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.

Topics covered

The two halves of liver disease in pregnancy
Intrahepatic cholestasis and its genetics
Diagnosis and the normal-GGT discriminator
Ursodeoxycholic acid treatment
Bile-acid-stratified delivery timing
Preeclampsia and HELLP
AFLP and the LCHAD mechanism
Hepatic rupture as the catastrophe

Key decisions

Intrahepatic cholestasis is diagnosed at total bile acids above ten micromol per liter, and a normal GGT with elevated bile acids and transaminases discriminates it from obstructive cholestasis, which lifts GGT and prompts ultrasound and MRCP.
Ursodeoxycholic acid ten to fifteen milligrams per kilogram per day is the treatment, with cholestyramine as second-line, and vitamin K is given around delivery because cholestasis impairs fat-soluble vitamin absorption.
Delivery timing follows the bile-acid tier: below forty deliver at thirty-nine weeks, forty to ninety-nine between thirty-six and thirty-nine, and at or above one hundred at thirty-six to thirty-seven weeks because stillbirth risk inflects sharply.
HELLP is defined by the Tennessee criteria of LDH at or above six hundred, AST at or above seventy, and platelets at or below one hundred thousand, and twenty percent of cases occur without hypertension.
Preeclampsia and HELLP are treated by delivery because the placental endothelial dysfunction does not resolve until the placenta is gone, with magnesium for seizure prophylaxis and platelet transfusion to above forty thousand for delivery.
AFLP is separated from HELLP by looking for mitochondrial failure, hypoglycemia, encephalopathy, coagulopathy, and lactic acidosis with an AST-to-ALT ratio above one, versus HELLP's schistocytes, high LDH, and deep thrombocytopenia.
Hepatic capsular rupture is triaged by hemodynamics: an unstable patient gets resuscitation with surgery or hepatic artery embolization, while a stable contained hematoma is managed conservatively with coagulopathy correction and serial imaging.

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - The two halves of liver disease in pregnancy
(01:02) - Intrahepatic cholestasis and its genetics
(02:53) - Diagnosis and the normal-GGT discriminator
(04:11) - Ursodeoxycholic acid treatment
(06:22) - Bile-acid-stratified delivery timing
(08:05) - Preeclampsia and HELLP
(11:19) - AFLP and the LCHAD mechanism
(16:00) - Hepatic rupture as the catastrophe