Endocrine 1 Flashcards
Where does the thyroid diverticulum arise from?
The thyroid diverticulum arises from the floor of the primitive pharynx.
Where does the thyroid diverticulum descend into?
The thyroid diverticulum descends into the neck.
What connects the thyroid diverticulum to the tongue?
The thyroid diverticulum is connected to the tongue by the thyroglossal duct.
What may persist from the thyroglossal duct?
The thyroglossal duct may persist as cysts or a pyramidal lobe of the thyroid.
What is the normal remnant of the thyroglossal duct?
The normal remnant of the thyroglossal duct is the foramen cecum.
What is the most common site for ectopic thyroid tissue?
The most common ectopic thyroid tissue site is the tongue (lingual thyroid).
What can removal of lingual thyroid tissue result in?
Removal may result in hypothyroidism if it is the only thyroid tissue present.
How does a thyroglossal duct cyst present?
A thyroglossal duct cyst presents as an anterior midline neck mass that moves with swallowing or protrusion of the tongue.
How does a thyroglossal duct cyst differ from a branchial cleft cyst?
A thyroglossal duct cyst is an anterior midline neck mass that moves with swallowing or protrusion of the tongue, while a branchial cleft cyst arises from a persistent cervical sinus in the lateral neck.
From which germ layer are thyroid follicular cells derived?
Thyroid follicular cells are derived from endoderm.
From which origin are parafollicular cells derived?
Parafollicular cells (C cells) are derived from neural crest.
What is the origin of the adrenal cortex?
The adrenal cortex is derived from mesoderm.
What is the origin of the adrenal medulla?
The adrenal medulla is derived from neural crest.
What are the zones of the adrenal cortex?
The zones of the adrenal cortex are Zona Glomerulosa, Zona Fasciculata, and Zona Reticularis.
What does GFR stand for in relation to adrenal cortex zones?
GFR stands for Salt (mineralocorticoids), Sugar (glucocorticoids), Sex (androgens).
What primarily regulates the zona glomerulosa?
The primary regulator of the zona glomerulosa is AT II.
What hormone class does the zona glomerulosa produce?
The zona glomerulosa primarily produces mineralocorticoids.
What is the primary hormone produced by the zona glomerulosa?
The primary hormone produced by the zona glomerulosa is aldosterone.
What primarily regulates the zona fasciculata?
The primary regulators of the zona fasciculata are ACTH and CRH.
What hormone class does the zona fasciculata produce?
The zona fasciculata primarily produces glucocorticoids.
What is the primary hormone produced by the zona fasciculata?
The primary hormone produced by the zona fasciculata is cortisol.
What primarily regulates the zona reticularis?
The primary regulators of the zona reticularis are ACTH and CRH.
What hormone class does the zona reticularis produce?
The zona reticularis primarily produces androgens.
What is the primary hormone produced by the zona reticularis?
The primary hormone produced by the zona reticularis is DHEA (Dehydroepiandrosterone).
What hormones does the anterior pituitary secrete?
The anterior pituitary secretes FSH, LH, ACTH, TSH, Prolactin, GH, and β-endorphin.
Where is Melanotropin (MSH) secreted from?
Melanotropin (MSH) is secreted from the intermediate lobe of the pituitary.
What are ACTH, MSH, and β-endorphin derivatives of?
ACTH, MSH, and β-endorphin are derivatives of proopiomelanocortin (POMC).
What is the origin of the adenohypophysis?
The adenohypophysis is derived from Rathke’s pouch.
What is the common subunit of anterior pituitary hormones?
The common subunit is the hormone subunit common to TSH, LH, FSH, and hCG.
What determines the specificity of anterior pituitary hormones?
The specific subunit of anterior pituitary hormones determines hormone specificity.
Which anterior pituitary hormones are secreted by basophils?
Basophils secrete FSH, LH, ACTH, and TSH.
Which anterior pituitary hormones are secreted by acidophils?
Acidophils secrete GH and PRL.
What hormones does the posterior pituitary store and release?
The posterior pituitary stores and releases vasopressin (ADH) and oxytocin.
Where are vasopressin and oxytocin made?
Both are made in the hypothalamus (supraoptic & paraventricular nuclei).
How are vasopressin and oxytocin delivered to the neurohypophysis?
They are delivered via neurophysins (carrier proteins).
What is the origin of the posterior pituitary?
