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Common complaints in pregnancy

  • Heartburn (30-70%) is a burning sensation caused by acidic or gastro-oesophageal reflux. Hormones in pregnancy lead to reduced sphincter muscle tone and compression of the stomach by the uterus. Eat smaller meals, ensure good posture, avoid eating within 3 hours of bed, stop smoking, antacids, elevate head of bed
  • Constipation (40%) is due to mechanical pressure on the colon and rectum and iron tablets. Also, progesterone relaxes intestinal smooth muscle, decreasing GIT motility; prolonged transit time allows increased water absorption.

Increase fluids, dietary fibre and activity; mild laxatives (e.g. prune juice)

  • Nausea and vomiting (60% >12 weeks, 9% <16weeks) is poorly understood, but may be due to gastric reflux, vitamin B6deficiency, overactive thyroid and high levels of estrogen or hCG. Eat frequent small meals, rehydrate, rest, B6 supplementation, eat ginger
  • Increased urine production (60%) due to increased fluid intake and GFR, bladder more irritable (hyperaemic, oedamatous and reduced tone) and compression by uterus (late pregnancy)
  • Nocturia –during the day, water and sodium accumulate in the lower extremities (gravity, venous stasis and pressure of the uterus on the large veins returning blood to the heart). Fluid is mobilised at night because upon lying down, this pressure is relieved so blood flow returns to the heart, then kidneys. Reduce evening fluids, limit intake of caffeine and other diuretics
  • Altered thermoregulation – more heat is produced as progesterone has thermogenic effects, maternal metabolism is altered and basal metabolic rate is increased. The extra heat is dissipated by vasodilation of peripheral vessels and increases in skin blood flow, making it feel warmer (hands and feet most affected).
  • Altered hair growth – during pregnancy, less hair is lost as estrogen slows the rate of growth. There is often postpartum hair loss as the normal cycle rate is resumed. There is generally complete regrowth by 6-15 months.
  • Dependant oedema (excessive fluid in/around cells) – several forces controlling movement of fluid out of capillaries into the interstitium are altered during pregnancy: capillary hydrostatic pressure (due to compression of iliac vein and IVC) and colloid osmotic pressure. Avoid the supine position (increases the pressure of the uterus on the iliac vein and IVC), and avoid the upright position for extended periods. Wear support stockings, exercise regularly (contracting muscles compress veins and facilitate venous return), limit salt consumption
  • Varicose veins are superficial veins that have become dilated and tortuous because of a defect in the valves or weakness of the vessel wall that allow backflow of blood. Progesterone dilates the veins and softens the valve leaflets and venous pressure is increased in the pelvis and lower extremities because of on the iliac vein and IVC. A family history of varicose veins also increases the likelihood of developing them.
  • Haemorrhoids are varicosities of the rectal veins, caused by obstruction of the large veins of the pelvic region by the pregnant uterus, and exacerbated by constipation.
  • Dizziness and fainting due to blood return from limbs being impeded (venous stasis, compression of large veins). This is exacerbated by standing still for a long period of time, without contractions of the lower limb muscles to help push blood towards the heart. The reduced venous return can lead to a drop in blood pressure and fainting if the pressure is not adequate to maintain cerebral blood flow.
  • Supine hypotension (8%) – when supine, the pregnant uterus compresses the aorta and IVC, compromising blood flow to the uterus and placenta, and impeding the return of blood to the heart (venous return). This causes a large drop in heart rate and blood pressure, causing weakness, lightheadedness, nausea, dizziness or fainting. A collateral circulation usually develops alongside the spine, and the utero-ovarian circulation is also dilated; these allow venous blood to bypass the inferior vena cava.
  • Anaemia in the mother generally does not affect the baby, as it is protect at cost to the mother. However severe anaemia may result in decreased fetal growth. It is mostly due to increased folate (3x) or iron requirements. Physiological/dilutional anaemia results
  • Dyspnoea (shortness of breath) can be due to anaemia or hyperventilation, as progesterone re-sets the respiratory centre in the brain. In late pregnancy, pressure of the uterus on the diaphragm restricts the movement of the lungs and can lead to breathlessness.
  • Lower back pain – from early on in pregnancy, relaxin and progesterone soften ligaments and increase the elasticity of connective tissue and collagen, and widening and increased mobility of the sacroiliac joints and pubic symphysis starts by the end of the first trimester. Later, weight of the uterus shifts the centre of gravity lower and placing a stress on the muscles and ligaments of the lower back and spine. There is an increased curvature of the lower spine (lordosis) to counteract the weight of the uterus, which is exacerbated by stretching and decreased tone of the abdominal muscles.
  • Pubic symphysis pain – the joint widens during pregnancy as ligaments soften and mobility of this and the other pelvic joints increases. The joint becomes very tender, causing pain on walking, turning in bed, and with other movement. Treatment depends on severity; good posture, care with bending and using pillows to support your pelvis when lying down can help, and a pelvic support belt is sometimes used.

