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Phase 2 3. Endocrinology > PBL 3 - Thyroid gland > Flashcards

PBL 3 - Thyroid gland Flashcards

1
Q

Where is the thyroid gland located?

A

anterior neck, spanning between the C5 and T1 vertebrae
Lies behind the sternohyoid and sternothyroid muscles, wrapping around the cricoid cartilage and superior tracheal rings.
Inferior to the thyroid cartilage of the larynx

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2
Q

Describe the gross structure of the thyroid

A

divided into two lobes, connected by an isthmus.

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3
Q

What structures are found in the visceral compartment of the neck?

A

thyroid, trachea, oesophagus and pharynx

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4
Q

What covers the thyroid gland?

A

loose fascia (pretrachial fascia), that secures the gland onto the trachea and larynx

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5
Q

What is the arterial supply to the thyroid gland?

A
  1. Superior thyroid artery
    - first branch of the external carotid artery. After arising, the artery descends toward the thyroid gland.
    - it ~ supplies the superior and anterior portions
  2. Inferior thyroid artery
    - arises from the thyrocervical trunk (a branch of the subclavian artery)
    - tends to supply the postero-inferior aspect.
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6
Q

Describe the venous drainage of the thyroid gland

A

superior, middle and inferior thyroid veins form a venous plexus.
The superior and middle veins drain into the internal jugular veins, whereas the inferior drains into the brachiocephalic vein.

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7
Q

Describe the innervation of the thyroid gland

A

branches derived from the sympathetic trunk.

NB: these nerves do not control endocrine secretion – release of hormones is regulated by pituitary gland.

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8
Q

Describe the histology of the thryoid gland

A
  • composed of large numbers of microscopic spherical sacs called thyroid follicles

Follicles are lined by cuboidal epithelial cells (primarily follicular cells) that secrete a substance called colloid into the interior of the follicle

A basement membrane surrounds each follicle.

When follicular cells become inactive, their shape is low cuboidal to squamous, but under the influence of TSH, they become active in secretion and range from cuboidal to low columnar shape.

The thyroid gland also contains C cells that secrete calcitonin

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9
Q

What does the colloid consist of?

A

primarily of thyroglobulin, a large glycoprotein that contains the thyroid hormones

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10
Q

Where are iodide ions absorbed?

A

from the GIT - delivered to the thyroid via bloodstream

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11
Q

How does the BM of thyroid follicular cells take up iodide?

A

cell uses a sodium-iodide transporter to actively take up iodide via secondary active transport (gradient is initiated by Na-K-ATPase)

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12
Q

What is iodide trapping?

A

process of concentrating iodide in the cell is called

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13
Q

What stimulates iodide trapping

A

TSH

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14
Q

How are iodide molecules transported into the follicle lumen?

A

by pendrin (a chloride-iodide counter-transporter)

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15
Q

What do thyroid epithelial cell secrete?

A

thyroglobulin into the follicle lumen

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16
Q

Where are the thyroid hormones formed?

A

within the thyroglobulin molecule, and are stored in colloid in this state

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17
Q

How does iodide bind to tyrosine?

A

iodide has to be oxidized so that it can bind to tyrosine

Iodide ions diffuse to the apical surface and are converted to the active (I+) by the enzyme thyroid peroxidase.

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18
Q

Where is iodide oxidised?

A

the location where thyroglobulin enters the follicle lumen, where the thyroid peroxidase is located within the apical membrane

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19
Q

What is organification of thyroglobulin?

A

binding of oxidised iodide to thyroglobulin

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20
Q

How does iodide contribute to the formation of thyroid hormones?

A

Tyrosine molecules and iodide ions are covalently linked together, forming the thyroid hormones (T3 & T4)

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21
Q

What process does tyrosine go through before forming thyroid hormones?

A

tyrosine is first iodised to monoiodotyrosine, then diiodotyrosine

Iodotyrosine molecules become coupled with one another

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22
Q

What is the storage capacity of thyroglobulin?

A

thyroglobulin contains up to 30 thyroxine molecules and a few T3 molecules

In this form, the thyroid gland stores enough thyroid hormones to supply the body for 2-3 months

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23
Q

How is T3 and T4 released?

