Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine & Reproduction II Exam #2 > Thyroid Pathology > Flashcards

Thyroid Pathology Flashcards

1
Q

Essential action of the thyroid

A

Increase BMR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is T3 and T4 released?

A

Thyroglobulin (Tg) is synthesized and stored in colloid.

Iodide is transported into the cell and incorporated into Tg to form iodinated tyrosines.

Tg is endocytosed and cleaved to release free T3 and T4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are 3 subtypes of Primary Hyperthyroidism?

A 
Diffuse hyperplasia (Graves disease)
Hyperfunctioning multinodular goiter
Hyperfunctioning thyroid adenoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which kind of hyperthyroidism is most common?

A

Primary hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the 1 secondary hyperthyroidism?

A

Pituitary adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the 3 variants of hyperthyroidism:

Apathetic hyperthyroidism

Regular hyperthyroidism

Thyroid storm

A

Apathetic hyperthyroidism - older adults w/ masked symptomatology; unexplained weight loss; CVD

Regular hyperthyroidism - sweating, flushing, psychiatric changes, palpitations/tachycardia, exophthalmos, jitters

Thyroid storm - extreme and abrupt episode of potentially life-threatening thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which drug can precipitate thyroid storm?

A

Amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the the levels of TH and TSH in primary and secondary hyperthyroidism?

A

Primary: elevated TH, low TSH

Secondary: elevated TH, high TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Treating the manifestations of hyperthyroidism:

Treating the underlying disease of hyperthyroidism:

A

Manifestation: beta-blockers, NSAIDs

Underlying Dz: high-doses of iodide (Wolff-Chaikoff effect), Thionamide, Radioiodine ablation, surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Graves disease is the most common…

What 3 things is it characterized by?

A

Etiology of hyperthyroidism.

  1. Hyperthyroidism w/ gland enlargement
  2. Infiltrative ophthalmopathy
  3. Pretibial myxedema - infiltrative dermopathy and scaly, indurated skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Graves disease-associated orbitopathy/ophthalmopathy is characterized by… (2)

A

Thickened EOM + Retraction of eyelids w/ associated proptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

5 steps of pathogenesis of Graves disease affecting the orbit

A
  1. Lymphocytes invade pre-orbital space
  2. Fibroblasts have TSH receptor
  3. EOM swelling
  4. Matrix accumulates
  5. Adipocytes expand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Levels of the following in Graves disease:

T3/4
TSH
TSI (thyroid-stimulating Ig)

A

T3/4 - high
TSH - low
TSI (thyroid-stimulating Ig) - high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Features of Congenital Hypothyroidism (Cretinism) (4)

Where is it endemic?

It can be a result of…

A

MR, GR, coarse facial features, umbilical hernias.

Areas without iodine supplementation (depends on time of onset in the mother).

Genetic alterations in normal thyroid metabolic pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Myxedema occurs in which ages?

What are symptoms? (4)

A

Adults and older children

Mental and physical sluggishness
Weight gain
Cold intolerance
Cardiac effect - lower CO, hypercholesterolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hashimoto thyroiditis =

It is the most common cause of…

How does the thyroid gland appear?

What is the level of thyroid function? Any exceptions?

What’s the progression?

A

Auto-Abs against thyroglobulin (Tg) and thyroid peroxidase (TPO).

Most common cause of hypothyroidism in iodide-sufficient areas.

Thyroid is diffuse, painless and enlarged.

Hypothyroid (usually), but can be hyperthyroid if Hashitoxicosis.

Progression:

  1. Immune-mediated insult
  2. Hyperactivity and enlargement
  3. Follicular cell exhaustion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does Hashimoto’s thyroiditis appear on histology? (2)

A

Lymphocytic infiltrate w/ germinal centers.

Atrophic cells with eosinophilic change (Hurthle cell metaplasia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What auto-antibodies are there in Hashimoto’s vs. Graves?

