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What are the 4 hormones excreted from the ovary?
- 1. Estrodiol
- 2. Progesterone
- 3. Testosterone
- 4. Inhibit
What are the 3 hormones excreted from the testicles?
- 1. Testosterone
- 2. Androgen binding protein
- 3. Inhibin
GnRH is affected by which 3 hormones NT and do they inhibit or stimulate?
- 1. Dopamine--> (-) inhibits
- 2. Endorphins--> (-) inhibits
- 3. NE--> (+) stimulates
Of the 2 estrogen receptors ER-a & ER-b, which is a negative feedback?
Negative feedback--> ER-a
Fast pulse of GnRH released from the hypothalamus produces FSH or LH? Slow pulses?
- Fast pulses--> LH
- Slow pulses--> FSH
Low levels of estrogen stimulate or inhibit FSH?
- Low levels E2--> stim FSH
- High levels E2--> inhibit FSH
Low levels of progesterone stim or inhibit FSH?
Low levels Pg--> STIM FSH
What are the 3 effects of FSH on the follicle?
- 1. Stimulate granulosa cells to release E2
- 2. Aromatizes androgens to E2
- 3. Induces LH receptors on theca cell
What is the effect of LH?
1. Stimulates ovulation (switches cells to Pg production)
What does the LH surge do?
- 1. Luteinizes theca & granulosa cells (produce Pg)
- 2. Inhibit further cell growth
- 3. Drives oocyte into 1st meiotic division
- 4. Weakens wall of follicle
What are 3 disruptions to the cycle?
- 1. Stress
- 2. Weight loss
- 3. Pituitary adenomas
What are the 3 types of estrogen and where are they excreted?
- 1. E2--> ovaries
- 2. E1--> fat
- 3. E3--> placenta
Where is a majority of estrogen excreted?
What are the adverse SE of synthetic E2 1st pass effect in liver?
- -Increased clotting factors
- -Increased plasma renin substrate
What is the MOA of synthetic estrogen?
- -Disassociates from SHBG--> binds to ERa or ERb--> changes conformation--> releases HSP
- -Binds to estrogen response elements--> often a promotor gene
Where is ERa mainly expressed? ERb?
- ERa--> uterus, liver, kidney, and heart
- ERb--> ovary, prostate, lung, GI, bladder, heme, CNS
Both--> mammary, epididymis, thyroid, adrenal, bone, some brain
What are 4 generalized effects of estrogen?
- 1. Female maturation
- 2. endometrial regulation
- 3. Metabolic/cardio effects
- 4. coagulation
- 5. Others: Pg receptor synthesis, libido, SNS well-being, fluid shifts (bloating)
What are the uses of Estrogen?
- 1. Primary hypogonadism
- 2. Postmenopausal HRT
- 3. Others: Hemorrage (ob)
- 4. Ovulation suppression
What are the benefits and risk of E2 only?
- B: ⇓ hot flashes, osteoporosis, Br Ca
- R: ⇑Blood clots, stroke, CAD
What are the risk/benefits of E2 + Pg?
- B: ⇓ Hot flashes, osteo, colorectal cancer
- R: ⇑ Blood clots, stroke, CAD, Br. Ca
What is the difference in risk fo E2 only and E+P?
E+P has increase risk for Breast Cancer
What is the difference in benefit between E2 only and E + Pg?
E+P has added benefit if decreased colorectal cancer risk
What are some random other uses of Estrogen?
- Breast cancer
- prostate cancer
- wound healing
- Growth in girls
- Trauma liver injury
Where is the primary source of progesterone synthesis?
- Ovary (CL)
- --> also in testis, adrenal gland, and placenta
How is progesterone excreted?
Renally (almost complete 1st pass in liver)
- -Ligand-receptor complex--> activate gene transcription
- -Depends on receptor coregulators
- -some splicing
T or F. Progestin has little impact on protein?
True--> favors fat deposition
What are the effects of progestin on carbs?
- -Increase basal insulin
- -Increase insulin response to glucose
- -Promote glycogen storage
- -promotes ketogenesis
T or F. Progestin competes w/ aldosterone & mineralocorticoid receptors.
True--> ⇓ NA reabsorption--> increase aldosterone secretion
T or F. Synthetic progestins don't alter respiratory function.
True--> natural do
What is the effect of progestin on the endometrium?
-maturation and secretion
What are the therapeutic uses of Pg?
- 1. hormone replacement
- 2. Contraception
- 3. Pregancy/infertility
What are 3 contraindication of Pg?
- 1. Increase BP in women
- 2. Androgenic synthetic Pg--> decrease HDL
- 3. Postmenopause--> Increase Br Ca risk
Inhibit increases or decreases FSH secretion?
Activin increases or decreases FSH secretion?
What is the action of Activin with FSH? Activin with LH?
Activin w/ FSH--> stimulates granulosa cells to synthesize Pg & aromotase
-Activin w/ LH--> ⇓ Pg, but markedly increases aromatase
- -Synthesized by luteinized granulosa cells
- -Found in ovary, placenta, uterus, & blood
- -Insulin-like--> increase glycogen, H20 reuptake in myometrium, decrease uterine contractility
- -Clinical trials--> dysmenorrhea, premature labor
What are the 2 Progestin families?
