Thyroid Gland Pathology

Question 1

What are the two types of endocrine cells in the thyroid gland? (2)

Answer 1

• Follicular cells (endoderm origin), surround protein-rich lakes of pink colloid
• C-cells (neural crest origin)

Question 2

What are thyroid follicular cells?

Answer 2

Question 3

What are the roles of the thyroid hormones (triiodothyronine, T3 and thyroxine, T4)? (4)

Answer 3

TSH tells thyroid follicular cells to increase the synthesis and secretion of thyroid hormones

Question 4

Physiology of the synthesis of thyroid hormones (5)

Answer 4

Question 5

What are thyroid C cells? (3)

Answer 5

Question 6

What is calcitonin? (3)

Answer 6

• Hypocalcemia, thyroid C cells accumulate secretory granules.
• Hypercalcemia, thyroid C cells will release these granules.
• Opposes the effects of parathyroid hormone (PTH).
  
  • C cells secrete calcitonin in response to hypercalcaemia
  • Long term hypercalcaemia results in hyperplasia of C cells

Question 7

Species variation in the shape of the thyroid gland (2)

Answer 7

• Cows = big, butterfly-shaped
• Cats = two little slugs on lateral surfaces of trachea

Question 8

What are the developmental malformations of the thyroid gland? (2)

Answer 8

• Ectopic thyroid tissue
• Thyroglossal duct cysts

Question 9

Answer 9

Question 10

What is ectopic thyroid tissue? (4)

Answer 10

Question 11

What are thyroglossal duct cysts? (5)

Answer 11

• Epithelium resembling thyroid follicles (if near the larynx)
• Usually less than 1 cm diameter
  
  • Can rupture – inflammation
  • Rarely undergo malignant transformation
• DDx for abscesses around the head and neck

Question 12

What causes hypofunction of the thyroid gland? (2)

Answer 12

• Lymphocytic (immune-mediated) thyroiditis (inflammation)
• Idiopathic follicular atrophy

Question 13

Answer 13

Question 14

Answer 14

Question 15

What is lymphocytic thyroiditis? (4)

Answer 15

Question 16

What is idiopathic follicular atrophy (4)

Answer 16

• Treatment (thyroid hormone replacement) exacerbates atrophy – negative feedback reduces TSH
• Few, small, follicles and fat infiltration

Question 17

What are the features of hypothyroidism? (4)

Answer 17

• Hypercholesterolaemia -> atherosclerosis
• Myxedema
• Sparse wool or hair
• Subnormal growth rate

Question 18

Answer 18

Question 19

Answer 19

Question 20

What are the features of hypothyroidism? (4)

Answer 20

• Hypercholestrolaemia -> athersclerosis
• Myxedema
• Sparse wool or hair
• Subnormal growth rate

Question 21

What is a goitre? (4)

Answer 21

Question 22

What causes follicular hyperplasia? (4)

Answer 22

• Iron deficiency
• Iodine excess
• Goitrogens - substances that cause goitres
• Congenital defects in synthesis of thyroid hormone

Question 23

What is a diffuse goitre?

Answer 23

Typically compensatory, TSH-induced response to hypothroidism

Question 24

What is a multinodular gotire? (3)

Answer 24

• Hyperplastic follicular cells acting autonomously (independent of TSH) to cause hyperthyroidism e.g. in old cats
• Groups of delinquent thyroid follicular epithelium ignore the hypothalamus & pituitary gland
• Rest of thyroid gland undergoes atrophy (negative feedback resulting in low TSH)

Question 25

Answer 25

Question 26

How does iron deficiency cause goitrogenesis? (3)

Answer 26

* Especially during foetal development (greatest need for thyroid hormone) – major cause of goitre in animals living in areas where iodine supplementation is required (take care not to give too much iodine because that also causes problems) * Deficient synthesis of T3 and T4 results in TSH-induced hyperplastic goitre * Not enough iodine -\> not enough thyroid hormone -\> no negative feedback loop, so the pituitary gland keeps shouting at the thyroid gland to produce thyroid hormone & thyroid follicular cells become super sensitive to iodine because they’re trying to extract every ion of it out of the blood

Question 27

How does excess iodine cause goitrogenesis? (3)

