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Endocrine System > Thyroid Gland physiology and disease > Flashcards

Thyroid Gland physiology and disease Flashcards

1
Q

what are the hormones secreted by the thyroid gland?

A
  • thyroxine (T3)
  • triiodothyronine (T4)
  • calcitonin
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2
Q

what are T3 and T4 made up of?

A
  • tyrosine residues and iodine (3 for T3 and 4 for T4)
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3
Q

how are T3 and T4 stored in the thyroid gland?

A

stored in colloid, attached to thyroglobulin protein

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4
Q

what triggers release of thyroid hormones?

A

hypothalamus secretion of TRH, which stimulates TSH from pituitary, which causes T3 and T4 to be endocytosed into follicular cells and secreted into the bloodstream

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5
Q

where in the thyroid gland is calcitonin secreted?

A

in parafollicular C cells

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6
Q

what is the purpose of T3 andT4?

A
  • promote futile energy producing catabolic and anabolic cycles at the same time
  • important for growth in utero and brain development
  • important for heat production in babies
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7
Q

what class of hormone are T3 and T4?

A
  • amine hormones which act like steroid hormones
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8
Q

what are the classic steroid hormone characteristics in T3 and T4?

A
  • need a protein carrier for transport in circulation
  • have intracellular receptors in target cells
  • alter nuclear transcription
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9
Q

what protein carrier transports thyroid hormones in the blood?

A

Thyroid Binding Globulin (TBG)

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10
Q

how much thyroid hormone is protein bound in the blood, and how much is free in circulation?

A
  1. 8% is protein bound

0. 2% is free

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11
Q

which thyroid hormone is more physiologically active and why?

A

T3 is more physiologically active than T4 because it binds more strongly to the intracellular receptors

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12
Q

what happens to T4 in the circulation?

A

T4 has a lower affinity to the target receptor, so it stays bound to its carrier and is converted to T3 by deionases when needed

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13
Q

which thyroid hormone is more abundant in the circulation?

A

T4

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14
Q

which thyroid hormone has a longer half-life and why?

A

T4, because it’s mostly bound to carrier proteins

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15
Q

what are the main causes of hypothyroidism?

A
  • autoimmune disease (Hashimoto’s thyroiditis, atrophic)
  • chronic iodine deficiency
  • iatrogenic (drugs, thyroidectomy)
  • congenital
  • subacute (de Quervain’s) thyroiditis
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16
Q

what are some of the symptoms of hypothyroidism?

A
  • dry skin/hair
  • weight gain
  • lethargy
  • slow reflexes
  • cold intolerance
  • heavy periods
  • constipation
  • bradycardia
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17
Q

what tests should be done to investigate hypothyroidism?

A
  • TSH levels and T3/T4 levels

- Thyroid Peroxidase Antibodies (TPO)

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18
Q

what would TSH and T3/T4 levels likely be in primary, secondary and subclinical hypothyroidism?

A
  • primary hypothyroidism: high TSH, low T3/T4
  • secondary hypothyroidism: normal/low TSH, low T3/T4
  • subclinical hypothyroidism: high TSH, normal T3/T4
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19
Q

what is the usual treatment for hypothyroidism?

A
  • levothyroxine (T4) tablets
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20
Q

what are some of the possible presentations of goitre?

A
  • diffuse
  • nodular
  • cystic
  • tumour
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21
Q

why should special care be taken with pregnant women or patients with heart disease when considering levothyroxine treatment?

A
  • pregnant women: will need higher levels

- heart disease patients: levothyroxine could aggravate heart symptoms through higher thyroid hormone action

22
Q

what investigations should be done for goitre?

A
  • FNA
  • TFT
  • ultrasound
  • isotope scan
23
Q

what are the possible results of an isotope scan for a single nodule goitre? what are their implications?

A
  • hot nodule –> takes up more iodine, unlikely malignant

- cold nodule –> not functioning properly, 20% likelihood malignant

24
Q

what are some of the types of thyroid cancer?

A
  • differentiated (papillary, follicular)
  • anaplastic
  • lymphoma
25
Q

what are the characteristics of papillary thyroid tumours?

A
  • multifocal lesion
  • spread locally or to lymph nodes
  • good prognosis
26
Q

what are the characteristics of follicular thyroid tumours?

