Thyroid Gland Pathology Flashcards

1
Q

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

A
  • Follicular cells (endoderm origin), surround protein-rich lakes of pink colloid
  • C-cells (neural crest origin)
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2
Q

What are thyroid follicular cells?

A
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3
Q

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

A

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

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4
Q

Physiology of the synthesis of thyroid hormones (5)

A
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5
Q

What are thyroid C cells? (3)

A
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6
Q

What is calcitonin? (3)

A
  • 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
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7
Q

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

A
  • Cows = big, butterfly-shaped
  • Cats = two little slugs on lateral surfaces of trachea
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8
Q

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

A
  • Ectopic thyroid tissue
  • Thyroglossal duct cysts
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9
Q
A
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10
Q

What is ectopic thyroid tissue? (4)

A
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11
Q

What are thyroglossal duct cysts? (5)

A
  • 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
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12
Q

What causes hypofunction of the thyroid gland? (2)

A
  • Lymphocytic (immune-mediated) thyroiditis (inflammation)
  • Idiopathic follicular atrophy
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13
Q
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14
Q
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15
Q

What is lymphocytic thyroiditis? (4)

A
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16
Q

What is idiopathic follicular atrophy (4)

A
  • Treatment (thyroid hormone replacement) exacerbates atrophy – negative feedback reduces TSH
  • Few, small, follicles and fat infiltration
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17
Q

What are the features of hypothyroidism? (4)

A
  • Hypercholesterolaemia -> atherosclerosis
  • Myxedema
  • Sparse wool or hair
  • Subnormal growth rate
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18
Q
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19
Q
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20
Q

What are the features of hypothyroidism? (4)

A
  • Hypercholestrolaemia -> athersclerosis
  • Myxedema
  • Sparse wool or hair
  • Subnormal growth rate
21
Q

What is a goitre? (4)

A
22
Q

What causes follicular hyperplasia? (4)

A
  • Iron deficiency
  • Iodine excess
  • Goitrogens - substances that cause goitres
  • Congenital defects in synthesis of thyroid hormone
23
Q

What is a diffuse goitre?

A

Typically compensatory, TSH-induced response to hypothroidism

24
Q

What is a multinodular gotire? (3)

A
  • 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)
25
Q
A
26
Q

How does iron deficiency cause goitrogenesis? (3)

A
  • 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
27
Q

How does excess iodine cause goitrogenesis? (3)

A

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

28
Q

What substances cause goitrogenesis? (Goitrogens) (3)

A
  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).

29
Q

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

A
  • 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
30
Q

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

A
  • Diffuse enlargement
  • Reddening (inc vascularity)
31
Q

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

A
  • Follicular epithelial cells become taller
  • Lumen of follicle reduced in size
  • Paler colloid than normal
32
Q

What are the features of hypothyroidism? (3)

A
  • Myxoedema - skin folds, swelling, tragic facial appearance
  • Hair loss
  • Atherosclerosis - thick + white blood vv.
33
Q
A
34
Q

What are colloid goitres? (4)

A
35
Q
A
36
Q

What is multinodular hyperplasia (“goitre”)? (5)

A
37
Q

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

A
  • Increased basal metabolic rate ->
  • Weight loss with polyphagia
  • Polyuria & polydipsia
  • Increased frequency of defecation
  • Increased volume of stools
  • Increased activity
38
Q

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

A

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

39
Q

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

A
  • Follicular cell adenomas
  • Follicular cell carcinomas
  • Thyroid C-cell neoplasia
40
Q
A
41
Q

What are follicular cell adenomas? (10)

A
  • Similar histological appearance to hyperplastic tissue
  • Cats = extra cells - hyperthyroidism + functional thyroid tumours -> hyperthyroidism, treated with a thyroidectomy, medical treatment or radioactive iodine
42
Q
A
43
Q

What are follicular cell carcinomas? (6)

A
44
Q

What is thyroid C-cell neoplasia (3)

A
  • 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
45
Q

Most common equine thyroid tumour

A

C-cell adenoma

46
Q

Most common canine thyroid tumour

A

Thyroid carcinoma

47
Q

Most common feline thyroid tumour

A

Thyroid adenoma

48
Q

Most common thyroid tumour in bulls

A

C-cell carcinoma (also found in dogs)

49
Q

Describe the pathogenesis of congenital dyshormonogenetic goitre

A

Adequate iodine in the face of defective thyroid hormone synthesis