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imed3004 > Thyroid Function > Flashcards

Thyroid Function Flashcards

1
Q

What are the anatomical features of the thyroid gland?

A

It wraps around the trachea

It is ~25 grams in adults (larger in females than males and increases in size with pregnancy)

2 large lateral lobes connected by a thin isthmus

Contains 4 parathyroid glands and receives very high blood flow.

Has an abundant supply of sympathetic and parasympathetic nerves

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2
Q

What does the thyroid gland have inside it?

A

Follicles with colloids surrounded by follicular cells and C cells on the outside of follicles (secrete calcitonin).

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3
Q

Where are Thyroid hormones synthesized?

A

In epithelial cells lining the follicle.

Follicle interior is filled with thyroglobulin (glycoprotein)

Each follicle is surrounded by a dense capillary network

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4
Q

What active hormones are produced from thyroglobulin?

A

Thyroxine (T4) [major secretory product that is not as active as T3 and it eventually transforms into T3]

Triiodothyronine (T3)

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5
Q

What are the 2 major components of thyroid hormone synthesis?

A
  1. Iodine: Thyroid hormone needs large amount of iodine.
  2. Thyroglobulin precursor (TGB): Thyroglobulin precursor is the major component for T3 and T4 synthesis. It is a big protein and is stored as colloid. It is made in follicle cells which is immediately exocytosed into follicle lumen.
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6
Q

How is iodine absorbed?

A

As iodide and oxidised to iodine. Thyroid glands have powerful iodide pumps to concentrate iodine within the thyroid gland.

This requires a lot of energy due to ATPase action.

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7
Q

What are the stages of thyroid hormone biosynthesis and secretion?

A

Iodine trapping

Oxidation of iodide

Synthesis of thyroglobulin

Iodination of tyrosine residues

Coupling of tyrosine residues (DIT +DIT = T4; MIT + DIT = T3)

Endocytosis and digestion of colloid

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8
Q

How does iodine trapping take place?

A

Using a Na/I symport pump - Pumps 2x Na, 1x I from plasma into follicle cell

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9
Q

How does iodide get oxidised?

A

Thyroid peroxidase oxidises iodide to iodine (I2) which is then transported into follicular lumen.

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10
Q

How is thyroglobulin synthesized?

A

In Golgi apparatus/ER and then secreted into lumen via exocytosis.

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11
Q

What is iodination?

A

Iodination of precursor to form mature thyroglobulin. During this stage either Diiodotyrosine is formed or Monoiodotyrosine.

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12
Q

What happens during coupling?

A

2 tyrosine residues are brought together to form mature hormones. DIT + DIT =T4 (90% of the time), MIT + DIT = T3 (10% of the time)

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13
Q

Why is colloid formed?

A

This allows large amounts of TH precursor to be stored so the body becomes independent of day to day availability of iodine

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14
Q

How are thyroid hormone precursors stored?

A

Tyrosine residues are bound to thyroglobulin which is a large carbohydrate that keeps them in the colloid.

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15
Q

How is thyroid hormone released?

A

When stimulated thyroglobulin is endocytosed. Endocytotic vesicles fuse with lysosomes.

Proteases then release T3 and T4 from TGB storage molecule

Thyroid hormone then migrates to the basal membrane to be exocytosed in circulation

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16
Q

How is thyroid hormone transported?

A

TBG (Thyroid Binding Globulin) (70%)

Transthyretin (10 - 15%)

Albumin (15 - 20%)

Free T3 (~0.03)

Free T4 (~0.3%)

It needs to be free to work

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17
Q

Why is most thyroid hormone in blood T4?

A

It has a longer half life (3.5 days for T3 vs 6.5 days for T4)

18
Q

How does thyroid hormone enter cells?

A

Via iodothyronine transporters:

Organic anion transporters (OATPs) are passive but probably involve ion exchange (not sure if it does)

Monocarboxylate transporter (MCT8/10) (This is an active transporter with powerful scavenging activity)

19
Q

How is T4 converted into T3?

A

Target cell deiodinase enzymes

20
Q

Where are TH receptors located?

A

They are ubiquitous

21
Q

How does thyroid hormone work?

A

Binds to intracellular nuclear receptor and regulates activity of specific genes which increase metabolic rate.

22
Q

What kinds of proteins does TH upregulate?

A

Na-K pump

gluconeogenic enzymes

Respiratory enzymes

Myosin heavy chain

Beta-adrenergic receptors

Many others

23
Q

What hormones and axis are involved in control of thyroid function?

A

Tonic basal release:

Hypothalamus -> TRH -> Anterior pituitary -> TSH -> thyroid gland -> T3 + T4 -> Systemic metabolic effects

Negative feedback:

T4 and T3 inhibit pituitary from releasing TSH.