The posterior pituitary is derived from neuroectoderm.
What are Islets of Langerhans?
Islets of Langerhans are collections of endocrine cells that arise from pancreatic buds.
What do alpha pancreatic cells produce and where are they located?
Alpha pancreatic cells produce glucagon and are located peripherally within the islets of Langerhans.
What do beta pancreatic cells produce and where are they located?
Beta pancreatic cells produce insulin and are located centrally within the islets of Langerhans.
What do delta pancreatic cells produce and where are they located?
Delta pancreatic cells produce somatostatin and are interspersed within the islets of Langerhans.
What is the synthesis process of insulin?
Preproinsulin (synthesized in RER) undergoes cleavage of ‘presignal’ to proinsulin (stored in secretory granules), then cleavage of proinsulin leads to exocytosis of insulin and C-peptide equally.
In what scenarios would levels of both insulin and C-peptide be increased?
Levels of both insulin and C-peptide would be increased in insulinoma and sulfonylurea use.
What happens to levels of insulin and C-peptide with exogenous insulin use?
Only insulin increases, as exogenous insulin lacks C-peptide.
How does insulin bind to its receptors?
Insulin is released from pancreatic beta cells, binds insulin receptors with tyrosine kinase activity, and induces glucose uptake into insulin-dependent tissue and gene transcription.
What are the insulin-dependent glucose transporters?
GLUT4 is the insulin-dependent glucose transporter found in adipose tissue and striated muscle.
How can exercise affect GLUT4 expression?
Exercise can increase GLUT4 expression.
What are the insulin-independent glucose transporters?
GLUT1, GLUT2 (bidirectional), GLUT3, GLUT5 (Fructose), SGLT1/SGLT2 (Na+-glucose cotransporters).
Which tissues express GLUT1?
GLUT1 is expressed in RBCs, brain, cornea, and placenta.
Which tissues express GLUT2?
GLUT2 is expressed in islet cells, liver, kidney, and small intestine.
Which tissues express GLUT3?
GLUT3 is expressed in the brain and placenta.
Which tissues express GLUT5?
GLUT5 is expressed in spermatocytes and the GI tract.
Which tissues express SGLT1/SGLT2?
SGLT1/SGLT2 is expressed in the kidney and small intestine.
What does the brain utilize for metabolism during starvation?
The brain utilizes glucose for metabolism but ketone bodies during starvation.
What do RBCs utilize for energy?
RBCs utilize glucose for energy as they lack mitochondria for aerobic metabolism.
What tissues have insulin-independent glucose uptake?
Tissues with insulin-independent glucose uptake include Brain, RBCs, Intestine, Cornea, Kidney, Liver, Islet cells, Placenta, and Spermatocytes.
What is insulin’s effect once in the placenta?
Unlike glucose, insulin does not cross the placenta.
What are the anabolic effects of insulin?
Insulin promotes glucose transport in skeletal muscle and adipose tissue, glycogen synthesis and storage, triglyceride synthesis, Na+ retention in kidneys, protein synthesis in muscles, cellular uptake of K+ and amino acids, and inhibits glucagon release.
What is the major regulator of insulin release?
The major regulator of insulin release is glucose.
Why is there a different insulin response with oral vs IV glucose?
The difference is due to incretins (e.g., GLP-1, GIP), which are released after meals and increase beta cell sensitivity to glucose.
What are incretins?
Incretins include glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which are released after meals and enhance beta cell sensitivity to glucose.
Which receptors regulate insulin secretion?
Insulin release is stimulated by GLP-1 and inhibited by somatostatin.
What is the mechanism of insulin secretion by pancreatic beta cells?
Glucose enters beta cells, generating ATP from glucose metabolism, which closes K+ channels, depolarizes the cell membrane, opens voltage-gated Ca2+ channels, and stimulates insulin exocytosis.
What is the source of glucagon?
Glucagon is made by alpha cells of the pancreas.
What is the function of glucagon?
Glucagon promotes glycogenolysis, gluconeogenesis, lipolysis, and ketone production, elevating blood sugar levels during fasting.
How is glucagon regulated?
Glucagon is secreted in response to hypoglycemia and inhibited by insulin, hyperglycemia, and somatostatin.
What is the function of ADH?
ADH increases water permeability of distal convoluted tubule and collecting duct cells in the kidney to enhance water reabsorption.
What is the stimulus for ADH secretion?
