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Neuro/Endo Leftovers-ish > 5. The Thyroid Gland > Flashcards

5. The Thyroid Gland Flashcards

1
Q

What is the primary secretory product of thyroid follicular cells?

A

T4

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2
Q

At what point would radio labeled iodine uptake peak if the patient had hyperthyroidism not related to Graves’ disease?

A

Roughly 18 hours.

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3
Q

Why might hypothyroidism contribute to type II diabetes?

A

Because thyroid hormone enhances insulin-dependent glucose uptake.

Hypothyroidism means more insulin is necessary to uptake the same amount of glucose, which can lead to glucose resistance.

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4
Q

How might hypothyroidism structurally damage the heart?

A

Thyroid hormone stimulates the construction of myosin.

Hypothyroidism results in deficits of myosin.

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5
Q

What amino acid is the backbone for all of the thyroid hormones?

A

Tyrosine.

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6
Q

What is the relationship between cholesterol/triglycerides and thyroid hormone?

A

They are inversely related. High thyroid hormone corresponds with low triglycerides/cholesterol.

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7
Q

What two precursor molecules come together to form tetraiodothyronine (T4)?

A

Diiodotyrosine + diiodotyrosine = tetraiodothyronine (T4).

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8
Q

Why would a thyroid binding resin test come back differently in a patient early on in pregnancy to a patient later on in pregnancy?

A

Early on, TBG levels increase, resulting in less free T3. Later on T3 and T4 synthesis increases, resulting in “clinically euthyroid” results.

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9
Q

What three clinical states are associated with reduced conversion of T4 to T3?

A

Fasting.

Medical and surgical stress.

Catabolic disease.

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10
Q

How might hypothyroidism damage the contractility of the heart?

A

Thyroid hormone stimulates the production of Ca2+ ATPase.

Hypothyroidism damages Ca2+ ATPase, which is necessary for proper cardiac contraction.

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11
Q

What would be the effect of hyperthyroidism on the intestines?

A

Diarrhea.

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12
Q

What should we suspect if we see a decreased T3 resin uptake?

A

Increased TBG.

Less T4 (hypothyroidism).

Pregnancy (early phases of high TBG, before T3 and T4 synthesis increases).

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13
Q

What would be the effect of excess thyroid hormone on bone?

A

Osteoporosis.

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14
Q

What are the effects of hypothyroidism on the skin?

A

Dry skin.

Myxedema.

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15
Q

What are the three functions of thyroid peroxidase?

A

Oxidizes I- (I- -> I2).

Binds I2 to thyroglobulin, forming MIT and DIT.

Uses MIT and DIT to make T3 and T4.

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16
Q

At what point would radio labeled iodine uptake into the thyroid gland peak if the patient was normal?

What percentage of the radio labeled iodine would be absorbed?

A

Roughly 12 hours.

25% of radio labeled iodine would be absorbed.

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17
Q

What are the symptoms of cretinism?

A

Feeding problems.

Respiratory difficulty.

Protruding tongue.

Curse facial features.

Growth and mental retardation.

Jaundice.

Dry skin.

Hypotonia.

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18
Q

On the most basic molecular level, what is responsible for the actions of thyroid hormone?

A

Thyroid hormone activates nuclear receptors and the cAMP second messenger system.

19
Q

If a patient presents with an anti-thyroid antibody, what disease should you immediately be thinking?

A

Hashimoto’s thyroiditis.

20
Q

What would the effects of hypothyroidism be in a fetus?

What would cause these issues?

A

Lack of proper bone formation due to a lack of thyroid hormone’s synergistic effects on growth hormone and somatomedin.

Abnormal synaptic development, decreased dendritic branching and myelination, and cretinism. This is due to thyroid hormone’s essential function in the development of the central nervous system.

21
Q

What would a T3 binding resin test show if the patient had hepatic failure?

A

Increase in the level of free T3 and T4, followed by inhibition of synthesis of T3 and T4.

22
Q

What would be the effect of hypothyroidism on the cardiovascular system?

A

Bradycardia.

Decreased contractility.

Decreased cardiac output.

Heart failure.

