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FHB - Endocrine & Reproductive > Lecture 7 (74): Thyroid > Flashcards

Lecture 7 (74): Thyroid Flashcards

1
Q

Where is the thyroid gland located?

What fuses the 2 symmetrical lobes?

A

Located anterior to cricoid cartilage

Two symmetrical lobes fused by the isthmus

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2
Q

What is the blood supply to the thyroid?

What is the innervation?

A

Blood Supply:

  1. Superior (ext. carotid) and
  2. Inferior (thyrocervical trunk) thyroid arteries

Venous plexus on surface gives rise to superior, middle, and inferior thyroid veins — drain into internal jugular vein

Innervation:
Middle and inferior cervical ganglion (sympathetic NS)

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3
Q

What is the thyroid derived from?

Epithelium is arranged in follicles that contain a large storage of what?

How do inactive follicles look? What type of epithelium?

Follicles become active when stimulated by what? What do they transform into?
(test)

A
  1. Derived from branchial pouch endoderm.
  2. large storage of thyroglobulin (colloid)
  3. Inactive follicles have flattened, SQUAMOUS epithelium.
  4. Stimulated by TSH, follicles become active.
    Follicular cells transform to CUBOIDAL epithelium
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4
Q

What epithelial cells surround the lumen of the thyroid gland?

What is the lumen filled with?

What other cells are found? What is the main function of the 2nd most abundant cell type?

A
  1. Follicle epithelial cells surrounding lumen
  2. lumen filled with COLLOID (thyroglobulin (TG) is major component)
  3. Parafollicular Cells (C Cells)
    - produce CALCITONIN
    - other proteins that maintain follicle

Other cells:
Epithelial cells, fibroblasts, lymphocytes, adipocytes

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5
Q

Parafollicular cells do not come into contact with what cells?

A

Parafollicular cells:
Do not touch colloid
Many small granules

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6
Q

Thyroid hormones are _______.

What 2 precursors are required?

What is a critical component of thyroid hormones?

What happens to most excess iodide?

A
  1. Iodothyronines
  2. Thyroglobulin (TG)
    & IODIDE
  3. Iodide is a critical component of THYROID hormones
  4. Most excess iodide is excreted in urine as iodine
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7
Q

What is the Wolf-Chaikoff Effect?

As iodide intake increases, what happens to gland transport and hormone synthesis?

Clinically, what are very high iodide doses used for?

A
  1. An intrathyroidal response that assures constancy of iodide storage in the face of changes in dietary iodide
    = AUTOREGULATION
  • stable at about 25-100 (uptake decreases after 100)
    2. Increases in iodide intake decrease gland transport and hormone synthesis (dashed line), and vice-versa
    3. Clinically: very high iodide doses are used to rapidly SHUT DOWN THYROID PRODUCTION in hyperthyroid patients
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8
Q

The following describes T4, T3, or rT3?

  1. Long half-life in plasma ~ 7-8 days
  2. Tightly bound to transport proteins in blood
  3. Binds to receptor with low affinity
A

T4

  • LONG Half life***
  • tightly bound to transport proteins which is why it has such a long half life
  • no biological activity on its own, but precursor to active form of T3
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9
Q

The following describes T4, T3, or rT3?

  1. Primary active form
  2. Most is converted intracellulary from T4
  3. Binds with high affinity, low capacity to receptor

Which of these is biologically inactive?

A

T3

  • converted intracellularly (low extracellular)
  • binds with HIGH affinity
  • do not need much to saturate the receptor

RT3
- reverse triidothyronine

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10
Q

T4 is peripherally deiodinated to T3 in the thyrotropes and brain by which deiodinase?

