Thyroid Gland Flashcards

1
Q

Describe the functional unit of the thyroid gland.

A

Thyroid follicle is the functional unit and it is surrounded by a single layer of epithelial cells. Follicular lumen is filled with colloid made of new synthesized thyroid hormones attached to thyroglobin.

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2
Q

What is difference between T3 and T4?

A

T4 is the precursor to the active molecule T3. T4 has a longer half life and 10x more is made than T3

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3
Q

How is hormone stored in the follicular colloid?

A

Stored as Iodinated thyroglobin, enough supply to last 2-3 months

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4
Q

How do you make T3?

A

One DIT and one MIT combine

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5
Q

How to make T4?

A

Two DIT combine

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6
Q

How is T4 converted to T3?

A

Deiodinase type one or two (Two is more predominant in the brain) converts T4 to T3. Reverse T3 iodinie is removed from inner residue and it is inactive. Active T3 has iodine removed from middle.

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7
Q

What is purpose of having peripheral conversion of T3 and 4?

A

T4 has a higher affinity for proteins that are used to create a store and carry them throughout the blood.

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8
Q

What clinical states are associated with a reduction in conversion of T4 to T3?

A

Fasting Medical and surgical stress Catabolic diseases

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9
Q

Steps to Thyroid hormone and location.

A
  1. Thyroglobin enters follicular lumen via rough ER and goligi
  2. Iodide gets in epithelial cell via “I-Trap” a sodium Iodide co transporter
  3. Iodide gets out via Iodide chloride transporter
  4. Thyroid Peroxidase combines Iodide with tyrosine? to make MIT or DIT and then DIT and MIT combine to make T3 and T4 and attach to Thyroglobin(in follicular lumen)
  5. TSH stimulation occurs and via pinocytosis the colloid is moved back into the epi cell and Proteoases break T4 and T3 off for circulation
  6. MIT and DIT get recycled with intrathyroidal deiodinase
    1. deficiency of intrathyroidal deiodincase mimics dietary deficiency
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10
Q

What happens when the availability of iodide is restricted?

A

Formation of T3 is favored

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11
Q

What is pendrin? Defects?

A

A chloriede/Iodide pump in the follicular epithelial cell apical membrane

  • Disruption in thyroid hormone synthesis
  • Hypothyroidism with goiter, also causes sensorineural hearing loss as channel is in cochlea
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12
Q

How do high levels of Iodide effect synthesis of thyroid hormones?

A
  • High iodide inhibits organification and synthesis of thyroid hormones this is called Wolff-Chalkoff effect
    • The expression of Thyroid Peroxidase is decreased
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13
Q

How do Perchlorate or Thiocynaate work and what are they used for?

A
  • It blocks I trap
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14
Q

What is used for treatment of hyperthyroidism?

A

Blocking TPO with PTU

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15
Q

Organification defect?

A

can take iodine up but cant process it into thyroid hormone, results in hypothyroidism

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16
Q

How is radioactive iodine uptake used?

A

32 minutes

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17
Q

How is thyroid hormone transported and what is active?

A
  • 99% is found bound to plasma proteins, main one is TBG
    • synthesized in the liver and has high affinity for T4
  • Trasnthyretin (TTR) more in brain carries 10-15%
  • Albumin carries 15-50%

Free is active

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18
Q

Describe the circulating thyroid hormone T4 half life and T3.

A
  • T4 halflife is 6 days due to the high affinity to TBG
  • T3 halflife is 1 day
19
Q

How are circulating levels of TBG indirectly assessed?

A
  • T3 Resin Test
  • T4 bound to TBG is most predominantly found in plasma and you add labeled free T3 to the sample
  • Incubate the sample
  • If we have low TBG the extra T3 will remain free bc there is a lack of binding sites
    • when put in the resin with antibody for T3 to absorb T3 will bind to that
  • If TBG is high we decrease the amount of T3 taken up on the resin bc there are plenty of spaces to bind
20
Q

In hyperthyroidism how does a resin uptake test look?

A
  • high T4
  • high T3 resin uptake
21
Q

How would a resin uptake test look in a person with hypothyroidism?

A
  • low T4
  • low T3 resin uptake
22
Q

How does hepatic failure impact TBG?

