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Questions and Answers
What is the effect of injecting Thyroxine on a person with no thyroid gland?
What is the effect of injecting Thyroxine on a person with no thyroid gland?
What is the effect of injecting PTU on a person with normal thyroid function?
What is the effect of injecting PTU on a person with normal thyroid function?
What is the characteristic of a person with Graves' disease?
What is the characteristic of a person with Graves' disease?
What is the effect of injecting TSH on a person with normal thyroid function?
What is the effect of injecting TSH on a person with normal thyroid function?
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What is the characteristic of a person with no adenohypophysis?
What is the characteristic of a person with no adenohypophysis?
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What is the effect of injecting Thyroxine on a person with no adenohypophysis?
What is the effect of injecting Thyroxine on a person with no adenohypophysis?
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What is the primary effect of injecting TSH on a person with normal thyroid function?
What is the primary effect of injecting TSH on a person with normal thyroid function?
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What is the primary mechanism of Propothyuricil (PTU) in reducing thyroid hormone production?
What is the primary mechanism of Propothyuricil (PTU) in reducing thyroid hormone production?
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What is the characteristic of a person with no thyroid gland in terms of TSH levels?
What is the characteristic of a person with no thyroid gland in terms of TSH levels?
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What is the effect of injecting Thyroxine on a person with normal thyroid function?
What is the effect of injecting Thyroxine on a person with normal thyroid function?
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What is the primary function of deiodinase enzyme in the tissue?
What is the primary function of deiodinase enzyme in the tissue?
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What is the characteristic of Graves' disease in terms of thyroid gland size?
What is the characteristic of Graves' disease in terms of thyroid gland size?
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What happens to the BMR when TSH is injected into a person with no thyroid gland?
What happens to the BMR when TSH is injected into a person with no thyroid gland?
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What is the effect of Propothyuricil on the conversion of T4 to T3 in the tissue?
What is the effect of Propothyuricil on the conversion of T4 to T3 in the tissue?
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What is the characteristic of a person with normal thyroid function when Thyroxine is injected?
What is the characteristic of a person with normal thyroid function when Thyroxine is injected?
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What is the effect of injecting PTU on a person with no adenohypophysis?
What is the effect of injecting PTU on a person with no adenohypophysis?
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What is the primary mechanism of Graves' disease?
What is the primary mechanism of Graves' disease?
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What is the effect of injecting TSH on a person with no thyroid gland?
What is the effect of injecting TSH on a person with no thyroid gland?
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Injecting TSH into a person with no thyroid gland will decrease their TSH levels.
Injecting TSH into a person with no thyroid gland will decrease their TSH levels.
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In a person with normal thyroid function, injecting PTU will increase their BMR.
In a person with normal thyroid function, injecting PTU will increase their BMR.
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A person with Graves' disease will have a lower TSH level due to negative feedback.
A person with Graves' disease will have a lower TSH level due to negative feedback.
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In a person with no adenohypophysis, injecting Thyroxine will stimulate the hypothalamus to produce more TRH.
In a person with no adenohypophysis, injecting Thyroxine will stimulate the hypothalamus to produce more TRH.
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Propothyuricil (PTU) blocks the conversion of T3 to T4 in the thyroid gland.
Propothyuricil (PTU) blocks the conversion of T3 to T4 in the thyroid gland.
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In a person with no thyroid gland, injecting TSH will stimulate the production of T3 and T4.
In a person with no thyroid gland, injecting TSH will stimulate the production of T3 and T4.
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In a person with normal thyroid function, injecting Thyroxine will eventually lead to suppression of the thyroid hormone production.
In a person with normal thyroid function, injecting Thyroxine will eventually lead to suppression of the thyroid hormone production.
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A person with no thyroid gland will have a low TSH level due to negative feedback.
A person with no thyroid gland will have a low TSH level due to negative feedback.
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In a person with no adenohypophysis, injecting TSH will stimulate the production of T3 and T4.
In a person with no adenohypophysis, injecting TSH will stimulate the production of T3 and T4.
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Propothyuricil (PTU) blocks the conversion of T4 to T3 in the thyroid gland.
Propothyuricil (PTU) blocks the conversion of T4 to T3 in the thyroid gland.
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In a person with Graves' disease, the hypothalamus will produce more TRH due to low T3 and T4 levels.
In a person with Graves' disease, the hypothalamus will produce more TRH due to low T3 and T4 levels.
