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Endocrinology > Thyroid gland > Flashcards

Thyroid gland Flashcards

1
Q

Where is the thyroid gland?

A

just below the cricoid cartilage

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2
Q

What structure joins the two lobes of the thyroid gland?

A

the isthmus

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3
Q

Describe the embryological development of the thyroid gland

A
  • first gland to develop
  • starts as epethilial proliferation in floor of pharynx at the base of the tongue at 3-4 weeks
  • then descends through the thyroglossal duct and passes in front of the hyoid bone
  • It remains connected to the thyroglossal duct during its migration but this then degenerates
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4
Q

Describe the histology of the thryroid gland

A
  • follicular cells arranged in spheres called thyroid follicles
  • the follicular cells secrete colloid (a deposit of thyroglobulin) into the follicles for storage
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5
Q

What is T3 and T4 made of?

A

T3- monoiodotyrosine (MIT) + diodotyrosine (DIT)
T4- DIT +DIT
MIT and DIT is tyrosine residues with thryoglobulin and iodine added, MIT has 1 iodine, DIT has 2, T3 has 3 and T4 has 4

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6
Q

Which thryoid hormone is secreted more from the thryroid gland and which is most active?

A

T4 is secreted more but T3 is more active

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7
Q

Where can T4 be converted to T3?

A

liver and kidneys

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8
Q

how does T3 and 4 travel in the blood?

A

bound to thyroxine binding globulin

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9
Q

Are thyroid hormones the only substances in the body to use iodine?

A

yeh

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10
Q

How is iodide taken up from blood into thyroid epithelium?

A

a sodium- iodide symporter

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11
Q

Describe synthesis, storage and release of thyroid hormone

A
  • iodide (I-) taken up by iondine- sodium symporter
  • tyrosine taken up from blood also and made into thyroglobulin
  • iondide and thryoglobulin excreted into follicles
  • iodide converted to iodine (I) by oxidation
  • iodine and thryoglobulin bound by iodination to make MIT/DIT which are coupled to make T3/4
  • pinocytosis of T3/T4
  • lysosome fuses with vesicle with T3/4 in
  • some T3/4 released, some degraded to release I- for more synthesis
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12
Q

Describe endocrine control of thyroid hormone release

A
  • hypothalamus secretes TRH
  • this travels by portal system to anterior pituitary where it stimulates release of TSH
  • TSH travels in blood to thyroid gland where in stimulates synthesis and release of thyroid hormone
  • t3/4 inhibts release of TSH and TRH when levels too high
  • TSH inhibits release of TRH when its levels are too high
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13
Q

What is the difference in structure of TSH, FSH and LH?

A

TSH, FSH and LH all have an alpha unit which is the same but the beta unit differs and provides specificity

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14
Q

What type of receptor does TSH bind to?

A

an s or q GPCR- both stimulate release of T3/T4

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15
Q

Describe the intra cellular process that occurs when TSH binds to a GPCR

A 
if S type:
- adenylyl cyclase activated
- cAMP produced
- PKA activated 
if Q type:
- phosphlipase C activated 
- PIP2--> DAG and IP3
- causes Ca2+ release via Ip3 receptor 
- and PKC activation

both routes result in thyroid hormone synthesis and release

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16
Q

What general effects do thyroid hormones have?

A
  • increase basal metabolic rate (except in brain, spleen and testis) by stimulating more and larger mitochondria and synthesis of enzymes in the respiratory chain
  • stimulates catabolic pathways- lipid metabolism and more insulin intake meaning more gluconeogenesis and glycogenolysis
  • increase catecholamine receptor synthesis so cells increase sympathetic output
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17
Q

What effects do thyroid hormones have on CVS?

A
  • increase sensitivity to sympathetic stimulation

- increase peripheral vasodilation to reduce temperature

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18
Q

What effects does thyroid hormone have on the CNS?

A
  • essential for development and adult function

- increases myelination of nerves for development of neurones

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19
Q

Where do thyroid hormones (amino acid derivatives) act?

A

in the nucleus - bind to hormone response elements to increase regulation of certain genes

20
Q

What is the role of thyroid peroxidase?

A
  1. oxidses iodide to iodine
  2. adds iodine to tyrosine
  3. couples MIT and DIT
21
Q

What are the symptoms of hypothyroidism?

A
  • excessive tiredness, feeling down
  • memory problems, depression, phycosis
  • weight gain
  • cold intolerance
  • gruff, croaky voice
  • puffy eyes, hands and feet
  • dry, flaky skin
  • hair loss (outer third of eye brows)
  • carpal tunnel symptoms
  • mennorrhagia
  • muscle weakness and cramps
22
Q

What are the signs of hypothyroidism?

A
  • may be none
  • pallor (peaches and cream face)
  • coarse facial featurea and perioorbital puffiness
  • bradychardia
  • non pitting odema- myxoedema
  • ascities or pericardial effusion (very rare)
23
Q

What are the common causes of pitting vs non pitting oedema?

