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Hormonal & Reproductive Week 1 - WLB > Thyroid Hormone Physiology and Pharmacology - Trachte > Flashcards

Thyroid Hormone Physiology and Pharmacology - Trachte Flashcards

1
Q

What are the components of the Thyroid Hormone Axis?

A
  1. Hypothalamus (TRH: thyrotropin releasing hormone)
  2. Anterior Pituitary (TSH: thyroid stimulating hormone)
  3. Thyroid gland
  4. T3/T4 hormone (T3: triiodothyronine/T4: thyroxine)
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2
Q

What are the main negative regulators of Thyroid hormones?

A

Block portal system => stop release of TSH

T3/T4 => negative feed back to stop release of TSH and TRH

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3
Q

What are some of the other negative regulators of Thyroid hormones?

A

Somatostatin, dopamine, and high glucocorticoids (adrenal cortex) all DECREASE TSH release

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4
Q

What is the function of TRH?

A

Tetrapeptide that stimulates release of TSH from thyrotrophs of the anterior pituitary

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5
Q

Why is Thyroid Hormone Axis important?

A

Has an important role in the regulation of energy homeostasis, feeding behavior, thermogenesis, and autonomic regulation.

TRH controls energy homeostasis mainly through stimulation of TSH and ultimately regulation of circulating thyroid hormone levels.

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6
Q

How does TRH stimulate the target cell?

A

Couples to PLC => phospholipase C-IP3
Cascade results in Ca++ release and rapid intracellular responses including release of secretory vesicles containing TSH.

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7
Q

TSH is similar to what other gonatotropin hormones?

A 
LH= luteinizing hormone  
hCG= human chorionic gonadotropin
FSH = follicle stimulating hormone
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8
Q

How does TSH stimulate the receptor signal transduction?

A

Receptors reside on plasmamembrane of thyroid follicular cells.

G(s)-coupled receptor => increase cAMP

TSH:TSH receptor binding stimulates many aspects of thyroid hormone synthesis and release.

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9
Q

What are the 7 steps of Thyroid Hormone synthesis?

A
  1. Iodide Uptake (via Na+ coupled symporter)
  2. Iodide Oxidation to Iodine (organification)
  3. Iodination of tyrosine-thryoglobulin
  4. Conjugation of MIT/DIT thyroglobulin
  5. Endocytosis of T3/T4-thyroglobulin
  6. Proteolysis to mature hormone
  7. Secretion of T3/T4 via exocytosis (?)
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10
Q

How do T3 and T4 compare?

A

T3 is more active than T4.

T4 is converted to T3 intracellularly.

T3 has a shorter circulating t1/2 T3~ 1 d; T4~ 6d

Both T3 and T4 bind thyroid hormone receptors but it is thought most T4 is converted into T3.

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11
Q

What are the transporters for thyroid hormone?

A

Thyroxine binding globulin (= TBG =thyroid binding globulin)
- binds 75% of T4 and 75% of T3

Transthyretin

Albumin

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12
Q

What three things does TSH stimulate the synthesis of in order to produce thyroid hormones?

A

Thyroid peroxidase synthesis

Thyroglobulin transcription

Na+/I- transport activity (increases I- availability to the follicular cell)

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13
Q

What are the main functions of thyroid hormone?

A

Promotes oxygen consumption, heat production and free radical formation

Regulation of BMR

Increased heat production

Increased glucose utilization, uptake and synthesis

Permissive sympathetic effects, ↑ heart rate, ↑ contractility (increases beta receptors)

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14
Q

Why do many states mandate newborn testing of thyroid function?

A

brain doesn’t develop/grow properly if low thyroid function

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15
Q

What happens if there is a congenital lack of thyroid hormone in infants?

A

(Cretinism) or maternal hypothyroidism:

  • profound mental retardation
  • short stature
  • delay in motor development
  • coarse hair
  • protuberant abdomens
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16
Q

What are the physiologic effects of low thyroid hormone in adults?

A

Lethargy

Somnolence

Slowed intellectual functions including speech

Stiffness and aching muscle

*Cold intolerance

Delayed deep tendon reflex relaxation

Anovulation and amenorrhea common, menorrhagia less common

17
Q

What are the physiologic effects of excess thyroid hormone in adults?

A

Increases heart rate (via funny Na+ channels)

Increase sensitivity to catecholamines via increase of number of beta adrenergic receptors in heart, skeletal muscle, adipose tissue and lymphocytes.

Amplifies catecholamine post-receptor action.

Increased O2 demand leads to increased production of erythropoietin and increases erythropoiesis.

Promotes GI motility resulting in increased defecation.

Promotes bone turnover with net bone loss and hypercalciuria.

Promotes increased protein turnover and net loss of skeletal muscle with myopathy (weakness, fatigue)

Increases hepatic gluconeogenesis and glycogenolysis and intestinal glucose absorption, therefore can worsen control of glucose levels with diabetes patients.

