Pathology of thyroid

Question 1

Histology of Graves’ Disease

Answer 1

• Follicular cells are taller and more crowded
• —> diffuse hyperplasia and hypertrophy
• —> may form papillae in lumen
• Widespread scalloping of colloid
• Colloid is paler
• Lymphocytic infiltrate

Question 2

Mechanism of Graves’ disease

Answer 2

• AI disease against TSH receptor on thyroid
• TSI (thyroid stimulating Ig)
• TGSI (thryoid growth stimulating Ig)
• Both bind and stimulates TSH receptor, mimics TSH

Question 3

Mechanism of Hashimoto’s

Answer 3

• Breakdown of tolerance to thyroid tissue (AI)
• causes damage by:
  1) CD8+ cytotoxic cell mediated death
  2) Cytokine mediated death (IFN-gamma)
  3) TSH- blocking Ab–> decrease thyroid function
• strong genetic component

Question 4

Hashimotos- what do we see clinically?

Answer 4

• Decreased fT4
• Increased TSH (less NF)
• Anti- TPO Ig (anti- thyroid peroxidase Abs)
• Anti- Tg Ig (anti thyroglobulin Abs)

Question 5

Hashimoto’s histology

Answer 5

• Germinal centres
• mononuclear cell infiltrate- equal proportions T and B cells
• Abundant, hypereosinophilic, granular cytoplasm in follicular cells
• fibrosis and scar tissue

Question 6

What is multinodular goitre?

Answer 6

• Simple goitre becomes MN
• Some follicles rupture and fibrose
• can get calcification, haemosidirin and cholesterol clefts

Question 7

What is TMNG?

Answer 7

Toxic multinodular goitre

- When nodules become autonomous and can start producing TH on their own, without TSH

Question 8

Diffuse ‘simple’ non- toxic goitre histology

Answer 8

• Follicular cells are hyperplastic
• overcrowded epithelia
• some follicles are larger than others
• large colloid filled cysts