A

Under the influence of TSH:

  • Follicle cells remove thyroglobulin from the follicles by endocytosis
  • lysosomal enzymes break down thyroglobulin, releasing free T3 and T4 into the cytoplasm
  • T3 and T4 diffuse across the basement membrane and into the bloodstream
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24
Q

How do follicle cells remove thyroglobulin?

A

by endocytosis.

the apical surface of thyroid cells sends out pseudopod projections that close around small portions of the colloid, forming pinocytic vesicles

These enter the thyroid cell

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25
Q

Describe how lysosomal enzymes break down thyroglobulin

A

Lysosomes in the cell fuse with the vesicles and release free T3 and T4 into the cytoplasm, as well as amino acids. These amino acids are recycled and used to synthesise more thyroglobulin.

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26
Q

How are thyroid hormones carried in the blood?

A

Most of the T3 and T4 are bound to thyroid-binding globulins (TBGs), and some are bound to transthyretin or albumin.

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27
Q

How is T3 formed?

A

5’ deiodination of T4 (one iodide ion is removed from T4 to make T3).

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28
Q

Describe the release of thyroid hormones to the tissues

A

Because plasma proteins have a high affinity for thyroid hormones, they are released to the tissue slowly

T3 is released faster than T4 because plasma proteins have a lower affinity for T3

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29
Q

How is thyroid hormone production regulated?

A

by the hypothalamus and pituitary gland.

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30
Q

Describe hypothalamic control of thyroid hormone synthesis

A

Hypothalamic thyrotropin-releasing hormone (TRH) stimulates

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31
Q

Describe the pituitary role in thyroid hormone production

A

anterior pituitary thyrotropin (TSH) synthesis and secretion.
TSH acts on the thyroid gland causing stimulation and secretion of T3/T4
acts directly on the TSH receptor (TSH-R) on follicular basolateral membrane
TSH regulates iodide uptake mediated by the sodium/iodide symporter, followed by a series of steps necessary for normal thyroid hormone synthesis and secretion

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32
Q

How is thyroid hormone production inhibited?

A

T3/T4 negatively feedback to the pituitary gland and hypothalamus to reduce its own production.

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33
Q

What happens in the absence of TSH?

A

thyroid follicles become inactive. Neither synthesis nor secretion occurs.

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34
Q

Where are thyroid receptors found?

A

almost every organ

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35
Q

What does thyroid hormone binding facilitate?

A

process regulates gene transcription and the subsequent production of various proteins that are involved in development, growth, and cellular metabolism

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36
Q

What proteins help transport thyroid hormones in the blood?

A

thyroxine-binding globulin [TBG], pre-albumin [transthyretin], and albumin

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37
Q

How do thyroid hormones enter cells?

A

through membrane transporter proteins

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38
Q

How do thyroid hormones modulate gene expression

A

The TH receptor normally forms a heterodimer with retinoid X receptor at specific thyroid hormone response elements on the DNA

Binding activates receptors and initiates transcription

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39
Q

What is the effect of thyroid hormones that bind to T3 nuclear receptors

A

activates genes that are involved in energy production and utilisation.

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40
Q

Where are T3 nuclear receptors found?

A

more sensitive tissues (pituitary, liver)

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41
Q

What is the calorigenic effect?

A

increase body heat production, which seems to result, at least in part, from increased oxygen consumption and rates of ATP hydrolysis.

= the calorigenic effect (calor, heat) of thyroid hormones

(because the cell consumes more energy and generates more heat. )

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42
Q

How do thyroid hormones effect cellular metabolic activity?

A

increased number and activity of mitochondria
increased active transport of ions through cell membranes
increased activity of Na-K-ATPase
this uses a lot of energy and also increases heat production
most cell membranes also become leaky to Na

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43
Q

How do thyroid hormones effect carbohydrate metabolism?

A

almost all aspects of carbohydrate metabolism are stimulated, probably due to overall increase in cellular metabolic enzymes
including enhancement of insulin-dependent entry of glucose into cells and increased gluconeogenesis and glycogenolysis to generate free glucose

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44
Q

How do thyroid hormones effect fat metabolism?

A

Increased thyroid hormone levels stimulate fat mobilization, leading to increased concentrations of fatty acids in plasma. They also enhance oxidation of fatty acids in many tissues

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45
Q

What is the effect of thyroid hormones on the plasma and liver fats?

