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David's mottershead > womens health 2 > Flashcards

womens health 2 Flashcards

1
Q

give an example of mechanicla and hormonal condom

A

Mechanical: condom
Hormonal: orally, transdermal patch, vaginal ring, IUD

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2
Q

Give an example of a 1st, 2nd, 3rd and 4th generation progestin drug?

A
  • 1st - norethisterone
    -2nd - noergestrel
    3rd - desogestrel
    -4th - drospirenone
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3
Q

How does combined estrogen and progestogen contraceptive work?

A
  • Supress GnRH, LH and FSH release at hypothalamic and pituitary level
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4
Q

progestin inhibits estrogen induced LH sureg and inhibits ovulation. TREU RO FALSE?

A

TREU

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5
Q

estrogen upregulates PGR, increasing negative feedback by progesterone (synergy). TREU OR FALSE?

A

TRUE

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6
Q

estrogen only promotes endometrial growth which can lead to endometrial cancer. TREU OR FALSE/

A

TRUE

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7
Q

in term of PK, what happens in Phase 1 for combined estrogen and progestogen contraceptive?

A
  • Extensive first pass by intestinal and hepatic P450
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8
Q

in terms of PK, what happens in phase 2 for combined estrogen and progestogen contraceptive?

A

-Sulfation and glucoronidation, followed by biliary secretion

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9
Q

conjugation prevents enterohepatic recirculation of for combined estrogen and progestogen contraceptive? TRUE OR FALSE?

A

TRUE

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10
Q

what is monophasic and multiphasic and explain each?

A
  • Monophasic: does of estrogen and prohestin does not vary
  • Multiphasic:
    bisphasic - dose of prgestin only vary
    Triphasic -3 different dose combinations
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11
Q

what are some ADRs for estrogen drugs?

A
  • Hypertension

- Risk of endometrial cancer (this is long term)

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12
Q

what are the ADRs for progestogen drugs?

A
  • Headache, nausea, vomiting
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13
Q

What are the ADRs for combined estrogen and progestogen drugs?

A
  • Thromboembolism
  • Hypertension
  • Cancer
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14
Q

what are some contranindications for combined estrogen and progestogen drugs?

A
  • Cardiovascular, thromboembolism, pregnacy
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15
Q

what are some drug interctions of combined estrogen and progestogen drugs?

A
  • drugs that induce P450 e.g riampicin
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16
Q

How do progestogen only contraceptives work?

A
  • Inhibit the release of GnRH from the hypothalamus
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17
Q

progestogen only contraceptives are useful when oestrogen is contranindicated. TREU OR FALSE?

A

TRUE

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18
Q

progestogen only contraceptives are more efficacious as the combined therapy. TREU OR FALSE?

A

FALSE

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19
Q

what are the ADRs with progestogen only contraceptives?

A
  • Breakthough bleedig may occur
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20
Q

Give two examples of depot parental formulations for progestogen only contraceptives?

A
  • Medroxyprogesterone

- Norethisterone

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21
Q

Norethisterone is an oil formulation used for short term contraceptive also used ot treat heavy periods. TREU RO FALSE?

A

TRUE

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22
Q

Why do Medroxyprogesterone and Norethisterone cause problems with returning to full fertility?

A
  • Because they are slow release formulations
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23
Q

with Subdermal implant for progestogen only contracepives feritility is restored on removal. TRUE OR FLASE?

A

TRUE

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24
Q

what does Intra-uterine device do?

A
  • Prevents endometrial thickening
25
Q

With IUD you can get dysmenorrhoea (period pain). TREU RO FALSE?

26
Q

what does copper IUD do?

A
  • Releases copper which prevents fertilization
27
Q

Give an example drug dor emergency contracetpive and what it does?

A
  • Levonorgestrol- high single dose,

- It blocks LH surge which prevents ovulationa nd implantation

28
Q

Ulipristal (SPRM) is an emergency contraception and is useful 120hr after intercourse. TREU RO FALSE?

29
Q

Emergency contraception not effective after implantation. TRUE OR FALSE?

30
Q

what is mifepristone and what is it used for?

