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Pharmacy Year 3 > Reproduction > Flashcards

Reproduction Flashcards

1
Q

When does ovulation occur?

A

Day 14 in a 28 day cycle

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2
Q

What is the corpus luteum and what does it produce?

A

The structure left in the ovary after the egg has been released. It produces oestrogen and progesterone.

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3
Q

Which hormone peaks 36 hours before ovulation?

A

Luteinising hormone

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4
Q

Which functional group do oestrogens have that other steroid hormones do not?

A

An aromatic ring

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5
Q

What are the common properties for all major classes of steroid hormone?

A
  • 2 binding sites, one for DNA and the other for steroid
  • binding of steroid ligand produces a complex that acts on DNA
  • binding of DNA complex to DNA sites alters the combination of genes being expressed by target cells
  • defines steroid receptors as transcription factors
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6
Q

Why do gonadotrophins need receptors at the cell surface?

A

To eventually produce effects that are seen

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7
Q

Describe the function of GnRH

A
  • acts at GnRH receptor (it is a GPC receptor)
  • release of hormones is pulsatile
  • stimulates the release of FSH and LH
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8
Q

What kind of frequencies is FSH stimulated by?

A

Slow GnRH pulse frequencies

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9
Q

What of frequencies if LH stimulated by?

A

Fast GnRH pulse frequencies

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10
Q

Give a use of GnRH agonists and antagonists

A

Used in ART to shut down the ovary in advance of a controlled cycle of ovulatory stimulation

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11
Q

What is Buserelin and what is it used for?

A

Buserelin is an antagonist at GnRH receptor, it reduces production of FSH and LH.
Gives a contraceptive effect and is used in HRT

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12
Q

What are the consequences of long term Buserelin use?

A
  • GnRHR down regulation
  • insensitivity to GnRH
  • loss of production of FSH and LH
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13
Q

Which hormone is released as levels of fat increase in girls?

A

Leptin

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14
Q

What does Leptin do?

A

Stimulates kisspeptin neurone to stimulate GnRH neurons to produce GnRH

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15
Q

What is early puberty associated with?

A

Higher risks for osteoporosis but lower risks for breast cancer

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16
Q

Describe the early follicular phase

A

There is low oestrogen, the follicle hasn’t really grown.
No negative feedback to the hypothalamus.
There are slow GnRH pulses giving rise to high levels of FSH and lower levels of LH

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17
Q

Describe the mid follicular phase

A

Oestrogen rises, there is negative feedback to the hypothalamus.
FSH is suppressed due to negative feedback.
Positive feedback as oestrogen increases at another areas in the hypothalamus
GnRH pulses increase

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18
Q

Describe the late follicular phase

A

Oestrogen and progesterone feedback negatively
High oestrogen and progesterone suppress the production of gonadatrophins
Positive feedback by steroid to the hypothalamus is followed by negative feedback

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19
Q

Describe steroid hormone action

A

Binding of steroid complex to the steroid response element (SRE) on DNA alters the rate of transcription so mRNA abundance is also altered

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20
Q

What happens when oestrogen binds to its receptor?

A

The receptor undergoes a conformational change, this can affect binding to DNA or its ability to recruit co-factors.

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21
Q

MoA of Faslodex

A

Binds to oestrogen receptor and blocks its ability to activate target genes. It binds in preference to estradiol

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22
Q

MoA of Tamoxifen

A

partial agonist/antagonist used for breast cancer, it is effective on oestrogen in the breast but not in the endometrium

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23
Q

Define menstruation

A

Shedding of superficial layer of endometrium

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24
Q

What does withdrawal of sex steroid lead to?

A

Vasoconstriction
Tissue hypoxia
Connective tissue breakdown
Fragmentation

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25
Q

Define endometriosis

A

The establishment and growth of endometrial tissue outside the uterus

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26
Q

What causes endometriosis?

A

Reflex menstruation - endometrial tissue fragments shed at menses passing through the fallopian tube then becoming established in ectopic sites

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27
Q

What are the symptoms for endometriosis?

A

Pelvic pain and infertility

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28
Q

What are the treatment options for endometriosis?

A

Surgical removal
Pain medication
Pharmacological blocking of hormone cycle with an aromatase inhibitor, COC or GnRH modulators

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29
Q

Define interstitial implantation

A

Implantation of developed blastocyst (the implantation window is ~4 days)

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30
Q

What produces hCG?

A

The placenta produces hCG from the hatched blastocyst stage

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31
Q

Where is hCG measurable?

A

Maternal blood and urine - only after implantation

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32
Q

What happens if implantation is too late?

A

The corpus luteum regresses and pregnancy fails

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33
Q

What is the role of progesterone in pregnancy?

