Histology Flashcards
What is the difference between how hydrophilic and hydrophobic hormones are transported in the blood?
Hydrophilics (proteins, glycoproteins, peptides, modified amino acids) can travel straight in the blood
Hydrophobic (steroid and thyroid hormones) must travel bound to protein carriers
How does the pituitary gland develop?
During the third week of development, a hypophyseal pouch (Rathke’s Pouch) buds up from the roof of the mouth (ectoderm) while a neurohypophyseal bud grows down from the diencephalon (ectoderm from floor of brain).
The mouth pouch becomes the anterior/glandular pituitary or Adenohypophysis (including pars distalis, pars tuberalis, and pars intermedia)
The brain pouch becomes the posterior pituitary or Neurohypophysis (including pars nervosa and infundibulum/stalk attached to the hypothalamus via the median eminence) which secretes hormones via neurons
Why do the anterior and posterior pituitary stain differently?
Anterior is glandular tissue which is full of hormone granules
Posterior does not produce any hormones because they all come from neurons that originate outside of the pituitary
What is the hypothalamic-hypophyseal tract? What hormones are involved?
Bundle of axons that travel from the supraoptic and paraventricular nuclei through the infundibulum to the neurohypophysis
Supraoptic nuclei produces ADH while paraventricular nuclei produces Oxytocin
Describe the blood supply of the pituitary gland (hypothalamic-hypophyseal portal system). What is the importance of this portal system?
The superior hypophyseal artery supplies a plexus that surrounds the median eminence and infundibulum. The hypophyseal portal veins connect the primary plexus to a secondary plexus that surrounds the pars distalis.
The inferior hypophyseal artery supplies a (mostly) separate plexus for only the posterior pituitary
The portal plexuses carry neuropeptides produced by the hypothalamus to the anterior pituitary to either stimulate or inhibit hormones.
What are the common features of endocrine organs?
Parenchyma: cords or clumps of cells
Highly vascular: fenestrated capillaries
Ductless glands: not like exocrine
Stroma: reticular connective tissue and some nervous tissue
Secretes hormones: peptides, amino acid derivatives, steroids
Name the two types of acidophils in the anterior pituitary
Somatotrophs: Growth Hormone
Mammotrophs/lactotrophs: Prolactin
Name the basophils in the anterior pituitary
Thyrotrophs: TSH
Gonadotrophs: FSH and LH
Corticotrophs: ACTH
Where do the nuclei in the pars nervosa come from? What are Herring bodies?
The only nuclei are from Pituicytes (supporting cells) and capillary endothelial cells
Herring bodies are the neurosecretory vesicles at nerve endings
What are chromophobes?
Cells of the adenohypophysis that do not stain because they are non-secretory
What types of cells are found in the pars tuberalis?
Mostly gonadotrophs
What is the difference between the corticotrophs of the pars intermedia and those of the pars distalis?
The ones in the pars intermedia cleave POMC into two types of melanocyte stimulating hormones (MSH): y-LPH and B-endorphin
The ones in the distalis cleave POMC into ACTH
Where are hypothalamic hormones produced? What hypothalamic hormones regulate which hormones of the pars distalis?
Paraventricular nucleus, medial preoptic nucleus, arcuate nucleus
TRH (Somatostatin inhibits)—> Thyrotrophs (TSH)
TRH (dopamine inhibits) —> Lactotrophs (Prolactin)
GnRH —> Gonadotrophs (FSH and LH)
CRH —> Corticotrophs (ACTH)
GHRH (somatostatin inhibits) —> Somatotrophs (GH)
What type of axons are found in the pars nervosa?
Unmyelinated
How does negative feedback of hormones work? Use thyroid hormone as an example
How else are pars distalis hormones regulated?
TRH stimulates TSH release which stimulates TH release.
Hypothalamus recognizes an increase in body temp and inhibits TRH release. At the same time, TH binds TRH receptors on thyrotrophs and inhibits the release of TSH.
Outside inhibitory (or stimulatory) factors can also regulate hormone release. Ex) ghrelin from the stomach mucosa stimulates somatotropin release
What happens to ADH and oxytocin after they are released?
They get taken up into fenestrated capillaries
What does oxytocin do?
Stimulates contraction of uterine smooth muscle during child birth and myoepithelial cells in the mammary gland
What regulates the daily rhythms of bodily activity (including light/dark cycles and release of melatonin)?
