Adrenal Gland Histology Flashcards
anatomy of the suprarenal glands
a. Suprarenal glands—AKA adrenal glands
i. Pair of triangular shaped glands, each about 2 inches long and 1 inch wide, superior to the kidney
ii. High vascularized
2 parts of the adrenal gland and their embryological origins
a. 2 parts of the adrenal gland (cortex and medulla) develop from 2 different origins—on posterior abdominal wall from the urogenital ridge
i. cortex—mesodermal
1. develops from the celomic epithelium o fthe posterior abdominal wall
ii. medulla—ectodermal
1. develops from the neural crest cells
fetal cortex of adrenal gland
a. by the 8th week of fetal development, these cortical elements have differentiated into a thin outer definitive cortex and a thick inner fetal cortex
i. fetal cortex actively produces fetal steroids during gestation, but involutes rapidly after birth
accessory adrenocortical nodules
a. accessory adrenocortical nodules—ectopic adrenal tissue, accessory cortical tissue, hamartoma, accessory adrenal gland, supernumary adrenal, and adrenocortical rest
i. frequently located in contact with the capsule at one pole of the adrenal but can occur completely separated from the adrenal gland in the retroperitoneal fat
adrenocortical rests
a. occur in up to 50% of newborn infants, but tend to atrophy and disappear in the postpartum period
i. the can be detected anywhere along the path of embryonic migration of adrenal cortex
development of adrenal zones of adrenal gland
a. the development of the adrenal zones occurs slowly after birth, in parallel with regression of the fetal cortex, and is not completed until late in the first year of life
functional adrenal cortex
a. definitive cortex persists and develops into the functional adrenal cortex, with distinct zonae glomerulosa and fasciculatae present at birth
i. zona reticularis develops during first year of life
3 developmental events that require glucocorticoids?
a. During the early stage of gestation, the adrenal cortex synthesizes dehydroepiandrosterone (DHEA)—precursor of the synthesis of estrogen of the placenta
b. Lack of 3beta-hydroxysteroid dehydrogenase (3beta-HSD) activity prevents the synthesis of progesterone, glucocorticoids, and androstenedience
c. Interaction b/w the fetal adrenal cortex and placenta—fetoplacental unit
congenital adrenal hyperplasia (CAH)
i. 3 beta hydroxysteroid dehydrogenase II deficient congenital adrenal hyperplasia (3-beta HSD CAH)
ii. results from a mutation in the gene for 3beta-HSD type II
iii. wide spectrum of clinical presentations
1. milder forms—result from incomplete loss of 3beta-HSD type II fcn
a. can produce virilization of genetically female infants
b. undervirilization of genetically male infants
i. only form of hypoadrenalism is the only form of CAH that can cause ambiguous genitalia in both sexes
glucocorticoids
i. either of maternal origin or synthesized from placental progesterone by the fetus and are essential for 3 events:
1. production of surfactant by type II alveolar cells after the 8th month of fetal life
2. development of functional hypothalamopituitary axis
3. induction of thymic involution
zona glomerulosa
a. outermost of cortex of adrenal gland
i. makes mineralocorticoids—aldosterone
1. produced in response to ACTH and angiotensin II
ii. lies under the capsule and is 10-15% of cortex
iii. cells aggregate into a glomerulus like arrangement and have a moderate amount of lipid droplets in the cytoplasm
iv. lacks the enzyme 17alpha hydroxylase—so cannot produce cortisol or sex steroids
v. aldosterone is made here and stimulates retention of Na in kidneys, retention of water, and renal secretion of K and H
zona fasiculata
i. 75% of cortex
ii. secretes glucocorticoids and androgens
iii. cells contain many lipid droplets of cholesterol (steroid precursor) in cytoplasm
iv. cells appear vacuolated—foamy appearance
1. so, cells are called spongiocytes
v. contains cuboid cells—with the structural features of steroid producing cell arranged in longitudinal cords separated by cortical fenestrated capillaries
zona reticularis
a. innermost of cortex of adrenal gland
i. innermost that is 5-10% of cortex
ii. cells in irregular cords that form anastomosing network
iii. secrete glucocorticoids and androgens
iv. although cells of ZF can synthesize androgens, the primary site of adrenal sex H production is the ZR
DHEA and androstenedione are the predominant androgens produced by cortex of adrenal gland
1. although DHEA and androstenedione are weak androgens, they can be converted to testosterone and even to estrogen in peripheral tissues
what characteristics are shared by ZF and ZR?
