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PBL SEM 4 > hypothyroidism/hyperthyroidism > Flashcards

hypothyroidism/hyperthyroidism Flashcards

1
Q

what does the hypothalamus release in the hypothalamus-pituitary-thyroid (HPT) axis? what does it act on?

A

releases TRH (thyrotropin releasing hormone) — acts on thyrotrophs in the anterior pituitary

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2
Q

what does the anterior pituitary release in the HPT axis and what does it act on?

A

releases TSH (thyroid stimulating hormone) — acts on thyroid

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3
Q

what do T4 and T3 do in the HPT axis?

A

provide -ve feedback to further regulate the production of TRH and TSH

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4
Q

what happens when TSH binds to its receptor on the basal membrane?

A
  • increases levels of cAMP —> triggers various intracellular effects

various processes occur:
- thyroglobulin synthesised
- iodide is actively recruited via an active transport process —> results in iodisation of thyroglobulin to create iodinated thyroglobulin
- thyroid peroxidase enzyme activity stimulated as part of intracellular effects

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5
Q

where is active thyroid peroxidase enzyme (TPO) located?

A

apical membrane (microvilli surface) of thyroid epithelial cells where it is secreted into colloid

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6
Q

how does I- enter the thyroid epithelial cell?

A

Na+/I- symporter on the basal membrane

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7
Q

what is active TPO enzyme stimulated by?

A

TSH

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8
Q

what does active TPO enzyme do?

A

assists the chemical reaction that adds I- to thyroglobulin to form thyroid hormone (thyroglobulin in complex with iodide)

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9
Q

what is TH stored as?

A

colloid

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10
Q

how is TH recycled?

A
  • thyroglobulin degradation —> active hormone is released into circulation (T3 and T4) and I- is recycled through pendrin across apical membrane
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11
Q
A
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12
Q

what is the active thyroid hormone name?

A

T3 = triiodothyronine

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13
Q

the critical I is on what carbon of T3?

A

5

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14
Q

what is T4 name?

A

thyroxine

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15
Q

what are the 2 inactive forms of T3 and T4?

A

T2 = diiodothyronine
reverse-T3 = triiodothyronine

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16
Q

80% vs 20% of hormone release by thyroid

A

80% = T4
20% = T3

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17
Q

where and how is T4 converted to T3?

A

in circulation of peripheral tissues

enzyme = type 1 selenodeiodinase (D1)

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18
Q

what enzyme converts T3 and T4 to their inactive counterparts?

A

D3 deiodinase

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19
Q

what are the inactive counterparts to T3 vs T4?

A

T3 —> T2

T4 —> rT3

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20
Q

what does T3 do when it enters the nucleus?

A
  • binds to thyroid hormone receptor (TR is in complex with RXR)
  • turns on/off gene expression to alter cell function
  • mRNA forms and enters cytoplasm
  • protein formation = what accounts for TH action

thyroid hormone action is therefore a SLOW process

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21
Q

what is the essential precursor to thyroid hormone?

A

tyrosine — (sequential iodination of tyrosine)

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22
Q

thyroid hormone is stored as ______ in gland

A

colloid

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23
Q

T4 vs T3

A
  • T4 is produced entirely by thyroid
  • T3 - peripheral T4 mono-deiodination (liver and kidney)
  • T3 is metabolically active
  • half life of T4 is longer (5-7 days vs 1-3 days) — therefore in treatment T3 has to be given 3 x a day vs once a day for T4
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24
Q

serum what is a long term and best indicator of thyroid?

A

serum TSH

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25
Q

what is the name of an enlarged thyroid gland?

A

goitre

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26
Q

what is hashimoto disease?

A

an autoimmune disorder that can cause hypothyroidism, or underactive thyroid

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27
Q

is hypothyroidism more common in men or women?

A

women

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28
Q

classic hashimoto vs atrophic thyroiditis

A
  • classic = goitrous
  • atrophic = non-goitrous (in relality, a mix of antibody mediated/T cell-mediated. TPO, TSHR, Tg auto-antibodies)
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29
Q

what causes goitre?

A

iodide deficiency

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30
Q

what drugs can induce hypothyroidism?

A

amiodarone, iodides, lithium

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31
Q

what antibody is most specific to autoimmune thyroid disease?

A

TSH receptor antibody — binds to receptor and blocks its function

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32
Q

what can cause genetic/developmental hypothyroidism?

A

Thyroid Transcription Factor 1 (TTF1), PAX8, Pendred syndrome, NIS (Na I Symporter)

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33
Q

what is pendred syndrome?

A

a disorder typically associated with hearing loss and a thyroid condition called a goiter in children

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34
Q

what else can cause hypothyroidism?

A

post-ablative radioiodine/post-operative

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35
Q

what are secondary/tertiary causes of hypothyroidism?

A
  • hypopituitarism and hypothalamic
  • pituitary adenoma, congenital deficiency, irradiation of pituitary gland
    (- sarcoid, infection)
36
Q

what are signs and symptoms of hypothyroidism?

