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Y1 DRE Endocrine > L3: the thyroid gland > Flashcards

L3: the thyroid gland Flashcards

1
Q

Relevance of thyroid disease to oral health

A

High percentage of patients with undiagnosed thyroid problems, meaning they are seen in the dental chair where routine treatment had the potential to result in adverse outcomes. E.g., spotting a goitre in the neck.

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2
Q

Where is the thyroid gland?

A
  • surround the trachea at the front of the throat
  • right and left lobe
  • largest gland in the body
    (3: 10)
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3
Q

Function of the thyroid gland

A

Function of the thyroid gland is to take iodine, found in many foods and use it to synthesis thyroid hormones: thyroxine (T4) and triiodothyronine (T3).
These are then release into the bloodstream and transported throughout the body where they control metabolism.

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4
Q

Thyroid histology

A

4:15, 5:30
2 types of cell in thyroid gland:
- follicular cells release and store thyroid hormone
- parafollicular cells (C cells) secrete calcitonin

Colloid is a glycoprotein (consisting of thyroglobulin) inside the follicular cells.

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5
Q

Thyroglobulin synthesis and transport

A

Min 8

  1. Iodine from the diet is present in the blood and enters the thyroid follicular cells via a sodium/iodine symporter
  2. Iodine is bound to a protein called pendrin which allows it to move into the colloid
  3. It is oxidised here by TPO (thyroid perioxidase) giving it a negative charge

Within the cell thyroglobulin is also being synthesised from the endoplasmic reticulum, which is also placed in the colloid by exocytosis. Thyroglobulin has many tyrosine residues on it that have a spatial orientation making them susceptible to iodisation in the colloid.

  1. In the colloid, TPO will iodinate the tyrosine residues, either at one or two sites (MIT or DIT)
  2. TPO will make the iodinated thyroglobulin undergo coupling to become either T3 or T4.
  3. These then undergo endocytosis, where they are cleaved up by lysosomes and then secreted.
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6
Q

Difference between the thyroid hormones

A

13:45 for chemical structure

T4 has 4 iodines on it. DIT + DIT = tetra-iodothyronine (T4/thyroxine)
T3 has 3 iodines on it. MIT + DIT = tri-iodothyronine (T3)

MIT = mono-iodo-tyrosine
DIT = di-iodo-tyrosine
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7
Q

Thyroid hormone storage and release

A

Thyroid hormones undergo endocytosis back into the thyrocyte/thyroid follicular cell. Lysosomes fuse with the vesicles and release the T3 and T4 from the thyroglobulin. Peptidases release T4 and T3 into the bloodstream to have their effect at numerous cells. Almost all cells in body. They will increase metabolism.

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8
Q

What is the active thyroid hormone?

A

Most of thyroid hormones release are T4, which is inactive. At the peripheral tissue in liver and kidneys, T4 needs to be converted to T3 to be active by peripheral de-iodisation. T3 is the active form.

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9
Q

How are thyroid hormones transported around the blood?

A

Thyroid hormones are lipid soluble so T3 and T4 must be bound to plasma carrying proteins = thyroid binding globulin, TBG, a glycoprotein synthesised in the liver.
Carried proteins allow maintenance of a stable pool of thyroid hormones from which the active, free hormones are released for uptake by target cells.

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10
Q

Peripheral deiodination

A

T3 and T4 will go to their target tissue, where the deiodinase (D1-3) enzymes are present. They will convert T4 into T3, which will bind to the receptor and activate a response.

D1 and D2 activate T4 to T3. D3 inactivates.

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11
Q

Thyroid hormone receptors

A
  • nuclear receptors for thyroid hormone (THR) belong to the same superfamily as steroid hormone receptors
  • in the absence of hormone binding, THR binds to DNA and represses transcription
  • hormone binding activates THR and initiates transcription
  • T3 enters the cell and binds to intracellular receptors found in the nucleus of a cell. Receptor hormone complex initiated gene transcription and protein synthesis (like steroid hormones).
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12
Q

Main actions of T3

A
  • increases basal metabolic rate (tells cells to burn more energy so temp. increases)
  • influences growth and development
  • influences nervous development
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13
Q

Control of thyroid function, a classical hypothalamo-pituitary axis

A

Min 22 flow diagram. Negative feedback.