- Contain 17alpha hydroxylase to make glucocorticoids (cortisol) and 17, 20 hydroxylase to make sex Hs
- Cortisol is not stored in cells and new synthesis, stimulated by ACTH, is required for achieving a hormonal increase in blood circulation
a. Cortisol is converted in hepatocytes to cortisone
b. Can be used synthetically as anti-inflammatory and anti-allergy
c. Effects of cortisol:
i. Metabolic—stimulates gluconeogenesis to increase the conc of glc in blood
ii. Anti inflammatory—suppresses tissue responses to injury and dec cellular and humoral immunity - Although the ZF is odten associated with glucocorticoid production—mainly cortisol—the ZR with androgen production, the distinctions are not precise
- Both layers stimulated by corticotropin (ACTH)
adrenal medulla
neuroectodermic
makes catecholamines
adrenal glands in women
major course of androgens in women—androgens stimulate growth of pubic and axillary hair during puberty
chromaffin cells
i. composed of polyhedral cells arranged in cords or clumps
ii. regarded as modified sympathetic postganglionic neurons without postganglionic axons
iii. derived from neural crest
iv. lost axons and dendrites during embryonic development and have become secretory cells
v. secretory granules of epinephrine and norepinephrine
vi. adrenal medulla is innervated by sympathetic preganglionic fibers that release acetylcholine
catecholamines
i. secreted into the blood instead of being secreted into a synapse, as in postganglionic terminals
ii. secreted in response to intense emotional rxns
iii. defensive rxn ot stress
iv. inc HR
v. dilates blood vessels of cardiac and skeletal M
vi. bronchiole dilation
vii. vasoconstriction of blood vessels supplying GI, kidneys, skin
3 sources of blood supply of adrenal gland
i. inferior phrenic A give rise to superior adrenal A
ii. aorta from with the middle adrenal A branches
iii. renal A which gives rise to inferior adrenal A
arterial plexus
a. all 3 sources enter the adrenal capsule and form an arterial plexus
i. 3 sets of branches from plexus
1. subcapsular plexus—one set supplies the capsule
2. short cortical A—second set enters the cortex forming the straight fenestrated capillaries/sinusoids, percolating b/w the ZG and ZF, and forming a capillary network in the ZR before entering the medulla
3. long cortical A—third set generates medullary As travel w/o branching and supplying blood only to the medulla
tumor in the zona glomerulosa*
a. ZG: tumor localized in the ZG can cause excessive secretion of aldosterone
i. Primary aldosteronism—Conn’s syndrome
ii. A more common cause of hyperaldosteronism is an increase in renin secretion—secondary hyperaldosteronism
tumor in the zona fasiculata*
a. ZF: increase in aldosterone, cortisol, and adrenal androgen production—secondary to ACTH production—occurs in Cushing’s Disease
i. Caused by an ACTH producing tumor of the anterior hypophysis
ii. Cushing’s syndrome—functional tumor of the adrenal cortex can also result in overproduction of cortisol, as well as of aldosterone and adrenal androgens
causes of Cushing’s Syndrome
a. Endogenous—overproduction of cortisol caused by:
i. Pituitary tumor— Cushing’s Dz
ii. Adrenal tumor
iii. Other causes
b. Exogenous—taking meds containing glucocorticoids, such as hydrocortisone
Addison’s Disease*
i. Chronic destruction of the adrenal cortex by an autoimmune process or TB
ii. ACTH secretion increases b/c of the cortisol deficiency
1. ACTH can cause skin pigmentation, in particular in the skin folds and gums
iii. Loss of mineralocorticoids leads to hypotension and circulatory shock
iv. Deficiency in cortisol causes muscle weakness
v. Symptoms:
1. Fatigue, lassitude, malaise, weakness, anorexia
2. Postural dizziness, syncope
3. GI symptoms: nausea, vomiting, abdominal pain, diarrhea, constipation
4. Myalgia, arthralgias
5. decreased libido, amenorrhea
vi. signs:
1. weight loss
2. hyperpigmentation
3. hypotension
4. thinning of axillary and pubic hair
5. vitiligo
pheochromocytoma*
i. benign tumor of the chromaffin cells
ii. episodic secretion of epinephrine and NE
iii. signs/symptoms are those of SNS hyperactivity: elevated HR, BP, palpitations, diaphoresis, anxiety, headaches, nausea, pallor
iv. b/c of excessive catecholamine secretion, pheochromocytomas may precipitate life threatening hypertension or cardiac arrhythmias
v. up to 25% of pheochromocytomas are familial
