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BRS > The thyroid gland > Flashcards

The thyroid gland Flashcards

1
Q

What are thyroid follicles made up of?

A

Follicular cells surrounding colloid.

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2
Q

Where are parafollicular cells found?

A

Thyroid gland

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3
Q

What do parafollicular cells do?

A

Regulate calcium levels.

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4
Q

What is the anatomical variant found sometimes in the middle of the thyroid gland called?

A

Pyramidal lobe.

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5
Q

What do parathyroid glands do?

A

Regulate calcium levels.

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6
Q

Explain the development of thyroid gland?

A

Originates from base of tongue. Development of thyroglossal duct. Divides into two lobes. Duct disappears leaving foramen caecum.

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7
Q

Explain production of T3 and T4 in thyroid gland.

A

TSH binds to TSH receptor. This activates sodium iodide channel protein resulting in active transport of iodide into follicular cell. Iodide ions travel across follicular cell and enter colloid by another channel protein. Binding of TSH also results in production of thyroglobulin, thyroid peroxidase and hydrogen peroxide. Iodide ions are oxidised by hydrogen peroxidase and thyroid peroxidase in colloid cell. Iodine is added to thyroglobulin in an iodination reaction to produce monoiodotyrosine (MIT) and diiodotyrosine (DIT) (catalyse by thyroid peroxidase and hydrogen peroxidase); both of which are bound to thyroglobulin. MIT and DIT undergo a coupling reaction to produce T3 and T4 both still bound to thyroglobulin (catalysed by thyroid peroxidase and hydrogen peroxidase). T3,T4 thyroglobulin complex makes it way back into follicular cell where a lysosome breaks down the peptide bonds holding thyroglobulin to T3 and T4. T3 and T4 are released in the bloodstream.

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8
Q

What is thyroglobulin?

A

Glycoprotein chain that contains tyrosine.

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9
Q

How is 3-monoiodotyrosine made?

A

Addition of one iodine atom to tyrosine.

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10
Q

How is 3,5 - diiodotyrosine made?

A

Addition of two iodine atoms to tyrosine.

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11
Q

How is T3 made?

A

Coupling reaction of MIT and DIT.

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12
Q

How is T4 made?

A

Coupling reaction of two DIT molecules.

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13
Q

What is the main hormone product released from thyroid gland?

A

T4.

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14
Q

What happens when T4 enters peripheral tissues?

A

De-iodination to T3.

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15
Q

What enzyme catalyses conversion of T4 to T3?

A

Deiodinases.

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16
Q

Why is T4 to T3 conversion important?

A

T3 is the bioactive form. T3 provides almost all thyroid hormone activity in target cells.

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17
Q

Differences between T3 and T4?

A

T4 is the inactive form of thyroid hormone while T3 is the active form. T4 has a greater half life.

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18
Q

What results in reverse T3?

A

Deiodination of T4 in different position.

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19
Q

How are T4 and T3 transported in the blood?

A

T3 and T4 are bound to plasma proteins in the blood. Unbound T3 and T4 is very low.

20
Q

What is the main protein that transports T4 and T3?

A

Thyroid binding globulin.

21
Q

What are the two proteins other than the main one that carries T4 and T3?

A

Albumin and prealbumin.

22
Q

How does thyroid hormone bring about its effect?

A

Binds to intracellular receptors. T4 is converted to T3 by deiodinases. T3 enters nucleus and bind to thyroid hormone receptor. This alters gene expression.

23
Q

What does thyroid hormone do?

A

Results in fetal growth and development especially in regards to the CNS. Increases basal metabolic rate. Increases catecholamine effect resulting in tachycardia and lipolysis. Increases heat production.

24
Q

What is it called when someone is born with an absent or underdeveloped thyroid gland?

A

Congenital hypothyroidism (cretinism).

25
Q

How is cretinism avoided?

A

Heel prick test that measures TSH within the few days of being born.

26
Q

What does release of T3 and T4 inhibit?

A

TSH and TRH.

27
Q

What inhibits release of TSH?

A

T3,T4 and somatostatin.

28
Q

What inhibits release of TRH?

A

T3 and T4.

29
Q

What inhibits release of T3 and T4?

A

Low TSH or Low TRH. High amounts of iodide (wolff chaikoff effect).

30
Q

What is primary hypothyroidism?

A

Autoimmune damage to thyroid gland resulting in low thyroxine and high TSH.

31
Q

Symptoms of hypothyroidism?

A

Fatigue, hair loss, bradycardia, weight gain.

32
Q

Two main types of autoimmune thyroid disease?

A

Graves disease and hashimotos thryoiditis.

33
Q

What does graves disease generally result in?

A

Hyperthyroidism.

34
Q

What does hashimotos thyroiditis generally result in?

A

Hypothyroidism.

35
Q

What can increase risk of autoimmune thyroid disease?

A

Sex, other autoimmune diseases.

36
Q

How could you treat hypothyroidism?

A

Levothyroxine.

37
Q

What is levothyroxine?

A

Synthetic T4.

38
Q

How would you manage someone of levothyroxine?

A

You would regularly check their TSH, check if they are taking the drug and alter dose.

39
Q

Levothyroxine mechanism?

A

Synthetic T4 that is converted to T3 in peripheral tissues and brings about thyroid hormone effects.

40
Q

How is levothyroxine administered?

A

Orally.

41
Q

How could levothyroxine be used to treat hyperthyroidism?

A

Block and replacement regimen. Use high doses of antithyroid drugs to block and switch off thyroid hormone production. Use levothyroxine as a replacement for lack of thyroid hormone production.

42
Q

What is hyperthyroidism?

A

High thyroxine and low TSH.

43
Q

Symptoms of hyperthyroidism?

A

Insomnia, weight loss, heart arrhythmia and heat intolerance.

44
Q

Causes of hyperthyroidism?

A

Graves disease, toxic multinodular goitre and solitary toxic nodule.

45
Q

What causes graves disease?

A

Antibodies bind to and stimulate TSH receptor in the thyroid.

46
Q

What other symptoms can be present with graves disease and how do these symptoms arise?

A

Exopthalmous - other antibodies bind to muscles in the eye. Pretibial myxoedema - other antibodies bind and stimulate growth of soft tissue of shins.

BRS (52 decks)

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