Pineal gland
What makes up the Pineal gland? What is corpora arenacea?
Stoma: connective tissue capsule (pia mater) and septae (contain blood vessels) that divide it into lobules; fenestrated capillaries; corpora arenacea (calcified concretions that don’t do anything, but they can be used to distinguish the pineal)
Parenchyma: Pinealocytes (90% of cells) arranged in clumps and cords with one to two cell processes that extend to fenestrated capillaries; glial like cells in the interstitium.
How is the release of melatonin regulated?
Postganglionic sympathetics from the superior cervical ganglion stimulate release of melatonin in response to darkness
How can you tell the difference between pinealocytes and astrocytes in the pineal gland?
The pinealocytes have euchromatic nuclei and are clumped together
Astrocytes have darker, more elongated nuclei and are only found in the connective tissue septa.
What makes up the stroma of the thyroid?
Fibroelastic c.t. capsule and septae (which contain blood vessels)
Reticular cells and reticular fibers
Fenestrated capillaries
What makes up the parenchyma of the thyroid? What is secreted by the thyroid?
Millions of small thyroid follicles lined with simple cuboidal or low columnar epithelium (thyrocytes) and filled with an acidophilic, gelatinous colloid of the protein thyroglobulin
Between the thyrocytes (or between the follicles), large pale-staining C cells (parafollicular cells) can be found which secrete calcitonin for calcium metabolism.
Thyroglobulin is stored within the follicles to later be converted into thyroxine (T4) and tri iodothyronine (T3) which both help determine the basal metabolic rate of the body.
What can be found between follicles in the thyroid?
Parafollicular cells and capillaries
What is the difference between low columnar and squamous follicular cells? Describe the TEM of a follicular cell.
Low columnar represents an active follicle while squamous follicles are hypoactive.
Tight junctional complex at the top, attached to a basal lamina at the bottom. Very well developed RER and Golgi along with many lysosomes. Also have microvilli facing the lumen
Where can C cells be found (think about TEM)? What do they look like?
Closely associated with the follicular cells and inside the basement membrane, but often not contacting the lumen.
Large nucleus, large Golgi apparatus, extensive RER, and many dark granules containing calcitonin
How is iodide taken up by thyrocytes in order to produce T4 and T3?
Na/I symporters in the basolateral cell membrane.
I-/Cl- transporter (pendrin pumps) pumps I- from the cell into the lumen
Describe the process by which thyroid hormones are produced
1) thyrocytes make thyroglobulin and secrete it into the lumen
2) iodide (from the diet) is pumped across the cells into the lumen
3) membrane bound thyroid peroxidases convert iodide to iodine which is then added to tyrosine residues on thyroglobin. This produces MIT and DIT
4) MIT and DIT come together to form T3 and two DITs come together to form T4. However, both T3 and T4 are still attached to the glycoprotein backbone
5) Iodinated Thyroglobulin is endocytosed and degraded into active T3 and T4 which is then released into the capillaries.
How do T3 and T4 enhance metabolic activity? Which is more prevalent?
Increase number and size of mitochondria in cells
90% of thyroid hormone is in the T4 form
What regulates the function of the thyroid gland?
TSH receptors on the basement membrane of thyrocytes bind TSH which stimulates growth of cell height and stimulates all stages of thyroid hormone synthesis.
Thyroid hormones inhibit release of TSH. Cold exposure increases release of TSH while heat and stressful stimuli decrease it.
What is Graves Disease?
Autoimmune disorder in which antibodies cause overstimulation of follicular cells (by binding to TSH receptors and causing cAMP release) and release of thyroid hormones. Marked by weight loss, heat intolerance, sweating, etc.
TSH goes down due to negative feedback by T3 and T4, but it doesn’t matter because this bypasses that system!
Hypothyroidism
Reduced thyroid hormone levels caused by inflammation or inadequate secretion of TSH. Results in tiredness, weight gain, intolerance of cold, and decreased concentration.
Primary hypothyroidism
Most commonly idiopathic
TSH receptor blocking autoantibodies
Hashimoto Thyroiditis
Autoimmune that targets thyroid peroxidase (T3 and T4 can’t be produced)
Causes goiter and hypothyroidism
Lymphoid follicle appears next to thyroid follicles
When is calcitonin released? How does it work?
