fertile Flashcards
semen deposition
□Generally into the posterior fornix of the vagina which is hostile:
•pH 5.5-6.0 due to presence of lactobacilli
• partly buffered by alkaline semen
•semen initially ‘clots’ breaks down in about 10-20 mins due to action seminal enzymes
□ Most semen is lost from vagina after sex □ 1% or less retained by cervix
semen analysis
- volume >1.5 ml
- density > 15 x 10^6/ml
- motility > 40% progressively motile
- morpholgy >4% normal
sperm capacitation
“Switching on” of sperm - HYPERACTIVE
Takes about 4 hours after ejaculation
Cholesterol loss and calcium influx
subfertility
Is an arbitrary diagnosis:
failure to conceive after 1 year regular unprotected intercourse
• Is a common problem: 1 in 7 couples
• Should be managed as a couple
causes of anovulation
• Hyperprolactinaemia - raised prolactin (PRL)
• Hypothyroidism - Low T4/T3: Raised TSH
• Hyperthyroidism -Raised T4/T3 Low TSH
• Hypogonadotrophic hypogonadism - Low FSH and LH and oestradiol
• Hypergonadotrophic hypogonadism (ovarian failure)
- Raised FSH and low oestradiol
• Polycystic ovary syndrome - tonic elevation of LH
- mildly elevated testosterone
• Anorexia - Low body mass & low FSH/LH
estrogens
○Cardiovascular adaptation to pregnancy: □↑blood vessel compliance → accommodates more blood □↑eNOs→ ↑NO
○Growth of uterus
○Primes uterus for labour → coordinates, synchronises uterine contractions
○weak antiinsulinic activity via ↑cortisol → creates [glu] gradient between mum and fetus
○onset of labour?
○cervical ripening
progesterone
○prepares, maintains endometrium for implantation
○initially produced by corpus luteum (up to 55d) then placenta
○may suppress maternal immune response to fetal antigens
○role in parturition
○a substrate for fetal adrenal gland production of glucocorticoids and mineralocorticoids
○growth of mammary glands
○maintains pregnancy → inhibits uterine contractions, prevents cervical ripening
○induces overbreathing → ↓CO2 maternal
kalmann syndrome
f isolated hypogonadotropic hypogonadism where there is an associated lack of sense of smell.
Hypogonadotrophic hypogonadism -> defective hypotalamic cells that secrete GnRH. Absence of sense of smell
progesterone normally not prego
During mestrual cycle:
Cause a rise in body temperature, the production of secretory endometrium and secretion of thick cervical mucus with leucocytes; has negative feedback on pituitary and hypothalamus
In pregnancy: cuases a reduction of contractions and reduces muscle tone. Rise in body temperature
Cellular effects:
Stimulates formation of 17-hydroxysteroid dehydrogenase whuch leads to inactivation of oestradiol in target tissue by converting it to oestrone
lactation
However, although prolactin levels are very high during pregnancy, lactation does not occur because estrogen and progesterone block the action of prolactin on the breast.
A_fter parturition, when estrogen and progesterone levels fall precipitously, their inhibitory effects on the breast are removed, and lactation can proceed._ As described in Chapter 9, lactation is maintained by suckling, which stimulates the secretion of both oxytocin and prolactin.
hCG
○rescues, maintains corpus luteum → entirely dependent on it
○stimulates maternal thyroid: □hCG binds TSH receptors □LH-hCG receptor is expressed in the thyroid
hPL human placental lactogen
○↑maternal lipolysis →↑NEFAs which are a source of energy for maternal metabolism, fetal nutrition
○anti-insulin/diabetogenic action: □↑maternal insulin, ↑protein synthesis, glucose transport for fetus ○angiogenic → formation of fetal vasculature
CRH corticotropin releasing hormone
○immnunosuppression? ○CRH levels rise near the end of gestation (CRH-binding protein ↓) → induces myometrical contractions? ○prostaglanding formation in placenta, amnion, chorion leave and deciduas is increased by CRH → controls timing of parturition?
Leptin
○secreted by cytotrophoblasts and syncytiothrophoblasts
○maternal levels are higher than normal and in fetus ○stimulates placental amino acid/NEFA transport
○fetal leptin levels correlate positively with birthweight ○role in development and growth
Maternal adrenala hormones increase
BP?
○Na retention →>>↑volume →>>↑CO:
□oestrogen →↑renin-aldosterone
_□progesterone, _ vasodilatory PGs→↑aldosterone
□shunting of blood to uterine circulation stimulates sympathetics →↑renin
□renal Na loss due to ↑GFR →↑renin □hCG→↑renin
○↓peripheral resistance: □↑NO, prostacyclin □relaxin?
□shear stress: mechanical transduction into chemical response: ↑PGI2→↑cAMP; ↑NO→↑cGMP; ↑EDHF → relaxation
◊preeclamptic women don’t have such vascular responses
○skin blood flow predominantly ↑ in hands and feet: ↑skin temperature, nail growth, %of hairs growing, disappearance of Raynauld’s syndrome, nose bleeds, stuffed, snoring
renal syst in pregnancy
○in pregnancy, there is no high diuresis because ADH is ↑↑, so low blood osmolarity is maintained.
○↑GFR because needs to excrete waste
○plasma markers: urea, creatinine
○glycosuria → GFR too high to have sufficient time to reabsorb ○calciuria ○urinary frequency ↑
○urinary stasis due to dilation of collecting system
pregnancy pulmonary fx
○↑tiadial volume due to progesterone
○respiratory rate unchanged ○↓expiratory reserve
○↓pCO2, ↑pO2, pH unchanged, (HCO3↓)
○costal margin and diaphragm altered
