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Flashcards in SPR L1 Thyroid Hormone Deck (30):
1

Thyroid Function - Human Structure and Function 1

Learning Outcomes

  • Outline the steps in the manufacture of thyroid hormones
  • Describe the structural and functional differences between T3 and T4
  • Outline the cellular mechanisms of action of T3 and T4
  • Explain how the hypothalamus and pituitary regulate circulating levels of thyroid hormones
  • Describe how thyroid hormones are transported in the plasma
  • Describe the metabolic effects of thyroid hormones
  • Describe the systemic effects of thyroid hormones
  • Relate the normal effects of thyroid hormones to the abnormalities seen with deficient and excess production

2

Where is the thyroid gland located?

Inferior to the larynx and superior to the trachea

Isthmus joins the two lobes

Brown because of the iodine necessary for thyroid hormone

Lumpy because of the lobes

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3

What is the thyroid gland made up of, and what are these filled with?

What are these lined by?

What other types of cells are present?

Comprised of lobules of spherical follicles that are filled with colloid

Lined by cubboidal epithelial cells

C cell / parafollicular cell - these produce calcitonin

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4

What is the primary constituent of colloid?

Thyroglobulin

 

2-3 month supply of thyroid hormone within the colloid within follicle within lobule within lobe

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5

What are the thyroid hormones?

T3 and T4

 

Tyrosine residues incorporated – means that these are AMINE hormones

6

What are the basic 'ingredients' for thyroid hormone synthesis?

tyrosine & iodine

 

(can't make iodine in the body - can get it from shellfish etc)

Salt is ionised to make sure thyroid hormone can be produced

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7

Outline the steps in the synthesis of T4 and T3

I  +  tyrosine => monoiodotyrosine (MIT)

MIT  +  I => diiodotyrosine (DIT)

DIT  +  DIT => thryoxine(T4)

DIT  +  MIT => triiodothyronine (T3)

8

Outline the steps in the synthesis and secretion of thyroid hormone

  1. Iodine is cotransported with Na+ from the capillary
  2. Diffusion across the follicle cell
  3. Iodine is oxidised and attached to rings of tyrosines in thyroglobulin (in the lumen of the follicle - colloid) Iodising agent HYDROGEN PEROXIDE. Enzyme catalysing oxidation of iodide to iodine = thyroid peroxidase. 
  4. The iodinated ring of one MIT or DIT is added to a DIT at another spot (in the lumen of the follicle- colloid)
  5. Endocytosis of thyroglobulin contains T3 and T4
  6. Lysosomal enzymes release T3 and T4 from TG
  7. T3 and T4 moves back out into the interstitial fluid

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9

What does T4 need to be converted into to exert its full biological activity?

What percentage is T4?

T3

90%

10

Give examples of organs that have cells with their own deiodinases

Liver and Kidney

11

How is T3 and T4 transported in the blood?

What is it bound to?

 

  1. What is the majority of T4 bound to?
  2. What is the majority of T3 bound to?

Almost 100% is bound - 0.02% isn't, but can still carry out a lot of biological effects

Thyroid Binding Globulin TBG

Thyroid Binding Prealbumin TBPA

Thyroid Binding Albumin TBA

  1. TBG
  2. TBA

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12

Intracellular Actions of Thyroid Hormones

Outline these

Increases the number of mitochondria and their efficiency 

 

Then also binds to nuclear receptors. Protein synthesis, enzyme activity altered. (increased sodium potassium ATPases). Acts like steroid hormones through Hormone Receptor Complex. Can exert genomic effects and non-genomic effects.

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13

Thyroid hormones affect all cells in the body - describe the metabolic actions of T3 and T4.

 

  • Increase O2 consumption - increased mitochondria
  • Increase BMR
  • Calorigenic effect
  • Carbohydrate metabolism:
    • increased absorption of glucose from GIT, increased insulin secretion, increased gluconeogenesis
    • glucose oxidation, glycogen degradation (hypersecretion)
  • Lipid metabolism:
    • lipolysis - increases circulating FFA levels, accelerates FFA oxidation
    • decrease cholesterol, triglycerides & phospholipids in plasma (hypersecretion)
  • Protein metabolism:
    • protein synthesis
    • breakdown (hypersecretion)

Na K ATPase is increased

14

Systemic effects of Thyroid Hormones

Give examples of how the following are effected 

  1. Heart
  2. Lungs
  3. GIT
  4. Reproductive 
  5. Musculoskeletal 
  6. Nervous System

  1. increase HR, CO, SBP and decrease DBP

    Increased blood flow to skin 

  2. increase ventilation rate 

  3. Increases appetite

    Increases secretion digestive juices

    Increases GIT motility

  4. Essential for normal reproduction and lactation

  5. promotes normal body growth and maturation of skeleton

    promotes normal function and development of muscles

  6. promotes normal neuronal development in feotus and infant (developmental)

    promotes normal neuronal function in adult - increases synaptic activity

    enhances effects of sympathetic nervous system – sympathomimetic: upregulates B1 adrenergic R in heartR

15

What regulates circulating levels of thyroid hormones?

The Hypothalamus and Pituitary

 

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16

The hypothalamus & pituitary regulate circulating levels of thyroid hormones

  1. What are the inputs?
    1. Negative
    2. Positive
  2. Where do they act?
  3. What does the Hypothalamus release?
  4. What does the ANT Pituitary Release?
  5. What does the Thyroid Gland release?
  6. What is the effect of T3 and T4?
  7. What does increased levels of T3 and T4 in the blood cause?

