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BMS200 > week 4, lecture 2 > Flashcards

week 4, lecture 2 Flashcards

1
Q

what does the thyroid develop from in embryo?

A

Originates from the endodermal lining of the primitive pharynx

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2
Q

where does the thyroid develop at (embryo)

A
  • The thyroid begins to develop as a pit at the base of the tongue in the midline (Foramen Cecum)
  • Begins as a small endodermal thickening in the floor of the pharynx, near the base of the tongue.
  • foramen cecum, between the 1st and 2nd pharyngeal pouches in the 3rd week
  • Here is when the the thyroid diverticulum forms, which descends through the neck.
  • The thyroid descends from the foramen cecum (at the tongue base) via the thyroglossal duct.
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3
Q

what week in embryo does the thyroid reach its final position in front of the trachea

A

7th week

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4
Q

what is the thyroid composed of

A

Thyroid develops into two lateral lobes connected by an isthmus.

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5
Q

what is the thyroglossal duct

A
  • Temporary duct that connects the developing thyroid to the tongue.
  • Normally, the duct disappears by the 10th week
  • In some, the pyramidal lobe is an extension fo the duct
  • but remnants of it can lead to thyroglossal duct cysts.
  • 7% of the population has this. A Midline swelling can possibly be apparent
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6
Q

by the 7th week in embryo what happens

A
  • the thyroid gland is in its final anatomical position.
  • Anterior to the trachea and Below the larynx
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7
Q

what does the thyroid consist of

A
  • Two lateral lobes * Isthmus
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8
Q

what does the thyroid look like

A
  • Shaped kind of like a butterfly, the isthmus usually lies below the cricoid cartilage

▪ Right and left lobes, connected via the Isthmus

▪ In some individuals, a pyramidal lobe extends superiorly from the isthmus (remnant of the thyroglossal duct)

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9
Q

arterial supply for thyroid

A
  • Superior thyroid artery (branch of external carotid artery). * Inferior thyroid artery (branch of subclavian artery).
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10
Q

venous drainage of thyroid

A
  • Superior thyroid vein.
  • Middle thyroid vein.
  • Inferior thyroid vein
    All drain into the SVC (superior vena cava) via the brachiocephalic trunk
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11
Q

what is a cricothyrotomy?

A

Cricothyrotomy is a “famous” urgent airway procedure

  • Locate the junction of the cricoid and the thyroid cartilage
  • Small incision provides quick and pretty save access to the trachea
  • The thyroid is extraordinarily vascular – if one slices indiscriminately in this area, hemorrhages happen
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12
Q

what is the capsule of the thyroid

A
  • The thyroid gland is enclosed by a thin fibrous capsule.
  • This capsule serves both as a protective layer and as an anchor for the gland to nearby neck structures.
  • The capsule is not just superficial—it sends septa (thin partitions) deep into the thyroid, dividing the gland into smaller lobules.
  • This internal structure helps compartmentalize the tissue for efficient blood flow and hormone production.
  • The capsule is also firmly attached to the cricoid cartilage and the upper part of the trachea
  • The thyroid moves up and down when you swallow, a key clinical sign used during physical examination of the gland.
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13
Q

what is the thyroid made up of

A

thyroid follicles

The functional units responsible for hormone production.

A follicle is a spherical structure, typically surrounded by a single layer of cuboidal epithelial cells (known as follicular cells or thyrocytes).

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14
Q

what are thyroid follicles filled with

A

colloid (fluid) that contains pro hormone thyroglobulin

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15
Q

what are follicular cells responsible at synthesizing

A

synthesizing and secreting thyroid hormones thyroxine (T4) and triiodothyronine (T3) via enzymes

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16
Q

what is in the parafollicular area

A

Between the follicles, in the interstitial spaces, are clusters of parafollicular cells (also called C cells).

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17
Q

what are parafollicular cells responsible for

A

These cells are responsible for producing calcitonin, a hormone that helps regulate calcium levels by inhibiting bone resorption when calcium levels are high

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18
Q

what do parafollicular/ c cells produce? and why?

A

calcitonin

regulate calcium levels (inhibit bone resorption when calcium levels are high)

calcitonin is not directly involved in metabolic processes but plays a role in calcium homeostasis.