A

decreases the concentration of cholesterol, phospholipids and TAG in plasma even though it increases FFA concentration
this might be achieved by increasing secretion into bile

46
Q

What is the effect of thyroid hormones on vitamin requirement?

A

increased requirement for vitamins because many bodily enzymes are upregulated. A relative vitamin deficiency can occur in hyperthyroid state

47
Q

What is the effect of thyroid hormones on respiration?

A

increased rate and depth of respiration due to increased oxygen consumption and CO2 production

48
Q

What is the effect of thyroid hormones on GI activity?

A

increased appetite and food intake
increases rate of digestive juice secretion
increase GI tract motility
hyperthyroidism can cause diarrhoea

49
Q

What is the effect of thyroid hormone on growth?

A

Thyroid hormones are clearly necessary for normal growth in children and young animals (growth-retardation is observed in thyroid deficiency). The growth-promoting effect of thyroid hormones is intimately intertwined with that of growth hormone. In growing children, thyroid hormones are essential for the development of skeletal, muscular and nervous systems.

50
Q

What is the effect of thyroid hormone on development?

A

normal levels of thyroid hormone are essential to the development of the foetal and neonatal brain.

51
Q

What is the effect of thyroid hormones on the cardiovascular system?

A

Thyroid hormones increases heart rate, cardiac contractility and cardiac output. They also promote vasodilation, which leads to enhanced blood flow to many organs.
Increased metabolism increases oxygen consumption in tissues, and more metabolic end products are released, causing vasodilation and increased blood flow
rate of blood flow to skin significantly increases due to need to eliminate heat
Increased heart rate - thyroid hormone has a direct excitable effect on the heart
NB: normal arterial pressure (systolic BP increases but diastolic BP decreases)

52
Q

What is the effect of thyroid hormones on the central nervous system

A

Both decreased and increased concentrations of thyroid hormones lead to alterations in mental state. Too little thyroid hormone, and the individual tends to feel mentally sluggish, while too much induces anxiety and nervousness

53
Q

What is the effect of thyroid hormones on the reproductive system

A

Normal reproductive behavior and physiology is dependent on having essentially normal levels of thyroid hormone. Hypothyroidism in particular is commonly associated with infertility.

54
Q

What is hyperthyroidism?

A

THYROTOXICOSIS (when symptomatic)

Overactivity of the thyroid gland, either due to a tumour, overgrowth of the gland, or Graves’ disease, that can lead to an excess of thyroid hormone secretion

55
Q

What is the most common cause of hyperthyroidism?

A

Graves’ disease

56
Q

What are the clinical causes of hyperthyroidism

A

Suppressed TSH levels

elevated T3 and T4 levels

57
Q

What are other causes of hyperthyroidism?

A

Toxic adenomas (rarely thyroid carcinomas)
Multinodular goitre (abnormal swelling of the neck)
Thyroiditis
Excessive administration of thyroxine (T4 must be kept within the reference limits)

58
Q

What is hypothyroidism?

A

Hypothyroidism is defined as an underactive thyroid gland, leading to deficient thyroid hormones.

59
Q

What is under-activity of the thyroid gland usually a result of?

A

usually primary, from disease of the thyroid, but may be secondary to hypothalamic-pituitary disease (reduced TSH drive)

60
Q

What are the main causes of hypothyroidism?

A
  • Autoimmune thyroid disease
  • Hashimoto’s Thyroiditis
  • Thyroiditis (viral)
  • Thyroidectomy
  • Following Radioactive Iodine therapy
  • Pituitary/Hypothalamic disease - secondary hypothyroidism
  • Severe Iodine Deficiency - ‘endemic goitre’
61
Q

What is Hashimoto’s Thyroiditis

A

destruction of the thyroid gland (anti-TPO antibodies are high). Lymphoid filtration of the thyroid gland and eventual atrophy and fibrosis. Especially common in middle aged women.

62
Q

What is Thyroiditis

A

inflammation of thyroid gland due to a viral cause

63
Q

What are the clinical symptoms of hypothyroidism?