Intracellular T3 then acts by negative feedback to inhibit _____ and _______

A

Type II deiodinase

T4 = thyroid hormone sensor

  1. inhibits TRH and TSH
    - dopamine and somatostatin also inhibit TSH release!
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11
Q

Describe the HPT Axis for Thyroid Hormone Regulation:

  1. TRH is released from neurons where? What does it bind after it is release and where does this occur?
  2. What signaling pathway is activated?
  3. What is synthesized after this?
  4. Where does it bind next?
  5. TSH stimulates what synthesis?
  6. What happens to T4?
  7. What does intracellular T3 then do?
A
  1. TRH release from neurons in the PVN bind G protein coupled receptors on the THYROTROPE cells in the ANTERIOR pituitary
  2. Activate DAG/IP3 signaling pathway
  3. Stimulate the synthesis and release of TSH
  4. Binds to basolateral membrane of follicular epithelial cells
  5. TSH stimulates T4/T3 synthesis and release from the thyroid follicle
  6. T4 is deiodinated to T3 in the thyrotropes and brain by Type II deiodinase which acts as a thyroid hormone sensor
  7. Intracellular T3 then acts by negative feedback to inhibit TRH and TSH
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12
Q

All steps in thyroid hormone synthesis are mediated by what?

A

TSH

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13
Q

What are the 7 steps of Thyroid Hormone Synthesis?

A
  1. Iodide trapping
  2. Transport
  3. Iodination
  4. Conjugation
  5. Endocytosis
  6. Proteolysis
  7. Secretion
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14
Q

What converts Iodase to Iodine?

A

Thyroid Peroxidase

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15
Q

Describe the major events in the following events of thyroid hormone synthesis:

  1. Iodide Trapping
  2. Transport

What inhibits the NIS symporter?

A
  1. Iodide Trapping
    - TSH stimulates iodide (I-) trapping by increasing the activity of the NIS co-transporter in the basal membrane of the follicular epithelial cell.
  2. Transport:
    I- transported to follicular lumen and oxidized by thyroid peroxidase (TPO) to form iodine (I).
    - Thyroglobulin is transported into the lumen

NIS symporter inhibited by LITHIUM!!

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16
Q

What is the function of Carbimizole?

What is it used as a treatment for?

A

Inhibits thyroid peroxidase (TPO)

  • Used as a treatment for HYPERTHYROIDISM
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17
Q

1 MIT and 1 DIT is what?

2 DIT is?

Options:

  1. T3
  2. T4
A
  1. T3

2. T4

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18
Q

If iodinated residue is on the OUTER RING what is formed?

Inner ring?

A
  1. REVERSE T3
    (2 I’s on the aromatic circle)
  2. T3
19
Q

Describe the major events in the following events of thyroid hormone synthesis:

  1. Iodination
  2. Conjugation
A
  1. Iodination
    - Iodination of Tyrosil residues on THYROGLOBULIN
  2. Conjugation
    - Conjugation of Iodinated TYROSINES to form T4 and T3 linked thyroglobulin
20
Q

Describe the major events in the following events of thyroid hormone synthesis:

  1. Endocytosis
  2. Proteolysis
  3. Secretion from thyroid follicular epithelial cells
A
  1. Endocytosis
    - Conjugated thyroglobulin with T4/T3 enters follicular epithelial cell
    - packaged in endosomes
  2. Proteolysis
    - TG, MIT, DIT, T4, T3 released from vesicle
  3. Secretion from thyroid follicular epithelial cells
    - T4/T3 secreted into circulation
21
Q

What is T3 formed from?

A

Coupling of one MIT and 2 DIT residues

  • reverse T3 is inactive and is distinguished from active T3 by the presence of two iodinated residues on the OUTER ring

T4 = formed from coupling of 3 DIT

22
Q

What is T3 formed from?

Reverse T3?

T4?

A

Coupling of one MIT and 2 DIT residues

  • reverse T3 is inactive and is distinguished from active T3 by the presence of two iodinated residues on the OUTER ring

T4 = formed from coupling of 3 DIT

23
Q

How does the radioactive Iodide uptake scan work?

What is it used to determine?

