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ACEM Primary Written > Endocrinology: Physiology - Thyroid gland > Flashcards

Endocrinology: Physiology - Thyroid gland Flashcards

1
Q

Two thyroid gland functions

A
  1. Secretion of thyroid hormones
  2. Secretion of calcitonin
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2
Q

Describe the anatomy of the thyroid gland

A

Two lobes separated by isthmus +/- pyramidal lobe arising from isthmus

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3
Q

Describe the difference in structure and appearance of the follicular thyroid when active vs inactive

A

Inactive: large follicles, abundant colloid, flat epithelial lining
Active: small follicles, “reabsorption lacunae” present where colloid draining from follicle, cuboidal or columnar epithelial lining

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4
Q

Which thyroid hormone is more abundant? Which has greater biologic activity?

A

T3 (triiodothyronine) produced in lesser amounts than T4 (thyroxine) but is more biologically active

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5
Q

What is the minimum daily intake of iodine required for normal thyroid function in adults?

A

150ug/day

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6
Q

What is the average daily iodine intake in adults in developed countries? How is this achieved?

A

500ug/day
Due to supplementation of table salt

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7
Q

Describe iodine metabolism (including specific values)

A

500ug ingested
120ug to thyroid -> 40ug to ECF, 80ug as T3 and T4
80ug as T3 and T4 received by liver and other tissues -> 60ug to ECF, 20ug to faeces as bile
480ug filtered and excreted by kidneys

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8
Q

How is iodine taken up by thyrocytes?

A

Taken up across basolateral membrane via Na+/I- symporter (NIS): this is a form of secondary active transport where energy is generated by Na+/K+ ATPase which pumps Na+ out to generate electrochemical gradient for inward movement

Then transported across apical membrane via Cl-/I- exchanger called pendrin

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9
Q

What is the effect of TSH on NIS expression?

A

Increases expression and retention in basolateral membrane

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10
Q

Describe the synthesis of thyroid hormones in thyrocytes

A

Iodine transported into colloid, then undergoes oxidation and incorporation into thyroglobulin via thyroid peroxidase
Produces monoiodotyrosine (MIT) and diiodotyrosine (DIT)
DIT + DIT -> T4
MIT + DIT -> T3
DIT + MIT -> RT3
Thyroid peroxidase also involved in the catalyse of these coupling reactions

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11
Q

What is the fate of MIT and DIT if not as thyroid hormones?

A

Deiodinated via iodotyrosine deiodinase
Iodine reutilised

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12
Q

What are the four functions of thyrocytes?

A
  1. Collect and transport iodine
  2. Synthesise and secrete (into colloid) thyroglobulin
  3. Generate thyroid hormones
  4. Remove thyroid hormones from thyroglobulin and secrete into circulation
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13
Q

Normal T4 level. How much of this is protein-bound?

A

8ug/dL (103nmol/L)
99.98% protein-bound, predominantly TBG

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14
Q

Normal T3 level. How much of this is protein-bound?

A

0.15ug/dL (2.3nmol/L)
99.8% protein-bound, predominantly TBG and some albumin

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15
Q

Which is more highly protein-bound: T3 or T4?

A

T4 (99.98% vs 99.8% for T3)

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16
Q

What feeds back to suppress TSH release?

A

Free thyroid hormones (not protein-bound)

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17
Q

What are the three plasma proteins that bind thyroid hormones? What are their respective half-lives?

A
  1. Albumin: t1/2 = 13 days
  2. Transthyretin (a prealbumin): t1/2 = 2 days
  3. Thyroxine-binding globulin (TBG): t1/2 = 5 days
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18
Q

Which of the plasma proteins has the highest capacity for binding thyroid hormone? Which has the highest affinity (and therefore carries the most)?

A

Highest capacity: albumin
Highest affinity: thyroid-binding globulin

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19
Q

List six factors which increase the concentration of thyroid-binding globulin

A
  1. Pregnancy
  2. Exogenous oestrogens
  3. Methadone
  4. Heroin
  5. Antipsychotics
  6. Clofibrate
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20
Q

List four factors which decrease the concentration of thyroid-binding globulin

A
  1. Glucocorticoids
  2. Androgens
  3. Danazol
  4. Asparaginase
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21
Q

List three drugs which inhibit T4 binding to TBG

A
  1. Phenytoin
  2. Salicylates
  3. 5-fluorouracil
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22
Q

What pattern of TBG concentration, total plasma thyroid hormone concentration, free thyroid hormone concentration, plasma TSH levels, and clinical state, is seen with:
a) hyperthyroidism
b) hypothyroidism
c) increased thyroid hormone binding proteins
d) decreased thyroid hormone binding proteins

A

a) normal, increased, increased, decreased, hyperthyroid
b) normal, decreased, decreased, increased, hypothyroid
c) increased, increased, normal, normal, euthyroid
d) decreased, decreased normal, normal, euthyroid

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23
Q

Why are patients with derangements in the concentration of thyroid hormone binding proteins usually euthyroid?

