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Endocrinology > Pathology of the Thyroid > Flashcards

Pathology of the Thyroid Flashcards

1
Q

Where does the thyroid gland develop?

A
  • at the base of the tongue and travels along the thyroglossal duct to the anterior neck.
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2
Q

What is a thyroglossal duct cyst?

A
  • cystic dilation of the thyroglossal duct remnant.

- presents as an anterior neck mass.

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3
Q

What is a lingual thyroid?

A
  • persistence of thyroid tissue at the base of the tongue.

- presents as a mass at the base of the tongue.

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4
Q

What is HYPERthyroidism?

A
  • increased level of circulating thyroid hormone.
  • increases BMR
  • increases sympathetic nervous system activity.
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5
Q

** How does hyperthyroidism increase BMR?

A
  • by increasing the Na+/K+ ATPase
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6
Q

** How does hyperthyroidism increase the sympathetic nervous system?

A
  • by increasing B1-adrenergic receptors.
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7
Q

What are the clinical features of HYPERthyroidism?

A
  • WEIGHT LOSS despite increased appetite.
  • HEAT intolerance and sweating
  • tachycardia with increased cardiac output.
  • arrhythmia (a-fib) in elderly
  • tremor, anxiety, insomnia, and heightened emotions.
  • staring gaze with lid lag.
  • diarrhea with malabsorption.
  • oligomenorrhea
  • bone resorption with hypercalcemia.
  • decreased muscle mass with weakness.
  • HYPOCHOLESTEROLEMIA
  • HYPERGLYCEMIA
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8
Q

Why does hyperthyroidism cause HYPOcholesterolemia and HYPERglycemia?

A
  • bc thyroid hormone causes both gluconeogenesis and glycogenolysis
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9
Q

What is the most common cause of hyperthyroidism?

A
  • Graves disease
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10
Q

*** What is Graves disease?

A
  • autoantibody (IgG) stimulates TSH receptor, leading to increased synthesis and release of thyroid hormone.
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11
Q

In what group of people does Graves disease most often occur?

A
  • women of childbearing age
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12
Q

What are the clinical features of Graves disease?

A
  • hyperthyroidism
  • diffuse goiter (due to massive hypertrophy and hyperplasia of the thyroid gland).
  • EXOPHTHALMOS and PRETIBIAL MYXEDEMA
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13
Q

** What causes exophthalmos and pretibial myxedema in Graves disease?

A
  • fibroblasts behind the eye and behind the shin have TSH receptors, and in response to the autoantibody to the TSH receptor will secrete excess glycosaminoglycans (pushing the eyes outward and giving the shins a dough like appearance and structure).
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14
Q

** What will you see on histology of the thyroid in Graves disease?

A
  • enlarged follicles with SCALLOPING of the colloid (looks white around the edges)
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15
Q

What labs will you see with Graves disease?

A
  • increased total and free T4
  • decreased TSH due to the increased T4 down-regulating TRH receptors in the anterior pituitary.
  • hypocholesterolemia
  • hyperglycemia
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16
Q

How do you treat Graves disease?

A
  • B-blockers
  • Thioamide= blocks peroxidase (enzyme which catalyzes the production of thyroid hormone in the follicular lumen).
  • Radioiodine ablation
17
Q

What is Thyroid Storm?

A
  • elevated catecholamines and massive hormone excess (stress; child birth or surgery)
  • arrhythmia, hyperthermia, and vomiting with hypovolemic shock.
18
Q

How do you treat thyroid storm?

A
  • PTU= inhibits peroxidase mediated oxidation, organification, and coupling, as well as the peripheral conversion of T4 to T3.
  • B-blockers
  • steroids.
19
Q

What is a multinodular goiter?

A
  • enlarged thyroid gland with multiple nodules due to relative iodine deficiency.
  • usually nontoxic (euthyroid), but rarely regions can become TSH-independent (toxic goiter)
20
Q

What is HYPOthyroidism?