Vaginal delivery vs. Caesarian section

Advantages Disadvantages Vaginal delivery

  • Higher maternal-infant interaction and maternal satisfaction at time of delivery; skin-to-skin interaction after birth leads to better infant physiological outcomes, positive attachment relationships and maternal breast feeding success
  • Shorter recovery time (1-2 days), earlier discharge
  • Significantly less postpartum complications and pain
  • May be immunological beneficial
  • Cheaper * Inability to schedule date of birth (unless induced)
  • Fear or apprehension of pain, harm or affect sex life
  • Genital area discomfort (esp. if tearing or episiotomy), hemorrhoids (30%), coccyx displacement (10%)
  • Anal sphincter laceration
  • Urinary or faecal
  • incontinence, pelvic floor disorders

Caesarian delivery

  • Convenience
  • Protection of pelvic floor, less anal sphincter trauma
  • Less moderate-severe urinary incontinence
  • Better fetal outcome in some situations (e.g. breech) To the mother:
  • Maternal mortality
  • Complications – surgical (bladder lacerations, ureteral injury, haemorrhage) and anaesthesia
  • Post-op complications – increased readmissions, infection, UTI, DVT, haemorrhage, sepsis, endometritis
  • Longer and more painful recovery (>6 weeks), chronic pelvic pain, dense adhesions (make subsequent surgery more difficult and may cause chronic pain and bowel obstruction
  • Increased risk in future pregnancies – more placental problems (previa, accrete, abruption), ectopic pregnancy, uterine rupture, stillbirth. Infertility
  • Delayed bonding, breastfeeding and skin-to-skin
  • Increased postpartum depression and psychosis
  • Increased neonatal respiratory distress and chance of developing asthma
  • Fetal injury (accidental laceration)
  • Premature birth – if dates not accurately calculated
  • Increased risk of congenital malformation/CNS injury

Indications for planned Caesarian delivery:

  • Baby too large for the pelvis
  • Abnormal fetal lie or presentation
  • Multiple pregnancies (more than twins)
  • Placenta lying over the cervix
  • Condition preventing maternal effort or vaginal birth
  • Maternal request
  • Previous CD, traumatic VD or uterine surgery

Medical reasons for emergency caesareans:

  • Maternal condition that risks lives of mother and fetus
  • Haemorrhaging
  • Fetal distress and failure to progress in labour
  • Failed induction of labour
  • Cord prolapse
  • Threatened uterine rupture

Australia (2007)

  • 57.9% vaginal births
  • 11.2% had an instrumental vaginal delivery (forceps or vacuum extraction)
  • 30.9% caesarean section births

Initiation of labour at term and preterm

Parturition requires both:

  • Coordinated contractions of the myometrium to increase uterine pressure
  • Cervical softening– prior to parturition, the cervix retains the fetus in the uterus. Cervical incompetence is a cause of preterm delivery

Myometrium weight increases 20x during pregnancy, particularly due to estrogens. There is muscle cell hypertrophy (from 50 to 500µm), hyperplasia and increasing glycogen deposition. The outer longitudinal muscle contractions exert force circumferentially and along the axis of the uterus. Muscle cells behave as a syncytium; they act together and are electrically coupled via special gap junctions. Spontaneous depolarising pacemaker potentials occur (i.e. nerve stimulation is not needed). Contractility can be altered by changing the pacemaker potentials, threshold and calcium release. Two hormones enhance uterine contractility:

  • Prostaglandins – enhance Ca2+ release from intracellular stores
  • Oxytocin – lowers threshold

The pivotal point in muscle cell contraction is MLCK (myosin light chain kinase), an enzyme causing phosphorylation of actin and myosin filaments.

