Thyroid Hormones Flashcards

1
Q

The release of the thyroid hormones starts with the hypothalamus; what does it release?

A

releases thyrotophin releasing factor straight into the bloodstream

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2
Q

Where do the TRH act and what does that cause the release of?

A

They act on the anterior pituitary which then produces thyroid stimulating hormone (thyrotrophin)

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3
Q

What do the TSH act on and what does this cause the release of?

A

The thyroid gland which releases thyroid hormones (T3 and T4) to target cells throughout the body

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4
Q

What kind of glands produce hormones?

A

Endocrine glands

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5
Q

Describe the structure of the thyroid hormones

A

Two rings linked by an oxygen with a carbon head group and a hydroxyl tail group
The T3 has three I2 groups and the T4 has four

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6
Q

The thyroid hormones are zwitterionic; what does this suggest about their hydrophobicity?

A

They are hydrophillic so will not cross the cell membrane

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7
Q

Why would radioactive iodine lead to thyroid cancer and what could be used to treat this?

A

Since all the iodine you take in from your food is concentrated here to make the T3 and T4 hormones any radioactive iodine would lead to cancer here which can be treated by iodine tablets to compete with the radioactive iodine

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8
Q

What does it mean by T3 and T4 have negative feedback?

A

They control how much TRH and TSH (thyrotropin) are released which ultimately controls the the production of the thyroid horomones

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9
Q

What do T3 and T4 act on to cause negative feedback?

A

The anterior pituitary to inhibit TSH and the hypothaamus to inhibit TRH

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10
Q

Describe a follicle of the thyroid and its role in synthesis and storage of thyroid horomes?

A

The follice contains a layer of cells surrounding a colloid filled with fluid.
The thyroid hormones are synthesised in the cells and then stored in the colloid

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11
Q

What form is iodine taken up into the cell in and what does that cause the release of to counteract?

A

Take up as iodide ions and Na+ is released to balance the charge

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12
Q

What is the iodide uptake into the follice cell stimulated by?

A

TSH

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13
Q

Once in the follice cell iodide is oxidised to iodine; what enzyme does this?

A

Peroxidase enzyme

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14
Q

Once iodide has been oxidised what happens?

A

Active transport of iodine into the colloid from the follice cell

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15
Q

Once in the colloid what protein is present and what important residues does it contain?

A

Thryoglobulin which contains tyrosine residues

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16
Q

What happens once the iodine is in the colloid and what does it produce?

A

It is transferred to tyrosine residues to produce mono-iodinated tyrosine (MIT) and di-iodinated tyrosine (DIT)

17
Q

How do MIT and DIT combine to form the thyroid hormones and where are these stored?

A

One MIT and DIT combine to make T3 whereas two DITs combine to make T4 - they are linked by enzymes
T3 and T4 are then stored on the thyroglobulin in the colloid

18
Q

How does TSH stimulate the release of the hormone?

A

When blood levels of T3 and T4 are low it stimulates the uptake of thyroglobulin into the follice cells where T3 and T4 are removed and released into the blood

19
Q

What receptors to T3 and T4 then act on? Which form of thyroid hormone is the ligand?

A

Nuclear receptors that can associate with DNA - T4 is converted into T3 because T3 is the ligand

20
Q

What effects does the T3 binding the nuclear receptor have?

A

It stimulates mRNA production and therefore protein synthesis

21
Q

Thyroid hormones act on all the cells of the body but what does this effects produced depend on?

A

The type of cell the thyroid hormones act on

22
Q

What sort of effects do thyroid hormones produce through regulation of the nuclear receptors they act on?

A
  1. Increased metabolism
  2. Increased heat production
  3. Increased glucose and amino acid uptake
  4. Increased number and size of mitochondria
23
Q

What is hypothyroidism?

A

An autoimmune disease when you have to little thyroid hormone

24
Q

What is hypothyroidism caused by?

A

The body making antibodies to attack and breakdown the thyroid gland leading to decreased production of thyroid hormones

25
Q

What sort of complications can hypothyroidism lead to?

A

Mental retardation and dwarfism in infancy and depressed metabolic rate leads patients being irritable/tired with low appetite

26
Q

How can hypothyroidism be treated?

A

With T4 tablets (thyroxine) which is converted to T3 after 6-8 weeks

27
Q

What is hyperthyroidism?

A

An autoimmune disease where you have too much thyroid hormones

28
Q

What is hyperthyroidism caused by?

A

Antibodies bind to TSH receptors meaning TSH is constantly being produced so therefore thyroid hormones are constantly being produced (not negative feedback)

29
Q

What is hyperthyroidism caused by?

A

Antibodies bind to TSH receptors meaning TSH is constantly being produced so therefore thyroid hormones are constantly being produced (not negative feedback)

30
Q

95% of thyroid hormones are attached to plasma proteins; what is one reason for this?

A

The elevated levels of thyroid hormones in the blood plasma is what causes the negative feedback of TSH

31
Q

Thyroid hormones can act on B-adrenoreceptors; what does this cause the release of?

A

Adrenaline

32
Q

What are the symptoms of hyperthyroidism?

A

Since there are more thyroid hormones the receptors they act on are more stimulated than normal which causes increased metabolism, cardiac output, appetite, patient is nervous

33
Q

Name 4 ways used to treat hyperthyroidism?

A
  1. Surgery
  2. Iradation with iodine 131
  3. Iodides
  4. Drugs which inhibit iodine synthesis
34
Q

Name three examples of drugs that inhibit iodine syntehsis?

A

Carbimazole, Methimazole, Propylthiouracil

35
Q

How do drugs that inhibit iodine synthesis work?

A
  1. They inhibit the peroxidase enzyme that convers iodine ions to iodine in the follicle cells
  2. they inhibit the tyrosine residues of thyroglobulin becoing iodinated
  3. they inhibit mit and dit iodinated tyrosine residues of thyroglobulin coming together to form T3 and T4
  4. They inhibit the conversion of T3 to T4 in the follice cell