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The thyroid (L7) Flashcards

1
Q

Blood supply to the thyroid

A

Superior from external carotid

Inferior from thyrocervical trunk

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2
Q

Venous drainage of thyroid

A

Superior, middle, and inferior thyroid veins that all drain into the internal jugular

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3
Q

Innervation of the thyroid

A

Middle and inferior cervical ganglia of sympathetic nervous system

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4
Q

Follicle of the thyroid

A

Epithelial cells surrounding a lumen filled with colloid

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5
Q

Major compound of the lumen

A

Thyroglobulin (TG)

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6
Q

Parafollicular cells (“C” cells)

A

Produce calcitonin and other proteins maintaining the follicle

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7
Q

Other cell types in the thyroid

A

Epithelial cells, fibroblasts, lymphocytes, adipocytes

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8
Q

What is the shape of follicular cells when activated by TSH?

A

Cuboidal

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9
Q

Microvilli

A

Extend into the colloid to facilitate transport of TG

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10
Q

Where are the parafollicular cells located?

A

In the basement membrane; no direct contact with the lumen

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11
Q

Two precursors necessary for thyroid hormone synthesis

A

Thyroglobulin and iodide

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12
Q

Daily dietary intake of iodine that results in thyroid deficiency

A
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13
Q

Wolf-Chaikoff effect

A

Intrathyroidal response that assures constancy of iodide storage in the face of changes in dietary iodide intake - increases in iodide intake decreases gland transport and hormone synthesis

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14
Q

How is the Wolf-Chaikoff effect used clinically?

A

High doses of iodine are used to shut down hormone synthesis in hyperthyroid patients

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15
Q

HPT axis

A

Hypothalamus: PVN releases TRH
TSH from anterior pituitary
T3/T4 feeds back on hypothalamus and pituitary

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16
Q

Intracellular “thyroid sensor”

A

Level of T3 in the anterior pituitary

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17
Q

Inhibition of thyroid stimulating hormone

A

Tonic inhibition by dopamine, somatostatin

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18
Q

T3 formation from T4

A

Peripherally deiodinated in thyrotropes and brain by type II deiodinase

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19
Q

How many steps in thyroid hormone synthesis are there?

A

7

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20
Q

NIS cotransporter

A

Takes up sodium and iodine on the basolateral surface of the follicle cell, “trapping” iodine inside

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21
Q

Thyroid peroxidase

A

Turns iodide to iodine

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22
Q

Movement of TG during T3/T4 synthesis

A

Transported from the follicle out the apical surface into the lumen

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23
Q

What is the fate of the iodine transported into the cell?

A

It leaves the apical membrane and is attached to the tyrosyl residues on TG

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24
Q

Once the tyrosyl residues are iodinated, what happens?