  • Stimulation – calcium, prostaglandin F, oxytocin
  • Inhibition of contraction – nitric oxide, relaxin, β-agonists, parathyroid hormone

Cervix resists stretch; must soften in preparation for labour:

  • ↓ collagen fibres
  • Changes in the matrix leading to loosening of the bundles and increased ability to stretch – ↑glycosaminoglycans, ↑ keratan sulphate, ↓ dermatan sulphate

Cervical softening (ripening) is caused by:

  • ↑metalloproteinases in the cervix (degrade collagen)
  • ↑ inflammatory cells, proinflammatory cytokines (IL2, IL8)
  • ↑ iNOS (inducible nitric oxide synthase = ↑NO. Pharmacological inhibition of iNOS prevents ripening
  • Prostaglandins PGE2 and PGF intravaginally or intracervically can induce labour, while PG inhibitors arrest premature cervical ripening

Oxytocin synthesis is in the SO and PV nuclei (hypothalamus)

  • Leader sequence of preprooxyphysin is removed ; remainder packaged into a secretory granule and is transported down the axons to the posterior pituitary gland
  • During transport, it is cleaved into oxytocins and Neurophysin I
  • Action potentials down the axon causes release of both products from the nerve endings and into the circulation

Maternal oxytocin plasma levels do not increase until after parturition has begun; it does not actually initiate labour. Actions of oxytocin:

  • ↑uterine contractions:
    • Acts directly on uterine smooth muscle cells (on oxytocin receptor) causing contraction
    • Stimulates formation of prostaglandins in the decidua; these enhance the oxytocin-induced contractions
  • Important for milk ejection – contracts the myoepithelial cells of the breast

Myometrial activation is the transformation of the myometrium to a state of responsiveness to endogenous stimulants (oxytocins, PGs), producing labour contractions.

A ↑estrogen/progesterone ratio is critical for parturition (E rises and P stays same). It causes:

  • number of oxytocin receptors – E increases number, P decreases
  • synthesis of PGs, via release of enzyme phospholipse A2 from lysosomes – E opens the lysosomes (=more PGs, P stabilises them)
  • release of PGs via ↑ number of oxytocin receptors (O stimulates PG release)
  • Induction of iNOS activity
  • Facilitation of the neuroendocrine (Ferguson) reflex
  • ↑ in CAP (contraction associated proteins) genes associated with uterine activation
    • Ion channels (Na+, Ca2+) = more contraction
    • Agonist receptors (for oxytocins, PG)
    • Gap junctions – help message pass from muscle to muscle

Endocrine changes alone are not sufficient; mechanical stretch also contributes to activation. This may explain increased incidence of preterm labour in multiples.

Timing of parturition: In sheep, the fetus itself determines the timing of parturition via maturational changes in its hypothalamic-pituitary-adrenal axis. CRH (corticotrophin releasing hormone) from the fetal hypothalamus stimulates an increase in ACTH in the last 14 days of gestation. The ACTH stimulates the fetal adrenals to produce cortisol, which goes to the placenta to cause ↓progesterone and ↑ estrogen.

  • Ablating the hypothalamus, pituitary, or disrupting the connection between them = prolonged pregnancy
  • Infusion with ACTH or cortisol = premature birth

In humans, timing is less well understood. Like in sheep, fetal and amniotic fluid \[cortisol\] increases in the last few weeks of pregnancy. However, prolonged pregnancy does not always occur with anencephaly or adrenal hypoplasia, and infusion of ACTH/glucocorticoids does not induce parturition.

Maternal estrogen rises progressively in gestation, but progesterone levels to not generally fall before parturition. Functional withdrawal of progesterone occurs due to a change in the balance of the two progesterone receptors. PR-B is the functional receptor, PR-A seems to oppose the B receptor. Towards term, there is more A = less progesterone attaching to the active B receptor

The initiating factor for time of labour may be placental CRH; maternal plasma levels increase exponentially with gestation. In the last month of pregnancy, levels of CRH binding protein drops, leading to a rise in free CRH. Women with preterm babies have higher CRH early on. CRH may cause labour by:

  • Stimulating the fetal pituitary gland (↑ ACTH Adrenocorticotropic hormone) and exerting a direct action on the adrenal cortex to lead to ↑DHEAS (dehydroepiandrosterone). DHEAS undergos conversion into estrogen = ↑E/P ratio
  • In the uterus, stimulation of CRH receptors =
    • ↑production of locally acting prostaglandins (especially PGE2and PGF2α)
    • Potentiates the contractile response of smooth muscle to oxytocins (via a PG-dependent mechanism)


