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Endocrine-W3 > Thyroid and Parathyroid Pathology > Flashcards

Thyroid and Parathyroid Pathology Flashcards

1
Q

parathyroid cells types (3)

A

-Chief cells
-Oxyphillic cells
-Adipose cells

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2
Q

Chief Cells (3)

A

-Functional cells
-Parathyroid hormone synthesis and release
-Contain calcium sensing receptors

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3
Q

Parathyroid hormone (4)

A

Regulates serum calcium
- promoting release of calcium (and phosphate) from bone
- increases production of vitamin D to enhance intestinal calcium absorption
- Deceases calcium loss in urine, increases phosphate excretion

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4
Q

Parathyroid Adenoma (3)

A

> 85% of primary hyperparathyroidism
-10% hereditary
MEN1, MEN2, MEN4, HPT-JT

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5
Q

Parathyroid Adenoma vs Hyperplasia (4)

A

-Can look identical
-Conventional wisdom used to limit adenoma diagnosis to single entity “assuming normality/suppression of remaining glands”
-multiple adenomas in hereditary hyperparathyroidism (ie MEN etc)
-These are now recognised as adenomas, not hyperplasia

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6
Q

Hyperplasia (2)

A

-Primary hyperplasia thought to be v.rare
-Secondary / compensatory hyperplasia associated with physiological stimulus (ie low serum calcium, high serum phosphate, vit D deficiency)

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7
Q

Parathyroid Carcinoma (4)

A

<1% of primary hyperthyroidism cases

Can be familial - 15% of HPT-JT patients will develop

Can be sporadic

CDC73 (usually deletion / inactivation)
-Codes for parafibromin tumour suppressor protein

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8
Q

Diagnostic criteria for parathyroid carcinoma (5)

A

showing at least one of the following:
-Angioinvasion
-Lymphatic invasion
-Perineural invasion
-Invasion of adjacent structures/organs
-Regional/distant metastasis

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9
Q

Atypical Parathyroid Tumour (4)

A

looks weird but doesn’t meet the diagnostic criteria for parathyroid carcinoma

-Atypial cytological and architectural features, extension into capsule (but not through and into surrounding tissue)

-But not to be overused

-Parathyroid adenomas can have variation in appearance / occasional mitoses

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10
Q

Thyroid histology (3)

A

Follicular cells
Parafollicular Cells

Colloid

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11
Q

Thyroid physiology (4)

A
  1. hypothalamus releases hormone TRH which stims pituitary gland

2.pituitary gland releases hormone TSH which stims thyroid gland

3.thyroid gland makes the thyroid hormone T3 +T4

  1. As T3 + T4 are made they signal hypothalamus + pituitary to stop stimulating e.g. when T3 + 4 are adequate no more needs to be made
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12
Q

Thyroid Pathology (4)

A

Non-neoplastic=
-Inflammatory / Autoimmune

Neoplasia= Benign + Malignant

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13
Q

Non Neoplastic (3)

A

Multinodular goitre

Hashimotos thyroiditis

Graves disease

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14
Q

Multinodular goitre (5)

A

Also called nodular / multinodular hyperplasia
-Colloid goitre, hyperplastic nodule etc
-All represent the same process

Diffuse or nodular enlargement of the gland

Often very distorted

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15
Q

Hashimoto Thyroiditis (4)

A

Autoimmune process
-Elevated circulating antiperoxidase + antithyroglobulin antibodies
-Female predominance

Hyperplastic gland, usually 2-3X normal size, usually diffuse and symmetrical enlargement.

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16
Q

Hashimoto Thyroiditis path (3)

A

lymphatic infiltrate with germinal centre

-follicular trophy
-hurthle cell

17
Q

Graves’ Disease (5)

A

Also known as diffuse hyperplasia

Autoimmune process
-Diffuse goitre, thyrotoxicosis, infiltrative opthalmopathy

From pathology perspective, important to know if patient has been treated
-Carbimazole can affect the way the cells look microscopically

18
Q

Neoplasms- Benign (2)

A

Follicular adenoma
-Oncocytic adenoma

19
Q

Neoplasms- Benignish (3)

A

NIFT-P
Thyroid Tumour of Uncertain Malignant Potential
Hyalising Trabecular Tumour

20
Q

Neoplasms- Malignant (7)

A

Papillary carcinoma

Medullary carcinoma

Follicular carcinoma
-Oncocytic carcinoma

High grade follicular cell derived non-anaplastic thyroid carcinoma
-Poorly differentiated thyroid carcinoma
-Differentiated high grade thyroid carcinoma

21
Q

Follicular adenoma (2)

A

Encapsulated neoplasm of thyroid follicular cells

Lacks capsular or vascular invasion

22
Q

Oncocytic adenoma (4)

A

Previously known as Hurthle cell adenoma

Used to be a subtype of follicular adenoma, now has its own category

Oncocytic cells = swollen and pink

Encapsulated, non invasive

23
Q

Follicular Carcinoma (4)

A

Looks like a follicular adenoma, but can have capsular invasion or vascular invasion

Or both

Can be widely invasive or minimally invasive, with or without vascular invasion

Additional variant “encapsulated with angioinvasion”

24
Q

Oncocytic Carcinoma (3)

A

Used to be a variant of follicular carcinoma

Now has its own category

Criteria for malignancy same as follicular adenoma, but lesion must have dominant oncocytic cell component

25
Q

Thyroid Tumours of Uncertain Malignant Potential (3)

A

Essentially used in situations where invasion is equivocal Or incomplete

For example, invasion into capsule, but not all the way through

Or tumour bulging into vessels but not fully into endothelial lined space

26
Q

Papillary Thyroid Carcinoma (PTC) (2)

A

Most common thyroid malignancy

Multiple subtypes based on architecture, many have prognostic implications

27
Q

PTC subtypes (11)

A

-Classic PTC
-Encapsulated PTC
-Diffuse sclerosing PTC
-Sold/trabecular PTC
-Warthin-like PTC
-Oncocytic PTC
-Spindle cell PTC
-PTC with fibromatosis/fasciitis-like/desmoid type stroma
-Tall cell PTC
-Hobnail PTC
-Columnar Cell PTC

28
Q

PTC Molecular (3)

A

BRAF p.V600E mutations most common
-Have treatment implications

-Other genes which may be involved include RET, TERT promoter mutations, NTRK

29
Q

Medullary Carcinoma (7)

A

C-cell derived neoplasm
Up to a quarter are associated with MEN2a or MEN2b
-Germline gain of function mutation in RET proto-oncogene

Often associated with increased serum calcitonon and or carcinoembryonic antigen (CEA)

Variable histological appearance
-Can show amyloid deposition

IHC often helpful – calcitonin positive along with neuroendocrine markers

30
Q

Anaplastic Carcinoma (3)

A

Undifferentiated thyroid carcinoma

Characterised by aggressive progression and extremely poor prognosis- Usually fatal outcome

Usually thyroid IHC markers are lost, sometimes PAX8 is retained

Endocrine-W3 (9 decks)

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