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pharmacology 2 > hormonal contraception > Flashcards

hormonal contraception Flashcards

1
Q

hypothalamus producing GnRH

A

produces it in a cyclical manner

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2
Q

GnRH acts on

A

anterior pituitary to make it produce FSH and LH

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3
Q

HPO axis

A

hypothalamo-pituitary-ovarian

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4
Q

FSH acts during

A

first half of the manstual cycle

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5
Q

LH acts during

A

2nd half of the menstrual cycle

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6
Q

FSH causes production of

A

oestrogen from granuloma cells in dominant follicle

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7
Q

LH causes production of

A

porgesterone>oestrogen

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8
Q

3 endogenous oestrogenen

A

E2 - 17b oestradiol, major
E1 - estrone, minor
E3 - oestriol, pregnancy

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9
Q

17b oestradiol E2

A

most abundant and potent

produced by ovarian granulosa cells

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10
Q

oestrone E1

A

produced by ovaries and adrenals

levels increase slightly after menopause

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11
Q

oestriol E3

A

placental - only in pregnancy

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12
Q

endogenous oestrogens are

A

18-carbon steroids
transported by SHBG
bind oestrogen receptors

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13
Q

oestrogen receptors

A

ERa and ERb
expressed redundantly in reproductive system and breast
expressed non-redundantly in CVS, skeleton, CNS and immune system - not reproductive effects of oral contraceptives
ERa/b are ligand activated transcription factors (target genes with EREs) - slow response time

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14
Q

ERa over expressed in

A

breast cancers
not ERb
anti oestrogen blocking ERa are widely used in breast cancer

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15
Q

oestrogen levels modulate

A

FSH and LH release
cyclical changes in uterus and breasts
induction of progesterone receptors

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16
Q

metabolic actions of oestrogen

A

increase bone mass by blocking bone resorption - why women are more susceptible to osteoporosis
improve TG profile - improve HDL:LDL ratio
increase coagulability - venous thrombosis embolism and stroke

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17
Q

progesterone

A

secreted mainly by the corpus luteum and placenta
secreted in the second half of the cycle
levels decrease before mestruation (unless pregnant)
transported by albumin and corticosteroid binding globulin CBG

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18
Q

progesterone receptor

A

ligand activated transcription factor expressed in female reproductive tract, breast and CNS

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19
Q

actions of progesterone

A

prepare for/maintain pregnancy
uterine/cervical effects
- endometrium, decreased proliferation, increase secretory changes
- cervix - thickens and decrease secretions, decrease sperm penetration
- myometrium - decrease uterine excitability
- breasts - glandular development
- hypothalamus - decrease LH surge and GnRH release, block ovulation
- CNS - increase body temperature

20
Q

2 types oral contraceptives

A
  • combined contraceptives (COCs) contain oestrogen and a progestogen
  • progestogen only contraceptives
21
Q

until recently, endogenous hormones were not used orally due to

A

their extensive 1st pass hepatic metabolic - very low bioavailability

22
Q

combined oral contraceptives

A

contain a synthetic oestrogen and a synthetic progestogen

23
Q

oestrogens used in the pilll

A

ethinyloestradiol and mestranol

24
Q

synthetic oestrogens

A

ethinylestradiol EE- derivative of estradiol, addition of ethinyl group to reduce hepatic metabolism and allow it to be taken orally
mestranol - pro-drug of EE - undergoes demethylation, less potent

25
Q

synthetic progestogens

A

multiple - differentiations in potency and spectrum of activity
1st generation - ethisterone - significant androgenic effects: acne, hirsutism, weight gain, no longer used
2nd generation - norethisterone, levonorgestrel - reduced androgenic side effects
3rd generation - desogestrel, gestodene - reduced androgenic and lipid effects but increased thromboembolic effects

26
Q

how does the combined pill work

A

inhibit ovulation - prevent release of FSH (follicle development) and LH (ovulation
synergistic effect of oestrogen (FSH) and progestogen (LH)
thickens cervical mucus - forms a barrier to sperm via progestogen effect
thin endometrial lining - reduce endometrial receptivity to inhibit implantation