  • Uterine contractures (Braxton-Hicks) are recurring contractile events of low amplitude and low frequency that occur during pregnancy. They last for 3-15 minutes and are not painful; most mothers are unaware of it
  • Labour contractions are high-frequency, high-amplitude, relatively short-lasting and painful (though not between contractions). The commencement of labour is signaled by 2-4 relatively intense contractions per 10 minutes and/or rupture of the fetal membranes. By this stage, the uterus has two functionally distinct segments
    • Upper uterine segment – muscular
    • Lower –thin and amuscular; unifies with vagina during labour to provide a passive fibromuscular birth canal

Stages of labour Stage 1 (longest stage, labour is usually 8-14 hours) begins with the onset of regular painful contractions associated with dilation and shortening of the cervix, and ends when the cervix is fully dilated (10cm). Subdivided into:

  • Latent phase (slow dilation until about 3cm)
  • Active phase (more rapid dilation after 3cm)

Each muscle cell becomes thicker and shorter, as after every contraction and relaxation, the original length is not regained. Fundal musculature becomes thicker and uterine volume decreases

Stage 2 (<1 hour) begins at full dilation of the cervix and ends at complete delivery of the fetus. Uterine contractions, aided by maternal abdominal wall contractions, push the fetus down and through the pelvis.

Stage 3 (very short) begins at the end of fetal expulsion, and ends at delivery of the placenta. A few minutes after delivery of the fetus and clamping of the cord, the placenta becomes detached from the wall. It is completely expelled by uterine contractions and the aid of the midwife or obstetrician. Active management involves steady traction and

  • Ocytocin or syntometrine injection helps to contract the uterus down; also used in C-sections

Delivery date (EDD) can be calculated by adding 7 days to the LMP, and adding 9 months (conception normally occurs 14 days after the start of the LMP). Full term is around 40 (37-41) weeks of amenorrhea. The accuracy of EDD is dependent on a regular 28-day cycle; if the cycle is shorter, the delivery date will be earlier (as ovulation occurred sooner than 14 days after the start of the LMP) and vice versa.

Risk factors for premature labour:

  • Premature rupture of the membranes; previous preterm labour or LBW
  • Uterine over-distention – multiple pregnancy, polyhydramnios (excessive amniotic fluid)
  • Infection – may be responsible for >40% of cases; includes bacterial vaginosis and UTI
  • Bleeding, e.g. placental abruption or abnormal placentation
  • In Vitro Fertilisation
  • Fetal abnormality/birth defect/intrauterine fetal death
  • Medically indicated – severe maternal hypertension, endangered fetus (growth restriction, fetal distress)
  • Minor – extreme stress, standing >2 hours/day, age <17 or >35, reduced BMI (<20), smoking and drug abuse, male fetus, low socioeconomic status, short conception cycle

Management of pre-term labour may include (depending on individual circumstances)

  • Corticosteroids (betamethasone – matures the lungs), antibiotics if membranes ruptured (risk of infection)
  • Tocolytic agents – inhibition of labour
    • Beta-agonists (salbutamol)
    • Prostaglandin synthase inhibitors
    • Calcium channel blockers
    • Oxytocins antagonists (abostatin)

Ectopic pregnancy

Risk factors Symptoms

  • History of ectopic pregnancy
  • Smoking
  • Age over 35
  • Inflammation and infection (PID, STIs, endometriosis)
  • Abnormalities of fallopian tubes
  • Contraceptive choice: pregnancies occurring despite tubal ligation/IUD
  • Fertility drugs or IVF
  • Prior spontaneous and medically induced abortions Mirror normal pregnancy, appearing 7 weeks after LMP – amenorrhoea, morning sickness, breast tenderness.
  • Unusual vaginal bleeding – "prune juice"
  • One-sided pain in the lower abdomen – severe and persistent stabbing sensation
  • Pain on urination

Stretching of uterine tubes may lead to rupture and internal bleeding

  • Shoulder, lower back, abdominal or pelvic pain (blood irritates nerves)
  • Dizziness and fainting with loss of blood

Higher risk of infertility and subsequent ectopic pregnancies

Gestational diabetes

GD is a temporary form of diabetes that happens during pregnancy (usually diagnosed in the 2nd and 3rd trimesters. It typically starts in the weeks 24-28, and goes away after the baby is born, though having GD does put you at risk for developing type II diabetes later in life. It affects between 5-10% of pregnancies in Australia. GD is pathophysiologically similar to type 2 DM – human placental lactogen (hPL) increases insulin resistance (increases in direct relation to length of gestation). Normally, insulin maintains glucose homeostasis, if this is insufficient you get hyperglycaemia and GD.