A

Levels of free thyroid hormones control TSH release: increased binding and therefore decreased free thyroid hormone leads to increased TSH release, which restores levels of free and thus active hormone (even if total concentration increased)

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24
Q

Describe the metabolism of thyroid hormones

A

T3 and T4 are deiodinated in the kidney, liver and other tissues by deiodinases (D1, D2 and D3)
Catabolises hormones but also increases local concentration of T3 which is the primary physiologic mediator

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25
Q

Which of the deiodinases is the primary deiodinase responsible for conversion of T4 to T3 in the periphery?

A

D1

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26
Q

What % of circulating T4 is converted to T3 in the periphery? What % is converted to RT3?

A

1/3 to T3
45% to RT3

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27
Q

What % of circulating T3 is secreted by the thyroid and what % is formed by deiodination in the periphery?

A

13% secreted from thyroid
87% from T4 in periphery

28
Q

What tissues have high T3/T4 ratios?

A

Pituitary
Cerebral cortex

29
Q

What is the difference in composition of circulating thyroid hormones during fetal life compared with adulthood? When does this change?

A

Relatively more RT3 and less T3
Ratio shifts ~6/52 post birth

30
Q

List 8 states which suppress deiodinases (thereby decreasing T3 +/- increasing RT3)

A
  1. Selenium deficiency
  2. Burns, trauma
  3. Advanced cancer
  4. Cirrhosis
  5. CKD
  6. MI
  7. Fever
  8. Starvation
31
Q

Describe the structure of TSH. What does it resemble and what is the clinical significance of this?

A

Alpha and beta subunits
Alpha subunit identical to that of LH, FSH and hCG
hCG-secreting placental tumours can cause mild hyperthyroidism

32
Q

What is the half-life of TSH?

A

60mins

33
Q

Describe the pulsatile secretion pattern of TSH

A

Peaks at midnight
Declines throughout the day

34
Q

What is the effect of longterm TSH on thyrocytes and thyroid overall?

A

Induces hypertrophy of thyrocytes
May result in goitre

35
Q

List five factors which decrease TSH secretion

A
  1. Free T3, T4
  2. Stress
  3. Glucocorticoids
  4. Somatostatin
  5. Dopamine
36
Q

Describe the regulation of thyroid hormone secretion in brief

A

Thyrotropin-releasing hormone stimulates release of thyroid stimulating hormone
TSH increases thyroid hormone production and release
Free thyroid hormones provide negative feedback to the pituitary to decrease TSH secretion

37
Q

How do thyroid hormones exert their effects on a cellular level?

A

Enter cell and bind to thyroid receptor in nucleus (T3 binds more avidly than T4)
Hormone-receptor complex then binds to DNA via zinc fingers and induces expression of specific genes

38
Q

How many more times potent than T4 is T3?

A

3-5x

39
Q

Describe the physiologic effects of thyroid hormones on the heart and how these are mediated

A

Positive chronotropy and inotropy via three mechanisms:
1. Increased expression of B-adrenergic receptors
2. Increased response to circulating catecholamines
3. Increased a-myosin heavy chain (higher ATPase activity)

40
Q

Describe the physiologic effects of thyroid hormones on adipose tissue

A

Increased lipolysis

41
Q

Describe the physiologic effects of thyroid hormones on muscle

A

Increased protein breakdown -> thyrotoxic myopathy
Also results in increased K+ in urine

42
Q

Describe the physiologic effects of thyroid hormones on bone

A

Promotes normal growth and skeletal development

43
Q

Describe the physiologic effects of thyroid hormones on the nervous system

A

Promotes normal brain development

44
Q

Describe the physiologic effects of thyroid hormones on the gut

A

Increased carbohydrate absorption

45
Q

Describe the physiologic effects of thyroid hormones on lipoprotein

A

Increased expression of LDL receptors in liver -> decreased circulating cholesterol

46
Q

Describe the physiologic effects of thyroid hormones on metabolism generally

A

Increased BMR
Increased O2 consumption by most metabolically active tissues
Increased Na+/K+ ATPase activity in many tissues
May precipitate vitamin deficiencies due to increased requirement

47
Q

Which metabolically active tissues do not increase O2 consumption in response to thyroid hormones?