Secreted in response to elevated blood calcium
Directly inhibits osteoclasts which resorb bone
Causes kidney to excrete more calcium and phosphate
Parathyroid gland structure
4 ovoid structures on posterior side of the thyroid
Connective tissue capsule and trabeculae
Stroma: reticular cells and fibers
Highly vascular with fenestrated capillaries
Parathyroid parenchyma
Chief cells— produce PTH; organelles typical of a protein secreting cell; pale staining
Oxyphils— large, very eosinophilic cells; filled with mitochondria; function unknown; more prevalent in older people. Usually degenerated derivatives of chief cells
Adipocytes— 50% of cells in older patients
How does PTH work?
Polypeptide hormone secreted by chief cells
Causes osteoblasts to secrete an osteoclast stimulating factor (RANK) which increases both the number and activity of osteoclasts
The increases resorption of bone matrix increases the levels of blood Ca2+ and serum alkaline phosphatase.
Also indirectly increases Ca2+ by increasing vitamin D activity in small intestine (increases Ca2+ uptake)
Increased Ca2+ inhibits PTH release
Primary Hypoparathyroidism vs pseudoparathyroidism
Deficiency in PTH secretion due to damage, hereditary, or autoimmune
Leads to dense bones, spastic muscle contractions, convulsions, tetany, death
Pseudoparathyroidism— rare; abnormal PTH receptors causes hypocalcemia although PTH levels are high
Primary hyperparathyroidism vs. malignant tumor
Usually a hormone secreting tumor of chief cells; causes thinning of bones, bone fractures. Deposits of bone in soft tissues
Malignant tumor (breast, lung, ovarian) may secrete a PTH related protein (PTHrP) leading to hypercalcemia
What effect does pineal destruction/tumor have on humans?
Precocious puberty in children
Contraception properties as well
A proper functioning pineal is important in defending against breast and prostate cancer
What is so nifty about the pineal gland?
It converts sensory information (light) into hormonal information (melatonin)
What type of drug might benefit a breast cancer patient with bone metastases?
PTH antagonist
Some breast cancer cells secrete PTHrP because they themselves have a PTH receptor that stimulates cell proliferation by PTHrP. However, the PTHrP also stimulates osteoblasts to oversecrete RANK
What is the endocrine function of the pancreas? Where does it occur?
Secrete insulin, glucagon, somatostatin, and pancreatic polypeptide
Occurs in the islets of Langerhans.
What makes up the islets of langerhans?
Parenchyma: clusters of cells scattered throughout pancreas
Stroma: reticular cells and reticular fibers
Highly vascularized with fenestrated capillaries
10% of islet cells have autonomic innervation. Gap junctions exist between islet cells.
Describe the 4 types of cells found in the parenchyma of the exocrine pancreas
A or alpha cells (20% of cells)— secrete glucagon; react with silver stain; found in periphery of islets
B or beta cells (70% of cells)— secrete insulin; located in interior of islets
D or delta cells (5% of cells)— secrete somatostatin; scattered throughout islet
F cells (<1%)— secrete pancreatic polypeptide which inhibits exocrine secretion of pancreas.
Type 1 vs. Type 2 diabetes (beta cells)
Type 1— decreased number of B cells (destroyed by antibodies) and increased leukocyte infiltration
Type 2— variable number of B cells (with amyloid deposits) and islet amyloid polypeptide (IAPP) deposits
What do the different zones of the adrenal cortex produce? What properties do all these cells share?
All produce steroid hormones
Zona glomerulosa— mineralcorticoids (aldosterone); stimulated by Ang II and high K+
Zona fasciculata— glucocorticoids (cortisol and corticosterone); stimulated by ACTH; exhibits negative feedback
Zona reticularis— sex steroids (weak androgens), DHEA (gets converted to testosterone in both men and women); stimulated by ACTH; exhibits neg feedback
Steroid producing cells have: Abundant SER, mitochondria with tubulovesicular cristae, lipid droplets (to supply the cholesterol precursor)
Primary hyperaldosteronism (Conn disease) affects which zone of the cortex?
Elevated aldosterone due to an adenoma of the zona glomerulosa
Cushing syndrome
Caused by administration of large doses of steroids to treat primary disease.
