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Phase 2 3. Endocrinology > Thyroid gland > Flashcards

Thyroid gland Flashcards

1
Q

What is the epidemiology of thyroid disorders?

A

Affect 5% of women and 0.5% of men in the population

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2
Q

Describe the thyroid gland

A

Two highly vascular lobes either side of trachea, weighing 10-20g

Contains follicles made up of single layer of cells surrounding a lumen containing colloid (largely
thyroglobulin)

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3
Q

What is a significant complication of a thyroidectomy?

A

bleeding following surgery can lead to compression of the trachea and
respiratory interruption.

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4
Q

Describe the follicular cells

A

When stimulated, these cells become columnar and the
lumen is depleted of colloid

When suppressed, the cells become flat and colloid
accumulates in the lumen

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5
Q

What is the role of iodine in the thyroid?

A

thyroid gland has evolved to take up and store iodine, the essential component of thyroid hormones
=> necessary for thyroid hormone synthesis

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6
Q

How is iodine used in thyroid hormone synthesis?

A
  • oral iodine is reduced to iodide in the GI tract and absorbed
  • Iodide is transported into follicular cells against a chemical gradient on the basolateral membrane by the
    sodium iodide transporter (active transport)
    o Allows follicular cells to concentrate iodide

Iodide then diffuses to apex of cell and is transported by prendrin into vesicles fused with the apical cell
membrane

Oxidation of iodide to iodine occurs in the vesicles and binds to tyrosine residues on thyroglobulin
o This process is called organification – catalysed by thyroid peroxidase

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7
Q

How are thyroid hormones synthesised?

A

Formation of DIT/MIT, then T3/T4 and endocytosis of thyroglobulin into cell

  • droplets fuse with lysosome and thyroglobulin is hydrolysed => release of T3, T4 into circulation
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8
Q

What happens to thyroid hormone synthesis in iodine deficiency?

A

the body makes predominantly T3 (uses less iodine and is more active)

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9
Q

What is thyroglobulin?

A

Polypeptide backbone for the synthesis and storage of thyroid hormones

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10
Q

What is the preliminary step of MIT and DIT formation?

A

Iodine attachment to tyrosyl residues on thyroglobulin

(Iodine combines with tyrosine to form mono or di-iodinated thyronine
These combine to form T3 and T4)

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11
Q

How are T3 and T4 released?

A

Proteolytic cleavage in lysosomes

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12
Q

Describe release of T4

A

released in greatest quantity, and solely, by the thyroid gland

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13
Q

Describe T3

A

T3 is the more active hormone, formed by peripheral 5’ deiodination of T4

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14
Q

Describe the circulating thyroid hormones

A

Free (0.5%) / bound (99.5%)
o Free component is the active and regulated component
o Bound to thyroid binding globulin, transthyretin and albumin

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15
Q

What happens to T4?

A

converted to T3 in the periphery. T3 then binds to its nuclear receptor

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16
Q

How are thyroid hormones regulated?

A

TSH from anterior pituitary stimulates synthesis and secretion of T4 and T3

TSH secretion is inhibited by T4 and T3 (negative feedback)

TRH from HPS stimulates TSH secretion

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17
Q

How is thyroid hormone action mediated?

A

by nuclear receptors

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18
Q

How is the majority of T3 generated?

A

locally from T4

varies between tissues

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19
Q

What is the action of T3?

A

Cytosolic T3 is transported into nuclei and binds to receptor

  • Alpha and beta T3 nuclear receptors vary between tissues
  • Binding increases protein synthesis, and proteins mediate the observed effects
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20
Q

How does thyroid hormone effect foetal development?

A

Foetus requires maternal thyroid hormones for brain

development

21
Q

What is the influence of thyroid hormones?

A

Influence on nearly every system (more T3 nuclear receptors in more
sensitive tissues, such as pituitary and liver)
o Skeletal - Bone turnover
o Cardiovascular - Heart rate
o Metabolic – lipids and glucose

22
Q

Briefly describe primary hypothyroidism

A

High TSH and low T4
o Disease is in the thyroid gland
o Treat with thyroxine

23
Q

Briefly describe secondary hypothyroidism

A

Low TSH and low T4
o Pituitary cause of disease
o May also have other pituitary axis hormone deficits
o Make sure their cortisol is okay before commencing thyroxine
treatment

24
Q

Briefly describe primary hyperthyroidism

A

Low TSH and high T4

25
Q

Briefly describe sick euthyrodism

A

low TSH and low T4
o Effect on thyroid hormones with other illness (e.g. malignancy), but not fundamental thyroid
disease

26
Q

What are the causes of hyperthyroidism?

A

Excess thyroid hormone

  • auto-immune (Graves’ disease)
  • toxin adenoma
  • multinodular goitre
  • thyroiditis
  • excess thyroxine
27
Q

What are the clinical manifestations of thryotoxicosis?

A 
o Weight loss
o Tachycardia
o Tremor
o Hypertension (high pulse pressure - high systolic and low diastolic BP)
o Heat intolerance
o Palpitations
o Diarrhoea
o Sweating
28
Q

What is toxic adenoma?

