Which of the following histologic changes would be expected in this patient's adrenal glands? A 33-year-old woman comes to the physician because of a 16-kg (35-lb)weight gain during the past 6 months despite dieting. She is 168 cm (5 fl 6 in) tall and now weighs 114 kg (230 lb); BMI is 37 kg/m2. Her blood pressure is 156/96 mm Hg. Physical examination shows a round, ruddy face with hirsutism, excess weight predominantly in the shoulders and abdomen: and purple striae over the abdomen. An MRI shows a mass in the pituitary gland. A CT scan of the abdomen shows enlarged adrenal glands.
A. Cortical hyperplesia
B. Cortical hypertrophy.
C. Cortical mstaplasia
D. Medullary hyperplasia
E. Medullary hypertrophy
F. Medullary metaplasia
Dx is Cushing disease based off of the classic sx(adbo stria, wt gain, htn,central obesity) therefore Answer is Cortical Hyperplasia.ACTH-secreting pituitary adenoma (Cushing disease); paraneoplastic ACTH secretion (eg, small cell lung cancer, bronchial carcinoids)—result in ACTH, bilateral adrenal hyperplasia.
You fell for the bait like many of us. Pituitary adenoma can be for any of the "FLAT PiG" hormones. This was specifically ACTH-secreting pituitary adenoma (Cushing disease).
Adrenal hypertrophy may be a result of stress or indeed may result from functional impairment of theadrenal cortexand reduced capacity to secrete glucocorticoids (in turn resulting in diminished negative feedback inhibition of ACTH and overstimulation of the gland
Pt would not have sx of Cushingfor a pituitary tumorbut rather Sx of which ever "FLAT PiG" hormone is excessivly spewing out ieProlactinoma -Headache gynacomastia galactorrhea.
Cortical hypertrophy.-the pituitary glands anterior lobe (adenohypophysis) is a true gland which produces and secretes six different hormones: thyroid-stimulating hormone (tsh), adrenocorticotropic hormone (acth), follicle-stimulating hormone (fsh), luteinizing hormone (lh), growth hormone (gh), and prolactin (prl).cushings diseaseis a cause of cushings syndrome characterised by increased secretion of (acth) from the anterior pituitary (secondary hypercorticism). this is most often as a result of a pituitary adenoma or due to excess production of hypothalamus crh (corticotropin releasing hormone) (tertiary hypercortisolism/hypercorticism). pituitary adenomas are responsible for 70% of endogenous cushings syndrome, that is, when excluding cushings syndrome from exogenously administered corticosteroids, which is the major cause of cushings syndrome.the primary cause of adrenocortical hypertrophy is increased (acth) stimulation. in toxicology studies, such a condition can arise as a result of the stress response, but it may also occur due to deficient glucocorticoid feedback regulation of acth due to toxicity to the adrenal cortex. this latter condition is defined as adrenocortical insufficiency and represents a serious adverse toxic effect on the function of the adrenal cortex. adrenocortical hypertrophy may occur in the absence of other adrenocortical lesions such that a toxicopathological mechanism is not obvious, for example by pharmacological inhibition of steroidogenesis at the biochemical level.hyperplasia , means increase in number of cells/proliferation of cells. it may result in the gross enlargement of an organ and the term is sometimes mixed with benign neoplasia / benign tumor.hyperplasia is a common preneoplastic response to stimulus. microscopically cells resemble normal cells but are increased in numbers. sometimes cells may also be increased in size (hypertrophy) hyperplasia is different from hypertrophy in that the adaptive cell change in hypertrophy is an increase in cell size, whereas hyperplasia involves an increase in the number of cells.