A

Regulates the transport of egg/embryo though the fallopian tubes.
Prepares the uterus to receive implanting blastocyst
Sustains uterine lining throughout pregnancy
Inhibits myometrial contractility

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34
Q

What happens at 7-9 weeks of pregnancy?

A

The placenta takes over production of oestrogen and progesterone from the CL - luteoplacental endocrine switch

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35
Q

What what point are miscarriages most likely?

A

At the luteoplacental endocrine switch, if abnormal placentas are produced they can’t produce the hormones required

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36
Q

At what point is a pregnancy viable?

A

From when the heart pulsations can be visualised within gestation sac

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37
Q

When can a transvaginal ultrasound be done?

A

5 weeks after last menstrual period

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38
Q

When can a transabdominal ultrasound be done?

A

6 weeks after last menstrual period

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39
Q

Why does ectopic pregnancy occur?

A

Occurs due to tubal infection / upper reproductive tract infection. Humans have a short cervix and so it doesn’t work as effectively as other animal species.

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40
Q

Which drug is used in ectopic pregnancy?

A

Methotrexate - used to prevent cell proliferation (blocks DNA synthesis)

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41
Q

What is mifepristone used for?

A

Termination of pregnancy

Structurally similar to progesterone and binds to its receptor but exerts different effects

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42
Q

How does mifepristone work?

A

Blocks preparation of endometrium for pregnancy

Counteracts effect of progesterone on myocetrial contractility

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43
Q

What does human placental lactogen (hPL) do?

A

Modulates intermediary metabolism by changing the level of insulin-like growth factor (IGF). Increases glucose and amino acid availability to foetus

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44
Q

What occurs in the embryonic stage?

A

Formation of major organs - lasts up to 10 weeks

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45
Q

What occurs in the foetal stage?

A

Maturation, development and growth - lasts 10 - 38 weeks

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46
Q

How is progesterone involved in labour?

A

Progesterone suppresses myometrial contractility till late pregnancy - the receptor is switched and the inhibitory receptor is lost.

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47
Q

How does the foetus stimulate labour?

A

Surfactants in the lung

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48
Q

What it oxytocin and how does it work?

A

Oxytocin is a peptide hormone released from the posterior pituitary gland.
Levels rise in the last trimester

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49
Q

How is oxytocin used?

A

Used with prostaglandin analogues to induce labour

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50
Q

What is used to mature foetal lungs in labour induction?

A

Glucocortioid treatment

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51
Q

Can drugs be used in pregnancy?

A

With caution but avoid anyway
Most drugs diffuse across the placenta and enter foetal circulation e.g. lipophilic, weakly basic drugs and larger molecules

52
Q

What are tocolytics used for?

A

Prolonging pregnancy for up to 48 hours

53
Q

What is a monophasic oral contraceptive?

A

Each pill has the same level of hormone

54
Q

Give examples of monophasic 21 day pills

A

Microgynon 30, Yasmine, Cilest

55
Q

What is Microgynon made up of?

A

Ethinylestradiol and Levonorgestrel

56
Q

Give an example of a monophasic 28 days pill

A

Microgynon 30 ED

57
Q

What is a phasic oral contraceptive?

A

Phasic pills contain two or three sections of different coloured pills in a pack. Each section contains a different amount of hormones.

58
Q

Give an example of a 21 day phasic pill and what is its composition?

A

Logynon

Ethinylestradiol and Levonorgestrel

59
Q

Give examples of 28 day phasic pills and their composition

A

Logynon ED - Ethinylestradiol and Levonorgestrel

Qlaira - Ethinylestradiol and Dienogest

60
Q

What are the 2 types of POP?

A

3 hour - traditional progesterone, has to be taken everyday within the same 3 hour window
12 hour - desogesterel, must be taken within 12 hours of the same time each day

61
Q

What is the difference between COC and POP in terms of number of pills and taking them?

A

POP need to be taken every day, there is no pill free period

62
Q

Give an example of a traditional POP

A

Noriday - noresthisterone

63
Q

Give an example of a newer POP

A

Cerazette - Desogestrel

64
Q

Give examples of non oral COCs

A

Contraceptive patches (Evra)
- 1 patch every 7 days for 21 days
Vaginal ring (NuvaRing)
- 1 ring for 3 weeks

65
Q

Give examples of POCs

A

Injection (Depo Provera - every 13 weeks)
Contraceptive implant (Naxplanon - every 3 years for 18-40 y/os)
IUS (Mirena every 5 years OR Jaydess every 3 years

66
Q

What is the mechanism of action for CHCs?

A

Primary action is to inhibit ovulation, they thicken cervical mucus and alter the endometrium.
Oestrogen causes endometrial proliferation and Progestogen opposes proliferation

67
Q

What is the mechanism of action for POCs?

