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Endocrinology > the thyroid > Flashcards

the thyroid Flashcards

1
Q

what type of protein is thyroid hormone?

A

a glycoprotein (a basophil)

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2
Q

what does an over-active thyroid look like?

A

tall columnar epithelium with very little colloid

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3
Q

what does an under-active thyroid look like?

A

flattened epithelium with excess colloid

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4
Q

what can occur if the thryoglossal duct does not atrophy?

A

if the upper portion does not atrophy (this can lead to a midline thryoglossal cyst) this is clinically distinguishable because it can move when the tongue is protruded.

some patients have a pyramidal lobe, this is the lower portion of the thyroglossal duct

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5
Q

what is an under-migrated thyroid?

A

lingual thyroid

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6
Q

what is an over migrated thyroid?

A

retro-sternal thryoid

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7
Q

what is a mutation that can cause congenital hypothyroidism?

A

PAX-8 mutation

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8
Q

what is a bruit an auscultation evident off?

A

this is evident of an over active thyroid, recall the thyroid has a very high blood supply from the superior and inferior thyroid arteries

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9
Q

what are the two main actions of thyroid perioxidase?

A

this causes organification:

  • oxidises the iodide
  • then adds this iodide to tyrosine residues exposed on the thyroglobulin.

causes coupling:

  • di-iodo-tryosine + di-iodo-tyrosine = T4
  • di-iodo-tyrosine + mono-iodo-tyrosine = T3
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10
Q

where is thyroid perioxidase synthesised?

A

this is synthesised in the follicular cell and packaged into a vesicle by the Golgi, it then becomes activated at the apical plasma membrane

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11
Q

where is thryoglobulin synthesised?

A

this is transcribed, translated and post translation mofiied and packaged into vesicles at the Golgi

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12
Q

where does iodine for thyroid hormone synthesis come from? and how does it reach the follicular lumen?

A

this comes from dietary supplied. it is concentrated in the follicular epithelial cells via the sodium/ iodide transporter and then transported into the lumen via pendrin

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13
Q

what can mutations in pendrin cause?

A

this can cause pendrin syndrome, which is a congenital form of hypothyroidism.

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14
Q

what are the effects of TSH on thyroid hormone secretion?

A

it causes an increase in the amount of the fresh thryoglobulin and thyroid hormone secretion. the secreted thyroid hormone is more active because it has higher proportion of T3:T4

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15
Q

what are the usual concentrations of free thyroid hormone within circulation

A

in picomolar and this is because 99.9% of the thyroid hormone is bound to plasma proteins

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16
Q

what are the physiological actions of thyroid hormone

A
  • positive chronotropic and ionotropic effects
  • increases BMR
  • is a CNS stimulant
  • promotes growth and development with GH
synergies with adrenaline to:
- increase lipolysis 
-increase glycogenolysis 
- increase heart rate
antagonises insulin

its secretion is reduced by GHRH

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17
Q

why can selenium deficiency cause a rare form of hypothyroidism

A

because selenium is required to deiodinate the outer ring of T4 to form T3

this is because T4 is the precursor for T3

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18
Q

there are several forms of De-iodinating enzymes:

what is the function of D1:

A

D1 is responsible for making most of the T3 in the body (found in the liver, kidney and muscle)

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19
Q

what is the function of D2?

A

this is responsible for negative feedback mechanisms and is found in the brain and pituitary

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20
Q

what is the function of D3

A

This ensures that once cells have taken up all the T3 they require they’re not under influence by circulating T3

they de-iodinate the inner ring of T4 to make inactive T3, or de-idoinate the inner ring of T3 to make T2 which is hormonally inactive and rapidly cleared from circulation

21
Q

what are long acting thyroid stimulators?

A

those are the type of antibodies produces in Grave’s disease:

  • they have prolonged action on the TSH-R
  • although the action of the auto-antibodies may take longer to manifest
22
Q

what are the specific symptoms associated with Grave’s disease

A

orbital pathology e.g. proptosis
pretibial myooxedema
thyroid acropachy

23
Q

what are the acute causes of hyperthyroid status?

A

Hashimoto’s disease and De Quervain’s
- those are thryoditis, initially may manifest as hyperthyroid but with time, there is glandular dysfunction and this leads to a hypothyroid status

24
Q

why does Grave’s disease sometimes have a relapsing-remiting disease course

A

because the auto-antibodies produced in Grave’s are not only stimulatory,TSI
but sometimes antibodies produced can be inhibitory; TBII

25
Q

what is poly-glandular autoimmune syndrome?