A

METABOLISM SLOWED

37
Q

why can the skin thicken in hypothyroidism? what can this lead to?

A

get deposition of glycosaminoglycans

—> can get compression of median nerve causing carpal tunnel syndrome

38
Q

what are examples of organ-specific autoimmune diseases? (must think about these if hypothyroidism diagnosed)

A
  • Graves’ disease
  • autoimmune hypothyroidism
  • pernicious anaemia
  • Addison disease
  • Autoimmune atrophic gastritis
  • type 1 diabetes mellitus
39
Q

what is addison disease?

A

autoimmune destruction of adrenal gland

40
Q

what is pernicious anaemia?

A

arises from autoimmune destruction of the parietal cell —> loss of intrinsic factor secretion and consequently vitamin B12 deficiency

41
Q

what would someone with congenital hypothyroidism look like?

A
42
Q

what can triglyceride and cholesterol levels be like in hypothyroidism?

A

elevated — hypothyroidism predisposes an individual to dyslipidaemia

43
Q

what investigations are carried out for hypothyroidism?

A
  • blood test (TFTs)
  • normochromic normocytic anaemia
  • macrocytosis, mixed dyslipidaemia

no need for ultrasound scan (or autoantibody measurement in UK)

consider other autoimmune endocrinopathies eg. adrenal, ovary, T1DM, (pernicious anaemia, vitiligo)

44
Q

what are RBCs like in pernicious anaemia?

A

large —> macrocytosis

45
Q

how is hypothyroidism treated?

A

REPLACE THYROXINE

  • once daily thyroxine, lifelong
  • usually 100mcg a day
  • rapid start in young, gentle increment in elderly
  • repeat blood tests after 4-6 weeks
46
Q

what is the goal of treatment in hypothyroidism?

A

normalise TSH

47
Q

what are the levels of T4/T3/TSH like in hypothyroidism?

A
  • T4 and T3 levels are low
  • TSH levels are raised due to lack of -ve feedback
48
Q

what happens in treatment if there are normal levels of T4 and T3 but TSH is raised?

A

compensated response

  • if symptoms, treat with thyroxine
  • if no symptoms, could wait and repeat test, subclinical hypothyroidism
49
Q

what would you consider if T4 and T3 levels are low but TSH are also low or normal?

A

consider potential pituitary disease/sick euthyroid syndrome

50
Q

what is sick euthyroid syndrome?

A

abnormal findings on thyroid function tests that occur in the setting of a nonthyroidal illness (NTI), without preexisting hypothalamic-pituitary and thyroid gland dysfunction

51
Q

what is vitiligo?

A

autoimmunity against melanocytes

52
Q

why does iodine deficiency cause a goitre?

A

the thyroid gland increases in size to attempt to capture as much iodide as possible

53
Q

what is thyrotoxicosis?

A

excess circulation thyroid hormone (NOT THE SAME AS HYPERTHYROIDISM)

54
Q

what is hyperthyroidism

A

an overactive thyroid gland

55
Q

what can cause hyperthyroidism?

A
  • graves’ disease (autoimmune, other associated features)
  • toxic nodule (possibly part of multi nodular goitre, no other features)
    (- pituitary adenoma or thyroid hormone resistance syndrome)
  • transient (viral eg. coxsackie, ECHO)
  • pharmacological (thyroid hormone - take too much levothyroxine)
56
Q

what is De Quervian subacute thyroditis?

A

a painful swelling of the thyroid gland thought to be triggered by a viral infection, such as mumps or flu

Subacute thyroiditis (also known as De Quervain’s thyroiditis, granulomatous thyroiditis, or giant cell thyroiditis) is inflammation of the thyroid characterised by a triphasic course of transient thyrotoxicosis, followed by hypothyroidism, followed by a return to euthyroidism

57
Q

subacute thyroditis:

The thyrotoxic phase is due to thyroid _______ damage and release of preformed thyroid hormone. This phase is characterised by ______ thyroid uptake on nuclear scan and _______ serum ___ or ___ levels

A

The thyrotoxic phase is due to thyroid follicular damage and release of preformed thyroid hormone. This phase is characterised by low thyroid uptake on nuclear scan and elevated serum ESR or CRP levels

58
Q

symptoms of hyperthyroidism

A
59
Q

examination for hyperthyroidism

A
60
Q

describe thyroid orbitopathy

A

autoimmune affecting muscles behind eyes — eyes pushed forwards

61
Q

what is pretivial myxoedema?

A

thickening of skin on shins

a skin condition that causes plaques of thick, scaly skin and swelling of your lower legs. This condition is a form of Graves’ disease and can affect people diagnosed with thyroid conditions

62
Q

describe bruit

A
  • very increased blood flow
  • only hear it in autoimmune graves’ disease affecting all of the gland
63
Q

what are the differential diagnoses of primary hyperthyroidism/thyroiditis?

