4. Pathology Of Thyroid

Front 1

Follicles lined with columnar epithelium. Between the follicles are a number of differently staining cells. What are they and what function do they serve?

Back 1

Parafollicular/C cells. These cells secrete calcitonin which opposes the action of PTH (increases calcium deposition in bone, decreasing calcium in circulation)

Front 2

What is the effect of thyroid hormone on carbohydrate catabolism, lipid catabolism, protein catabolism? How does it exert its effects?

Back 2

T3 & T4 circulate bound to TBG. Thyroid response elements (TREs) at target tissues bind thyroid hormone (usually T3).

Increases catabolism of protein, increases catabolism of lipids, increases SYNTHESIS of protein (not catabolism)

Front 3

Calcitonin's effect on calcium? How does it exert its effects?

Back 3

Decreases calcium in circulation. Inhibits osteoclasts (less Ca liberated from bone), inhbits intestine (less Ca absorbed), inhibits renal tubule cells (less Ca absorbed, more excreted in urine)

Front 4

Difference between thyrotoxicosis and hyperthyroidism?

Back 4

Both indicate an increase in T4. Hyperthyroidism indicates that the problem is an increased thyroid function (increased synthesis).

Front 5

Difference between primary and secondary hyperthyroidism? Examples?

Back 5

Primary- excess production of T3/T4 by thyroid (Graves, goiter, toxic adenoma)

Secondary- disorder outside thyroid gland (TSH-secreting adenoma)

Front 6

Primary vs. secondary vs. thyroiditis- how do these levels change?

Free thyroid hormone, TSH, radioactive iodide uptake

Back 6

Primary- increased free thyroid hormone, decreased TSH, increased radioactive iodide uptake

Secondary- increased free thyroid hormone, increased TSH, increased radioactive iodide uptake

Thyroiditis- increased free thyroid hormone, decreased TSH, decreased iodine uptake

Front 7

Signs & symptoms of hyperthyroidism

Back 7

Increased metabolic rate, increased HR, heat intolerance, anxiety, osteoporosis, diarrhea

Front 8

Primary vs. secondary vs. tertiary hypothyroidism

Back 8

Primary- at level of thyroid (developmental problem, synthesis problem, iodine deficiency, hashimoto's, drugs, thyroid ablation)

Secondary- problems at level of pituitary (decreased TSH)

Tertiary- problems at level of hypothalamus (decreased TRH)

Front 9

What is cretinism? What does it tell us about the role of thyroid hormone?

Back 9

A manifestation of hypothyroidism in utero or early life. Pts have mental retardation, short stature, coarse features, protruding tongue.

Verifies essential role of thyroid hormone in development (especially of brain)

Front 10

What is myxedema? What is it typically associated with?

Back 10

Due to hypothyroidism. Seen with fatigue, weight gain, decreased exercise capacity, coarse features, constipation

Due to deposition of glycosaminoglycans!

Front 11

Is thyroiditis painful? What is it caused by?

Any other systemic symptoms?

Back 11

YES! Acute- bacteria. Chronic- mycobacterium or viruses

Fever

Front 12

Increased risk of Hashimoto's in which of the following karyotypes (may be more than 1 correct answer):

a- XXY
b- Trisomy 13
c- Trisomy 16
d- Trisomy 21
e- XXYY
f- XO

Back 12

D & F- Turner and Down

hashimoto's TURNs DOWN your thyroid

Front 13

True or false, in Hashimoto's the thyroid is attacked via cell mediated, cytotoxic and antibody dependent pathways.

True or false, Hashimoto's is painful

True or false, the thyroid gets bigger in Hashimotos

Back 13

True

False

True, moderately enlarged

Front 14

microscopic changes in a hashimoto's thyroid.

Back 14

Look for germinal centers (filled with lymphocytic cells), Hurthle cells (epithelial metaplasia) and fibrosis

Front 15

A patient with Hashimoto is at an increased risk of developing which malignancy?

Back 15

B cell, MALT lymphoma (non-hodgkin)

Front 16

Cause of dequervains thyroiditis? How can it be distinguished microscopically?

Back 16

Viral infection --> cytotoxic T cell injury

Dequervains presents with multinucleated giant cells around residual colloid

Giant cells=macs
MACquerVains thyroiditis (v for viral)

Front 17

True or false, Dequervains is painful. What symptoms are seen?

