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Endo/Repro Exam 1 > 5. Thyroid Gland > Flashcards

5. Thyroid Gland Flashcards

1
Q

What hormones does the thyroid gland make?

A

The thyroid gland makes iodothyronines.

  1. T4 (tetraiodothyronines)- a prohormone (90%)
  2. T3 (Triiodothyronine)- an active hormone.

Deiodinase is required for conversion

  1. C cells (parafollicular cells)- secrete calcitonin
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2
Q

Describe the blood supply of the thyroid gland.

A

Rich blood supply.

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3
Q

What is the functional unit of the thyroid gland?

A
  • The functional unit of the thyoid gland is the thyroid follicle.
  • Lined by: cuboidal epithelial cells.
  • Lumen is filled with colloid, iodine and thyroid hormone precursors.
  • The size of the epithelial cells and colloid change depending on the activity of the thyroid follicle.
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4
Q

Thyroid hormones contain a large amount of _______.

A

iodine

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5
Q

Where does synthesis of thryoid hormones occur?

A

Follicular epithelial cells: partly intracellular and extracellular with T4 being the main product secreted.

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6
Q

What is the colloid made up of?

A

Newly made thyroid hormones attached to thryoglobulin.

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7
Q

Describe the conversion of T4 -> T3.

A
  • Conversion of T4 -> T3 occurs d/t deiodinase.
  • 80% is peripherally converted; 10-20% is directly secreted as T3.
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8
Q

Typically deiodinases work fine.

However, what can prevent them from converting T4-> T3?

A
  1. Fasting
  2. Medical and surgical stress
  3. Catabolic diseases

Cause a decrease in active thyroid secretion.

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9
Q

________ is the backbone for all of the thyroid hormones.

A

Tyrosine

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10
Q

How do we make monoiodotryosine and diodotyrosine?

A

Iodine + tyrosine.

Iodine + iodine + tyrosine.

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11
Q

__________ + ________ = tetraiodothyronine** (T4).**

A

Diiodotyrosine + diiodotyrosine = tetraiodothyronine (T4).

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12
Q

___________ + ____________ = triiodothyronine (T3).

A

Diiodotyrosine + monoiodotyrosine = triiodothyronine (T3).

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13
Q

The synthesis of thyroid hormones is more complex than that of most hormones.

There are three unusual features of the synthetic process:

A

1. Thyroid hormones have a lot of iodine, which we must get thruu diet.

2. Synthesis is intracellular and extracellular, with completeed hormones stored extracellularly in the follicular lumen until stimulated.

3. T4 is the the main secretory product, but no the active form.

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14
Q

What is thyroglobuin?

A
  • A glycoprotein w/ alot of tyrosine, is made in the thyroid follicular epithelial cells and is pushed into the follicular lumen – awaiting iodination.
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15
Q

What transporters are located on the BL membrane of the thyroid follicular epithelial cell, facing the blood?

A
  1. NIS symporter
  2. Na/K+ ATPase
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16
Q

What transporters/enzymes are located on the apical membrane of the thyroid follicular epithelial cell, facing the follicular lumen?

A
  1. Pendrin (Cl/I- countertransporter)
  2. Thyroid peroxidase.
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17
Q

What is organification?

A

Process of binding iodine with TG.

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18
Q

Describe the process of thyroid hormone synthesis.

A
  1. Thyroglobulin (TG), a glycoprotein with a lot of tyrosine, is made on the rER and golgi apparatus of the thyroid follicular epithelial cells. It is then put inside secretory vesicles and pushed into across the apical membrane into the [follicular lumen], awaiting iodination of thyroglobulin to form precursors of thryroid hormones.
  2. Na+/I- symporter (NIS) on the BL membrane actively moves in 1 I- (against gradient) and 2 Na+ into the thyroid follicular cell. Known as I trap.
    • Activity is regulated by I- levels. Low levels stimulate pump, attempting to compensate for deficiency.
    • If the dietary deficiency is too severe, the pump cannot compensate and synthesis of thyroid hormones will decrease.
  3. Oxidation of I (iodide)- -> I2 (iodine): I- then moves through the apical membrane of the thyroid follicular cell via pendrin (a Cl-/I- counter transporter) where it is oxidized to I2 by thyroid peroxidase (TPO), which also catalyzes the next two steps.
  4. Organification of I2: I2 then passes through the apical membrane and immediately meets the tyrosine of thyroglobulin in the lumen. I2 + tyrosine of TG -> MIT (monoiodotyrosine) and DIT via t_hyroid perixoidase_. MIT and DIT remain attached to thyroglobulin in the follicular lumen until the thyroid gland is stimulated to secrete its hormones.
  5. Two coupling reaction occurs via thyroid peroxidase, while still attached to thyroglobulin.
      • DIT + DIT -> T4
        • DIT + MIT -> T3
        • The first reaction is faster, which is why we make 10x more T4 than T3.
        • Portion of MIT and DIT does not couple (left overs) and remains attached to thyroglobulin.
        • After coupling, thyroglobulin contains T3, T4 and leftover MIT and DIT.
        • Iodinated thyroglobulin is stored in the follicular lumen as colloid until thryroid gland is stimulated by TSH.
  6. Endocytosis of thryglobulin: When the thyroid gland is stimulated, iodinated thyroglobulin with its attached T4, T3, MIT, and DIT, is endocytosed back into the follicular epithelial cells.
  7. Thyroglobulin (+ T3, T4, MIT and DIT) is hydrolyzed into component by lysosomal enzymes: While in the cell, lysosomal membranes fuse with thyroglobulin. Lysosomal proteases then hydrolyze peptide bonds to release T4, T3, MIT, and DIT from thyroglobulin.
    • T4 and T3 are transported across the basal membrane and into the bloodstream.
    • MIT, DIT, remain in the follicular cell
  8. Deiodination of MIT and DIT inside the cell by thyroid deiodinase.
    • Tyosine and I- are salvaged by the intrathryroidal deiodinase to make new thyroglobulin.
    • I- made is recycled, increases in the cell and is used to export out via pendrin.
    • Tyrosine are used to make new thyroblobulin next cycle.
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19
Q