Also caused by ACTH secreting adenoma (corticotrophs) or adrenal cortical adenoma
Congenital adrenal hyperplasia
Caused by mutations in genes for steroid synthesizing enzymes—> increased level of androgens
Primary adrenal insufficiency (Addison) vs. secondary insufficiency
Primary— caused by autoimmune destruction of adrenal cortex; disrupts glucocorticoid feedback and causes oversecretion of ACTH
Secondary— hypothalamus or adenohypophysis disorder leading to decreased ACTH
Chromaffin cells
Make up the adrenal medulla
“Modified sympathetic ganglion” cells that secrete epinephrine and norepinephrine
What distinguishes chromaffin cells from adrenal cortex cells? Which is bigger, NE or Epi granules?
Chromaffin cells stain lighter and are larger and clumped together in larger clumps than cortex cells
NE granules are bigger and darker than Epi
What is the origin of chromaffin cells? What about adrenal cortex?
Neural crest: they are modified postganglionic neurons that have lost their dendrites and axons
Cortex: comes from mesoderm
What neurotransmitter triggers the release of catecholamines from the adrenal medulla?
ACh
Pheochromocytoma
Catecholamine producing tumor (secretes both epinephrine and NE) of the adrenal medulla
What is the importance of the blood supply of the adrenal gland?
Short arteries supply the cortex but only leave venous blood by the time it reaches the medulla
Long arteries bypass the cortex to supplement the medulla
The short arteries allow glucocorticoids from the cortex to be taken to the medulla because they are needed to for maintenance of the enzyme that produces Epi and NE. Also needed to inhibit development of neuronal cell processes.
Neuroblastoma
Neoplasm containing primitive neuro blasts (40% occur in the adrenal medulla)
What makes up the structure of the adrenal glands?
Dense connective tissue capsule that sends trabeculae into the parenchyma (that contain blood vessels and neurons probably)
Stroma: reticular fibers and reticulocytes
Parenchyma: cells that produce steroid hormones and catecholamines
What’s so special about the mitochondria of the adrenal cortex cells?
Tubulovesicular cristae instead of the shelf like kind.
Not only produce ATP but also contain enzymes for converting cholesterol to pregnenolone (along with the Smooth ER)
What primarily increases aldosterone secretion?
Angiotensin II and high K+ levels (only weakly stimulated by ACTH)
What are the functions of the ovary?
Production of oocytes
Production of hormones: sex steroids (estrogen and progesterone); protein hormones (relaxin, Inhibin, activin)
What are the functions of the ovary?
Production of oocytes
Production of hormones:
Sex hormones: estradiol and progesterone
Protein hormones: activin, Inhibin, relaxin
What is the flow of development in the ovary from primordial follicle to corpus luteum?
Primordial follicle-> early primary follicle-> primary follicle-> secondary follicle-> mature Graafian follicle-> ruptured follicle (releases oocyte)-> corpus hemorrhagicum-> corpus luteum
How many follicles are you born with? How many lost per cycle? How many at menopause?
Born with 1 million
1,000 lost per cycle
1,000 left at menopause
When does the Ovarian cycle start? What are the different phases?
Day 1 of menses (sloughing off of the endometrial wall)
Follicular phase- days 1-14
Ovulation phase- days 14-15
Luteal phase- days 15-28; luteal regression usually begins around day 24
Any variation in cycle length is due to follicular phase. Luteal phase is always 14 days
What happens during the follicular phase? What phases of the uterine cycle does it correspond with?
FSH stimulates growth and maturation of a follicle (LH helps a little bit) until ovulation
Menstrual phase (days 1-5) and Proliferative phase (days 6-14)
What happens during the luteal phase? What uterine phases does it overlap with?
LH promotes ovulation (with help of FSH) and proliferation of the corpus luteum
Secretory phase (days 15-26) and Pre-menstrual phase (days 27-28)
What are the different layers of the ovary?
Outer epithelium (mesothelium) of simple cuboidal cells
Tunica albuginea (like testes)— dense connective tissues capsule
Cortex— cellular connective tissue where primordial follicles reside
Medulla— inner loose connective tissue with blood vessels entering from the hilum
Primordial follicle
Present since fetal life; arrested in Prophase of Meiosis I since week 11-12 of development (46, 4N)
Found in cortex of ovary; 25um in diameter with large nucleus in the middle (primary oocyte arrested in prophase)
Single layer of flat, squamous follicular cells surround oocyte; separated from vascularized stroma by basal lamina
Primary Follicle
Stimulated by FSH (only during follicular phase), a primary oocyte starts to increase in size and number of organelles (but stays in Prophase I)
Unilaminar primary follicle— follicular cells undergo mitosis and become single cuboidal layer. Bigger than primordials.
