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Y2S1-CVS-Pathology > Thyroid diseases > Flashcards

Thyroid diseases Flashcards

1
Q

Which endocrine gland is superficial?

A

The thyroid gland

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2
Q

What are the functions of the thyroid hormone?

A

1) Increases glucose in the blood and its uptake

2) Increases fatty acids in the blood due to its induction of lipolysis and increases its uptake by the liver

3) Normally it causes protein anabolism but in HYPERthyroidism it would cause protein destruction, whether muscle or the heart

4) Increases the basal metabolic rate

5) Increases O2 consumption by all body tissues

6) It is needed for all kinds of development whether physical, mental, or sexual

7) It increases the potency of catecholamines such as epi & Norepi which is why one of the treatments we give to HYPERthyroidism patients are beta-blockers

8) Increases HR, the force of contractions, and everything in the CVS but again in HYPERthyroidism due to its protein catabolism effect it would destroy the heart therefore decreasing everything

9) Increases alertness in the CNS but in hyperactive cases, it can cause nervousness and even tremors

10) Increases GIT motility so in hyperactive cases can cause diarrhea

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3
Q

What is meant by thyrotoxicosis?

A

An increase in thyroid hormone due to anything

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4
Q

What is the cause of hyperthyroidism?

A

When there is thyrotoxicosis with hyperthyroidism

  • It could be primary or secondary
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5
Q

What are the different primary causes of hyperthyroidism?

A

1) Graves’ disease

2) Toxic multinodular goiter

3) Toxic adenoma of the thyroid

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6
Q

What are the secondary causes of hyperthyroidism?

A

Pituitary adenoma secreting TSH

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7
Q

What is thyroiditis?

A

Destruction of the follicular cells due to an inflammatory process leading to transient thyrotoxicosis due to the release of T3 & T4 independent of a hyperactive gland

  • Thyroiditis in the beginning causes hyperthyroidism but after continuous destruction, you’ll have no more glands left hence you end up with hypothyroidism
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8
Q

What is meant by a toxic multinodular goiter?

A

The nodules in the thyroid gland are enlarged and if it starts releasing thyroid hormone it becomes “Toxic”

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9
Q

What are the manifestations of hyperthyroidism?

A

1) Calorinergic effects:

  • Heat intolerance
  • Soft, warm, flushed skin
  • Weight loss despite increased appetite

2) Systemic:

  • CVS: inc.HR, Cardiomyopathy, valvulopathy
  • NMS: Nervousness, Tremors, Irritability, Muscle weakness
  • GIT: Diarrhea + Steatorrhea (Fat in still, described as not easily flushed with a foul smell)
  • Thyroid: Goiter (not seen in thyroiditis)

3) Raises serum calcium (like in nephrogenic DI where we have hypercalcemia and hypokalemia)

4) Raised blood glucose serum (it also increases it uptake and increases the insulin metabolism)

5) Lowers the cholesterol (increases the uptake by the liver, which could lead to gallstones)

6) Contraction of the eyelid muscle making a wide stare gaze

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10
Q

What are the investigations of hyperthyroidism?

A

1) Serum TSH

  • First line, if it is low then primary or thyroiditis “due to negative inhibition”, if it is high then secondary

2) Free T3 & T4 hormone assay

3) Measuring the activity by seeing the uptake of radioactive Iodine (diffuse uptake in Graves disease, only the adenoma in toxic adenoma, in Toxic MNG only the nodules will uptake it, low uptake thyroiditis)

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11
Q

What is Graves disease?

A
  • Most common cause of hyperthyroidism
  • Autoantibodies against TSH receptor stimulating the thyroid gland
  • There is a triad in Graves disease

1) Hyperthyroidism “diffuse hyperplasia

2) Infiltrative ophthalmology (leads to exophthalmos)

3) Localized dermopathy (pretibial myxedema “Scaly thickening of the dermis due to deposition of GAGs and infiltration by lymphocytes”)

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12
Q

What is the pathogenesis of graves disease?

