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endocrine > thyroid evaluation and disorders > Flashcards

thyroid evaluation and disorders Flashcards

1
Q

active T3

A

free T3

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2
Q

total T3

A

active and inactive T3 (inactive T3 bound to thyroid binding globulin, albumin and transthyretin)

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3
Q

TSH test

A

the most sensitive test

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4
Q

thyroid stimulating immunoglobulin

A

causes autoimmune Grave’s hyperthyroidism- excessive thyroid hormone production and thyroid enlargment

*** produces all the effects og TSH

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5
Q

Anti-thyroid peroxidase (TPO) Abs, a.k.a. anti-microsomal Abs
Anti-thyroglobulin Abs
elvated in?

A

Hashimoto’s

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6
Q

radiocative iodine

  1. uptake
  2. scan
  3. why is it used?
A
  1. Uptake = How much radioactive iodine is taken up into the gland (low, normal, high)?
  2. Scan = Where is the radioactive iodine being taken up?
  3. Single best test to determine etiology of hyperthyroidism
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7
Q

radioactive scan in graves

A

high uptake and diffuse pattern

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8
Q

radioactive scan in subacute thyroiditis

A

low uptake

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9
Q

Fine Needle Aspiration (FNA) Biopsy purpose

A

distinguish a benign from a malignant nodule

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10
Q

what happens if we do a thyroid nodule evaluation and it turns up HOT?

A

Don’t biopsy. Hot nodules are almost never malignant

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11
Q

The volume of both the extraocular muscles and retroocular tissue is increased seen in Graves, due to (3)

A

fibroblast proliferation, inflammation, and the accumulation of glycosaminoglycans, secreted by fibroblasts

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12
Q

radioactive iodine ablation

A

use I-131

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13
Q

which drug inhibits the thyroid leading to hypothyroidism

A

lithium

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14
Q

A hyperplastic process stimulated by autoantibodies leading to diffuse hyperplasia of follicular cells

A

grave’s disease

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15
Q

A destructive process mediated mostly by cytotoxic lymphocytes leading to shriveled, damaged follicular cells

A

Hashimoto’s disease

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16
Q

what do we see on hist o with graves?

A

increase in height of cells to form tall columnar cells forming pseudopillary buds

  • irregular follicles with a scalloped appearance
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17
Q

is lymphocytic infiltration common in graves?

A

yes but it is more in Hashimoto’s

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18
Q

histo for hashimoto’s

A

hurthle cells and fibrosis

Gland symmetrically or asymmetrically enlarged and tan or gray tan due to inflammatory cell infiltrate

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19
Q

what are hurthle cells?

A

it is where follicular cells accumulate mito and become oxyphilic

seen in hypo

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20
Q

what happens to the thyroid parenchyma in hypo?

A

it is replaced by intense infiltration by lymphocytes and plasma cells

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21
Q

de Quervain’s thyroiditis

A

Subacute granulomatous thyroiditis

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22
Q

“silent” or “painless”thyroiditis

A

Subacute lymphocytic thyroiditis

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23
Q

Riedel’s thyroiditis

A

IgG4 disease

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24
Q

thyroiditis:

usually presents as a painful neck mass in middle-aged women often preceded by URI/viral etiology leading to thryoid tissue destruction.

_ we see a neutrophilic followed by lymphoplasmacytic infiltrate, with foreign body granulomatous response to colloid from disrupted follicles

  • remits within a few months but sometimes progresses to hypo
A

Subacute Granulomatous Thyroiditis (de Quervain’s thyroiditis)

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25
Q

Incidental asymptomatic finding in up to 20% of adult autopsies. Most common in elderly women.

