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PT4023 CA1 > L6 Thyroid Hormones 1 > Flashcards

L6 Thyroid Hormones 1 Flashcards

1
Q

What hormones are produced by the thyroid follicle?

A

The iodothyronine hormones thyroxine (T4) and 3, 5, 3’-triiodothyronine (T3)

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2
Q

Role of T4 and T3 hormones

A
  • essential for normal growth and development
  • play an important role in energy metabolism
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3
Q

What happens when thyroid hormones are synthesised?

A

They are then stored as amino acid residues of thyroglobulin, a protein constituting the vast majority of the thyroid follicular colloid

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4
Q

What makes the thyroid a unique gland?

A

It has the ability to store great quantities of potential hormone as amino acid residues of thyroglobulin

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5
Q

How does the hypothalamus control T3 and T4 hormones?

A
  • TRH is produced by the hypothalamus
  • TRH stimulates the pituitary gland via the portal system
  • This stimulates TSH production
  • TSH acts directly on the thyroid, causing production of both T3 & T4
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6
Q

Role of thyroperoxidase (TPO)

A

TPO catalyses the iodination of thyroxine residues, and the coupling of iodothyronines to form either T3 or T4

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7
Q

How do anti-thyroid drugs work?

A

By blocking the iodination of thyroglobulin, which will prevent the production of T3 and T4. Anti-thyroids have direct effects on individual cells within the endocrine gland to prevent the production of their effector hormones.

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8
Q

What enzymes are used as substrates for conversion of thyroid hormones?

A

Deiodinase enzymes (D1, D2 & D3)
- associated with specific tissues
- each have very distinct actions

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9
Q

Which deiodinase enzymes are decreased in hypothyroidism?

A

D1 and D3
(D2 is increased)

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10
Q

Which deiodinase enzyme is responsible for T3 degradation?

A

D3

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11
Q

Quantity of thyroid hormone per litre in the thyroid pool

A

~8000µg

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12
Q

What is hypothyroidism?

A

A clinical syndrome resulting from a deficiency of thyroid hormones, which results in widespread organ-specific effects

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13
Q

Hypothyroidism in infants/children is characterised by?

A

marked slowing of growth and development, with serious permanent consequences, including mental retardation and short stature

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14
Q

Hypothyroidism with onset in adulthood leads to?

A
  • diminished calorigenesis and oxygen consumption
  • impaired cardiac, pulmonary, renal, GI & neurological functions
  • deposition of glycosaminoglycans in intracellular spaces (particularly in skin & muscle)
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15
Q

What is myxedema?

A

Occurs in extreme cases of hypothyroidism - patients exhibit multiple organ abnormalities and progressive mental deterioration, skin appears very swollen and puffy

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16
Q

Classification of hypothyroidism

A
  1. Primary (most common)
  2. Secondary (pituitary TSH deficiency)
  3. Tertiary (hypothalamic TRH deficiency)
  4. Peripheral thyroid hormone resistance
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17
Q

Most characteristic pathological finding of hypothyroidism

A

the accumulation of glycosaminoglycans, mostly hyaluronic acid, in interstital fluids

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18
Q

What causes the accumulation of glycosaminoglycans, and what does it lead to?

A

The accumulation is due to decreased metabolism of glycosaminoglycans. The accumulation of this hydrophilic substance and the increased capillary permeability to albumin leads to interstitial non-pitting oedema in the skin, heart muscle and striated muscle.

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19
Q

What term is applied to newborn infants with hypothyroidism, and what is it characterised by?

A

‘Cretinism’
Severe iodine deficiency, mental retardation, short stature, characteristic puffy appearance of face & hands, frequently deaf mutism

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20
Q

Possible causes of neonatal hypothyroidism

A
  • spontaneous
  • exposure during pregnancy to iodides
  • anti-thyroid drugs given to the mother
  • inadvertent administration of radioactive iodine for thyrotoxicosis or thyroid cancer
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21
Q

Signs of neonatal hypothyroidism

A

respiratory difficulty, cyanosis, jaundice, poor feeding, hoarse cry, umbilical hernia, marked retardation of bone maturation

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22
Q

Hypothyroidism in children and adolescents is characterised by?

A

retarded growth and short stature

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23
Q

Common features of hypothyroidism in adults

A

easy fatiguability, cold sensitivity, weight gain, constipation, menstrual abnormalities (especially menorrhagia), muscle cramps

24
Q

Physical findings of hypothyroidism in adults

A
  • cool, rough, dry skin
  • puffy face and hands
  • hoarse, husky voice
  • slow reflexes
25
Q

Cardiovascular signs of hypothyroidism

A
  • impaired ventricular contraction
  • bradycardia
  • increased peripheral resistance
  • diminished cardiac output
  • low voltage of QRS complexes and P and T waves
  • cardiac enlargement (due in part to interstitial oedema)
26
Q

What is often seen in patients with myxedema coma?