A

this is collection of syndrome of heterogenous groups of autoimmune conditions affecting more than one endocrine gland: not linked to a single gene but possessing certain alleles increases the risk of developing the syndrome

syndrome includes:

  • Grave’s disease-
  • addisson’s disease
  • pernicious anaemia
  • T1DM
26
Q

what are the specific and non-specific autoantibodies?

A

specific: anti-TSH-R autoantibodies
non-specific: anti-thyroid perioxidase antibodies
non-specific: anti-thryoglobulin antibodies

27
Q

how will a scintigram, which uses iodine be able to identify Grave’s disease?

A

because there will be increased equal uptake of the iodine

28
Q

how is Lugol’s iodine used to treat hyperthyroidism?

A

you block the production of T3 and T4 using injection of excessive iodine (Wolff-Chaikoff effect)

effect only lasts for a few days then patient becomes hyperthyroid (Jod-basedow)

29
Q

how is primary hyperthyroidism diagnosed?

A

low TSH (assuming that T3 and T4 high)

30
Q

how is primary hypothyroidism diagnosed?

A

high TSH (assuming TSH and T4 are low)

31
Q

what are the two main differences between Grave’s disease and Hashimoto’s disease?

A

Grave’s disease is mediated by the presence of plasma cells secreting antibodies to receptors.

In hashimoto’s it is associated with T-cell infiltrated and b cell actively killing the thyroid tissue - in grave’s there is no tissue destruction

32
Q

what is autoimmune polyendocrine syndrome Type II?

A

this is a syndrome in which there is autoimmunity to more than one endocrine gland, it is not associated with a single gene but possessing certain HLA types increases the risk of developing the syndrome:

includes;

  • Pernicious anaemia
  • Addison’s
  • Grave’s
  • Hashimoto’s
  • vitiligo
33
Q

how can the thyroid compensate within limits for hypothyroidism?

A

increase iodine uptake, increased iodine recycling. preferential making of T3 over T4

34
Q

What thyroid function tests show for a secondary hypothyroidism?

A

LOW T3 and T4 and abnormally normal TSH (this could reflect insensitivity of the feedback mechanisms)

35
Q

what is the general treatment for hypothryodisim?

A

levothyroxine (with a half life of 1 week)

liothyroxine (with a half life of 3-6hrs)

36
Q

on histopathology of a sample: carvio-embyronic antigens are found as well as calcitonin? what is this indicative of?

A

a medullary carcinoma

37
Q

what symptoms (physical is medullary carcinoma indicative of?)

A

diarrohea and flushing

38
Q

how is ultra-sound used in identifying nodules?

A

this is a very sensitive technique used to identify nodules most nodules found are benign, but it is used to guide FNA

39
Q

How is FNA used?

A

this looks at cellular morphology

40
Q

How is FNA used?

A

this looks at cellular morphology

bengin: abundant colloid
suspicious: THY3 (enlarged follicular cell or Hurthle cells)

malignant: irregular follicular or papillary cells (THY4 AND THY5)

41
Q

what is is the only to distinguish between the benign and malignant tumour?

A

via surgery

42
Q

what determines whether a nodule is toxic or non-toxic

A

according to the thyroid function tests

43
Q

patient comes in:

  • previous history of neck irradiation
  • positive for RET/PTC translocation
  • goitre moves on swalloing
  • what is this?
A

this is a papillary carcinoma

  • the RET/PTC translocation presents a constantly active tyrosine kinase receptor causing massive proliferation.
  • BRAF mutations = worse prognosis
44
Q

patient comes in:

  • history of chronic iodine deficiency
  • histopathology shows enlarged follicular cells with capsular invasion
  • what can this be?
A

this is a follicular carcinoma (An adenoma would show no capsular invasion)
- this carcinoma spreads

45
Q

why is treatment of differentiated thyroid cancers much more successful than non-differentiated cancers?

A

because differentiated thyroid cancers express the symporter (Na/I-)radioactive I-131 (So they can accumulate can cause death of the overactive cells)

you;d follow up by giving T3 and T4 to suppress TSH secretion which would cause thyroid proliferation

non-differentiated cancers will not express the symporters

46
Q

what are RET mutations associated with?

A

multiple endocrine neoplasia type II
include medullary carcinoma and phaechromocytoma

25% of medullary carcinomas are associated with hereditary mutations

47
Q

what is primary thyroid lymphoma associated with?

A

associated with Hashimoto’s

48
Q

what is primary thyroid lymphoma associated with?

A

associated with Hashimoto’s

some T-cell turn malignant and they require external beam therapy

Endocrinology (6 decks)

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