Deficiency in thyroid deiodinase mimics what?

A

Dietary I- deficiency.

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20
Q

___ is a growth factor of the thyroid gland, which can cause goiters.

A

TSH

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21
Q

When the availability of iodide is restricted, the formation of ____ is favored.

A

T3

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22
Q

When the availability of iodide is too high, what happens?

A

Wolff-Chaikoff effect: describes how the thyroid peroxidase is inhibited by a large bolus of dietary iodine. This inhibits organification and we do not make a lot of thyroid hormone.

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23
Q

What can inhibit NIS?

A

Perchlorate and thiocynate.

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24
Q

What is PTU (propylthiouracil)?

A

PTU is used to treat hyperthyroidism by inhibiting thyroid peroxidase (TPO).

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25
Q

We will take ____ ug of iodide from ECF -> thyroid gland

____ ug of iodide will leak from the thyroid gland -> ECF.

A

We will take 120ug of iodide from ECF -> thyroid gland

60ug of iodide will leak from the thyroid gland -> ECF.

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26
Q

Where is iodine stored?

A

Iodine is stored iodinated as tyrosine of thyroglobulin in follicular colloid.

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27
Q

Enough hormone is stored as iodinated TG in colloid to last the body______

A

2-3 months

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28
Q

Activity of the thyroid gland can be assessed by radioactive iodine uptake.

  • Hyperactive thyroid gland (hyperthyroidism/graves dz)–>
  • Hypothyroididm thyroid gland –>
A
  • Hyperactive thyroid gland (hyperthyroidism/graves dz) tends to take up more radioactive iodine.
  • Hypothyroididm thyroid gland will not take up a lot of radioactive iodine.
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29
Q

How do we transport thyroid hormones?

A
  • They circulate in the blood stream bound to plasma protein (99%) or free (1%). There is a equilibrium between bound and free circulating T3 And T4.
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30
Q

What are the thyroid hormone binding proteins?

A
  1. Thyroxin-binding protein (TBG) is the most predominant one. It is made by the liver and preferentially binds T4.
  2. Transthyretin (TTR)
  3. Albumin.
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31
Q

Most circulating thyroid hormone is T4. Thus, T3 and T4 half life and what are they affected by?

A
  • ½ for T4 bc binds to TBG preferentially: 6 days.
  • ½ for T3 is 1 day.
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32
Q

T3 resin uptake test can help us differentiate between: hypo/hyperthyroidism and levels of TBG.

Hyperthyroidism:

Hypothyroidism:

A
  • Hyperthyroidism: High T4 (free and bound) and high T3 resin uptake
    • ​More total T4 available. Thus, there are fewer spaces on the TBG got T3. So more T3 will bind to resin as more T3 is free
  • Hypothyroidism: Low T4 (free and bound) and low T3 resin uptake
    • Less total T4. is available. Thus, more space on TGB for T3. Thus, less T3 will bind to resin as more binds to TGB.
33
Q

High TBG

A

means there will be more bound T3 ANDT4, resulting in a decreased T3 resin uptake.

High TBG: high T4 (but normal free); low T3 resin uptake

34
Q

Low TBG

A

low T4 (but normal free) and high T3 resin uptake

35
Q

Hepatic failure

A

Decreased levels of TBG; thus, the patient will have a transient increase in the level of free T3 and T4. Negative feedback will then inhibit the synthesis of T3 and T4.

Hepatic failure: low TBG and high T3 resin uptake.