Risk factors
  • Mothers of certain ethnic backgrounds — Indian, Chinese, Vietnamese, Middle Eastern, Polynesian/Melanesian, and indigenous Australians more at risk than Anglo-Celtic women
  • Being overweight
  • Family history of type 2 diabetes
  • Gestational diabetes in a previous pregnancy
  • Difficulty carrying a pregnancy to term
  • Age >30
  • Previously having a very large baby (>4.5kg).
  • GD is usually asymptomatic, so it is important o be tested between weeks 26-28. Possible symptoms may include excessive fatigue, being thirsty all the time and increased urination
  • Screening is by a glucose challenge test; this involves drinking a glucose solution and taking a blood sample after an hour. If the one-hour blood glucose reading is high, a glucose tolerance test is recommended to confirm diagnosis
  • Maternal GD should not cause birth defects in the unborn child; it occurs late in pregnancy when the child is already well developed. However, if undiagnosed and untreated, there is a higher risk of:
    • High birth weight (may necessitate early delivery and/or C-section)
    • Hypoglycaemia after birth – extra maternal glucose crosses the placenta, the baby responds by producing extra insulin. After birth, the extra glucose is no longer being supplied, but the infant's pancreas is still secreting insulin, leading to hypoglycaemia
    • Child at increased risk for developing type 2 diabetes later in life
  • Treatment for GD is usually control of blood glucose by diet and exercise, but some may have to take insulin. Self-monitoring is also important

Maternal and Perinatal mortality

  • Maternal death – death of a woman while pregnant or within 42 days of termination of pregnancy from any cause related to or aggravated by the pregnancy or its management; <1% in developed countries
  • Maternal mortality ratio – per 100,000 live births; measure of mortality risk once pregnant (World 400, Aus 4)
  • Maternal mortality rate – per 100,000 of women of reproductive age
  • Lifetime risk of maternal death – considers probability of becoming pregnant and probability of dying as a result of that pregnancy culminated across a woman's reproductive years
  • Live birth – 400g or 20 weeks showing signs of life such as heartbeat or breath
  • Neonatal death – death within 28 days of birth
  • Perinatal mortality – stillbirth (400g or 20 weeks with no signs of life) and neonatal deaths/1000 births
  • Miscarriage – any pregnancy <20weeks that fail to continue

More than 500,000 women die each year from maternal causes. Direct complications leading to maternal deaths:

  • Haemorrhage (25%) is the most common
  • Infection or sepsis (15%) a result of poorly-performed abortion, unsterile delivery or prolonged labour where membranes have ruptured and delivery is not within 24 hours
  • Unsafe abortion (13%) with unsanitary conditions or instruments
  • Eclampsia (12%) high BP may lead to eclampsia (convulsions) during pregnancy, which must be treated early
  • Obstructed labour (8%) requires treatment at a facility that can perform operative delivery

Newborns are often disabled because of poor maternal heath and lack of skilled care; most deaths due to infections.

Cervix in health and disease

In nulliparous woman, the external os of the cervix is small and round. During parturition, its fibromuscular tissue is stretched by powerful contractions of uterine muscles; becomes effaced and dilates to around 9cm. After a vaginal delivery, the external os is widened, with a horizontal slit-like appearance

The epithelium of the ectocervix is non-keratinising squamous and the endocervix is columnar mucinous. The squamo-columnar junction is not the same as the transformation zone. At birth, the junction is high up, and moves down during young adulthood. With age related hormonal changes and the vaginal acidity, the columnar epithelium metaplases into squamous. This squamous metaplasia area is the transformation zone.

