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Y2B1 - Endocrine 📕 > Pathology 🩺 > Flashcards

Pathology 🩺 Flashcards

1
Q

what are thyroid gland disorders?

A
  1. Functional disorders:
    - Hyperthyroidism (thyrotoxicosis and thyroid storm)
    - Hypothyroidism (cretinism, myxedema)
  2. Thyroiditis
  3. Goiter
  4. Neoplasms
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2
Q

what are the causes of hyperthyrodism?

A

Primary:
- Graves disease
- Toxic multinodular goiter
- Toxic follicular thyroid adenoma

Secondary “in parts rather than the thyroid gland”
- TSH-secreting pituitary adenoma

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3
Q

what are the causes of hypothyrodism?

A

Primary:
- Iodine deficiency “people leaving away from seas”
- Hashimoto thyroiditis
- Postablative
- Genetic defects in thyroid develpment
- Dyshormonogenetic goiter.
- Thyroid hormone resistance

Secondary:
- Pituitary failure.

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4
Q

Incidence of Hashimoto Thyroiditis

A
  • The most common cause of Hypothyroidism after iodine deficiency.
  • More common in females
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5
Q

Pathogenesis of Hashimoto Thyroiditis

“inhibit thyroglubulin & oxidation of iodide”

A
  • Auto-immune thyroiditis

————————

  • Activation of helper (CD4+) T lymphocytes sensitized to thyroid antigens:

a) CD4+ helper T lymphocytes stimulate proliferation of cytotoxic (CD8+) T lymphocytes, which attack thyroid follicular cells.

b) CD4+ helper T lymphocytes T lymphocytes also recruit reactive B lymphocytes to produce antibodies against thyroid antigens as anti-thyroglobulin and anti-thyroid peroxidase.

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6
Q

Gross appearence of Hashimoto Thyroiditis

“enlarged,firm & loss of glistening app. + late atrophy”

A

Early: symmetrical diffuse enlargement of the thyroid gland with vague nodularity
a) The affected areas are white gray or yellow brown and firm
b) They lack the glistening appearance of colloid

Late: The gland becomes symmetrically atrophic

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7
Q

Microscopic appearence of Hashimoto Thyroiditis

“lymphocytes + Hurthe cells”

A
  • follicles are atrophied.
  • Follicles are lined by large cubical cells with eosinophilic granular cytoplasm (Hurthle cells).
  • Inflammatory cells (lymphocytes, plasma cells, macrophages).
  • Reactive lymphoid follicles.
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8
Q

what are the complications of Hashimoto Thyroiditis?

A
  1. Hypothyroidism
  2. Neoplasms (papillary thyroid carcinoma, lymphoma).
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9
Q

what is the definition of Sub acute Granulomatous (de Quervain) Thyroiditis?

“tender thyroid”

A

A self-limited (resolve on its own) disorder in which patients present with a tender thyroid.

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10
Q

what is the etiology of Sub acute Granulomatous (de Quervain) Thyroiditis?

A

is not known but clinical features of preceding respiratory infection suggest a possible Viral etiology.

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11
Q

gross appearence of Sub acute Granulomatous (de Quervain) Thyroiditis

focal enlargment + moderate asymmetrical growth

A
  • Moderate enlargement of the gland which is often focal and asymmetrical.
  • The cut surface of the involved area is firm and yellowish-white.
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12
Q

Microscopic appearence of Sub acute Granulomatous (de Quervain) Thyroiditis

granulomatous shape

A
  • Early, Acute inflammatory destruction of the thyroid follicles.
  • Late, Granulomas consist of central colloid material surrounded by histiocytes and scattered multinucleate giant cells.
  • advanced cases: Fibrosis.
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13
Q

Etiology of Riedel thyroiditis

“fibrous thyroiditis”

A

Rare chronic disease of unknown cause, Riedel’s thyroiditis may be part of multifocal idiopathic fibrosclerosis.

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14
Q

Gross appearance of Riedel thyroiditis

A

The gland is stony hard and adherent to the surrounding structures.

may be mistaken for cancer

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15
Q

Microscopic appearence of Riedel thyroiditis

A
  • Follicles are atrophied
  • Excess fibrous tissue may extend outside the gland
  • Lymphocytic infiltrate
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16
Q

complications of Riedel thyroiditis

A

Compression manifestations: dysphagia, dyspnea, recurrent laryngeal nerve paralysis and stridor.

mediastinal syndrome

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17
Q

what is the morphologic appearence of Palpation Thyroiditis?

A

Morphologically similar appearance to de Quervain thyroiditis

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18
Q

what causes Palpation Thyroiditis?

usually in patients with goiter

A

May be produced in cases where vigorous thyroid palpation initiate mechanical trauma to the thyroid follicles

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19
Q

what is the definition of goiter?

A

Non inflammatory, non neoplastic enlargement of the thyroid gland

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20
Q

what are the types of goiter?

A
  • Simple (non toxic)
  • Toxic (associated hyperthyroidism)
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21
Q

what is the definition of Simple (non toxic) Goiter?

A

Enlargement of the thyroid gland without toxic manifestation.

22
Q

incidence of Simple (non toxic) Goiter

A

Common in females

23
Q

what are the causes of Simple (non toxic) Goiter?

