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Endocrinology Quiz 4 > Thyroid Hormones > Flashcards

Thyroid Hormones Flashcards

1
Q

Hormones secreted by the Thyroid gland

A
  • 3,5,3’,5’-tetraiodothyronine (thyroxine, T4) - major
  • 3,5,3´-triiodothyronine (T3)
  • 3,3´,5´-T3 (reverse T3) - trace amount
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2
Q

Functional Thyroid Hormone

A
  • A substantial fraction of the secreted T4 is converted to T3 and rT3 in peripheral tissues
  • T3 is the major hormone bound to the thyroid hormone (TH) receptors.
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3
Q

Effects of Thyroid Hormone

A
  • T3 is the hormone that is primarily responsible for the physiological effects of the TH.
  • These effects include the control of metabolic processes and heat production, and normal growth and development.
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4
Q

Mechanisms of Action of Thyroid Hormone

A

• T4 and T3 are transported into cells by specific TH transporters (MCT and OATP transporters).
• Target cells contain nuclear TH receptors (TRs), which have an affinity for T3 that is five to
ten times that for T4.
• Association of ligand with the TRs bound to TH-response elements (TREs) located on specific genes results in enhancement or suppression of transcription.
• However, the unliganded receptor is not necessarily inactive. In the absence of ligand, TRs can have the opposite effect to that which it exerts in the presence of ligand. For example if the liganded TR stimulates the transcription of specific gene, transcription may be suppressed in the absence of ligand.
• The effects of the unliganded receptors are thought to be critical in TH-dependent brain development.

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5
Q

Biosynthesis of Thyroid Hormone

A
  1. Active concentration of plasma iodide across the basal membrane of the thyroid by the sodium-iodide symporter (NIS).
  2. Peroxidation of thyroidal I- to form an iodinating agent (I2 or I+).
  3. Iodination of tyrosine residues contained in the thyroidal protein (thyroglobulin) to yield monoand
    diiodotyrosine (MIT and DIT).
  4. Coupling of two DIT or one DIT and one MIT molecules to form T4 or T3.
  5. Enzymic hydrolysis of thyroglobulin to yield its constituent amino acids including T4 and T3, MIT
    and DIT.
  6. Some T3 may be also formed by the intrathyroidal monodeiodination of T4 to yield T3.
  7. The MIT and DIT released from the thyroglobulin are rapidly deiodinated within the thyroid by a
    specific iodotyrosine deiodinase and are NOT released into the circulation. The iodide can be
    recycled into TH biosynthesis.
  8. The T4 and T3 are released into the serum when the appropriate signal is given.
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6
Q

Control of Synthesis and Secretion of Thyroid Hormone - Autoregulation

A

• A sudden increase of iodide in the system, such as occurs following intake of KI, or a large amount of seaweed, results in a marked but temporary decrease in iodide uptake and organification in the thyroid.
• The exact mechanism is not clear, but it is due in part to the direct suppressive effect of iodide on the NIS, and on the peroxidation system essential for tyrosine iodination.
• A sudden high level of iodine also markedly suppresses the release of T4 and T3, and
decreases the total blood content in the thyroid.
• All these effects are independent of TSH and are TEMPORARY. If the iodine level is maintained, the gland “escapes” from the effect and TH synthesis and release resume. In humans the iodide effect lasts only 48-72 hours.

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7
Q

Control of Synthesis and Secretion of Thyroid Hormone - Extrathyroidal regulation

A
  • Appropriate regulation of TH synthesis and release is achieved primarily through the stimulating action of the pituitary hormone thyrotropin (thyroid-stimulating hormone, TSH).
  • TSH binds to receptors in the membrane of the thyroid cell, and most of its effects are mediated by cAMP: effects include enhancement of hormone biosynthesis and secretion, thyroidal intermediary metabolism, phospholipid and RNA synthesis and growth and vascularity of the gland.
  • In abnormal circumstances, a variety of autoantibodies can bind to the TSH receptor and mimic OR block the effects of TSH.
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8
Q

Control of Synthesis and Secretion of TSH -

Thyrotropin-releasing hormone (TRH).

A

• TRH from the hypothalamus is carried by the
hypophysial portal system to the anterior pituitary, where it binds to cell membrane receptors, and
enhances both the release of TSH and its synthesis via the phosphatidylinositol 4,5 bisphosphate
second messenger system.
• TRH is rapidly inactivated by enzymes present in plasma so that its concentration in the peripheral circulation is very low.

