Thyroid Flashcards

1
Q

where is the thyroid gland?

A

at base of neck (butterfly shape)

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2
Q

what are the two main classes of thyroid hormones?

A
  1. T3 and T4 thyroid hormones

2. calcitonin

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3
Q

is T3 or T4 more active on THR?

A

T3

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4
Q

what are T3 vs T4 aka?

A

T3: triiodothryonine
T4: thyroxine

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5
Q

what is the highest-circulating thyroid hormone?

A

T4T

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6
Q

What is the HPT axis for thyroid hormones?

A

TRH released from hypothalamus stimulates ant pit to release TSH which stimulates thyroid (follicular cells) to release T3/T4 (neg feedback on hypo and ant pit)

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7
Q

what are T3 and T4 collectively called?

A

thyroid hormone

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8
Q

what are 3 physiological effects of thyroid hormone?

A

incr basal metabolic rate, sensitization to catecholamines (NA: incr HR, CO, breathing rate), growth and development

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9
Q

are thyroid hormones synthesized from free tyrosine molecules?

A

No, synthesized from precursor protein (thyroglobulin)

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10
Q

How many modified tyrosine molecules make up thyroid hormones?

A

2 (have iodine molecules)

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11
Q

What is the process of thyroid hormone synthesis?

A

tyrosines undergo enzymatic iodination/iodide undergoes organification into MIT (1 I2) or DIT (2 I2), iodinated tyrosines are enzymatically coupled into T3 (MIT + DIT) or T4 (2 DIT)

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12
Q

What position on the aromatic tyrosine ring are iodines added to?

A

3 and 5

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13
Q

what stimulates T3 or T4 synthesis?

A

TSH stimulation causes thyroglobulin endocytosis and processing into T3 or T4 (> released)

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14
Q

what is the basic unit of the thyroid gland? (3) and what occurs in each part?

A

apical side of follicle: iodination and coupling of thyroglobulin (lumen)
follicle cell: thyroglobulin processing
basolateral side: T3/4 released into bloodstream

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15
Q

how does the thyroid gland concentrate iodide into follicle lumen?

A

from bloodstream via Na/I cotransporter (basolateral, Na down, I up)

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16
Q

what is the thyroid hormone receptor?

A

intracellular (TF w/ TH binding)

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17
Q

how is the THR an exception to most intracellular receptors?

A

T3/4 are not lipid-soluble and require a transport protein to reach THR

18
Q

what is THR bound to at rest (unactivated)?

A

thyroid response elements (TREs) on DNA and corepressors (homodimers)

19
Q

what occurs to T4 when it enters the cell?

A

de-iodinated to T3 (enzyme)

20
Q

what occurs when T3 binds to the THR?

A

recruitment of RXR (retinoic acid receptor) to form heterodimer (1 THR replaced) and coactivator binding (incr transcription)

21
Q

what are the 4 most common causes of hypothyroidism?

A

iodine deficiency, autoimmunity towards thyroid (Hashimoto’s thyroiditis), developmental defect, inappropriate hormonal regulation (decr TRH/TSH)

22
Q

what are 4 symptoms of hypothyroidism?

A

fatigue, weight gain (decr met rate), hypersensitivity to cold, bradycardia

23
Q

how are thyroid diseases diagnosed? (2)

A

measure TSH (THR circ never high-acts directly on ant pit) or anti-TSH antibodies for hyperthyroidism

24
Q

what is a cause and features of primary hypothyroidism?

A

cause: defect in thyroid function
feature: low T3/4, high TSH (low neg feedback)

25
Q

what is a cause and features of secondary hypothyroidism?

A

cause: central defect (hypo/ant pit)
features: low TSH, low T3/4 (decr TSH)

26
Q

what is a treatment for hypothyroidism?

A

hormone replacement

27
Q

which hormone is used for hormone replacement in the treatment of hypothyroidism?

A

T4/thyroxine (main circ form)

28
Q

what is the name of the drug prescribed for hypothyroidism?

A

levothyroxine

29
Q

what are 2 most common causes of hyperthyroidism?

A

Grave’s disease (autoimmune response to TSHR-activates) and hyperplasia (thyroid adenoma, goiter-excessive growth)

30
Q

what are 5 symptoms of hyperthyroidism?

A

sleep difficulty, heat intolerance, tachycardia, weight loss, tremor (incr met rate)

31
Q

what’s the cause and features of Grave’s disease?

A

cause: thyroid activation by anti-TSHR Abs
features: high T3/4, low TSH (neg feedback)

32
Q

whats the cause and features of thyroid hyperplasia?

A

cause: benign tumour in/on thyroid
features: high T3/4, low TSH (neg feedback)

33
Q

whats the cause and features of secondary hyperthyroidism?

A

cause: central defect (incr TSH from ant pit)
features: incr TSH, high T3/4

34
Q

whats the difference btwn Grave’s disease and Hashimoto’s thyroiditis?

A

both autoimmune
Grave’s: Abs stimulate TSHR
Hashimotos: Abs damage thyroid

35
Q

what are 2 special diagnostic features of Grave’s disease?

A

exophthalmos (bulging eyes): autoimmune damgae to eye muscle/fibroblasts
goiter (swelling of neck): overactive thyroid (stim Abs)

36
Q

t/f: goiter is only seen in Grave’s disease

A

false, also seen in hypothyroidism (iodine deficiency) if TSH incr (stim thyroid)

37
Q

what is the surgical approach for hyperthyroidism and its drawbacks?

A

approach: part/all of thyroid is resected
drawbacks: require hormones replacement (hypothyroidism), disruption to parathyroid (Ca disturbances/hypoparathyroidism)

38
Q

what is the radioactive iodine treatment approach for hyperthyroidism and its drawbacks?

A

approach: I^131 concentrates in thyroid, radiation destructs thyroid
drawbacks: hormone replacement, not for pregnancy/nursing (damage to infant)

39
Q

what is the anti-thyroid drug (methimazole) approach for hyperthyroidism and its drawbacks?

A

approach: prevents synthesis of T3/4
drawbacks: diverse

40
Q

what is the symptomatic B-blocker approach for hyperthyroidism and its drawbacks?

A

approach: B-blockers help tachycardia
drawbacks: doesn’t treat underlying cause of disease

41
Q

how do thioamides (methimazole) treat hyperthyroidism?

A

inhibits thyroperoxidase enzyme (iodination/organification+coupling of thyroglobulin into colloid)