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Hannah's Endocrine > Thyroid Hormones > Flashcards

Thyroid Hormones Flashcards

1
Q

Which dietary element is essential for thyroid hormone synthesis? Where is it primarily found?

A

Iodine, abundant in the sea

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2
Q

What is the effect of circulating T3/T4 on TRH and TSH release?

A

Feeds back to hypothalamus to reduce TRH release and to the anterior pituitary to reduce TSH release

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3
Q

What are 2 alternative uses of iodine besides dietary in thyroid hormone production?

A

As an antiseptic, and for X-ray contrast

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4
Q

How does iodine act as an antiseptic?

A

The active form, I2, is a potent oxidiser which reacts in electrophilic reactions with enzymes of the respiratory chain, and AAs in the cell membrane and cell wall proteins; this destroys the cell integrity

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5
Q

What is the effect of excessive iodine intake?

A

Interferes with thyroid function and may cause goitre; can cause goitre in the fetus during pregnancy sufficient to block the airways

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6
Q

What is the upper level for dietary iodine intake?

A

1100ug/day

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7
Q

What is a goitrogen? In what kind of foods are they found?

A

A substance that inhibits iodine uptake in the thyroid and usually magnifies the severity of any iodine deficiency; found in soy, cabbage, kale and brussel sprouts

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8
Q

What is cretinism?

A

A congenital disorder caused by maternal iodine deficiency and marked by dwarfism and severe mental retardation

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9
Q

How do thyroid hormones alter energy level?

A

By elevating ATP, acetyl-CoA, NADH and NADPH

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10
Q

What are the metabolic effects of thyroid hormone?

A

They alter energy levels by inducing enzyme synthesis (especially the protein of oxidative phosphorylation)

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11
Q

What are the 2 functions of the thyroid gland?

A

Secretion of thyroid hormones and calcitonin

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12
Q

Describe the cellular structure of the thyroid gland

A

Follicular cells surrounding colloid with C cells located in interstitial spaces

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13
Q

Describe the steps involved in thyroid hormone synthesis

A

1) Follicular cells synthesise enzymes and thyroglobulin which are then exocytosed into the colloid
2) A Na+/I- symporter brings iodide (I-) into the follicular cell and the pendrin transporter moves it into the colloid
3) Iodide is oxidised to chemically reactive iodine (I2) by thyroperoxidase (TPO)
4) Iodine reacts with tyrosines in thyroglobulin to form MIT (1 iodine) and DIT (2 iodines)
4) TPO enzymatically condense DIT and MIT to form T3, and 2 DITs to form T4; inactive “reverse T3” is also produced to remove excess iodine
5) The modified thyroglobulin is taken back up into the follicular cells in vesicles
6) Intracellular enzymes hydrolyse peptide links to liberate free AAs and the di-tyrosyl moieties T3 and T4 from the thyroglobulin backbone
7) Free T3 and T4 diffuse into the circulation

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14
Q

What proportions of T3 and T4 are produced respectively?

A

10% and 90%

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15
Q

What is the difference between T3 and T4 in terms of their actions?

A

T4 (thyroxine) is a prohormone which can be cleaved to produce the 4x more active product, T3

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16
Q

What % of circulating T3 is derived from T4?

A

80%

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17
Q

Where does most of the circulating T3 come from?

A

Produced via Type I deiodinase activity in the liver and kidney

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18
Q

What effect does stress have on the thyroid hormone pathway?

A

Decreases TRH secretion

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19
Q

What effect does cold in infants have on the thyroid hormone pathway?

A

Increases TRH secretion

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20
Q

What effect does circulating T3 and T4 have on the hypothalamus and anterior pituitary?

A

Provide negative feedback to reduce TRH and TSH secretion from the hypothalamus and anterior pituitary, respectively

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21
Q

How are thyroid hormones transported in the blood?