36
Q

Pregnancy

A
  • Increased levels of TBG;
  • Increased bound forms, > decreasing free T3 and T4 -> increase in synthesis and secretion of T3 and T4 ->
  • Increases total levels of T3 and T4, but levels of free, physiologically active thyroid hormones are normal. (clinically euthyroid)

pregnancy= high TBG and low T3 resin uptake

37
Q

What is the role of TSH?

A
  1. Enlarges the thyroid gland (trophic effect)
  2. Causes the secretion of thyroid hormone
38
Q

Major control of the synthesis & secretion of thyroid hormones is via the _________

A

HPT axis.

39
Q

What regulates TSH?

What is the 2nd MSNGR for TSH?

A
  1. TRH.
  2. Free T3 via negative FB

The 2nd msnger is CAMP.

40
Q

TSH secretion, in contrast to the secretion of GH, occurs a what rate?

A

a steady!

41
Q

What stimulates thyroid hormone secretion?

A
  1. TSH
  2. Thyroid-stimulating immunoglobins
  3. Increased TBG levels (during pregnancy)
42
Q

What inhibits thyroid hormone secretion?

A

1. I- deficiency

2. Deiondinase deficiency

3. Excessive I- intake (Wolff Chaikon effect)

4. Percholrate/ thiocyante.

5. PTU

6. Decreased TBG levels (liver failure)

43
Q

What. are the actions of TH? (6)

A
  1. Activate nuclear receptors and cAMP second MSGR.
  2. Increase metabolic activity; BMR, carbohydrate/lipid metabolism
  3. Growth; fetus, neonate and adolescence
  4. Increase CO
  5. GI motilty
  6. Development of CNS
44
Q

What intracellular changes are included in the actions of TH?

A
  • Thyroid hormones help to make new proteins such as: Na/K ATPase, transport proteins, B1 adrenergic, lyosomal enzymes, proteolytic proteins and structural.
  • In cardiac muscle, it helps to make B-adrenergic R, myosin, Ca2+ ATPase.
  • Liver and adipose tissue: metabolix enzymes.
45
Q

How does thyroid hormones affect BMR?

A
  1. Increase in BMR mainly d/t in increase Na/K ATPase
  2. Increase in Na/K ATPase will cause an
    • Increase O2 consumption
    • Increase heat consumption
46
Q

Plasma concentration of cholesterol and TAGS are _________correlated with thyroid hormones.

A

INVERSELY CORRELATED.

High cholesterol= hypothyroidism

47
Q

Hyperthyroidism leads to ____ BMR.

Hypothyroidism leads to ____ BMR.

A

high

low

48
Q

How does thyroid hormones affect metabolism?

A

Carb metabolism:

    1. Increase in glucose absorption–> Increase glycogenolysis –> Increase gluconeogenesis TO MAKE FREE GLUCOSE
    1. insulin-dependent glucose uptake

Fat metabolism

  • Lipolysis (fat mobilization) and increase oxidation of FA –> increases concentration of FA in plasma.
49
Q

How do thyroid hormones affect cardiovascular?

A

Main: Increase CO.

It will have direct and indirect effects.

  • Decrease in systemic/peripheral vascular resistance –> decrease diastolic BP–> + RAAS–> increase in blood volume (also d/t direct effect of T3) and increase in B-adrengeric R (increase contractiility) will increase HR and CO.
    *
50
Q

The increase in BMR made by a single dose of thyroxine (T4) occurs after _________ but it is _______.

A

Occurs after several hours

but is is long lasting. (>6 hours)

51
Q

Patients who are HYPOTHYROID can suffer from blindness and yellow skin. Why?

A

Thyroid hormones are needed to convert carotene–> vit A.

52
Q

Thyroid hormones stimulate the synthesis of B-adrenergic receptor on the heart. What does this result in?

A

It will be more sensitive to sympathetic stimulation: and thus, there will be an increase in chronotropy and ionotropy.

53
Q

How does TH affect growth?

A

Works together with GH and somatomedins to promote bone formation.

54
Q

TH is important for CNS maturation. Decrease of these hormones during perinatal period can lead to what?

A

1. abnormal devlopment of synapses.

2. Decrease in dendritic branching and myelination.

These changes are irreversible and can lead to cretinism unless replacement is started SOON after birth.

55
Q

Hyperthyroidism will affect metabolism and bone in what key question ways?

A
  • Metabolism: weight loss, heat intolerance, high BMR
  • Bone: osteoporosis
56
Q

Hyperthyroidism will affect CNS and Skin in what key question ways?

A

CNS: agitation, anxiety, difficulty concentrating, hyperreflexia

Skin: sweating

57
Q

Hyperthyroidism will affect CV system and intestine in what key question ways?

