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61 Cards in this Set

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  • Back
The Thyroid gland maintains metabolic homeostasis by regulating these 3 things
1. Growth & development

2. Body temperature

3. Energy levels
What hormones are involved in accomplishing the functions of the thyroid gland?
1. Triiodothyronine = T3

2. Tetraiodothyronine = T4 = Thyroxine
What is the molecular composition of T3?
one Monoiodotyrosine (MIT) + one Diiodotyrosine (DIT)
What is the molecular composition of T4?
2 Diiodotyrosine (DIT)
What is the Thyroglobulin ratio of T3 and T4?
1 T3 molecule for every 5 T4 molecules


T3:T4 = 1:5
How much Iodide (I-) does the Thyroid gland remove from the extracellular pool each day?
75 mg
Thyroid hormone synthesis:
-Iodide is taken up by Thyroid follicular cells via a membrane __1__ transporter
-Iodide is coupled to __2__ residues on the __3__ molecule (=organification)
-formation of __4__ &__5__
-__6__ catalyzes coupling of 2 DIT molecules to form T4 or one molecule each of MIT and DIT to form T3
-Thyroglobulin is stored as __7__ in the lumen
-__8__ signals secretion to hydrolyze Thyroglobulin to free MIT, DIT, T3 & T4
1. Na+/I-
2. tyrosine
3. thyroglobulin
4. MIT = monoiodotyrosine
5. DIT = diiodotyrosine
6. Thyroid peroxidase
7. colloid
8. TSH
Plasma T3 and T4 are REVERSIBLY bound to __1__

Why is most of the thyroid hormone that is released T4?
Thyroxine-binding globulin

T4:T3 ratio in Thyroglobulin is 5:1
The peripheral metabolism of T4 is mainly by what mechanism?

What 2 things does it form?

1. T3 = 3-4 times more potent than T4
2. rT3 = metabolically inactive
Give 2 reasons why the total serum levels of T4 are higher than T3
1. more of it is released (5:1 ratio)

2. metabolic clearance of T3 is much higher
Just know which one is higher and which one is lower
Explain Hypothalamic-Pituitary-Thyroid Regulation
1. Paraventricular nuclei in the Hypothalamus secrete TRH
2. TRH stimulates the Anterior Pituitary to release TSH
3. TSH acts on Thyroid to release T3 & T4
4. T3 & T4 act by negative feedback to inhibit formation of TRH & TSH
Describe the Autoregulation within the Thyroid gland
Modifies Thyroid hormone synthesis through blood iodine levels
-high iodine levels → inhibit iodide organification → reduced T3/T4 synthesis → hypothyroidism

**counterintuitive b/c the same substance, iodine, has opposite effects and
the effects depend on the concentration --> higher plasma Iodine = lower T3/T4
Explain Grave's Disease
Autoantibody to the TSH receptor in the Thyroid causes increased T3/T4 release

**TRH and TSH levels will be decreased due to negative feedback of T3/T4
Explain Hashimoto's Disease
Destructive Autoantibody causing decreased T3/T4 release

**TRH and TSH will be elevated b/c T3/T4 are not present for negative feedback
Thyroid hormone receptors located in all cells are monomers that interact with ___1____ to form heterodimers

In the absence of T3 the heterodimer associates with a __2__ complex that binds to DNA to __3__

In the presence of T3 the __4__ dissociates, while __5__ form to stimulate __6__
1. Retinoic Acid X Receptor (RXR)
2. co-repressor
3. inhibit gene expression
4. co-repressor
5. coactivators
6. Gene expression

** = T3 stimulates gene expression
T3 receptors belong to a superfamily of __1__ receptors (c-erb which includes receptors for __2__ and __3__)
1. nuclear

2. steroid hormones

3. Vitamins A & D
Describe the Thyroid Hormone Mechanism of action (6 steps)
1. T3/T4 are dissociated from thyroid-binding proteins
2. T3/T4 enter target cells by diffusion or transport
3. in cytoplasm 5'-deiodinase converts T4 to T3
4. T3 enters the nucleus to bind to T3 receptors
5. increased formation of RNA
6. increased protein synthesis
Circulating iodine is 95% __1__ and 5% __2__
1. organic iodine

2. iodide = I-
Of the circulating iodine in the Organic form 95% is __1__ while the other 5% is __2__
1. T4

2. T3
What protects circulating T3 and T4?
Thyroxin binding globulin (TGB)

*free or unbound hormones are minimal
*only the unbound hormones have metabolic activity
In peripheral tissues what converts T4 to T3?

