the thyroid Flashcards

(48 cards)

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
what is poly-glandular autoimmune syndrome?
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
what are the specific and non-specific autoantibodies?
specific: anti-TSH-R autoantibodies non-specific: anti-thyroid perioxidase antibodies non-specific: anti-thryoglobulin antibodies
27
how will a scintigram, which uses iodine be able to identify Grave's disease?
because there will be increased equal uptake of the iodine
28
how is Lugol's iodine used to treat hyperthyroidism?
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
how is primary hyperthyroidism diagnosed?
low TSH (assuming that T3 and T4 high)
30
how is primary hypothyroidism diagnosed?
high TSH (assuming TSH and T4 are low)
31
what are the two main differences between Grave's disease and Hashimoto's disease?
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
what is autoimmune polyendocrine syndrome Type II?
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
how can the thyroid compensate within limits for hypothyroidism?
increase iodine uptake, increased iodine recycling. preferential making of T3 over T4
34
What thyroid function tests show for a secondary hypothyroidism?
LOW T3 and T4 and abnormally normal TSH (this could reflect insensitivity of the feedback mechanisms)
35
what is the general treatment for hypothryodisim?
levothyroxine (with a half life of 1 week) | liothyroxine (with a half life of 3-6hrs)
36
on histopathology of a sample: carvio-embyronic antigens are found as well as calcitonin? what is this indicative of?
a medullary carcinoma
37
what symptoms (physical is medullary carcinoma indicative of?)
diarrohea and flushing
38
how is ultra-sound used in identifying nodules?
this is a very sensitive technique used to identify nodules most nodules found are benign, but it is used to guide FNA
39
How is FNA used?
this looks at cellular morphology
40
How is FNA used?
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
what is is the only to distinguish between the benign and malignant tumour?
via surgery
42
what determines whether a nodule is toxic or non-toxic
according to the thyroid function tests
43
patient comes in: - previous history of neck irradiation - positive for RET/PTC translocation - goitre moves on swalloing - what is this?
this is a papillary carcinoma - the RET/PTC translocation presents a constantly active tyrosine kinase receptor causing massive proliferation. - BRAF mutations = worse prognosis
44
patient comes in: - history of chronic iodine deficiency - histopathology shows enlarged follicular cells with capsular invasion - what can this be?
this is a follicular carcinoma (An adenoma would show no capsular invasion) - this carcinoma spreads
45
why is treatment of differentiated thyroid cancers much more successful than non-differentiated cancers?
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
what are RET mutations associated with?
multiple endocrine neoplasia type II include medullary carcinoma and phaechromocytoma 25% of medullary carcinomas are associated with hereditary mutations
47
what is primary thyroid lymphoma associated with?
associated with Hashimoto's
48
what is primary thyroid lymphoma associated with?
associated with Hashimoto's some T-cell turn malignant and they require external beam therapy