27
Q

3 mechanisms of combined pill

A

inhibit ovulation
thicken cervical mucus
thin endometrial lining

28
Q

efficacy of COC

A

> 99% with perfect use
effectiveness reduced by
- compliance
- delayed start of the next pack - decrease HPO suppression
- missed pills
- vomiting - decreases intestinal absorption
- broad spectrum antibiotics (ampicillin) - decreases enterohepatic circulation (probably more a theoretical than a real problem)
- CYP3A4 induction - griseofulvin, anti-epileptics (phenytoin, carbamazepine), TB drugs (rifampicin), st john’s wort

29
Q

regimens and dose of COC

A

21 days OC and 7 days placebo
7 days hormone free - withdrawal bleed (not a period)
no biological reason for a withdrawal bleed and extended OCP regimens may increase compliance

30
Q

COC formulations

A 
monophasic - same daily dose of EE and progestogen 
phased regimens (biphasic and triphasic) - dose varies to mimic cyclical endogenous hormone secretion 
biphasic - constant EE, progestogen in 2nd half of cycle 
triphasic - increase EE in middle to decrease breakthrough bleeding plus stepwise increase in progesterone 
no contraceptive advantage
31
Q

breakthrough bleeding

A

treat by increasing oestrogen or progesterone

32
Q

nausea

A

treat by reducing oestrogen dose to take the pill at night with food

33
Q

fluid retention, breast tenderness

A

treat by decreasing oestrogen dose

34
Q

chloasma

A

treat by avoiding sun, use sun screen

35
Q

androgenic and antiandrogenic side effects

A

ance
depression, irritability and fatigue
reduction in libido

36
Q

enhanced coagulation

A

dose related risk
metabolic side effect of oestrogen
older contraceptives had more of a problem with this
increases clotting - DVT, pulmonary embolism, MC, stroke
increase risk in obesity, long haul travel and underlying genetic clotting abnormalities eg. factor 5 laden
MI risk increases >35yo, smoker, hypertensive

37
Q

breast cancer and oestrogen

A

oestrogen promotes breast cancer - early menarche, nulliparity, late age of 1st pregnancy, lack of breast feeding - all increases risk of breast cancer
role of progestogen is more complex
increased risk of breast cancer in usage of the pill
reduction in risk when pill is stopped

38
Q

cervical cancer risk

A

causal link not established

may be behavioural in origin - OC users more sexually active, use barrier contraceptive methods less, exposed to HPV

39
Q

protective risk effects of COC

A

decreased ovarian risk, endometrial, colorectal
decreased risk os long term - does not diminish when pill is ceased

reduced risk of PID, salpingitis and ectopic pregnancy
improvement in acne
improvement in menstrual problems: cramps, heavy flow, endometriosis, premenstual syndrome, iron deficiency anaemia

40
Q

contraindications of the COC

A
  • pregnancy
  • history of VTE or Stroke
  • CVD - coronary artery disease, valvular disease
  • major elective surgery - stop 1 month beforehand
  • oestrogen dependant breast cancer sufferer
  • migraine with aura - increase stroke risk
  • hepatic disease - acute hepatitis, severe cirrhosis
    >35 years old, obese, smoker with HT and DM
41
Q

progestogen only OC

A

minipill
contain no oestrogen
useful with COC is contraindicated or not tolerated

42
Q

progestogen only OC mechanism of action

A
  • inhibitor of ovulation due to inhibition of LH surge
  • thickens and decreases amount of servical mucous, impedes sperm penetration
  • endometrium thins - decreases implantation rate

30-40% of progestogen only OCs still ovulate, so less effective than combined OCs

requires more meticulous compliance

43
Q

minipill

A

progestogen only OC

44
Q

long acting reversible contraceptives

A

LARCs
IUDs, progestogen implants
more effective reversible contraceptive
20x more effective than OC
safe for most women, including adolescents, post partum, post abortion
menstrual cycle disturbance is common, with irregular bleeding but decreased bleeding over time
levonorgestrel IUD often decreases bleeding - used therapeutically

45
Q

antisperm antibodies

A

some women naturally produce antibodies to sperm
immunological infertility
topically delivered trap >99.9% of sperm
still in clinical trials

pharmacology 2 (19 decks)

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