A

Bound to plasma proteins (70-80% bound to thyroid-binding globulin, rest to albumin or transthyretin)

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22
Q

Which of the 2 thyroid hormones has a shorter half-life?

A

T3 (the more potent form)

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23
Q

What cells and tissues of the body are targeted by thyroid hormones?

A

Most cells and tissues

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24
Q

What class of receptors do thyroid hormones act on?

A

Nuclear receptors

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25
Q

What is the cellular action of thyroid hormones?

A

To increase the production and therefore activity of metabolic enzymes and Na+/K+/ATPase

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26
Q

What are the whole body/tissue actions of the thyroid hormones?

A

Increased BMR and oxygen consumption
Thermogenesis
Protein catabolism in adults and anabolism in children
Sympathomimetic effects including increased HR and CO
Involved in normal development of the nervous system
Permissive role in GH and IGF action in infants and children

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27
Q

What are the 2 causes and what are the biochemical findings in primary hypothyroidism?

A

Caused by thyroid gland failure (may be due to a variety of underlying pathologies, including Hashimoto thyroiditis) or dietary iodine deficiency
Findings would be decreased T3/T4 and increased TSH

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28
Q

How can primary and secondary hypothyroidism be distinguished clinically?

A

There is no goitre in secondary hypothyroidism

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29
Q

What are 2 causes of secondary hypothyroidism and what are the biochemical findings?

A

Caused by hypothalamic or anterior pituitary failure/tumour

Findings would be decreased T3/T4 and decreased TSH +/- decreased TRH

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30
Q

What is the result of maternal hypothyroidism?

A

Cretinism at birth

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31
Q

List 5 causes of congenital hypothyroidism

A

Maternal iodine deficiency
Fetal thyroid dysgenesis
Inborn errors of thyroid hormone synthesis
Maternal antithyroid antibodies that cross the placenta
Fetal hypopituitary hypothyroidism

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32
Q

List 12 symptoms of hypothyroidism

A 
Fatigue
Decreased appetite
Weight gain
Constipation
Cold intolerance
Bradycardia
Angina
CHF
Decreased mentation and depressed mood
Decreased reflexes
Myxoedema (puffy appearance)
Alopecia
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33
Q

What is the basis of myxoedema in hypothyroidism?

A

Decreased protein synthesis (decreased oncotic pressure) and accumulation of mucopolysaccharides under the skin

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34
Q

How is hypothyroidism treated?

A

By replacing thyroid hormone and ensuring adequate dietary iodine

35
Q

What is the most common cause of primary hyperthyroidism and what are the biochemical findings?

A

Caused by Graves’ disease most commonly (60-80%)

Findings would be increased T3/T4 and decreased TSH

36
Q

What is the pathological mechanism of Graves’ disease? Make reference to the 3 different types of Abs found in Graves’

A

Thyroid-stimulating immunoglobulin (TSI) or thyroid growth-stimulating immunoglobulins (TGI) act on TSH receptors to stimulate T3/T4 production
TSH-binding inhibitor immunoglobulins may also be present and can stimulate or inhibit the TSH receptor (so can present with hypothyroidism)

37
Q

What are 2 causes of secondary hyperthyroidism and what are the biochemical findings?

A

Caused by hypothalamic or anterior pituitary excess

Findings would be increased T3/T4 and increased TSH +/- increased TRH

38
Q

How can primary and secondary hyperthyroidism be distinguished from hyperthyroidism caused by a hypersecreting tumour in terms of the clinical presentation?

A

Primary and secondary hyperthyroidism can present with goitre, whilst a hypersecreting tumour will not cause goitre

39
Q

List 5 possible causes of thyroid overactivity?

