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Block 3 Week 6 Meg > O'Driscoll: Thyroid Gland > Flashcards

O'Driscoll: Thyroid Gland Flashcards

1
Q

The thyroid gland is located immediately below the (blank) on each side of and anterior to the trachea

A

larynx

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2
Q

Thyroid gland is made up of the following cell types: (blank) cells which synthesize thyroid hormone, (blank) cells which line the capillaries, (blank) cells which produce calcitonin, and fibroblasts, lymphocytes, and adipocytes.

A

follicular; endothelial; C cells

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3
Q

Follicular cells are closed follicles filled with (blank), whose major constituent is thyroglobulin. They are lined with cuboidal epithelial cells.

A

colloid

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4
Q

Thyroid epithelial cells are morphologically and functionally (blank). Their apical surface faces the follicular lumen, where (blank) is stored. Their basolateral surface faces the interstitium and is exposed to the (blank).

A

polarized; colloid; bloodstream

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5
Q

Cellular and tissue organization is critical to understanding the relationship between (blank) accumulation and hormone biosynthesis.

A

Iodide

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6
Q

Most (93%) of thyroid secretion; most is converted to T3 in the tissues

A

tetraiodothyronine (thyroxine; T4)

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7
Q

7% of total thyroid secretion; similar function as thyroxine but much more potent

A

T3

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8
Q

Is [plasma] greater for T3 or T4?

A

T4

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9
Q 
TSH
Thyroglobulin
Iodine
Membrane transporters
Enzymes
A

Factors involved in hormone synthesis

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10
Q

(blank) plays an important role in the synthesis and storage of thyroid hormone

A

thyroglobulin

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11
Q

Thyroglobulin is a large glycoprotein containing multiple (blank) residues. It is synthesized in the thyroid (blank) cells, is secreted through the (blank) membrane into the follicular lumen, and is stored in the colloid. It’s a scaffold.

A

tyrosine; follicular epithelial; apical

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12
Q

Thyroid hormones incorporate (blank) into their structure. Adequate (blank) intake is required for normal thyroid hormone production. (blank) deficiency is the world’s most prevalent, yet easily preventable cause of brain damage.

A

Iodine (x3)

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13
Q

Where does the biosynthesis of thyroid hormones take place?

A

In both the colloid and follicular epithelial cells

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14
Q

Stage 1 in thyroid hormone synthesis; transport of iodides from the blood into the thyroid cells and follicles

A

Iodide trapping

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15
Q

(blank) actively pump iodide into the cytosol; energy for transporting iodide against a concentration gradient comes from the (blank) pump. Iodide is transported into the follicle lumen by (blank) (a chloride-iodide counter-transporter).

A

sodium iodide symporters (NIS); Na+/K+ ATPase; pendrin

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16
Q

Process of concentrating iodide in the cell; influenced by TSH

A

Iodide trapping

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17
Q

Iodide transcellular transport relies on the functional/morphological (blank) of the cell

A

polarization

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18
Q

Concentration of iodide inside the thyroid cells is normally (blank) times higher than in the blood

A

30x

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19
Q

Stage 2: Formation and secretion of (blank)

A

thyroglobulin

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20
Q

ER and Golgi synthesize and secrete (blank) into the follicular colloid. Each molecule of thyroglobulin contains about 140 (blank) amino acids - some are major substrates that combine with iodine to form the thyroid hormones.

A

thyroglobulin; tyrosine

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21
Q

Where do thyroid hormones form?

A

Within the thyroglobulin molecule!

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22
Q

Stage 3: (blank) of iodide and coupling of iodine with thyroglobulin

A

oxidation

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23
Q

Iodide exits the apical membrane and is oxidized by (blank). Oxidized iodine combines directly with multiple tyrosine amino acids within the thyroglobulin molecule (organification), and within secs to mins, 20% of the tyrosines are (blank)

A

thyroperoxidase; iodinated

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24
Q

Formation of T3 and T4 requires successive stages of (blank) and coupling of iodotyrosine residues

A

iodination

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25
Q

Tyrosine is first iodinized to monoiodotyrosine and then to diiodotyrosine. What is formed when two molecules of DIT are coupled together? What is formed when one molecule of MIT is coupled with one molecule of DIT? Small amounts of (blank) are formed but this has little activity

A

T4; T3

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26
Q

Catalyzes the oxidation of iodide
Iodination of tyrosines on thyroglobulin (organification)
Synthesis of T4 or T3 from two iodotyrosines

A

thyroperoxidase (TPO)

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27
Q

What happens if TPO is blocked or absent?

A

Rate of formation of thyroid hormones is zero

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28
Q

(blank) in the colloid acts as storage form of thyroid hormones

A

thyroglobulin

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29
Q

Thyroid hormones remain part of the thyroglobulin molecule during storage in the (blank). High storage capacity of thyroid. If no iodine available, how long can thyroid hormone secretion be maintained?

