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FHB Exam 4 > Endocrine 7: Thyroid and HPT > Flashcards

Endocrine 7: Thyroid and HPT Flashcards

1
Q

Where is the thyroid gland located?

A
  • anterior to the trachea and cricoid cartilage
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2
Q

What does the thyroid gland look like?

A
  • 2 symmetrical lobes connected by an isthmus
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3
Q

Describe the blood supply of the thyroid gland.

A
  • superior and inferior thyroid arteries (external carotid and thyrocervical trunk)
  • venous plexus on anterior surface gives rise to superior, inferior, and middle thyroid veins => jugular vein drainage
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4
Q

What is a bruit and thrill?

A

In thyroid hypertrophy, the anterior venous plexus becomes vasodilated.

  • bruit = you can hear the sound of blood through this area
  • thrill = you can feel the blood moving through
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5
Q

How is the thyroid gland innervated?

A

middle and inferior cervical ganglia

- sympathetic

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6
Q

Describe the structure of the thyroid gland cells.

A
  • colloid/lumen
  • surrounded by follicular epithelial cells
  • parafollicular cells
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7
Q

How are follicular epithelial cells activated?

A
  • when inactivated, they are flat and squamous

- when activated by TSH, they become cuboidal

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8
Q

Define colloid.

A

lumen of thyroid cellular components

  • large storage of TG
  • surrounded by FECs
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9
Q

Define follicular epithelial cells.

A
  • surround the colloid
  • where TG is made and secreted into the colloid
  • microvilli extend into the colloid to deliver iodide and TG
  • close to fenestrated capillaries to deliver hormones directly to blood
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10
Q

Define parafollicular cells.

A
  • C cells
  • produce calcitonin
  • do NOT line the colloid
  • maintain the follicles
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11
Q

How is iodide intake and thyroid hormone production related?

A
  • thyroid hormones are iodothyronines
  • thyroid hormone production requires TG and iodide
  • excess dietary iodide is mostly excreted
  • thyroid keeps 3-4 months worth of iodide
  • iodized salt is main dietary source
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12
Q

Describe the Wolf-Chaikoff effect.

A
  • autoregulatory effect inside the thyroid to control iodide intake and maintain iodide storage
  • low iodide dose = thyroid takes as much as it can
  • high iodide dose = thyroid stops taking it in, and might even stop altogether
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13
Q

Describe the clinical use of the Wolf-Chaikoff effect.

A
  • treat hyperthyroidism
  • give high dose iodide to shock the thyroid gland to stop taking in iodide => prevent further production of thyroid hormones
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14
Q

Why is iodide intake important?

A
  • need it to make thyroid hormones
  • most common cause of mental retardation worldwide
  • iodized salt
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15
Q

Define the HPT axis.

A

H - hypothalamus - PVN secretes TRH
P - pituitary - thyrotrophs respond to TRH and secrete TSH
T - thyroid - responds to TSH and makes T3/T4/rT3

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16
Q

What are the negative feedback mechanisms of the HPT?

A
  • T4 goes to pituitary => converted to T3 inside thyrotrophs = stops TSH secretion
  • T3/T4 negative feedback on PVN
  • tonic inhibition by dopamine and SS
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17
Q

Define Thyroxin.

A
  • T4
  • long half-life
  • VERY tightly bound to transport protein
  • mostly inactive (low affinity binding to thyroid receptor inside cells)
  • converted to T3 inside cells
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18
Q

Define Triiodothyronine.

A
  • T3
  • long half-life
  • VERY tightly bound to transport protein
  • primarily active thyroid hormone (high affinity, low capacity to thyroid receptors inside cell)
  • most intracellular T3 source is converted from T4
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19
Q

Define rT3.

A
  • reverse T3
  • DIT on outer, MIT on inner
  • inactive
  • used to keep thyroid balance in check in fetus, brain, etc.
20
Q

Why are follicular epithelial cells polarized?

A
  • basolateral membrane = intake of I from the bloodstream; moves I against concentration gradient via NaI symporter; subsequent release of T3, T4 after hormone synthesis
  • apical membrane = releases TG and I (NaI symporter) into colloid; reuptake of iodinated TG
21
Q

List the mechanism of action of thyroid hormone synthesis.

A
  1. Iodide Trapping - TSH stimulates NaI symporter on the basolateral membrane to move Iodide into the FEC against its concentration gradient
  2. Transport - TG and iodide (via pendrin protein) are transported to colloid/lumen; thyroid peroxidase (TPO) converts iodide to iodine
  3. Iodination/Organification - tyrosine residues of TG are iodinated
  4. Conjugation - conjugation of iodinated tyrosines to form T3 or T4 (combining MIT and DIT)
  5. Endocytosis - T3/T4-TG are packaged into endosomes via megalin protein
  6. Proteolysis - cleavage of T3 and T4 from TG (TG, MIT, DIT are recycled)
  7. Secretion - T3 and T4 released from basolateral membrane
22
Q

Describe conjugation of iodinated TG.

A
  • if one Iodine is added = MIT
  • if 2 iodine are added = DIT
T3 = MIT + DIT
T4 = DIT + DIT
rT3 = DIT + MIT (double I on outer ring)
23
Q

How does lithium relate to thyroid hormone production?

A
  • blocks NIS

- can’t make hormone b/c no iodide

24
Q

Define carbimazole.