A

1. Absolute iodine deficiency: in area away from seas or due to intake of goitrogenic agents e.g cabbage and cauliflower

2. Relative iodine deficiency: due to increase demand for thyroid hormones as at puberty, pregnancy and lactation

24
Q

pathogenesis of Simple (non toxic) Goiter

A
  • Deficient thyroid hormones —-> excessive TSH stimulation.
  • This leads to hyperplasia of follicular epithelium & formation of new thyroid follicles.
  • Diffuse enlargement of the thyroid gland (maintains the euthyroid state).
  • Cyclic hyperplastic stage followed by involution stage.
  • Involuted nodules undergo fibrosis, calcification, hemorrhage & cystic degeneration.
25
Q

what is the gross morphology of multi-nodular Goiter?

A
  • The thyroid gland is asymmetrically enlarged with nodular surface.
  • The cut surface shows numerous irregular nodules contain glistening colloid.
  • Fibrosis, calcification, chronic inflammation, hemorrhage & cystic degeneration may be present.
26
Q

what is the microscopic appearence of toxic Goiter?

A
  • Nodular thyroid gland with fibrous tissue.
  • Hyperplastic nodules, tall columnar follicular epithelium, papillary structures, formation of small new follicles.
  • Involuted nodules, large follicles distended by colloid and lined by flat follicular epithelium. Large colloid-containing follicles may fuse to form colloid cysts.
  • Calcification, chronic inflammation, hemorrhage & cystic degeneration are common in the old standing cases.
27
Q

what are the Complications of toxic Goiter?

A

1. Pressure effects: on trachea, esophagus and recurrent laryngeal nerve

2. Hyper functioning nodules: and cause secondary hyperthyroidism (no exophthalmos)

3. Malignancy: rare in 2% of cases

28
Q

what is the definition of Grave’s disease?

A

autoimmune disease, affecting young females.

29
Q

etiology of Grave’s disease

A
  • Due to auto-antibodies (TSI; thyroid stimulating immunoglobulin.
  • They stimulate TSH receptors leading to diffuse hyperplasia and hyper functioning thyroid follicles with excess thyroid hormone secretion
30
Q

what are the pathologic features of grave’s disease?

A
  • N/E & M/E
  • Exophthalmous
  • Pretibial myxedema
  • Other manifestations of Hyperthyroidism
31
Q

what is the gross appearence of Grave’s disease?

A
  • The thyroid gland is symmetrically enlarged.
  • The gland appears fleshy.
  • Cut surface is firm and dark red.
  • Loss of the normal translucence of stored colloid
32
Q

what is the microscopic appearence of Grave’s disease?

A
  • the gland is diffusely Hyperplastic and highly vascular.
  • The epithelial cells are tall and columnar.
  • Hyperplastic papillae that project into the lumen of the follicles.
  • The colloid is depleted and appears scalloped or( moth-eaten) at the periphery.
  • Lymphocytes and plasma cells infiltrate the interstitial tissue and may form reactive lymphoid follicles.
33
Q

what causes exophthalmous in Grave’s disease?

A

It is caused by retro ocular edema, fibroblasts and lymphocyte infiltration. The increased orbital contents displace the eye forward (proptosis).

34
Q

pretibial myxedema of Grave’s disease

A

Thickening of the skin on the shin of the tibia

35
Q

what are examples of thyroid tumors?

A
36
Q

what is the most common begnin thyroid tumor?

A

follicular adenoma

37
Q

N/E of follicular adenoma

A
38
Q

M/E of follicular adenoma

A
39
Q

what is a characteritic feature for follicular adenoma?

A
  • no invasion of blood vessels
  • no invasion of capsule
40
Q

what are the risk factors of thyroid carcinoma?

A
  • Iodine excess
  • TSH
  • External radiation
  • Genetic basis
41
Q

genetic basis of thyroid carcinoma

A

papillary carcinoma: RET gene
Follicular carcinoma: RAS gene
Medulary carcinoma: RET gene
Anaplastic carcinoma: P53 gene

42
Q

M/E of thyroid carcinoma (types under microscopre)

A
  1. papillary carcinoma
  2. follicular carcinoma
  3. medullary carcinoma
  4. anaplastic carcinoma
43
Q

papillary carcinoma

  • Incidence
  • Age & Sex
  • Prognosis
  • Spread
  • N/E
  • M/E
A
44
Q

M/E of papillary carcinoma

A

Papillary pattern: Branching - Thin fibrovascular core

Nuclear features: Elongation & Overlapping - Nuclear clearing (Washed out or Ground Glass - Longitudinal groove - Nuclear Pseudo-inclusion

Psammoma bodies: Concentric Calcified spherules

45
Q

Follicular carcinoma

  • Incidence
  • Age & Sex
  • Prognosis
  • Spread
  • N/E
  • M/E
A
46
Q

how is follicular carcinoma diffrentiated from follicular adenoma?

A

based on demonstration of invasion of blood vessels & capsular invasion

47
Q

medullary carcinoma (Neuro-endocrine tumor)

  • Origin
  • Incidence
  • Mutation
  • Cases
  • Prognosis
  • Spread
  • N/E
  • M/E
A
48
Q

what is another name for medullary carcinoma?

A

Neuro-endocrine

49
Q

cases of medullary carcinoma

A

(90% are sporadic - 10% are familial)

  • Sporadic cases: Occur in middle and old age (5th & 6th decades) - Unilateral
  • Familial cases: Occur in younger age 2nd & 3rd decades) - Bilateral Multicentric - Associated Multiple Endocrine Neoplasia (MEN syndrome)
50
Q

anaplastic “undiffrentiated” carcinoma

  • Incidence
  • Age & Sex
  • Prognosis
  • Spread
  • N/E
  • M/E
A

Y2B1 - Endocrine 📕 (7 decks)

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