The stimulus for ADH secretion is plasma osmolality, except in cases of SIADH.
What is the function of CRH?
CRH stimulates ACTH, MSH, and β-endorphin secretion.
What decreases CRH levels?
CRH levels decrease in chronic exogenous steroid use.
What is the function of dopamine?
Dopamine inhibits prolactin and TSH secretion.
What can dopamine antagonists cause?
Dopamine antagonists can cause galactorrhea due to hyperprolactinemia.
What is the function of GHRH?
GHRH stimulates GH secretion.
What is GHRH analog used to treat?
GHRH analog (tesamorelin) is used to treat HIV-associated lipodystrophy.
What is the function of GnRH?
GnRH stimulates FSH and LH secretion.
What suppresses GnRH?
GnRH is suppressed by hyperprolactinemia.
What is the effect of tonic vs pulsatile GnRH?
Tonic GnRH suppresses the HPG axis, while pulsatile GnRH leads to puberty and fertility.
What is the function of MSH?
MSH stimulates melanogenesis by melanocytes.
Why does MSH cause hyperpigmentation in Cushing disease?
MSH and ACTH share the same precursor molecule, proopiomelanocortin.
What is the function of oxytocin?
Oxytocin causes uterine contractions during labor and is responsible for the milk letdown reflex in response to suckling.
What is the function of prolactin?
Prolactin stimulates milk production in the breast and inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release.
What symptoms does pituitary prolactinoma cause?
Pituitary prolactinoma causes amenorrhea, osteoporosis, hypogonadism, and galactorrhea.
What is the function of somatostatin?
Somatostatin inhibits GH and TSH secretion.
What are somatostatin analogs used to treat?
Somatostatin analogs are used to treat acromegaly.
What is the function of TRH?
TRH stimulates TSH and prolactin secretion.
What can increase TRH secretion?
TRH may increase prolactin secretion in primary or secondary hypothyroidism.
Where is prolactin secreted from and what is it structurally homologous to?
Prolactin is secreted mainly by the anterior pituitary and is structurally homologous to growth hormone.
What is the function of PRL?
PRL stimulates milk production in the breast and inhibits ovulation and spermatogenesis.
What inhibits prolactin secretion?
Prolactin secretion is tonically inhibited by dopamine from the tuberoinfundibular pathway of the hypothalamus.
How does prolactin inhibit its own secretion?
Prolactin inhibits its own secretion by increasing dopamine synthesis/secretion from the hypothalamus.
What effect does TRH have on PRL secretion?
TRH increases prolactin secretion.
What can inhibit prolactin secretion and be used to treat prolactinoma?
Dopamine agonists (e.g., bromocriptine) can inhibit prolactin secretion.
What drugs stimulate prolactin secretion?
Dopamine antagonists (e.g., most antipsychotics) and estrogens (e.g., OCPs, pregnancy) stimulate prolactin secretion.
Where is growth hormone (somatotropin) secreted from?
Growth hormone is secreted by the anterior pituitary.
What is the function of growth hormone (GH)?
GH stimulates linear growth and muscle mass through IGF-1 secretion by the liver.
What is a side effect of growth hormone?
GH can cause insulin resistance (diabetogenic).
How is GH released?
GH is released in pulses in response to growth hormone-releasing hormone (GHRH).
When is GH secretion increased?
GH secretion increases during exercise, deep sleep, puberty, and hypoglycemia.
What inhibits GH secretion?
GH secretion is inhibited by glucose and somatostatin release via negative feedback by somatomedin.
What can excess secretion of GH cause?
Excess GH secretion may cause acromegaly in adults or gigantism in children.
How is excess GH treated?
Excess GH is treated with somatostatin analogs (e.g., octreotide) or surgery.
What is the function of ghrelin?
Ghrelin stimulates hunger (orexigenic effect) and GH release via GH secretagogue receptor.
Where is ghrelin produced?
Ghrelin is produced by the stomach.
How does ghrelin exert its effects?
Ghrelin acts via the lateral area of the hypothalamus to stimulate appetite.
How do sleep deprivation and Prader-Willi syndrome affect ghrelin?
Sleep deprivation or Prader-Willi syndrome increases ghrelin production.
What is the function of leptin?
Leptin is a satiety hormone produced by adipose tissue.
How does leptin exert its effects?
Leptin acts via the ventromedial area of the hypothalamus to decrease appetite.
