Liver Issues Flashcards
liver diseases associated with pregnancy
*hyperemesis gravidarum
*intrahepatic cholestasis of pregnancy (ICP)
*preeclampsia
*acute fatty liver of pregnancy (AFLP)
*HELLP syndrome
normal effects of pregnancy on LFTs
*serum alkaline phosphate INCREASES (due to placental production)
*GGT should be normal
*AST and ALT should be NORMAL
*serum albumin DECREASES due to hemodilution
*spider angiomata and palmar erythema can occur in the absence of liver disease due to estrogen excess
hyperemesis gravidarum
*intractable vomiting in the first trimester:
-loss of 5% of body weight, ketonuria, severe enough to require IV hydration
*abnormal LFTs in up to 50% of patients (elevated ALT and AST up to 100, occasional jaundice)
*tx: supportive care
intrahepatic cholestasis of pregnancy - overview
*cardinal sx = PRURITUS
-due to elevated bile acid levels
-affects all parts of the body, but itching of palms & soles predominate
*jaundice & elevated AST and ALT
intrahepatic cholestasis of pregnancy - risk to fetus
*main risk in ICP is to the fetus
*fetal distress, occurs in 20-40%
*fetal complications include placental insufficiency, premature labor, sudden fetal death
intrahepatic cholestasis of pregnancy - treatment
*UDCA (ursodeoxycholic acid)
preeclampsia
*new onset during pregnancy of:
-HTN
-proteinuria
*liver involvement in preeclampsia is unusual but signifies severity and need for immediate delivery
HELLP syndrome - acronym
*H - hemolysis (LDH > 600)
*E and L - elevated liver enzymes (ALT and AST of 70-6000)
*L and P - low platelets (platelets < 150K)
HELLP syndrome - pathophysiology
*pathophysiology is related to endothelial injury and intravascular fibrin deposition, resulting in hepatic hemorrhage and necrosis
HELLP syndrome - clinical presentation
*typically presents in the 3rd trimester
*most common presenting sx:
-epigastric & RUQ abdominal pain
-nausea, vomiting, headache, malaise
-usually occurs in the setting of preeclampsia
HELLP syndrome - treatment
*immediate delivery (most require a C-section)
*complications if not treated: DIC, abruptio placenta, eclampsia, perinatal mortality
acute fatty liver of pregnancy - pathophysiology
*microvesicular fatty infiltration of the liver
*due to abnormal fatty acid oxidation in the mitochondria of the hepatocytes (LCHAD complex)
acute fatty liver of pregnancy - clinical presentation
*sudden onset in the 3rd trimester
*sx: anorexia, nausea, vomiting, RUQ pain, headache
*exam: HTN, jaundice, edema, ascites, encephalopathy
*lab: ALT-AST 300-1000, bilirubin < 5
*histologic dx, but liver biopsy usually not necessary
acute fatty liver of pregnancy - treatment
*immediate delivery (C-section)
*maternal mortality and fetal mortality significant
*25% chance of recurrence in subsequent pregnancies
vascular diseases of the liver
*ischemic hepatitis
*portal vein thrombosis
*congestive hepatopathy
*Budd-Chiari syndrome
*sinusoidal obstruction syndrome
ischemic hepatitis
*the dual blood supply (hepatic artery, portal vein) prevents isolated vascular lesions (thrombosis, embolism) from resulting in hepatic infarction
*ischemic hepatitis is almost always associated with profound systemic hypotension, resulting in decreased hepatic artery and portal vein flow
*characterized by a rapid rise in AST and ALT to > 1000, with rapid return to normal
portal vein thrombosis - causes
*CIRRHOSIS (related to sluggish portal vein flow)
*hypercoagulable states
*oral contraceptive use
*hepatocellular carcinoma
*intraabdominal infection or inflammation (IBD, pancreatitis)
acute vs. chronic portal vein thrombosis
*acute: abdominal pain, fever (RARE)
*chronic: cavernous transformation of the portal vein
portal vein thrombosis - clinical manifestations
*most often subclinical, discovered accidentally on imaging
