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.

Topics covered

Hepatitis A and vaccination safety
Hepatitis B and the tenofovir decision
Hepatitis C and universal screening
Hepatitis E and genotype severity
Disseminated HSV and empiric acyclovir
Autoimmune hepatitis and PBC continuation
Wilson disease and chelation
Cirrhosis and portal hypertension

Key decisions

Maternal antiviral therapy for hepatitis B is added when HBV DNA exceeds two hundred thousand international units per milliliter by week twenty-eight, using tenofovir disoproxil fumarate three hundred milligrams daily started at twenty-eight to thirty-two weeks.
All infants of HBsAg-positive mothers receive HBIG plus the first vaccine dose within twelve hours of birth, taking transmission from over ninety percent down to under five percent, and cesarean delivery is not indicated for HBV alone.
Ribavirin is essentially absolutely contraindicated as a teratogen requiring two forms of contraception for six months, and HCV is screened universally but treated before conception or after pregnancy, while hepatitis E genotypes one and two carry twenty to thirty-three percent third-trimester maternal mortality by geography.
Disseminated HSV produces anicteric liver failure with transaminases twenty-five to forty times normal and bilirubin below three, and empiric IV acyclovir is started before PCR returns because it cuts mortality from thirty to fifty percent down to eight to twenty-five percent.
Azathioprine is continued because the fetal liver cannot activate it, while mycophenolate is strictly contraindicated with a six-month pre-conception washout, and methotrexate-class exposure is avoided.
In Wilson disease chelation must continue with trientine preferred over penicillamine, the dose reduced twenty-five to fifty percent in the third trimester, copper IUDs contraindicated, and levonorgestrel IUDs preferred.
For variceal prophylaxis in cirrhotic pregnancy propranolol is preferred over nadolol, and vasopressin is avoided because it activates myometrial V1 receptors and induces contractions.

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

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(00:00) - The incidental half and hepatitis A
(00:34) - Virus-specific decisions begin
(01:21) - Hepatitis B and the tenofovir decision
(04:18) - Hepatitis C and universal screening
(05:54) - Hepatitis E and genotype severity
(07:23) - Disseminated HSV and empiric acyclovir
(08:45) - Pre-existing liver disease principles
(11:50) - Wilson disease and chelation
(14:15) - Cirrhosis and portal hypertension