A
  • low thyroid hormone
21
Q

*** What is Cretinism?

A
  • HYPOthyroidism in NEONATES and INFANTS.
22
Q

** What are the clinical features of Cretinism?

A
  • mental retardation (bc thyroid hormone is important for brain development).
  • short stature with skeletal abnormalities
  • coarse facial features
  • enlarged tongue
  • umbilical hernia
23
Q

What are the causes of Cretinism?

A
  • maternal HYPOthyroidism during early pregnancy.
  • thyroid agenesis
  • dyshormonogenetic goiter (deficiency in ability to produce thyroid hormone).
  • iodine deficiency
24
Q

*** What is the most common enzyme that is deficient in dyshormonogenetic goiter (causing Cretinism)?

A
  • thyroid peroxidase (important for oxidation, organification, and coupling)
25
Q

*** What is Myxedema?

A
  • HYPOthyroidism in older CHILDREN or ADULTS.
26
Q

*** What are the clinical features of Myxedema?

A
  • Myxedema= edematous tissue with dough-like appearance due to excess glycosaminoglycans (especially in the LARYNX; deep voice, and TOUNGE).
  • WEIGHT GAIN despite normal appetite.
  • slowing of mental activity.
  • muscle weakness
  • COLD intolerance with decreased sweating.
  • bradycardia with decreased cardiac output
  • oligomenorrhea
  • HYPERcholesterolemia (ATHEROGENIC profile)
  • constipation.
27
Q

What can cause Myxedema?

A
  • iodine deficiency
  • HASHIMOTO THYROIDITIS
  • drugs (LITHIUM)
  • surgical removal or radioablation of thyroid
28
Q

** What is Hashimoto thyroiditis?

A
  • autoimmune destruction of thyroid gland; associated with HLA-DR5.
  • CD8+ T cells, cytokines produced by CD4+ T cells, and antithyroid antibodies all contribute to thyroid cell death.
29
Q

*** What are the clinical features of Hashimoto thyroiditis?

A
  • INITIALLY may present as HYPERthyroidism (due to leakage of thyroid hormone as the gland is initially destroyed).
  • progesses to HYPOthyroidism; decreased T4 and increased TSH.
  • antithyroglobulin and antimicrosomal antibodies are often present; just markers that damage is present.
  • symmetric/diffuse PAINLESS enlargement of thyroid.
  • remember anytime T4 goes down, TSH goes up due to negative feedback.
30
Q

** What will histology of the thyroid gland look like in Hashimoto thyroiditis?

A
  • chronic inflammation with GERMINAL CENTERS

- Hurthle cell changes= pink color change to cells that surround the thyroid follicle.

31
Q

For what disease are pts with Hashimoto thyroiditis at an increased risk?

A
  • B CELL Non-Hodgkin LYMPHOMA, bc you are generating post-germinal center B cells, which eventually form a MARGINAL ZONE.
32
Q

*** What is Subacute (deQuervain) Granulomatous Thyroiditis?

A
  • granulomatous thyroiditis that follows a viral infection.
  • NEUTROPHILIC infiltrate.
  • presents as TENDER/PAINFUL THYROID with transient hyperthyroidism.
  • self-limited (does NOT progress to HYPOthyroidism) :)
33
Q

What is Reidel Fibrosing Thyroiditis?

A
  • chronic inflammation with extensive asymmetric fibrosis of thyroid.
  • presents as HYPOthyroidism with ‘HARD as WOOD,’ nontender thyroid gland.
  • classically a YOUNG FEMALE.
34
Q

To where may fibrosis extend in Reidel Fibrosing Thyroiditis?

A
  • local structures (e.g. airway).
35
Q

If you had the same presentation as Reidel Fibrosing Thyroiditis, but in an older pt, what would you think instead?

A
  • anaplastic carcinoma of the thyroid
36
Q

What is the most common cause for CONGENITAL HYPOthyroidism?

A
  • IODINE DEFICIENCY
37
Q

What is ACQUIRED HYPOthyroidism?

A
  • surgical or radiation induced ablation of the thyroid.

- drugs given intentionally to decrease thyroid secretion.

38
Q

What normally causes a goiter?

A
  • dietary deficiency of iodine. TSH rises in an attempt to make more thyroid hormone, leading to hypertrophy.

Endocrinology (18 decks)

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