A

1) Autoantibodies against the TSH receptor (TSI), will lead to hyperthyroidism in three different ways:

1a) TSI binds to TSH receptor increasing the secretion of thyroid hormones

1b) Thyroid growth-stimulating Ig, binds to TSH receptor proliferation of thyroid follicular epithelium = diffused hyperplasia

1c) TSH-binding inhibitor Ig:

  • This could stimulate the thyroid function (hyperthyroidism) and it can also inhibit it leading to (hypothyroidism)
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13
Q

What are the different types of immunoglobulins found in graves disease?

A

1) Thyroid-stimulating IgG

  • Binds to TSH receptors to release the hormone

2) Thyroid growth-stimulating Ig

  • Causes hyperplasia of the gland

3) TSH-binding inhibitor Ig

  • Firstly, it blocks the TSH receptors and prevents the normal TSH from binding, then sometimes it will mimic the TSH and trigger the release of thyroid hormone and sometimes it BLOCKS its action even from its autoantibody brothers. This is why patients with graves have attacks of Hyper AND hypothyroidism
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14
Q

Exopthalmous is due to infiltrative ophthalmology, what is infiltrative ophthalmology?

A
  • When the volume of the retroorbital connective tissue and the extraocular muscles increase in volume and mass due to:

1) Infiltration via T-cells

2) Accumulation of hydrophilic glycosaminoglycans

3) Increase in adipocytes

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15
Q

What are the changes in the thyroid gland that occur?

A

1) Grossly:

  • Diffuse and systemic enlargement of the thyroid

2) Microscopically:

  • Thyroid follicles follicular epithelial cells that are crowded with small papillae that do not have a fibrovascular core (pseudo papillae)
  • Colloid with scalloped margin
  • Stroma is infiltrated by lymphocytes, plasma cells with the formation of lymphoid follicles
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16
Q

Summarize graves disease

A
  • Triad (hyperthyroidism, exophthalmos, pretibial myxedema)
  • Gross diffuse hyperplasia, microscopic pseudo papillae with colloid scalloped border
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17
Q

What are the different causes of hypothyroidism?

A

1) Primary

1a) Congenital (like in thyroid dysgenesis or Dyshormonogenetic goiter)

1b) Autoimmune (Hashimoto thyroiditis)

1c) Iatrogenic (Surgical or in radiation-induced ablation of the thyroid parenchyma)

2) Secondary

  • Arises from a hypothalamic or pituitary disease
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18
Q

What are the clinical manifestations of hypothyroidism?

A

1) Cretinism (hypothyroidism in infancy or early childhood)

2) Dwarf

3) Puffiness of the eyelids

4) Depressed nasal bridge

5) Big lips

6) Protruding tongue

7) severe mental retardation

8) Impotent

9) Myxedema (hypothyroidism in older children and adults)

10) Calonergic effects (like cold intolerance, decreased sweating, dry cold skin, loss of outer 1/3 of the eyebrows, brittle nails, weight gain)

11) Systemic: (Decreased HR, CO, slow mentation, poor memory, hypersomnia, steatorrhea, galactorrhea, goiter, Hypoglycemia, hyperprolactinemia “Galactorrhea? This means increased prolactin but what is the link? Low T3 & T4 will stimulate positive feedback to release TRH and when this is elevated it will induce more TSH + GH + PL. So expect to see galactorrhea and gynecomastia”)

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19
Q

Describe the pathogenesis of Hashimoto thyroiditis

A
  • The mechanisms of thyrocyte death are:

1) T-cell mediated cell death (CD8+ cytotoxic T-cells, Type 4 hypersensitivity rxn)

2) Cytokine-mediated cell death (Increased number of CD4+, recruiting and activating macrophages)

3) Antibody-dependent cell-mediated cytotoxicity (anti-thyroglobulin and antithyroid peroxidase antibodies “Type-2 hypersensitivity)

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20
Q

What are the clinical presentations of Hashimoto thyroiditis?

