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Colin Endo/Repro > PHYS - Thyroid Gland > Flashcards

PHYS - Thyroid Gland Flashcards

1
Q

What is T4?

A

Tetraiodothyronine is a prohormone synthesized by the thyroid gland

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2
Q

What is T3?

A

Triiodothyronine is an active hormone synthesized by the thyroid gland

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3
Q

What are parafollicular C cells?

A

Cells outside the follicles of the thyroid gland that secrete Calcitonin

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4
Q

Which cells synthesize the thyroid hormones?

A

Follicular epithelial cells that surround the follicles containing colloid

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5
Q

What is colloid composed of?

A

Colloid is composed of newly synthesized thyroid hormones attached to thyroglobulin

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6
Q

What is the ratio of synthesized thyroid hormone (T4:T3)

A

T4:T3

10:1

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7
Q

What is the enzyme responsible for converting T4 into T3?

A

Deiodinase enzyme

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8
Q

What is the inactive form of T3?

A

Reverse T3 is inactive

It has an iodine missing from the wrong benzene ring

1% of synthesized thyroid hormone is made into Reverse T3

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9
Q

What are the sources of T3?

A

80-90% of T3 is produced via peripheral conversion (via deiodoinase)

10-20% of T3 is directly secreted from the thyroid gland

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10
Q

What can cause a decrease in conversion of T4 to T3?

A

Fasting
Medical and Surgical stress
Catabolic disease

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11
Q

What is the NIS channel?

A

It is a Na+/I- symporter on the apical membrane of the follicular cells of the thyroid gland

It transports 2 Na+ for every I-

It is also called the Iodine trap

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12
Q

What are Pendrin channels?

A

They are channels found on the basolateral membrane of the follicular cells of the thyroid gland

They are responsible for secreting I- anions into the thyroid follicles

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13
Q

What is the role of Thyroid peroxidase?

A

Thyroid Peroxidase is an enzyme that takes two Iodide (I-) anions and forms molecular Iodine (I2)

Molecular I2 can be added MIT/DIT/Thyroglobulin in the follicle to form the colloid

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14
Q

What specifically does TSH do to follicular cells?

A

TSH stimulates pinocytosis of colloid fluid into the follicular cell which then gets acted on by proteases (lysosomes) to remove the T3 and T4 from the thyroglobulin molecule

T3 and T4 are then secreted into the blood

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15
Q

What is thyroglobulin?

A

Thyroglobulin is a binding protein that is synthesized in the follicular cells of the thyroid gland.

It is translated in the rough ER and packaged in the Golgi before being secreted into the follicle

Thyroglobulin binds to MIT, DIT, T3, and T4 in the follicle. The collection of thyroid hormone and its precursors bound to thyroglobulin is what makes up the colloid fluid

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16
Q

Describe the process of thyroid hormone synthesis and secretion

A

NIS Channel (iodine trap) on the basolateral membrane (facing the blood) brings in one I- anion with two Na+ cations into the follicular cell

Thyroglobulin binding protein is synthesized in the follicular cell and secreted into the follicle

Pendrin channel on the apical membrane (facing the follicle) is an I- anion channel that sends I- into the follicle

Peroxidase enzyme takes two I- anions to form molecular Iodine (I2)

Molecular I2 binds with MIT (to form DIT), DIT (to form T3), and T3 (to form T4)

MIT, DIT, T3, and T4 bind with thyroglobulin binding molecules in the follicle forming the colloid

TSH signaling induces Follicular cells to conduct pinocytosis of the colloid fluid.

Thyroglobulin molecules collected in the follicular cells from pinocytosis interact with proteases to break down the binding proteins, freeing up the thyroid hormone molecules for secretion.

MIT and DIT do not get secreted; instead they interact with deiodinase enzymes, which remove the iodoine molcules from MIT and DIT in order to be recycled back into the follicle

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17
Q

What is PTU?

A

Propylthiouracil

It is a drug that is used to treat hyperthyroidism

PTU blocks the actions of thyroid peroxidase, therefore inhibiting the oxidation of iodide (I-) anions into molecular Iodine

18
Q

What is the function of Perchlorate and Thiocynate?

A

Perchlorate and Thiocynate are drugs that block the NIS channel on the basolateral membrane of the follicular cells of the thyroid gland, preventing Iodine uptake from the blood into the cell

19
Q

What happens to thyroid hormone synthesis when iodide availability is restricted?

A

T3 is favored over T4

20
Q

How is thyroid gland activity assessed?

A

Radioactive iodine uptake test

21
Q

In what state does thyroid hormone travel in the blood?

A

99% bound to plasma proteins

1% free

22
Q

How do the half lives of T3 and T4 compare?

A

T4 has a greater half life than T3

T4 = 6 days
T3 = 1 day
23
Q

What are the main binding proteins that carry thyroid hormone in the blood?

A

TBG (Thyroxine-binding Globulin) - 70%

  • Synthesized in the liver
  • Has a higher affinity for T4 than T3

Transthyretin (TTR) - 10-15%

Albumin - 15-20%

24
Q

What happens to T4 when it is delivered to the tissues?

