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McCune-Albright Syndrome

clinical: GNAS mut on 20q -> mut Gsalpha + oths -> var hyperfx endocrine glands, cafe-au-lait spots, polyostotic fibrous dysplasia

humoral

hormone release: []ecf

neural

hormone release: nn innerv gland

hormonal

hormone release: release of oth hormones

GH (growth hormone)

hormone: stim by GHRH, inhib by SS (both from somatotrophs of HypThal), JAK2 -> STAT -> Tyr Kinase, involves inc IGFs (somatomedins) -> inc mm AA uptake, lipolysis, [Glc]bl

IGFs (insulin-like growth factors)

hormone: works w/ GH to inc cartilage, bone growth, prot synth + cell growth, can be used to indirectly meas GH levels

Prolactin

hormone: INHIB by dopa from HypThal (poss stim by E2 -> TRH + PRF) -> made by lacto(mammo)trophs -> JAK2 -> STAT -> TyrKinase -> dev breasts + make milk

Oxytocin

hormone: nursing or cervical P -> hypthal -> pos. pit -> inc Ca2+ -> Gq -> smooth mm contract

parafollicular cells

thyroid cells: secrete calcitonin

follicular cells

thryoid cells: secrete T3 (tri-iodothyronine) and T4 (thyroxine)

TRH (thyroid releasing hormone)

hormone: PVN of Hypthal synth -> Ant. Pit. Gq on Thyrotrophes -> inc TSH, pulsatile circadian rel, neg feedback, t1/2 = 5min

TPO (ThyroPerOxidase)

enzyme: conv Iodine -> Iodide to combo w/ TG (ThyroGlobulin)

NIS

pumps iodine in to cell against [] grad. by coupling w/ Na+

T3 (triiodothyronine)

hormone: the more active thyroid hormone, but makes up 10% of ecf [], can be made from oth thyroid hormone via deiodinase

Graves Disease

clinical: TSH-R ABs -> high T3, T4 but low TSH (vs. thyrotrophoma = high T3, T4 and high TSH)

Aldosterone

hormone: stim by AII or K+ (min ACTH from corticotrophs) -> Z. glomerulosa -> inc Na+ reabs + K+ secr in DCT + CD Principal cells, 50% bound to prots, 15 min t1/2

CRH

hormone: synth in Ant PVN, stored imn median eminence -> corticotrophs -> Gs -> synth POMC, pulsatile diurnal rel

ACTH

hormone: synth from POMC -> Melaocortin-2 Gs Rs on adrenal gland -> + P prots and activate StAR (but only in Z. fasiculata + reticularis)

StAR (Sterioid Acute Regulatory protein)

mitoch memb Chol chan so Chol can be converted to Pregnenolone in mitoch, activated by ACTH in Z. fasiculata + reticularis, and by AII or K+ in Z. glomerulosa

CYP11A

enzyme: converts Chol -> Pregnenolone, aka Chol Side-Chain Cleavage Enzyme)

CYP17A (17-alpha-hydroxylase)

enzyme: converts Pregnenolone to DHEA and Progesterone to Androstenedione

3-B-HSD II (3-beta-Hydroxysteroid deHydrogenase)

enzyme: converts Pregnenolone to Progesterone and 17-alpha-pregnenolone to 17-alpha-progeterone

CYP21A2 (21-hydroxylase)

enzyme: converts Progesterone to to 11-Deoxycorticosterone and 17a-OH Progesterone to 11-Deoxycortisol, defic = dec Ald + cortisol -> Virilizing Congenital Hyperplasia

CYP11B1 (11-beta-hydroxylase)

enzyme: converts 11-Deoxycorticosterone to Corticosterone and 11-Deoxycortisol to Cortisol

CYP11B2 (Aldosterone synthase)

enzyme: converts Corticosterone to Aldossterone

HSD11B

enzyme: converts Cortisol to Cortisone (inactive metabolite) in kidneys, inhib by licorice => can result in mineralocorticoid excess

Conn Syndrome

clinical: Z. glomerulosa tumor (low renin)or inc renin secrete (HIGH renin)-> inc Ald -> hypertension, hypervolemia, hypokalemia, slight hypernatremia

Addison's disease

clinical|: autoimmune adrenal or granuloma-> dec adrenal hormones -> polyuria, dehydration, hypotension, hyperkalemia, hyponatremia, weak, stressed, anorexia, dark skin

mitochondria

location of CYP11A (Chol-Side-chain Cleavage Enzyme) + 11-beta-HSD

smooth ER (SER)

location of steroidogensis enzymes that are NOT CYP11A (Chol-Side-chain Cleavage Enzyme) + 11-beta-HSD

glucocorticoids

hormone: class of hormones from Z. fasiculata that includes Cortisol, norm bound to plasma prots like CBG (Cortisol Binding Globulin = Transcortin), 8% bound to albumin, 5% free -> conj by liver -> excr by kidney

androgens

hormone: sex hormones from Z. reticularis, norm bound to albumin -> degraded or metabolized in to more active products, NO neg feedback on ACTH or CRH => reg by glucocorticoids

cortisol

hormone: primary glucocorticoid, inc Glc production by liver (hypOglycemia) or inc Glc storage (hypERglycemia), inc proteolysis, lipolysis, [Glc]bl (by opposing Insulin on most tissues), stim surfactant, lactation, inc contractility, inhib immune + inflamm response (inhib PLA-2), inc appeptite, neg Ca2+ bal

Cushing's Syndrome

clincal: var probs assoc w/ inc Cortisol (ACTH-indy), could be due to overuse of corticosteroids or small oat cell carcinoma

Cushing's Disease

clinical: Ant Pit Tumor -> hyper ACTH -> hyper cortisol (ACTH-dep)