A
  • Decreases TBG resulting in transient increase of free T3 and T4
  • Followed with negative feedback normalizing levels over time
23
Q

How does pregnancy affect TBG and T3/4?

A
  • Increase TBG synthesis so decrease free thyroid hormones
  • Decreasing resin uptake of T3
  • The transient decrease in free T3 and 4 causes an increase in synthesis and secretion of T3 and T4
    • increasea total levels of T3 and 4 but levels of free active thyroid hormones are normal
    • Clinically euthyroid
24
Q

Role of TSH and regulation?

A
  • Regulates growth of thyroid gland (trophic effect) and increase secretion of thyroid hormones
  • Regulated by TRH and Free T3
    • PVN releaseas TRH to ant. pit which releases TSH to thyroid gland releasing T3 and 4 for negative fb on ant pit and hypothalamus
  • Secretion of TSH is released at a steady rate
25
Q

Actions of TSH on thyroid gland?

A
  • Increase synthesis and secretion of thyroid hormones
  • Trophic effect of thyroid gland
26
Q

What are the inhibitory factors of secreting thryoid hormones?

A
  • Iodide deficiency
  • Deiodinase deficiency
  • Excessive iodide intake
  • Perchlorate, thiocyanate (Itrap inhibition)
  • PTU (Peroxidase inhibition)
  • Decrease TBG levels
27
Q

Stimulatory factors for Thyroid hormones?

A
  • TSH
  • Immunoglobins
  • Increased TBG levels such as in pregnancy
28
Q

What does thyroid hormone do in cardiac muslce cells?

A
  • synthesizes myosin
  • b1 adrenergic receptors
  • Ca ATPase

Increase CO

29
Q

In the liver and adipose tissue what does thyroid hormone do?

A

Increase synthesis of metabolic enzymes

30
Q

In most tissues what does thyorid hormone cause synthesis of?

A

Na K ATPase

31
Q

What are the effects of T3 on metabolism?

A
  • Glucose absorption
  • Glycogenolysis
  • Gluconeogenesis
  • Lipolysis
  • Protein synthesiss and degradation
32
Q

What is the effect of T3 on the cardiovascular system?

A

Increase CO upregulation of B1 adrenergic receptors

33
Q

What accounts for the increase of BMR?

A

Increased activity of Na K ATPase leading to increase O2 consumption and heat production

34
Q

Throid hormone on Lipid metabolism?

A
  • Fat mobilization-increase FA concentration in plasma
  • Enhance oxidation of FA
  • Plasma concentration of cholesterole and triglycerides are inversely correlated with thyroid hormones
    • Increase blood cholesterol in hypothyroidism
35
Q

How does thyroid hormone effect growth?

A

Acts synergistically with growth hromone and somatomedins to promote bone formation

36
Q

How does thyroid hormone effect CNS?

A
  • slide 671
37
Q

Most common cause of Thyrotoxicosis?

A

Graves disease

Primary Hyperthyroidism

38
Q

What causes secondary hyperthyroidism?

A

Could be a TSH secreting tumor

39
Q

How do TSH levels look in hyperthyroidism?

A
  • Decreasaed due to negative FB of T3 on anterior lobe of pituitary with Graves
  • With an adenoma or anterior pituitary defect TSH is increased
40
Q

How do you distinguish between Graves disease and adenoma’s?

A

Presence of circulating TSI, exophthalmos and periorbital edema

41
Q

Sheehan syndrome?

A
  • Postpartum hypopituitarism due to necrosis of pituitary gland
  • Most patients present with agalactorrhea, amenorrhea, hypothyroidism
  • Other endocrnie dysfxn may be present
42
Q

Hashimoto’s?

A
  • Thyorid hormone synthesis is imparired by TG or TPO antibodies leading to decrease of T3 and T4 levels
  • TSH leevels are high bc T3/4 are low leading to goiter
43
Q

What thyroid disorders have a goiter associated with them and why?

A
  • Graves disease due to
  • Secondary hyperthyroidism from Adenoma due to TSH production
  • Primary hypothyroidism (Hashimotio’s) due to decreased T3/4 leading to increase in TSH
  • Iodine Deficiency due to decrease in T3/4 to increase TSH