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
Q

Once the TG is conjugated, what occurs?

A

The compound is transported back into the follicular cell and packaged into an endosome

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26
Q

Once inside the cell, what happens to the T3/T4 conjugated TG?

A

Proteolysis - TG, MIT, DIT, T3, and T4 released from vesicle

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27
Q

Final step in T3/T4 synthesis

A

Transport of T3 and T4 across basolateral membrane and release into blood

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28
Q

Thyroxine’s half-life

A

Long - ~7 days

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29
Q

Circulation in blood - thyroxine

A

Tightly bound to transport proteins; binds receptors with low affinity

30
Q

Triiodothyronine - receptor activity

A

Binds with high affinity, low capacity

31
Q

rT3

A

Reverse T3: biologically inactive

32
Q

Carbimazole

A

Inhibits thryoid peroxidase; used as treatment for hyperthyroidism

33
Q

T3 hormone structure

A

Formed by the combination of one MIT and one DIT residue

34
Q

How is rT3 distinguished from T3?

A

Two iodinated residues on the outer ring instead of the inner ring, only one on the inner ring

35
Q

T4 hormone structure

A

Formed by the coupling of two DIT residues

36
Q

Radioactive iodine uptake scan

A

Used to test the function of the thyroid gland; use pertechnetate

37
Q

Hot nodule

A

Area of increased iodine uptake and thyroid hormone synthesis; usually benign

38
Q

Cold nodule

A

Area of dysfunctional/inactive iodine uptake and decreased thyroid hormone synthesis; can be benign or malignant

39
Q

Normal uptake of radioactive iodine

A

25% after 24 hours

40
Q

Parameters for hyper/hypothyroidism based on radioactive iodine uptake

A

> 60%: hyperthyroid

41
Q

Organification defect

A

Iodine cannot be added to tyrosyl residues; tested with perchlorate (NIS inhibitor)

42
Q

Type 1 deiodinase

A

Outer and inner ring deiodinase found in the liver, kidney, thyroid, and skeletal muscle

43
Q

Type 2 deiodinase

A

Outer ring deiodinase found in brain, pituitary, placenta, and cardiac muscle
(THYROID SENSOR IN PITUITARY)

44
Q

Type 3 deiodinase

A

Inner ring deiodinase found in brain, placenta, and skin

45
Q

What is the difference between inner and outer ring deiodination?

A

Inner ring: deactivates (rT3 formation)

Outer ring: activates (T3 formation)

46
Q

Which is in higher storage, T3 or T4?

A

T4; long half life

47
Q

How much of T4 is switched over to T3?

A

80% peripherally; T4 has low affinity

48
Q

How much of thyroid hormone is bound peripherally?

A

More than 99%

49
Q

Breakdown of proteins binding thyroid hormone

A

TBG: 70%
Transthyretin: 10%
Albumin: 15-25%

50
Q

Which form, T3 or T4, binds more tightly to carrier proteins?

A

T4; half life of 7 days vs T3’s half life of 1 day

51
Q

How long is TBG?

A

394 AA glycoprotein

52
Q

What factors affect concentration of TBG?

A

Hepatitis, estrogen: increase

Nephrotic syndrome, steroids: decrease

53
Q

Changes in TBG and effects on T3/T4

A

Bioavailable T3 usually doesn’t change, but total levels of T3 and T4 do

54
Q

To what family of receptors does the thyroid hormone receptor belong?

A

Nuclear receptor hormones; same as steroids

55
Q

With what does the THR heterodimerize?

A

Retinoic acid receptor (RXR)

56
Q

What type of cell expresses THR?

A

Almost every type

57
Q

Physiologic effects of thyroid hormone

A

T3 increases mitochondrial activity and generates futile cycles, increasing oxygen consumption and heat production

58
Q

Neurologic effects of thyroid hormone

A

Necessary for proper neural development

  • Induces neural cell migration/differentiation
  • Myelination
  • Synaptic transmission
59
Q

Cretinism

A

Iodine deficiency during development, causing short stature, mental retardation, and delayed motor development

60
Q

Physiologic effects on the heart

A

Increased cardiac output by increase in resting heart rate and stroke volume

61
Q

Consequence on the heart of hyperthyroidism

A

Possible development of arrhythmias

62
Q

Etiology of goiter production

A

Thyroid cancer (3:1 women:men)
Hyperthyroidism; Graves’ disease
Hypothyroidism; Hashimoto’s

63
Q

Etiology of Graves’ disease

A

Autoimmune disorder that causes stimulation of TSH receptors by long-acting thyroid stimulator (LATS)

64
Q

Symptoms of Graves’ disease

A
Diffuse bilateral goiters
Irritability
Nervousness
Hyperactivity
Muscle wasting
Weight loss
Heat intolerance
Tachycardia
Ophthalmopathy
65
Q

Histology of Graves’ thyroid

A

Scant colloid, tall columnar follicular cells, infiltration of lymphocytes

66
Q

Etiology of Hashimoto’s thyroiditis

A

Autoimmune disorder; antibodies against TPO and TG. Causes destruction of thyroid tissue

67
Q

Symptoms of Hashimoto’s

A
Lethargy
Fatigue
Weight gain
Decreased appetite
Hair loss
Brittle nails
Cold intolerance
68
Q

What is thyroid storm?

A

An emergency life-threatening situation in which hyperthyroidism is coupled with severe, acute illness

69
Q

Symptoms of thyroid storm

A
Tachycardia
High fever
Altered mental status
Severe nausea, vomiting, diarrhea
Severe circulatory collapse --> death
70
Q

Treatment for thyroid storm

A

Carbimazole
Propylthiouracil (PTU) - acute treatment
Beta blockers to restore normal heart function