Podcast
Questions and Answers
What effect does hyperprolactinemia have on men?
What effect does hyperprolactinemia have on men?
- Leads to loss of libido, erectile dysfunction, and infertility (correct)
- Causes weight gain and fatigue
- Enhances growth hormone secretion
- Increases libido and fertility
Which diagnostic test is definitive for confirming acromegaly?
Which diagnostic test is definitive for confirming acromegaly?
- Prolactin level measurement
- IGF-1 secretion assessment
- Oral glucose tolerance test (correct)
- An MRI scan of the pituitary gland
Which of the following treatments is a long-acting analogue used for the suppression of growth hormone secretion?
Which of the following treatments is a long-acting analogue used for the suppression of growth hormone secretion?
- Insulin
- Lanreotide (correct)
- Pasireotide
- Octreotide
What is a common misdiagnosis regarding elevated prolactin levels in men?
What is a common misdiagnosis regarding elevated prolactin levels in men?
How do normal subjects differ from patients with acromegaly during an oral glucose tolerance test?
How do normal subjects differ from patients with acromegaly during an oral glucose tolerance test?
What effect does somatostatin analogues have on insulin secretion?
What effect does somatostatin analogues have on insulin secretion?
What is the primary action of bromocriptine in relation to dopamine receptors?
What is the primary action of bromocriptine in relation to dopamine receptors?
What is a consequence of administering pasireotide related to glucose metabolism?
What is a consequence of administering pasireotide related to glucose metabolism?
How is bromocriptine's absorption affected by first-pass metabolism?
How is bromocriptine's absorption affected by first-pass metabolism?
Bromocriptine's elimination half-life is best described as:
Bromocriptine's elimination half-life is best described as:
How do somatostatin analogues impact glucose tolerance in most patients?
How do somatostatin analogues impact glucose tolerance in most patients?
Which therapeutic action is NOT associated with bromocriptine?
Which therapeutic action is NOT associated with bromocriptine?
What is a potential consequence of increased glucagon-like peptide 1 secretion?
What is a potential consequence of increased glucagon-like peptide 1 secretion?
Which mechanism primarily regulates growth hormone secretion?
Which mechanism primarily regulates growth hormone secretion?
What role does Insulin-like Growth Factor 1 (IGF-1) play in growth hormone regulation?
What role does Insulin-like Growth Factor 1 (IGF-1) play in growth hormone regulation?
Where is somatostatin (SST) synthesized?
Where is somatostatin (SST) synthesized?
How does IGF-1 interact with cells to mediate its actions?
How does IGF-1 interact with cells to mediate its actions?
What is the intrinsic activity of the type 1 IGF receptor?
What is the intrinsic activity of the type 1 IGF receptor?
Which substance primarily stimulates somatostatin secretion?
Which substance primarily stimulates somatostatin secretion?
What effect does hypoglycemia have on growth hormone levels?
What effect does hypoglycemia have on growth hormone levels?
Which hormone is closely related to the type 1 IGF receptor?
Which hormone is closely related to the type 1 IGF receptor?
Which physiological state is least likely to influence growth hormone release?
Which physiological state is least likely to influence growth hormone release?
Which of the following does NOT represent a direct way IGF-1 affects tissue?
Which of the following does NOT represent a direct way IGF-1 affects tissue?
What is the typical starting dose of Insulin-like Growth Factor 1 for adults?
What is the typical starting dose of Insulin-like Growth Factor 1 for adults?
Which factor can lead to a decrease in IGF-1 dosage during therapy?
Which factor can lead to a decrease in IGF-1 dosage during therapy?
What is the significance of mecasermin and mecasermin rinfabate in therapy?
What is the significance of mecasermin and mecasermin rinfabate in therapy?
What is the effect of estrogen on growth hormone action?
What is the effect of estrogen on growth hormone action?
What must be monitored during GH therapy to adjust the IGF-1 dosage?
What must be monitored during GH therapy to adjust the IGF-1 dosage?
How is mecasermin primarily administered in patients?
How is mecasermin primarily administered in patients?
What potential effect does GH treatment have on insulin sensitivity?
What potential effect does GH treatment have on insulin sensitivity?
Which condition is mecasermin not typically indicated for?
Which condition is mecasermin not typically indicated for?
Which scenario contraindicates the use of GH therapy?
Which scenario contraindicates the use of GH therapy?
What type of protein binds IGF-1, influencing its therapeutic use?