A

1) Hypothyroidism (decreased T3 & T4, while there is an increased in TSH)

2) Hashtoxicosis (sometimes preceded by hyperthyroidism, it has an increased T3, and T4 while a decreased TSH)

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21
Q

Describe the morphology of Hashimoto thyroiditis

A

1) Gross:

  • Diffuse and symmetric enlargement of the thyroid

2) Microscopically:

  • The thyroid follicles are atrophied and lined with hurthle cells “follicular cells that tried to fight off the lymphocytes by becoming big cells with red cytoplasm”(eosinophilic cytoplasm)
  • Scanty colloid
  • The stroma is filled with inflammatory cells (lymphocytes, plasma cells) + formation of lymphoid follicles
  • Fibrosis
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22
Q

Summarize Hashimoto thyroiditis

A
  • Hyperthyroidism then hypo
  • Grossly diffuse enlargement and microscopically lymphocytes + Hurthle cells (Hurthle cells are the follicular cells that tried to fight off the lymphocytes by becoming big cells with red cytoplasm)
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23
Q

How to differentiate between Graves disease and Hashimoto?

A

Hashimoto can have T-cell infiltration but in graves, there are no T-cells

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24
Q

Summarize the causes of Hashimoto’s thyroiditis

A

1) CD8+ cytotoxic cell-mediated cytotoxicity

2) Cytokine-mediated thyrocyte injury

3) Antibody-dependent cell-mediated cytotoxicity

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25
Q

What are the different causes of goiter?

A

1) Endemic:

  • Colloid goiter
  • iodine deficiency (in geographic areas where the iodine is low, the thyroid gland can’t make the thyroid hormone so to compensate TSH will increase enlarging the gland)
  • Goitrogens (ingestion of substances that interfere with the synthesis of the thyroid hormone)

2) Sporadic, females

  • Physiologically like in adolescence, pregnancy (where there is an increased metabolic demand for T4)
  • Drug-induced goiter (lithium, sulfonamides, and phenylbutazone)

3) Genetic factors

  • Dyshormogenetic goiter (where there is an inherited enzymatic defect that interferes with the synthesis of the thyroid hormone)
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26
Q

What are the different types of goiter?

A

1) Simple

  • Diffuse and non-toxic

2) Multinodular

  • Irregular enlargement of the thyroid due to recurrent episodes of hyperemia and involution
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27
Q

Describe the morphology of the diffuse goiter

A

1) Gross

  • Diffuse goiter
  • Symmetric enlargement

2) Microscopically

  • Hyperplastic follicular epithelium that can pile up and form projections
  • Involution, where the follicular epithelium becomes flattened and cuboidal with abundant colloid
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28
Q

Describe the morphology of the multinodular goiter

A

1) Gross:

  • Multiple nodules of varying sizes
  • One lobe of the thyroid might be more involved
  • One nodule may become prominent and appear as a solitary nodule
  • Goiters may grow behind the sternum and clavicle producing an intrathoracic/plunging goiter
  • A cut section will reveal nodules of varying sizes (colloid nodule/colloid cyst)

2) Microscopically:

  • Multiple variable-sized non-capsulated nodules with variable number and size of follicles with a variable colloid separated by a fibrous septa
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29
Q

Summarize the multinodular goiter

A
  • Multiple nodules grossly
  • Microscopically also various shaped nodules, colloids, follicles and are not encapsulated (Non-capsulated is important because in the thyroid if you have papillae its cancer. If you have a capsule, it’s a tumor that can be malignant or benign)
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30
Q

What are the congenital diseases of the thyroid?

A

1) DiGeorge syndrome:

  • Chromosomal disorder due to 22q11.2 deletion, due to the failure of the development of the 3rd and 4th pharyngeal pouch

2) Thyroglossal Duct (TGD) cyst

  • Cystic lesion that is lined by the respiratory epithelium, with a midline swelling

3) Branchial cleft cyst

  • Anterolateral neck mass in children and young adults
  • Microscopically the cyst is lined by a squamous, columnar, ciliated epithelium with abundant lymphoid tissue
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31
Q

What are the different types of thyroid neoplasms?

A

1) Cold nodule

2) Warm nodule

3) Hot nodule (benign)

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32
Q

What is a follicular adenoma?