A
  • transient thyroiditis — viral infections
  • Graves’ disease
  • toxic nodule (part of MNG)
  • pituitary adenoma
  • thyroid hormone resistance syndrome
64
Q

what are T4,T3,TSH levels like in primary hyperthyroidism?

A
  • T4 and T3 are elevated
  • TSH is slow
65
Q

what are T3,T4,TSH levels in subclinical (compensated) hyperthyroidism?

A

T4 + T3 are normal

TSH is low

66
Q

what are thyroid autoantibodies like in hyperthyroidism?

A

TSH receptor antibodies — stimulate receptor

graves vs toxic multi nodular goitre

67
Q

what does an ultrasound scan show in hyperthyroidism? Graves vs MNG

A

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

68
Q

uptake scan (low dose radioiodine or other radionuclide) : graves vs MNG

A

graves - homogenous
single/MNG - isolated ‘hot nodule’

69
Q

treatment of hyperthyroidism

A

block thyroid hormonogensis

  • Thionamide: Carbimazole (most common) or proprylthiouracil
  • goal = restore normal thyroid hormone levels. in time TSH should normalise
  • definitive treatment options (radioiodine or surgery)
70
Q

how does carbimazole work?

A

Carbimazole is a pro-drug as after absorption it is converted to the active form, methimazole. Methimazole prevents thyroid peroxidase enzyme from iodinating and coupling the tyrosine residues on thyroglobulin, hence reducing the production of the thyroid hormones T3 and T4 (thyroxine).

they are thionamides

71
Q

when is propylthiouracil preferred over carbimazole in hyperthyroidism treatment?

A

if trying for pregnancy or pregnant

carbimazole can (albeit rarely) have adverse effects on the skin of a developing baby

72
Q

what is Graves’ disease associated with? (autoimmune characteristics)

A

T1DM, Addison’s disease, vitiligo, pernicious anaemia, alopecia areata, myasthenia gravis, coeliac disease

73
Q

what is the major auto antigen in Graves’ disease?

A

TSH receptor

74
Q

is graves’ disease more commin in men or women?

A

women

0.8/1000 vs <0.1/1000

75
Q

characteristics of graves’ disease

A
  • waxing and waning inflammatory autoimmune stimulation of the thyroid (not constant — wavers)
  • 20-40 years old
  • more aggressive in children and males
76
Q

symptoms and signs of graves’ disease

A

same as for primary hyperthyroidism

plus

  • thyroid bruit
  • thyroid eye disease/Graves orbitopathy
  • pretivial myxoedema
77
Q

treatment of Graves’ disease

A
  • carbimazole
  • high dose carbimazole + thyroxine (block and replace)
  • beta blockers for symptomatic relief
  • monitor thyroid function test
  • trial off treatment
  • 1/3 cure, 1/3 relapse sometime, 1/3 relapse soon
78
Q

possible adverse blood effect of carbimazole?

A

agranulocytosis

it is immunosuppressive

79
Q

what is proptosis?

A

eye further forward than it should be = not as bad as eye being pushed back (could press on optic nerve)

80
Q

describe graves orbitopathy/thyroid eye disease

A
  • inflammation of the extraocular muscles, causing increased retro-orbital pressure
  • proptosis or optic enrve damage, diplopia, corneal ulceration
  • usually associated weight thyroid upset, but can be entirely separate
  • higher frequency and worse outcome with cigarette smoking
  • radioiodine aggravates — choose surgery over this
  • treated with artificial tears, immunosuppression, debatable effects of radiotherapy
  • ultimately ‘burns itself out’
81
Q

how does graves’ disease change throughout pregnancy?

A

exacerbated in early pregnancy, but ameliorated in later pregnancy

82
Q

how can graves’ disease affect pregnancy/foetus?

A
  • spontaneous abortion rates increase
  • premature labour
  • small birth weight
  • congestive cardiac failure
  • pre-eclampsia
83
Q

why is graves’ disease worse at the start of pregnancy?

A

hCG also simulates the thyroid

84
Q

T3/4, TSH levels in pregnancy

A

normal T4/3, low TSH is normal in pregnancy

85
Q

how is graves’ disease treated/not treated in pregnancy?

A
  • not radioiodine — foetal thyroid present at 8-10 weeks gestation
  • not beta blockers — foetal bradycardia, hypoglycaemia, respiratory depression, IUGR (intrauterine growth restriction)
  • surgery if intolerant of thionamide/agranulocytosis
86
Q

what do 1% of Graves’ pregnancies generate?

A

foetal hyperthyroidism — get placental crossing of TSHR stimulating Abs

  • foetal HR >160 bpm, goitre, advanced neonatal bone age, craniosynostosis
  • even if maternal thyroidectomy, might still have lots of antibodies, measure at start of 2nd trimester? (if >5 fold normal, significant risk of foetal hyperthyroidism, can be treated by maternal thionamide)
87
Q

what are the 3 thionamides?

A

carbimazole, methimazole, propylthiouracil

PBL SEM 4 (50 decks)

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