A

pitting: water retention: heart failure, varicose veins, pregnancy ect
non pitting: lymph node dysfunction, myxodema in hypothyroidism

24
Q

What is the most common cause of hypothyroidism in the UK?

A
  • hashimotos disease
  • auto immune destruction of thryoglobulin and thyroid perioxidase in blood. In early stages there may be a small diffuse goitre but this may not happen
  • more common in women
25
Q

How is hypothyroidsm treated?

A

oral T4 (not broken down in intestine)

26
Q

What is the most common cause of hypothyroidism globally? What other effects come with this cause?

A

severe iodine deficiency

  • leads to a usually nodular goitre
  • if in children leads to cretinism as well as hypothyroidism: mental retardation, deaf, mute, short stature due to developmental impairment
27
Q

What is the difference between thyrotoxicosis and hyperthyroidsm?

A

Hyperthyroidism (over active thyroid gland) always leads to thyrotoxicosis (high thyroid hormone). But there are other causes of thyrotoxicosis.

28
Q

What are the symptoms of hyperthyroidism?

A
  • overactivity, tiredness
  • nervouseness, anxiety, insomnia
  • shaking, trembelling
  • heart intolerance
  • increased sweating- warm sweaty hands
  • palpitations, rarely angina
  • weight loss inspite of increased appetite
  • diarrhoea
  • amenorrhea
  • proximal muscle weakness
29
Q

What are the signs of hyperthyroidism?

A
  • weight loss
  • warm sweaty hands
  • fine hand tremour
  • tachycardia
  • AF - irregular pulse
  • bounding pulse
  • proximal myopathy
  • lid lag (delay in eyelid movement down when eye moves down due to more sympathetic stimulation)
  • staring eyes
30
Q

How are the signs of anxiety different to hyperthyroidism?

A
  • cold and sweaty hands
  • weight loss is due to eating less
  • history
  • otherwise symptoms similar
31
Q

Why is it rare for a pituitary adenoma (affecting TSH production) to present with hypo or hyperthyroidism?

A
  • not hyperthryoidism because its very rare for it to secrete more TSH
  • not hypothyroidism because if adenoma is affecting hormone release then other stuff is likely to go more wrong more quickly
32
Q

What is measured in blood to diagnose hyper or hypothyroidism?

A

TSH- if high then hypothroidism as the gland is underfunction so less T3/4 so more TSH release

33
Q

What are the 3 key causes of hyperthyroidism?

A
  • graves disease
  • toxic multi nodular goitre
  • toxic adenoma of thyroid gland
34
Q

What is graves disease and what are key differentiating signs?

A
  • auto immune condition producing thyroid stimulating immmunoglobulin so more T3/4 released
  • exopthalmos (bulding eyes) and pretibial myxoedema (not in every case)
  • sometimes a diffuse goitre
35
Q

Why is myxodema found in hypothyroidism?

A

deposition of mucopolysaccharides

36
Q

when and how does a toxic multinodular goitre develop?

A
  • low T4 from mild iodine deficiency
  • thryoid cell hyperplasia to adjust
  • increased replication predisposes TSH receptor mutation
  • TSH receptor mutation makes it consitiutively active
37
Q

What will a toxic adenoma of the thyroid gland look like on a radioactive iodine scan?

A
  • looks like one lobe/ area much larger than the other

- as the adenoma takes up most of the iodine and surpresses most of the gland

38
Q

How is hyperthyroidism treated?

A
  • carbimazol
  • prevents thyroid peroxidase coupling iondinated tyrosines
  • so less T4 production
39
Q

What is the prognosis of adenoma of thyroid gland?

A

97% cure rate

1% malignancy rate

40
Q

should the thyroid gland be able to be felt or seen?

A

no

41
Q

Why does the thyroid gland normally move up and down on swallowing?

A
  • it is enclosed in the pre-tracheal fascia which also attaches to the trachea and larynx (and thryroid cartilage)
  • this moves it moves up on swallowing with the thyroid cartilage
42
Q

How can the thyroid gland be observed?

A
  • ultrasound scan
  • technetium scinitgraphy: technetium is similar to iodine but radioactive so can be detected, this can give impression of size and activity of thyroid
43
Q

What is a thyroglossal duct cyst?

A
  • when the thyroglossal duct persists after birth and fills with fluid (creates cyst)
  • creates bulge on/ near midline near/ under hyoid bone
  • will move up when you stick your tongue out due to where it attaches to mouth floor
44
Q

WHat are the three types of goitre?

A
  • diffuse (both nodes enlarge equally)
  • multinodular (many nodules to goitre)
  • single nodular
45
Q

When are small goitres normal?

A
  • pregnancy
  • menopause
  • after/ during a girls first period
46
Q

What is the most common cause of goitre globally and in UK?

A
  • globally: iodine deficiency
  • Uk: multinodular goitre of unknown cause: normal thryoid function but after many years it may lead to toxic multinodular goitre and so cause hypertyroidism
47
Q

What is a major complication of goitres?

A
  • they enlarge backwards
  • cause retrosternal goitre
  • cause tracheal compression

Endocrinology (7 decks)

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