A

Hashimoto’s:

  • TSHR-Ab (TSI) - 10-20%
  • hTg-Ab - 80-90%***
  • hTPO-Ab - 90-100%***

Graves:

  • TSHR-Ab (TSI) - 80-95%***
  • hTg-Ab - 50-70%
  • hTPO-Ab - 50-80%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Subacute lymphocytic thyroiditis presents how?

Example:

What may it progress to?

A

A transient period of thyroid hormone irregularities.

  • hyperthyroidism (occasionally hypothyroidism)
  • goiter

Postpartum thyroiditis.

May progress to permanent hypothyroidism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Granulomatous (de Quervain’s) thyroiditis presents how?

What is its origin?

What does it usually get lumped in with?

A

Painful granulomata.

Possibly viral (i.e. mumps).

Subacute thyroiditis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Associated disease with HLA-B35 =

A

Granulomatous (de Quervain’s) thyroiditis

22
Q

What occurs to the thyroid tissue in Riedel thyroiditis?

What cells are in high concentration?

Which group of disease is it in? What are the hallmarks?

A

It is a fibrosing process that extends into the adjacent tissue. “Feels like cement”.

Plasma cells and lymphocytes (in addition to fibrosis).

IgG4-related disease - fibrosis and IgG4+ plasma cells are hallmarks of these diseases.

23
Q

Hashmoto’s in review

Cause
Histology
Thyroid state
Level of TPO Ab’s

A

Cause: autoimmune
Histology: lymphocytes
Thyroid state: hypothyroid
Level of TPO Ab’s: high titer

24
Q

Subacute lymphocytic thyroiditis in review

Cause
Histology
Thyroid state
Level of TPO Ab’s

A

Cause: autoimmune
Histology: lymphocytes
Thyroid state: hypo- or hyperthyroidism
Level of TPO Ab’s: high titer

25
Q

Granulomatous (de Quervain’s) thyroiditis

Cause
Histology
Thyroid state
Level of TPO Ab’s

A

Cause: unknown (viral?)
Histology: granulomata
Thyroid state: hypo- or hyperthyroidism
Level of TPO Ab’s: low or absent titer

26
Q

Riedel thyroiditis

Cause
Histology
Thyroid state
Level of TPO Ab’s

A

Cause: unknown (IgG4-related)
Histology: fibrosis
Thyroid state: euthyroid (normal function)
Level of TPO Ab’s: variable

27
Q

Diffuse non-toxic goiter

What “types” of goiter can it be?

A

Endemic goiter - iodine deficiency
-Goitrogens: Cassava root (thiocyanate) and Brassicaceae (broccoli, cauliflower, cabbage and radishes)

Sporadic goiter: more common in females and unknown etiology.

28
Q

What symptoms often come with diffuse goiters?

What is the thyroid function like?

A

Symptoms due to mass effect: dysphagia, hoarseness, stridor, SVC syndrome.

Usually euthyroid.

29
Q

What are some features of a multinodular goiter? (3)

What symptoms?

What is unique about them?

A

Hyperplasia, regression (involution) cycle.
Varied response of nodules to stimuli.
Neoplastic nature of some nodules (adenomas).

Mass effect symptoms - same as diffuse goiters.

May become strikingly large!

30
Q

What does Radioisotope scanning (thyroid scintigraphy) used for?

What “types” of nodules might it reveal? (2)
What should be done if you find one of these nodules?

A

Determining which nodule is responsible for hyperfunction (if so, it can be treated w/ excision or ablation).

Hot or cold nodules.

  • hot nodules will be treated with iodine or surgery.
  • cold nodules are more likely to be neoplastic and get a US and FNA.
31
Q

Benign thyroid nodules (2)

A

Hyperplastic (adenomatoid) nodules + Follicular adenomas

32
Q

Follicular adenomas =

They are benign, but what must you evaluate to be certain? (2)

A

Discrete clonal population of follicular cells w/ “thyroid autonomy”.

  1. Capsule intact - no growth pattern of follicular carcinoma.
  2. No nuclear features of papillary carcinoma.
33
Q

What is the most common malignant tumor of the thyroid gland?

What age do they most often occur?

How do they present?

What imaging should be ordered?