A
  • Tumor in a gland that originates from the follicular epithelium
  • It could be Hot or Cold nodule
  • It could be toxic or nonfunctioning
33
Q

Which thyroid neoplasms are hot

A

1) Follicular adenoma

34
Q

Which thyroid neoplasms are cold

A

1) Follicular adenoma

35
Q

Which thyroid neoplasms are warm

A
36
Q

Describe the pathogenesis of follicular adenoma

A
  • Due to genetic factors (shared with follicular carcinoma), it could be due to mutations in:
  • Non-functioning adenoma:

RPPP

1) Ras

2) PIK3CA

3) PAX8-PPARG fusion gene (PPFP)

  • Toxic adenoma

1) Mutations in TSH receptor signaling

37
Q

Which gene mutations are associated with non-functioning follicular adenomas?

A

RPPP

1) Ras

2) PIK3CA

3) PAX8-PPARG fusion gene (PPFP)

38
Q

Which gene is mutated in toxic adenomas?

A

The TSH receptor signaling pathway

39
Q

Describe the morphology of follicular adenoma

A

1) Gross:

  • Solitary
  • Capsulated
  • Compresses the adjacent thyroid gland

2) Microscopic:

  • Well-formed capsule encircling the tumor
  • The lining cells could be eosinophilic cytoplasm in follicles
40
Q

What are the different investigations for follicular adenoma?

A

1) US

2) Fine needle aspiration

3) Radioactive uptake, depending on how much it uptakes it is classified as hot or cold

41
Q

Thyroid carcinomas are derived from which cell of origin?

A

1) Thyroid follicular epithelium

  • Papillary carcinoma
  • Follicular carcinoma
  • Anaplastic carcinoma

2) Parafollicular

42
Q

What are the causes of papillary carcinoma?

A

1) Ionizing radiation

2) Activation of MAP kinase pathway:

  • Rearranging the RET to other genes creating a RET/PTC fusion oncogenes
  • Activating point mutations in BRAF V600E
  • it loves to metastasize into adjacent cervical lymph nodes and lungs
43
Q

What are the causes of follicular thyroid cancer?

A

1) Low iodine in diet

2) Activation of the PI3K/AKT pathway & PAX8-PPARG fusion gene

  • RAS
  • Papillary is strange to a thyroid gland so it will need a MAP. (a way to remember)
44
Q

What is anaplastic carcinoma?

A
  • Arises de novo/progression
  • Highly aggressive
  • Molecular changes are similar to those found in well-differentiated carcinomas but occur at a higher rate
  • Other genetic factors could include the inactivation of p53 or mutations of b-catenin and TERT)
  • Just remember that it is very aggressive and undifferentiated, and it’s associated with p53
45
Q

Which gene mutation is associated with medullary thyroid cancer?

A
  • RET gene mutation, due to the constitutive activation of tyrosine kinase receptor leading to the proliferation of the cells
  • It could be due to the germline in familial medullary thyroid carcinomas in MEN-2 (Multiple endocrine neoplasm) and thus if you find MTC you should look for cancers in the parathyroid, medullary thyroid carcinomas, and pheochromocytoma
  • The RET gene here is due to MUTATION but in PTC it was chromosomal rearrangement
46
Q

Describe the morphology of papillary carcinoma

A
  • Papillary carcinoma is the only cancer where you consider their nuclei when suspecting it (white nuclei are called orphan Annie)
  • The morphology of follicular carcinoma are similar of that in follicular adenoma, but the difference is in the carcinoma you’d find cells piercing the capsule

1) Gross

  • Solitary or multifocal
  • Some are encapsulated while others are infiltrated

2) Microscopic

  • It has papillae with a fibrovascular core, covered by epithelial cells with nuclei (E O CIS)

1) Enlarged

2) Oval

3) Chromatin clearing (empty/ground glass nuclei)

4) Nuclear membrane irregularity

5) It has psammoma bodies (calcified structures within the core of the papillae

47
Q

What are the different types of papillary thyroid cancer?

