with pink,
homogenous colloid
8. Hypothyroidism:
• Causes:
– structural or functional
– 95% are due to:
• Surgical or radiation ablation
• Hashimoto’s thyroiditis
• Primary idiopathic hypothyroidism
9. Cretinism
• This is uncommon disease of
childhood due to failure of thyroid to
synthesize thyroid hormones
hypothyroidism
13. Hyperthyroidism
• Excess thyroid hormone
(Thyrotoxicosis)
• Causes:
– primary diffuse toxic hyperplasia
(Grave’s disease) > 95%
– toxic multinodular goiter
– toxic adenoma
– certain form of thyroiditis
– secondary to pituitary or hypothalamic
lesion
14. •Clinical features:
• nervousness and emotional instability
• menstrual changes
• fine tremors of the hands
• heat intolerance with warm skin and
sweating
• weight loss despite a good appetite
15. • Eye changes: (exopthalmos, widened
palpebral fissures, staring gaze)
• Cardiac changes: (tachycardia,
palpitations, atrial fibrillation and
thyrotoxic cardiomyopathy----- cardiac
failure)
• skeletal muscle atrophy and fatty
infiltration
• lymphadenopathy
• fatty change of the liver
• Osteoporosis
19. Diffuse Goiter
• Characterized by diffuse
symmetrical enlargement of thyroid
(200 - 300 gm) with normal thyroid
function.
• Hypofunction may occur early in the
course .
• Usually occurs in: Endemic areas
( iodine & goiterogens) or
• Sporadic (physiological
20. Multinodular Goiter
• Characterized by
nodular
asymmetrical
enlargement of
thyroid (up to 1000
gm)
• Slowly evolves
from diffuse
goiter.It can be
toxic or non-toxic
27. Hashimoto’s thyroiditis
• This is an autoimmune most
common type of thyroiditis
characterized by symmetrical
modesty enlarged thyroid
responsible for most cases of
primary goiterous
hypothyroidism.
28. Pathogenesis
• B cells autoantibodies against
microsomes and thyroglobulin.
• Cell-mediated destruction of the
gland
• ♀ : ♂ = 10 : 1 middle-aged
• Higher incidence of autoimmune
disease
29. Clinical Course
• Euthyroid--- hypothyroid
• Moderate goiter
• Hashitoxicosis(hyperthyroidism)
occasionally
• 5% - B cell lymphoma or rarely
papillary carcinoma of thyroid
35. Papillary Carcinoma
60-70%
• The most common type
• Young age 20-50y , F:M=3:1
• Forming papillae and psammoma bodies
• Cells typically show ground-glass
appearance with clear grooved nuclei
“Orphan Annie” and intranuclear inclusion
• 50% at presentation Cervical LN
metastasis
• Haematogenous spread is rare (not
common)
36. •Follicular variant of
papillary carcinoma :
No papillary formation .
The nuclei shows typical nuclear
ground glass appearance of papilary
crcinoma.
•Grow slowly with indolent course
•Occult microscopic variant
38. Follicular Carcinoma
• Macroscopically often encapsulated
similar to adenoma
• Histologically : composed of follicles
with no papillary formation and no
groundglass nuclear changes.
• sometimes the cells are oncocytic
(Hurthle cell carcinoma).
39. Follicular Carcinoma
• Haematogenous spread (lung, bone, liver.
. )
• Poorer in prognosis than papillary
carcinoma.
• Represent approximatly 15%
• Most patients are >40y
• TYPES:
1- minimally invasive FC.
2- widely invasive FC.
40. Medullary Carcinoma of
thyroid <5%
• Derived from calcitonin – secreting
C-cells
• Characterized by formation of
amyloid material from calcitonin,
surrounded by small to medium sized
cells with round to spindle shaped
nuclei forming sheets, nests or cords
42. Medullary Carcinoma
• It has slow but progressive growth
• Both lymphatic and hematogenous
metastasis occurs
• 10-20% are familial, multicenteric in
young age, associated with MEN 2&3
• Immuno: +ve calcitonin
• 80-90% sporadic, solitary, old age
43. Anablastic carcinoma 5-10%
0ccurs in patient > 60 y
• Poorly differentiated, highly malignant tumour
usually forms bulky necrotic mass often
disseminate extensively through blood
• death occurs within 1-2 years (<10% survive for
10y)
•Histological variants:
• Giant cells, spindle cells(sarcomatoid), squamoid
cells
48. Hyperparathyroidism
- Primary Hyperparathyroidism:
Increase PTH due to parathyroid lesion
(Adenoma/hyperplasia) Hypercalcaemia
PTH Hypercalcaemia :
– osteoclast to mobilize Ca++ from bone
– Ca++ reabsorption in the kidney
– Ca++ absorption in Git .through vit .D.
– excretion of phosphate in urine .
• Part of MEN I & II
• F : M = 3 : 1 > 40y
51. Adenoma & Hyperplasia
In adenoma one gland, Hyperplasia >one gland
• Frozen section (intraoperative consultation)
required to confirm presence of parathyroid
tissue.
Carcinoma of parathyroid:
* Rare
– Invasion and metastasis
– Bands of collagen in the stroma
– High mitotic figures.
54. MULTIPLE ENDOCRINE
NEOPLASIA (MEN)
• MEN are syndromes characterized by
hyperplasic or neoplastic involvement of
at least two endocrine glands and
sometimes associated with non-endocrine
lesions.
55. • MEN I: Wermer ’ s Syndrome
– Parathyroid adenom/hyperplasia .
– Pituitary adenoma .
– Pancreatic lesions (hyperplasia
adenoma , carcinoma )
– Mutant gene(MEN1) locus at 11q13
– Autosomal dominnant
56. • MEN II (IIa): Sipple Syndrome
– Medullary carcinoma of thyroid
– Pheochromocytoma .
– Occasionally parathyroid lesion
(30%)
– Mutant gene locus at 10q11.2
(RET proto-oncogen)
– Autosomal dominant
57. • MEN III (IIb):William syndrome:
similar to MEN II plus
– Marfanoid bodily habitus
– Multiple mucocutanenous
ganglioneuromas
– Parathyroid involvement :
(none/rare).