Answer 27

Excess iodine blocks release of thyroid hormones -\> decreased T3 & T4 -\> increased pituitary TSH

Question 28

What substances cause goitrogenesis? (Goitrogens) (3)

Answer 28

1. Plants (genus Brassica) - by-products of metabolism are goitrogens. 2. Thiocyanates, perchlorate and some ion - compete with iodine for uptake into thyroid follicular cells (act like iodine, so the thyroid follicles think they’re iodine –but they’re not. So when the thyroid follicular cells take them up, there is no T3 & T4 spat out the other end -\> no negative feedback loop so the pituitary gland starts raging. 3. Phenobarbital (used to treat seizures), rifampin and some other drugs - increase degradation of T3 and T4 Iodine deficiency increases the sensitivity to goitrogens (iodine-deficient animals will require less iodine supplementation because of their increased sensitivity to iodine. i.e. A dose of iodine that’s normal for an animal will be excessive in an iodine-deficient animal).

Question 29

What are congenital goitres and what are they caused by? (3)

Answer 29

* Congenital hypothyroidism caused by defective thyroid hormone synthesis, even with adequate dietary iodine * Linked to genetic defects - autosomal recessive in sheep and goats, rare in cattle, dogs and cats * Affected animals born with massive TSH-induced hyperplastic goitre

Question 30

What are the gross typical findings in diffuse follicular hyperplasia? (2)

Answer 30

* Diffuse enlargement * Reddening (inc vascularity)

Question 31

What are the gross typical findings in diffuse follicular hyperplasia? (3)

Answer 31

* Follicular epithelial cells become taller * Lumen of follicle reduced in size * Paler colloid than normal

Question 32

What are the features of hypothyroidism? (3)

Answer 32

* Myxoedema - skin folds, swelling, tragic facial appearance * Hair loss * Atherosclerosis - thick + white blood vv.

Question 33

Answer 33

Question 34

What are colloid goitres? (4)

Answer 34

Question 35

Answer 35

Question 36

What is multinodular hyperplasia ("goitre")? (5)

Answer 36

Question 37

What are the clinical signs of multinodular hyperplasia (goitre)? (6)

Answer 37

* Increased basal metabolic rate -\> * Weight loss with polyphagia * Polyuria & polydipsia * Increased frequency of defecation * Increased volume of stools * Increased activity

Question 38

What does the physical examination for multinodular hyperplasia involve? (4)

Answer 38

Tachycardia - thyrotoxic cardiomyopathy - lumen of heart gets smaller, muscle gets bigger

Question 39

What are the different neoplasms of the thyroid gland? (3)

Answer 39

* Follicular cell adenomas * Follicular cell carcinomas * Thyroid C-cell neoplasia

Question 40

Answer 40

Question 41

What are follicular cell adenomas? (10)

Answer 41

* Similar histological appearance to hyperplastic tissue * Cats = extra cells - hyperthyroidism + functional thyroid tumours -\> hyperthyroidism, treated with a thyroidectomy, medical treatment or radioactive iodine

Question 42

Answer 42

Question 43

What are follicular cell carcinomas? (6)

Answer 43

Question 44

What is thyroid C-cell neoplasia (3)

Answer 44

* Mainly aged bulls & horses & occasionally in dogs * Commonly develop with other endocrine neoplasms, particularly pheochromocytoma, resembles the human multiple endocrine neoplasia type II (MEN2) * Hyperplasia of C cells may precede the development of C-cell neoplasia, C-cell hyperplasia is a response to chronic hypercalcemia; bulls fed a high-calcium diet are prone to develop C-cell hyperplasia + neoplasia e.g. dairy bulls

Question 45

Most common equine thyroid tumour

Answer 45

C-cell adenoma

Question 46

Most common canine thyroid tumour

Answer 46

Thyroid carcinoma

Question 47

Most common feline thyroid tumour

Answer 47

Thyroid adenoma

Question 48

Most common thyroid tumour in bulls

Answer 48

C-cell carcinoma (also found in dogs)

Question 49

Describe the pathogenesis of congenital dyshormonogenetic goitre

Answer 49

Adequate iodine in the face of defective thyroid hormone synthesis