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In a person with normal thyroid function, injecting PTU will decrease the metabolic rate.
In a person with normal thyroid function, injecting PTU will decrease the metabolic rate.
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Study Notes
Normal Thyroid Function
- BMR and hormone production are unaffected
- Injecting Thyroxine (T4) leads to:
- 2x thyroid hormone production
- Eventually, suppression/dependency of the system
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function
- Injecting PTU leads to:
- Decreased metabolic rate
- Decreased T3/T4 conversion in thyroid
- Decreased T4 to T3 conversion in tissue
No Thyroid (Hypothyroidism)
- Increased TSH (no binding site)
- Decreased/absent T3/T4 (no stimulation)
- Signals to hypothalamus that levels are low
- Injecting Thyroxine (T4) leads to:
- Increased metabolic rate
- Increased T3/T4
- Injecting TSH has no effect (no thyroid to bind to)
- Injecting PTU has no effect (no T3 to convert, already decreased T4)
No Adenohypophysis (Hypopituitarism)
- Low/no TSH
- Increased TRH (no binding site)
- T3/T4 levels are low, signaling hypothalamus to produce TRH
- Injecting Thyroxine (T4) leads to:
- Increased T3/T4
- Decreased TRH
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function (if present)
- Injecting PTU has no effect (no TSH to produce T3/T4)
Propylthiouracil (PTU) and Thyroid Hormone Production
- PTU blocks tyrosine iodination, preventing T4 production
- PTU also blocks deiodinase enzyme, preventing T4 to T3 conversion in tissue
- Storage forms of T4 are low due to PTU
Graves' Disease
- Autoantibody overstimulates TSH signal on thyroid
- Leads to excessive T3 production
- Thyroid gland becomes too large due to TSH stimulation
- T3 vs T4 ratio: 1:9 (T4 to T3), with T3 being the most effective
Normal Thyroid Function
- BMR and hormone production are unaffected
- Injecting Thyroxine (T4) leads to:
- 2x thyroid hormone production
- Eventually, suppression/dependency of the system
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function
- Injecting PTU leads to:
- Decreased metabolic rate
- Decreased T3/T4 conversion in thyroid
- Decreased T4 to T3 conversion in tissue
No Thyroid (Hypothyroidism)
- Increased TSH (no binding site)
- Decreased/absent T3/T4 (no stimulation)
- Signals to hypothalamus that levels are low
- Injecting Thyroxine (T4) leads to:
- Increased metabolic rate
- Increased T3/T4
- Injecting TSH has no effect (no thyroid to bind to)
- Injecting PTU has no effect (no T3 to convert, already decreased T4)
No Adenohypophysis (Hypopituitarism)
- Low/no TSH
- Increased TRH (no binding site)
- T3/T4 levels are low, signaling hypothalamus to produce TRH
- Injecting Thyroxine (T4) leads to:
- Increased T3/T4
- Decreased TRH
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function (if present)
- Injecting PTU has no effect (no TSH to produce T3/T4)
Propylthiouracil (PTU) and Thyroid Hormone Production
- PTU blocks tyrosine iodination, preventing T4 production
- PTU also blocks deiodinase enzyme, preventing T4 to T3 conversion in tissue
- Storage forms of T4 are low due to PTU
Graves' Disease
- Autoantibody overstimulates TSH signal on thyroid
- Leads to excessive T3 production
- Thyroid gland becomes too large due to TSH stimulation
- T3 vs T4 ratio: 1:9 (T4 to T3), with T3 being the most effective
Normal Thyroid Function
- BMR and hormone production are unaffected
- Injecting Thyroxine (T4) leads to:
- 2x thyroid hormone production
- Eventually, suppression/dependency of the system
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function
- Injecting PTU leads to:
- Decreased metabolic rate
- Decreased T3/T4 conversion in thyroid
- Decreased T4 to T3 conversion in tissue
No Thyroid (Hypothyroidism)
- Increased TSH (no binding site)
- Decreased/absent T3/T4 (no stimulation)
- Signals to hypothalamus that levels are low
- Injecting Thyroxine (T4) leads to:
- Increased metabolic rate
- Increased T3/T4
- Injecting TSH has no effect (no thyroid to bind to)
- Injecting PTU has no effect (no T3 to convert, already decreased T4)
No Adenohypophysis (Hypopituitarism)