A

They suppress ovulation by thickening the cervical mucus, they delay the transport of the ovum - affect the way cilia work.
They change the environment of the endometrium to make implantation unlikely.

68
Q

Which contraceptive methods have a high risk of user failure?

A

Pill
Patch
Vaginal ring

69
Q

Which contraceptive methods are independent of user (LARCs)?

A

Injection
Implant
IUD and IUS

70
Q

Give examples of non hormonal contraceptive methods

A

Male / female condom
Diaphragm/cap + spermicide
Natural family planning
Sterilisation

71
Q

Define lactational amennorhoea

A

Temporary postnatal infertility that occurs when a woman is amenorrheic and fully breastfeeding.
Up to 98% effective

72
Q

What are the advantages of CHCs?

A
  • menstrual period regular, lighter and less painful
  • decrease in acne, functional ovarian cysts and benign ovarian tumours
  • decreases risk of ovarian, uterine and colon cancer
73
Q

What are the disadvantages of CHCs?

A
  • Minor ADRs

- increases risk of high BP, MI, stroke, VTE, breast cancer and cervical cancer

74
Q

What are the advantages of POCs?

A
  • High efficacy
  • suitable when COCs aren’t
  • decreased risk of endometrial cancer
75
Q

What are the disadvantages of POCs?

A
  • ADRs

- menstrual irregularities

76
Q

What is classed as a missed COC pill?

A

> 24 hours

77
Q

What is classed as a missed POC pill?

A

3 hours late for tradition

12 hours late for newer

78
Q

When is EHC indicated for missed COCs?

A

If 2 or more are missed in >24 hours and UPSI occurs

79
Q

What is advice for missed POP?

A

Continue pills with 2 days of barrier protection

80
Q

When is EHC indicated for missed POCs?

A

If 1 or more active pills are missed and UPSI occurs before 2 tablets have been taken correctly

81
Q

What is the UKMEC Category 4?

A

UK medical eligibility criteria

Category 4 - a condition which presents an unacceptable health risk if a contraceptive is used.

82
Q

What are the UKMEC Category 4 conditions?

A 
Breast feeding women
Women >35 y/o + 15 cigarettes a day
Multiple CVS risks
Consistently elevated BP
Vascular disease and history of VTE
Migraine with aura
Current breast cancer
DM w/ nephropathy, retinopathy or neuropathy
Benign hepatocellular adenoma and malignant hepatoma
83
Q

What is the advice for starting on COC?

A

Start on day 1 of natural cycle
If starting on day 1-5, no additional precautions needed
Quick starting (> day 6) then use additional precautions for 7 days

84
Q

What is the advice for starting traditional POPs?

A

Start at anytime, no extra precautions needed

85
Q

What is the advice for starting newer POPs?

A

If starting on day 1-5 no precaution needed

But if starting > day 6, additional precaution needed for 2 days

86
Q

Changing from COC to POP?

A

Make sure previous contraception has been taken effectively OR exclude pregnancy. Additional precaution needed for 2 days if in pill free period.

87
Q

Changing from COC non ED to POP?

A

For immediate cover, ignore PF period and start immediately

88
Q

Changing from COC to Cerazette?

A

For immediate cover, no need for PF period

89
Q

Changing from POP to Qlaira?

A

Additional precautions for 9 days

90
Q

Changing from POP to Zoely and other COC?

A

Additional precautions for 7 days

91
Q

What are the types of emergency contraception?

A

IUS - up to 120 hours post UPSI
ellaOne - up to 120 hours post UPSI
Levonelle - up to 72 hours post UPSI

92
Q

Which forms of contraception do DDIs with enzyme inducers occur?

A

Patches
Vaginal rings
Oral tablet
Implant

93
Q

Which forms of contraction have no DDIs with enzyme inducers?

A

Injection
IUS
IUD

94
Q

Which drugs decrease the effectiveness of contraceptives through DDIs with hepatic enzyme induction?

A 
Carbamazepine
Oxcarbazepine 
Phenytoin 
Phenobarbital
Primidone
Topiramate 
Neviprine
Ritonivir
Rifabutin
Rifampicin
95
Q

Which CHCs are first line?

A

Microgynon 30 Ed
Brevinor
Marvelon

96
Q

Which CHCs are second line?

A

Cilest
Logynon
Loestrin

97
Q

Which CHCs are third line?

A

Evra - patch

Better for younger patients

98
Q

Which POCs are first line?

A

Micronor

Depo-Provera (injection, but not for adolescents)

99
Q

Which POCs are second line?

A

Cerazette

Mirena - IUD

100
Q

Which POCs are third line?

A

Jaydess - use if woman wants period or is having issues with Mirena

101
Q

What are the advantages and disadvantages of the contraceptive injection?

A

Adv: lasts 8-13 weeks and may reduce heavy, painful periods
Disadv: fertility may take time to come back

102
Q

What are the advantages and disadvantages of the implant?