Multilaminar primary follicle— continues to grow and follicular cells develop into multiple cell layers called granulosa cells. Cells communicate through gap junctions. Still a vascular and retains basal lamina. Zona pellucida (a glycoprotein layer required for sperm binding and fertilization) separates the oocyte and the granulosa layer. Oocyte and granulosa can communicate through this layer. Stroma surrounding follicle starts to differentiate into theca interna and theca externa. Bigger than unilaminar.
What does the theca interna do? Theca externa?
Theca interna is well vascularized endocrine tissue that secretes androstenedione. Molecule diffuses through basement membrane where granulosa cells convert it into estrogen via aromatase. This is FSH dependent. The estrogen then leaves back into the theca layer and into the capillaries.
Theca externa is a layer containing fibroblasts and smooth muscle that blends into the stroma around it.
What happens to multilaminar primary follicles as they continue to grow?
They move deeper into ovarian cortex and antri (antrum) start to appear and fill with follicular fluid containing GAG, plasminogen, fibrinogen, heparin sulfate, and high concentrations of steroids (progesterone and estrogen)
Now called Secondary Follicle. Primary oocyte still in Prophase I
Cumulus oophorus and corona radiata?
As the secondary follicle matures, the antrum starts to outgrow the granulosa layer and the layer becomes thinner. The oocyte juts out into the antrum while staying surrounded by a layer of granulosa known as the Cumulus oophorus
The corona radiata is the layer that immediately surrounds the oocyte and stays with it after ovulation. Cell processes from the corona and microvilli from the oocyte extend into the zona pellucida and communicate with one another.
Mature Graafian follicle (and polar body)
Once a follicle reaches a certain size (2cm) it is considered a mature follicle. It pushes up against the wall of the ovary and forms a bulge that is visible through ultrasound. Just before ovulation, this bulge becomes ischemic and is called the STIGMA.
Just before ovulation, the oocyte becomes a secondary oocyte by completing meiosis I (becomes 23, 2N). One daughter oocyte is much larger than the other. The smaller is called the first polar body and undergoes atresia. The larger oocytes is ovulated but remains suspended in metaphase of meiosis II until fertilization.
Follicular atresia
Begins during fetal life and continues partly into menopause. Can occur at any stage of follicular development.
Of the 1000 follicles that start during each menstrual cycle, 999 undergo atresia while 1 is ovulated (but they can still secrete hecka estrogen for a while before they die).
Includes apoptosis of granulosa cells, loss of zona pellucida, autolysis of oocyte, and invasion by macrophages to clean up.
Where does GnRH originate? How does puberty onset?
Arcuate and Preoptic nucleus; pulsatile release stimulates release of FSH and LH (especially during ovulation)
Pulsatile release of GnRH leads to onset of puberty
How is GnRH regulated during follicular development? What are the roles of estrogen and progesterone?
At low levels, estrogen exhibits neg feedback on GnRH during the follicular phase but once a mature follicle, it reaches a threshold and starts to positively feedback causing GnRH release to increase and an LH surge (triggers ovulation). During the luteal phase, progesterone exhibits negative feedback on FSH and GnRH
Other inhibitors: dopamine, endorphins, melatonin, CRF
Other stimulators: norepinephrine
Estrogen (from the granulosa cells) increases endometrium proliferation during the follicular phase while progesterone and estrogen (from corpus luteum) stimulate endometrium proliferation even more during luteal phase.
Why doesn’t estradiol positive feedback also result in an FSH surge?
During the follicular phase, granulosa cells also secrete Inhibin B which has a negative feedback effect on FSH release (as well as low levels of estrogen). During the luteal phase, progesterone and Inhibin A from corpus luteum have negative feedback effects on both FSH and GnRH
Nothing directly inhibits LH secretion
How does estradiol synthesis decrease as a result of the LH surge?
LH receptors on theca cells become completely occupied during LH surge which leads to suppression of LH induced androgen precursor synthesis.
Loss of androgen precursors leads to decrease in estradiol synthesis after LH surge.
What happens during ovulation?
Cause by LH surge
Meiosis I is completed
Granulosa cells secrete more prostaglandins and hyaluronan which causes the antrum to swell and loosens the outer layer of cells
Ovarian wall weakens due to plasminogen from capillaries
Smooth muscle contractions begin in the theca externa stimulated by the prostaglandins.
The cells of the ovulated follicle give rise to the corpus luteum under stimulation of LH.
