Thyroid Flashcards
Parafollicular cells
Occasional scattered C cells
- Slightly larger cells with clearer cytoplasm
- Secrete calcitonin
- Lower serum Ca but in practise is of little significance
Causes of Hyperthyroidism
Graves disease Hyperfunctioning nodules/tumours Thyroiditis TSH secreting pituitary adenoma (rare) Ectopic production (struma ovarii) Factitious (exogenous intake)
Struma ovarii
Literally a goitre of the ovary, containing thyroid tissue
Palpation thyroiditis
Palpation thyroiditis refers to the development of thyroid inflammation due to mechanical damage to thyroid follicles. This can occur by vigorous repeated palpation (as with thyroid examination) or surgical manipulation (as can occur with radical neck dissection)
Subacute lymphocytic thyroiditis
Subacute lymphocytic thyroiditis features a small goiter without tenderness. This condition tends to have a phase of hyperthyroidism followed by a return to a euthyroid state, and then a phase of hypothyroidism, followed again by a return to the euthyroid state. The time span of each phase can vary; however, each phase usually lasts 2-3 months
Can be diagnosed by radioactive iodine uptake test
During hyperthyroid period, uptake is suppressed. During hypothyroid it is incresased
de Quervains Thyroiditis
Hyperthyroid
Hypothyroid
Euthyroid
Distinguishing between subacute thyroiditis and Graves disease
The clinical presentation during the hyperthyroid phase can mimic those of Diffuse Toxic Goiter or Graves’ disease. In such cases, a radionuclide thyroid uptake and scan can be helpful, since subacute thyroiditis will result in decreased isotope uptake, while Graves’ disease will generally result in increased uptake. Distinguishing between these two types of disease is important, since Graves’ disease and Diffuse Toxic Goiter can be treated with radioiodine therapy, but subacute thyroiditis is usually self-limited and is not treated with radioiodine.
Riedel’s Thyroiditis
Riedel’s thyroiditis is characterized by a replacement of the normal thyroid parenchyma by a dense fibrosis
Who does Grave’s disease tend to affect?
F:M 10:1
Age 20-40
When might you see antibodies to TSH receptor, thyroid peroxisomes and thyroglobulin?
Grave’s Disease
Anti-TSH receptor antibodies
Thyroid stimulating immunoglobulin
Relatively specific (unlike peroxisome and thyroglobulin abs)
Thyroid growth stimulating immunoglobulin
TSH binding inhibitor immunoglobulins
May explain episodes of hypofunction
Triad of features of Grave’s disease
Hyperthyroidism with diffuse enlargement of the thyroid
Eye changes (exophthalmos)
Pretibial myxoedema
Why do you get eye changes in hyperthyroidism?
The eye changes result from fibroblasts etc expressing TSH receptors
Hashimoto’s Thyroiditis
Affects middle aged women
Associated with other AI disease
Associated with HLA – DR3 and DR5
Causes of hypothyroidism
Hashimoto’s Thyroiditis
Iodine deficiency, drugs, post therapy (surgery, 131 I, irradiation)
Congenital abnormalities
Inborn errors of metabolism
Which has a longer half life, T3 or T4?
T4.
T4 is also the major form of thyroid hormone in the blood
People most likely to develop Hashimoto’s thyroiditis?
F:M 10-20:1
Ages 45-60
Gene Polymorphisms associated with Hashimoto’s Thyroiditis?
CTLA-4
PTPN-22
What may preceded hashimoto’s thyroiditis?
Hashitoxicosis
What does hashimotos thyroiditis put you at a greater risk of?
Other autoimmune diseasea
Increased risk of developing B cell non- Hodgkin’s lymphoma in affected gland
What are goitre’s often caused by?
Lack of iodind
Diffuse Goitre
Endemic - >10% population affected
Sporadic – F > M, puberty and young adults
Ingestion of substances limiting T3/T4 production
Inborn errors of metabolism (dyshormonogenesis)
Most cases – cause unknown
Usually euthyroid – present with mass effects
T3 / T4 normal but TSH high or upper limit of normal
In children dyshormonogenesis may cause cretinis
T3/T4 and TSH levels in diffuse goitre?
T3/T4 levels normal
TSH high or upper limit of normal
Multi-nodular goitre differential diagnosis?
Thyroid neoplasm
Multi-nodular goitre
Evolution from long standing simple goitre
Recurrent hyperplasia and involution
Enlargement can be impressive
DDx thyroid neoplasm
Variation of response of follicular cells to external stimuli
Mutations of TSH signaling pathway.
Rupture of follicles, haemorrhage, scarring, calcification
Mass effects
Cosmetic
Airway obstruction, dysphagia, compress vessels
May develop autonomous nodule – hyperthyroid
10% after 10 years
Low risk of malignancy (<5% but not 0)