23
Q

What are the possible causes of goiter discussed in class?

A

TSH excess - such as from a pituitary adenoma or Hashimoto’s

Iodine deficiency.

24
Q

If the thyroid is not producing T4, what hormone would we expect to be increased?

A

Thyroid stimulating hormone.

T4 inhibits thyroid stimulating hormone, so its absence increases thyroid stimulating hormone.

Thyrotropin releasing hormone (TRH) does not appear to be elevated as a result of absent or reduced T4.

25
Q

What are some of the potential causes for cretinism?

A

Iodide deficiency.

Maternal intake of anti-thyroid medications.

Impaired development of the thyroid gland.

Inherent deficit in the synthesis of thyroid hormones.

26
Q

What is inhibited by perchlorate and thiocyanate?

A

Na+/I- co-transporter.

27
Q

What percentage of radio labeled iodine would be absorbed by the thyroid gland in a patient with hypothyroidism?

A

Roughly 5 to 10%.

28
Q

What effects do thyroid hormone have on the cardiovascular system?

A

Increased β1-adrenergic activity (contractility, force of contraction, etc.).

Decreased systemic vascular resistance.

Ultimately increased blood volume.

29
Q

Where do we find type I and type II deiodinases, respectively?

A

Type I deiodinases are in the periphery.

Type II deiodinases are located on the anterior pituitary.

30
Q

What is the basic cause of cretinism?

A

Fetal hypothyroidism.

31
Q

Is Graves’ disease primary or secondary hyperthyroidism?

A

Primary hyperthyroidism.

32
Q

How might lack of thyroid hormone lead to night blindness?

A

Thyroid hormone is required for the conversion of carotene to vitamin A, which is necessary to prevent night blindness.

33
Q

What is the negative feedback system in the hypothalamus-pituitary thyroid axis?

A

T3 and T4 inhibit the anterior pituitary from secreting thyroid stimulating hormone directly, and the hypothalamus from secreting thyrotropin releasing hormone by increasing metabolic actions.

34
Q

After how many hours would radio labeled iodine in the thyroid gland peak if the patient had Graves’ disease?

A

Roughly 5 hours.

35
Q

How might hypothyroidism damage the sympathetic nervous system’s ability to interact with target organs (such as the heart)?

A

Thyroid hormone stimulates the production of β1-adrenergic receptors.

Hypothyroidism results in reduced β1-adrenergic receptors.

36
Q

What is the Wolff-Chaikoff effect?

A

Describes how iodine inhibits thyroid peroxidase.

(Specifically inhibits “organification.” I2 + thyroglobulin -> thyroglobulin + MIT + DIT)

37
Q

How does iodine get into the thyroid follicular cell?

A

Na+/I- symporter, down the concentration gradient created by the Na/K ATPase.

38
Q

What is the function of the drug PTU (propylthiouracil)?

A

Inhibits thyroid peroxidase to reduce the amount of T3 and T4 released into the bloodstream.

(Treat hyperthyroidism / Graves’ disease)

39
Q

What is the function of pendrin?

A

Pendrin shuttles I- out of the thyroid follicular cells and into the follicle, in exchange for a Cl-.

Cl-/I- counter-transporter.

40
Q

What is the basic pathophysiology of Graves’ disease?

A

Thyroid stimulating immunoglobulins attach to the receptor for thyroid stimulating hormone on the thyroid follicular cells without thyroid stimulating hormone being present.

41
Q

What is the basic pathophysiology of Hashimoto’s thyroiditis?

What lab test results would be expect to find?

A

Autoantibodies against either thyroid peroxidase or thyroglobulin – preventing production of T3 and T4.

High TSH, possibly even leading to goiter on physical exam.

42
Q

What inhibits the Na+/I- co-transporter?

A

Perchlorate.

Thiocyanate.

43
Q

What ubiquitous transporter is stimulated by thyroid hormone?

A

Na/K ATPase.

(Many other transport proteins as well.)

44
Q

What three proteins carry thyroid hormone in the blood?

A

Thyroxine binding protein.

Transthyretin.

Serum albumin.

Neuro/Endo Leftovers-ish (15 decks)

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