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19
Q

what happens to the follicular cells when they are inactive vs active

A
  • Inactive: flat cells, lots of colloid
  • Active: cells become cuboidal or columnar as they take up the colloid via “reabsorption lacunae”
  • Fenestrated capillaries
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20
Q

what are the main ingredients to make thyroid homrone

A

tyrosine and iodine

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21
Q

what is produced in a high amount but less active and what is produced in low amounts but is more active ; t3 or t4

A

t4: * High amount is produced, but it is less active

t3: * Very little is produced, but it is VERY active

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22
Q

how can t4 be converted into t3

A
  • Can be converted into T3 in the periphery by deiodination
    (removal of iodine)
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23
Q

what is reverse t3

A
  • Produced in the periphery; small amount; activity unclear
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24
Q

what are thyroid hormones the derivative of

A

tyrosine

  • Thyroid hormones (T3 and T4) are derivatives of the amino acid tyrosine.
  • Tyrosine is an aromatic amino acid that forms the backbone of the thyroid hormones.
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25
Q

amino acid to make thyroid hormones

A

tyrosine

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26
Q

what are thyroid hormones made of

A

The production of thyroid hormones involves the coupling of two tyrosine molecules that undergo a series of modifications, particularly iodination.

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27
Q

what is the structure of tyrosine? what are the carbon positions where it can get iodinated?

A
  • Each tyrosine molecule has an aromatic ring structure with carbon atoms at positions 1 through 6.
  • For thyroid hormone synthesis, iodination occurs specifically at the 3- and 5-carbon positions on the ring.
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28
Q

what is iodination

A

Iodination refers to the process where iodine atoms are added to these carbon positions.

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29
Q

what is monoiodotyrosine (MIT)

A

A tyrosine molecule with one iodine at the 3-carbon.

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30
Q

what is diiodotyrosine DIT

A

A tyrosine molecule with two iodines, at both the 3- and 5-carbons.

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31
Q

what is T3 made of (i.e. DIT or MIT)

A

Formed when one MIT combines with one DIT, resulting in a molecule with three iodine atoms.

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32
Q

what is T4 made of (i.e DIT or MIT)

A

Formed when two DIT molecules combine, creating a molecule with four iodine atoms.

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33
Q

t3 vs t4 for DIT and MIT

A

t3= dit and mit
t4 = 2 dit

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34
Q

where does the coupling process of adding mit and dit to make t3 and t4 happen

A

takes place within the colloid of the thyroid follicles.

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35
Q

what is thyroid hormone derived from

A
  • Two tyrosine molecules “stuck” together with variable levels of iodination on the 3- and 5-carbon of aromatic ring
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36
Q

what are tyrosine initially part of

A

a larger protein known as thyroglobulin

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37
Q

what is thyroglobulin

A
  • Thyroglobulin is a large glycoprotein that acts as a precursor and scaffold for thyroid hormone synthesis.
  • It is a large protein, containing about 2750 amino acids, and is synthesized and secreted by follicular cells into the colloid of the thyroid follicles.
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38
Q

how many tyrosine residues in thyroglobulin; how many can be used

A

123
4-8

  • Within the thyroglobulin protein, there are 123 tyrosine residues available.
  • However, not all of these residues are used for hormone synthesis.
  • Only 4-8 tyrosine residues within thyroglobulin are actually iodinated and incorporated into the final thyroid hormones (T3 and T4).
  • These specific tyrosine residues are selectively iodinated, and the iodinated tyrosine pairs are linked together to form T3 and T4.
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39
Q

where is thyroglubin made and stored?

A

Synthesis and Storage: Thyroglobulin is produced in the follicular cells and secreted into the colloid, where the tyrosine residues undergo iodination and coupling to form hormone precursors.

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40
Q

why is thyroglobulin endocytose

A

Endocytosis and Proteolysis: When thyroid hormones are needed, the thyroglobulin is taken back into the follicular cells via endocytosis.

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41
Q

where is thyroglubin released itno

A

Release: Inside the follicular cells, enzymes cleave the thyroglobulin, releasing the active hormones (T3 and T4) into the bloodstream.

