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07. Endocrine > 7.05 Thyroid Function > Flashcards

7.05 Thyroid Function Flashcards

1
Q

What is the function of the thyroid gland?

A
  • Secrete thyroid hormones to regulate metabolism
  • Secrete calcitonin to regulate calcium levels (not considered a thyroid a hormone)
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2
Q

Describe the anatomy of the thyroid gland

A

It is a glandular tissue shaped like a butterfly. It is composed of 2 lobes joined by isthmus. It sits just below the larynx infront of the thyroid cartilage of the larynx

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3
Q

Describe the internal anatomy of the thryoid gland

A
  • They thryoid gland is made up of follicular cells that surround colloid
  • Colloid (glycoprotein mix) contains thyroglobulin (Tg) which is an important precursor to the thyroid hormones
  • C cells in interstitial spaces secrete calcitonin
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4
Q

Describe the steps in thyroid hormone synthesis

A
  1. Iodine flowing in the blood stream is pumped into thryoid follicular cells
  2. Iodine binds to tyrosine to give Monoiodotyrosine (MIT)/ and di- (DIT)
  3. 2DIT molcules combine to form T4 (and 1 MIT +DIT form T3) this all occurs on the thyroglobulin of the colloid
  4. Thyroglobulin is taken back into the follicular cells (endocytosed)
  5. Intracellular enzymes separate T3 and T4 from thyroglobulin
  6. T3 and T4 diffuse into the blood
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5
Q

How does iodine enter the follicular cell and then exit the follicular cell (to the colloid)

A
  • It enters the follicular cell from the bloodstream through the I-/Na+ symport channel
  • It leaves the follicular cell cytoplasm and enters the colloid through the pendrin transporter
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6
Q

What enzymes catalyses iodonisation of tyrosine to produce the thyroid hormones?

A

Thyroid peroxidase

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7
Q

Describe how the T3 and T4 molecules get out of the follicular cell and how they travel in the blood

A

They are lipophilic hormones and thus diffuse through the membrane into circulation

They bind to plasma proteins:

  • Thyroid binding globulin (TGB),
  • Albumin
  • Transthyretin
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8
Q

What are the two absolute essentials that make up thyroid hormone? What are the source of these?

A
  • Iodine (diet, only known use in body)
  • Tyrosine (amino acid in body) derivative also in diet
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9
Q

What are the two thyroid hormones?

Describe their potency and their relative abundance in synthesis

A

Tetraiodothyronine (T4) = Thyroxine

  • (prohormone) - not as potent
  • Synthesised at 90%

Triodothyronine (T3) (most potent) 10%

  • Not synthesised in abundance in the thyroid gland
  • 80% of T3 is derived from T4
  • Deiodinase (iodine removal from T4) occurs to increase potency
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10
Q

Draw the hypothalamic-pituitary-thyroid axis

A
  • TRH is produced by the hypothalamus in medial neurons of the paraventricular nucleus
  • This travels through the portal system to the anterior pituitary and stimulates the production and release of Thyroid stimulating Hormone (TSH)
  • TSH travels to the thyroid gland and stimulates the thyroid to produce T3 and T4
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11
Q

What is the major regulator of the hypothalamic-pituitary-thyroid axis?

A

TSH stimulates all steps in thyroid hormone synthesis

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12
Q

Describe the concept of negative feedback of the hypothalamic-pituitary-thyroid gland axis

A

High levels of T3 and T4 provide negative feedback to both the pituitary and hypothalamus

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13
Q

How is TRH release regulated?

A

It is normally tonically released by the paraventricular nuclei of the hypothalamus. It is regulated by negative feedback.

  • Cold in infants only factor to 􏰀increase levels TRH
  • Stress 􏰁can decrease TRH tonic release
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14
Q

What are the major actions of thyroid hormone? [3]

A
  • 􏰀BMR & oxygen consumption (Calorigenic / heat producing effects)
  • Modulates metabolism
  • Sympathomimetic effect: increases heart rate and cardiac output
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15
Q

Is thyroid hormone essential for life? How so?