Selective inhibition of pituitary
T or F. Progestin only may NOT inhibit ovulation.
What are the 3 physical effects of combined E+P?
- 1. Mimics pregnancy--> inhibits ovulation
- 2. Alters cervical mucous
- 3. Alters tubal motility
T or F. Progestin only alters tubal motility?
False (E+P does)
What is the effect of progesterone on the uterus?
Atrophic endometrium (unless E added)
What is the effect of progestin on the binding globulins in the body?
Increased! (TBG, CBG, SHBG)
What are the effect of progestin on lipids?
-Increase TG and HDL
T or F. Pg causes increased insulin resistance.
True (and decreased carb absorbed from gut)
What is the effect of progestin on the RAAS?
-Increase plasma renin--> increase aldosterone
What is the effect of Pg on the cardio system?
-Increased BP, HR (may be profound in some women)
What are "mild" adverse side effects of Pg?
- -Nausea, mastalgia, BTB, edema (E effects)
- -H/A, worsening migraines
What are some "moderate" effects of Pg (+E)?
- -BTB only in Pg
- -Wg gain (depo)
- -pigmentation (cholasma, linea nigra)
- -Bacturia (ureteral dilation)
Severe Adverse SE of Pg (+E).
- -Thromboembolism (VTE, MI, CVA)
- -GI: jaundice, gallbladder
- -Cancer (reduced ovarian/endo)
Contradindations for OCPs?
- -Thrombophlebitis, coagulopathy
- -Cardio issues
- -Unexplained vag bleeding
- -cancer (e-dependent)
- -Avoid: liver dx, asthma, eczema, migraine, DM, HTN, optic/retrobulbar neuritis, seizure d/o
What drug is a competitive partial agonist inhibitor working at the Estrogen receptor?
Which drug is a partial E2 agonist?
Which is the effect of clomid?
inhibits negative feedback--> increasing FSH (good to improve ovulation)
What are the adverse effects of clomid?
- -Hot flashes
- -H/A, constipation, allergic skin rxn
- -Increase endometrial implant growth
- -N/V, depression, fatigue, breast tenderness, wt gain
- -Mult gestation
What is the MOA of Mifepristone?
Binds tightly to Pg receptor (inhibiting Pg activity)
What are the uses of Mifepristone?
- -Misoprostol--> abortifactant
- -Experimental--> endometriosis, cushings, Br Ca
What are the adverse effects of Mifepristone (Pg inhibitor)?
- -V/D, abdominal/pelvic pain
- -heavy bleeding
-Binds to androgens, progesterone & glucocorticoid receptors
What are the effects of Danazol?
- -Suppress ovarian function (inhibit LH surge)
- -Inhibit gonadal function
What is Danazol used for?
- -Breast pain, hemophilia, Xmas Dx, ITP, angioneurotic edema
What are adverse effects of Danazol?
1. Wt gain, edema, decrease breast size, acne, increased hair growth, deepening voice, H/A, hot flashes, libido changes, muscle cramps, adrenal suppression
What is the effect of Aromatase Inhibitors? When is it used?
- -Inhibits estrogen synthesis
- -Uses in Breast Cancer
What weak estrogens are produced in the testis?
- 1. Androstenedione
- 2. DHEA
**majority secreted from adrenal glands
Discuss Androstenedione, DHEA, DHEAS
- -Produced in adrenal gland
- -Important for "well-being"
- -⇑ SHBG binding w/ ⇑ E, thyroid hormone, cirrhosis
- -⇓ SHBG binding w/ ⇑ androgen, GH, obesity
- -33% bound to albumin
What substance converts Androgen to dihydrotestosterone?
What substance converts Androgens to Estrodiol?
Aromatase (fat, liver, hypothalamus regulation)
What are 5 effects of androgens?
- 1. Growth (ht, wt, lean m. mass)
- 2. Genital (growth, prostate, seminal vesicle)
- 3. Skin (puberty hair, sebaceous glands, darkening of skin
- 4. Larynx & vocal cords thicken
- 5. Sexual function
What are the uses of synthetic androgens?
- 1. anabolic effects
- 2. hormone replacement
When is androgen replacement used?
- -Hypopituitarism (gradually increase dose for growth spurt & 2nd sexual characteristics
- **only use GnRH if spermatogensis is goal
Adverse effects of Androgens?
- -Women: masculinization, progestational activity, endometrial bleeding, atherosclerotic dx
- -Infants--> over/under masculinzation of genitalia
- -Men--> acne, sleep apnea, erythrocytosis, gynecomastia, azoospermia
- -Everyone--> Na+ retention/edema, hepatic dysfunction
What are cautions/contraindications of Androgen replacement?
- -NOT in pregnancy
- -Prostate/Breast Ca
- -young children
- -Renal/cardiac disease
- -Hepatocellular ca
When is androgen suppression use?
- -Advanced Prostate cancer
- -Androgen overproduction (use steriod synthesis inhibitor like ketoconazole)
What are 3 ways to suppress androgen and a drug example of each?
- 1. Steroid synthesis inhibitors (ketoconazole)
- 2. Halt steroid conversion (Finasteride)
- 3. Receptor inhibitors (Flutamide & spironolactone)