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

Natural and hormonal family planning Flashcards

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
Q

differentiate withdrawal bleeding from breakthrough bleeding

A

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
Q

noncontraceptive benefits of OCP

A
  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
Q

most common SE of OCP

A

nausea (effect of estrogen on CNS)

28
Q

SE of OCP

A 
Nausea
Breast tenderness
Fluid retention
Melasma
Mood changes
Wt gain
Acne
Nervousness
Failure of withdrawal bleeding
29
Q

newer gen of OCP poses a higher risk for

A

thrombosis

30
Q

how does estrogen increase risk for thrombosis

A

it increases the production of several globulins (clotting factors) by the liver - thrombosis

31
Q

how can ocp increase BP

A

it can lead to and increase in the conversion of angiotensinogen to angiotensin

32
Q

the higher the dose of progestin, the greater the impairment of

A

glucose metabolism that’s why it’s not given to px with uncontrolled DM

33
Q

if px has DM what gen of progestin will you give

A

it is best to avoid progestins n px with DM

34
Q

effects of estrogen in terms of lipid metabolism

A

inc HDL, tri G and total chol; dec LDL

35
Q

effects of progestin in terms of lipid metabolism

A

dec HDL, triG and total chol; inc LDL

36
Q

effects of progestin on coagulation parameters

A

No effect

37
Q

effects of estrogen on coagulation parameters

A

inc synthesis of several coag factors including fibrinogen (px w/ history of VTE should not be given OCP_

38
Q

most common cardiovascular effects of OCP

A

arterial thrombosis

39
Q

nicotine and estrogen would increase the risk for

A

stroke

40
Q

if the px stopped taking OCP how long before she can get pregnant again

A

if they ovulated regularly they can do so w/in 3 mo

41
Q

OCP has a protective effect on the dev of what CA

A

endometrial CA and Ovarian CA

42
Q

absolute contraindications for OCP

A 
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
Q

it is recommended to start taking OCP how long after menses

A

within 7 days following the onset of menses

44
Q

px delivered 10 wks fetus, when can she take OCP?

A

she can start immediately (<12 wks)

45
Q

why combined OCP is not a good choice in lactating moms

A

it reduces quantity and quality of breastmik

46
Q

if the woman is fully breastfeeding how soon can you give OCP

A

after 6 mo

47
Q

provides sustained release of the steroids and result in a relatively constant sserum lvls that are less than peak lvls seen in oC

A

contraceptive patch

48
Q

example of contraceptive patch

A

ethinyl estradiol + norelgestromin

49
Q

example of contraceptive vaginal ring

A

EE + etonorgestrel

50
Q

examples of injectable suspension

A

DMPA (depomedroxyprogesterone acetate)
Norethindrone ethanate
Progestin estrogen injectable formulation

51
Q

MOA of DMPA

A

inhibition of ovulation
produces thin endometrium
makes cervical mucus thick and viscous

52
Q

examples of subdermal implants

A

implanon

norplant

53
Q

subermal implant that contains single rod; 68mg etonogestrel

A

implanon

54
Q

subbdermal implant that contains 36mg levonorgestrel

A

norplant

55
Q

MOA of epostane as emergency pill

A

it blocks production of progesterone

56
Q

most effective emergency contraceptionif treatment is begun 72 hrs after an isolated midcycle act of coitus

A

steroids

57
Q

examples of emergency contraceptive pills

A 
EE+norgestrel
Levonorgestrel (plan B)
Danazol
Mifepristone
Epostane
58
Q

char of cervical mucus after menses

A

opaque thick sticky

59
Q

char of cervical mucus close to ovulaion

A

slippery, lubricative, transparent

60
Q

char of cervical mucus after ovulation

A

dry mucus

61
Q

physiology of lactational amenorrhea

A

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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