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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?

A

TRUE

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?

A

TRUE

29
Q

Emergency contraception not effective after implantation. TRUE OR FALSE?

A

TRUE

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?

A

TRUE

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?

A

TRUE

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?

A

TRUE

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?

A

true

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?

A

TRUE

46
Q

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

A

TRUE

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?

A
  • ERa

- ERb

50
Q

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

A

TRUE

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?

A

TRUE

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?

A

TRUE

54
Q

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

A

TRUE

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?

A

TRUE

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?

A

TRUE

David's mottershead (3 decks)

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