Thyroid gland Flashcards

1
Q

what is the structure of the thyroid?

A

sits on top of the trachea. is bilobed with isthmus connecting both lobes. Another lobe may be present in some people called the pyramid which sticks up vertically from the isthmus.

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2
Q

what is the thyroid made from?

A

thyroid follicles and parafollicular cells. follicular cells line the follicles and inside is known as the colloid.

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3
Q

what does the apical membrane of the follicular cells line?

A

the colloid

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4
Q

what is the basolateral membrane of follicular cells in contact with

A

blood supply

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5
Q

what is thyroglobulin?

A

thyroid hormone precursor, this protein contains tyrosine residues which get iodinated when the rest of the protein is cleaved.

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6
Q

Describe the formation of T3 and T4 in the follicles

A

TSH arrives from the blood and binds to the TSHR at on the basolateral surface of the follicular cells, this triggers:

  • Uptake of iodide from the blood via Sodium Iodide symporters on the basolateral surface. This iodide is converted into I2 and diffuses across the cell and is transported into the colloid via transporters on the apical surface.
  • synthesis of thyroglobulin which diffuses into the colloid
  • iodination using H2O2 of TG by thyroperoxidase to form monoiodotyrosine thyroglobulin (MIT TG) and diiodotyrosine thyroglobulin (DIT TG).
  • coupling reaction using thyroperoxidase and hydrogen peroxide to form T3 and T4 thyroglobulin.
  • T3 TG and T4 TG are taken back into the follicular cell and the rest of the protein is cleaved using lysosome activity forming active T3 and T4 which diffuse into the blood.
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7
Q

what are T3 and T4?

A

iodoTHYRONINES

T4 is also known as thyroxine.

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8
Q

how are these hormones transported in the blood?

A
  • bound to Thyroid Binding Globulin plasma protein (75%)
  • then some bound to albumin
  • some bound to prealbumin (transthyretin)
  • VERY LITTLE FREE BIOACTIVE T3 and T4 in blood.
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9
Q

what is active form (have biological effect) of the thyroid hormones?

A

T3

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10
Q

which of the iodothyronines are mostly produced by the thyroid gland?

A

T4

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11
Q

what needs to happen to T4/thyroxine for it to be active?

A

needs to be deiodinated to T3 in peripheral tissues.

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12
Q

what is reverse T3?

A

sometimes when T4 is deiodinated, it forms inactive reverse T3.

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13
Q

how does T3 trigger a cellular response?

A

T3 diffuses into the cell and binds to a thyroid hormone receptor within the nucleus, this complex acts as a transcription factor.

T3 interacts with mitochondria directly to stimulate metabolic activity

T3 also interacts with ion channels on the cell surface membrane.

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14
Q

why is Thyroid hormone needed for infants and foetuses?

A

needed for growth and development

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15
Q

examples of thyroid hormone action in adults?

A

increases basal metabolic rate
protein, carb and fat metabolism
increases cells’ sensitivity to chatecholamines
effects on the GI, CNS and reproductive system maturation

NOTE TH affects all organs.

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16
Q

what is the latent period of a hormone?

A

time taken from release to biological effects to show

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17
Q

what is the latent period for thyroid hormones?

A

T3 ~ 12 hours

T4 ~ 72 hours

18
Q

what is the half life of T3 and T4?

A

T3, around 2 days

T4, around 7-9 days

19
Q

describe the thyroid axis

A
  • Hypothalamus produces TRH which stimulates release of TSH from thyrotrophs oestrogen also stimulates TSH production. Somatostatin and glucocorticoids decrease production of TSH.
  • TSH stimulates production of T3 and T4
  • the thyroid hormones negatively feed back directly on the pituitary and indirectly on the hypothalamus
20
Q

what is the Wolff-Chaikoff effect?

A

high levels of iodide in the blood causes inhibition of Thyroid hormone production.

21
Q

which nerves run close to the thyroid, meaning you have to take care in surgical procedures such as a thyroidectomy?

A

Superior and recurrent laryngeal nerves

if these are damaged, patient might lose voice.

22
Q

where is the thyroid gland embryologically derived from?

A

out pouching from the back of the tongue, descending down the neck via thyroglossal duct then forms two lobes. this finishes by week 7.

23
Q

when the thyroglossal duct disappears, what does it leave?

A

the caecum foramen

24
Q

what is it called when the out pouching of the tongue to from the thyroid is still there?

A

the lingual thyroid.

25
Q

how many thyroid lobes are there?

A

4, each 2.5cm x 2.5cm

26
Q

which lobe is bigger?

A

right

27
Q

what is the average weight of a healthy adult thyroid gland?

A

20g

28
Q

where are the parathyroid glands located?

A

4, embedded in the thyroid gland.

29
Q

name some problems with thyroid gland development

A
  • Agenesis (complete absence)
  • incomplete descent
  • thryoglossal cyst (segment of duct stays)
30
Q

if we remove the thyroid gland, what do we need to give the patient?

A

lifetime supply of thyroid hormone

31
Q

what is cretinism?

A

neonates with thyroxine defficiency causing irreversible brain damage and slow growth and development.

32
Q

how can cretinism diagnosed and treated?

A

heel prick test, high TSH means low thyroxine hence thyroxine treatment is given.

33
Q

facts about thyroid disease

A

affects 5% of population

4: 1 females to males
1: 1 underactive to overactive

34
Q

why are females more likely to develop thyroid diseases?

A

most thyroid disease is autoimmune, females have tolerance due to pregnancy hence higher chance of autoimmune diseases.

35
Q

what is primary hypothyroidism/myxoedema?

A

primary thyroid failure due to autoimmune or surgery. this means thyroxine levels are low therefore TSH is high.

NB, myxoedema doesn’t mean swelling

36
Q

symptoms of primary hypothyroidism?

A
  • deepening of voice,
  • depression and tiredness,
  • cold intolerance
  • weight gain, reduced appetite,
  • constipation
  • bradycardia
  • may become unconscious as BMR slows and not enough glucose produced for brain.
  • cholesterol levels increase

EVERYTHING SLOWS DOWN.

37
Q

treatment for hypothyroidism

A

daily 100mg thyroxine tablet and alter to TSH levels

38
Q

what is the difference between thyrotoxicosis and hyperthyroidism?

A

hyperthyroidism is where the thyroid produces excess thyroid hormone. thyrotoxicosis can be due to extrinsic sources of thyroxine too. both show decrease in TSH levels.

39
Q

features of hyperthyroidism

A

raised BMR leads to:

  • raised temperature
  • increased appetite but weight loss
  • palpitations due to increased heart rate
  • myopathy due to muscle protein breakdown
  • mood swings
  • diarrhoea
  • tremor due to increased effect of adrenaline
  • sore eyes
  • goitre
40
Q

what is graves disease?

A

causes hyperthyroidism where whole gland is smoothly enlarged (goitre) and overactive (measured using scintigram)

41
Q

cause of graves disease?

A

autoimmune where antibodies bind to TSHR and stimulate thyroid hormone production.

42
Q

additional symptoms for graves disease?

A

antibodies bind to muscles behind the eyes causing EXOPHTHALMOS
Pretibial Myxoedema: antibody stimulates shin soft tissue hypertrophy causing non pitting swelling