A
  • blocks TPO
  • can take in iodide, but can’t convert to iodine
  • iodide trapped in colloid…can’t make hormone
  • organification defect => hypothyroid
25
Q

What is the ratio of T3:T4 in blood?

A

mostly T4

26
Q

Define cold and hot spots.

A
  • normal = bilateral uptake;
  • cold spots = one section has no iodide uptake; more indicative of malignancy
  • hot spots = much more uptake on one side, diffuse in the other;
27
Q

How can radioactive iodide uptake scans help in making diagnoses?

A
  • normal = 25% uptake after 24 hours
  • hypothyroid = 60%
  • hyperstimulation/Graves Disease = rapid rise, plateau; high turnover
  • organification defect = normal rise in intake, but declines after
28
Q

Define Type 1 Deiodinases.

A
  • can act on either outer or inner ring
  • makes T3 or rT3
  • present in liver, kidney, thyroid, skeletal muscle
  • primary source of circulatory T3
29
Q

Define Type 2 Deiodinases.

A
  • can only act on outer ring
  • makes T3
  • expressed in brain, pituitary, placenta, cardiac muscle
  • in locations where T3 activity is needed, negative feedback
30
Q

Define Type 3 Deiodinases.

A
  • can only act on inner ring
  • makes rT3
  • expressed in brain, placenta, skin
  • in locations where you need to protect from excess T3
31
Q

How are thyroid hormones transported?

A
  • mostly thyroid binding globulin (TBG)
  • some on transthyretin (TTR)
  • some on albumin
  • rarely free
32
Q

Describe the structure of TBG.

A
  • same family as CBG
  • tightly bound, high affinity
  • surrounds the thyroid hormone
  • synthesized in liver (hence, affected by liver function)
  • stimulated by TSH and estrogen
  • reversible (can bind more right away)
33
Q

Describe the mechanism of action of thyroid hormones inside its target cells.

A
  1. TBG delivers T3/T4 to cell
  2. Type 1 and 2 deiodinases convert T4 to T3
  3. T3 goes to nucleus and binds to thyroid hormone receptor (THR)
  4. THR and retinoic acid receptor (RXR) form a heterodimer and act as TF
34
Q

Describe the affinity of thyroid hormones to THR.

A
  • high affinity, low capacity for T3

- very low affinity for T4 (must be converted)

35
Q

What are the general physiological effects of thyroid hormone?

A
  • maintain BMR by continuous futile cycle of energy storage and breakdown
  • —> gluconeogenesis, lipolysis, proteolysis ==> increased energy consumption and thermogenesis
  • promotes CNS maturation
  • upregulation of B-adrenergic receptors in heart, skeletal muscle, adipose tissue
36
Q

Describe the physiological effects of thyroid hormone on metabolism.

A
  • T3 increases energy consumption, oxygen consumption, and thermogenesis by increasing mitochondrial activity
37
Q

Describe metabolic effects of hypothyroidism.

A
  • decreased BMR
  • decreased gluconeogenesis, decreased glycolysis = no change
  • decreased lipolysis, decreased lipogenesis = high cholesterol
  • decreased proteolysis, decreased muscle mass formation = no change
  • decreased thermogenesis = cold intolerance
38
Q

Describe metabolic effects of hyperthyroidism.

A
  • increased BMR
  • increased gluconeogenesis, increased glycolysis = no change
  • increased lipolysis, increased lipogenesis = low cholesterol
  • increased proteolysis, increased protein synthesis = muscle wasting (weight loss)
  • increased thermogenesis = hot intolerance
39
Q

What are the CNS physiological effects of thyroid hormones?

A
  • normal brain development
  • neural cell migration
  • neural cell differentiation
  • myelination
  • synaptic transmission
40
Q

Define cretinism.

A
  • iodide deficiency during development
  • hypothyroidism
  • short stature
  • impaired bone formation
  • mental retardation
  • delayed motor development
41
Q

Describe thyroid hormone physiological effects on the CVS.

A
  • upregulation of beta adrenergic receptors
  • increased CO
  • increased RHR, SV
  • increased contractility
  • hyperthyroidism can cause arrhythmias
42
Q

Define goiter.

A
  • enlarged thyroid gland

- either hypo or hyper can cause

43
Q

Define Graves Disease.

A
  • hyperthyroidism
  • symmetrical goiter
  • autoimmune disorder
  • LATS antibodies bind to and activate TSH receptors in the thyroid gland
  • rapid overproduction of T3/T4
  • constant stimulation of thyroid leads to hypertrophy
  • Sx: goiter, tachycardia, bugged eyes, irritability, heat intolerance, muscle wasting, low TSH b/c excess T3/T4 negative feedback
44
Q

Define Hashimoto’s Thyroiditis.

A
  • hypothyroidism
  • autoimmune destruction of thyroid follicles
  • antibodies against TG and TPO (can’t make thyroid hormones)
  • Sx: goiter, lethargy, fatigue, hair loss, brittle nails, cold intolerance, weight gain
45
Q

Define Thyroid Storm.

A
  • occurs in individuals who are already hyperthyroid
  • in acute stress, surge of catecholamines combined with elevated T3/T4 baseline leads to rapid tachycardia and arrhythmias, N/V, fever
  • life threatening
  • Tx
    • propylthiouracil (PTU) - blocks TPO, only acute
    • carbimazole - blocks TPO
    • beta blockers

FHB Exam 4 (16 decks)

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