Physiological changes of pregnancy UC San Diego 妊娠的生理变化迭戈.pptVIP

Pregnancy is “diabetogenic”. Why? Placental hormones plus obesity may overwhelm adaptive capacity of pancreatic insulin output. Hyperglycemia Obesity Inflammation Insulin resistance Placental vascular damage Atherosclerosis Nephropathy Retinopathy Neuropathy Immune dysfunction Poor wound healing Pancreatic beta cell damage Decreased insulin output Genetic predisposition Two vicious cycles of type II DM in pregnancy: #1 #2 “Glucotoxicity” Placental hormones Gestational DM: Appears in 4% of pregnancies. Possibly due to inability to make enough insulin to counteract the “counteregulatory hormones” which increase in pregnancy—placental lactogen, placental GH, cortisol and progesterone. Gestational DM tends to recur in subsequent pregnancies. Gestational DM increases risk for type 2 DM later in life. Pregestational DM: Insulin requirements increase rapidly after the 26th week of gestation. Insulin requirement at term is about 50% more than pre-pregnant requirements. Insulin requirements fall during first stage of labor, but rise during second stage of labor. Insulin requirement falls up to 40% the day after delivery. Placental hormones are “diabetogenic”. Urinary system Renal infections increase in incidence. Progesterone relaxes ureters Compression of ureters at pelvic brim? obstruction? infection GI tract Decreased gastric emptying Increase GERD Full stomach precautions Avoid aorto-caval compression: useleft uterine displacement (LUD) LUD helps venous return. C/S as part of resuscitation? LUD decreases chance of DVT LUD increases O2 delivery to fetus: Increases uterine artery pressure and decreases uterine venous pressure. Why we don’t do it: It doesn’t look right! Colman-Brochu S 2004 Chestnut chap. 2 The End * * Physiological changes of pregnancy Tom Archer, MD, MBA UCSD Anesthesia Outline Normal changes CV Respiratory Hematologic Endocrine Urinary GI Implications for pathological conditions. Pregnancy as a “stress test for life” Unveils prob