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9
Q

Control of Synthesis and Secretion of TSH -

Feedback control of TSH

A

• Feedback control occurs at the pituitary AND the
hypothalamus and both T4 and T3 are involved.
• In the hypothalamus TH suppresses the release of
TRH.
• In the pituitary, TH inhibits both the synthesis and secretion of TSH and antagonizes the action
of TRH. The latter effect results from a decrease in TRH receptor concentration.
• T3 inhibits TSH synthesis by inhibiting the transcription of the genes for both the TSH-a and the TSH-b subunits.
• Inhibition by T4 in both the hypothalamus and pituitary is dependent on its intrapituitary conversion to T3 (vide infra).

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10
Q

TH in the circulation

A
  • The major circulating iodothyronine is T4 together with some T3 and traces of rT3.
  • Greater than 99.95% of T4 (99.5% of T3) is bound to plasma proteins.
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11
Q

Thyroide Hormones binding protiens

A

• T4 is normally bound to three proteins in the ratio of ~ 60:30:10:
• Thyroxine-binding globulin (TBG),
(which in contrast to the TRs has a higher
affinity for T4 than for T3).
• Thyroxine-binding prealbumin (TBPA)
• Albumin

• T3 is bound only to TBG and albumin

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12
Q

Thyroid Hormone binding and half life

A

• The binding of T4 and T3 in plasma is reversible and the extent of the binding governs the half life of
each hormone in plasma (in humans T4: 9 days; T3: 1 day).
• Only free (unbound) T4 or T3 is available
to the target cells

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13
Q

Peripheral Distribution of TH

A

T4 and T3 are present in every tissue of the body

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14
Q

Metabolism of TH

A

T4 and other iodothyronines are metabolized by three types of deiodinase: D1, D2 and D3

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15
Q

D1

A
  • D1 is an outer-ring or 5’-deiodinating enzyme
  • D1 is found primarily in liver, kidney and thyroid, and is responsible for the production from T4 of some of the T3 circulating in plasma.
  • D1 also has inner ring deiodinase activity with a substrate preference for the sulfate conjugates of the iodothyronines.
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16
Q

D2

A
  • D2 is an outer-ring or 5’-deiodinating enzyme
  • D2 is found primarily in the pituitary, CNS and brown fat and is responsible for the local generation of T3 from T4 in these tissues.
17
Q

D3

A
  • D3 is an inner-ring or 5-monodeiodinating enzyme that converts T4 and T3 to their inactive derivatives, rT3 and 3,3’-T2, respectively
  • D3 is found in high levels in placenta and pregnant uterus, and at lower levels in several tissues, in particular brain,during development.
18
Q

Excretion of Thyroid Hormones

A

• Significant fractions of the circulating T4, T3 and other iodothyronines are conjugated in the liver
with glucuronic acid and to a lesser extent sulfates. • The conjugated forms are excreted as such into
the bile.
• As they pass through the intestine, the conjugates are hydrolyzed releasing the original
hormones, some of which can be reabsorbed into the bloodstream.
• The unabsorbed iodothyronines pass through the GI tract and are excreted in feces.

19
Q

Physiological Effects of TH

Metabolic Effects

A 
TH participates in the regulation of:
• BMR and heat production
• water and ion transport
• calcium and phosphorus metabolism
• cholesterol and fat metabolism
• nitrogen metabolism
• carbohydrate metabolism
20
Q

Physiological Effects of TH

Growth-Promoting and Developmental Effects

A

TH is essential for:
• growth of many vertebrate tissues;
• amphibian metamorphosis;
• maturation of CNS.

21
Q

TH deficiency during development

A
  • It results in mental retardation and this is the one known effect of TH deficiency that is irreversible.
  • If a baby is born with congenital hypothyroidism and is NOT treated immediately it will suffer from, among other problems, severe metal retardation and stunted growth.
  • Treatment is initiated with T4 and continued for life
22
Q

TH deficiency during pregnancy

A

• If iodine deficient during pregnancy; depending on the severity of the deficiency the fetus may exhibit only mild but irreversible neurological damage sometimes coupled with a slightly reduced IQ, to severe neurological effects that greatly impair movement and quality of life.
• In these children, euthyroidism is achieved if adequate iodine is supplied as their own thyroids are not impaired. However, the damage already
incurred cannot be reversed.

23
Q

Miscellaneous Effects of TH

A 
TH influences:
• the cardiovascular system
• respiration
• the GI tract
• muscle function

Endocrinology Quiz 4 (2 decks)

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