A

CV: tachycardia, a-fib, palpitation, high output heart failure

Intestines: diarrhea

58
Q

Hypo thyroidism will affect bone and CNS and CV system in what key question ways?

A
  • bone- stunted growth
  • CNS- cretinism, adults: slowed movement, impaired memory and decreased mental capacity
  • CV: bradycardia, decreased contractility, decreased CO, HF
59
Q

In general, hyperthryoidism (too much TH in blood) causes

A

increased speed of body fxs: weight loss, sweating, high HR, high BP,

60
Q

In general, hypothyroidism (not enough TH in blood) causes

A

body fxs to slow down: fatgigue, weight gain, cold interance,.

61
Q

TRH (hypothalamus) –> TSH (thyrtrophs of AP) –> T3 and T4 (thyroid).

How is TSH secreted at a steady rate?

A

TSH is going to be regulated by:

  1. TRH from the hypothalmus
  2. Negative feedback of free T3 inhibiting the secretion of TSH by downregulating the TRH receptor on thyrotrophs of the AP. Thus, this decreases sensitivity to TRH.
62
Q

What is primary hyperthyroidism and give an example.

A

Primary hyperthyroidism- the endocrine gland (thyroid) is secreting too much T3 and T4.

Ex. Graves Dz.

63
Q

What is secondary hyperthroidism and give an example?

A
  • Secondary hyperthyroidim is d/t the AP.
  • TSH-secreting pituitary is secreting too much TSH.
64
Q

What is Graves disease?

A
  • Thyroid-stimulating immunoglobins stimulate the TSH receptor on the thyroid gland, without TSH present.
  • Thyroid release alot of TH

Results

  • TH is high.
  • TSH is low (because the high levels of TH inhibit TSH secretion).
65
Q

What are the presentation of Graves dz?

A
  1. Exophthalmos (abnormal protrustion of eye ball) and preorbital edema d/t anti-TSH R Ab

Diagnosed by: High serum free and total T4/3 and signs of a goiter. Also presence of TSI (thyroid-stimulating immunoglobins).

  • TSI helps to distinguish drom adenoma of pituitary.
66
Q

Causes of hypothryoidism.

A
    1. Agenesis
    1. Gland destruction (primary cause) which can be d/t hasimoto thyroiditis.
    1. Inhibition of TH synthesis and release
    1. Pituiary dz (sheehans)
    1. Resistance to TH
    1. Transient; after surgey, postpartum, thyroiditis
67
Q

How can we replace hypothyroidism AND WHAT SHOULD WE BE CAUTIOUS OF?

A
  • Replacement dose of T4: bc metabolism of T4 decreases with age and plasma half-life increases with age. Thus, higher doses in younger kids.
  • CAREFUL: overprescribing T4 to post-menopausal W can cause osteoporosis.
68
Q

What is an example of hypothyroidism?

A
  • Hashimoto’s thyroiditis
  • Cretism
69
Q

What is Hashimoto Thyroiditis?

A
  • Thyroglobulin or TPO antibodies impairs TH synthesis, decreasing T3/T4 secretion.
  • B/c of low T3/T4, we will have high TSH levels -> goiter.
70
Q

What cretinism?

A
  • Caused by: iodide deficiency, mom intakes _anti-thyroid med_s, impaired development of thyroid gland–> deficit in synthesis of TH.
  • Sx: feeding problems, resp problems, protruding tongue, growth/mental retardation
71
Q

Untreated postnatal hypothyroidism can lead to what?

A

cretinism

72
Q

Iodine deficiency can cause what?

A

hypothyroidism;

Iodine deficiency -> transient decrease in synthesis of TH -> THUS, we will have high TSH -> goiter.

73
Q

With I- defiency, you can get a goiter.

If the enlarged gland can maintain normal blood levels of TH (d/t high TSH) -> that person will be ________ and _______.

If the gland cannot maintain normal levels of TH, the person will be ________.

A

If the enlarged gland can maintain normal blood levels of TH (d/t high TSH) -> that person will be clincally euthyroid and assymptomatic.

If the gland cannot maintain normal levels of TH, the person will be clinically. hypothroid. .

74
Q

a TSH producing tumor is _____ hyperthyroidism.

A

secondary

75
Q

TSH-secreting tumor.

____ levels of TSH

____ levels of T4/T3

Goiter?

A

Increase

increase

yes

76
Q

Ingestion of T4

____ levels of TSH

____ levels of T4/T3

Goiter?

A

Decreased

Increased

No.

77
Q

Autoimmune thyroiditis

____ levels of TSH

____ levels of T4/T3

Goiter?

A

Increased (d/t neg feedback)

Decreased

Yes. it enlarges even though its not making TH!

78
Q

TSH Deficiency

____ levels of TSH

____ levels of T4/T3

Goiter?

A

Low

Low

No

Endo/Repro Exam 1 (14 decks)

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