Clinical Flashcards

1
Q

Describe the anatomy of the thyroid gland? Its shape, location and whether it is palpable or visible in life?

A

It is a butterfly shaped organ which lies across the trachea at the base of the larynx.

It is neither visible nor palpable in health.

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2
Q

What two cell types are present in the thyroid gland?

A
  1. C (clear) cells which secrete calcitonin (Ca regulating hormone)
  2. Follicular cells which support thyroid hormone synthesis and surround hollow follicles
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3
Q

Describe the structure of thyroid follicles?

A

They are spherical structures whose walls are made of follicular cells.

The centre of the follicle is filled with colloid.

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4
Q

What is colloid composed of?

A

Sticky glycoprotein matrix.

It contains 2-3 months supply of TH.

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5
Q

What two things do the follicular cells make?

A
  1. The enzymes which make thyroid hormones

2. Thyroglobulin

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6
Q

What happens to the products of the follicular cells?

A

The enzymes and thyroglobulin are packaged into vesicles and exported from F cells to the colloid.

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7
Q

How does iodine get to the colloid and what happens when it does?

A

Follicular cells actively concentrate iodide from the plasma and transport it into the colloid where it combines with tyrosine residues to form thyroid hormones

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8
Q

Where is tyrosine derived?

A

From the diet.

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9
Q

How is iodide obtained by the body?

A

From the diet.

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10
Q

How does iodide enter the follicular cells from the plasma?

A

Through a NA+/I- transporter (symport).

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11
Q

Is the uptake of iodide by follicular cells with/against the concentration gradient?

A

Against the concentration gradient (via symport transporter).

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12
Q

How is iodide transported into the colloid?

A

Via the pendrin transporter.

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13
Q

What happens when iodide becomes iodine?

A

Loses an electron

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14
Q

What is formed when one iodine molecule is added to tyrosine residues on the thyroglobulin molecule?

A

Monoiodotyrosine (MIT)

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15
Q

What is formed when two iodine molecules are added to tyrosine residues on the thyroglobulin molecule?

A

Diiodotyrosine (DIT)

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16
Q

How is triiodothyronine or T3 formed?

A

Reaction between MIT and DIT.

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17
Q

How is tetraiodothyronine or thyroxine (T4) formed?

A

DIT + DIT

18
Q

What enzyme catalyses thyroid hormone synthesis and where is it located?

A

Thyroid peroxidase which is located in the apical membrane of the follicular cells.

19
Q

Are T3 and T4 lipid soluble or lipid insoluble?

A

Lipid soluble (so can pass follicular cell membrane into the plasma)

20
Q

What happens when TSH acts on the colloid?

A

Portions of the colloid are taken back into the follicular cells by endocytosis.

Within the cells they form vesicles which contain proteolytic enzymes that cut the thyroglobulin to release the thyroid hormones.

21
Q

What is the name of the main plasma protein which thyroid hormones bind to?

A

Thyroxine binding globulin

22
Q

Thyroxine binding globulin (TBG) has high affinity for T3 or T4?

A

T4 - so it is released slowly into plasma (longer half-life)

23
Q

Can bound hormones in the plasma exert an inhibitor effect on TSH and TRH?

A

No, only free hormone can.

24
Q

Which thyroid hormone is there more of (free and bound)

A

50x more T4 in plasma

25
Q

90% of which thyroid hormone binding to receptors inside cells?

A

T3 - TH receptor has a much higher affinity for T3 making it 3-5x more physiologically active

26
Q

Where is T4 deiodinated?

A

50% is deiodinated in plasma while the remaining is deiodinated in the target cells

27
Q

What are the effects of cold, exercise and pregnancy on TRH?

A

They increase the release of tropic hormones which act of TRH, which increases TSH release and thus increasing T3/T4 release.

28
Q

How does somatostatin inhibit the regulation of thyroid hormone release?

A

It inhibits TSH

29
Q

How do glucocorticoids inhibit the regulation of thyroid hormone release?

A

They inhibit TSH and the conversion of T4 to T3

30
Q

How do TH influence metabolic rate and thermogenesis?

A

Raises metabolic rate and promotes thermogenesis, typically through promoting futile cycles of simultaneous catabolism and anabolism

31
Q

What effect do TH have on gluconeogenesis and blood glucose?

A

Increased hepatic gluconeogenesis but no effect on BG providing the pancreas is releasing adequate insulin

32
Q

Why are TH critical for growth?

A

Lack of TH result in retarded growth (it stimulates GH receptor expression)

33
Q

Why is TH essential for brain development in utero?

A

Maternal iodine deficiency is found to cause congenital hypothyroidism/cretinism.

Although physical growth can be corrected after birth, mental growth and development can never be fully recovered.

34
Q

What are the main causes of hyperthyroidism?

A

Graves Disease (most common)

Thyroid adenoma (rare) = hormone-secreting thyroid tumour

35
Q

What is Grave’s disease?

A

Antibodies are produced that mimic TSH and continually activate the thyroid gland - increased release of TH switches off TSH release from the anterior pituitary so plasma [TSH] is very low – may have enlarged thyroid gland.

36
Q

What are the symptoms of hyperthyroidism

A
  1. Increased metabolic rate and heat production
  2. Increased protein catabolism
  3. Altered nervous system function
  4. Elevated CVS function (TH permissive to epinephrine)
37
Q

What are the main causes of hypothyroidism?

A
  1. Hashimoto’s Disease (autoimmune attack on thyroid gland)
  2. Deficiency in dietary iodine (only 50mg/year)
  3. Idiopathic
38
Q

What are the symptoms of hypothyroidism?

A
  1. Decreased metabolic rate and heat production
  2. Disrupted protein synthesis
  3. Altered nervous system function
  4. Reduced CVS function
39
Q

What is a Goitre and how is it caused?

A

Enlargement of the thyroid gland and is caused by increased trophic action of TSH on thyroid follicular cells (hypo) or over-activity due to Grave’s.

40
Q

Are hypothyroid and hyperthyroid primary or secondary endocrine disorders?

A

Both are primary (direct effect on endocrine gland producing end hormone)