What type of protein binds IGF-1, influencing its therapeutic use?
Which of the following statements about dose increase during therapy is true?
Which of the following statements about dose increase during therapy is true?
What must adults demonstrate to be considered for GH treatment?
What must adults demonstrate to be considered for GH treatment?
How does the modification in somapacitan affect its pharmacokinetics?
How does the modification in somapacitan affect its pharmacokinetics?
Which patient demographic typically requires a higher starting dose of IGF-1?
Which patient demographic typically requires a higher starting dose of IGF-1?
Which of the following conditions would disqualify a patient from receiving GH therapy?
Which of the following conditions would disqualify a patient from receiving GH therapy?
What could be a necessary adjustment when initiating GH therapy?
What could be a necessary adjustment when initiating GH therapy?
What is the primary reason for contraindicating GH use in patients with closed epiphyses?
What is the primary reason for contraindicating GH use in patients with closed epiphyses?
Which statement best describes the nature of somapacitan?
Which statement best describes the nature of somapacitan?
What condition is characterized by severe nonproliferative diabetic retinopathy?
What condition is characterized by severe nonproliferative diabetic retinopathy?
Which factors can lead to the exclusion of a patient from GH treatment?
Which factors can lead to the exclusion of a patient from GH treatment?
Study Notes
Growth Hormone and Prolactin Disorders
- Growth Hormone (GH) Regulation: GH secretion is controlled by negative feedback loops, involving GH itself, Insulin-like Growth Factor 1 (IGF-1), and Somatostatin (SST). Sleep, stress, hypoglycemia, exercise, and sex steroids increase GH secretion.
- IGF-1 Role: IGF-1 inhibits GH secretion predominantly in the anterior pituitary and to some extent in the hypothalamus. IGF-1 interacts with receptors in virtually all tissues, interacting with related Growth Factor IGF-2. The type 1 IGF receptor is similar in structure to the insulin receptor.
- GH Treatment Considerations: In adults, GH treatment is indicated for organic etiologies of GH deficiency, demonstrated low GH production, or three or more pituitary hormone deficiencies. GH treatment may decrease insulin sensitivity, so adjusting insulin and other hypoglycemic agent doses might be necessary. GH is contraindicated in pediatric patients with closed epiphyses, acute critical illness, active malignancy, and specific retinopathy cases.
Growth Hormone Treatment
- Somatropin Analogues: Somapacitan is a GH analogue with an extended half-life due to albumin binding, administered every 4 weeks
- Octreotide and Lanreotide: These are long-acting SST analogues that suppress GH secretion. Octreotide may reduce tumor size but growth often resumes after treatment stops. Lanreotide is administered every 4 weeks.
Prolactin Disorders
- Hyperprolactinemia: Elevated prolactin levels can have non-pituitary causes, besides PRL-producing adenomas
- Diagnosis: The oral glucose tolerance test is a key diagnostic tool. Normal subjects suppress GH levels (<1 ng/mL) in response, while those with acromegaly show either no suppression or a paradoxical increase. Diagnosis requires identifying increased circulating growth hormone (GH) or IGF-1.
- Bromocriptine: A dopamine receptor agonist used to treat hyperprolactinemia. It's a semi-synthetic ergot alkaloid that inhibits prolactin release (primarily through D2 receptors).
- Bromocriptine Administration: Well absorbed orally, but extensive first-pass metabolism (only 7% reaches the systemic circulation). Short half-life (2-8 hours), requiring divided doses or a slow-release form (outside the US) and can be administered vaginally.
SST Analogues and Effects
- Effect on Insulin Secretion: SST analogues decrease insulin secretion.
- Effect on Glucose Tolerance: Overall impact on glucose tolerance can vary depending on the specific SST analogue and the relative effects on insulin secretion vs. resistance.
- Pasireotide- Decreases the secretion of glucagon-like peptide 1 and glucose-insulinotropic peptide (incretins); leading to significant worsening of glucose tolerance and often necessitating antihyperglycemic therapy
- Effect on Cushing disease: Pasireotide is effective treatment for Cushing disease (excessive cortisol production) in patients not suitable for surgery.
Insulin-like Growth Factor 1 (IGF-1)
- Therapeutic Use: Recombinant human IGF-1 (mecasermin) and a combination of recombinant human IGF-1 with its binding protein, IGFBP-3 (mecasermin rinfabate) FDA-approved for therapy.
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