A
  • weight gain
  • depression
  • lethargy
  • constipation
  • cold intolerance
  • poor concentration
  • hoarseness
  • menorrhagia
64
Q

What are the clinical signs of hypothyroidism?

A
  • weight gain
  • bradycardia
  • dry skin
  • coarse, thin hair
  • anaemia
  • slow relaxing reflexes
  • may have goitre
65
Q

What are the clinical findings of primary hypothyroidism?

A

Primary Hypothyroidism - High TSH, Low T4

66
Q

What are the clinical findings of secondary hypothyroidism?

A

Secondary Hypothyroidism - Low TSH, Low T4

67
Q

List the complications of hypothyroidism

A
  • goitre
  • heart problems
  • mental health issues
  • myxedema
  • birth defects
68
Q

How can a goitre develop?

A

Constant stimulation of thyroid to release more hormones may cause the gland to become enlarged. Generally not uncomfortable, but a large goitre can affect appearance/interfere with swallowing or breathing

69
Q

How can heart problems occur in hypothyroism?

A

High levels of LDL can occur in hypothyroidism. Untreated hypothyroidism can lead to an enlarged heart and, possibly, heart failure.

70
Q

What are the mental health effects of hypothyroidism

A

Depression may occur early in Hashimoto’s disease and may become more severe over time. Libido may also decrease in both men and women and can lead to slowed mental functioning.

71
Q

What is myxedema?

A

rare, life-threatening condition can develop due to long-term hypothyroidism. Its signs and symptoms include drowsiness followed by profound lethargy and unconsciousness.

72
Q

What is the treatment for hypothyroidism?

A

Thyroxine replacement therapy is given for life

Levothyroxine (synthetic thyroxine) is given by oral administration.

73
Q

How does Hashimoto’s thyroiditis cause hypothyroidism?

A

characterized by the destruction of thyroid cells by various cell- and antibody-mediated immune processes.
Inflammation from Hashimoto’s disease, known as chronic lymphocytic thyroiditis, often leads to hypothyroidism

74
Q

What causes Hashimoto’s thyroiditis?

A

genetic susceptibility and environmental factors.

75
Q

What are the genetic links to Hashimoto’s thyroiditis?

A

People who get Hashimoto’s often have family members who have thyroid disease or other autoimmune diseases.

76
Q

What are the hormone links to Hashimoto’s thyroiditis?

A
  • effects about seven times as many women as men, suggesting that sex hormones may play a role
77
Q

What is the link between iodine and Hashimoto’s thyroiditis?

A

Excessive iodine. certain drugs and too much iodine, may trigger thyroid disease in susceptible people

78
Q

What is the link between Hashimoto’s thyroiditis and radiation exposure?

A

Increased cases of thyroid disease have been reported in people exposed to radiation, including the atomic bombs in Japan, the Chernobyl nuclear accident, and radiation treatment for Hodgkin’s disease.

79
Q

What is the link between Hashimoto’s thyroiditis and Graves’ disease?

A

The familial association with Graves’ disease and the fact that Graves’ disease may sometimes evolve into Hashimoto’s thyroiditis (and vice versa) indicate that the two disorders are closely related pathophysiologically,

80
Q

What is the pathophysiology of Hashimoto’s thyroiditis?

A

immunologic attack typically aggressive and destructive

lymphocytic infiltration and destruction of thyroid tissue with secondary antibodies to thyroid peroxidase, thyroglobulin, and other thyroid antigens

Hashimoto’s thyroiditis occurs in two varieties:

  • an atrophic variety
  • a goitrous form
81
Q

What is Graves’ disease?

A

autoimmune disease characterized by hyperthyroidism due to circulating autoantibodies.

82
Q

How does Graves’ disease cause hyperthyroidism?

A

Thyroid-stimulating immunoglobulins (TSIs) bind to and activate thyrotropin receptors, causing the thyroid gland to grow and the thyroid follicles to increase synthesis of thyroid hormone

83
Q

What causes Graves’ disease?

A

Graves’ disease is caused by a combination of genetic (80%) and environmental factors (20%) and a number of gene regions have consistently been linked to Graves’ hyperthyroidism.