A

Focal Lymphocytic Thyroiditis

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26
Q

Incidental asymptomatic finding most common at institutions with lots of residents!
Scattered lymphohistiocytic aggregates and occasional giant cells formed in response to damage of follicles by palpation

A

Palpation Thyroiditis

27
Q

painless goiter where the thyroid shows dense fibrosis and mild inflammatory process involving thyroid and it extends into adjacent neck strucutres. It might present with sclerosing in other locations

A

riedel’s thyroiditis

28
Q

Enlarged thyroid gland, which can be due to a number of etiologies.
aka “thyromegaly”

A

goiter

29
Q

goiter can compress the (3)

A
  1. trachea
  2. esophagus
  3. blood vessels- pemberton’s sign–> you get red with raised arm
30
Q

what happens if the goiter if there are compressive symptoms?

A

surgery to remove it

31
Q

the most common type of goiter

A

adenomatous goiter- irregularly enlarged thyroid with multiple soft large nodules

32
Q

Histo presentation of goiter:

Many nodules with absent or
incomplete capsules,
Irregular, variable size follicles
No compression of surrounding follicles

A

adenomatous goiter

33
Q

histo presentation of goiter:

Solitary
 Complete capsule
 No invasion through capsule
 Follicles uniform
 Compression of surrounding tissue
 Often different morphology
A

adenoma

34
Q

differentiating goiters

A

fine needle aspiration biopsy

35
Q

allele that can be present with family history of thyroid cancer

A

MEN2

36
Q

most aggressive type of thyroid cancer

A

anaplastic

37
Q

histo of thyroid cancer:
Complex branching fronds with fibrovascular core and epithelial covering (Latin, papilla, nipple)
Calcificatons with concentric lamination: psammoma bodies Greek, psammos, sand)
Little colloid
Distinctive nuclei

A

papillary thryoid carcinoma

38
Q

artefact from formalin fixation of FINELY DISPERSED CHROMATIN

A

orphan annie eyes (vesicular/optically clear)

seen in follicular variant PTC

39
Q

histo of thyroid cancer:

Partially or non-encapsulated
Prominent capsular and/or vascular invasion
Frequently metastatic, often distant spread
Up to 20% have distant mets at presentation
May grossly resemble adenoma or may be widely invasive
May histologically resemble normal thyroid or may be more cellular
BUT DO NOT HAVE ORPHAN ANNIE EYE NUCLEI

A

follicular carcinoma

40
Q

besides in hypo, where else can you see hurthle cells?

A

in adenoma/carcinoma

41
Q

thyroid cancer:

Mainly elderly, >60 yrs, F/M ~ 1.5:1
OFTEN ARISES FROM A PRE-EXISTING PTC OR FTC
Rapidly growing, hard, fixed irregular mass, frequently invasive with distant metastases
Solid growth pattern with giant, spindle and squamoid cells, necrosis, numerous and atypical mitoses. NO RESEMBLANCE TO NORMAL THYROID
Does not take up radioactive iodine

A

anaplastic thyroid carcinoma

42
Q

cancer that is derived from C-cells and not follicular epithelium there is some family hx associated with MEN2A/B

A

medullary thryoid CA

43
Q

C cells

A

neuroendocrine cells that produce calcitonin

44
Q

thyroid cancer physical description:

Firm, white gray, sometimes fleshier than other thyroid CA

A

medullary carcinoma

45
Q

In medullary carcinoma the definitive marker is calcitonin but it also produces other neuroendocrine substances. We can often see _____ stroma due to it being derived from calcitonin precuros

A

amyloid

46
Q

________________ prior to carcinoma formation in familial MTC

A

Multifocal with C cell hyperplasia

47
Q

Disease states or drugs may affect thyroid binding proteins and metabolism which can change TFTs. Oral estrogens and acute hepatitis may ________ binding proteins. Malnutrition, cirrhosis and nephrotic syndrome may __________ binding proteins.

A

Disease states or drugs may affect thyroid binding proteins and metabolism which can change TFTs. Oral estrogens and acute hepatitis may increase binding proteins. Malnutrition, cirrhosis and nephrotic syndrome may decrease binding proteins.

48
Q

Thyroglobulin is made in the thyroid and is most commonly used as a

A

tumor marker for differentiated thyroid cancers.

