case 9 - thyroid gland and thyroid hormone Flashcards

1
Q

where is TRH released from

A

the hypothalamus and acts on the anterior pituitary

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2
Q

what does the anterior pituitary then release

A

TSH from the anterior pituitary

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3
Q

what does this TSH do

A

it activates the thyroid - T3 and T4 secretion

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4
Q

what is thyroid hormone formed from

A

sequential iodination of tyrosine

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5
Q

what is thyroid hormone stored as in the thyroid gland

A

colloid

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6
Q

what is T4 produced by

A

entirely by the thyroid

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7
Q

what is T3 produced by

A

partially by the thyroid, however peripheral T4 mono-deiodination in the liver and kidney make it metabolically active??

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8
Q

what is the half life of T3 and T4

A

half life of T3 is 1-3 days and half life of T4 is 5-7 days

T3 has to be given three times daily, T4 once daily

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9
Q

what does TR do

A

acts in the nucleus on gene expression, therefore thyroid hormone effects are slow

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9
Q

what does TR do

A

acts in the nucleus on gene expression, therefore thyroid hormone effects are slow

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10
Q

what is the HPT axis regulated according to

A

the principles of negative feedback; for primary thyroid disorders, TSH indicates thyroid status - a biomarker

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11
Q

what is a goitre

A

an enlarged thyroid gland

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12
Q

what is the active form of thyroid hormone

A

T3

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13
Q

where does T4 get converted

A

in the peripheral tossues

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14
Q

what does T3 do

A

regulates gene expression - for it to have effect it has to get into the cell and turn genes on - it is a slow process

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15
Q

what is the aetiology of primary hypothyroidism

A

autoimmune thyroiditis (Hashimoto disease)
4.1/1000 females; o.6/1000 males per year over 20 years, increasing
5% of over 60s
Classic Hashimoto (goitrous)
Atrophic (non-goitrous)
In reality, a mix of antibody mediated/ T cell mediated
TPO, TSHR, Tg auto-antibodies - most important one is TSH

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16
Q

what drugs can cause hypothyroidism

A

drugs (amiodarone, iodides, lithium) - these can cause hypothyroidism

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17
Q

what is the aiteology of secondary hypothyroidsm

A

pituitary adenoma, congenital deficiency, irradiation
Sarcoid, infection

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18
Q

what are the symptoms and signs of hypothyroidism

A

insidious
Weight gain
Cold intolerance, particularly at extremities
Fatigue, leathery
Depression
Mentally slowed, dull, expressionless
Coarse skin, puffy, (possible carpal tunnel syndrome) - aminoglycans
Dry, brittle, thinning hair
Hoarse voice
Constipation, faecal loading
Menstrual disturbance
Muscle stiffness, cramps, slow-relaxing reflexes
Generalised weakness and paraethesias
Cerebellar ataxia
Bradycardia
Macroglossia

family history
History of other autoimmune disorders

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19
Q

what are some examples of organ-specific autoimmune diseases that increase the risk

A

graves disease
Autoimmune hypothyroidism
Pernicious anaemia

Addison disease
Autoimmune atrophic gastritis
Type 1 diabetes mellitus

20
Q

what does pernicious anaemia arise from

A

arises from autoimmune destruction of the parietal cells, loss of intrinsic factor secretion and consequently vitamin B12 deficiency

21
Q

what are the investigations done

A

blood tests
(TFTs)
Normochromic normocytic anaemia
Macrocytosis (also to do with B12 deficiency), mixed dyslipidaemia
Consider other autoimmune endocrinopathies
Adrenal, ovary, T1DM, pernicious anaemia, vitiligo
no need for an ultrasound scan

22
Q

what is the treatment for hypothyroidism

A

once daily thyroxine, lifelong, usually 100 mcg; young, rapid start; elderly, gentle increment
Goal; normalise TSH, repeat blood tests after 4-6 weeks

