Hormones Pharm part I, Linger Flashcards

1
Q

What are the estrogens we have for drugs

A

conjugated E- premarin
estradiol valerate
ethinyl estradiol
mestranol

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2
Q

what are the progestin drgus

A

desogestrel(inactive etonogestrel(active)
drospinenone
medroxyprogresterone, norethindrone, norgestimate
norgestrel (L-norgestrel, levonorgestrel)

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3
Q

what are the E and P inhibitors

A

Mifepristone

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4
Q

what are the selective E R modulators

A

raloxifene
tamoxifen
toremifene

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5
Q

what are the selective E R downregulators

A

clomiphene

fulvestrant

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6
Q

what are the aromatase inhibitors

A

anastrazole
exemestane
letrozole

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7
Q

how do synthetic E work

A

bind to the SHBG and lower affinity to albumin so there is more unfound E around

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8
Q

why are vaginal and transdermal modes for effective for giving E

A

because avoid the first pass metabolism of the liver

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9
Q

MOA E

A

binds ER and activates gene transcription

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10
Q

how do E Receptros work

A

homodimerize and bind promoter regions or bind to other transcription factors which bind to the promoter regions

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11
Q

endometrial effects of E

A

bleeding and shedding

continuous exposure will lead to hyperplasia of the endometrium leading to abnormal bleeding patterns

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12
Q

metabolic effects of E

A

decrease rate of bone resoprtion because promotes apoptosis of osteoclasts
stimulate adipose tissude production of letpin
stimulates increase production of the cortisol globulin, thyroxine binding globulin, sex hormone binding protein
increase HDL and TG, reduce LDL

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13
Q

vascular effects of E

A

enhance coagulability of blood
increases factors II CII IX and X, decrease antithrombin III
icnrease plasminogen

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14
Q

When do we use E for Tx

A

primary hypogonadism
postmenopausal hormone replacement
suppress ovulation in patients with intractable dysmenorrhea or suppress ovarian function in cases of hirsutism and excessive ovary androgen secretion

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15
Q

E and P replacement decreases risk of what

A

osteoporotic fractures of hip vertebrae, and wrist

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16
Q

adverse effects estrogens

A

uterine bleeding, breast and endometrial cancer

nausea, breast tenderness, hyperpigmentation, increased migraine frequency, cholestasis, gallbladder disease and HTN

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17
Q

how is endometrial hyperplasia from administration of E prevented

A

give progestin too

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18
Q

does adding P to E Tx prevent breast cancer

A

not, may actually increase risk of breast cancer

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19
Q

Contraindications to E

A

patients with E dependent neoplasms (endometrial carcinoma and breast cancer)
patients with unDx genital bleeding, liver disease, history of thromboembolic disorder and heavy smokers

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20
Q

what sideeffects are decreased in transdermal preparations of e

A

does not increase renin levels, corticosteroid binding substrate and thyroxine binding substrate

21
Q

Where is P naturally made

A

in ovary (corpus luteum), testis and adrenal Cx

22
Q

how are pharmacokinetics of P different than E

A

rapid regardless of PO or IM

23
Q

MOA progesterone

A

activates gene transcription via nuclear R

24
Q

isoforms of Progesterone R

A

A and B

25
Q

physiologic effects of progesterone

A
  • dec frequency of GnRH pulses
  • onset menstruation with its abrupt decline
  • maintains pregnancy and mammary gland development
  • stimulates lipoprotein lipase and favors fat deposition
  • increases basal insulin levels and insulin response to glucose
  • promotes glycogen storage and ketogenesis
  • can compete for mineralocorticoid R (dec in Na reabsorption)
26
Q

clincal uses of progestins

A

HRT and hormone contraception

long term ovarian suppression

27
Q

how are progestins used for Dx testing

A

can be used to test E secretion

causes bleeding after 5-7 days progesterone if endometrium has been stimulated by E

28
Q

dosage and drug used for long term ovarian suppression

A

150mg medroxyprogesterone acetate IM every 90 days

29
Q

adverse effects of progestins

A

breakthrough bleeding
increase BP
reduce HDL in women

30
Q

2 types of oral contraception preparations

A

combinations E and P or just P without E

31
Q

what is monophaseic? bi? tri?

A

mono is constant dose of both E and P in pills
biphasic changes once
triphasic changes twice

32
Q

what hormones are in the transdermal preparation of contraception

A

ethinyl estradiol and norelgestromin

33
Q

adverse effects with ransdermal patch

A

breast discomfort, dysmenorrhea, nausea, vomiting and skin irritation

34
Q

What drugs are in the NuvaRing

A

ethinyl estradiol and etonogestrel

35
Q

adverse effects for injectable preparations for contraceptin

A

unpredictable spotting or bleeding
return of fertility can take 18 mo after last injection
increased risk atherosclerosis

36
Q

What drug is in IUD and how long is it effective

A

levonorgestrel

effective for 5 years

37
Q

with IUD at increased risk for

A

ovarian cyst

38
Q

what drug is in the implantable contraceptions

A

eronogestrel
good for 3 years
bleeding abnormalities are common

39
Q

what drugs are in the day after pills

A

E alone
P alone
E and P
P R modulators

40
Q

adverse effects of day after pills

A

nausea, vomiting, HA, dizziness, breast tenderness, abdominal and leg cramps

41
Q

what is in plan B

A

levonorgestrel

42
Q

how does plan B work

A

not sure

cannot reverse pregnancy that has already occurred (post implantation)

43
Q

What is Ella and how does it work

A

Ulipristal acetate, partial agonist at P R, inhibits ovulation when taken up to 5 days after intercourse, may block implantation

44
Q

adverse effects Ella

A

HA and abdominal pain

45
Q

main MOA E and P contraceptive pills

A

selective inhibition of pituitary function (negative feedback)
change cervical mucus, uterine endometrium and motility of uterine tubes

46
Q

effects of E and P on ovary

A

depress ovarian function

47
Q

effects oe E and P on uterus

A

prolonged use may cause hypertrophy of cervix and polyp formationl
glandular atropy and decreased bleeding are common depending on preparation

48
Q

E and P contraception effects on breast

A

stimulate enlargement and suppress lactation

49
Q

other effects of E and P contraception

A

mood changes
increased urinary exretion of free cortisol, increased renin, increased aldosterone
increased coagulability of blood
increase certain lipids