A

follicular colloid; 2-3 months

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30
Q

Stage 4: (blank) of thyroglobulin into the follicular cell via pseudopodia, fusion with lysosomes, digestion of thyroglobulin, and release of thyroid hormones into the bloodstream

A

endocytosis

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31
Q

Stage 5: (blank) of iodine

A

recycling

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32
Q

(blank)% of iodinated tyrosine in thyroglobulin never becomes T3 or T4 (remains as MIT or DIT). When thyroglobulin is digested, MIT and DIT are freed in the cytosol but are not secreted into the blood. Iodine is cleaved from MIT and DIT via (blank) and recycled

A

75%; deiodinase enzyme

33
Q

This can cause iodine deficiency due to failure of recycling process

A

congenital absence of deiodinase

34
Q

In the blood stream, >99% of T3 and T4 combine with plasma proteins synthesized by the liver. Less than 1% of thyroid hormone is found free. What is the most common plasma protein?

A

Thyroxine binding globulin

35
Q

Binding proteins are (blank), and acute changes in hormone secretion have very little effect on free hormone concentrations

A

unsaturated

36
Q

What are two things that can alter an individual’s binding-hormone capacity?

A

disease

hormonal changes

37
Q

If hormone levels increase, binding protein synthesis will also increase to maintain (blank) of free and bound hormone. Dynamic changes occur throughout the life of an individual in health or disease.

A

equilibrium

38
Q

The binding proteins cause thyroid hormones to be released to the tissue cells slowly. Which thyroid hormone has a greater affinity for the binding protein? Which has a longer halflife?

A

T4 (10x higher!)

T4 has a longer half life

39
Q

Binding of thyroid hormones to plasma proteins ensures these two things

A
  1. a circulating reserve

2. delays their clearance

40
Q

What percentage of thyroid hormone released by the gland is T4? What is the main source of circulating T3?

A

93%; peripheral deiodination of T4 by deiodinases

41
Q

There is a sequential deiodination process beginning with T4, leading first to the more active form (blank) and finally to complete inactivation (blank).

A

T3; T2

42
Q

This deiodinase is found in liver, kidney, and thyroid. Catalyzes both outer and inner ring deiodination. Takes T4–>T3, T4–>rT3, and T3–>T2
MAJOR SOURCE OF CIRCULATING T3

A

deiodinase type I

43
Q

This deiodinase is found in brain, pituitary, and thyroid, skeletal and cardiac muscle. Only deiodinates outer rings. Takes T4–>T3
MAJOR SOURCE OF LOCAL T3 IN TISSUES

A

deiodinase type II

44
Q

This deiodinase is found in brain, placenta, and fetal tissues. Only deiodinates inner rings. Inactivates T3, allows placental protection of the fetus by decreasing T3 levels, and protects adult brain from high thyroid hormone conc.

A

deiodinase III

45
Q

Thyroid hormones have a (blank) onset and a (blank) duration of action. Actions of T3 are much quicker than T4, which has a long latency period.

A

SLOW; LONG

46
Q

Principle regulator of thyroid hormone

A

TSH

47
Q

Action of TSH

A

binds to TSH receptor; binding initiates cAMP second messenger system; increases activity of thyroid glandular cells

48
Q

TSH has both genomic and non-genomic effects. Its genomic effects include PROMOTING GENE TRANSCRIPTION of these things…

A

Iodide pump
thyroglobulin
NO synthase
Local growth factors

49
Q

TSH has non-genomic effect via an increase in cAMP. It increases proteolysis of (blank), increases (blank) activity, and increases iodination of tyrosine

A

thyroglobulin; iodide pump

50
Q

What type of feedback controls thyroid hormone synthesis and release

A

negative feedback

51
Q

Increased thyroid hormone in the body decreases secretion of (blank). Thyroid hormone inhibits these three things via negative feedback.

A

TSH

  1. TRH secretion from hypothalamus
  2. Gene expression for TSH and for TRH receptor on pituitary
  3. TSH release from the pituitary
52
Q

Thyroid hormone receptors have a higher affinity for (blank). TRs are (blank) receptors, and bind enhancer elements on DNA (thyroid response elements). TRs initiate trx and formation of new proteins.

A

T3; nuclear

53
Q

Which effects of thyroid hormone are slower? Genomic + non-genomic?

A

Genomic

54
Q

Genomic effects are mediated primarily by (blank) of a large number of genes. The net result is increase in functional activity throughout the body.

A

transcriptional regulation

55
Q

Non-genomic effects are faster and are independent of their effects on (blank). Appear to involve activation of secondary messengers and protein kinase signaling cascades. Regulation of ion channels and transporters.

A

gene trx

56
Q

Thyroid hormones increase activity of almost all tissues. What effects do they have?

