GI in Pregnancy

Episode one of the GI in Pregnancy chapter sets the physiologic baseline that every later stem depends on. The organizing idea is that pregnancy shifts a predictable set of labs, so any deviation pregnancy does not itself cause is by definition pathologic. From there it walks the volume, CBC, and liver-test changes, the fetal-protective imaging menu, and the antiemetic sequence for nausea and hyperemesis. The through-line is that you interpret a pregnant patient against a moved reference range, and you treat vomiting on a mechanistic ladder that ends with an absolute safety rule.

Episode two takes the upper-GI symptom that rides on the same pregnancy physiology as hyperemesis. GERD dominates because progesterone loosens the lower esophageal sphincter while estrogen strengthens the gastric mucosal barrier, so ulcers stay uncommon. The management is a stepwise sequence built on local-then-systemic safety logic, and the reasoning is that the rules fall out of mechanism rather than memorization. The one hard contraindication anchors the section: misoprostol is off the table because the same prostaglandin effect that heals ulcers induces labor.

Episode three covers the liver diseases that exist only because pregnancy is occurring, the syndromes for which delivery is the definitive treatment. It opens on intrahepatic cholestasis, where a stillbirth-risk curve inflecting at bile acids of one hundred drives delivery timing and a normal GGT separates it from obstruction. It then works through the preeclampsia, HELLP, and AFLP spectrum, teaching the distinction as a mechanism problem: vascular fibrin-and-shear versus fetal LCHAD-driven mitochondrial overwhelm. It closes on hepatic capsular rupture, the catastrophic complication that hemodynamic status triages.

Episode four takes the hepatic disease that is not caused by pregnancy but is reshaped by it. Viral hepatitis turns on virus-specific decisions: the tenofovir-plus-HBIG-and-vaccine stack that decisively cuts HBV vertical transmission, universal HCV screening with treatment deferred, genotype-driven HEV severity, and the empiric acyclovir that any pregnant patient with high transaminases and low bilirubin earns before HSV PCR returns. The pre-existing diseases follow an immune and pharmacokinetic principle: continue what is working and swap out the teratogens, with the specifics being mycophenolate out, azathioprine acceptable, trientine over penicillamine, and propranolol not nadolol.

Episode five flips a deeply intuitive instinct: pregnancy is not the time to back off immunosuppression, because the measured danger to the fetus is active maternal disease, not active maternal medicine. Once that principle is in place the medication rules become predictable, anything that maintained remission is continued and a small set of mechanism-toxic drugs is held. The molecular centerpiece is FcRn-mediated placental transfer, which loads IgG anti-TNF into cord blood by term but spares the Fab-fragment certolizumab, and that fact drives dose timing near term and infant vaccine decisions.

Episode six closes the chapter on two luminal problems governed by anatomy and timing. Post-bariatric pregnancy reads every rule off what the surgery changed: bypassed duodenum drops iron and calcium, reduced parietal cell exposure drops B12, the bypassed pylorus invalidates the OGTT, and mesenteric defects plus a gravid uterus produce internal hernia, so right upper quadrant pain after gastric bypass is internal hernia until proven otherwise. Cholelithiasis is governed by the trimester window: conservative when mild, second-trimester laparoscopic cholecystectomy when complicated, and ERCP built around keeping fetal dose under one milligray.