Pregnancy Physiology Flashcards
What systems undergo adaptations for pregnancy?
Endocrine
Immune
CVS
Resp
Haemotological
GI
Urinary
What is responsible for these maternal adaptations?
HORMONES:
hCG
Oestrogen
Progesterone
Relaxin (softens ligaments)
hPL (involved in fat breakdown for glucose)
What are the adaptations within the immune system in pregnancy?
Fetus= hemi allograft- recognised by the maternal immune system
Placental progesterone changes balance between Th1 cells (cytotoxic) and Th2 cells (non-cytoxic)–> this causes reduction in Th1 and increase in Th2–> provides immune tolerance–> don’t have an immune response to baby
Consequences of pregnancy being an immunosupressed state?
Higher attack rate and severity of certain viral pathogens ie. varicella
May improve certain autoimmune conditions (cytotoxic mediated conditions) e.g.g graves
Adaptations in resp system during pregnancy?
Tidal volume- increases by 30-40%
Minute ventilation- increase by 40-50%
PaO2- increase
PCo2- decrease
Expiratory reserve volume- decrease by 20%
Total lung capacity: decrease by 5% as baby pushes up on diaphragm
Consequences of adaptations in the resp system in pregnancy?
Dyspnea- due to hyperventilation due to increase CO2 production- not major shouldn’t happen at rest
Need to consider pathology if it marked:
Physiological e.g. anaemia
Primary cardiac or resp condition e.g. asthma
Is it an acute condition in pregnancy? e.g. PE, pneumonia, ARDS?
Maternal adaptations in CVS due to pregnancy
Cardiac output increases:
Early pregnancy–> increase volume
Later–> increase HR
Progesterone: smooth muscle relaxation
Causes decreases systemic vascular resistance
Drop in diastolic BP during the first and second trimester of pregnancy
RAAS activated
Leading to increased sodium levels and water retention–> total blood volume increases
Affect of pregnancy on clotting factors?
Increased procoagulants: fibrinogen, factor VIII, vWF)
Decreased anticoagulants (protein s)
Reduced fibrinolysis
Consequences of adaptations in CVS/clotting?
Increase RAAS: peripheral oedema
Change in plasma volume: dilution anaemia
Clotting: hyper coagulable state–> risk of thromboembolic events
Adaptation of Renal system in pregnancy?
Systemic vasodilation= increased renal blood flow:
Increased GFR–> 50%
Decrease serum urea and creatinine by 25%
Decrease PCT absorption:
Glucosuria
Structural: smooth muscle relaxation + obstruction
Increased size of kidneys R>L
Decreased speed of urine passage- cause stasis–> more UTIs
Maternal adaptations in GI system when pregnant?
Structural- gravid uterus displaces the bowel- can cause mechanical obstruction
Slow transit due to progesterone effects and increased water absorption- constipation
LFTs: ALP increased due to placental synthesis
Decreased LES tone- GORD, Aspiration
Decreased gallbladder contractility: Gallstones
Maternal adaptations in endocrine system in pregnancy?
Fetus reliant on maternal thyroxine until 8-12 weeks–> takes up a lot of free thyroxine
Increased oestrogen results in increase of hepatic production of TBG–> more free T3 and T4 bind to the TBG–> more TSH to be release–> free T3 and T4 increases but total stays the same
Maternal adaptations in endocrine system in pregnancy?
Fetus reliant on maternal thyroxine until 8-12 weeks–> takes up a lot of free thyroxine
Increased oestrogen results in increase of hepatic production of TBG–> more free T3 and T4 bind to the TBG–> more TSH to be release–> free T3 and T4 increases but total stays the same
Maternal changes to glucose regulation?
Pregnancy= diabetogenic
Insulin resistance as need more glucose to shunt to the baby
Increased insulin secretion
Increased risk of ketoacidosis
Why is there insulin resistance in pregnancy?
As need more glucose to shunt to the foetus
Increase in human placental lactogen, prolactin, cortisol levels- ANTI-INSULIN HORMONES–> increase resistance