A

They are conjugated with T4 and T3

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25
Once the TG is conjugated, what occurs?
The compound is transported back into the follicular cell and packaged into an endosome
26
Once inside the cell, what happens to the T3/T4 conjugated TG?
Proteolysis - TG, MIT, DIT, T3, and T4 released from vesicle
27
Final step in T3/T4 synthesis
Transport of T3 and T4 across basolateral membrane and release into blood
28
Thyroxine's half-life
Long - ~7 days
29
Circulation in blood - thyroxine
Tightly bound to transport proteins; binds receptors with low affinity
30
Triiodothyronine - receptor activity
Binds with high affinity, low capacity
31
rT3
Reverse T3: biologically inactive
32
Carbimazole
Inhibits thryoid peroxidase; used as treatment for hyperthyroidism
33
T3 hormone structure
Formed by the combination of one MIT and one DIT residue
34
How is rT3 distinguished from T3?
Two iodinated residues on the outer ring instead of the inner ring, only one on the inner ring
35
T4 hormone structure
Formed by the coupling of two DIT residues
36
Radioactive iodine uptake scan
Used to test the function of the thyroid gland; use pertechnetate
37
Hot nodule
Area of increased iodine uptake and thyroid hormone synthesis; usually benign
38
Cold nodule
Area of dysfunctional/inactive iodine uptake and decreased thyroid hormone synthesis; can be benign or malignant
39
Normal uptake of radioactive iodine
25% after 24 hours
40
Parameters for hyper/hypothyroidism based on radioactive iodine uptake
>60%: hyperthyroid
41
Organification defect
Iodine cannot be added to tyrosyl residues; tested with perchlorate (NIS inhibitor)
42
Type 1 deiodinase
Outer and inner ring deiodinase found in the liver, kidney, thyroid, and skeletal muscle
43
Type 2 deiodinase
Outer ring deiodinase found in brain, pituitary, placenta, and cardiac muscle (THYROID SENSOR IN PITUITARY)
44
Type 3 deiodinase
Inner ring deiodinase found in brain, placenta, and skin
45
What is the difference between inner and outer ring deiodination?
Inner ring: deactivates (rT3 formation) | Outer ring: activates (T3 formation)
46
Which is in higher storage, T3 or T4?
T4; long half life
47
How much of T4 is switched over to T3?
80% peripherally; T4 has low affinity
48
How much of thyroid hormone is bound peripherally?
More than 99%
49
Breakdown of proteins binding thyroid hormone
TBG: 70% Transthyretin: 10% Albumin: 15-25%
50
Which form, T3 or T4, binds more tightly to carrier proteins?
T4; half life of 7 days vs T3's half life of 1 day
51
How long is TBG?
394 AA glycoprotein
52
What factors affect concentration of TBG?
Hepatitis, estrogen: increase | Nephrotic syndrome, steroids: decrease
53
Changes in TBG and effects on T3/T4
Bioavailable T3 usually doesn't change, but total levels of T3 and T4 do
54
To what family of receptors does the thyroid hormone receptor belong?
Nuclear receptor hormones; same as steroids
55
With what does the THR heterodimerize?
Retinoic acid receptor (RXR)
56
What type of cell expresses THR?
Almost every type
57
Physiologic effects of thyroid hormone
T3 increases mitochondrial activity and generates futile cycles, increasing oxygen consumption and heat production
58
Neurologic effects of thyroid hormone
Necessary for proper neural development - Induces neural cell migration/differentiation - Myelination - Synaptic transmission
59
Cretinism
Iodine deficiency during development, causing short stature, mental retardation, and delayed motor development
60
Physiologic effects on the heart
Increased cardiac output by increase in resting heart rate and stroke volume
61
Consequence on the heart of hyperthyroidism
Possible development of arrhythmias
62
Etiology of goiter production
Thyroid cancer (3:1 women:men) Hyperthyroidism; Graves' disease Hypothyroidism; Hashimoto's
63
Etiology of Graves' disease
Autoimmune disorder that causes stimulation of TSH receptors by long-acting thyroid stimulator (LATS)
64
Symptoms of Graves' disease
``` Diffuse bilateral goiters Irritability Nervousness Hyperactivity Muscle wasting Weight loss Heat intolerance Tachycardia Ophthalmopathy ```
65
Histology of Graves' thyroid
Scant colloid, tall columnar follicular cells, infiltration of lymphocytes
66
Etiology of Hashimoto's thyroiditis
Autoimmune disorder; antibodies against TPO and TG. Causes destruction of thyroid tissue
67
Symptoms of Hashimoto's
``` Lethargy Fatigue Weight gain Decreased appetite Hair loss Brittle nails Cold intolerance ```
68
What is thyroid storm?
An emergency life-threatening situation in which hyperthyroidism is coupled with severe, acute illness
69
Symptoms of thyroid storm
``` Tachycardia High fever Altered mental status Severe nausea, vomiting, diarrhea Severe circulatory collapse --> death ```
70
Treatment for thyroid storm
Carbimazole Propylthiouracil (PTU) - acute treatment Beta blockers to restore normal heart function

Endocrine (11 decks)

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