Samenvatting hele semester gynaecologie gnk 2.2

, ENDORCINOLOGY

Pregnancy: oestrogen raised -> increases prolactin but inhibits it effect on lactation; birth: low
oestrogen, still high prolactin = lactation

GnRH: pulsatile release -> constant in males, varies in females with menstrual cycle
 Low frequecy pulses increase FSH while high frequency pulses of GnRH increases LH


WOMEN'S REPRODUCTIVE HEALTH - GYNAECOLOGY H1

Menarche to menopause
 These years earlier incidence of puberty, especially in high income countries: by better
general health and socioeconomic circumstances
 Maternal age menarche: major determinant of offspring age menarche (same for
menopause) -> but genetic influence is decreasing while environmental influence is
increasing: changes in utero-endocrine environment by excessive maternal weight gain, DM,
smoking preg, endocrine environmental disturbances

 Small for gestational age: earlier menarche bij hormonal changes: bijv. increase DHEAS
 High BMI infant/childhood: earlier menarche because increased leptin -> influences GnRH
 Nulliparous women: earlier menopause, while multiparous women later menopause

Unnatural menopause: in 20% of women, bijv. by medical procedures like hysterectomy ->
medically induced menopause


Infertility: 10-20% of women
 Riskfactors: PCOS, obesity, endometroisis, pelvic inflammatory disease (bijv. by SOA)
o Environmental: low education, socioeconomic, western diet, sedentary, smoking,
alcohol
 Women with low fertility who eventually become pregnanct have a higher risk of pregnancy
complications: miscarriage, low gestational weight, gestational DM
 Suboptimal maternal health characteristics are more common in women from ethnic
minority groups -> more pregnancy complications
 Infertility, especially by PCOS, can lead to endometrial cancer, CVD, psychiatric disorders



Menarche & menopause:
 Menopause: at least 1 year of amenorrhoea
 Menopause & postmenopause phase 1=reduced ovarian function, lower oestrogen ->
oestrogen is necessary for organ functions so reduced oestrogen causes urogenital
symptoms, oesteoporosis CVD
 Younger age at menarche: cancer, metabolic disease, CVD, premature death, obesity
 Younger age at menopause/older age at menarche: osteoporosis
 Young age at menarche + old age at menopause: BC, endometrial cancer
 So: intervak between age menarche and menopause is related to risk of chronic disease later
in life

 Women with excess gestational weight/gest DM/h.t: increased risk of obesity, CVD, DM2
o The Children with high birth weight: obesity, h.t, DM2, asthma
 Women with low birht weight infants: increased risk of CVD

, o The Children with low birth weight: increased risk of CVD, metabolic, osteoporosis,
cancer
 Infants who are proportionally smal: adverse effects early in pregnancy
 Infants who are disproportionally smal: adverse effects late in pregnancy

Pregnancy periods:
 Embryonic periods: early in pregnancy -> earliest development rates = may be specific critical
period in pregnancy for development programming
 Boys grow faster from an early stage onwards -> more vulnerable to suboptimal in-utero
environment -> higher risk adverse birth outcomes
 Preconception, embryonic, foetal development, infancy are independent critical periods for
developmental programming
 Foetal and infancy periods: most important period of developmental plasticity -> individual
adapts to early environmental cues to develop phenotype best suited for survival
o Mistmatch hypothesis: when subsequent environment in child and adult is similar,
likely to remain healthy, if not (low birth weight and postnatal obesity) -> increased
risk of adverse health outcomes and crhonic disease later
 Another examples is hygiene hypothesis
 Epigenetic modifications by environmental factors (bijv. maternal nutrition) = developmental
adaptation
 Changes in foetal nutrients and O2 supply -> blood preferentially gredistributed to brain and
heart -> less to lower body parts = asymmetry growth restriction with head size big and risk
chronic diseases later

Development origins of health and disease hypothesis: adverse health outcomes in adulthood
originate in early life-> adverse exposure in foetal development either by restricted nutrition
environment in utero or excess nutrition -> increased risk of non-communicable disease later in
life

Pregnancy is physiologic stress model -> poses physiologic burden on women's body to sustain
fetal growth and development


ETHICS OF PRECONCEPTION CARE - GYNAECOLOGY H3

Preconception care PCC: to be effective, preferrably adopted before conception

2 types of PCC:
1. Individual:
a. Reprodictive genetic counselling:
i. Prevention: reduced children born with genetic defects
1. Ethical: reduced suffering
2. Health economic motivation: reduce societal costs
3. Critique: population eugenics
ii. Autonomy view = dominant: used now by current non-directive genetic
counselling
iii. Exceptional situation where advice is justified, like severe risk situations
b. Incompentent client (no ability to decide with reasonable assessment) = other
principles -> chose in best interes of patient
c. Nonvoluntary anti-conception/sterilisation: in client incompentend with regard to
reproduction and parenting and measure is in best interest client

, d. Confidentialitiy: only inform family members of genetic defects if everything has
been tried to convice patient, if otherwise would cause harm, if certain that
informing reduces or prevents harm, profressional is conscient stricken by keeping
the secret, not more of secret revealed than necessary
e. PCC as primary prevention: different ethical framework than counselling b/c nothing
eugenic in trying to avoid AVOIDABLE harm and mother have responsibility to
protect future children from harm
f. Prenatal child protection measures
i. Pressure: TRY to influence behavior, but without denying client a choicein
the matter -> regular visits
ii. Coercion: hospitalisation bijv to avoid further exposure or avoid perinatal
care
iii. Level of restriction on mother's freedom must be proportional to harm
prevented
iv. Protect future child, not foetus
In order to not intervene with women's right to have a termination, prenatal child protection
measures can only be taken after legal limit of abortion

2. General population: not aimed at risk group but at healthy person with average risk
profile -> folic acid, iron in diet, rubella vaccine, housing, screening
 Critique: medicalisation pre-pregnancy period
 Carrier testing: test people with risk personal/family history
 Carrier screening: test those without specific risk


Fertility preservation:
 Cryopreservation: preserve for after loss fertility; but only if cancer treatment can be
delayed and disease doesnt prohibit hormone stimulation
 Proactive IVF: combine egg of infertile mother with donor sperm -> embryo grow and freeze
for future use
 Oocyte harvesting: only option of fertility preservation for prepubertal girls -> followed by
IVM (in vitro maturation) or auto-transplantation
 Must create more embryos than needed in IVF to increase efficiency (more likely healthy
embryos for next cycle) and reduce burden for women
 Sperm donors dont have health risk but egg donors do:
 Ovarion hyperstimulation syndrome (OHSS): lethal risk but very avoidable
 Infection at ovum pick-up: very rare

Reasonable wellfare: professional can refrain from assisted reproduction if believed that it
would cause high risk of seriously diminished QoL for future child (if mother smokes, not
enough of a reason)

Fertility tourism/cross border reproductive care: by limited services in home country or legal
restrictions

 Surrogacy:
 Partial/traditional: use egg of surrogate with sperm of husband, not always assisted
reproduction needed
 Full/gestational: use egg of infertile wife and sperm of husband, grow embryo in
uterus surrogate
 Indications:
 If wife has no uterus