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Lily BRS Endo > The Thyroid Gland > Flashcards

The Thyroid Gland Flashcards

1
Q

What is the anatomy of the thyroid gland?

A

Sits in the neck below the thyroid cartilage (Adams Apple)

Two lives joined by the isthmus

Some people have a pyramidal section in the middle

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2
Q

What makes up the thyroid gland?

A

Lots of follicular cells arranged into spheres with colloid in the middle. Each of these is a follicle

The colloid is an extracellular fluid

There are also some parafollicular cells that produce calcitonin

Follicles are surrounded by lots of blood vessels

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3
Q

Which anatomical structures are anatomically close to the thyroid gland?

A

On the underside of the thyroid there are two pairs of parathyroid glands

The superior and inferior parathyroid glands. These produce parathyroid hormone which is important in the absorption of calcium

The recurrent laryngeal Nerva also runs close behind the thyroid gland. This supplies the vocal chords

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4
Q

What is the embryology of the thyroid gland? (How is it formed)

A

Midline outpouching from floor of pharynx (originated from base of tongue)

This develops into the thyroglossal duct

This divides into two lobes

The duct disappears leaving the foramen caecum

It is in its final position by 7 weeks

Then the thyroid gland develops

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5
Q

What are the thyroid hormones?

A

T3 - tri-iodothyronine

T4 - tetra-iodothyronine (aka thyroxine)

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6
Q

How are the thyroid hormones made?

A

TSH (from anterior pituitary) binds to TSH receptors on basolateral membrane of follicular cells

Sodium and iodine ions in the blood also enter the follicular cell

The iodide enters the colloid and undergoes iodination to form iodine

Thyroglobulin (TG) is released from the nucleus. It is a pro hormone and goes into the colloid

TPO (thyroid peroxidase enzymes) are also released into the colloid. This helps the iodination and coupling reactions

The iodine and thyroglobulin undergo iodination to form MIT (monoiodotyrosine) and DIT (di…)

These undergo coupling reactions to form T3 and T4 which then enter the blood

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7
Q

Simply what is needed for thyroid hormone synthesis?

A

TSH

Thyroglobulin

Iodide ions

Thyroid peroxidase And hydrogen peroxide

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8
Q

How do the coupling reactions work?

A

Thyroglobulin has around 100 tyrosine residues on it. Around 20 of these can be iodinated

They can be iodinated once or twice to form
MIT ( monoiodotyrosine) and DIT (diiodotyrosine)

MIT and DIT undergo a coupling reaction to form Tri-iodothyronine (T3)

DIT and DIT couple to form tetra-iodothyronine (T4) (thyroxine)

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9
Q

What is the difference between T3 and T4?

A

T4 (thyroxine) is like a pro hormone. It is biologically inactive. It is made into T3

T3 is the bio active form

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10
Q

How is T4 turned into T3?

A

Deiodination

One of the iodine’s is removed to form T3

Done by a deiodinase enzyme present in body cells

(It can also be deiodinated in a different position to produce reverse T3 which is inactive)

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11
Q

What proportion of T3 comes from where?

A

80% comes from deiodination of T4

20% from direct thyroid secretion

T3 is responsible for pretty much all the thyroid hormone activity in target cells

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12
Q

How are the thyroid hormones transported in the blood?

A

Bound to plasma proteins

  1. thyroid binding globulin (TBG) (70-80%)
  2. Albumin (10-15%)
  3. Prealbumin (transthyretin)

Only 0.05% of T4 and 0.5% of T3 are unbound

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13
Q

How to the thyroid hormones have an effect on gene expression?

A

T4 and T3 enter the target cells

T4 is deiodinated to T3 by deiodinase enzymes present in target cells

These enter the nucleus and bind to the TRE (thyroid responsive element)

This leads to altered gene expression

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14
Q

How do thyroid hormones effect foetal development?

A

Essential for growth and development, especially that of the CNS

Untreated congenital hypothyroidism: cretinism

But this isn’t seen often anymore as at 5 days every new born in England has a heel prick test to measure TSH levels

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15
Q

What are the actions of T3?

A

Increase basal metabolic rate (sodium potassium ATPase, oxygen consumption, heat production)

Increase metabolism (glucose absorption, protein carbohydrate and fat metabolism)

Potentiate actions of carecholamines (increases cardiac output and heart rate)

Also GI, CNS and reproductive systems

The half life of T4 is 8 days, T3 is 2 days

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16
Q

How does the hypothalamic-pituitary-thyroid axis work?

A

Hypothalamus releases TRH

Anterior pituitary releases TSH

Thyroid releases T3 and T4

17
Q

What factors inhibit thyroid output?

A

Somatostatin (decreases production of TSH)

T3 and T4 (decrease production of TRH and TSH)

High levels of iodide (decrease production of T3 and T4) (wolff-chaikoff effect)

18
Q

Are thyroid disorders more common in men or women?

A

Women

Most are auto immune

Women carry babies so are exposed to more antigens. This means we are more likely to experience glitches in the system

19
Q

What is more common hyper or hypothyroidism?

A

They are equally common

20
Q

What is primary hypothyroidism?

A

Auto immune damage to the thyroid

Thyroxine levels decline. TSH levels increase

Commonly caused by Hashimoto’s thyroiditis

21
Q

What are some symptoms of primary hypothyroidism?

A

Hair loss

Fatigue and depression

Swollen face and eyes

Deep voice

Slow heart rate (Bradycardia)

Weight gain and constipation

Low sex drive

Rough skin and muscle cramps

Cold intolerance (always warm)

Eventual myxoedema coma

22
Q

How is hypothyroidism treated?

A

Levothyroxine

Almost identical to T4 so can be turned into T3

Used in hypothyroidism. Sometimes in hyperthyroidism radioiodine will be used which causes hypothyroidism so levothyroxine will be used for the rest of life)

Dose is adjusted until TSH levels are in normal range. But usually started at 100 micro grams a day.

Most commonly administered orally (tablet)

Side effects: weight loss, headache. Heart attack and tachycardia. (These usually only happens if too high a dose is given)

There is no evidence that T3 is better, and it is more expensive. So not used

23
Q

What is hyperthyroidism?

A

Thyroxine levels rise. TSH levels decrease

Can be caused by Graves’ disease (whole gland enlarged and overactive). Also toxic multi modular goitre. And solitary toxic nodule

24
Q

What are some symptoms of hyperthyroidism?

A

Hair loss

Depression

Enlarged thyroid (goitre)

Tachycardia and high blood pressure

Weight loss and diarrhoea

Fragile nails and tremor of hands

Warm moist skin

Heat intolerance

Sore eyes

25
Q

What is graves disease?

A

Autoimmune disease

Antibodies bind to and stimulate TSH receptor in the thyroid

Smooth diffuse goitre

Enlargement of thyroid

Causes hyperthyroidism

Other antibodies bind to muscles behind eye : exophthalmos

Some antibodies stimulate growth of soft tissue of shins: Pretibial myxoedema

Lily BRS Endo (10 decks)

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