A
  • Histological variations

1) Microcarcinoma

  • Very small PTC (<1cm)

2) Encapsulated

  • Surrounded by a capsule

3) Follicular

  • Cells arranged in follicles
48
Q

What is the investigation for PTC?

A
  • Immunohistochemistry
  • It is positive CK19 & Galectin 3
49
Q

What is the clinical presentation of papillary thyroid cancer?

A

Painless mass in the neck

50
Q

Describe the morphology of follicular carcinoma

A

1) Gross:

  • Solitary nodule
  • Well-circumscribed or it can infiltrate

2) Microscopic:

  • The cells are Uniformed, arranged in small follicles
  • Mushroom-shaped invasion, infiltrating the capsule or blood vessel
51
Q

What is medullary thyroid carcinoma?

A
  • MENullAry CALCinoma of the thyroid

1) Associated with MEN (multiple endocrine neoplasms)

2) Tumor is surrounded by Amyloid

3) Produces CALCItonin

4) Tumor of C-Cells

  • NE tumor that is derived from the parafollicular C-cells
  • Due to point mutation in the RET gene (could be sporadic or familial), in familial it is associated with MEN 2A or 2B, calcitonin screening should be done for relatives

In any scenario with increased serum calcitonin, you have one option which is medullary carcinoma

52
Q

Describe the morphology of the medullary thyroid cancer

A

1) Gross:

  • Solitary nodule/spindle-shaped cells
  • It forms nests/trabeculae
  • Amyloid is found in the adjacent stroma (Amyloid the most imp striking feature of this cancer)
  • Congo red stain is used under polarized light giving an apple-green birefringence
53
Q

How to confirm the diagnosis of medullary carcinoma?

A

1) Start with hemotoxin and eosin, it will turn it red

2) Congo red stain (know this) turns the amyloid into orange

3) Looked at under a polarized light will appear green

  • Only then you can confirm this diagnosis (Medullary carcinoma, think of high calcitonin and amyloid)
54
Q

Describe the morphology of the anaplastic carcinoma

A
  • Undifferentiated tumors that are aggressive and found in elder people

1) Grossly: A bulky mass

2) Microscopic: Highly anaplastic cells

55
Q

What is NIFTP?

A
  • Non-invasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP)
  • A RAS lineage tumor, with no BRAF V600E mutation
56
Q

Describe the morphology of NIFTP

A

1) Nuclear features of papillary thyroid cancer

2) Follicular growth pattern

3) Encapsulated

  • To diagnose it you need surgical samples, Remember when we said we can never diagnose PTC by fine needle aspiration? This is because of NIFTP, firstly its benign so excision of the lobe affected is curative. It is formed of follicular cells with papillary LIKE NUCLEAR features. You can never differentiate between them by fine needle. How to describe the microscopic pic? Read the name backward, tumor cells with nuclear-like features of papillary carcinoma, arranged in follicles in the thyroid
57
Q

What are the parathyroid glands composed of?

A

1) Chief cells (produces PTH)

2) Oxyphil cells (larger than the chief cells with an acidophilic cytoplasm, it appear at puberty with an unknown function

  • A key normal feature is having adipose tissue, any disease in the parathyroid you won’t find fat and that is abnormal and signifies hyperplasia or benign or malignant tumor.
58
Q

What is the function of the parathormone?

A

parathormone increases blood calcium by activating osteoclasts, it also does so by stimulating the formation of active vitamin D3 which increases calcium absorption in the intestine

59
Q

What are the types of hyperparathyroidism?

A

1) Primary

  • Hyperplasia, Adenoma, Carcinoma of the parathyroid

2) Secondary

  • Decreased Vitamin D or Calcium in the diet
  • Chronic renal failure (retention of phosphate in the blood which will decrease serum calcium, metabolic acidosis will mask the hypocalcemia)
  • FYI: in secondary PTH is high but calcium is normal ( corrected) or its still low and this is what differentiated between it and primary because in primary calcium is high

3) Tertiary

  • Irreversible parathyroid hyperplasia due to long secondary hyperthyroidism, causes an increase in PTH and Ca

4) Ectopic

  • Paramalignant (like in small cell lung cancer)
60
Q

What are the effects of hyperthyroidism?