What effect does a mutation of the leptin gene have?
A mutation of the leptin gene can lead to congenital obesity.
What effect does sleep deprivation have on leptin?
Sleep deprivation or starvation decreases leptin production.
What is the effect of endocannabinoids?
Endocannabinoids act at cannabinoid receptors in the hypothalamus and nucleus accumbens to increase appetite.
What is the source of ADH (vasopressin)?
ADH is synthesized in the hypothalamus (supraoptic and paraventricular nuclei) and stored/secreted by the posterior pituitary.
What does ADH regulate and which receptors does it use?
ADH regulates serum osmolality via V2-receptors and blood pressure via V1-receptors.
What can cause nephrogenic DI?
Nephrogenic DI can be caused by a mutation in the V2-receptor.
What is the primary function of ADH?
The primary function of ADH is serum osmolality regulation.
What is the source of ADH (vasopressin)?
Synthesized in hypothalamus (supraoptic and paraventricular nuclei), stored/secreted by posterior pituitary.
What does ADH regulate and which receptors does it use?
Regulates serum osmolality (V2-receptors) and blood pressure (V1-receptors).
What can cause nephrogenic diabetes insipidus (DI)?
Mutation in V2-receptor.
What is the primary function of ADH?
Regulates serum osmolality (ADH ? serum osmolality, ? urine osmolality) via regulation of aquaporin channel insertion in principal cells of renal collecting duct.
How do ADH levels differ in central vs nephrogenic diabetes insipidus (DI)?
ADH level is decreased in central DI, normal or decreased in nephrogenic DI.
What is desmopressin used to treat?
Central diabetes insipidus and nocturnal enuresis.
What regulates ADH secretion?
Osmoreceptors in hypothalamus and hypovolemia.
What enhances the conversion of cholesterol into pregnenolone?
Steroidogenic acute regulatory protein (STAR) enhances this conversion by mediating cholesterol transport from outer to inner mitochondrial membrane.
What is synthesized in the zona glomerulosa?
Mineralocorticoids.
What is the first step in the mineralocorticoid synthesis pathway?
Cholesterol desmolase catalyzes the conversion of cholesterol to pregnenolone.
What regulates cholesterol desmolase activity?
ACTH enhances the activity of cholesterol desmolase.
What drug inhibits the conversion of cholesterol to pregnenolone?
Ketoconazole (azole antifungal, blocks several steps in steroidogenesis).
What is synthesized in the zona fasciculata?
Glucocorticoids.
What drug inhibits the conversion of 11-deoxycortisol to cortisol?
Metyrapone inhibits 11?-hydroxylase.
What drug inhibits the conversion of cortisol to cortisone?
Glycyrrhetinic acid (found in black licorice).
What is synthesized in the zona reticularis?
Androgens.
What is the conversion of androstenedione in peripheral tissue?
Androstenedione converts to estrone (aromatase) and testosterone converts to estradiol (aromatase) or dihydrotestosterone (DHT) (5? reductase).
What drugs inhibit the conversion of androstenedione to estrone and testosterone to estradiol?
Aromatase antagonists such as anastrozole and exemestane.
What drug inhibits the conversion of testosterone to DHT?
5? reductase antagonist: finasteride.
What regulates aldosterone synthase?
Angiotensin II (ATII) upregulates aldosterone synthase.
What characterizes all congenital adrenal enzyme deficiencies?
Skin hyperpigmentation (due to increased MSH production) and bilateral adrenal gland enlargement (due to increased ACTH stimulation).
What is the effect of 17?-hydroxylase deficiency on mineralocorticoids?
Mineralocorticoids: decreased.
What is the effect of 17?-hydroxylase deficiency on cortisol?
Cortisol: decreased.
What is the effect of 17?-hydroxylase deficiency on sex hormones?
Sex hormones: decreased.
What is the effect of 17?-hydroxylase deficiency on blood pressure?
Blood pressure: increased.
What is the effect of 17?-hydroxylase deficiency on potassium levels?
What is the lab finding for 17?-hydroxylase deficiency?
Labs: increased androstenedione.
What is the presentation of 17?-hydroxylase deficiency in XY individuals?
Ambiguous genitalia and undescended testes.
What is the presentation of 17?-hydroxylase deficiency in XX individuals?
Lacks secondary sexual development.
What is the most common steroidogenic enzyme deficiency?
Not specified in the provided text.
