The thyroid gland (12) Flashcards Preview

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Flashcards in The thyroid gland (12) Deck (24)
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1
Q

Where is the thyroid located?

A

in neck, around trachea, below thyroid cartilage

N.B. superior and inferior parathyroid glands embedded in thyroid
and recurrent laryngeal nerve runs close- supplies vocal cords

2
Q

How can we describe the structure of the thyroid gland?

A

isthmus separates the 2 lobes

roughly 10-30% people have extra lobe - pyramidal lobe- embryological variant

3
Q

How does the thyroid develop? (embryology)

A
  • originates from base of tongue
  • thyroglossal duct descends
  • divides into 2 lobes
  • duct disappears, leaving foramen caecum
  • final position of thyroid gland at week 7 of gestation, then develops
4
Q

How can we describe the histology of the thyroid gland?

A

follicles in thyroid- made up of follicular cells which surround spheres/sticky colloid (where thyroid hormone made)
also parafollicular cells- secrete calcitonin

5
Q

How is thyroid hormone made?

A
  • TSH secreted from anterior pituitary, arrives via bloodstream and binds TSH-R on follicular cell–> triggers production of thyroglobulin TG (a prohormone with tyrosine residues) AND activates enzyme TPO (thyroperoxidase)–> travels into colloid + catalyses iodination reactions
  • IODIDE ions also arrive- transported into follicular cell–> then enters colloid
  • iodide oxidised to iodine
  • iodine sticks onto tyrosine residues of TG–> forms MIT and DIT–> couple to form T3 (active) and T4
  • T3 and T4 move back into follicular cell- protein bonds broken down to release from TG–> then enter systemic circulation
6
Q

What are MIT and DIT and what happens when you combine them?

A

monoiodotyrosine and diiodotyrosine (iodine/2 iodine been added to tyrosine)

if you combine MIT and DIT–> triiodothyronine (T3)
if you combine DIT and DIT–> tetraiodothyronine/thyroxine (T4)

7
Q

What is reverse T3?

A

inactive hormone

- T4 has been deiodinated in a different position

8
Q

Where do the proportions of circulating T3 come from?

A

N.B. a healthy adult thyroid gland secretes T3 AND T4

T4= prohormone- converted into more active T3 by deiodinase enzyme in peripheral tissues

! 80% of T3 comes from deionisation of T4 !
! 20% from direct thyroidal secretion !

9
Q

How does thyroid hormone travel around the body?

A
  • mostly bound to plasma proteins e.g. thyroid-binding globulin (TBG), albumin, and prealbumin
  • less than 1% thyroid hormone is unbound, so very small amount actually active
10
Q

How does thyroid hormone affect gene transcription?

A

T3 and T4 enter target cell via receptors–> T4 activated by deiodinases- becomes T3–> enters nucleus and binds to thyroid hormone receptor in nucleus

11
Q

Why do we need thyroid hormone?

A
  • essential for fetal growth and development, esp. CNS
    (N.B. untreated congenital hypothyroidism= cretinism)
    (heel prick test measures TSH in babies)
  • increases basal metabolic rate
  • protein, carbohydrate and fat metabolism
  • effects on GI, CNS, reproductive systems
  • affect sympathetic nervous system by potentiating actions of catecholamines (e.g. tachycardia, lipolysis)
12
Q

What controls thyroid hormone production?

A
  • hypothalamus produces TRH–> enters anterior pituitary–> stimulates thyrotrophs to release TSH (thyrotropin)–> TSH enters systemic circulation–> arrives at thyroid–> T3 and T4 production
  • T3 and T4 negative feedback to anterior pituitary and hypothalamus- ‘hypothalamo-pituitary thyroid axis’
  • somatostatin inhibits TSH production
  • iodide inhibits hormone production
13
Q

Are thyroid disorders more common in men or women?

A

women (4:1 ratio) bc more at risk for autoimmune disorders

14
Q

Is an hypothyroidism or hyperthyroidism more common?

A

equally prevalent

15
Q

What is the main cause of primary hypothyroidism?

A

autoimmune damage to thyroid–> thyroxine levels dec. –> TSH levels inc. (bc wants to make T4)

also from surgery (if thyroid removed)

16
Q

What are the commonest forms of autoimmune thyroid disease?

A

Hashimoto’s thyroiditis (hypo) and Graves’ disease (hyper)

N.B. presence of 1 autoimmune disease inc. risk of others

17
Q

What are the symptoms and signs of hypothyroidism?

A
  • deepening voice
  • depression and tiredness
  • intolerance to cold
  • weight gain w/ reduced appetite
  • constipation
  • bradycardia
  • eventual myxoedema coma
18
Q

How do we treat hypothyroidism?

A

tablet- levothyroxine (same as T4)… sometimes used for hyperthyroidism (blocking+replacement regimen)
N.B. don’t need T3 as deiodinase enzymes in whole body

19
Q

What is the common dosage of levothyroxine?

A
  • adjusted according to TSH (to get into normal range)
  • mostly administered orally (sometimes intravenously if emergency- give T3)
  • common dose 50-100 micrograms
20
Q

What are potential complications of levothyroxine?

A

if given too much- minor: can cause weight loss and headache

major: heart attack/ rapid HR

21
Q

What happens in hyperthyroidism?

A

thyroid makes too much thyroxine–> thyroxine levels rise–> TSH levels drop

22
Q

What are the causes of hyperthyroidism?

A
  • Graves’ disease- autoimmune- thyroid gland enlarged–> overactive
  • nodules that release too much thyroxine (multi or singular)
23
Q

What is Graves’ disease?

A

autoimmune disease

  • antibodies bind to and stimulate TSH receptor in thyroid (should normally just respond to TSH)
  • -> disrupts negative feedback loop
  • causes smooth goitre (enlargement of gland)
  • other antibodies bind to muscles behind eye (exophthalmos)
  • other antibodies stimulate growth of soft tissue of shins (pretibial myxoedema)
24
Q

What are the symptoms and signs of hyperthyroidism?

A
  • really hot
  • weight loss w/ inc. appetite
  • diarrhoea
  • palpitations
  • mood swings
  • myopathy (muscle weakness)
  • sore eyes, goitre