23
Q

what is *fT4↓; fT3↓; TSH↑ treated with

A

thyroxine

24
Q

what is *fT4 →; fT3 →; TSH treated with

A

nothing - this is normal - never treat with thyroxine

25
Q

what does *fT4 →; fT3 →; TSH↑ mean

A

compensated response -

if there are symptoms - treat with thyroxine
if there are no symptoms - wait and repeat test

26
Q

what does *fT4↓; fT3↓; TSH ↓ or → mean

A

consider potential pituitary disease / sick euthyroid syndrome

27
Q

what is a major cause of goitre and hypothyroidism

A

iodine deficiency

28
Q

what is thyrotoxicosis

A

excess circulation thyroid hormone - this is not hyperthyroidism

29
Q

what is hyperthyroidism

A

an over active thyroid gland

30
Q

what are symptoms of hyperthyroidism

A

(From most common to less usual)
*Irritability, nervousness
*Hyperactivity
*Heat intolerance, sweating
*Palpitations
*Weight loss
*Dyspnoea
*Fatigue, weakness
*Increased appetite
*Increased bowel frequency
*Altered mood
*Insomnia
*Oligo/amenorrhoea
*Hair loss
*
*Sore throat
*Family history
*History of other autoimmune disorders (Graves disease)

31
Q

what would inspection show if got hyperthyroidism

A

Inspection: (clothing, weight, hair loss, eye disease, obvious goitre, ask patient to swallow)

32
Q

what would hands show if got hyperthyroidism

A

Hands: (warm moist palms, fine tremor, palmar erythema, onycholysis, pulse rate and rhythm)

33
Q

what does percussion have

A

retrosternal goitre

34
Q

what are the extra findings

A

Extra findings: (hyperreflexia, muscle weakness, congestive cardiac failure)

35
Q

what are the Graves specific findings

A

Graves-specific: (thyroid orbitopathy, pretibial myxoedema, vitiligo)

36
Q

what is the integrate clinical thyroid statuses

A

Hyperthyroid
Euthyroid
Hypothyroidism

37
Q

what is the differential diagnosis for primary hyperthyroidism

A

(transient thyroiditis)
Graves disease
Toxic nodule (part of multinodular goitre)
Pituitary adenoma
Thyroid hormone resistance symtoms

38
Q

what would thyroid function test show

A

fT4 increases, fT3 increases, TSH decreased
fT4 —>; fT3—> TSH decreased: subclinical hyperthyroidism
thyroid auto-antibodies (stimulatory, mimic TSH) - helps distinguish

39
Q

what would an ultrasound of primary hyperthyroidism show

A

Increased echogenicity: homogenous (Graves) or heterogenous (MNG)

40
Q

what is the treatment for hyperthyroidism

A

block thyroid hormonogenesis
- Thionamide: Carbimazole or propylthiouracil (use PTU if trying for pregnancy)
- Goal: restore normal thyroid hormone levels; in time TSH should normalise
Definitive treatment options (radioiodine or surgery; radioiodine is very useful for toxic nodule)

41
Q

what is Graves diseae

A

autoimmune characteristics
Associated with T1DM, Addison’s disease, vitiligo, pernicious anaemia, alopecia areata, myasthenia gravis, coeliac disease

42
Q

what is the major autoantigen involved in graves disease

A

TSHR

43
Q

what are the symptoms of graves disease

A

Thyroid eye disease / Graves orbitopathy
pretibial myxoedema

44
Q

what is the treatment for Graves disease

A

–Carbimazole (immunosuppressive; N.B. agranulocytosis)
–Carbimazole + thyroxine
–Beta blockers for symptomatic relief
–Monitor thyroid function test
–Trial off treatment
–1/3 ‘cure’; 1/3 relapse sometime; 1/3 relapse soon

45
Q

what is graves orbitopathy

A

inflammation of the extra ocular eye muscles, causing increases retro-orbital pressure - proptosis or optic nerve damage

46
Q

what are the aggravates in graves orbitopathy

A

radioiodine aggravates

47
Q

what is it treated with

A

Treated with artificial tears, immunosuppression, debatable effects of radiotherapy