What are the 3 main organs that do this?
Iodothyronine 5'-deiodinase

Liver, Thyroid, Kidneys
What is the active hormone in most target tissues?
List the 4 main effects of Thyroid Hormone
1. Nervous, musculoskeletal, and reproductive issues

2. Calorigenic effect

3. Sympathetic hyperactivity

4. Metabolic effects
List the Nervous, musculoskeletal, and reproductive effects Thyroid hormone has
Emotional lability
Muscle weakness & fatigue
Menstrual irregularities
Describe the Calorigenic effect thyroid hormone causes
increased Oxygen consumption

Describe the Sympathetic hyperactivity effects Thyroid Hormone causes
Up-regulates B1-adrenergic receptors in the heart
-increased stroke volume & CO
-high-output heart failure

**may want to use B-adrenergic blocking agent (propranolol) as an adjunct treatment for hyperthyroidism
Describe the Metabolic effects Thyroid Hormone causes
Decreased Cholesterol and TG's

Increased BMR


Preparation of choice for Replacement and Suppression therapy for Hypothyroidism
Synthetic Levothyroxine (T4)
Why is Levothyroxine the preparation of choice for replacement therapy of Hypothyroidism?
1. Stable
2. Uniform content
3. Low cost
4. Long half-life (7 days)
5. conversion to produce both T3 and T4
Thyroid preparation though inexpensive, is not recommended for replacement therapy b/c of its antigenicity, instability, and variable hormone content
Dessicated Thyroid
Thyroid replacement that is 3-4 times more active than Levothyroxine but is not recommended for routine replacement therapy
Liothyronine (T3)
Why is Liothyronine not recommended for routine thyroid replacement therapy?
1. High cost
2. Shorter half-life (24 hrs vs. 7 days)
3. **Cardiotoxicity** potential
4:1 combination of synthetic T4 and T3, is also expensive with the same disadvantages as Liothyronine
List the 2 Thioamides (anti-thyroid drugs)

Where do the 2 Thioamides accumulate readily?
Thyroid gland for treatment of Thyrotoxicosis
Thioamide that is 10X more active than the other
What are the plasma half-lives for the 2 Thioamides?
Methim-azole = 6 hrs

Propyl-thio-uracil = 1.5 hrs
How long does it take for the Thioamides to have an effect?
Slow onset!!! ➡ 3-4 weeks to deplete T4 stores
What are the mechanisms of action of the Thioamides? (3)
1. Inhibits peroxidase rxns = blocks Iodine Organification (conversion of I- to I2)
2. blocks Iodotyrosine coupling
3. Inhibit peripheral deiodination of T3 and T4

***Mechanism 1 is the major action
What is the most common adverse effect of the Thioamides?
Maculopapular pruritic rash
What are the rare adverse effects of the Thioamides?
Urticarial rash, vasculitis, arthralgia, lupus-like rxn, jaundice, hepatitis, hypothrombinemia
What is the most dangerous adverse effect of the Thioamides?
What 2 mechanisms of Potassium Iodides render them effective in Hyperthyroidism treatment?
1. inhibition of hormone release by reducing Thyroglobulin proteolysis

2. decrease the size and vascularity of the Hyperplastic gland
With Iodide treatment thyrotoxic symptoms improve within __1__, but should not be used alone b/c the gland "escapes" from iodide block after __2__
1. 2-7 days

2. 2-8 weeks
Why should chronic use of Iodides to treat Hyperthyroidism not be used in pregnancy?
Iodide crosses the placenta and could cause Fetal Goiter
What are 4 advantages of Iodide treatment for Hyperthyroidism?
1. simplicity
2. inexpensive
3. relatively nontoxic
4. Absence of glandular destruction
List the adverse rxns of Iodide treatment
1. Acneiform rash
2. Swollen salivary glands
3. Mucous membrane ulceration
4. Conjunctivitis
5. Rhinorrhea
6. Metallic taste
7. Drug fever
8. Bleeding disorders
9. Anaphylaxis
What are the disadvantages of Potassium Iodide treatment? (4)
1. "escape"
2. Aggravation of Thyrotoxicosis
3. Allergic rxns
4. Increased intraglandular iodine which can delay the onset of Thioamide therapy or prevent use of radioactive iodine therapy for several weeks
The only radioactive isotope used for treatment of Thyrotoxicosis
Radioactive Iodine
How is RAI administered?
Oral solution
-RAI is rapidly absorbed and concentrated in the Thyroid gland
What becomes evident within weeks after Radioactive Iodine treatment?
Thyroid parenchymal destruction
-epithelial swelling
-follicular disruption
-Leukocyte infiltration
What does the therapeutic effect of RAI depend on?
Emission of Beta rays
-penetration range of 400-2000 micrometers
-effective half-life of 5 days
What are 4 advantages of RAI?
1. easy administration = oral solution
2. Effectiveness
3. Low expense
4. Absense of pain
What is the major disadvantage of RAI?
induction of Hypothyroidism
What is the main contraindication of RAI?
Pregnancy b/c RAI crosses the placenta and is also excreted in Breast Milk
What is the mechanism of action of the Anion Inhibitors (Perchlorate, Pertechnetate, Thiocyanate)?
competitively inhibit the iodide transport mechanism and therefore block Iodide uptake

*effectiveness is unpredictable
List 3 Anion Inhibitors
1. Thio-cyanate
2. Per-chlorate
3. Per-tech-netate
Anion Inhibitor that is no longer used clinically because it causes Aplastic Anemia
Potassium Perchlorate
Though not FDA approved these act by inhibiting conversion of T4 to T3 in the liver, kidney, pituitary, and brain
Iodinated Contrast media
-Ipodate = by mouth
-Dia-triz-oate = IV
Since many symptoms of Thyrotoxicosis result from sympathetic hyperactivity, what have also been used for treatment?
B-adrenergic blockers or Guan-ethi-dine