Back 17

True.

Fever, malaise, myalgias, subclinical hypothyroidism

Front 18

Painless thyroiditis with germinal centers

Back 18

Subacute thyroiditis- may be a precursor to hashimoto's

Thyroid does NOT enlarge much (unlike hashi)

Front 19

Notable features of Riedel thyroiditis?

Back 19

FIBROSIS of thyroid gland and adjacent structures of neck

Front 20

Graves disease- common in what demographic? Any genetic susceptibility?

Back 20

Common in young-middle aged women.

Certain HLA antigens as well as CTLA-4 variants (normally a T cell inhibitor)

Front 21

Graves is technically caused by 3 different types of autoantibodies. Explain what each one does

Back 21

TSI- Binds & stimulates @ TSH receptor --> increase thyroid hormone release
TGI- causes thyroid hyperplasia
TBII- stimulates or inhibits thyroid follicular cell function

Front 22

What causes opthalmopathy in graves patients?

Back 22

Autoimmune T cell reaction against fibroblasts + synthesis of glycosaminoglycans (different than lid lag, seen in other hyperthyroidism)

GAGs are also responsible for pretibial myxedema

Front 23

Characteristic microscopic finding in Graves disease

Back 23

Scalloped edges of follicles

Front 24

Pathogenesis of goiter- explain

Back 24

Thyroid gland is struggling to make thyroid hormone. More TSH is synthesized leading to hypertrophy & hyperplasia of thyroid follicular cells. Growth is uneven

Patients may manage to remain euthyroid or develop hypothyroidism

Front 25

Causes of goiter

Back 25

IODINE deficiency (uncommon in US since we iodinate our water)
Enzyme defects
Injestion of goitrogens (brussel sprouts, cauliflower, cassava)
Idiopathic

Front 26

Micro appearance of goiter

Back 26

Alternating regions of follicular hyperplasia and areas of inactivity with HUGE amounts of colloid accumulation

Front 27

most common demographic with goiter

Back 27

Women. young adults- diffuse goiter, older- multinodular

Front 28

Plummer syndrome

Back 28

A person with goiter that develops a hyperactive autonomous nodule

Front 29

Thyroid neoplasia- 4 types

More often benign of malignant

More often in males of females?

Back 29

1. Follicular adenoma
2-4. papillary/medullary/anaplastic carcinoma

More often benign and found in females

Front 30

Describe follicular adenoma, gross & micro

Clinical features

Back 30

Gross- well circumscribed mass with obvious fibrous capsule

Micro- no capsular or vascular invasion

Clinical- usually not detected, most are nonfunctional (cold)

Front 31

Papillary carcinoma- risk factors?

Gross?
Microscopic?
Clinical?
Behavior?

Back 31

Previous radiation exposures (esp. at young age)

Gross- Variable appearance, often cystic
Micro- ground glass/orphan Annie nuclei (grooved) + psammoma bodies
Clinical- asymptomatic cold nodule, Behavior- CAN METASTASIZE to regional lymph nodes (but prognosis is good)

Front 32

Follicular carcinoma- risk factors?

Gross?
Micro?
Clinical?
Behavior?

Back 32

Risk- iodine deficient countries

Gross- wide range (well circumscribed to infiltrative)
Micro- varying (well differentiated to obvious neoplasm)
Clinical- painless, cold, slowly enlarging
Behavior- METS hematogenously (not lymphatics)

Front 33

Anaplastic carcinoma- risks?

Micro?
Clinical?
Behavior?

Back 33

Least common, Usually older adults with previous thyroid carcinoma

Micro-Tons of pleomorphic anaplastic spindle shaped cells
Clinical- RAPIDLY enlarging mass (may infiltrate structures of neck- SERIOUS)
Behavior- widespread, very poor prognosis (<1 year)

Front 34

Medullary carcinoma- risk?

Gross?
Micro?
Clinical?

Back 34

Neuroendocrine origin, mutation of RET oncogene (usually sporadic)

Gross- heterogeneous and infiltrative
Micro- salt and pepper chromatin + AMYLOID + C CELL HYPERPLASIA
Clinical- thyroid mass, often in pts with other endocrine tumors