- Low/no TSH
- Increased TRH (no binding site)
- T3/T4 levels are low, signaling hypothalamus to produce TRH
- Injecting Thyroxine (T4) leads to:
- Increased T3/T4
- Decreased TRH
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function (if present)
- Injecting PTU has no effect (no TSH to produce T3/T4)
Propylthiouracil (PTU) and Thyroid Hormone Production
- PTU blocks tyrosine iodination, preventing T4 production
- PTU also blocks deiodinase enzyme, preventing T4 to T3 conversion in tissue
- Storage forms of T4 are low due to PTU
Graves' Disease
- Autoantibody overstimulates TSH signal on thyroid
- Leads to excessive T3 production
- Thyroid gland becomes too large due to TSH stimulation
- T3 vs T4 ratio: 1:9 (T4 to T3), with T3 being the most effective
Normal Thyroid Function
- BMR and hormone production are unaffected
- Injecting Thyroxine (T4) leads to:
- 2x thyroid hormone production
- Eventually, suppression/dependency of the system
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function
- Injecting PTU leads to:
- Decreased metabolic rate
- Decreased T3/T4 conversion in thyroid
- Decreased T4 to T3 conversion in tissue
No Thyroid (Hypothyroidism)
- Increased TSH (no binding site)
- Decreased/absent T3/T4 (no stimulation)
- Signals to hypothalamus that levels are low
- Injecting Thyroxine (T4) leads to:
- Increased metabolic rate
- Increased T3/T4
- Injecting TSH has no effect (no thyroid to bind to)
- Injecting PTU has no effect (no T3 to convert, already decreased T4)
No Adenohypophysis (Hypopituitarism)
- Low/no TSH
- Increased TRH (no binding site)
- T3/T4 levels are low, signaling hypothalamus to produce TRH
- Injecting Thyroxine (T4) leads to:
- Increased T3/T4
- Decreased TRH
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function (if present)
- Injecting PTU has no effect (no TSH to produce T3/T4)
Propylthiouracil (PTU) and Thyroid Hormone Production
- PTU blocks tyrosine iodination, preventing T4 production
- PTU also blocks deiodinase enzyme, preventing T4 to T3 conversion in tissue
- Storage forms of T4 are low due to PTU
Graves' Disease
- Autoantibody overstimulates TSH signal on thyroid
- Leads to excessive T3 production
- Thyroid gland becomes too large due to TSH stimulation
- T3 vs T4 ratio: 1:9 (T4 to T3), with T3 being the most effective
Normal Thyroid Function
- BMR and hormone production are unaffected
- Injecting Thyroxine (T4) leads to:
- 2x thyroid hormone production
- Eventually, suppression/dependency of the system
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function
- Injecting PTU leads to:
- Decreased metabolic rate
- Decreased T3/T4 conversion in thyroid
- Decreased T4 to T3 conversion in tissue
No Thyroid (Hypothyroidism)
- Increased TSH (no binding site)
- Decreased/absent T3/T4 (no stimulation)
- Signals to hypothalamus that levels are low
- Injecting Thyroxine (T4) leads to:
- Increased metabolic rate
- Increased T3/T4
- Injecting TSH has no effect (no thyroid to bind to)
- Injecting PTU has no effect (no T3 to convert, already decreased T4)
No Adenohypophysis (Hypopituitarism)
- Low/no TSH
- Increased TRH (no binding site)
- T3/T4 levels are low, signaling hypothalamus to produce TRH
- Injecting Thyroxine (T4) leads to:
- Increased T3/T4
- Decreased TRH
- Injecting TSH leads to:
- Increased BMR
- Stimulation of thyroid function (if present)
- Injecting PTU has no effect (no TSH to produce T3/T4)
Propylthiouracil (PTU) and Thyroid Hormone Production
- PTU blocks tyrosine iodination, preventing T4 production
- PTU also blocks deiodinase enzyme, preventing T4 to T3 conversion in tissue
- Storage forms of T4 are low due to PTU
Graves' Disease
- Autoantibody overstimulates TSH signal on thyroid
- Leads to excessive T3 production
- Thyroid gland becomes too large due to TSH stimulation
- T3 vs T4 ratio: 1:9 (T4 to T3), with T3 being the most effective
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Description
This quiz covers the effects of injecting thyroxine, TSH, and PTU on thyroid hormone production, metabolic rate, and thyroid function. Understand how the thyroid system responds to different hormones and medications.