Increase in LDL receptor # and thereby accelerates LDL clearance.

Hyperthyroidism promotes aromatization of androgens to estrogens and increases sex hormone binding globulins which can contribute to gynecomastia in men.

18
Q

What is Thyrotoxicosis?

A

any cause of excessive thyroid hormone concentration and its effects on organ systems

19
Q

What is Thyroid Storm?

A

Thyroid storm represents the extreme manifestation of thyrotoxicosis

20
Q

What are the potential etiologies of Hypothyroidism?

A

***Primary hypothyroidism (i.e., problem lies in thyroid gland): Congenital defects, Gland destruction (surgical, radioactive, external radiation), Iodine deficiency, Autoimmune (Hashimoto thyroiditis=chronic lymphocytic thyroiditis)

*Secondary/tertiary (i.e., problem lies in pituitary gland or hypothalamus, respectively) usually associated with other pituitary deficiencies

Thyroid hormone resistance syndromes (with normal hormone production): receptor resistance

21
Q

What happens to TRH, TSH and TH levels in primary hypothyroidism?

A

TRH levels increase

TSH levels increase

TH levels decrease

22
Q

What happens to TRH, TSH and TH levels in secondary hypothyroidism (i.e. pituitary deficiencies)?

A

TRH increase

TSH and TH decrease

23
Q

What happens to TRH, TSH and TH levels in thyroid hormone resistance hypothyroidism?

A

ALL INCREASE

Increase TRH release (no inhibitory)

Increase TSH

Increase TH

24
Q

What are the potential etiologies of Hyperthyroidism?

A

Hyperthyroidism that results in toxicosis in target tissues is called thyrotoxicosis.

Graves’ disease = Production of thyroid stimulating immunoglobulins (TSI)

25
Q

What happens to TRH, TSH and TH levels in hyperthyroidism due to Graves’ disease?

A

TRH decrease
TSH decrease
TH increase

T cells become sensitive to thyroid antigen and stimulate B cells to produce antibodies that mimic TSH. Result is hyperstimulation of thyroid hormone production, consequently causing strong negative feedback.

26
Q

Why does goiter develop in the case of iodine deficiency?

A

Increase in TRH and TSH with no negative feedback stimulates thyroid gland to maximize function and enlarge

27
Q

Why does goiter develop in the case of Graves’

disease?

A

The gland grows big and maximizes function due to thyroid stimulating immunoglobulins
-direct stimulation of the thyroid gland

28
Q

TSH test. Normal range is 0.5 to 6 U/dL.
If the level is higher than this, what does that mean?
If the level is lower than this, what does that mean?

A

Higher => Hypothyroidism

Lower => Hyperthyroidism

29
Q

When do you test T3 and T4 levels?

A

If TSH test is abnormal

30
Q

What does Thyroid-stimulating immunoglobulin (TSI) test for?

A

Graves’ disease

31
Q

What is a Thyroid scan used for?

A

A thyroid scan shows how and where iodine is distributed in the thyroid. The images of nodules and other possible irregularities help the health care provider diagnose the cause of a person’s hyperthyroidism.

32
Q

What is a Radioactive iodine uptake test used to assess?

A

The radioactive iodine uptake test measures the amount of iodine the thyroid collects from the bloodstream. Low levels of iodine uptake might be a sign of hypothyroidism, whereas high levels could support Graves’ disease diagnosis.

33
Q

What are the hypothyroidism and thyroid hormone replacement preparations?

A

Levothyroxine (T4) => long half life

Liothyronine (T3) (doesn’t last as long)

34
Q

What are Thioamides (aka Thionamides) used for?

A

treatment of hyperthyroidism and to prepare for thyroid surgery by preventing Iodide organization and thyroid peroxidase reactions to iodinate Tyrosines (shrinks thyroid)

35
Q

What are the three Thioamides that we need to know?

A
  1. Methimazole and Carbimazole (metabolizes to methimazole)
  2. Propylthiouracil (PTU)
  3. Potassium Iodide (KI)
36
Q

What are radioactive Iodines used for?

A

131-I Used for thyroid ablation (destroy gland, results in hypothyroidism)

123-I Used for thyroid imaging

37
Q

What do Methimazole and PropylThioUracyl block?

A

inhibit thyroid peroxidase - oxidation of iodide and conjugation reactions producing T3 & T4

38
Q

What are the five types of anti-thyroid drugs?

A

***Drugs that inhibit thyroid synthesis (thioamides)

Drugs that impair release and proteolysis of thyroid hormones (iodides)

Drugs that interfere with T4 to T3 conversion (iodinated contrast media 123-I)

Drugs that alleviate peripheral symptoms of thyrotoxicosis (beta blockers)

Drugs that destroy the thyroid gland (radioactive 131-I).

Hormonal & Reproductive Week 1 - WLB (13 decks)

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