The Thyroid Gland

Question 1

Pendrin

Answer 1

Molecular transporter on the apical surface of follicle cells that transports I- into the follicle lumen

*TG is transported out in a secretory vesicle

Question 2

Thyroid peroxidase

Answer 2

Oxidizes I- to I after it travels thru pendrin; also catalyzes the formation of T4 and T3 from MIT and DIT

-Process requires H2O2

Question 3

Thyroid Oxidase

Answer 3

Catalyzes the formation of H2O2 required for the iodination of MIT and DIT

Question 4

Colloid

Answer 4

Contains thyroglobulin and is an important reservoir for I-

Question 5

Secretion of T3

Answer 5

Colloid is taken up into endocytic vesicles at the apical membrane and then fuse w/ lysosomes that digest colloid liberating T3 and T4 which diffuse into circulation

Question 6

Iodotyrosine deiodinase

Answer 6

Deiodinates MIT and DIT to conserve I-

*People deficient in this enzyme will excrete excess MIT and DIT in their urine

Question 7

TBG

Answer 7

Synthesized in the liver and binds most T3 and T4

• T4 affinity >T3
• Synthesis stimulated by estrogens; down-regulated by malnutrition

Question 8

Salicylates and TBG

Answer 8

Decreases binding of thyroid hormone to TBG

Question 9

Iodothyronine deiodinases

Answer 9

Peripheral enzymes that convert T4 to either T3 (D1&D2) or rT3; occurs mostly in the liver and kidneys

*Allows tissues to self-regulate and degrade their thyroid hormone concentration

Question 10

Synthetic T4

Answer 10

Given to hypothyroid patients because it is not intestinally broken down but is converted to T3 at the pts. tissues

Question 11

Major Pathway of TH degradation

Answer 11

Stepwise deiodination of thyronine that releases I- back into the circulating pool

-Thyronine will be excreted

Question 12

Actions of TSH

Answer 12

Instant: Iodide trapping
Endocytosis of Colloid

Delayed: Increased transcription of TBG, TPO, and NIS genes

Chronic: Increased vessel growth
Follicle cell proliferation

Question 13

Principal regulation of TH

Answer 13

T3 and T4 negative feedback @ the pituitary

• Causes a down-regulation of TRHR and encodes the B-subunit of TSH that includes inhibitory portion
• Occurs at the other sites too tho

Question 14

Wolff-Chaikoff effect

Answer 14

Increased ingestion of iodide => suppression of TH synthesis; eventually will be overridden to resume normal production

*Used to treat thyrotoxicosis

Question 15

Iodide Trap

Answer 15

NIS removes I- from circulation via a gradient formed by Na+/K+-ATPases on the basolateral surface of follicle cells

*Transport can be blocked by HClO4-, CNS-, and TcO4-

Question 16

THRs

Answer 16

Bound to TREs along w/ RXRs and are activated/suppressed when T3 binds to the ligand-activation zone

*Normally bound to Histone deacetylase and CoRs; binding of T3 induces a conformational change that releases these factors and cause CoAs to bind

Question 17

Genes activated w/ T3 binding

Answer 17

Na+/K+-ATPases and B2 receptors among many others

Question 18

Bone age in hypothyroid children

Answer 18

Retarded growth

Question 19

Placental transfer of T3

Answer 19

Low; placenta has increased D3 (iodothyrine deiodinase) and converts T3 to metabolically inactive constituents

Question 20

Unchanged BMR in tissues exposed to T3

Answer 20

Brain, spleen, and testes

*Normally leads to increased CO and HR to compensate for increasedd BMR

Question 21

Treatment for hyperthyroidism

Answer 21

B-adrenergic blocking drugs

*T3 => Increased B-adrenergic receptors to potentiate effects of catecholamines

Question 22

Congenital hypothyroidism

Answer 22

Infants born w/ no thyroid tissue or defective TSH; leads to severe growth and mental retardation

*Babies commonly screened to prevent this

Question 23

Hashimoto’s Thyroiditis

Answer 23

Production of anti-TPO and anti-TG destroys thyroid follicles; can assay serum for these antibodies

Symptoms include: weight gain, reduced muscle tone, joint pain, *facial puffiness & periorbital swelling (build up of mucopolysaccharids) and hypercholesteremia

Question 24

Endemic Goiter

Answer 24

Common in third world countries w/ dietary deficiencies of iodine; caused by excess stimulation by TSH

Question 25

Myxedemic Coma

Answer 25

Severe mental deterioration alongside bradycardia, hypothermia, and respiratory depression

*Triggered by severe stress in chronically undertreated hypothyroidism

Question 26

Graves Disease

Answer 26

Primary cause of thyrotoxicosis; pts have proptosis (triggered by AI mechanisms) and lid retraction

• Serum contains TSI; stimulus TSH- receptors inducing increased production to thyroid hormone and increased sensitivity to catecholamines
• Other symptoms include: tachycardia, weight loss, muscle weakness, heat intolerance, and oligomenorrhea

Question 27

Assessment of iodide trap

Answer 27

Administer radioactive I- and scan the thyroid to examine the uptake