A
  • Progesterone receptor antagonist

- Used for abortion

31
Q

how does mifepristone work?

A
  • Blocks progesterone receptor causing decay of decidua and embroy dies and detaches
32
Q

mifepristone can be used with misprostol to induce contractions. TRUE OR FALSE?

33
Q

what are the ADRs for mifepristone?

A
  • Causes serious bleeding
34
Q

estrogen receptor agonist can be natural and synthentic and can be used for hormonal replacement therapy. TRUE OR FALSE?

35
Q

What does SERMs stand for?

A
  • Specific estrogen receptor modulators
36
Q

SERMs are medicines with selectivity for different tissues. TRUE OR FALSE?

37
Q

what is Raloxifene a agonist and antagoist for?

A
  • Agonist in bone

- Antagonist in breast and uterus

38
Q

what is Tamoxifen a agonist and antagoist for?

A
  • Agonist in bone and uterus

- Antagonist in breast

39
Q

when does menopause occur?

A
  • When all follicles have been depleted
40
Q

in menopause there is decreased estrogen and inhibin which leads to less FSH and LH. true or false?

41
Q

what does estrogen synthesis depend on?

A
  • Aromatase synthesis in adipose tissue

- Hence less estrogen which is previous source of granulosa cells in follicles

42
Q

what are symtpoms of menopause?

A
  • Hot flushes

- Vaginal dryness

43
Q

what is involved in hormonal replacement therapy?

A
  • Progestin and estrogen to prevent risk of cancer
44
Q

what are the ARDs for HRT?

A
  • Stroke, breast cancer, increased risk of coronary heart disease
45
Q

there are reduced hip fractures from osteoproisis with HRT. TREU RO FALSE?

46
Q

Tamoxifen is an ER antagonist that inhibits estrogen dependent growth of breast cancer. TRUE OR FALSE?

47
Q

Why is tamoxifen use limited to 5 years?

A
  • Because of tis increased risk of endometrium cancer
48
Q

How do SERMs work?

A
  • Tissue specific pattern of estrogen receptors
  • Tissue speciif cpattern of co-regulator expression
  • Effects on ER stability and degradation
49
Q

what are the two Tissue specific pattern of estrogen receptors identified?

50
Q

SERMs have different affinties for ERa and ERb homodimers and ERa and ERb heterodimers. TREU OR FALSE?

51
Q

The pattern of genes activated by ER activation is regulated by the expression of what?

A
  • Co-regulatory proteins
52
Q

Co-regulatory repertoire varies from tissue to tissue (genes activated in bone are different from those in breast. TRUE OR FLASE?

53
Q

Co-regulator recruitment may be ligand dependent, thus a ligand may recruit co-activators specific to one tissue but co-repressors specific to another. TRUE OR FALSE?

54
Q

Some ER antangonists have been shown to increases the rate of ER degradation. TREU RO FALSE?

55
Q

Describe how SERMs achieve selectivity?

A
  • Differential SERMs effects on estrogen receptor dimers (either ERa ERb homodimer or heterodimer
  • Co-activator complex alters gene expression and response to SERM
  • Differential effects on ER degradation (depedent on receptor subtype and co-activator complex)
56
Q

what are the good and bad effects of Tamoxifen?

A
  • Good:
  • Reduces breast cancer risk
  • Lowers LDL cholesterol
  • strengthens bones

Bad:

  • Increases uterine cancer risk
  • Inreases blood clot risk
57
Q

what are the good and bad effects of Raloxifene a newer SERM?

A
  • Good:
  • Strengthens bones
  • Lowers LDL cholesterol
  • Reduces risk for invasive breast cancer
  • Fewer uterine cancers than tamoxifen
  • Fewer blood clots than tamoxifen

Bad:
- Blood clots, hot flushes, teratogenic

58
Q

The antagonistic activity of Raloxifene in breast and endometrium does not increase risk of endometrial cancer. TRUE RO FALSE?

59
Q

The agonist activity of Raloxifene in bone decreases bone resorption which is used to delay and prevent progression of osteoporosis in post menausal women. TREU OR FALSE?

David's mottershead (3 decks)

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