  1. Inputs
    1. Stress - less TH in blood to reduce stress on heart
    2. Cold
  2. Upon the hypothalamus
  3. TRH
  4. TSH
  5. T3 and T4
  6. Increase BMR, protein synthesis, and sympathetic tone
  7.  Negative feedback loop

17

TSH action on the thyroid gland  

What actions does TSH have on..,

  1. Iodide trapping and binding
  2. T3 and T4 Synthesis
  3. Thyroglobulin secretion into colloid
  4. Colloid endocytosis into follicular cells
  5. Size and Number of Follicular Cells
  6. Blood Flow at Thyroid

  1. Increase
  2. Stimulation
  3. Promotion
  4. Promotion
  5. Increased
  6. Increase

18

What are the actions of TSH on the Thyroid Gland?

  • Increase in iodide trapping and binding
  • Stimulation of T3 and T4 synthesis
  • Promotion of thyroglobulin secretion into colloid
  • Promotion of colloid endocytosis into follicular cells
  • Increased size and number of follicular cells
  • Increase in blood flow at thyroid

19

Abnormalities of Thyroid Function

Hypothyroidism

  1. What is Primary Hypothyroidism?
  2. What is Secondary Hypothyroidism?
  3. What is Tertiary Hypothyroidism?

  1. problem within the thyroid gland itself - failure of thyroid gland to respond to TSH

  2. deficient TSH production ​- thyroid atrophy

  3. deficient TSH production due to deficient TRH secretion

20

Abnormalities of Thyroid Function

Primary Hypothyroidism

  1. What is it?
  2. Give 4 causes
  3. What are the TSH levels as a result, and why?
  4. What happens to the thyroid gland itself?

  1. problem within the thyroid gland - failure of thyroid gland to respond to TSH

  2. Thyroiditis eg. Hashimoto’s Disease => targets thyroid peroxidase enzyme and the thyroglobulin itself. (Autoimmune disease)

    Severe iodide deficiency

    Severe deficiency of one or more synthesis enzymes

    Removal or destruction of thyroid gland

  3. Elevated TSH levels – reduced negative feedback

  4. Thyroid enlarges – goitre formation

21

Developmental consequences of hypothyroidism

Give two examples

  • Congenital Hypothyroidism
    • early diagnosis is essential - blood tests for all newborns
  • Adult Cretinism
    • Brain, bone and other development

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22

Hyperthyroidism or thyrotoxicosis

What are the three main causes?

 

What is the commonest cause?

  1. Autoimmune disease – Grave’s Disease

  2. Thyroid adenoma

  3. Inappropriate TSH secretion (rare)

 

Grave's Disease

23

What is the commonest cause of hyperthyroidism?

Grave's Disease

24

Outline the Pathogenesis of Grave's Disease

Antibody Producing Cells

Thyroid Stimulating Antibodies

THYROID

Excess T3 and T4 (and very low TSH via feedback to the pituitary) 

Hyperthyroidism

25

Give two key clinical features of Grave's Disease

Toxic Goitre

Exophthalmos

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26

Give signs and symptoms of Hyperthyroidism: increased T3 and T4 secretion

 

  • Increased BMR
  • Weight Loss with good appetite
  • Anxiety, physical restlessness, mental excitability
  • Hair loss
  • Tachycardia, palpitations, AF
  • Warm sweaty skin, heat intolerance
  • Diarhoea
  • Exopthalamos in Grave's Disease (MPS behind eyes)
  • Fast tendon reflexes
  • Muscle weakness
  • Fine tremor
  • Eye staring - eyelids up
  • UNTREATED = Thyrotoxic storm - high temperature

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27

Give signs and symptoms of Hypothyroidism: decreased T3 and T4 secretion

  • Decreased BMR
  • Weight gain, anorexia 
  • Depression, psychosis, mental slowness, lethargy 
  • Dry skin, brittle hair
  • Bradycardia
  • Cold skin, prone to hypothermia
  • Constipation
  • Slow tendon reflexes
  • Muscle weakness
  • Muscle stiffness
  • Voice deep and slow
  • UNTREATED = Myxoedema Coma - Hypothermia

28

What is a sign of untreated

  1. Hyperthyroidism?
  2. Hypothyroidism?

  1. THYROTOXIC STORM - High temperature

  2. MYXOEDEMA COMA – Hypothermia

29

The hypothalamic-pituitary thyroidal axis is affected by thyroid disorders

Outline how release rate of T4, TSH and TRH are affected in the following:

  1. Primary Hypothyroidism
  2. Pituitary Hypothyroidism (2ry)
  3. Hypothalamic Hypothyroidism (3ry)
  4. Grave's Disease

  1. Decreased, Increased, Increased
  2. Decreased, Decreased, Increased
  3. Decreased, Decreased, Decreased
  4. Increased, Decreased, Decreased

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30

Why is this knowledge important for dentists?

Oral Manifestations of Thyroid Gland Disorders are common

Hyperthyroidism: We must restrict the use of adrenaline and avoid severe stress situations and the spread of infectious foci. In patients treated with propylthiouracil, a complete blood count is usually recommended. NSAIDs and aspirin should be used with caution. Treatment should be discontinued if signs or symptoms of a thyrotoxic crisis develop

Hypothyroidism: a complete blood count before performing dental treatment is recommended. We must restrict the use of adrenaline and avoid oral infection and central nervous depressant drugs. We should know the drug interactions of thyroxine. If myxedematous coma develops, we will only carry out emergency dental treatment.

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