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Pharmacology > Gonadal Hormones and Inhibitors > Flashcards

Gonadal Hormones and Inhibitors Flashcards

1
Q

what happens when there is release of CRH

A
  • anterior pituitary releases ACTH, MSH, beta-endorphine
  • which cause a release of mineralcorticoids, glucocorticoids, and sex hormones

basically ACTH causes release of hormones from adrenal gland

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2
Q

what happens with increased dopamine

A

increased dopamine –> decreased prolactin –> increased GnRH –> increased spermatogenesis and ovulation

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3
Q

stimulus that causes an increase in GHRH

A
  • increased exercise and sleep

- decreased somatostatin and glucose

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4
Q

what is general mechanism of gonadal hormones - estrogen, progesterone, and androgens

A
  • they bind to their cytosolic receptor
  • the hormone-receptor complex (HRC) then travels into the nucleus
  • in nucleus, it is activated –> transcription of the steroid hormone regulated genes
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5
Q

what occurs in 17 alpha hydroxylase deficiency and symptoms it leads to

A

(17 years olds are salty they can’t have sex)

  • increase in aldosterone –> high BP and low K+
  • decrease in androgens and cortisol –> cryptochordism and indistinct genitalia in males while females lack secondary sexual characteristics
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6
Q

how do you treat males and females with 17 alpha hydroxylase deficiency

A

males: anti hypertensives, androgens, and glucocorticoids
females: anti hypertensives, estrogen

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7
Q

what occurs in 21 hydroxylase deficiency and what symptoms it leads to

A

(21 year olds can only have sex)

  • increase in androgens –> over masculinization and pseudo-hermaphroditism in females
  • decrease in cortisol and aldosterone –> low BP, high K, high renin activity, and volume depletion
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8
Q

how do you treat 21 hydroxylase deficiency

A

fluids and salt repletion and give cortisol to decrease ACTH

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9
Q

what occurs in 11 beta hydroxylase deficiency and what symptoms manifest

A

(11 beta is similar to 21 alpha)

  • increase in androgens –> over masculinazation
  • decrease in cortisol and aldosterone but increase in 11-deoxycorticosterone –> high BP because of the 11-deoxycorticosterone (how it differs from 21 hydroxylase deficiency)
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10
Q

how do you treat 11 beta hydroxylase deficiency

A

anti hypertensives and estrogen

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11
Q

what are the main estrogen synthesized within the body

A

estrone
estradiol (not seen after menopause)
estriol (seen in pregnancy)

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12
Q

what are the estrogen that can administered

A

CEMD

Conjugated estrogen
Ethinyl estradiol
Mestranol
Diethylstilbestrol

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13
Q

what is mestranol and its importance

A

prodrug converted –> ethinyl estradiol (seen in some contraceptives) –> increases bioavailability and half life, decreases FSH and LH via feedback

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14
Q

what metabolizes estrogen and the importance

A

CYP450 metabolizes estrogen –> if given an inducer, it can decrease the effect of contraceptives since estrogen seen in contraceptives

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15
Q

clinical uses of estrogen

A
  • long acting ones used in female hypogonadism
  • oral contraceptives together with progestins
  • postmenopausal HRT –> decrease hot flashes, prevent bone loss and fracture, decrease urogenital atrophy
  • dysmenorrhea, uterine bleeding, prostate cancer, and acne
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16
Q

adverse effects of estrogen

A
  • thromboembolism
  • breast cancer
  • endometrial hyperplasia and cancer (unless progestins added as well)
17
Q

adverse effect seen using estrogen diethylstilbestrol during pregnancy

A

if pregnant with female child –> infertility and vaginal cancer

18
Q

contraindications of estrogens

A
  • Thromboembolism
  • Breast and Endometrial cancer
  • Pregnancy
  • Liver Disease
19
Q

what are the SERMs (selective estrogen receptor modulator) and mechanism

A

RoTTC

Raloxifene
Tamoxifen
Toremifene
Clomiphene

they exhibit agonist behavior in some tissues and antagonist in others

20
Q

mechanism of tamoxifen and what it is used for

A
  • estrogen receptor antagonist in breast and agonist in bone and endometrium
  • used to treat breast cancer or for prophylaxis in high risk patients
21
Q

adverse effects of tamoxifen

A
  • risk of endometrial cancer
  • hot flashes (antagonist)
  • thrombosis (agonist)
22
Q

mechanism and uses of Toremifene and Raloxifene

A

-Toremifene: treatment and prophylaxis of breast cancer

  • Raloxifene: estrogen antagonist in breast and agonist in bone and no effect in endometrium
  • prophylaxis against breast cancer
  • prevention of post menopausal osteoporosis
23
Q

estrogen antagonist in all tissue and its use

A

fulvestrant: treatment of breast cancer in tamoxifen resistant patients

24
Q

adverse effect of fulvestrant

A

hot flushes, pain at injection site, headache

25
Q

what are the aromatase inhibitors and their exact mechanism

A

inhibits conversion of androgens to estrogen

Anastrozole - reversible
Letrozole - reversible
Exemestane - irreversible aromatase inhibitor

26
Q

use of aromatase inhibitors (name them) and their adverse effects

A

anastrozole, letrozole, exemestane

  • used in treatment of estrogen dependent breast cancer
  • AE: hot flushes, decreased bone mineral density
27
Q

mechanism and use of clomiphene

A
  • fertility drug used in tx of anovulatory infertility
  • estrogen antagonist in hypothalamus and anterior pituitary –> prevents feedback inhibition of GnRH release by hypothalamus –> continued release of GnRH from hypothalamus –> increased LH and FSH from pituitary –> ovulation
28
Q

adverse effect of Clomiphene

A
  • Ovarian hyper stimulation leading to enlargement of ovary

- Multiple pregnancy

29
Q

what are the progestins

A

PMNNNDD

Progesterone
Medroxyprogesterone
Norgestrel
Norethindrone
Norgestimate
Desogestrel
Drospirenone
30
Q

what is the anti progestin

A

Mifepristone

31
Q

what are the newer progestins that lack androgenic and antiestrogenic effects

A

MNNND

Medroxyprogesterone
Norgestrel
Norethindrone
Norgestimate
Desogestrel
32
Q

mechanism of drospirenone

A

spironolactone derivative used as an oral contraceptive and antagonizes aldosterone effect –> used in females for acne

33
Q

AE for long term use of progestins

A

HAD WAGE

  • HDL high, low LDL, and hypertension
  • Androgenic - hirsutism and acne
  • Depression
  • Weight gain
  • Anti estrogenic - blocks lipid change
  • Glucose intolerance
  • Edema and acne
34
Q

mechanism of mifeprostone

A

competitive inhibitor of progesterone AND glucocorticoid receptor

35
Q

use of mifeprostone

A
  • morning after drug abortifacient

- with prostaglandins, increases myometrial contraction

36
Q

AE of mifeprostone

A

Excessive bleeding

GI effects: anorexia, abdominal pain etc

Pharmacology (79 decks)

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