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42
Q

overview of formation and secretion of thyroid hormone

A
  1. Iodide absorption and transport
  2. Iodide uptake by the follicular cells + thyroglobulin synthesis (not “connected”)
  3. Transport of thyroglobulin and iodide into the follicle (not “connected”)
  4. Iodination of tyrosine residues on thyroglobulin
  5. Endocytosis of thyroglobulin (now with iodinated thyronine residues on it)
  6. Lysosomal destruction of endocytosed thyoroglobulin release of thyroid hormone into the cytosol
  7. Thyroid hormone enters the circulation and is carried to peripheral tissues via transport proteins
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43
Q

what symporter helps bring iodide from the diet into the follicular cell

A

a significant proportion of the iodide in the diet is absorbed into the follicular cell from the circulation by a very high-affinity sodium-iodide symporter

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44
Q

where is iodide mostly secreted to

A
  • Iodide is mostly secreted into the urinary system, some into bile
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45
Q

how does iodide circulate

A
  • As thyroid hormone is metabolized, iodide is liberated and circulates
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46
Q

where is iodine absorbed

A

small intestine

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47
Q

where is iodine stored/ used

A

Thyroid (for thyroid hormone production)
Up to 2 months supply Kidneys (excreted in urine)

Secondary locations: salivary glands, gastric mucosa, placenta, ciliary body of eye, choroid plexus, mammary glands (physiological role of iodine in these tissues is unclear)

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48
Q

how is iodine excreted

A

Liver metabolizes thyroid hormones and releases some iodine into bile attached to the metabolites (some is reabsorbed)

80% is excreted via kidneys

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49
Q

how is iodide absorbed and transported

A
  • Dietary iodide is rapidly absorbed through the gastrointestinal (GI) tract into the bloodstream.
  • Most dietary iodide comes from sources like iodized salt, seafood, and dairy products.
  • Once in the bloodstream, iodide is transported to the thyroid gland, where it is actively concentrated for thyroid hormone synthesis.
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50
Q

how is iodide uptake by follicular cells

A

Na/I cotransporter (NIS)

sodium iodide symporter

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51
Q

where is the sodium iodide symporter located?

A
  • Located on the basolateral membrane of the thyroid follicular cells (the side facing the blood).
  • The NIS (also known as SLC5A5) is a specialized Na+/I− cotransporter responsible for actively transporting iodide from the blood into the follicular cells.
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52
Q

which way does the iodine and sodium go in the Na/I symporter (NIS)

A
  • The NIS moves two Na+ ions and one iodide ion (I−) simultaneously into the cell.
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53
Q

where is iodide concentration highest (in blood or cell)? hint- active transport occurs

A
  • Iodide transport by the NIS occurs against its electrochemical gradient, meaning iodide is moved into the cell even though its concentration inside the follicular cell is already higher than in the blood.
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54
Q

what energy is needed to actively transport iodide into the cell

A
  • The energy for this process is provided by the sodium gradient, which is maintained by the Na+/K+ ATPasepump located on the basolateral membrane.

Sodium gradient:
* The Na+/K+ ATPase pumps sodium ions out of the follicular cell in exchange for potassium ions.
* This creates a low intracellular Na+ concentration, which drives the movement of Na+ into the cell along with iodide.

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55
Q

once iodide gets into the follicular cell how does it get into the lumen

A

Cl-/I- exchanger AKA pendrin

Once inside the follicular cell, iodide needs to be transported into the lumen of the thyroid follicle (colloid), where it will be used for hormone synthesis.

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56
Q

what is the purpose of pendrin

A
  • Iodide is transported across the apical membrane (the side facing the follicular lumen) by the Cl−/I− exchanger, known as pendrin.
  • Pendrin moves iodide (I−) into the follicle in exchange for chloride (Cl−) ions.
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57
Q

pendrin: Cl-/I- exchanger

A
  • Pendrin is a protein located on the apical surface of the follicular cell, responsible for secreting iodide into the follicle lumen.
  • Pendrin (SLC26A4) exchanges one chloride ion (Cl−) for one iodide ion (I−), allowing iodide to leave the cell and enter the colloid where it is used for thyroid hormone synthesis.
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58
Q

pendred syndrome (mutations in pendrin) symptoms

A

-goiter
-hearing loss
-Impaired iodide transport can lead to hypothyroidism or compensatory goiter, as the thyroid enlarges in an attempt to capture more iodide.

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59
Q

pendred syndrome

A
  • Caused by mutations in the SLC26A4 gene, which encodes the pendrin protein.
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60
Q

where is thyroglobulin made? what groups does it contain? and how is it made into t3 and t4?

