Reproductive pathophysiology Flashcards
(30 cards)
WHO preterm definition
before 37 weeks
Why are lungs an issue?
Lack of surfactant
Layers of the pregnant uterus
Amnion, chorion, decidua, myometrium
Infections associated with preterm birth?
Gram positive (ureaplasma parvum, ureaplasma urealyticum, strep), salmonella typhirium, Gardenerella vaginalis (bac. vaginosis). Tox plasmosis and malaria in developing countries. Can have two hit mechanism with initial candida/adenovirus initial infection
How do infections stimulate labour?
Inflammatory pathways enable return to pre-preg. state, but bacterial LPS activate TLR4, stimulate IL-6/TNF alpha (via NFkB) - pro inflammatory) as well as IL-1beta
Fetal fibronectin
produced in decidua, reaches upper cervix. Possible indiciator of pre-term labour/short cervix
Tocolysis
medical therapy to delay labour. Includes CCBs (L type), atosiban (oxytocin receptor antagonist), COX-2 inhib (inhibi prostg), NO donors (promote relaxation). None beneficial to fetus, just give some time
No proved benefit to Abx or other channel modulators
Prevention
Progesterone admin, cervical clercage
Pre-eclampsia
Dx criteria are HT+proteinuria (or underlying renal dysfunction). Early onset is <34, late is >34 weeks. Eatrly onset is worse.
Other symptoms are oedema, epigastric pain, thrombocytopoenia, cerebral/visual disturvance, headache, sudden weight gain, muscle twitch, pulmonary oedema. May have raisedliver enzymes.
Pathophysiology of pre-eclampsia
In pergnancy, should be very little resistance to flow to placenta. Dysfunction thought to be due to trophoblast debris entering maternal circ. Poor trophoblast invasion, poor vasodilatory response, endothelial dysfunction (arteries don’t dilate fully, endothelial damage). Ros and peroxides also implicated.
Pre-eclampsia risk factors
New partner, family Hx, maternal age (either extreme), CVD, renal disease, obesity
Pre-eclampsia treatment
low dose aspirin. Magnesium sulphate given for severe pre-eclampsia. Only real treatment is delivery of placenta (and baby).
Preeclamptic mothers and offspring have increased stroke risk
Intrauterine growth restriction
below 10th centile. Need serial growth measurements.Shares pre-eclampsia aetiology.
Asymmetrical IUGR
Typically late onset. Brain spared at expense of other organs. Examples are chronic hypoxia, malnutrition
Symmetrical IUGR
LEss common than asymmetrical. Typically early onset (<32 weeks). Normal ponderal index (HC/AC, both perameters reduced). Can be genetic disorders, drug use, or TORCH (toxoplasmosis, rubella, CMV)
Fetal undernutrition sequalae
Increases cortisol, pancreas/liver/kidneys/blood vessels underdeveloped, predisposes to insulin resistance, central obesity and HT/hyperlilidaemia. Increased risk of T2D
Dystocia
Responsible for 50% of C sections.
uncoordinated uterine contractions lead to abnormal fetal presentation (head hasn’t turned), but can also be cephalopelvic disproportion (head:pelvis ratio). Oxytocin and Pgs may help
Shoulder dystocia
Different from dystocia. More common in larger babies, and with diabetes/maternal obesity
Gestational diabetes
new onset of glucose intolerance in pregnancy. Tends to produce macrosomia (large baby). Increased T2D risk
Zika
Viral, causes microcephaly. Transmission via mosquito/sexual/blood/semen, placenta.
Symptoms - rash, myalgia, arthalgia, fever. Dx by PCR Causes developmental delay in babies.
Gestational HT
new onset HT after 20weeks pregnancy without pre-eclampsia features
superimposed pre-eclampsia
pre-eclampsia in women with chronic HT/renal disease
Key feature of pre-eclampsia
proteinuria. Heavily associated with IUGR
Role of Angiotensin 2 in pre-eclampsia
In pregnancy, sensitivity to AG2 is lost (angiotensin 2 counters local vasodilator PGs). Pre-ecmaptic women retain AG2 sensitivity