A

solitary nodule over secreting thyroid hormones

29
Q

What is multinodular goitre?

A

can be either a toxic multinodular goiter (causes hyperthyroidism) or non-
toxic (does not make too much thyroid hormone).

30
Q

What is thyroiditis?

A

generally caused by an attackonthe thyroid, resulting in inflammation and damage
to the thyroid cells

31
Q

What symptoms are specific to Graves’ disease?

A

Dysthyroid eye disease
o Dermopathy – In 1-2% patients
 red, swollen skin, usually on the shins and tops of the feet.
 The texture of the affected skin may be similar to that of an orange
peel

32
Q

What is Graves’ opthalmopathy?

A

autoimmune inflammatorydisorderof the orbit and periorbital tissues

characterized by:
o Lid retraction / lag and periorbital oedema
o Proptosis (30%) = Exophthalmos
o Diplopia (10%) = double vision
33
Q

What is the pathophysiology of Graves’ ophthalmopathy?

A

-Autoantibodies target the fibroblasts in the eye muscles, which can differentiate into adipocytes.
-Fat cells and muscles expand and become inflamed.
-inflammation results in a deposition ofcollagenandglycosaminoglycans in the muscles, which leads to
subsequent enlargement andfibrosis
-This increases in volume of the intraorbital contents within the confines of the bony orbit
-Veins become compressed, and are unable to drain fluid, causingoedema

34
Q

What is Thyroid acropachy

A

soft tissue swelling of the hands and clubbing of the fingers

35
Q

How is Graves’ managed?

A

Antithyroid drugs
Surgery – will lead to hypothyroidism
Radio iodine - will probably lead to hypothyroidism

36
Q

Which anti-thyroid drugs are used in the treatment of hyperthyroidism?

A

Thionamides

carbimazole, propylthyouracil

37
Q

Describe radioiodine therapy for Graves’ disease

A

 Destroys thyroid tissue by beta emission
 May worsen eye disease – ensure steroid cover and avoid hypothyroidism
 Defer conception for at least 4 months
 Hypothyroidism is main side effect
o May be transient in first 6 months
 50% patients given high dose at one year

38
Q

What are the complications of thyroid surgery?

A

o Haemorrhage 0-1.3%
o Rec laryngeal palsy 0-4.5%
o Permanent hypocalcaemia 0.6%
o Hypothyroidism

39
Q

What are the causes of hypothyroidism?

A
  • auto-immune
  • thyroiditis
  • thyroidectomy
  • radioiodine therapy
  • drug induced
  • pituitary disease
  • severe iodine deficiency
40
Q

What is Hashimotos?

A

Autoimmune thyroid disease

o Destruction of the thyroid gland (anti TPO antibody)
o May be positive family history, more common in females

41
Q

What drugs can induce hypothyroidism?

A

o Amiodarone (antiarrhythmic drug, contains a lot of iodine)
o Lithium
o Sunitinib

42
Q

What are the symptoms of hypothyroidism?

A 
 Weight gain
 Depression
 Lethargy
 Constipation
 Cold intolerance
 Poor concentration
 Hoarseness
 Menorrhagia - menstrual periods with abnormally heavy or prolonged bleeding
43
Q

What are the signs of hypothyroidism?

A 
 Weight gain
 Bradycardia
 Lethargy
 Dry skin
 Coarse, thin hair
 Anaemia
 Slow relaxing reflexes
 May have goitre
44
Q

What is goitre?

A

 Swelling in the neck resulting from an enlarged thyroid gland.
 Not only seen in hypothyroidism
 May be hyperthyroid or euthyroid with nodular disease

45
Q

What investigations are done in hypothyroidism?

A

Measure:
o Free T4
o TSH

  • Primary hypothyroidism = High TSH and low T4
  • Secondary hypothyroidism = Low TSH and low T4
46
Q

What is the main treatment for hypothyroidism?

A

levothyroxine

47
Q

What is the typical dosage regimine of levothyroxine?

A

o Generally need 1.7-2.0 micrograms / kg / day (with no gland whatsoever)
o Best taken on an empty stomach
o Avoid taking with proton pump inhibitors, ferrous sulphate or calcium
 Start lower, especially in elderly and in cardiac disease
o Increased thyroxine increases the load on the heart

48
Q

What are the treatment goals of hypothyroidism?

A

o Goal is to render patient euthyroid – Resolve symptoms and normalise TSH
o Normal TSH is controversial
 Range is 0.5 -5mU/L
 Some suggest that a TSH around 2mU/L more appropriate
 Full suppression of TSH is associated with Atrial fibrillation and osteoporosis

49
Q

What are the different types of thyroid cancer?

A 
 Differentiated (good prognosis)
o Papillary 17%
o Follicular 13-20%
o Mixed 50%
o Medullary Carcinoma of Thyroid 6%
 Undifferentiated 15% (poorer prognosis)
o Anaplastic
o Small cell
 Misc – Lymphoma, Sarcoma, Metastatic

Phase 2 3. Endocrinology (25 decks)

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