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Diseases > Thyroid disease > Flashcards

Thyroid disease Flashcards

1
Q

How common is thyroid disease?

A

200 million people worldwide have some form of thyroid disease

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2
Q

What does untreated thyroid disease increase the risk of?

A

Cardiovascular disease, osteoporosis and infertility

Increases chance of miscarriage, premature delivery and developmental problems

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3
Q

Describe the thyroid gland

A

Made of follicular cells and parafollicular cells

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4
Q

What do follicular epithelial cells do?

A

Secrete thyroid hormones

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5
Q

What do parafollicular epithelial cells do?

A

Secrete calcitonin

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6
Q

Describe the histology of thyroid follicules

A

A follicular epithelial layer of cells surrounds the colloid which contains thyroglobulin and thyroid hormone

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7
Q

How is the thyroid controlled?

A

The hypothalamic-pituitary axis
Hypothalamus senses low circulating T3 and T4
Releases thyrotropin releasing hormone
Stimulates pituitary to release thyroid stimulating hormone
T3 and T4 have a negative feedback loop on the hypothalamus

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8
Q

How are thyroid hormones synthesised?

A

TSH binding to the TSHR receptor stimulates Na/I symporter
Iodine is taken up from blood by pendrin
TSH stimulates thyroglobulin expression in the follicular cells
Exocytosed into the lumen
In the lumen thyroid peroxidase oxidises the iodine so that it can be incorporated into tyrosine residues of thyroglobulin
Thyroid peroxidase also catalyses conjugation of monoiodotyrosine or diiodotyrosine to form T3 or T4
TSH stimulates endocytosis of T3 and T4 still attached to thyroglobulin, proteolysis and transport to the blood

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9
Q

What does TSH drive?

A

Thyroid cell proliferation

Hormone release

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10
Q

What genes are upregulated by TSH?

A

Thyroglobulin
Thyroid peroxidase
Sodium iodide symporter
100+ identified in microarray analysis

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11
Q

List diseases of the thyroid

A 
Hyperthyroidism
Hypothyroidism
Thyroiditis
Autoimmune disorders: Graves's disease, Hashimoto's thyroiditis
Thyroid cancer
Cowden disease
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12
Q

What is a goitre?

A

A non-specific term for enlargement of the thyroid gland

Either diffuse or nodular. All previously mentioned thyroid diseases can cause goitre

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13
Q

What drives goitre formation?

A

Iodine deficiency

Increases TSH to drive TH synthesis

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14
Q

How common are goitre?

A

Palpable
4-8% of women
1-2% of men
As high as 30-40% and 20-30% in low iodine areas

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15
Q

What are different class of nodules?

A 
Benign nodules
Hyperplastic nodules
Adenomas
Cysts
Carcinomas
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16
Q

Describe thyroid cancer

A

Majority forms in follicular cells, specifically papillary cancer

17
Q

How are nodules classified?

A

Hot 85%
Warm 10%
Cold 5%
Based on their iodine levels and functional status

18
Q

Describe hot nodules in Graves’ disease

A

There are none as it is a diffuse nodular disease

19
Q

What are the different stages of thyroid goitre disease?

A

Simple goitre
Multinodular goitre: euthyroid (normal TSH and free TH levels), toxic multinodular (subclinical or overt hyperthyroidism)
Subclinical goitre

20
Q

What do subclinical and overt mean?

A

Subclinical: low TSH and normal free TH
Overt: low TSH and elevated free TH

21
Q

What happens to hot nodules?

A

They escape normal control by the pituitary gland. Produce TH in an uncontrolled manner.
Autonomously functioning thyroid nodules

22
Q

What factors influence nodular growth?

A

Lack of iodine, smoking, radiation, high BMI, selenium/iron/vitamin A deficiency, nutritional goitrogens
Women>men 4:1
Age
Genetics

23
Q

What causes hot thyroids?

A

Anti-TSHR antibodies
Point mutations of TSHR and subsequent coupled G-proteins
TSHR/TH crosstalk
Inactivation of TGFbeta1 signalling

24
Q

Give an example of a TSHR mutation

A

Constitutive activation of adenylyl cyclase

25
Q

What is familial non-autoimmune hyperthyroidism?

A

17 activating TSHR mutations identified in 24 families. Causes early onset of hyperthyroidism

26
Q

What is sporadic non-autoimmune hyperthyroidism?

A

Rare, first case reported in 1995
10 different mutations in 14 subjects
De novo germline mutation

27
Q

Describe signal modulation of the TSHR pathway

A

Desensitised TSHR signalling with beta-arresting and GRKs

Both over expressed in toxic thyroid nodules

28
Q

What are beta-arrestins?

A

Block the binding of G proteins and links the receptor to internalisation machinery

29
Q

What are GRKs?

A

Phosphorylate receptors eg. TSHR to activate them to bind to beta arrestins

30
Q

What causes cold thyroid nodules?

A

2-3x greater risk of being cancerous

Lack of uptake by the Na/I symporter

31
Q

How is NIS activity suppressed?

A

Altered mRNA expression
Activation of signalling pathways eg PI3kinase, Brafv600E
Hypermethylation (30% of maximal transcriptional activity)
Inhbition of NIS mRNA expression by protooncogenes
When PBF binds to NIS it causes localisation away from the membrane

32
Q

Evaluate animal models of thyroid disease

A 
Mouse models are used
Realistic. Homology between mice and human genes
Similarity of amino acid sequences
Time, expensive, ethics
Paper work
Differences in genes and disease
Homozygote might not be viable
33
Q

What is a PBF-Tg mouse?

A 
PTTG binding factor (PBF)
Overexpressed in thyroid tumours (and others)
Model of overexpression in a mouse
Increased goitre formation
Lesions of thyroid were hyperplastic
PBF was elevating the TSHR mRNA
Also increased pAkt activity 3 fold
34
Q

What is Cowden disease?

A

Over 60% of patients have multi nodular or follicular adenomas
10% lifetime risk of thyroid cancer
1 in 200,000
80% have inherited PTEN mutation

35
Q

What is PTEN?

A 
An inhibitor if PI3K activation of Akt
Disrupted PTEN elevates Akt activity
KO mouse had goitrogenesis
No tumours
Kras KO PTEN KO had tumours
36
Q

What is Graves’ disease?

A

Autoimmune condition
Causes hyperthyroidism
Affects 1 in 200 in the US
Thyroid stimulating immunoglobulin

37
Q

What is Hashimoto’s disease?

A

Autoimmune condition
Causes hypothyroidism
Affects 1 in 20 in the US

38
Q

What happens if hypothyroidism isn’t treated?

A

Develop myxedema coma

Diseases (5 decks)

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