A
  • Thyroglobulin (TG) is a glycoprotein synthesized by the follicular cells of the thyroid gland.
  • It contains the tyrosyl groups (tyrosine residues) that will be iodinated to form thyroid hormones (T3 and T4).
  • It contains 123 tyrosine residues, but only 4-8 of these will be used to form the thyroid hormones.
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61
Q

where is thyroglobulin synthesized and where is it packaged? how is it transported to then get exocytosed?

A
  • TG is synthesized in the rough endoplasmic reticulum (RER) and packaged in the Golgi apparatus of the follicular cell.
  • It is transported in secretory vesicles that carry it to the apical membrane, where it is exocytosed into the follicle lumen (colloid).
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62
Q

what is thyroid peroxidase? where is it located?

A
  • Along with TG, the secretory vesicles also carry the enzyme thyroid peroxidase (TPO), which is an integral membrane protein.
  • TPO is anchored in the apical membrane of the follicular cell, with its catalytic domain facing the follicle lumen (colloid), where iodination occurs.
63
Q

what is the function of thyroid peroxidase?

A

turn iodide into iodine

  • TPO catalyzes the oxidation of iodide (I−) into iodine (I*), which is a key step in thyroid hormone synthesis.
  • The oxidized iodine forms a highly reactive iodine radical (I*), which is essential for attaching to tyrosine residues on thyroglobulin.
64
Q

what turns iodide into iodine

A

thyroid peroxidase

65
Q

what is DUOX2

A

membrane protein used to help thyroid peroxidase do the oxidation reaction

  • The oxidation reaction carried out by TPO requires the activity of another apical membrane protein, known as DUOX2 (Dual Oxidase 2).
  • DUOX2 generates hydrogen peroxide (H2O2), which is necessary for TPO to oxidize iodide into the iodine radical.
66
Q

how are the iodinated tyrosines (DIT and MIT formed)

A

TPO gets iodide into iodine radical which can be added to tyrosines

Once the iodine radical is formed, it reacts with the tyrosine residues on thyroglobulin in the follicle lumen.
* This process is catalyzed by TPO and leads to the formation of iodinated tyrosines:
* Monoiodotyrosine (MIT): Tyrosine with one iodine attached. * Diiodotyrosine (DIT): Tyrosine with two iodines attached.

67
Q

what DIT and MIT make T4 and T3

A
  • TPO then facilitates the coupling of iodinated tyrosines:
  • Two DIT molecules combine to form T4 (thyroxine).
  • One MIT and one DIT combine to form T3 (triiodothyronine).
68
Q

what stimulates iodinated thyroglobulin to get endocytosed

A

TSH

Endocytosis of Iodinated Thyroglobulin
* Thyroglobulin has been iodinated and contains some coupled MIT and DIT residues (forming T3 and T4) remains in the colloid until the thyroid is stimulated to release hormones.
Endocytosis:
* When stimulated by TSH (thyroid-stimulating hormone), the iodinated thyroglobulin is taken back into the follicular cell via endocytosis.
* This forms vesicles containing TG, which are transported into the cell for further processing.
*

69
Q

what do the iodinate thryoglubin fuse with to break it down and release T3 and T4

A

lysosomes

70
Q

what is lysosomal hydrolysis of iodinated thyroglobulin for?

A

release t3 and t4 into cytosol

  • Once inside the follicular cell, the vesicles containing iodinated thyroglobulin fuse with lysosomes.
  • Lysosomal enzymes hydrolyze the thyroglobulin, breaking it down and releasing T3 and T4 into the cytosol.
71
Q

what happens to t3 and t4 when lysosomes hydrolyze them from thryroglublin? what happens to the unmodified part of the TG?

A
  • T3 and T4 are freed from the thyroglobulin backbone
  • While unmodified tyrosyl residues (MIT and DIT) are deiodinated and recycled within the follicular cell.
72
Q

how does t3 and t4 get into blood

A

unknown… but in blood bind thyroxine-binding globulin, transthyretin and albumin to get to periphery

After being released from thyroglobulin, T3 and T4 need to leave the follicular cell and enter the bloodstream to exert their effects on target tissues.
Transport Mechanism:
* The exact mechanism of how T3 and T4 leave the cell is not fully understood.
* In the bloodstream, T3 and T4 bind to transport proteins like thyroxine-binding globulin (TBG), transthyretin, and albumin to be carried to peripheral tissues.

