Thyroid disorders Flashcards

1
Q

Describe the anatomy of the thyroid gland
Include
-embryological origin
-how can the thyroid gland be distinguished from other neck lumps
- anatomical relations to nerves and other glands
- vascular supply
- what the thyroid tissue is made up and what it contains
- which cells synthesise the contents of thyroid gland
- what do neuroendocrine cells (C cells) secrete and in which disease is this substance elevated.

A

Embryological origin: back of tongue, migrates downwards to midline and sits anteriorly to thryoid cartilage in neck.
-distinguish: left and right lobe joined by central isthmus. Distinguished as moves up with swallowing.
- anatomical relations: recurrent laryngeal nerve lies laterally on each side, parathyroid glands lie posteriorly (both at risk during thyroid surgery)
- vascular supply: inferior and superior thyroid arteries
-thyroid tissue made up of colloid which contained iodinated thyroglobulin
- follicular cells synthesis thyroglobulin, which then is turned into thyroxine and stored in colloid
- C cells secrete calcitonin
which is elevated in medullary thyroid cancer

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2
Q

What are the thyroid hormones made up of? What are the 2 main thyroid hormones? Which one is the “main” circulating one?

A

iodinated tyrosine molecules to form thyroxine (T4) and triiodothyronine (T3).

T4 is the main circulating hormone, -converted peripherally to the more potent and shorter-acting T3.

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3
Q

Which molecules do thyroid hormones bind to? What does the FREE hormone act on?

A
  • thyroxine binding globulin [TBG]
  • transthyretin
  • albumin.

free hormone acts on intracelullar thyroid receptors - TRα and TRβ

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4
Q

What are the actions of thyroid hormones?

A

increase the basal metabolic rate, heart rate

effects on CNS, reproductive system

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5
Q

Summarise the pituitary thyroid axis

A

Negative feedback system

TRH > TSH secretion > T3 and T4 secretion

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6
Q

What is the difference between primary and secondary hypothyroidism?

A

Primary hypothyroidism - problem with thyroid gland itself, auto- immune in origin - low T4 + high TSH.
remember prIMary - IMmune

Secondary hypothyroidism -TSH deficiency -pituitary disease: low T4 levels and non elevated TSH.

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7
Q

What is hyperhtyroidism also known as?

What is hyperthyroidism in context of thyroid levels?

A

Thyrotoxicosis

Primary hyperthyroidism - increased T3/T4 levels and low TSH.

If TSH not suppressed in high T3/T4 - UNUSUAL - TSHoma, throid hormone reistance or assay interference.

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8
Q

Give some factors affecting thyroid results

A

Acute illness may impact results - so best interpreted when patients relatively well

Medication eg lithium, amiodarone

Pregnancy

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9
Q

What are the 3 most common caues of hyperhyroidism?

A

Autoimmune (Grave’s) disease most common

  • TSH receptor stimulating antibodies.
  • Young women
  • Relapsing-remitting

Nodular thyroid disease

  • older age
  • autonomous secretion of T3 / T4 either from a solitary toxic nodule, or nodules within a toxic multi- nodular goitre.

Thyroiditis

  • inflammation of the thyroid gland causing a release of thyroxine.
  • viral infection, medication (e.g amiodarone) or following childbirth (post- partum thyroiditis).
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10
Q

What are the symptoms of hyperthyroidism?

A

a range of symptoms caused by increased sympathetic action . Classical features include weight loss with increased appetite, insomnia, irritability, anxiety, heat intolerance, palpitations and tremor. Other symptoms include pruritus, increased bowel frequency and loose motions, menstrual disturbance and reduced fertility. Elderly patients may present atypically with reduced energy levels (termed apathetic thyrotoxicosis). Hyperthyroidism is less common in children than adults, and may present with classical symptoms, or with accelerated growth and behavioural disturbance. General signs of hyperthyroidism include a resting tachycardia (sinus rhythm or atrial fibrillation), warm peripheries, resting tremor, hyper-reflexia and lid lag. Lid-lag maybe seen in any cause of hyperthyroidism, due to increased sympathetic tone of the upper eyelid. Lid retraction and proptosis are only seen in Graves disease. Patients may have hypertension and a flow murmur. Patients often appear agitated and hyperkinetic. Specific clinical signs of Graves disease include thyroid eye disease, and skin changes (dermopathy) characterised by pre- tibial myxoedema as well as nail changes similar to clubbing (thyroid acropachy). These are a result of cross-reactivity with TSH receptors in the back of the orbit and skin.

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11
Q

What are the hormone levels when investigating hyperthyroidism?

A

High T3 + T4 and low TSH = hyperthyroidism

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