Corpus Luteum (of menstruation). What effect does it have on FSH?
After ovulation and under stimulation of LH, the granulosa layer and theca layer fold in on themselves and blood clots appear in the antrum
Granulosa cells increase in size, become well vascularized, and are called granulosa lutein cells which take up 80% of the corpus luteum. LH stimulates these cells to synthesize progesterone and estradiol that target the reproductive tract for preparation of fertilization, preimplantation development and implantation.
The theca interna becomes theca lutein cells which are half as big as granulosa lutein cells. LH causes these cells to make large amounts of weak androgens
The LH surge causes corpus luteum to secrete progesterone for 10-12 days. After that, if no pregnancy occurs, it undergoes apoptosis. This is called the Corpus luteum of menstruation. The decrease in progesterone after apoptosis causes sloughing of the endometrial lining (menstruation).
The estrogen produced by the corpus luteum inhibits FSH. FSH also stimulates Inhibin A to inhibit itself. So after it is gone, FSH goes back up.
What happens if GnRH secretion becomes continuous? Which is more important in GnRH secretion, magnitude or frequency?
FSH and LH levels are not maintained (they require pulsatile stimulation).
Frequency
What does FSH do in the early and later follicular phases?
Targets granulosa cells:
Early follicular phase: NO effect on primordial follicle (it grows spontaneously). Begins at primary follicle;
- stimulates mitosis and cell proliferation
- induces FSH receptors
- induces gap junction formation
- induction of aromatase to produce estradiol
- stimulates Inhibin B synthesis which stimulates androgen production by theca interna and decreases FSH release through negative feedback
Late phase: estrogen levels are elevated— induces LH receptors on granulosa cells resulting in low level progesterone production.
What does LH do during the early follicular phase and late follicular phase?
Targets both theca and granulosa cells
Early Follicular phase: targets theca interna— stimulates steroid hormone production (mainly androgens)
Late follicular phase: targets granulosa cells to initiate luteinization and progesterone synthesis
- LH surge: high occupancy of LH receptors on theca cells blocks androgen precursors needed for estradiol synthesis
How is estrogen created through side-chain cleavage?
Cholesterol side-chain is cleaved to 21 carbon progesterone. Cleaved some more into 19 carbon androstenedione or testosterone. Aromatase cleaves those into 18 carbon estradiol
What changes occur in the dominant follicle due to the LH surge?
Oocyte completes first mitotic division resulting in secondary oocyte and first polar body
Transformation of granulosa cells into lutein cells with an increase in progesterone production
Activation of proteolytic enzymes that degrade the follicular wall with formation of the stigma
Oocyte with cumulus detaches from the wall of the follicle and floats in the liquor follicular
Rapid accumulation of fluid in the antrum
Corpus albicans
Without LH, the corpus luteum dies
LH surge causes increase in progesterone from granulosa cells which exhibits negative feedback on GnRH release and down regulates GnRH receptors in pars distalis
LH secretion decreases. Corpus luteum degenerates into inactive corpus albicans that has NO NUCLEI
Corpus luteum of pregnancy
Human chorionic gonadotropin (hCG) from the implanting blastocyst RESCUES the corpus luteum (hCG acts similar to LH)
Steroid hormone production is continued and maintains the endometrial lining in the uterus
Corpus luteum of pregnancy continues to enlarge and increase hormone production throughout the first trimester
What’s the difference between Inhibin B and Inhibin A?
Inhibin B— granulosa cells; inhibits FSH secreting gonadotrophs
Inhibin A— granulosa lutein cells; inhibits both FSH and LH secreting gonadotrophs
What can a granulosa lutein cell make that a granulosa cell can’t? Why? What is weird about progesterone and estrogen synthesis in granulosa lutein cells?
FSH allows granulosa cells to convert androgens into estradiol via aromatase BUT LH allows granulosa lutein cells to take up cholesterol and form progesterone
HOWEVER, the granulosa lutein cells do not have the enzyme necessary to turn progesterone into androgens. Therefore, the androgens that become estradiol in the granulosa lutein cells still comes from theca lutein cells.
Clinical considerations of the ovary
Ovarian cysts— fluid filled cavities resulting from unruptured Graafian follicles
Polycystic ovary syndrome— elevated androgens and LH but no FSH means bilateral ovarian enlargement due to follicular cysts (that never matured)
Ovarian tumors
Menopause— ovarian follicles fail to develop
