Answer to Question 1
Correct Answer: 1,2
Rationale 1: Consistent high amounts of corticosteroid medications provide continuous negative feedback to the hypothalamus and pituitary, shutting down the secretion of ACTH.
Rationale 2: Without stimulation by ACTH, the adrenal cortex shrinks and stops secreting endogenous corticosteroids.
Rationale 3: Acute adrenocortical insufficiency is not caused by rebound ACTH secretion.
Rationale 4: Acute adrenocortical insufficiency is not caused by excessive secretion of ACTH.
Rationale 5: Mineralocorticoids do not cause acute adrenal insufficiency.
Global Rationale: Consistent high amounts of corticosteroid medications provide continuous negative feedback to the hypothalamus and pituitary, shutting down the secretion of ACTH. Without stimulation by ACTH, the adrenal cortex shrinks and stops secreting endogenous corticosteroids. Acute adrenocortical insufficiency is not caused by rebound ACTH secretion, by excessive secretion of ACTH, or by mineralocorticoid levels.
Answer to Question 2
Correct Answer: 1,2
Rationale 1: Open-angle glaucoma is a frequent adverse effect of long-term corticosteroid therapy.
Rationale 2: Cataracts are a frequent adverse effect of long-term corticosteroid therapy.
Rationale 3: Detached retina is not an adverse effect of long-term corticosteroid therapy.
Rationale 4: Retinopathy is not an adverse effect of long-term corticosteroid therapy, although it might occur as an effect of uncontrolled blood glucose levels, as seen in diabetes mellitus.
Rationale 5: Macular degeneration is not an adverse effect of long-term corticosteroid therapy.
Global Rationale: Open-angle glaucoma and cataracts are frequent adverse effects of long-term corticosteroid therapy. Retinopathy is not an adverse effect of long-term corticosteroid therapy, although it might occur as an effect of uncontrolled blood glucose levels, as seen in diabetes mellitus. Macular degeneration and detached retina are not adverse effects of long-term corticosteroid therapy.