A

T4 is a prohormone

T4 is converted to the active form of thyroid hormone, T3, in the tissues

OR sometimes it is converted to reverse T3 (inactive)

25
Q

How does a T3 resin uptake test work?

A

A known amount of labelled, free T3 is added to blood.

T3 will bind to TBG as long as there are unboundsites available

Once all sites are filled, anti-T3 antibodies are added and precipitate out of solution.

This allows you to determine the amount of TBG in the blood

26
Q

What happens to TBG levels in hepatic failure and what effect does this have on thyroid hormone function?

A

Hepatic failure decreases blood levels of TBG (which is synthesized in the liver

This causes an increase in levels of free T3 and T4

Increased levels of free T3,T4 provide negative feedback, inhibiting thyroid hormone synthesis

27
Q

What happens to TBG levels during pregnancy, and what effect does this have on thyroid hormone funtion?

A

TBG levels increase during pregnancy

This causes a decrease in levels of free T3,T4

Decreased levels of free T3,T4 promote thyroid hormone synthesis and secretion

Total levels of T3, T4 increase, but levels of free T3,T4 remain normal

28
Q

What type of receptor does TSH interact with?

A

GPCR - specifically Gs

Activates Adenylyl cyclase, which causes an increase in cAMP, which activates PKA, which phosphorylates target proteins

29
Q

What is the Wolff-Chaikoff effect?

A

An inhibitory effect on thyroid hormone synthesis due to excessive Iodine intake

30
Q

What action of thyroid hormone is primarily responsible for the increase in basal metabolic rate?

A

Thyroid hormones cause an increase in synthesis of Na-K-ATPase channels, which are primarily responsible for the increase in BMR seen with Thyroid Hormone

31
Q

What affect does thyroid hormone have on cardiac tissue?

A

Increases heart rate and cardiac output

Promotes synthesis of cardiac Beta-adrenergic receptors making the cardiac tissue more sensitive to sympathetic innervation

32
Q

What is the pathophysiology of hyperthyroidism?

A

Metabolism:

  • Heat intolerance
  • Weight loss
  • Increased BMR

Bone:
- Osteoperosis

CNS:

  • Agitation
  • Anxiety
  • Difficulty concentrating
  • Hyperreflexia

Skin:
- Sweating

CV System:

  • Tachycardia
  • Atrial Fibrulation
  • Palpitations
  • High-output cardiac failure

Intestine:
- Diarrhea

33
Q

What is the pathophysiology of hypothyroidism?

A

Metabolism:

  • Cold intolerance
  • Weight gain
  • Decreased BMR

Bone:
- Stunted growth

CNS:

  • Slowed movement
  • Impaired memory
  • Decreased mental capacity

Skin:
- Dry

CV System:

  • Bradycardia
  • Decreased contractility
  • Decreased cardiac output Heart Failure

Intestine:
- Constipation

34
Q

What is Primary Hyperparathyroidism vs Secondary Hyperthyroidism?

A

Primary = Graves Disease - Excessive secretion of TH from the thyroid gland (TSH levels will be decreased due to negative feedback)

Secondary = Excessive secretion of TSH from the anterior pituitary gland

35
Q

What is Grave’s Disease?

A

Thyroid Stimulating Immunoglobulins (TSIs) that are analogous to TSH will stimulate the TSH receptor on the thyroid gland promoting synthesis and secretion of TH despite lack of actual TSH signaling from the anterior pituitary gland

Major clinical signs:

  • Exophthalmos (protrusion of eyeball)
  • Periorbital edema
36
Q

What is Sheehan’s syndrome?

A

Hypothyroidism due to pituitary necrosis secondary to blood loss during or after delivery of baby (no TSH secretion from anterior pituitary, and therefore no TH secretion from thyroid gland)

37
Q

How do you treat hypothyroidism?

A

T4 supplementation

In older women, over prescribing T4 supplements can cause osteoporosis

38
Q

What is Hashimoto’s Thyroiditis?

A

Autoimmune disorder

Antibodies produced to fight against Thyroglobulin protein in colloid or Thyroid Peroxidase enzyme

Prevents synthesis of Thyroid hormone

Excessive TSH secretion occurs, causing production of a goiter

39
Q

What is cretinism?

A

Cretinism is congenital hypothyroidism

Caused by iodine deficiency, impaired development of thyroid gland

Symptoms:

  • Mental retardation
  • Growth retardation
  • Dry skin
  • Protruding tongue
  • Respiratory difficulty
  • Feeding problems
40
Q

What causes goiters?

A

TSH receptor activation causes hypertrophy of thyroid gland (goiter)

Anyway TSH receptor is activated excessively will cause a goiter, whether or not it is TSH that is activating it

(Graves disease causes goiter even though it is an Immunoglobulin that activates the TSH receptor, not actual TSH)

Colin Endo/Repro (12 decks)

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