A

It is not essential for life but it is essential for child growth & development

  • Growthpromoting: Fetal life
  • Nervous system development (Before & after birth)
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16
Q

What is goiter?

A

An abnormal enlargement of your thyroid gland as a result of overstimulation of the thyroid tissue (thyromegaly)

17
Q

Does goiter occur in hypothyroidism or hyperthyroidism?

A

It can occur in both

18
Q

What are the major types of Primary Hypothyroidism?

A
  • Thyroid failure
  • Iodine deficiency (very common)
19
Q

Describe how Primary Hypothyroidism causes goiter:

A

Thyroid dysfunction & Iodine deficiency have the same mechanism of causing goiter:

  • There is a dysfunctional thyroid gland or not enough ability to produce hormones (no iodine) leading to decreased production of T3 and T4.
  • This limits the negative feedback onto TRH and TSH thus they are present in high levels
  • TSH is both a trophic factor to increase thyroid hormone production AND thyroid gland hyperplasia
  • Thus leads to goitre
20
Q

What are the means of developing a secondary hypothyroidism? [2]

A
  • Hypothalamic or anterior pituitary failure
  • Tumor
21
Q

Can secondary hypothyroidisms cause goiter?

A

No

The deficiency of thyroid hormones is because there is a deficiency in the TRH (and possibly TSH) production. and thus there is no driving factor for thyroid gland hypertrophy

22
Q

What happens when there is a congenital deficiency of thyroid hormones (hypothyroidism)?

A

Cretinism

  • Dwarfism, severe mental retardation
  • congenital hypothyroidism is one of most common causes of preventable mental retardation
  • Newborns tested for thyroid deficiency
23
Q

What are the Physiological Affects of hypothyroidism?

A

SLOWED METABOLIC RATE:

  • Decreased BMR and O2 consumpation
  • Decreased energy and fatigue
  • Increased weight
  • Cold intolerance
  • Sympathetic effects: decreased HR
  • Central effects: decreased mentation (mental activity) & reflexes
  • Decreased􏰁 protein synthesis
  • Accumulate mucopolysaccharides under skin = puffy appearance of myxedema
24
Q

What is the current treatment for hypothyroidism?

A
  • replace thyroid hormone
  • adequate dietary iodine
25
Q

What is the main causes of primary Hyperthyroidism?

A

Grave’s disease

An autoimmune disease that overstimulates the thyroid:

  • Thyroid‐stimulating immunoglobulin (TSI)
  • From B lymphocytes
  • targets TSH receptors
26
Q

How does Grave’s Disease (hyperthryoidism) cause goitre?

A

The autotimmune thyroid‐stimulating immunoglobulin (TSI) mimics TSH to cause hypertrophy of the thyroid gland (as well as overproduction of the thyroid hormones)

27
Q

What are some secondary causes of hyperthryoidism?

A
  • Hypothalamic or anterior pituitary excess
  • Hypersecreting tumor
28
Q

Do the secondary hyperthyroidisms cause goiter?

  • Hypothalamic or anterior pituitary excess
  • Hypersecreting tumor
A

Hypothalamic or anterior pituitary excess

  • Increased stimulation of the thyroid gland due to high levels of TRH (and TSH) leading to hyperthyroidism and thus goiter

Hypersecreting tumor of the thyroid gland

  • The thyroid gland is the pathology causing a high level of thyroid hormone to be released
  • There is not a high level of TRH or TSH (there would likely be a deficincy because of negative feedback)
  • No Goitre
29
Q

What are the physiological implications of Hyperthyroidism?

A

INCREASED METABOLIC RATE:

  • Increased BMR & O2 consumption
  • Increased appetite with weight loss
  • Muscle weakness
  • heat intolerance
  • Increased heart rate, alertness, irritability, and hyperexcitability
  • Graves’ disease exophthalmos = bulging eyes (due to water retaining carbohydrates behind eyes)
30
Q

What are current treatments for hyperthyroidism?

A
  • Remove thyroid / tumour
  • Use radioactive iodine to destroy gland
  • Anti thyroid drugs (block TH synthesis or conversion T4 to T3)

07. Endocrine (10 decks)

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