A 
Solitary toxic adenoma
Toxic multinodular goitre
Hashimoto thyroiditis
TSH-secreting pituitary tumour
Mutations causing constitutive activation of the TSH receptor
40
Q

List 13 symptoms of hyperthyroidism

A 
Fatigue
Increased appetite
Weight loss
Diarrhoea
Muscle weakness and tremor
Osteoporosis
Heat intolerance
Tachycardia
AF
Cardiomegaly
CHF
Increased alertness, irritability and hyperexcitability
Anxiety, insomnia and emotional lability
41
Q

What is an additional symptom of hyperthyroidism caused by Graves’ disease? What is the underlying mechanism?

A

Exophthalmos/proptosis (bulging eyes)
Caused by retro-orbital deposition of hydrophilic mucopolysaccharides (leading to oedema) and fat, fibrosis and accumulation of lymphocytes
Fibroblasts appear to be the target and effector cells as they express TSH-like Ags and can produce hyaluronic acid (GAG) and transform into adipocytes

42
Q

How is hyperthyroidism treated?

A

Removal of thyroid (subtotal thyroidectomy) or tumour
Radioactive iodine ablation
Anti-thyroid drugs (e.g. carbimazole) to block synthesis and/or conversion from T4 to T3
Reduction of sympathetic overactivity (e.g. with B-blockers)
Thyroid arterial embolisation

43
Q

What is the normal mass of the thyroid?

A

~20g (+/- 5-10g)

44
Q

What is the difference between follicular and C (parafollicular) cells in terms of their cell type?

A

Follicular cells are epithelium

C cells are neuroendocrine in origin

45
Q

Describe the normal (inactive) histological appearance of the thyroid

A

Roud-to-oval follicles of various sizes, lined by cuboidal epithelium
Follicles filled with colloid containing thyroglobulin (stains bright pink)
Thin fibrous septa with a rich blood supply (many capillaries) surround the follicles

46
Q

Can C cells be seen on histological section?

A

Not on H&E; require a special stain or must be visualised using EM

47
Q

What 2 features are characteristic of an active thyroid follicle on histological section?

A

Tall cuboidal to columnar cells

“Scalloping” of colloid

48
Q

What is the difference between hyperthyroidism and thyrotoxicosis?

A

Thyrotoxicosis strictly refers to an elevated circulating T3/T4
Hyperthyroidism refers to the overactivity of the gland/pathway

49
Q

What is diffuse non-toxic (“simple”) goitre? What are the common biochemical findings? Is it reversible or irreversible?

A

Impaired synthesis of thyroid hormone causing elevation of TSH and compensatory enlargement of the thyroid
Patients are usually euthyroid but may have a slightly elevated TSH
Thyroid involutes if TSH and T3/T4 return to normal

50
Q

What is the definition of endemic simple goitre?

A

> 10% of the population are affected (usually due to iodine deficiency)

51
Q

List 2 causes of sporadic simple goitre

A

Congenital biosynthetic defects

Goitrogens

52
Q

What are the histological findings in a diffuse non-toxic (“simple”) goitre?

A

Cellular hyperplasia
Follicles lined by crowded cells
Some follicles larger than others; large colloid-filled cysts may be present

53
Q

What is the fate of the follicles in a diffuse non-toxic (“simple”) goitre if the high TSH is resolved vs. unresolved?

A

Follicles involute with resolution of high TSH

Can rupture and haemorrhage or grow larger with persistent stimulation

54
Q

How does simple goitre transition to multinodular goitre?

A

With cycles of hyperplasia and involution, some follicles become large nodules, and some rupture and fibrose

55
Q

What is the abnormality in TMNG?

A

Autonomous thyroid nodules

56
Q

How does TMNG present on a NM?

A

With “hot” patches in the thyroid

57
Q

What is a positive Pemberton’s sign? What is the underlying mechanism?

A

Facial congestion, cyanosis and respiratory distress after ~1 minute of the patient raising their arms above their head
Caused by SVC compression (often due to a retrosternal goitre but can be caused by any mediastinal mass)

58
Q

What is the difference in regression between simple goitre vs. TMNG?

A

Simple goitre regresses over 3-6 months

>1/3 of the thyroid regresses in TMNG

59
Q

What is the secondary risk in TMNG?