Which one is more predictive of thyroid cancer, cold or hot nodule?

A
  1. Iodide uptake in thyroid epithelial cell

Iodide is transported by the sodium iodide symporter (NIS)

Radioactive iodide (131I, 123I) and anions like pertechnetate (TcO4) can be transported by NIS

  1. Used to determine function of thyroid gland
  2. COLD NODULE
24
Q

What is the normal percentage of Iodide uptake after 24 hours?

What percentages qualify someone as hyperthyroid?
Hypothyroid?

Accelerated turnover of thyroid is seen in hyper stimulated thyroid gland or what disease?

A
  1. Normal uptake is 25% after 24 hours
  2. > 60% = hyperthyroid
  3. Grave’s Disease
25
Q

What is the Organification Defect?

How does the graph look?

A

Organification defect - iodine cannot be incorporated into tyrosine. Test by blocking NIS with inhibitor (i.e. perchlorate)

  • Add percolate, and the levels fall significantly (flat orange dashed line)

**inject radioisotope & block the SYMPORTER (NIS)

over time = no more uptake
anything put into the cell will DIFFUSE RIGHT BACK OUT
- so see nothing on the scan dashed line!!!

26
Q

State the following for Type I Thyroid conversion:

  1. Outer or inner ring deiodinase or both
  2. Where is it found primarily?
  3. Function?
A

TYPE I:

  1. OUTER AND INNER ring deiodinase
  2. Liver, kidney, thyroid, skeletal muscle (3)
  3. Primary source of T3 in circulation
27
Q

State the following for Type II Thyroid conversion:

  1. Outer or inner ring deiodinase or both
  2. Where is it found primarily?
  3. Function?
A

Type II:
1. OUTER ring

  1. Brain
    pituitary
    placenta
    cardiac muscle
  2. THYROID HORMONE SENSOR
28
Q

State the following for Type III Thyroid conversion:

  1. Outer or inner ring deiodinase or both
  2. Where is it found primarily?
  3. Function?
A

TYPE III:

  1. INNER RING
  2. Brain, placenta, skin
29
Q

More _____ produced and stored in thyroid

T4 has ____ receptor affinity (low/high)

Reverse T3 has no ______

______ is the thyroid hormone “sensor” in the pituitary

A
  1. T4
    - 80% of T4 is peripherally deiodinated to T3
  2. low
  3. biological activity
  4. Type II deiodinase
30
Q

What is the point of making reverse T3 if it is biologically inactive?

A

If making too much, use it to turn off the signal

- enzymes decide if making active or inactive hormone

31
Q

What are the 3 main transport proteins of Thyroid Hormone.

More than 99% of Thyroid Hormone is BOUND or UNBOUND in circulation?

A
  1. Thyroxine-binding globulin (TBG) (70%)
    - HIGH AFFINITY for thyroid even though less around
  2. Transthyretin (TTR) (10%)
  3. Albumin (15 – 25%)
    - T4 tightly bound = longer half-life approx. 7 days; T3 approx. 1 day
32
Q

TBG
1. 394 AA glycoprotein made in the _____

  1. What has highest affinity for it even though TBG is lowest in concentration?
  2. Estrogen and hepatitis increase or decrease TBG?
  3. Nephrotic syndrome, steroid increase or decrease TBG?
  4. What is unique about TBG?
A
  1. LIVER
    - if liver disease = no TBG
    - 99% of T4 and T3 are bound to TBG
  2. T4
  3. INCREASE
  4. DECREASE - but no net change in “free” T4/T3
  5. TBG can reversibly release T4 to target tissues
33
Q

Thyroid Hormone Receptor (THR)

What type of receptor? This is the same as what?

Forms HETERODIMERS with what?

Expressed in what cell types?

High/low affinity?
High/low capacity for T3?