A 
increase size and number of mito so increased ATP production
increase active transport of ions
increase synthesis of metabolic proteins
increase O2 consumption
increase BMR and heat production
57
Q

Thyroid hormones increase metabolism of (blank), (blank), and (blank). This leads to increased O2 consumption and increased BMR.

A

carbohydrates, lipids, nitrogen

58
Q

Excess thyroid hormone can cause a relative (blank) deficiency and an increased (blank), leading to a drop in body weight. With greater thyroid hormone, almost always drop in body weight.

A

vitamin; metabolism

59
Q

Normal levels of thyroid hormone are essential for growth and development of the fetal and neonatal (blank). Also essential for the skeletal system!

A

brain

60
Q

Effects of thyroid hormone on cardiovascular system include increased (blank), (blank), (blank), (blank). What portion of pulse pressure will rise? What portion will drop?

A

blood flow; cardiac output; heart rate; heart strength

systolic BP, diastolic BP

61
Q

When thyroid hormone is (blank), heart muscle strength becomes depressed because of long-term excessive protein catabolism

A

increased

62
Q

Other effects of thyroid hormone.

One of the most characteristic signs of hyperthyroidism

A

increased respiration, increased GI motility, effects on sleep, muscle vigor, CNS, ANS
fine muscle tremor

63
Q

In the pancreas, hyperthyroidism can cause increased need for (blank) secretion. In the pituitary, stimulates (blank) production and inhibits (blank)

A

insulin; growth hormone; TSH

64
Q
  • Diffuse toxic goiter (Grave’s disease)
  • Hyperfunctioning thyroid nodules (e.g. toxic adenoma, toxic multinodular goiter) → autonomous hypersecretion of thyroid hormones, LOW TSH
  • Therapy induced hyperthyroidism
A

Primary hyperthyroidism

65
Q
  • TSH secreting pituitary adenomas

- HIGH TSH, T4 and T3

A

Secondary hyperthyroidism

66
Q

antibodies calledthyroid-stimulating immunoglobulins(TSIs) form against the TSH receptor in the thyroid gland
T4 and T3 high, TSH low

A

Grave’s disease

67
Q

Signs and symptoms of Grave’s disease, including enlargement of the thyroid gland, virtually all result from direct and indirect effects of hyperthyroidism except these three

A

goiter
pretibial myxedema (cutaneous/dermal edema)
Grave’s opthalmopathy (eyeball probs)

68
Q

(protrusion of the eyeballs): Autoimmune reaction causes edematous swelling of retro-orbital tissues and degeneration of extraocular muscles

A

exophthalmos

69
Q

(inability to achieve or maintain convergence, limited superolateral or upward gaze), blurred or double vision, feeling of pressure behind the eyes
Irritation/ulceration of the cornea

A

thyroid stare

70
Q 
High excitability
Intolerance to heat
Sweating
Mild/extreme weight loss
Increased bowels
Muscle weakness
Hand tremor
Fatigue, but sleepless
A

Signs of hyperthyroidism

71
Q

Hashimoto’s disease – autoimmune disease

Endemic Colloid Goiter- dietary iodine deficiency

Congenital hypothyroidism- Cretinism

A

Primary hypothyoidism

72
Q

Disorders of the anterior pituitary or hypothalamus → lack of stimulation of the TSH receptor due to impaired TSH release –> low TSH, T4 and T3

A

Secondary hypothyroidism

73
Q

LOW T3 and T4, HIGH TSH

autoantibodies against thyroglobulin, thyroperoxidase, TSH receptor (blocking type)

A

Hashimoto’s disease

74
Q 
Fatigue 
Sluggishness
Slow heart rate
Weight gain
Constipation
Myxedema
Intolerance to cold
Goiter
Hypercholesterolemia
A

Symptoms of hypothyroidism

75
Q

What can cause endemic colloid goiter?

A

Iodide deficiency

76
Q

Deficient iodide-trapping mechanism
Deficient peroxidase system
Deficient coupling of iodinated tyrosines in the thyroglobulin molecule
Deficieny deiodinase enzyme

A

Abnormalities that can lead to colloid goiter

77
Q

Cause: Extreme hypothyroidism during fetal life and infancy due to congenital lack of thyroid gland or dietary iodine insufficiency

Symptoms & signs: neonate may have normal appearance and function (maternal thyroid hormones)
Symptoms appear a few weeks after birth:
sluggish movements, retarded physical
and mental development

Unless treatment begins immediately, mental
growth remains permanently and severely retarded
(CRITICAL TIME WINDOW)

A

Congenital hypothyroidism: CRETINISM

78
Q

autoimmune “thyroiditis” (thyroid inflammation) → progressive deterioration and finally fibrosis of the gland, with resultant diminished or absent secretion of thyroid hormone

A

Other causes of primary hypothyroidism

79
Q

How much iodide is recommended in the diet per year?

A

50 mg

Block 3 Week 6 Meg (7 decks)

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