73
Q

what do t3 and t4 bind to (3 things) to get carried to target tissue in bloodstream

A

thyroxine-binding globulin (TBG), transthyretin, and albumin

74
Q

effects of increased secretion of TSH from anterior pituitary

A

▪ Increase the activity of the sodium-iodide symporter
▪ Increases the synthesis of thyroglobulin
▪ Increases the activity of thyroid peroxidase
▪ Increases endocytosis of “iodinated” thyroglobulin
▪ Increases the proteolysis of thyroglobulin
▪ Stimulates the growth of the follicular cells and gland in general

75
Q

what are the active vs inactive forms of thyroid hromones

A

inactive- mit and dit
active- t3 and t4

Inactive Forms:
* MIT and DIT represent half of the iodinated tyrosines, are not secreted, and are recycled within the thyroid cells.
Active Forms:
* T3 and T4 constitute the other half, with T4 being the predominant hormone released into the bloodstream.

76
Q

t3 and t4 function vs reverse t3

A
  • T3 and T4 regulate critical physiological functions, whereas rT3 serves as a regulatory metabolite in certain conditions.
77
Q

are t3 and t4 hydrophilic or hydrophobic

A

hydrophobic

  • T3 (triiodothyronine) and T4 (thyroxine) are hydrophobic molecules due to their structural composition
  • This limits their solubility in aqueous environments like blood plasma.
  • Only a very small fraction of these hormones exists in their free (unbound) form within the bloodstream.
78
Q

how do t3 and t4 travel in blood

A

99% are bound to plasma proteins

  • Approximately 99.98% of T4 and 99.8% of T3 in circulation are bound to plasma proteins.
  • This high degree of binding protects the hormones from rapid metabolism and excretion, prolonging their half-lives.
79
Q

what’s more tightly bound, t3 or t4

A

t4 is tighter

  • T3 is less tightly bound to carriers compared to T4.
  • This results in a higher proportion of free T3 available to tissues for immediate action.
80
Q

longer vs shorter half life of t3 and t4

A

t4 longer, t3 shorter

  • T4 has a longer half-life
  • T3 has a shorter half-life
  • The shorter half-life of T3 makes it more readily available for tissues that require immediate responses, even though it circulates at lower concentrations.

t3 is also less tightly bound

81
Q

is t3 or t4 more available

A

t3

  • The free (unbound) fractions of T3 and T4 are biologically active and capable of entering target cells to exert their effects
    .
  • The relatively higher availability of free T3 allows it to more quickly influence metabolic processes in various tissues.
82
Q

what is the primary carrier for t3 and t4

A

albumin; is the most abundant protein in the blood

83
Q

what is the affinity albumin has for t3 and t4

A

low

While it has a lower affinity for thyroid hormones compared to other carriers, its abundance means it plays a significant role in transporting these hormones.

84
Q

transthyretin; affinity for t3 and t4

A
  • Transthyretin is another important transport protein that binds both T3 and T4.
  • It has a moderate affinity for these hormones and helps in stabilizing their levels in circulation
85
Q

what transport protein has the highest affinity for t4

A

thyroid binding globulin (TBG)

86
Q

what does thyroid binding globulin bind for with high affinity

A

t4

  • TBG has the highest affinity for T4 among all transport proteins, meaning it binds T4 more tightly than T3.
  • As a result, TBG is responsible for carrying the majority of T4 in circulation, which helps maintain its stable concentration over time.
87
Q

how do thyroid hormones enter cells

A

diffusion or transportes

  • While some studies suggest that thyroid hormones may enter cells via simple diffusion due to their lipophilic nature
  • it is increasingly recognized that specific transporters may facilitate their uptake but still being characterized
88
Q

what happens when t4 enters the target tissues

A

deoiodination

a process that removes iodine atoms to convert T4 into its more active form, T3, or its inactive form, rT3.