*esophageal variceal hemorrhage
*ascites (rarely)
*propagation of clot into the SMV, resulting in bowel infarct
portal vein thrombosis - management
*evaluate for underlying etiology
*screen for esophageal varices
*consider anticoagulation for acute PVT
congestive hepatopathy
*classically seen with chronic heart failure (R-sided failure “cor pulmonale”)
*often asymptomatic with minor LFT abnormalities
*increased unconjugated bilirubin, increased ALT and AST < 2x upper limit of normal, increased INR
*can present with RUQ pain, jaundice, ascites
*on exam:
-hepatomegaly
-jugular venous distension
-hepatojugular reflex
-pulsatile liver with tricuspid regurgitation
Budd-Chiari syndrome - overview
*occlusion of the major HEPATIC VEINS (carry blood from liver to heart), most often thrombosis
*underlying etiologies include: hypercoagulable states, oral contraceptive use
Budd-Chiari syndrome - diagnosis
*presentation: abdominal pain, hepatomegaly, ascites
*LFT abnormalities
*ultrasound with doppler evaluation of hepatic veins
Budd-Chiari syndrome - management
*anticoagulation, thrombolytics
*interventional radiology
*angioplasty, stents
*TIPS
*liver transplant?
sinusoidal obstructive syndrome (SOS)
*seen almost exclusively FOLLOWING BONE MARROW TRANSPLANTATION
*presentation: RUQ pain, jaundice, hepatomegaly, ascites, edema, weight gain
*increased bilirubin, increased AST + ALT, increased INR
benign lesions of the liver
*liver cyst
*cavernous hemangioma
*focal nodular hyperplasia
*hepatic adenoma
*hepatic abscess
liver cyst
*benign lesion of the liver
*usually discovered incidentally with abdominal imaging
*most are solitary and < 5 cm in size
*no clinical significance, except to distinguish from cystic neoplasms
cavernous hemangioma
*benign lesion of the liver
*most common tumor of the liver
*most are solitary and < 5 cm in size
*usually discovered incidentally with abdominal imaging
*of no clinical significance, except avoid biopsy and distinguish from malignant neoplasms
focal nodular hyperplasia
*not a true neoplasm
*seen most often in women (8:1)
*most are solitary and < 5 cm in size
*usually discovered incidentally with abdominal imaging
*of no clinical significance, except avoid biopsy and distinguish from malignant neoplasms
hepatic adenoma
*uncommon benign tumor of the liver seen in young women, characterized by plates of normal-appearing hepatocytes, without the typical architecture of a liver lobule
*STRONGLY ASSOCIATED WITH ORAL CONTRACEPTIVES
*can enlarge under influence of estrogen (OCP or pregnancy); can regress with d/c of OCPs
*can undergo malignant transformation
*dx based on imaging
*tx: stop estrogens; consider surgical resection
hepatic abscess
*2 major categories: pyogenic & parasitic
*pyogenic result from hematogenous, biliary, or penetrating traumatic introduction of bacteria (untreated appendicitis or diverticulitis); now commonly seen with biliary disease
*parasitic in immigrants; usually amebic or echinococcal infection
*presentation: RUQ pain, fever
*tx: antimicrobials, drainage of abscess
malignant lesions of the liver
*hepatocellular carcinoma (HCC)
*cholangiocarcinoma
*metastatic cancer - most common cancer of liver
risk factors for hepatocellular carcinoma (HCC)
*cirrhosis of any etiology:
-cirrhosis due to HBV, HCV the highest risks
-cirrhosis due to alcohol, PBC, and hereditary hemochromatosis
*hepatitis B carriers without cirrhosis
guidelines for hepatocellular carcinoma (HCC)
*patients with risk factors should be entered into surveillance program:
-ultrasound & alpha-fetoprotein screening at 6 month intervals
hepatocellular carcinoma (HCC) - diagnosis
*almost always based on imaging; rarely biopsied
hepatocellular carcinoma (HCC) - treatment
*surgical resection
*radiofrequency ablation
*liver transplantation