A

respiratory failure

27
Q

What can occur as a result of slowed peristalsis in hypotension?

A

chronic constipation and occasionally severe faecal impaction in ileus

28
Q

What can occur as a result of impaired renal function and decreased GFR in hypothyroidism?

A

impaired ability to excrete a water load, which predisposes the patient to hyponatremia, particularly from water intoxication if excessive free water is administered

29
Q

4 mechanisms that may contribute to anaemia in patients with hypothyroidism

A
  1. Impaired haemoglobin synthesis as a result of T4 deficiency
  2. Increased iron loss with menorrhagia, as well as impaired intestinal absorption of iron
  3. Folate deficiency
  4. Pernicious anaemia, with vitamin B12-deficient megaloblastic anaemia
30
Q

How does hypothyroidism affect the reproductive system?

A
  • impairs the conversion of oestrogen precursors to oestrogens, resulting in altered FSH & LH secretion, which can lead to anovulatory cycles and infertility
  • associated with menorrhagia
  • men may have decreased libido and erectile dysfunction
31
Q

Low serum FT4 and high serum TSH indicates?

A

primary hypothyroidism

32
Q

Low serum FT4 and normal/low serum TSH indicates?

A

secondary hypothyroidism

33
Q

How is hypothyroidism treated?

A

with T4
Levothyroxine is one of the most common synthetic T4 hormones

34
Q

What is the advantage of administering T4 in hypothyroidism?

A

T4 is converted to T3 in peripheral tissues. Therefore, by giving T4 you have both hormones available even though only one is being administered.

35
Q

What is the dose of levothyroxine based on?

A

The age of the patient. In a developing child, much higher levels of thyroxine are vital.

36
Q

Effects of levothyroxine

A
  • increases metabolic rate
  • decreases TSH production from anterior pituitary
  • converted to T3 in peripheral tissues
  • replaces thyroid hormones in hypothyroidism
37
Q

Is T3 or T4 more potent?

A

T3 is four times more potent than T4

38
Q

Levothyroxine interactions

A

aluminium hydroxide, calcium supplements, cholestyramine, ferrous sulphate and sucralfate - all alter the rate of absorption of levothyroxine

39
Q

What is the major toxic effect of T4 therapy?

A

Overdose - patients then can switch from having the symptoms & signs of hypothyroidism to hyperthyroidism e.g. palpitations & arrhythmias

40
Q

How do you correct an overdose of synthetic T4?

A

by omitting the daily dose of T4 for about 3 days

41
Q

What is thyrotoxicosis?

A

A clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormones (toxicity of thyroid hormones). It results in a generalised acceleration of metabolic processes.

42
Q

What causes most cases of thyrotoxicosis?

A

Hyperthyroidism

43
Q

What is the most common presentation of thyrotoxicosis/hyperthyroidism?

A

Grave’s disease (diffuse toxic goitre)

44
Q

What is known as Plummer disease?

A

Toxic adenoma

45
Q

What is Grave’s disease characterised by?

A

an increase in T3 and T4 production

46
Q

Why is Grave’s disease often considered an immune disorder?

A

TSH receptor antibodies will bind to TSH receptors, producing B cells with TSH receptor antibodies. These T cells multiply, and there is a genetic lack of suppressor T cells.

47
Q

Why are significant ophthalmology presentations often associated with Grave’s disease?

A

TSH-R Abs can bind to receptors in the retro-orbital connective tissue, stimulating inflammatory cytokine production, which causes accumulation of glycosaminoglycans and swelling in the muscle & CT located behind the eyes

48
Q

How is hyperthyroidism treated?

A
  • anti-thyroid drugs (thioamides)
  • radioiodine treatment (Iodine-131)
49
Q

Examples of thioamides

A

Carbimazole
Methimazole
Propylthiouracil

50
Q

How do thioamides work?

A
  • inhibit iodination of tyrosine-Tg
  • reduce deiodination of T4 to T3
  • immunosuppressive effects in Grave’s disease
51
Q

Most common adverse effect of thioamides

A

agranulocytosis (granulocyte count can be less than 250/µl)
(benign leukopenia is also observed)

52
Q

Radioiodine treatment is contraindicated in?

A

children and pregnant women

53
Q

What is a toxic adenoma?

A

A functioning adenoma which hypersecretes both T3 and T4 hormones, causing significant hyperthyroidism

54
Q

Toxic adenoma gradually suppresses __ secretion.

A

endogenous TSH

55
Q

Treatment for toxic adenoma

A

Mainly radioiodine therapy (in doses of 20-30 mCi) or surgery, as opposed to purely anti-thyroid drugs

56
Q

When is surgery for toxic adenoma considered?

A

if the nodule is very large and causing symptoms such as dysphagia, neck pressure or difficulty breathing

57
Q

High FT4 and low TSH suggests?

A

hyperthyroidism

PT4023 CA1 (8 decks)

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