89
Q

what does t4 become when it gets deiodinated

A

t3

90
Q

what are the enzymes for deiodination

A
  • Deiodinase type 1 (D1) * Deiodinase type 2 (D2).

and also
deiodinase type 3 (slightly different role)

91
Q

what does deiodinase type 1 do

A

convert t4 to t3

can also produce small amount of reverse t3

92
Q

where is deiodinase type 1 found

A
  • D1 is predominantly found in the liver, kidneys, thyroid, and pituitary gland.
93
Q

what is the significance of deiodinase type 1 (D1)

A
  • By generating T3, D1 helps maintain the physiological effects of thyroid hormones in tissues where T4 levels are higher.
  • The presence of D1 in the liver is particularly important for the regulation of systemic thyroid hormone levels.
94
Q

where is deiodinaase type 2 found

A
  • D2 is primarily found in the brain, pituitary gland, and brown adipose tissue.
95
Q

deiodinase type 1 vs 2 vs 3 location

A
  • D1 is predominantly found in the liver, kidneys, thyroid, and pituitary gland.
  • D2 is primarily found in the brain, pituitary gland, and brown adipose tissue.

Deiodinase Type 3 (D3) is predominantly found in the brain and reproductive tissues.

96
Q

deiodinase type 2 role

A

convert t4 to t3

97
Q

role of deiodinase type 2

A

D2 plays a crucial role in local T3 production in the brain, which is important for regulating metabolism and overall brain function.

98
Q

what adaptive mechanism does deiodinase type 2 have

A
  • The expression of D2 can be influenced by various physiological conditions (e.g., caloric intake, temperature), allowing the body to adapt thyroid hormone availability to its metabolic needs.
99
Q

where is deiodianse type 3 found

A

Deiodinase Type 3 (D3) is predominantly found in the brain and reproductive tissues.

100
Q

what is deiodianse type 3 role

A

convert t4 into reverse t3 and inactivate t3

101
Q

deiodinase type 1 2 and 3 what do they convert

A

3 converts t4 tp reverse t3 and also inactivate t3

1 and 2 convert t4 to t3

102
Q

importance of deioidanse type 3 and producing reverse t3

A
  • D3 facilitates the removal of iodine from T4, leading to the formation of rT3, which is biologically inactive.
  • This function is particularly important in contexts where reduced metabolic activity is needed, such as during stress or illness.
103
Q

what cofactor do the deiodinases (D1, D2, D3) alll need for their enzymatic activity

A

selenium

104
Q

why does selenium as a cofactor for the deiodinases (D1, D2, D3)

A

due to the presence of selenocysteine residues in their active sites, which are essential for the deiodination process.

105
Q

what residues do thyroid hormones have that need selenium

A

selenocysteine resideus

106
Q

selenium importance

A
  • Selenium is a vital trace mineral that plays a crucial role in thyroid hormone metabolism and overall endocrine health.
  • A deficiency in selenium can impair the function of deiodinases, leading to altered thyroid hormone levels and potentially contributing to conditions such as hypothyroidism.
107
Q

how is reverse t3 formed? is it active or inactive?

A
  • rT3 is formed during the deiodination of T4, typically when one iodine atom is removed from the outer ring of T4.
  • Although rT3 is considered an inactive metabolite, its levels can rise in certain conditions, such as fasting or illness, serving as a mechanism to downregulate metabolism.
108
Q

what is the physiological role of reverse t3? what does it do to reduce t3

A
  • rT3 competes with T3 for receptor binding but does not activate the thyroid hormone receptors, thus effectively reducing metabolic activity during times of stress or caloric restriction.
109
Q

what are deiodinases influenced by

A

▪ Age (less T3 made during fetal life)
▪ Drugs
▪ Selenium deficiency
▪ Illness (burns, trauma, advanced cancer, cirrhosis, chronic kidney disease, MI, febrile state)
▪ Diet
* Fasting: reduces T3 by 50% in 3-7 days (rT3 is increased)
* Overfeeding: increases T3 and reduced rT3

110
Q

impact of fasting vs overfeeding on t3 and rt3

A
  • Fasting: reduces T3 by 50% in 3-7 days (rT3 is increased)
  • Overfeeding: increases T3 and reduced rT3
111
Q

what has a higher affinity for thyroid hormone receptor in the cell; t3 or t4

A

t4 has lower affinity than t3

112
Q

what type of receptor is TSH recepetors

A

g-protein coupled receptor

113
Q

what activates the GPCR of the TSH receptor

A

phospholipase C

114
Q

what do TSH receptors GCPR increase?