A
  • single lesion
  • spread to bone/bone
  • good prognosis if resected
27
Q

what are the characteristics of anaplastic thyroid tumours?

A
  • aggressive
  • locally invasive
  • do not respond to RAI
  • poor prognosis
28
Q

what are the three main treatment principles for thyroid cancer?

A
  • debulk (surgery)
  • destroy (RAI)
  • suppress (thyroxine)
29
Q

what are the main causes of hyperthyroidism?

A
  • Graves’ disease (80%)

- Toxic multinodular goitre (20%)

30
Q

what antibodies should be tested for Graves’ disease?

A

TPOAb - thyroid peroxidase antibodies

TRAb - TSH receptor antibodies

31
Q

what antibodies should be tested for Hashimoto’s thyroiditis?

A

TPOAb - thyroid peroxidase antibodies

32
Q

what is the pathophysiology of Graves’ disease?

A

TRAb mimic effect of TSH and trigger uncontrolled release of thyroid hormones

33
Q

what is the pathophysiology of Hashimoto’s thyroiditis?

A

auto-immune condition with TPOAb attacking the thyroid gland

34
Q

what are some of the symptoms of hyperthyroidism?

A
  • weight loss
  • irritability/anxiety
  • heat intolerance
  • palpitations
  • light periods
  • frequent bowel movement
  • hyperreflexia
  • greasy hair
  • sweaty skin
  • thyroid eye problems
35
Q

what tests should be done to confirm a diagnosis of hyperthyroidism or Graves’ disease?

A

TSH and T3/T4
TPOAb
TSH receptor Ab

36
Q

what would the TSH and T3/T4 levels show in primary, secondary and subclinical hyperthyroidism?

A

primary: low TSH, high T3/T4
secondary: high TSH, high T3/T4
subclinical: low TSH, normal T3/T4

37
Q

what are the treatment options for hyperthyroidism?

A
  • surgery (thyroidectomy)
  • ATD (anti-thyroid drugs)
  • RAI (radioiodine)
38
Q

when should RAI not be considered in patients with hyperthyroidism, and why?

A

RAI not appropriate in patients with severe thyroid eye disease, because RAI may release Ab into the circulation which could precipitate eye problems

39
Q

what are the two main drugs used to treat hyperthyroidism?

A
  • carbimazole

- propylthiouracil

40
Q

what are the different ATD treatment regimes for hyperthyroidism?

A
  • titration (start high and lower as needed)

- block/replace (high dose drug then replace with thyroxine)

41
Q

what are the main side effects of carbimazole and propylthiouracyl in treatment of hyperthyroidism?

A
  • agranulocytosis (important!)

- rash

42
Q

what are the different RAI treatment regimes for hyperthyroidism, and what are their benefits?

A

ablative dose - higher curative percentage, higher hypothyroidism percentage
variable dose - lower curative percentage, lower hypothyroidism percentage

43
Q

what are the benefits and drawbacks of the different ATD treatment regimes?

A

both titration and block/replace have a 50% curative rate and a 30% hypothyroidism incidence, but block/replace comes with higher risk of side effects

44
Q

which patient groups should be more carefully monitored when treated for hyperthyroidism?

A
  • elderly patients with brittle bones

- patients with heart disease

45
Q

which patient population is most likely to get thyrotoxicosis from a toxic multinodular goitre?

A

elderly people

46
Q

what are common physiological causes for goitre in young people?

A

pregnancy and puberty

47
Q

what are some of the pathological causes for goitre?

A
  • autoimmune (Graves’, Hashimoto’s)
  • physiological (puberty, pregnancy)
  • thyroiditis
  • iodine deficiency
48
Q

what is de Quervain’s thyroiditis?

A
  • inflammation of the thyroid following a viral infection, causes short lived hyperthyroidism followed by a few months of hypothyroidism
49
Q

which hormones inhibit the activity of thyroid hormones?

A
  • somatostatin (GHIH)

- cortisol

50
Q

what are the treatment options for medullary thyroid cancer?

A

thyroidectomy

51
Q

which cells are affected in medullary thyroid cancer?

A

parafollicular C cells

52
Q

what test result would be expected in medullary thyroid cancer?

A

raised serum calcitonin levels

Endocrine System (6 decks)

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