Acute Adrenal Insufficiency

clinical: sudden withdrawal corticosteroids -> hypovolemic shock, postural hypO tension

VMAT (vesicular monoamine transporter)

transports dopa and Epi in to secretory vesicles in chromaffin cells

uptake-1

catech breakdown: in synaptic clefts/nerve terms -> MAO -> VMAT

uptake-2

catech breakdown: in target cells -> MAO + COMT

pheochromocytoma

clinical: chromaffin tumor -> inc NE rel (+ Epi, Dopa) -> hypertension, headache, chest pains, anxiety, perspiration, high Bp, hyperglycemia, glucosuria

C-peptide

component of endogenous insulin that is fully excr => good marker for insulin

GLUT2

insulin-independent Glc transporter

sulfonureas

drug: DM2 pt -> block K-ATP chan -> inc intracell K+ -> depol -> Ca2+ influx -> make insulin

GLUT4

insulin-sensitive (dep) Glc transporter

amino acids

major stimulus for alpha -> glucagon release

muscle

organ/system that glucagon has NO effect on but insulin does

osteoblasts

increase bone production (remove free ionized Ca2+ from bl)

osteoclasts

inc Ca2+ resorption in bone

osteocytes

involved in Ca2+ turnover in bone (bring Ca2+ back to bl)

chief cells

cells that synth PTH

PTH (parathyroid hormone)

hormone: secreted by chief cells, stored in secr granules in response to dec ionized Ca2 via weird reverse Gq mech (since it's not INC but DEC Ca2+ that stim rel) -> Gaq + Gas R on osteoblast -> inc M-CSF, RANK, IL-6 (stim osteoclasts) -> inc Ca2+ resorption, also helps resorb the 10% of Ca2+ that reaches the DCT, inc 1-a-hydroxylase (calcitriol synth)

phosphate

ion: PTH -> released from bone and dec resorb from kidneys => excr VS VitD -> inc GI + kidney absorption -> inc

Calcitriol (Vitamin D)

vitamin: 7-dehydroCho in skin -> Cholecalciferol from diet --25-hydroxylase (liver)--> 25-OH-Cholecalciferol --1-hydroxylase--> 1,25-dihydrocholecalciferol, stim by PTH (low ionized Ca2+) in PCT of kidney -> inc Ca2+ + PO4- absorb in gut, req for norm bone form, inc Ca2+ resorb in DCT

LH

hormone: stim by high freq GnRH rel, Gs on Leydigs or Theca cells-> conv Pregnenolone -> E2

GNRH (GRH)

hormone: 10aa peptide synth in arcuate nu -> stored in vesicles -> portal -> ant pit gonadotrophs -> Gq, pulsatile release, 2-4min t1/2

FSH

hormone: stim by low freq GnRH -> Gs on Sertolis or Granulosa cells-> inc Inhibin, Aromatase, ABP, GFs, activin, follistatin

ABP (androgen binding protein)

stim by FSH -> maint high androgen levels in tubles, carries testoterone to epididymis

epidymus

where 10% of the ejaculate (just sperm) is stored

ductus deferens

where 60% of the ejaculate is formed: Frc, PGs (inc contract smooth mm), CFs

prostate gland

where 30% of ejaculate is formed, + alkaline (neut acidic vagina), semen clotters (keep semen in vagina), unclotters (ex: fibrinolysin to swim to ova)

bulbourethral gland

secretes mucus to aid in lubrication during sex

theca cells

have LH Rs (Gas)-> Chol --CYP11A--> Progesterone --CYP17--> androstenedione which can be taken up by Granulosa cells to be converted to E2

Granulosa cells

have FSH Rs (Gas) -> converte androstenedione from theca cells to E2 (aromatase), also have LH Rs during Luteal phase => can directly make their own Progesterone, secrete Inhibin,

Progesterone

hormone: made from Chol via CYP11A, PRE-ovul = LH surge, inhib E2, OVUL = collagenase + PGs -> rupture, uterine excitability, alveoli cells, endometrium secr, PREG = uterus endometrial, maint preg, cervical mucus plug, breast dev

E2 (estradiol, estrogen)

hormone: product of T -> aromatase -> PUBERTY = inc reprod organs, breast dev, epiphyseal fusion, change uterine cells, protect vaginal epith, POST-puberty = inc cil cells in oviduct, in protsynth, subcut. fat deposit, ovarian fx, PREG = prep for parturition, dev breast, inhib make milk

hCG (human Chorionic Gonadotropin)

hormone: synth by embryo before implantation and syncytiotrophoblasts after implantation, sim to LH but perserves Corpus Luteum (=> inc E2, P)

hCS (human Chorionic Somatomammotropin, hPL)

hormone: aka human Placental Lactogen, HCS1,2 Rs, sim to GH, inc breast, dec insulin sensitivity, inc Glc for fetus

DHEA-S

hormone: used by placenta to produce estrogens, synth mostly in fetal cortex

pre-eclampsia

clinical: hypertensive pregnancy after 20th week -> headache, confusion, ab pain, fetal growth retardation

oxytocin

hormone: 9AA stored in pos pit -> imp for parturition and lactation, Gq -> maint contract, or post-birth -> suckling mechRs in nipple -> hypthal -> PosPit. -> rel -> milk let-down reflex

dystocia

clinical: abnorm or diff labor, norm due to cephalopelvic disprorportion or labor anesth

Prolactin

hormone: stim by suckling mechanoRs on nipple -> hyThal -> inc PRF/dec dopa -> Ant Pit -> secrete, dec GnRH (=> ammenorrhea, dec E2 + Prog which inhib lactogenesis), lactogenesis

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