T4 and T3 also inhibit hypothalamus from releasing TRH

Somatostatin inhibits TRH formation and can be produced in response to stress or starvation.

24
Q

What does TSH do?

A

Increases thyroid activity in 3 ways:

Increases hormone synthesis by increasing NIS iodide pump activity and thyroglobulin production

Increases thyroid hormone secretion by increasing vesicular uptake and exocytosis.

increases blood flow to the thyroid.

25
Q

What does TH do?

A

Increases metabolic rate and activity of growth hormone and adrenergic hormones. They maintain optimum metabolic rate by increasing or decreasing rate of synthesis of certain porteins within the cell.

26
Q

Why doesn’t the excess ATP production caused by thyroid hormone just get shut down by presence of too much ATP (Negative feedback)?

A

It is used to generate ion gradients by upregulating transporters such as Na+/K+-ATPase and SERCA pumps.

Uncoupled ADP phosphorylation in the mitochondria: TH induces uncoupling protein expression so protons are pumped but they leak back out.

27
Q

How does TH affect CHO, Lipid, and Nitrogen metabolism?

A

CHO metabolism: Accelerates T3 use by increasing GIT glucose absorption and oxidation in the liver, fat, and muscle cells. T3 acts by increasing the synthesis of specific metabolic enzymes. In the liver it increases lipid and glycogen breakdown.

Lipid metabolism: Optimal TH levels determine rates of lipolysis and lipgenesis in the liver and stimulates mobilisation of fat cells.

Nitrogen metabolism increases rate of protein synthesis and degradation is TH dependent.

28
Q

What sensory afferent connections does the hypothalamus receive?

A

Somatic and visceral information

Olfactory information (smell of food)

Emotional/olfactory (amygaloid nucleus)

Hippocampal input via fornix - mammillary body.

Cerebral cortex

29
Q

How does TH affect the skeletal system?

A

T3 acts synergistically with GH, IGF, and other growth factors to signal increased bone formation and maturation (closure of epiphyses)

30
Q

How does TH affect CNS?

A

TH is essential for normal brain development. (Low TH in pregnancy affects foetal brain development)

Low adult TH reduces neuroplasticity

Foetal H-P-T reaches full functionality between 11 - 18 weeks GA. (reduces problems caused by maternal hypothyroidism)

31
Q

What happens in hypothyroidism (eg Hashimoto’s disease)?

A

Lack of energy

Fatty acid mobilisation decreases leading to increased body weight

Decreased sensory capacity, impaired memory and psychosis may occur

Poor tolerance of cold

Oedema (fluid retained due to hyaluronic acid and condroitin sulfate: myxoedema)

32
Q

What are the symptoms of TH deficiency in children?

A

Short stature, mental and physical retardation (severe hypothyroidism), bone retardation, malformed facial bone structure.

33
Q

How can hypothyroidism in children be treated?

A

By using exogenous thyroxine

34
Q

What are the symptoms of hypothyroidism due to iodine deficiency?

A

Goiter, due to lots of precursors acting on the thyroid.

35
Q

What other conditions can cause hypothyroidism?

A

Deiodinase deficiency (cells can’t convert T4 -> T3

Severe selenium deficiency (deiodinases are selenoproteins)

Allan-Herndon-Dudley syndrome (MCT8 mutations so cells can’t actively take up TH.

36
Q

What are the primary problems caused by Allan-Herndon-Dudley syndrome?

A

Particularly affects CNS resulting in severe intellectual impairment, aphasia, and ataxia

Highly limited IQ, patients may never talk/walk and 50% need a feeding tube despite having normal lifespan.

37
Q

What causes hyperthyroidism?

A

Overproduction of THs this is known as Grave’s disease

38
Q

What are the symptoms of hyperthyroidism?

A

Poor heat tolerance (higher BMR)

Muscle wasting (Higher catabolism)

FA mobilisation

Exaggerated autonomic responses (Higher CO, HR, and contractility)

Goiter

Bone age prematurely advanced

Exophthalmos: Oedematous fluid retention behind the eyes causing them to bulge.

39
Q

What causes hyperthyroidism?

A

Autoimmune hyperthyroidism (production of thyroid stimulating immunoglobulins that bind to TSH receptor to directly activate TSH receptors increasing TH production.

40
Q

How is hyperthyroidism treated?

A

Antithyroid drugs (carbimazole and methimazole which block I2 coupling)

Beta-blockers

Surgery, radioiodine

41
Q

What happens to T3, T4, TRH, and TSH in hyperthyroidism?

A

T3 and T4 are elevated

TRH and TSH are reduced

42
Q

What sensory afferent connections does the hypothalamus receive?

A

Somatic and visceral information

Olfactory information (smell of food)

imed3004 (50 decks)

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