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BMS 200 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

where does the thyroid originate from embryology?

A

endodermal lining of the primitive pharynx. It descends via the thyroglossal duct and reaches its final position in week 7.

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2
Q

Remnants of the thyroglossal duct can remain, leading to what?

A

thyroglossal duct cysts, 7% of populations. Midline swelling can be apparant.

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3
Q

How is it that the thyroid can move up and down when you swallow?

A

Capsule: its enclosed by a thin ribrous capsule that serves as a protective layers and is attached the the cricoid cartilage and upper part of trachea.

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4
Q

what are the functional units responsible for hormone production in the thyroid?

A

Follicles: surrounded by a cubodial epithelial cells aka follicular cells or thyrocytes that synthesize and secrete thryoid hormones T4 and T3

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5
Q

what are the parafollicular cells (aka C cells) responsible for?

A

producing calcitonin to help regulate calcium levels by inhibiting bone resorption

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6
Q

How and where are hormones produced in the thyroid? (histology)

A

The colloid is the center of thyroid hormone production

Hormones are produced in the colloid when atoms of the mineral iodine attach to a glycoprotein, called thyroglobulin that is secreted into the colloid by the follicle cells.

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7
Q

What is the role of iodine and tyrosine in the colloid?

A

In the colloid, peroxidase enzymes link the iodine to the tyrosine amino acids in thyroglobulin to produce two intermediaries: a tyrosine attached to one iodine and a tyrosine attached to two iodines.

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8
Q

what are the are 2 intermediaries produced during iodination of tyrosine?

A

MIT (monoiodityrosine) 1 iodine

DIT (diiodotyrosine) 2 iodines

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9
Q

what is produced from these intermediaries linked by covalent bonding?

A

T3: triiodothyronine (3 iodines)
MIT + DIT

T4: thyroxine (4 iodines)
DIT + DIT

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10
Q

T/F: T4 is produced in a high amount and is less active
T3 which is produced less but is very active

A

True

NOTE: T4 can be converted into T3 in periphery by deiodination (removal of iodine)

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11
Q

when active thyroid hormones are needed, what happens to thyroglobulin?

A

the thyroglobulin is taken back into the follicular cells via endocytosis, here enzymes cleave the thyroglobulin via proteolysis releasing T3 and T4 which diffuse into blood

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12
Q

Where is iodine absorbed, stored, and excreted?

A

small intestine
stored in the thyroid (up to 2 months) and kidneys (excreted in urine), the liver metabolized thyroid hormones and releases some iodine into the bile but 80% is excreted by the kidneys

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13
Q

what is the role of NIS (Na/I cotransporter)?

A

this is a sodium/iodide symporter that actively transports iodide from blood into follicular cells.

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14
Q

once inside the follicular cell, how does iodide reach the colloid where it can be used for hormone synthesis? what is the clinical relevance of this?

A

Pendrin - the Cl-/I- exchanger
it moves iodide into follicle in exchange for chloride

mutations in the pendrin gene can lead to congenital disorder Pendred syndrome: goiter, hearing loss, impaired iodine transport so hypothyroidism or compensatory goiter.

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15
Q

what is the role of thyroid peroxidase (TPO) and iodination?

A

TPO catalyzes the oxidation of iodide into iodine so it can attach to tyrosine residues on thyroglobulin.

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16
Q

what is the role of DUOX2?

A

the oxidation rxn by TPO requires DUOX2 another apical membrane protein that generates hydrogen peroxide so iodide can become the iodine radical.

17
Q

review: what are the inactive and active forms of thyroid hormones?

A

inactive: MIT and DIT
active: T3 and T4

18
Q

what protects T3 and T4 from rapid metabolism and excretion once they are in the bloodstream?

A

they are bound to plasma proteins, prolonging half-life

NOTE: T4 has longer half life
T3 has shorter half life (makes it more readily available)

19
Q

what are 3 major transport proteins for thyroid hormones? what is the main one? which has highest affinity?

A
  1. albumin - main one due to abundance
  2. Transthyretin (TTR)
  3. Thyroid binding globulin (TBG) - highest affinity for T4
20
Q

what 2 enzymes mediate the deiodination of T4 to make T3 once its in target tissues?

A

Diodinase type 1 (D1)
Diodinase type 2 (D2)

21
Q

where are D1 and D2 primarily found? what is special about D2?

A

D1 - liver, thyroid, kidneys, pituitary
D2 - brain, pituitary, brown adipose

D2 can be influenced by physiological conditions like caloric intake, temperature and its crucial for T3 production in brain

22
Q

what is D3 and its role? (hint reverse T3)

A

found in brain and reproductive tissues, it converts T4 to rT3 and inactivates T3. Role in regulation to reduce metabolic activity during stress or illness.

23
Q

describe the relevance of selenium to thyroid hormone deiodination?

A

All diodinases (D1. D2, D3) all require selenium for their enzymatic activity.

Too little = hypothyroidism

24
Q

impact of diet on deiodinases?

A

fasting: reduces T3 by 50% in 307 days (rT3 is increased)

overfeeding: increases T3 and reduced rT3

25
Q

TSH receptors are G-protein coupled receptors (Gs) and are activated by what? what happens if there chronic high stimulation of the TSH receptors?

A

phospholipase C

Hypertrophy or goiter

26
Q

what is the stimulus for T4 production?

A

TSH secreted by anterior pituitary in response to TRH (thyrotropin-releasing hormone) from hypothalamus. TSH binds to receptors in thyroid follicular cells

27
Q

describe the feedback mechanism of Free T4 and TSH regulation?

A

free T4 in bloodstream regulates TSH secretion, when T4 levels rise -> negative feedbackon anterior pituitary

28
Q

regulation of TSH: when does pulsatile secretion of TSH peak?

A

starts to rise at 9pm, peaks at midnight.

29
Q

what are the main calorigenic action of T4 and T3?

A

increase O2 comsumption in almost all tissues
increase metabolic rate
increase requirements for all viamins

30
Q

what is the most common cause of hypothyroidism in developed world?

A

Hashimoto’s thyroiditis

autoimmune inflammation of thyroid gland.

31
Q

what is myxedema in hashimoto’s? vs myxedema coma?

A

non-pitting edema

a myxedema coma is a rare and serious complication of long term hypothyroidism plus often infection or another precipitating factor

32
Q

when thyroid hormones are low, what does the hypothalamus do?

A

the hypothalamus produces thyrotropin-releasing hormone (TRH).
TRH stimulates the pituitary gland to produce thyroid stimulating hormone (TSH).
TSH stimulates follicular cells in the thyroid gland to produce more thyroid hormones.

BMS 200 (7 decks)

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