  • hypothalamus recognises the cold or stress
  • this releases TRH
  • TRH acts on the pituitary gland which releases TSH
  • TSH goes to the thyroid gland to stimulate the synthesis of T3 and T4
  • these increase BMR (so temp.), protein synthesis and sympathetic tone
  • T3 and T4 will also feedback and stop the anterior pituitary and hypothalamus from releasing TSH and TRH.
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14
Q

Effect of TSH on the thyroid gland

A
  • binding of TSH to its receptors on thyroid cells stimulates synthesis of the iodine transporter (so more iodine taken up), thyroid peroxidase and thyroglobulin
  • the magnitude of the TSH signal also sets the rate of endocytosis of colloid - high concentrations of TSH lead to faster rates of endocytosis, and hence, thyroid hormone release into circulation
  • conversely, when TSH levels are low, rates of thyroid hormone synthesis and release diminish
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15
Q

Disorders of thyroid function

A

Pituitary adenoma thyroid hormone resistance causes high TSH and high T3/T4 caused by hypothalamus/pituitary problems
Hypopituitarism causes low TSH and low T3/T4, caused by hypothalamus/pituitary problems.
Hyperthyroidism causes low TSH and high T3/T4 and is caused by thyroid problems.
Hypothyroidism causes high TSH and low T3/T4, caused by thyroid problems.

RELATE TO NEGATIVE FEEDBACK SYSTEM

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16
Q

What is used to determine thyroid function?

A

Serum TSH

17
Q

Clinical causes associated with the thyroid gland

A
  • hyperthyroidism - overactive thyroid
  • hypothyroidism - underactive thyroid
  • goitre - an enlarged thyroid (3x at least) indicative of disease but not the underlying cause. Can be hyper or hypothyroidism
  • thyroid nodules - lumps in the thyroid gland
  • thyroid cancer - malignant thyroid nodules or tissue
  • thyroiditis - inflammation of the thyroid
18
Q

Clinical features of hyperthyroidism (thyrotoxicosis)

A
  • common symptoms - fatigue, heat intolerance, sweating, weight loss, hyperphagia (eating more), nervousness, tachycardia, tremor
  • causes - Graves’ disease, toxic modular goitre (areas that produce too much T3/T4).
  • diagnosis - increased T4 and decreased TSH
  • treatment - radioactive iodine (destroys the thyrocytes), anti-thyroid drugs (inhibits TPO), surgery to remove thyroid gland.
19
Q

What is Graves’ disease?

A
  • thyroid cells stimulated by an abnormal antibody targeted at the TSH receptor
  • stimulates excess hormone production and thyroid enlargement (goitre)
  • graves opthalmopathy - stary eyes from fat around the eyes, start to pop out, drying cornea from not being able to shut eyelids and eventually causing blindness
20
Q

Symptoms of hypothyroidism

A

General tiredness, weight gain but poor appetite, hair sparseness, skin puffy and dry, husky voice, cognitive impairment, depression, poor tolerance of cold, possible goitre, low cardiac output and slow pulse, myxoedema (skin swelling/inflammation)

21
Q

Treatment of hypothyroidism

A

Thyroxine replacement by tablets

22
Q

Causes of hypothyroidism

A
  • worldwide: dietary iodine deficiency
  • in countries that use iodised salts, Hashimoto’s thyroiditis is the most common cause = autoantibodies against thyroglobulin or TPO causing progressive destruction of gland. The inflammatory response can cause goitres.
  • side effect of treatment for an overactive thyroid or for thyroid cancer
  • rare - insufficient secretion of TSH from pituitary.
23
Q

Iron deficiency hypothyroidism in children

A

If mother is pregnant with iodine deficiency or children are born iodine deficient, can cause mental retardation, and underdevelopment due to severe brain damage.
Does not usually occur in UK due to national screening at birth, and diet high in fish and plants.

24
Q

Oral manifestations of hyperthyroidism

A 
Increased caries
Periodontal disease
Presence of extraglandular thyroid tissue
Accelerated tooth eruption
Burning mouth syndrome
25
Q

Oral manifestations of hypothyroidism

A 
Salivary gland enlargement
Macroglossia (large tongue)
Glossitis (tongue inflammation)
Delayed tooth eruption
Compromised periodontal health
Dysgeusia (distortion of the sense of taste)

Y1 DRE Endocrine (7 decks)

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