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PMCOL 200 > 30 Thyroid Gland Pharmacology > Flashcards

30 Thyroid Gland Pharmacology Flashcards

1
Q

What are the two main classes of hormones released by the thyroid gland?

A
  1. Thyroid hormones
    • T3 (triiodothyronine - Most Active) and T4 (thyroxine)
    • T4 has higher levels circulating but not the most active
  2. Calcitonin
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2
Q

What are the three levels of control for thyroid hormone production?

A
  1. TRH (thyrotropin releasing hormone from the hypothalamus)
  2. TSH (thyroid stimulating hormone from the anterior pituitary)
  3. T3 and T4 exert negative feedback on both upstream glands
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3
Q

What are three powerful physiological effects of the thyroid hormone?

A
  1. Increased basal metabolic rate
  2. Sensitization to catecholamines (increased cardiac output, heart rate, breathing rate)
  3. Important role in growth and development
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4
Q

Thyroid hormones are made up of __________ from the precursor protein _______

A

Thyroid hormones are made up of 2 modified tyrosine molecules from the precursor protein thyroglobulin (tyrosine rich)

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5
Q

Tyrosines that make up thyroid hormones are _____________ and then _________

A

Tyrosines that make up thyroid hormones are enzymatically iodinated (1 or 2 iodines per ring) and then enzymatically coupled (2 linked rings)

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6
Q

TSH stimulation causes ______ to be endocytosed and processed followed by the release of ___ and ___

A

TSH stimulation causes precursor protein (thyroglobulin) to be endocytosed and processed followed by the release of T3 and T4 (T4 is predominant)

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7
Q

What happens at the apical side of the follicle lumen?

A

Iodination and coupling of thyroglobulin

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8
Q

What happens in the intracellular space of the thyroid follicle?

A

Processing of thyroglobulin after it has been iodinated and coupled

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9
Q

What happens on the basolateral side of the thyroid follicle (by the bloodstream)

A

Release of T4 and T3 after being generated from thyroglobulin

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10
Q

How does the thyroid gland accumulate and concentrate iodine from the bloodstream?

A

Using a Na+/I- co-transporter

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11
Q

The thyroid hormone receptor is an ________ type receptor - acts as a _________ after binding of thyroid hormone

A

The thyroid hormone receptor is an intracellular type receptor - acts as a transcription factor after binding of thyroid hormone

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12
Q

T3 and T4 are not very lipid soluble, so how do they reach their receptors?

A

Thyroid hormone receptors are intracellular. T3 and T4 don’t easily diffuse across the membrane

  • need to be taken up into cells by a transporter protein in order to reach their receptors
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13
Q

At rest, unbound thyroid hormone receptors can associate with ________ and recruit ________

A

At rest, unbound thyroid hormone receptors can associate with response elements (TRE) and recruit co-repressors (weakens gene transcription)

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14
Q

What happens after T4 and T3 are taken up into the cell by a transmembrane receptor?

A
  1. T4 is typically de-iodinated to T3
  2. T3 binding in the nucleus causes recruitment of RXR (retinoic acid receptor) to form a heterodimer with the thyroid hormone receptor
  3. Recruitment of co-activators leads to enhanced transcription of target genes
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15
Q

What is hypothyroidism?

A
  • Deficient thyroid fxn = insufficient release of thyroid hormone
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16
Q

Four common causes of hypothyroidism?

A
  1. iodine deficiency (dietary)
  2. Autoimmunity towards thyroid (Hashimoto’s thyroiditis)
  3. Congenital defect
  4. Inappropriate hormonal regulation (insufficient TSH or TRH)
17
Q

What are common symptoms of Hypothyroidism?

A
  1. Fatigue
  2. Weight Gain
  3. Hypersensitivity to cold
  4. Bradycardia (reduced cardiac output)
18
Q

What is the difference between primary and secondary hypothyroidism?

A
  • Primary Hypothyroidism
    • Caused by a defect in thyroid function
    • Features: Low T4 and T3, High TSH
  • Secondary Hypothyroidism
    • Caused by Central defect (poor function of anterior pituitary or hypothalamus)
    • Features: Low T4 and T3, Low TSH
19
Q

What is hyperthyroidism?

A

Overactive thyroid fxn (excessive production of thyroid hormone)

20
Q

What are two most common causes of Hyperthyroidism?

A
  1. Graves’ disease
    • Stimulatory auto-antibodies against TSH receptor (ant pit)
      • activate the receptor leading to excess thyroid hormone release
  2. Hyperplasia of the thyroid leading to excess thyroid hormone release (thyroid adenoma, goiter)
21
Q

What are five common symptoms of hyperthyroidism?

A
  1. Sleep difficulty
  2. Heat (temperature) intolerance
  3. Tachycardia
  4. Weight loss
  5. Tremor
22
Q

How does measuring TSH help determine the underlying cause of Hyperthyroidism?

A
  • Graves’ disease
    • Caused by stimulation of thyroid by anti-tsh receptor antibodies (stimulatory)
    • Features: High T4 and T3, Low TSH
      • Detection of anti-TSH receptor antibodies which cause bulging eyes (exophthalmos)
  • Thyroid hyperplasia
    • Caused by Thyroid adenoma or goiter
    • Features High T4 and T3, Low TSH
  • Secondary hyperthyroidism (uncommon)
    • Caused by central defect (excessive production of TSH by ant pit)
    • Features High T4 and T3, High TSH
23
Q

What is the difference between Graves and Hashimotos thyroiditis?

A
  • Graves:
    • Autoimmune
    • Antibodies (anti-TSH antibodies) cause stimulation of the TSH receptor
  • Hashimotos
    • Autoimmune
    • Antibodies recognize other thyroid-specific proteins and lead to damage of the thyroid
24
Q

What are four treatment approaches for hyperthyroidism?

A
  • Surgery
    • resection of part or all of the thyroid followed by hormone replacement
  • Radioactive iodine tx
    • Iodine (131I) is concentrated within the thyroid, radiation leads to destruction of the thyroid
  • Anti-thyroid drugs (methimazole)
    • Prevents several steps in T4/T3 synthesis
  • Symptomatic tx with beta-blockers (short term)
    • May help with issues such as tachycardia
25
Q

What are thioamides? provide an example:

A

Thioamides (eg Methimazole) prevent iodination and coupling steps (mediated by thyroperoxidase enzyme)

  • methimazole inhibits thyroperoxidase enzyme preventing iodination and coupling

PMCOL 200 (30 decks)

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