84
Q

Describe the pathophysiology of Graves’ disease

A

autoantibodies bind to the TSH receptor, leading to the overstimulation of the thyroid hormones.
The thyrotropin receptor itself is the primary autoantigen of Graves disease and is responsible for the manifestation of hyperthyroidism.
These thyroid-stimulating antibodies cause release of thyroid hormone and thyroglobulin and they also stimulate iodine uptake, protein synthesis, and thyroid gland growth.

They remain bound to the TSH receptor and continuously influence the product of thyroid hormones.
Anti-TSH receptor antibodies cause thyroid hormone hyperproduction as well as thyroid hypertrophy and hyperplasia of thyroid follicular cells

85
Q

How does Graves’ disease effect the thyroid macroscopically?

A

In this condition, the thyroid gland is symmetrically enlarged and its vascularity markedly increased.
The gland may double or triple in weight.

86
Q

What are the microscopic changes in Graves’ disease?

A

Microscopically, the follicular epithelial cells are columnar in appearance and increased in number and size
In response to high circulating T3 and T4 hormones, there is negative feedback to the pituitary gland and suppressed secretion of TSH.

87
Q

What symptoms are specific to Graves’ disease?

A

Eyelid retraction or lid lag → noticeable “stare”

Periorbital oedema

Graves’ ophthalmopathy
caused by lymphocytic infiltration of the periorbital tissues and activation of fibroblasts to secrete osmotically active hyaluronic acid.
This increases the pressure and pushes the eye forward, resulting in proptosis

88
Q

What can TFTs tell you?

A

Suppressed or elevated TSH confirms presence of thyroid dysfunction but not its cause

89
Q

What is a low TSH level indicative of?

A

Low TSH level usually indicates that the person has an overactive thyroid gland (hyperthyroidism).
Occasionally, a low TSH may result from an abnormality in the pituitary gland, which prevents it from making enough TSH to stimulate the thyroid (secondary hypothyroidism).

90
Q

What is a high TSH level indicative of?

A

A high TSH level indicates that the thyroid gland is failing because of a problem that is directly affecting the thyroid (primary hypothyroidism).

91
Q

What is the best way to measure T3/T4 in terms of thyroid functioning?

A

The free fraction is the most important to determine how the thyroid is functioning

92
Q

What are T3 tests helpful for?

A

often useful to diagnose hyperthyroidism or to determine the severity of the hyperthyroidism.

93
Q

What common antibodies can cause thyroid problems?

A

Antibodies directed against thyroid cell proteins: thyroid peroxidase and thyroglobulin.

94
Q

What is Radioactive iodine uptake (RAIU) and scan

A

Usually ordered in the setting of thyrotoxicosis to help identify the underlying aetiology.
measures the amount of radioactive iodine (usually I-123) that is taken up by the thyroid gland.
High uptake may indicate hyperthyroidism

95
Q

what is TRH stimulation test

A

Used to evaluate TSH response to TRH stimulation in the setting of central hypothyroidism.
may also help differentiate TSH secretory tumour from resistance to thyroid hormone syndrome (RTH).
In RTH, the TSH response is normal. TRH stimulation test is not a specific test.

96
Q

Why is calcitonin measured?

A

usually a marker of medullary thyroid cancer.

97
Q

How is hyperthyroidism treated?

A

Antithyroid Drugs (Thionamides)

98
Q

Name types of Antithyroid Drugs (Thionamides)

A

Carbimazole

Propylthiouracil (PTU)

99
Q

Describe carbimazole

A

Drug of choice
A prodrug which is converted to the active metabolite, thiamazole via first pass metabolism.
Half life of thiamazole is 12-15 hours.

  • also has immunosuppressive properties therefore useful in treatment of Graves’ disease.
100
Q

What are the side effects of carbimazole?

A

It has some serious side effects (skin aplasia, rash, nausea etc).

101
Q

Describe Propylthiouracil (PTU)

A

Less active and shorter half life so twice the dosing is required. It is usually second line.
PTU also reduces the conversion of T4 → T3 peripherally giving some more acute effects.
T4 has a long half-life (7 days) and therefore treatment with antithyroid drugs can take from 10-20 days for any clinical benefit to be seen.

102
Q

What is the role of beta blockers in hyperthyroid treatment?

A

These reduce symptoms if there is symptomatic overactivity & does not affect hormone levels.