A

Papillary thyroid carcinoma

25-50 y/o

Typically w/o symptoms as a palpable nodule.

Order a US.

34
Q

What histologic finding is seen in Papillary thyroid carcinoma?

What are 2 mutations associated with it?

A

Psammoma bodies and papillary architecture.

RET-PTC mutations + BRAF mutations

35
Q

What is the diagnostic feature allowing for a diagnosis of Papillary thyroid carcinoma?

A

Nuclear characteristics - enlarged nuclei w/ “clear” appearance.

“Orphan Annie Eye nuclei”

36
Q

Follicular variant of Papillary thyroid carcinoma have which histological features?

What genetic changes are common?

A

Follicular architecture, but nuclear features of papillary carcinoma.

More cases w/ RAS mutations (similar to follicular carcinomas/adenomas) - less with RET-PTC and BRAF mutations

37
Q

Tall cell variant of Papillary thyroid carcinoma has a predilection for which age group?

A

Older patients

38
Q

Which thyroid carcinoma is considered highly aggressive?

A

Tall cell variant of papillary carcinoma

39
Q

Diffuse sclerosing variant of Papillary carcinoma

What age groups?

Where are the metastases?

What is the disease survival rates at 10 years?

A

Kids and young adults.

Greater incidence of distant mets (10-15%) - lung, brain, bone and liver. Despite these mets, mortality rates are comparable to those of conventional PTCs.

93% survival rate at 10 years.

40
Q

Follicular carcinomas are more common in which areas?

Which mutations are associated?

How common are they?

A

More common in areas w/ goiter from iodide deficiency.

PAX8/PPARG mutations.

Less common than PTC (5-15%).

41
Q

What classic histological findings are found in Follicular carcinoma? (2)

It is still considered a…

A

Invasive properties: invasion of the capsule (mushroom) and angioinvasion.

Differentiated thyroid carcinoma.

42
Q

What are therapeutic options for differentiated thyroid carcinoma? (2)

What if refractory? (2)

A

Surgery + radioactive iodine

Chemotherapy + tyrosine kinase inhibitors (in progress)

43
Q

Anaplastic carcinoma tends to affect which age group?

How common?

What is the progression?

What mutations are common?

A

Elderly patients.

Uncommon - 5% of thyroid carcinoma.

Highly aggressive - present w/ mass effect and patients die within 1 year of local invasion.

TP53

44
Q

Genetics/mutations and thyroid malignancies:

RET/PTC rearrangements + BRAF (MAP kinase signaling) =

PAX8-PPARG =

RAS + PTEN =

TP53 =

A

RET/PTC rearrangements + BRAF (MAP kinase signaling) = Papillary carcinoma

PAX8-PPARG = Follicular carcinoma

RAS + PTEN = non-specific follicular neoplasms

TP53 = Anaplastic carcinoma

45
Q

What is the function of C cells?

A

Secretion of calcitonin

46
Q

What kind of cancer is thyroid medullary carcinoma (MTC)?

What are 3 histological findings in thyroid medullary carcinoma?

A

NE carcinoma derived from C cells

Histology:

  • blue cells w/ dispersed chromatin
  • amyloid
  • C-cell hyperplasia
47
Q

Sporadic MTC makes up how many cases of MTC?

What “kind” of tumors there they?

Mean age:

Progression:

A

70-80% of MTC cases

Unifocal tumors

Mean age = 50 y/o

Aggressive - 50% rate of LN mets at time of diagnosis.

48
Q

Familial MTC has the…

What “kind” of tumors are they?

Mean age:

A

Best prognosis of all forms (100% at 15 years)

Multifocal tumors

Mean age = 43 y/o

49
Q

10-year survival rates of MTC when…

Confined to the thyroid
Spreads to cervical LNs
Mets at distant sites

A

Confined to the thyroid - 90%
Spreads to cervical LNs - 70%
Mets at distant sites - 20%

50
Q

What mutation of which gene, on which chromosome, are found in familial MTC?

A

RET proto-oncogene on chr. 10

Endocrine & Reproduction II Exam #2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions