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Endocrinology semester 1 > thyroid gland and thyroid gland dysfunction > Flashcards

thyroid gland and thyroid gland dysfunction Flashcards

1
Q

what does the thyroid gland consist of?

A

numerous spheres each of which form a follicle.

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2
Q

what do the walls of follicles consist of?

A

single layer of cuboidal cells

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3
Q

what makes up the centre of the lumen?

A

colloid made up of protein called thyroglobulin

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4
Q

what are some of the amino acids in thyroglobulin?

A

they have some thyroid hormones such as thyroxine and triiodothyronine

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5
Q

what secretes calcitonine?

A

parafollicular or C-cells

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6
Q

what is calcitonine involved in?

A

calcium balance

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7
Q

what are the thyroid hormones?

A
  • Thyroxine or T4 or tetraiodothyronine
  • Triiodothyronine or T3
    3,5,3’-Triiodothyronine
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8
Q

what is the first major step in the synthesis of thyroid hormones?

A

uptake of iodide ion by the thyroid gland

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9
Q

what is the second major step in the synthesis of thyroid hormones?

A

Oxidation of iodide and the iodination of tyrosyl groups of thyroglobulin

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10
Q

what is the third major step in the synthesis of thyroid hormones?

A

Coupling of iodotyrosyl residues by ether linkage to generate iodothyronine

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11
Q

what is the fourth major step in the synthesis of thyroid hormones?

A

Proteolysis of thyroglobulin and the release of thyroxine (T4) and T3

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12
Q

what is the normal daily intake of iodine?

A

150 µg

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13
Q

how is iodine absorbed?

A

Iodine is absorbed from the GI tract and reaches the circulation in the form of iodide.

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14
Q

how is iodide transported?

A

Thyroid gland efficiently and actively transports the ion.

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15
Q

what stimulates the transport mechanism of iodine?

A

thyroid-stimulating hormone (TSH or thyrotropin)

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16
Q

what is another mechanism the thyroid gland has?

A

The gland also have a mechanism (independent of TSH) to regulate the iodide uptake which depends on the iodine concentration in the blood

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17
Q

how are thyroid hormones transported in the blood?

A

highly bound to plasma protein

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18
Q

what are the 3 plasma proteins associated with thyroid hormone transport?

A
  • Thyroxine-binding globulin (TBG)
  • Thyroxine binding prealbumin (TBPA)
  • Albumin
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19
Q

why is protein binding good for the thyroid hormone?

A

High protein binding protect thyroid hormone from metabolism and excretion

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20
Q

where is thyroxine converted to T3?

A

liver

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21
Q

what % of thyroid secretions are

A

triiodothyronine (T3).

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22
Q

what is the main biologically active level at the cellular level?

A

T3

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23
Q

what do most peripheral targets use?

A

Most peripheral target tissues utilize T3 derived from the blood supply.

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24
Q

where is 80% of circulating T3 derived from?

A

from the circulating T4.

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25
Q

what happens under normal condition to T4?

A

Under normal conditions about 41% of T4 is converted to T3 about 38% to reverseT3 and 21 % via other pathways such as conjugation

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26
Q

what is the half life of thyroxine?

A

6-7 days

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27
Q

what is the half life of triiodothyronine?

A

1 day

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28
Q

what happens to the half life of thyroid hormones in hyperthyroidism?

A

reduced protein binding causes a decrease in the half-life

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29
Q

what happens to the half life of thyroid hormones in hypothyroidism?

A

increases binding resulting in an increase in the half-life

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30
Q

what is the mechanism of action for thyroid hormones?

A

Thyroid hormone produces most of its effects through control of DNA transcription and ultimately, protein synthesis.

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31
Q

what are the physiological actions of thyroid hormones?

A

Virtually every body tissue is affected either directly or indirectly

Primary determinant of the body’s overall metabolic rate

Essential for normal growth and development

32
Q

what are the effects of thyroid hormones?

A

Calorigenic effects
Effects on intermediary metabolism
Effects on cardiovascular system
Effects on growth and development

33
Q

what are the calorigenic effects of thyroid hormones?

A

Increases body’s overall basal metabolic rate.

Increases bodies O2 consumption (heart, skeletal muscle, liver and kidney plays the major role) and leads to increased heat production

The action of thyroid hormones is sluggish

34
Q

what are the effects of thyroid hormones on intermediary metabolism?

A

Thyroid hormone modulates the rate of many specific reactions involved in fuel metabolism. It also modulate the actions of other hormones such as insulin, glucagon, glucocorticoids and catecholamines

35
Q

what are the effects of thyroid hormones on carbohydrate metabolism?

A

Stimulate almost all aspect of carbohydrate metabolism

36
Q

what are the effects of thyroid hormones on fat metabolism?

A

Essentially all aspect of fat metabolism is also enhanced by thyroid hormone

Thyroid hormone increases the cholesterol secretion in bile. Increased thyroid hormone decreases the quantity of cholesterol in the plasma

37
Q

what are the effects of thyroid hormones on mucopolysaccharide metabolism?

A

Thyroid hormones affect both synthesis and degradation of hyaluronic acid (HA) in connective tissues

38
Q

what are the main effects of thyroid hormones on cardiovascular system?

A

Increased cardiac function

Increased heart rate

Increased force of contraction

Decreased peripheral resistance

39
Q

how is decreased peripheral resistance caused?

A

Resulting from increased myocardial gene expression and increased number of β-adrenergic receptors.

40
Q

what are the effects of thyroid hormones on growth and development?

A

Essential for normal growth and development of all tissues including the brain.

It also plays a permissive role for the growth hormone. The hormone is essential for the normal growth in children.