A

Increases iodide binding
Increases synthesis of T4 and T3
Increases secretion of thyroglobulin into colloid
Increases blood flow to thyroid

115
Q

what does chronic high stimulation of the TSH receptors do

A

hypertrophy or goiter

116
Q

where is TSH secreted from and in response to what

A

Thyroid Stimulating Hormone (TSH) is secreted by the anterior pituitary gland in response to Thyrotropin-Releasing Hormone (TRH) from the hypothalamus.

117
Q

where is TRH come from and what does it stimulate

A

hypothalamus and stimulate TSH in anterior pituitary

118
Q

where does TSH from anterior pituitary bind to and what does it cause secretion of

A
  • TSH binds to receptors on the thyroid follicular cells, stimulating the synthesis and secretion of thyroxine (T4).
  • T4 is the primary hormone produced by the thyroid and is largely responsible for regulating metabolism throughout the body.
119
Q

once t4 is secreted into the bloodstream; what are the 2 forms that it can exist as

A

free t4 or bound t4

120
Q

what is free t4

A

The unbound form, which is biologically active and able to enter cells and exert effects.

121
Q

what is bound t4

A

The majority of T4 binds to plasma proteins, such as thyroid- binding globulin (TBG), transthyretin, and albumin. This binding helps regulate the availability of T4 and provides a reservoir for hormone storage.

122
Q

what is the majority of t4 in the bloodstream; bound or unbound

A

bound

to plasma proteins, such as thyroid- binding globulin (TBG), transthyretin, and albumin

123
Q

equilibrium between free t4 and bound t4

A
  • There is a dynamic equilibrium between free T4 and bound T4.
  • Changes in protein levels (such as during pregnancy or illness) can alter the amount of free T4 available, affecting physiological responses.
124
Q

how does free t4 help regulation TSH

A

negative feedback

  • The levels of free T4 in the bloodstream are critical for regulating TSH secretion
  • When free T4 levels rise, they exert a negative feedback effect on the anterior pituitary gland.
  • This feedback mechanism inhibits the secretion of TSH, thus reducing stimulation of the thyroid gland and decreasing T4 production.
  • This ensures that hormone levels remain within a normal physiological range.
125
Q

how does t3 regulate TSH secretion

A

negative feedback

  • T3, like free T4, also has a negative feedback effect on the pituitary gland, further inhibiting TSH secretion.
  • This feedback mechanism is vital for maintaining the delicate balance of thyroid hormones and ensuring that metabolic processes function optimally.
126
Q

how is TSH similar to LH, FSH and hCG

A

Alpha subunit is identical, beta subunit is unique (glycoprotein tropic hormone)

127
Q

what is the half life of TSH, where is it excreted

A

60 mins and excreted in kidneysh

128
Q

how is TSH secreted? when is its peak?

A

peak at midnight

  • Pulsatile secretion, pulses increase in amplitude, frequency at night (peaks at midnight) Degraded and excreted mostly via kidneys
    Pulsatile secretion with rise at 9pm, peak at midnight and decline after
129
Q

t3 and t4 effects on the heart

A

chronotropic and ionotropic

increased number of beta andrengeric receptors

enhanced response to circulating catecholamines

increased proportion of alpha myosin heavy chain (with higher ATPase activity)

130
Q

t3 and t4 effects on adipose tissue

A

catabolic

stimulated lipolysis

131
Q

t3 and t4 effects on muscle

A

catabolic

increased protein breakdown

132
Q

t3 and t4 effects on bone

A

developmental

promote normal growth and skeletal devleopment

133
Q

t3 and t4 effects on the nervous system

A

devlopmental

promote normal Brian devleopment

134
Q

t3 and t4 effects on the gut

A

metabolic

increased rate of carbohydrate absorption

135
Q

t3 and t4 effects on lipoprotein

A

metbaolic

formation of LDL receptors

136
Q

t3 and t4 effects on calories and metabolism

A

calorigenic

stimulated oxygen consumption by metabolically active tissues

increased metabolic rate

137
Q

t3 activities

increase or decrease BMR

A
  • Increase basal metabolic rate
  • Greatly aid in normal growth and development
138
Q

hyperthyroid and hypothryoid- decrease or increase BMR

A

hyper-increase
hypo-decrease

139
Q

hyperthyroid and hypothryoid effect on carb metabolism

GNG
glycogenolysis
serum glucose

A

hyper
-increase GNG and glycogenolysis
-serum glucose norma;

