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Pathology
Congenital adrenal hyperplasia
Primary adrenal insufficiency
Waterhouse-Friderichsen syndrome
Hyperaldosteronism
Adrenal cortical carcinoma
Cushing syndrome
Conn syndrome
Thyroglossal duct cyst
Hyperthyroidism
Graves disease
Thyroid eye disease (NORD)
Toxic multinodular goiter
Thyroid storm
Hypothyroidism
Euthyroid sick syndrome
Hashimoto thyroiditis
Subacute granulomatous thyroiditis
Riedel thyroiditis
Postpartum thyroiditis
Thyroid cancer
Hyperparathyroidism
Hypoparathyroidism
Hypercalcemia
Hypocalcemia
Diabetes mellitus
Diabetic retinopathy
Diabetic nephropathy
Hyperpituitarism
Pituitary adenoma
Hyperprolactinemia
Prolactinoma
Gigantism
Acromegaly
Hypopituitarism
Growth hormone deficiency
Pituitary apoplexy
Sheehan syndrome
Hypoprolactinemia
Constitutional growth delay
Diabetes insipidus
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Precocious puberty
Delayed puberty
Premature ovarian failure
Polycystic ovary syndrome
Androgen insensitivity syndrome
Kallmann syndrome
5-alpha-reductase deficiency
Autoimmune polyglandular syndrome type 1 (NORD)
Multiple endocrine neoplasia
Pancreatic neuroendocrine neoplasms
Zollinger-Ellison syndrome
Carcinoid syndrome
Pheochromocytoma
Neuroblastoma
Opsoclonus myoclonus syndrome (NORD)
Adrenal insufficiency: Pathology review
Adrenal masses: Pathology review
Hyperthyroidism: Pathology review
Hypothyroidism: Pathology review
Thyroid nodules and thyroid cancer: Pathology review
Parathyroid disorders and calcium imbalance: Pathology review
Diabetes mellitus: Pathology review
Cushing syndrome and Cushing disease: Pathology review
Pituitary tumors: Pathology review
Hypopituitarism: Pathology review
Diabetes insipidus and SIADH: Pathology review
Multiple endocrine neoplasia: Pathology review
Neuroendocrine tumors of the gastrointestinal system: Pathology review
Polycystic ovary syndrome
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anovulation p. 669
antiandrogens p. 681
clomiphene p. 680
endometrial hyperplasia p. 665
ovarian neoplasm risk p. 670
Simone Taylor
Sam Gillespie, BSc
In polycystic ovary syndrome, “poly” means many, and “cystic” refers to cysts.
So you might think that having many ovarian cysts is a crucial part of polycystic ovary syndrome.
But while some people with polycystic ovarian syndrome do have ovarian cysts, ovarian cysts are no longer a necessary characteristic of the condition.
Instead, polycystic ovary syndrome is a dysfunction in the hypothalamic-pituitary-ovarian axis, which are the hormones that regulate the menstrual cycle.
A normal menstrual cycle can be divided into two phases: the follicular phase, which takes place before ovulation, and the luteal phase, which takes place after ovulation.
During the follicular phase, the hypothalamus secretes gonadotropin-releasing hormone, or GnRH.
GnRH makes the anterior pituitary gland secrete two other hormones, called gonadotropins, in roughly equal amounts, which it releases in pulses.
One of these gonadotropins is the luteinizing hormone, or LH.
The other is the follicle-stimulating hormone, or FSH.
LH and FSH travel to the follicles in the ovaries.
The follicles are small clusters of theca and granulosa cells that protect the developing oocyte, or egg.
The theca cells develop LH receptors which allow them to bind LH, and in response they secrete a hormone called androstenedione.
Granulosa cells develop FSH receptors, which allow them to bind to FSH and produce an enzyme called aromatase, which converts the androstenedione into 17β-estradiol - a member of the estrogen family.
Polycystic ovary syndrome or just PCOS, refers to a set of symptoms due to excessive androgen production in women. Signs and symptoms of PCOS include irregular or no menstrual periods, heavy periods, excess body and facial hair, acne, pelvic pain, trouble getting pregnant, and patches of thick, darker, velvety skin. Associated conditions include type 2 diabetes, obesity, obstructive sleep apnea, heart disease, mood disorders, and endometrial cancer. Management for PCOS may involve lifestyle modifications such as diet and exercise, hormone therapy, and medications.
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