A

Testes
Uterus
Lymph nodes
Spleen
Anterior pituitary (may slightly decrease consumption due to negative feedback on TSH production/release)

48
Q

What is the syndrome of congenital hypothyroidism also called and what are the two main features?

A

Cretinism
Results in dwarfism and mental retardation

49
Q

List five causes of congenital hypothyroidism

A
  1. Maternal iodine deficiency
  2. Fetal thyroid dysgenesis
  3. Inborn errors of thyroid hormone synthesis
  4. Maternal antithyroid antibodies
  5. Fetal hypopituitary hypothyroidism
50
Q

What are the two broad classifications (and sub-classifications) of hypothyroidism causes in adults? Which of these are responsive to TSH?

A
  1. Primary thyroid disease
  2. Secondary hypothyroidism:
    - Pituitary hypothyroidism*
    - Hypothalamic hypothyroidism*
  • responsive to TSH
51
Q

What level of iodine intake will produce hypothyroidism?

A

<50ug/day

52
Q

What causes goitre: hypothyroidism or hyperthyroidism?

A

Both can cause
E.g. iodine deficiency goitre or goitre with other primary hypothyroidism (increased circulating TSH), Graves disease hyperthyroidism

53
Q

What is the most common cause of hyperthyroidism and what % of cases does this represent?

A

Graves’ disease
60-80% of cases

54
Q

Is Graves’ disease more common in men or women?

A

Women

55
Q

What is the underlying pathophysiology of Graves’ disease?

A

Due to presence of anti-TSH-R antibodies which cause activation of the receptor thereby increasing free T3 and T4 (and decreasing TSH levels due to negative feedback)

56
Q

What is the hallmark clinical feature of Graves’ disease: in what % of cases does it occur?

A

Exophthalmus, which can precede other features of hyperthyroidism
Seen in 50% of patients with Graves’ disease

57
Q

What Abs may be seen in Graves’ disease?

A

Anti-TSH-R (primarily)
Anti-thyroglobulin
Anti-thyroid peroxidase (anti-TPO)

58
Q

Does Hashimoto’s thyroiditis cause hyperthyroidism or hypothyroidism?

A

Causes initial transient hyperthyroidism due to inflammation of gland
Later causes hypothyroidism due to destruction of gland by antibodies (classically anti-TPO) and cytotoxic T cells

59
Q

How might hyperthyroidism be treated?

A
  1. Drugs: thioureylenes (e.g. prophylthiouracil, methimazole)
  2. Radioactive iodine
  3. Surgery
60
Q

How does propylthiouracil work?

A

Competitively inhibits MIT iodination and blocks coupling reaction
D2 deiodinase inhibitor

61
Q

Nine clinical features of hypothyroidism

A
  1. Myxoedema (non-pitting oedema of skin)
  2. Decreased BMR (40%)
  3. Coarse, sparse hair
  4. Dry skin
  5. Carotenaemia
  6. Muscle weakness
  7. Cold intolerance
  8. Slow mentation, poor memory
  9. Increased cholesterol
62
Q

What % of normal BMR may be seen in hypothyroidism vs hyperthyroidism?

A

Hypothyroidism: 40%
Hyperthyroidism: +10% to +100%

63
Q

Nine clinical features of hyperthyroidism

A
  1. Weight loss
  2. Polyphagia
  3. Increased BMR (110-200%)
  4. Fine tremor
  5. Warm, soft skin
  6. Muscle weakness
  7. Heat intolerance
  8. Nervousness
  9. Increased pulse pressure
64
Q

Describe the Wolff-Chaikoff effect

A

Large doses of iodine act directly on thyroid to cause, mild transient inhibition of organic iodine binding and therefore thyroid hormone synthesis

65
Q

List six causes of hyperthyroidism due to thyroid overactivity, and two extrathyroidal causes

A

Thyroid overactivity:
1. Graves’ disease
2. Solitary toxic adenoma
3. Toxic multinodular goitre
4. Early Hashimoto’s
5. TSH-secreting pituitary tumour
6. Mutations causing constitutive activation of TSH-R

Extrathyroidal:
1. T3/T4 administration
2. Ectopic thyroid tissue

ACEM Primary Written (160 decks)

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