A

Adv: works for 3 years, fertility and period go back to normal
Disadv: small procedure to fit and remove

103
Q

What are the advantages and disadvantages of the intrauterine system?

A

Adv: 3-5 years depending on type and fertility goes back to normal on removal
Disadv: irregular bleeding/spotting in first 6 months and some can get ovarian cysts

104
Q

What are the advantages and disadvantages of the intrauterine device?

A

Adv: 5-10 years and fertility return to normal
Disadv: period may be heavier or longer and more painful

105
Q

What are the procedures for female sterilisation?

A

Fallopian tubes are cut, seals or blocked

106
Q

What are the advantages and disadvantages of female sterilisation?

A

Adv: periods are unaffected and it can’t easily be reversed
Disadv: other contraceptives until procedure is effective and there is a risk of ectopic pregnancy if sterilisation fails

107
Q

What are the procedures for male sterilisation?

A

Vas deferent are cut, sealed or tied

108
Q

What is a disadvantage of male sterilisation?

A

Need to use contraceptive until a semen tests show that there are no sperm left and this can take up to 8 weeks.

109
Q

Define precocious puberty

A

Gives <8 years old who have started menstruation

110
Q

What is primary dysmenorrhoea?

A

Cramping, pain to thighs and back with GI symptoms, headaches, fatigue/faintness
Peak incidence in teens to 20s

111
Q

What is secondary dysmenorrhoea?

A

Consequence of other pelvic pathology. Pain may begin before menstruation.
Peak incidence in 30s - 40s

112
Q

Describe the cause of primary dysmenorrhoea

A

Higher concentrations of prostaglandin in menstrual fluid
Increased myometrial contractility
Other mediators
- endothelins: vasoactive peptides regulate synthesis of prostaglandin
- vasopressin: stimulates uterine activity and decreases uterine blood flow

113
Q

Pharmacological management of primary dysmenorrhea

A 
NSAIDs 
OTC: Feminax
POM: naproxen, mefanamic acid
Oral contraceptives
Antispasmodics
114
Q

Describe the cause of secondary dysmenorrhea

A 
Prostaglandin involvement
Underlying pelvic pathology 
- PID
- endometriosis
- fibroids
- uterine polyps
115
Q

Pharmacological management of secondary dysmenorrhea

A

Surgery: ablation or laser therapy
Symptomatic relief
Non analgesic treatment

116
Q

Describe the causes of endometriosis

A

Development at embryological stage
Retrograde menstruation
Reflux menstrual loss
Increased prevalence with outflow obstruction

117
Q

Describe the symptoms of endometriosis

A 
Pain
Fatigue
Subfertility 
Dyspareuria
Dyschezia
Dysurria
Chronic pelvic pain 
Menstrual irregularities
118
Q

How is endometriosis diagnosed?

A

Pelvic exam
Pelvic ultrasound
Diagnostic laparoscopy

119
Q

What are the grades of endometriosis?

A

Grades 1-2
Minimal-mild, poorly visualised on ultrasound. Uterine and ovarian implantation

Grades 3-4
Moderate-severe, commonly associated with adhesions.
Rectovagincal endometriosis and bowel invasion

120
Q

What are the aims of surgery in the treatment of endometriosis?

A

Restore normal pelvic anatomy, divide adhesions and ablate endometrial tissue

121
Q

What are the aims of medicinal treatment in endometriosis?

Give examples

A

Provide symptomatic relief and improve fertility

1st line: NSAIDs
2nd line: 'shrinkers' 
Contraceptives
Progestogens or antiprogestogens
GnRH
SARMs - selective androgen receptos
Modulators - target biosynthetic pathways
122
Q

Describe the potential causes of menorrhagia

A 
Dysfunctional uterine bleeding (DUB)
Menopause, fibroids, PID, miscarriage/ectopic pregnancy, IUD, adenomyosis
Hepatic, renal or thyroid disease
PCOS 
Blood thinning medication
123
Q

Define menorrhagia

A

Menstrual blood loss >80ml per month

124
Q

What are the symptoms of menorrhagia?

A 
Irregular disease
Sudden change in blood loss
Intramentrual bleeding
Dyspareuria
Pelvic pain
Pre-menstrual pain
125
Q

How is menorrhagia diagnosed?

A 
Blood tests
Cervical smear
Biopsy
Ultrasound
Sonohysterography
Hysteroscopy
126
Q

How is menorrhagia managed?

A

If contraception is required: CHC, POC, IUS/pararenteral progesterone

If contraception is not required: trxnexamic acid

Mefanamic acid

Oral progestogen: norethisterone

Antiprogestogens: Gestrinone / danazol

Pharmacy Year 3 (11 decks)

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