41
Q

what is the main important function of thyroid hormone?

A

to promote growth and development of the brain during first few years of postnatal life.

42
Q

what is the speed of onset for hypothyroidism?

A

gradual onset

43
Q

what is the speed of onset for hyperthyroidism (thyrotoxicosis)?

A

develops acutely

44
Q

what is goitre?

A

Goitre is the name given to any enlargement of the thyroid gland

45
Q

what does goitre result from?

A

It results from the excessive stimulation of thyroid by either TSH or Thyroid Receptor Antibodies (also called Thyroid Stimulating Immunoglobulin) resulting in hypertrophy and hyperplasia.

46
Q

what is goitre associated with?

A

Hypothyroidism,

Hyperthyroidism or

Normal thyroid function (Euthyroidism)

47
Q

is a goitre present in all cases of thyroid dysfunctions?

A

not present in all cases of hypothyroidism or hyperthyroidism

48
Q

what are the primary causes of hypothyroidism?

A

congenital, acquired, drug induced, iodine deficiency

49
Q

what are the secondary causes of hypothyroidism?

A

Hypothalamic and pituitary diseases

TSH deficiency

50
Q

what is an example of an acquired cause of hypothyroidism?

A

Hashimoto’s thyroiditis (an autoimmune disorder and the most common cause of hypothyroidism in western countries)

51
Q

what are the most common drugs that cause hypothyroidism?

A

Amiodarone and Lithium

52
Q

what is cretinism?

A

Arrested physical and mental development due to congenital lack of thyroid secretion

53
Q

what are features of cretinism?

A
  • Dwarfed with short extremities
  • Mentally retarded
  • Inactive, uncomplaining and listless
  • The face is puffy and expressionless
  • Enlarged tongue
  • Dry and cool skin with a yellowish hue
  • Slow heart rate
  • Constipation is frequent
54
Q

what is the most common cause of hyperthyroidism?

A

Graves disease

55
Q

what is Graves’ Disease?

A

An autoimmune disorder and develop due to the presence of thyroid stimulating antibodies (thyroid receptor antibodies) that react with TSH receptors in the thyroid gland in the same manner as TSH

56
Q

what are other causes of hyperthyroidism?

A
  • Toxic multinodular goitre
  • Solitary toxic nodules
  • Amiodarone-induced thyrotoxicosis
  • Thyroiditis
57
Q

what is toxic multinodular goitre?

A

Multiple over active thyroid nodules

58
Q

what is solitary toxic nodules?

A

Single over active thyroid nodule

59
Q

what is the treatment of hypothyroidism?

A

Replacement therapy with synthetic thyroid hormones, unless due to iodine deficiency which is treated with iodide

60
Q

what are the available drugs for hypothyroidism treatment?

A

Levothyroxine (The drug of choice)

L-Triiodothyronine (liothyronine)

61
Q

what are the characteristics of Levothyroxine?

A

Orally active

Cheap

Takes long time to achieve steady state and dose adjustment is made only after 3-4 weeks

62
Q

what are the characteristics of L-Triiodothyronine?

A

Can be given orally or IV

Quicker action but only advantageous in severe hypothyroid cases, but may cause wide fluctuation in plasma concentration between doses

63
Q

what are the 3 main treatments of Thyrotoxicosis?

A
  • antithyroid drugs
  • radioactive iodine
  • surgery
64
Q

what are examples of antithyroid drugs?

A

Carbimazole and Propylthiouracil

Beta adrenoceptor antagonists

Iodine

65
Q

which of the antithyroid drugs inhibit thyroid hormone synthesis?

A

Carbimazole and propylthiouracil

66
Q

what is carbimazole converted to?

A

active compound methimazole

67
Q

what does iodine do in terms of antithyroid drug?

A

Iodine blocks release of thyroid hormone and reduce vascularity of thyroid gland

68
Q

what does propylthiouracil inhibit?

A
  • thyroid hormone synthesis

- peripheral conversion of T4 to T3

69
Q

how do beta adrenoreceptor antagonists function?

A

Beta adrenoceptor antagonists functionally antagonise the target organ effects of thyroid hormones.

70
Q

what is the gradual dose titration anti drug regimen?

A

Initial dose of 15-40 mg carbimazole daily, after 4-8 weeks dose is progressively reduced to 5-15 mg daily. The therapy usually last for 12-18 months.

About 50% of patients relapse, usually within next 2 years.

71
Q

what is the block and replace regimen?

A

With this regimen a full dose of antithyroid drugs (40-60 mg) is given to suppress thyroid completely while replacing thyroid activity with T4 (50-150 µg). The therapy is again given for 18 months. This regimen is claimed to have lower incidence of relapse. Not suitable during pregnancy

72
Q

what can be done if carbimazole is not tolerated?

A

propylthiouracil can be used at 10 times carbimazole dose

73
Q

when can surgery be done?

A

Surgery should only be performed in patients who have been rendered euthyroid

74
Q

what happens to antithyroid drugs in preparation for surgery?

A

Antithyroid drugs are stopped 10-14 days before surgery and Lugol’s iodine is given which reduce vascularity of the gland

75
Q

what does radioactive iodine do to the gland?

A

odine 131 accumulates in the gland and destroys the gland by local radiation

76
Q

what must be determined before radioiodine therapy?

A

Patient must be rendered euthyroid before the therapy.

Antithyroid drugs are stopped about 5 days before radioiodine

77
Q

why can’t carbimazole be taken for 2-3 days after radioiodine therapy?

A

because it will prevent radioiodine uptake by the gland. Beta-blocker may be used in this period.

Endocrinology semester 1 (10 decks)

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