hypo
-decrease GNG and glycogenolysis
-serum glucose normal

140
Q

hyperthyroid and hypothryoid

protein metabolism impact

A

hyper- increase synthesis and proteolysis
-muscle wasting present

hypo
-decrease synthesis and proteolysis

141
Q

hyperthyroid and hypothryoid impact on lipid metabolism

lipogeneissi, lipolysis and cholestero

A

hyper
-decrease lipogenesis and cholesterol
-inceased lipolysis

hypo
-increased lipogenesis and cholesterol
-decreased lipolysis

142
Q

hyperthyroid and hypothryoid impact on thermogeneiss

A

hyper- increased
hypo- decreawsed

143
Q

hyperthyroid and hypothryoid impact on ANS (catecholamines)

A

hyper- increased expression of catecholamine recepeotrs

hypo- globally reduced catecholamine signalling

144
Q

calorigenic (heat-producing actions of t3 and t4

A
  • Increase energy (oxygen) consumption in almost all tissues except for the brain (including pituitary) and adult reproductive organs
145
Q

what are calorigenic effects

A

▪ Increased fatty acid mobilization
▪ Increased activity of the sodium/potassium ATP-ase… everywhere
▪ Increased cardiac output & sympathetic nervous system effectiveness
▪ Activation of uncoupling protein in brown fat and perhaps other cells more prominent effect in young children

146
Q

calorigenic action

A

Increase O2 consumption in almost all tissues

Increase Na+ K+ ATPase activity

Increase fatty acid metabolism

Increase metabolic rate
–May result in weight loss if intake of nutrients doesn’t match
–Small amounts of T3 stimulate growth, but high amounts promote catabolism

Increase requirement for all vitamins
–>Thyroid hormones are also needed for liver’s metabolism of carotene into vitamin A

Other general effects:
Facilitates normal menstrual cycle Allows for milk secretion
Support normal skin structure

147
Q

cardiovascular impacts of t4 and t3

A

▪ Vasodilation –>decreased peripheral resistance –>modestly increased sodium and water reabsorption (increased blood volume)
▪ As mentioned, increased effectiveness of SNS on the heart –>

148
Q

neurological impacts of t3 and t4

A

▪ very, very important in early neurological development in the fetus and infant
* CNS,basalganglia,specialsenses(cochlea)
▪ Increases arousal and activation of reticular activating system, overall neuronal “excitability” (i.e. hypothyroidism –>

149
Q

t4 and t3 on carb metabolism

A

▪ Increased absorption of carbohydrates from GI, increased gluconeogenesis, increased glycogenolysis

  • However, blood glucose tends to remain normal, likely due to increased consumption
150
Q

impact of t3 and t4 on muscle growth, skeletal growth, cholesterol

A
  • Lower circulating plasma cholesterol
    ▪increased synthesis of LDL receptors
  • Muscle growth
    ▪ Hard to characterize–seems to both aid development but also lead to
    increased protein turnover (hyperthyroidism muscle weakness)
  • Skeletal growth
    ▪ Key for normal growth in childhood and skeletal maturity ▪ Facilitates function of growth hormone
  • Also has impacts on skin appearance/structure, milk secretion, and the normal menstrual cycle
151
Q

impact of congenital hypothryoid on normal delvoepment

A

This is a graph of developmental age— that is, the age that the child appears based on height, bone radiograph, and mental function—versus chronological age.
For a euthyroid child, the relationship is the straight line in red
The three green curves are growth curves for a child with thyroid hormone deficiency
* At age 4.5 years thyroid hormone replacement therapy was initiated. Notice the “catching up” of bone and height parameters, but the lag in cognitive parameters

152
Q

Other thyroxine, TSH, and TBG notables

A
  • Increased metabolic rate due to hyperthyroidism –>increased requirements for all vitamins
  • TSH release is induced by cold (in infants)
  • TSH release is inhibited by cortisol and stress
    ▪ Impacts on pituitary and hypothalamus
  • TBG can be increased with elevations in estrogen (and during pregnancy) and with some medications

▪ Increases “store” of bound thyroxine, no impact on free levels

  • TBG can be decreased by glucocorticoids, androgens, and other medications
    ▪ Still no impact on free levels of hormone
153
Q
A

BMS200 (19 decks)

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