Adrenal Glands Flashcards
What are the three layers of the adrenal cortex from the capsule in and what types of steroids are produced in each layer?
Zona glomerulus which produces aldosterone.
Zona fasciculata which produces cortisol
Zona reticularis which produces estrogens and androgens
What type of cells reside in the medulla and what hormones does the medulla produce?
Chromaffin cells which produce catecholamines, mainly epi and a little nor epi
What are the most common causes of ACTH independent causing syndrome?
Primary adrenal neoplasms, two most common being an adrenal adenoma and carcinoma.
In what situation would we see atrophy of the adrenal glands and why?
Cushing syndrome due to exogenous glucocorticoid administration because the exogenous steroids are suppressing the HPA axis.
In what situation would we find diffuse hyperplasia of the adrenal glands and why?
In ACTH dependent cushing syndrome because ACTH is constantly being secreted.
2 big differences between an adrenocortical adenoma and a carcinoma associated with Cushing’s syndrome?
Adenoma is much smaller and has a capsule.
Carcinoma is much bigger and does not have a capsule
What is the most common clinical manifestation of primary hyperaldosteronism?
Elevation is BP
What is the most common cause of primary aldosteronism and explain whats gong on? Also, what are two characteristics of the typical presenting patient?
Bilateral idiopathic. Bilateral nodular hyperplasia of both adrenal glands.
Older patients with less severe hypertension.
What is the second most common cause of primary aldosteronism? What are 2 characteristics of the typical presenting patient? What is the name of this syndrome?
Solitary adenoma
Women and middle adult life.
Conn syndrome.
What is the rare cause of primary hyperaldosteronism?
Mutation that causes ACTH lead to the production of aldosterone.
What are two other clinical symptoms of primary hyperaldosteronism besides hypertension?
Hypokalemia and hypomagnemia
Explain what is going on with secondary hyperaldosteronism?
There is increased aldosterone because the renin angiotensin system is being chronically being activated
What are 5 clinically significant cause of the renin system always being turned on?
Diuretic use, low renal perfusion, low blood volume, pregnancy, and renin secreting tumors.
3 morph/histo features she wants us to know about aldosterone-secreting adenomas?
Small and solitary
Found on the left more than right
Spironolactone bodies (build up of the drug after being prescribed for HTN)
What is the typical patient presenting with an aldosterone secreting adenoma? 2 things.
30s and 40s, women more than men
What is a big time long term effect of hyperaldosteronism?
IHD
The androgens secreted by the adrenal gland are stimulated by what mechanism?
ACTH
What are the 3 causes of excess secretion of androgens from the adrenal gland?
Cushing disease, adrenal adenoma or carcinoma (more common), and CAH
What is the biochemical problem with congenital adrenal hyperplasia?
Autosomal recessive error of metabolism. Each error has a deficiency or complete absent or an enzyme responsible for the synthesis of a steroid, usually cortisol. So every steroid precursor behind the defect is directed over to produce sex steroids. At the same time, the drop in cortisol production stimulates more ACTH which causes hyperplasia of the adrenal gland.
What is the most common enzyme deficiency in CAH?
21 hydroxylase
What is the salt wasting syndrome with 21 hydroxylase deficiency? What are the 4 clinical signs/symptoms?
Total lack of the enzyme, so no mineralcorticoids (aldosterone) and no cortisol production. Salt wasting Hyponatremia Hyperkalemia (acidosis) Hypotension
How does this salt wasting syndrome present in girls and boys differently?
Immediately this is noticed in females, because virilization is going on and that is easily seen at birth or even in uterus. Takes a few days to notices the other symptoms in boys.
What is simple virility syndrome?
Partial lack of the hydroxylase enzyme, so some mineralcorticoids and small amount of cortisol but not enough to suppress ACTH so you still get virlization. No salt wasting.
What is non classic or late onset virilism form of CAH?
Most common. Partial lack of enzyme. Can be asymptomatic of mild. Usually at puberty.