A

<5% of autonomous nodules are malignant and require removal

60
Q

What are the 3 main histological findings in Hashimoto thyroiditis?

A 
Mononuclear inflammatory infiltrate with lymphocytes (T and B), plasma cells and formation of germinal centres
Hurthle cells (follicular cells with abundant, eosinophilic, granular cytoplasm)
Increased interstitial connective tissue (fibrosis)
61
Q

What is the gross pathology of Hashimoto thyroiditis?

A

Initially enlarged but eventually atrophic gland
Firm, pale (fibrotic), tan-yellow surface (like a LN)
Somewhat nodular

62
Q

What is the underlying pathology in Hashimoto thyroiditis?

A

Loss of tolerance to thyroid tissues causing CTL- and cytokine-mediated cell death
TSH-blocking Abs including anti-TG and anti-TPO

63
Q

What is the typical age of onset of Hashimoto thyroiditis? What are 2 other risk factors?

A

45-65 years
Female gender
Genetic factors (e.g. family history of Hashimoto thyroiditis or other autoimmune conditions)

64
Q

What is the secondary risk in Hashimoto thyroiditis?

A

Increased risk of B-cell non-Hodgkin lymphoma

65
Q

What are 2 clinical symptoms specific to Graves’ disease?

A 
Exophthalmos
Pretibial myxoedema (only seen in 5%)
66
Q

What are the histological findings in Graves’ disease?

A

Cellular hypertrophy and hyperplasia (tall follicular cells)
Formation of papillae in follicle lumen
Widespread scalloping of colloid (colloid may be paler-staining)
Lymphocytic infiltrates

67
Q

What is the gross pathology of Graves’ disease?

A

Diffuse symmetrical enlargement with a “soft, meaty” cut surface

68
Q

What is the typical age of onset of Graves’ disease? What are 3 other risk factors?

A

20-50 years
Female gender
Genetic factors
Smoking

69
Q

What type of hypersensitivity is Graves’ disease?

A

Type II (IgG-mediated)

70
Q

What type of hypersensitivity is Hashimoto thyroiditis?

A

Type IV (cell-mediated)

71
Q

Which isotypes of iodine are used for NM scans and thyroid ablation respectively?

A

123 (gamma radiation only) and 131 (beta and gamma radiation)

72
Q

How do THs increase sympathetic innervation?

A

By upregulating expression of catecholamine receptors and directly enhancing catecholamine effects

73
Q

What effect do THs have on adipose tissue?

A

Stimulate differentiation to brown adipose tissue and the generation of heat by this brown adipose

74
Q

What is the effect of long term starvation on TH production?

A

Depresses output of THs

75
Q

Where is TPO located in the thyroid?

A

Embedded in the membrane of the follicular cell

76
Q

What is the protective role of the colloid surrounded by follicular cells?

A

Sequesters highly reactive free iodine and H2O2

77
Q

What drives the NIS symport for iodine uptake?

A

An Na+ gradient, maintained by 3Na+/2K+ ATPase

78
Q

What is the target in anti-thyroid drug therapy?

A

Inhibits TPO and/or deiodinase

79
Q

What is the most common combination of therapies in anti-thyroid drug therapy?

A

Propylthiouracil

Methimazole

80
Q

Where does most of the T3 acting in cells come from?

A

Produced via Type II deiodinase in the brain, brown adipose tissue and pituitary

81
Q

Where is the TH receptor located and what does it do in the absence and presence of THs?

A

The thyroid hormone receptors bind DNA and usually produce transcriptional repression in the absence of hormone
Hormone binding causes a conformational change leading to transcriptional activation

82
Q

How long do the THs take to produce an effect? How long does this alteration last?

A

1-10 hours to produce an effect

Effect may last several days

83
Q

What term is used to describe normal levels of THs?

A

Euthyroid

Hannah's Endocrine (8 decks)

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