A
  • Hypercalcemia
  • BKM

1) Bone: It will increase the osteoclastic activity leading to bone erosion (mainly the phalanges)

  • Microscopically, you will see aggregates of osteoclasts and hemorrhagic debris (brown tumor)

2) Kidney: Calcinuria, leading to urinary stones, and the calcification of the renal interstitium

3) Metastatic calcification: Blood vessels, lungs, stomach

61
Q

What is the clinical presentation of hyperthyroidism?

A

1) Diuresis (polyuria, polydipsia)

2) Renal stones

3) Peptic ulcer and pancreatitis

62
Q

What are the investigations done for hyperparathyroidism?

A

1) In primary hyperthyroidism:

  • Increased PTH
  • Hypercalcemia
  • Hypophosphatemia

2) Secondary hyperparathyroidism (الجسم عم بفرز PTH عشان عنا قليل من مشاكل فالأكل او الكلى):

  • Decreased/Normal Ca
  • Hyperphosphatemia
  • Increased PTH

3) In urinalysis:

  • Increased Ca and PO4
63
Q

What are the causes of hypoparathyroidism?

A

1) Primary

  • DiGeorge syndrome
  • Polyglandular deficiency syndrome

2) Secondary

  • Damage to the parathyroid gland due to radiation or Post-surgical

3) Pseudohypoparathyroidism

  • Defective response to PTH
64
Q

What are the effects of hypoparathyroidism?

A
  • Due to low calcium, sodium will excite the muscles leading to a hyperactive muscular system

1) Tetnay, due to increased NM excitability due to decreased ionized calcium

2) Tingling around the mouth and distal limbs

3) Muscle twitches

4) Muscle spasm

5) Latent tetany (Trousseau’s sign, chovstek’s sign)

  • Trousseaus sign: the patient has a carpal spasm when you measure the BP
  • Chvostek’s sign: you tap on the facial nerves and their face twitches
65
Q

What is parathyroid hyperplasia?

A

Enlargement of all 4 glands, proliferation of the chief cells, stromal fat is decreased within hyperplasia

66
Q

What are the different parathyroid neoplasms?

A

1) Adenoma

2) Carcinoma

67
Q

What is the parathyroid adenoma?

A
  • Due to abnormalities in 2 genes (cyclin D1 and MEN1)
  • Grossly it is well-circumscribed, capsulated, and confined to a single gland
  • Microscopically it has a fibrous capsule, composed of chief cells and the stromal fat is decreased in adenomas
68
Q

Describe the parathyroid carcinomas

A
  • Grossly circumscribed/difficult to distinguish from adenomas OR they might be invasive neoplasm, grey-white, with irregular masses
  • Microscopically the cells resemble normal parathyroid cells, enclosed in a fibrous capsule, with necrosis and vascular invasion
69
Q

What type of cancer is it when there is elevated calcitonin?

A

Medullary thyroid carcinoma

70
Q

Follicles piercing the capsule, so is follicular carcinoma associated with it?

A

RAS, PI3KCA, PI3K/AKT, PAX8-PPARG fusion gene

71
Q

Medullary carcinoma as you can see the amyloid associated with?

A

RET point mutation

72
Q

Papillary carcinoma associated with?

A

MAP, BRAF V600E, RET rearrangement

73
Q

NFTIP associated with?

A

RAS

74
Q

What is the criteria for follicular carcinoma?

A

Capsular or vascular invasion

75
Q

What are the criteria for medullary carcinoma?

A
  • Calcitonin + Amyloid
76
Q

What are the criteria for papillary carcinoma?

A
  • Enlarged, Oval, CIG
77
Q

Which antibody do we test for graves?

A

TSH receptor-stimulating antibodies

78
Q

Which gene mutation is associated with extra-axial cystic mass?

A

B-caterin

79
Q

amenorrhea, galactorrhea with a 1.2cm pituitary mass, what are the lab findings?

A

1) Elevated serum prolactin

2) Normal GH

3) Reduced FSH and LH

Y2S1-CVS-Pathology (12 decks)

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