103
Q

Describe drug induced thyrotoxicosis

A

Amiodarone (anti-arrhythmic drug) induced thyrotoxicosis may result from autoimmunity (type 1) or a destructive thyroiditis with release of preformed thyroid hormones (type 2).
More often than not these conditions are self limiting, and timely investigation saves patients from unnecessary treatment.

104
Q

Describe thyroiditis

A

Thyrotoxicosis associated with thyroiditis is transient, often progresses through a hypothyroid phase, and then resolves spontaneously.
Antithyroid drugs are ineffective and should be avoided
Treatment is often limited to symptom control with β blockers.
In subacute thyroiditis, non-steroidal anti-inflammatory drugs and occasionally systemic glucocorticoids may be required to control pain.

105
Q

Describe Toxic multinodular goitre and solitary toxic nodule

A

Antithyroid drugs do not lead to long term remission of thyrotoxicosis in toxic multinodular goitre or solitary toxic nodules.
Radioiodine is the treatment of choice for most patients with these conditions.
When treatment with radioiodine is not possible, the alternatives are a long term small dose of carbimazole (or methimazole) or thyroid surgery

106
Q

Describe the use of surgery in the treatment of thyrotoxicosis

A

Total (or near total) thyroidectomy is a highly effective and predictable treatment for Graves’ disease, particularly for patients:
who have relapsed after adequate medical treatment
with active Graves’ ophthalmopathy
with a cosmetically undesirable goitre

Long term complications of thyroidectomy include:
- hypocalcaemia as a result of hypoparathyroidism, which is most often transient
- vocal cord paresis due to operative compromise of the recurrent laryngeal nerve.
Patients need to be rendered euthyroid before surgery

107
Q

What are the long term effects of radioactive iodine treatment?

A

Radioactive Iodine and partial thyroidectomy run the long-term risk of hypothyroidism, as the remaining thyroid tissue may be insufficient to meet the body’s demands.
may develop in 50-90% of people as an expected consequence of treatment

108
Q

What are the short term effects of radioactive iodine?

A

rarely, some soreness around the thyroid gland
In the month after radioiodine treatment there is a small risk of thyrotoxicosis being exacerbated (or even a thyroid storm being precipitated) due to the release of preformed hormone.
To reduce this risk it is recommended that patients with large goitres, severe thyrotoxicosis, ischaemic heart disease, heart failure, or arrhythmia should be pretreated with thionamide until they are euthyroid.
Patients receiving a standard dose of radioiodine are also advised to take several precautions to minimise the perceived deleterious effects of ionising radiation to others.
For example, close and prolonged contact with children and pregnant women should be avoided for about three weeks

109
Q

Which patients is radioactive iodine therapy contraindicated in?

A

Pregnant women - radioiodine crosses the placenta and can affect the thyroid gland developing in the baby
Patients are advised to avoid a new pregnancy for six months after treatment.
Breast-feeding women - the radioactive iodine passes via the milk to the baby’s thyroid gland
Anyone who is vomiting or incontinent
People with active thyroid eye disease as it may worsen the eye disease unless steroids are given at the same time
release of thyroid antigen and subsequent hypothyroidism may be associated with deterioration of eye disease.
The risk of ophthalmopathy is much higher in smokers, but can be abrogated by a short course of prednisolone

110
Q

Describe radioactive iodine therapy

A

131Iodine is given in an empirical dose because of variable uptake and radio-sensitivity of the gland.
The 131Iodine is rapidly concentrated by the thyroid after oral ingestion and destroys the gland by local radiation (beta emission) although it takes several months to be effective.
The β radiation has a 2mm radius of activity and induces DNA damage leading to death of thyroid cells.
Six weeks to six months after radioiodine treatment most patients with Graves’ disease are rendered sequentially euthyroid and then hypothyroid
Patients with large goitres, however, may need higher or repeated doses to achieve euthyroidism
If the thyroid gland is very over-active, radioactive iodine can cause dangerously high levels of thyroid hormone, a condition known as thyroid crisis or storm.
doctor will therefore prescribe antithyroid drugs to control the hyperactivity first
Potassium Iodide - Reduces thyroid hormone release acutely and therefore used pre-operatively

Phase 2 3. Endocrinology (25 decks)

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