- Joined
- May 2, 2021
- Messages
- 1,224
BASIC PHYSIOLOGY
1. Hypothalamus releases thyrotropin-releasing hormone (TRH).
a. Binds to the thyrotropin-releasing hormone receptor (TRHR) in the anterior pituitary.
2. Pituitary releases thyroid-stimulating hormone (TSH) into the bloodstream.
3. TSH stimulates the thyroid to produce thyroxine (T4) and triiodothyronine (T3), which stimulates the metabolism.
4. T3 and T4 act via somatostatin to inhibit hypothalamic TRH in a negative feedback loop.
MECHANISMS OF THYROID HYPERPLASIA
1. Chronic TSH stimulation can produce hyperplasia of the thyroid gland
2. Catecholamines: not fully understood, except at the dopamine receptor.
a. Norepinephrine stimulates the release of TRH from the hypothalamus, which is likely how the cold speeds up our metabolism faster.
b. Dopamine regulates TSH
i. Dopamine and dopamine receptor agonists suppress TSH synthesis while dopamine antagonists minorly enhance TSH synthesis.
1. Schizophrenics have higher T3and T4 levels.
ii. Note that dopamine may lower GH pulses.
1. Dopamine agonists are used to treat gigantism, inhibiting GH more effectively than IGF-1 think of using nandrolone sans GH now!
2. Acutely, they cause growth hormone release in healthy people
3. IGF-1:
a. Type 1 IGF-1 receptor is mostly expressed in the thyroid gland[13].
b. IGF-1R overexpression in the thyroid increases gland weight, decreases TSH, increases serum T4, suggesting that IGF-1 and the IGF-1R stimulate thyroid function
c. Epidemiologic studies reveal IGF-1 levels are associated with goiter
d. In acromegaly:
i. Acromegalic people have increased thyroid vascularity
ii. In a study of 62 Italian acromegalics: thyroid volume is associated with the duration of acromegaly, 78% of patients had thyroid disorders (particularly non-toxic nodular disorder), and thyroid carcinoma was more common
iii. A study of 37 acromegalics found goiters to be common.
1. Early in the course of the disease, a diffuse goiter develops.
2. Thyroid autonomy and nodule formation begin – growth can continue without TSH.
3. Attenuating GH secretion can reduce thyroid size, but this is limited by the extent of nodularity
e. In hypopituitary patients given GH, IGF-1 does not independently stimulate thyroid growth but enhanced proliferation of thyroid cells by potentiation the mitogenic effects of TSH.
f. In women but not obese people, GH administration suppresses TSH.
g. IGF-1 levels are dose-dependently associated with the risk of thyroid enlargement and nodule formation in non-acromegalic people
1. Hypothalamus releases thyrotropin-releasing hormone (TRH).
a. Binds to the thyrotropin-releasing hormone receptor (TRHR) in the anterior pituitary.
2. Pituitary releases thyroid-stimulating hormone (TSH) into the bloodstream.
3. TSH stimulates the thyroid to produce thyroxine (T4) and triiodothyronine (T3), which stimulates the metabolism.
4. T3 and T4 act via somatostatin to inhibit hypothalamic TRH in a negative feedback loop.
MECHANISMS OF THYROID HYPERPLASIA
1. Chronic TSH stimulation can produce hyperplasia of the thyroid gland
2. Catecholamines: not fully understood, except at the dopamine receptor.
a. Norepinephrine stimulates the release of TRH from the hypothalamus, which is likely how the cold speeds up our metabolism faster.
b. Dopamine regulates TSH
i. Dopamine and dopamine receptor agonists suppress TSH synthesis while dopamine antagonists minorly enhance TSH synthesis.
1. Schizophrenics have higher T3and T4 levels.
ii. Note that dopamine may lower GH pulses.
1. Dopamine agonists are used to treat gigantism, inhibiting GH more effectively than IGF-1 think of using nandrolone sans GH now!
2. Acutely, they cause growth hormone release in healthy people
3. IGF-1:
a. Type 1 IGF-1 receptor is mostly expressed in the thyroid gland[13].
b. IGF-1R overexpression in the thyroid increases gland weight, decreases TSH, increases serum T4, suggesting that IGF-1 and the IGF-1R stimulate thyroid function
c. Epidemiologic studies reveal IGF-1 levels are associated with goiter
d. In acromegaly:
i. Acromegalic people have increased thyroid vascularity
ii. In a study of 62 Italian acromegalics: thyroid volume is associated with the duration of acromegaly, 78% of patients had thyroid disorders (particularly non-toxic nodular disorder), and thyroid carcinoma was more common
iii. A study of 37 acromegalics found goiters to be common.
1. Early in the course of the disease, a diffuse goiter develops.
2. Thyroid autonomy and nodule formation begin – growth can continue without TSH.
3. Attenuating GH secretion can reduce thyroid size, but this is limited by the extent of nodularity
e. In hypopituitary patients given GH, IGF-1 does not independently stimulate thyroid growth but enhanced proliferation of thyroid cells by potentiation the mitogenic effects of TSH.
f. In women but not obese people, GH administration suppresses TSH.
g. IGF-1 levels are dose-dependently associated with the risk of thyroid enlargement and nodule formation in non-acromegalic people
(Hoping this is appropriate? - If not I will delete)
