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Block 14 module 7 > Natural and hormonal family planning > Flashcards

Natural and hormonal family planning Flashcards

(61 cards)

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1
Q

Most widely used method of reversible contraception

A

oral steroid contraceptives

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2
Q

EE with an extra methyl group. It
requires bioactivation in the liver, where the
methyl group is cleaved, releasing the active
agent, EE

A

Mestranol

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3
Q

Norethindrone and its derivatives

A

Norethindrone acetate

Ethinyldiol diacetate

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4
Q

derivative of spironolactone
diuretic; progesterone agonist but a
mineralocorticoid & androgen antagonist

A

Drospirenone

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5
Q

used as transdermal patch
and more potent than norgestimate (parent
compound)

A

Norlgestromin

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6
Q

components of first gen oral steroid contraceptive

A

50 ug of ethinyl estradiol or
Mestranol or a higher form of progestin; Contains
very high levels of estrogen and progestin

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7
Q

components of 2nd gen oral steroid contraceptive

A

decreased the amount of
estradiol and combined other forms of progestin
20 to 35 ug ethinyl estradiol; progestin except 3
newest levonorgestrel derivatives (desogestrel,
gestodene, norgestimate)

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8
Q

components of third gen oral steroid contraceptive

A

20 to 35 ug ethinyl estradiol plus
either Norgestimate, Desogestrel or Gestodene; may
contain drosperinone or cyproterone acetate

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9
Q

estrogen has negative feedback on

A

FSH

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10
Q

Progestin has neg feedback on

A

LH

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11
Q

how does oral steroid contraceptives inhibit ovulation by inhibiting the midcycle gonadotropin surge

A

it interferes with the GnRH release from the hypothalamus

and it has an inhbitor y effect on gonadotropin producing cells of the pituitary gland

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12
Q

synthetic compounds that mimic effect of natural pregesterone but differ structurally

A

gonane group

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13
Q

this require bioactivation, converted to etono-gestrel

A

desogestrel

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14
Q

how does the progetins differ from one another

A

affinities for estrogen, androgen and progesterone receptors
their ability to inhibit ovulation
ability to substitute for progesterone and to antagonize estrogen

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15
Q

aldosterone derivative

A

cyproterone acetate

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16
Q

spironolactone derivative

A

drospirenone

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17
Q

progesterone agonist but a mineralocorticoid and androgen antagonist

A

drospirenone

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18
Q

alternative to cyproterone acetate in PCOS

A

drospirenone

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19
Q

most widely used and more effective formulation of ocp

A

multiphasic progestins

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20
Q

what is the rationale for use of multiphasic formulations

A

they lower the total dose of steroid w/o increasing the incidence of unscheduled uterine bleeding

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21
Q

bleeding that occurs during the time that active pills are ingested

A

unscheduled, intracyclic or breakthrough bleeding

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22
Q

Minipill is a form of progestin that contains

A

progesterone only, no estrogen

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23
Q

MOA of OCP

A
  1. it inhibits ovulation by inhibiting the midcycle gonadotropin surge
  2. renders the endometrium unfavorable for implantation
  3. affects motility of the uterus and oviduct
  4. alters ovarian responsiveness to gonadotropin
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24
Q

why is estrogen usually taken with progestin

A

estrogen has a proliferative effect on the endometrium while progestin opposes it

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25
differentiate withdrawal bleeding from breakthrough bleeding
withdrawal B occurs at hormone free period while Breakthrough B occurs during the time the woman is taking the active pill or a hormone-containing pill
26
noncontraceptive benefits of OCP
1. reduction of endometrial and ovarian CA 2. Fewel menstrual d/o, complaints of dysme disappear 3. Less symptoms of PMS 4. Less incidence of IDA due to less blood loss
27
most common SE of OCP
nausea (effect of estrogen on CNS)
28
SE of OCP
``` Nausea Breast tenderness Fluid retention Melasma Mood changes Wt gain Acne Nervousness Failure of withdrawal bleeding ```
29
newer gen of OCP poses a higher risk for
thrombosis
30
how does estrogen increase risk for thrombosis
it increases the production of several globulins (clotting factors) by the liver - thrombosis
31
how can ocp increase BP
it can lead to and increase in the conversion of angiotensinogen to angiotensin
32
the higher the dose of progestin, the greater the impairment of
glucose metabolism that's why it's not given to px with uncontrolled DM
33
if px has DM what gen of progestin will you give
it is best to avoid progestins n px with DM
34
effects of estrogen in terms of lipid metabolism
inc HDL, tri G and total chol; dec LDL
35
effects of progestin in terms of lipid metabolism
dec HDL, triG and total chol; inc LDL
36
effects of progestin on coagulation parameters
No effect
37
effects of estrogen on coagulation parameters
inc synthesis of several coag factors including fibrinogen (px w/ history of VTE should not be given OCP_
38
most common cardiovascular effects of OCP
arterial thrombosis
39
nicotine and estrogen would increase the risk for
stroke
40
if the px stopped taking OCP how long before she can get pregnant again
if they ovulated regularly they can do so w/in 3 mo
41
OCP has a protective effect on the dev of what CA
endometrial CA and Ovarian CA
42
absolute contraindications for OCP
``` VTE systemic dse affecting the vascular sys (SLE) Smokers .35 uncontrolled HPN elevated triG DM w/ retinopathy/nephropathy/neuropathy undiagnosed uterine bleeding known or suspected brest and endomet CA functional HD active liver dse migraine, headache w/ focal symptoms ```
43
it is recommended to start taking OCP how long after menses
within 7 days following the onset of menses
44
px delivered 10 wks fetus, when can she take OCP?
she can start immediately (<12 wks)
45
why combined OCP is not a good choice in lactating moms
it reduces quantity and quality of breastmik
46
if the woman is fully breastfeeding how soon can you give OCP
after 6 mo
47
provides sustained release of the steroids and result in a relatively constant sserum lvls that are less than peak lvls seen in oC
contraceptive patch
48
example of contraceptive patch
ethinyl estradiol + norelgestromin
49
example of contraceptive vaginal ring
EE + etonorgestrel
50
examples of injectable suspension
DMPA (depomedroxyprogesterone acetate) Norethindrone ethanate Progestin estrogen injectable formulation
51
MOA of DMPA
inhibition of ovulation produces thin endometrium makes cervical mucus thick and viscous
52
examples of subdermal implants
implanon | norplant
53
subermal implant that contains single rod; 68mg etonogestrel
implanon
54
subbdermal implant that contains 36mg levonorgestrel
norplant
55
MOA of epostane as emergency pill
it blocks production of progesterone
56
most effective emergency contraceptionif treatment is begun 72 hrs after an isolated midcycle act of coitus
steroids
57
examples of emergency contraceptive pills
``` EE+norgestrel Levonorgestrel (plan B) Danazol Mifepristone Epostane ```
58
char of cervical mucus after menses
opaque thick sticky
59
char of cervical mucus close to ovulaion
slippery, lubricative, transparent
60
char of cervical mucus after ovulation
dry mucus
61
physiology of lactational amenorrhea
suckling of infant elevates prolactin which in turn reduces GnRH release= Reducing LH release = inhibiting follicular maturation

Block 14 module 7 (6 decks)

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