49
Q

In primary hypothyroidism, TSH is _____ while T4 and free T4 are_______. T3 levels may not be ____ due to an increase in deiodinase converting T4 to T3. Thus, T3 is less useful for biochemical diagnosis of hypothyroidism.

A

In primary hypothyroidism, TSH is elevated while T4 and free T4 are low normal or low. T3 levels may not be low due to an increase in deiodinase converting T4 to T3. Thus, T3 is less useful for biochemical diagnosis of hypothyroidism.

50
Q

is a state of decompensated hypothyroidism requiring intravenous thyroid hormone and other supportive therapy

A

Myxedema coma

51
Q

why is it important to check T3 if hyperhtyroidism is suspected?

A

In mild cases, T4 and free T4 might be at the upper end of the normal range while T3 is elevated.

52
Q

why are beta blockers used un treatment of hyperhtyroidism?

A

help control symptoms

53
Q

thyroid storm treatment

A

corticosteroids and cold iodine

54
Q

Propylthiouracil (PTU) and methimazole (mostly methimazole) are the antithyroid medications used for treatment in the United States. They both interfere with thyroid hormone synthesis at multiple steps. what is the other effect that PTU has that methimazole does not?

A

PTU also blocks T4 to T3 conversion (methimazole does not)

55
Q

____________ is a destructive process mediated mostly by cytotoxic T-lymphocytes. Glands show dense lymphocytic infiltrate, follicular destruction, Hürthle cell metaplasia of residual follicular epithelium.

A

Hashimoto’s thyroiditis

56
Q

____________ is a hyperplastic process caused by agonist antibodies against TSH receptor. Tissue infiltration by lymphocytes is variable and less dense than in Hashimoto’s.

A

Graves’ disease

57
Q

is the most common type of thyroid cancer and has a very good prognosis in the vast majority of patients.

A

Papillary thyroid carcinoma

58
Q

______________ is mostly used as a tumor marker for differentiated thyroid cancer. Calcitonin is a tumor marker for ______________

A

Serum thyroglobulin is mostly used as a tumor marker for differentiated thyroid cancer. Calcitonin is a tumor marker for medullary thyroid cancer

59
Q

__________ are encapsulated, often look different from adjacent thyroid, do not have “Orphan Annie” nuclei, are not invasive. Entire capsule must be sampled to distinguish from follicular carcinoma. which can be diagnosed only by capsular invasion.

A

Adenomas

60
Q

in benign multinodular (adenomatous) goiter have absent or incomplete capsules, variable size and morphology, often look like adjacent thyroid, do not have “Orphan Annie” nuclei.

A

“Adenomatous nodules”

61
Q

PTC and FTC are distinguished from each other by _______________, not follicular architecture. “Follicular variant” of PTC has ________________ (FTC does not), behaves mostly like classic PTC (lymphatic vs hematogenous spread).

A

PTC and FTC are distinguished from each other by nuclear morphology, not follicular architecture. “Follicular variant” of PTC has Orphan Annie nuclei (FTC does not), behaves mostly like classic PTC (lymphatic vs hematogenous spread).

62
Q

PTC and FTC are considered “well differentiated”. ______________ is by definition undifferentiated, does not resemble anything in normal thyroid morphologically or immunohistochemically (no thyroglobulin, no RAI uptake).

A

Anaplastic carcinoma

63
Q

Abnormal genes in thyroid cancers include BRAF and RET/PTC in______________________, RAS and PAX8-PPARγ1 in_____________________ and p53 in _____________________

A

Abnormal genes in thyroid cancers include BRAF and RET/PTC in papillary thyroid carcinomas, RAS and PAX8-PPARγ1 in follicular carcinomas and p53 in anaplastic thyroid carcinoma

64
Q

___________________ are developmentally distinct from thyroid follicular cells, synthesize calcitonin and give rise to medullary thyroid carcinoma

A

C-cells (C stands for calcitonin)

endocrine (19 decks)

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