Human Papilloma Virus infection

  • >100 types; infects cells of the anogenital tract, also involved with anal, perianal, vulvar and penile carcinoma
    • Low risk types (6, 11, 42, 44) – genital warts; rarely progress to malignancy
    • High risk types (16,18, 31, 45) – pre-invasive lesions and invasive carcinomas
  • HPV is sexually transmitted; often associated with multiple sexual partners. Infection is common – 4 out of 5 will encounter it at some stage; majority unknown, clears within 9-15 months
  • Main risk factor for cervical carcinoma (as well as cigarette smoking, immunodeficiency, no screening)
  • HPV interferes with basal cell maturation, leading to a koilocytic change (enlarged and irregular nuclei, pleomorphic and hyperchromatic) and Cervical Intraepithelial Neoplasia (CIN 1 low grade, CIN 2 and 3 high grade) = squamous intraepithelial lesion

The Pap smear is a highly effective mass screening test for cancer, based on cytology of cells scraped from the cervical transformation zone. HPV DNA testing of the samples may be done, but will only tell you positive/negative not the type; only recommended for those with established abnormality. They should not be taken within a week of menstruation; the transformation zone (not the vaginal wall) is sampled. Sample is smeared onto a slide and quickly sprayed with liquid fixative. If not fixed, the cells dry out and acquire abnormal morphological appearances.

  • Colposcopy if abnormal result – colposcope magnifies the cervix, sometimes revealing a high grade abnormality that may require a biopsy and/or treatment. Usually, it will just confirm the presence of a low grade abnormality/ normal that will not need treatment – only monitoring each year until the Pap smear returns to normal.
  • Wire loop excision – removes abnormal cells using a wire loop under local anaesthetic
  • Cone biopsy – cone-shaped section of the cervix is removed, usually under GA. Recommended when the abnormal cells are higher in the cervical canal, to make sure there is no cancer involved
  • Laser or Diathermy– abnormal cells destroyed using heat or heat from a laser beam

Gardasil is a quadrivalent vaccine for HPV types 6, 11, 16 and 18; protection is against HPV responsible for 70% of cancers, so Pap smears must be continued. Gardasil is funded under the national vaccination program for females 14-26 years, not for males.

Failure of fertilized eggs

For every 100 eggs fertilized in vivo, less than 15 babies are born. This is because humans have low fecundity and egg potential decreases with age.

  • Very early loss (prior to missed period) – uncertain causes, but possibly chromosomal or implantation failure
  • Trimester 1 loss (from positive pregnancy test to 12 weeks) – 1 in 6 pregnancies fail after diagnosis (miscarriage)
    • Clinical presentation – bleeding, crampy abdominal pain
    • Cervical assessment to determine if threatened, inevitable, incomplete, complete
    • Diagnosis –distinguish from ectopic pregnancy; ultrasound confirms with presence of heartbeat
    • Treatment –uterine evacuation (dilatation and curettage) often required
    • Recurrent miscarriage is 3 or more consecutive miscarriages, caused by:
      • Random embryonic aneuploidy >60%
      • Parental aneuploidy 1:100-500
      • Antiphospholipid syndrome 1:6
      • Maternal disease – thyroid, diabetes rare
  • Trimester 2 loss – only 1% of pregnancies lost in T2; due to fetal abnormality, cervical incompetence, uterine abnormality or infection
  • Late pregnancy loss – causes:
    • Prematurity, birth trauma, cord accident, infection, hypoxia, meconium aspiration
    • Placental insufficiency or abruption, fetal abnormality


  • Fertility – the number of births that occur to an individual or a population (Australia 1.8/couple)
  • Fecundity – the physiological ability to have children
  • Crude birth rate – annual number births/average population x1000 (relates to whole population)
  • General fertility rate – number of births/women aged 15-49 x1000 (relates to women of childbearing age only)

Age and fecundity 'Age and fetal abnormality'

  • Couple aged 24 will conceive after an average 6 cycles (1-11)
  • Couple aged 34 will conceive after 10 (1-19)
  • Couple aged 39 will conceive after 20 (1-9) * Age 20 – chance of abnormality is 1/500
  • Age 40 – 1/65 chance
  • Age 45 – 1/20 chance
  • Age 49 – 1/8 chance

Infertility is the inability to conceive after one year of attempting to do so; affects 1/6 couples. Causes:

  • Male – sex dysfunction, sperm (marijuana, mumps, obesity, steroids, alcohol)
  • Female – mucous, tubal (blocked or damaged), endometriosis, anovulation (anorexia, excessive exercise, genetic causes, Polycystic Ovarian Syndrome)
  • Unexplained – 26%