____ affinity for T4.
Very little biological activity at physiological conditions.

A
  1. Nuclear receptor family
    - same as steroid hormones
  2. forms heterodimers with
    retinoic acid receptor (RXR)
  3. Expressed in nearly every cell type
  4. High affinity, low capacity for T3
  5. Low affinity for T4 – very little biological activity at physiological concentrations
34
Q

What are the 3 major affects of Thyroid Hormone on PHYSIOLOGICAL FUNCTIONS?

A
  1. Increase BMR
  2. Promote Brain (CNS) Maturation
  3. Increases B-Adrenergic receptors
    - heart, skeletal muscle, adipose tissue
35
Q

How specifically does Thyroid hormone affect BMR? (4)

A
  1. Stimulates hepatic gluconeogenesis (like cortisol)
  2. Stimulates proteolysis
  3. Stimulates lipolysis
  4. Overall increased energy/oxygen consumption, increased thermogenesis (hyperthyroid people are very HEAT INTOLERANT)
36
Q

By increasing mitochondrial activity, what 2 major things does T3 increase?

A
  1. Increase cellular Oxygen consumption

2. Increase Heat production

37
Q

T3 is critical for normal brain development, as seen in what disease that is caused by iodine deficiency?

What 3 things does T3 do in the brain?

A

Cretinism

Iodine deficiency during development

Short stature/impaired bone formation

Mental retardation

Delayed motor development

  1. Neuronal cell migration/differentiation
  2. Myelination
  3. Synaptic Transmission
38
Q

What are the main effects of T3 on the heart?

How can hyperthyroidism cause arrhythmias?

A
  1. Increases Cardiac Output
  2. Increases Resting Heart Rate and stroke volume
    - Hyperthyroidism can cause arrhythmias due to increase beta-adrenergic receptors
39
Q

What is a goiter?

What disease are associated with the following:

  1. Hyperthyroidism
  2. Hypothyroidism
A
  1. Enlarged thyroid
  2. Grave’s disease
  3. Hashimoto’s thyroiditis, idoine deficiency
40
Q

Graves Disease:

  1. What stimulates TSH
  2. What is elevated
  3. Hyperthyroid or Hypo? What are some associated symptoms?

What is the histology of the thyroid gland from a patient with graves disease?

A
  1. ANtibodies stimulate TSH receptor
  2. ELevated T4/T3
  3. HYPERTHYROID
    Diffuse symmetrical goiters with hyperthyroid symptoms:

tachycardia, opthalmopathy, irritability, hyperactivity, heat intolerance, weight loss, nervousness, muscle wasting

41
Q

Why is there a goiter in both Hyperthyroid and Hypothyroid patients?

A

Due to NEGATIVE feebdack

  1. HYPOTHYROID
    - not enough thyroid hormone
    - no negative feedback on anterior pituitary
    INCREASED PRODUCTION OF TSH = hyperactive follicular cells that result in goiter formation
  2. Hyperthyroid:
    also making more thyroid hormone
    - not due to negative feedback though, just more production of thyroid hormone in general
42
Q

Autoimmune Hasimotos Thyroiditis:

  1. Autoimmune destruction of what?
  2. Antibodies against? (2)
  3. Hyperthyroid or Hypothyroid?
A
  1. Destruction of thyroid follicles
  2. Antibodies against TPO, TG
  3. Diffuse goiter with hypothyroid symptoms: lethargy, fatigue, hair loss, cold intolerance, brittle nails decreased appetite, weight gain
43
Q

What is a THYROID STORM?

What is coupled?

What are the symptoms?

Tx?

A

Emergency life-threatening situation

HYPERTHYROID coupled with severe acute illness

Symptoms:

  1. High fever
  2. Tachycardia
  3. Altered Mental Status
  4. Severe Nausea, vomiting, diarrhea
  5. Severe circulatory collapse (resulting in death)

TX:

  1. PTU (propylthiouracil)
  2. Carbimazole (methimazole)
  3. Beta Blockers to restore normal heart function

FHB - Endocrine & Reproductive (17 decks)

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