Disorders of the Liver Flashcards
What is the percentage of the liver must be destroyed before life is threatened?
80%
Yellowish coloration of sclera, skin, mucous membranes due to
hyperbilirubinemia
Jaundice
Bilirubin needs to be around what level before you see jaundice?
2.5
What are the three main categories of jaundice?
Pre-hepatic - Due to increased bilirubin production
Hepatic – deficient bile production or bilirubin metabolism due to liver disease
Post-hepatic – due to bile drainage blockage
Complex neuropsychiatric syndrome
Symptoms range from mild confusion to lethargy, stupor, and coma
Specific cause unknow
Graded 1-4
Two forms: Acute and reversible, Chronic and progressive
Hepatic Encephalopathy
What is the pathophysiology of hepatic encephalopathy?
Increased arterial ammonia level is the main cause of symptoms and correlates with severity of the dysfunction?
Synthetic, non-digestible sugar used in the treatment of chronic constipation and hepatic encephalopathy
In treating hepatic encephalopathy, this treatment helps “draw out” anomia (NH3) from the body
Lactulose
Often develops with severe hepatic encephalopathy
Leads to increased ICP 🡪 decreased perfusion of the brain 🡪 cerebral
hypoxia
A major cause
Cerebral edema
What is the treatment for cerebral edema?
IV Mannitol infusion
Pathologic accumulation of fluid within the peritoneal cavity
An osmotic gradient occurs across the pleura, leads to intraabdominal collection of Na, H20, and protein
Ascites
List some causes of ascites
Advanced liver disease
Portal HTN
Malignancy
infection
What is a complication of ascites we worry about?
spontaneous bacterial peritonitis
This occurs in the absence of an intra-abdominal source (appendicitis, etc)
Bacteria translocates across gut wall to ascitic fluid
spontaneous bacterial peritonitis
List some organisms responsible for spontaneous bacterial peritonitis
Almost all are monomicrobial infections
Anaerobic bacteria not involved
Gram negative: E. coli, Klebsiella pneumonia
Gram positive: Streptococcus pneumonae, Viridians streptococcus
What are some risk factors for spontaneous bacterial peritonitis?
Cirrhosis that is decompensating
Cirrhosis/chronic liver failure on PPI long term
What is an important factor to consider in cases of bacterial peritonitis?
Important to distinguish from secondary bacterial peritonitis
from an intra-abdominal source
What are some ways to distinguish the different types of bacterial Peritonitis?
spontaneous bacterial peritonitis: Almost all are monomicrobial infections
secondary bacterial peritonitis: for secondary, will see multiple organisms
What is the mortality rate of spontaneous bacterial peritonitis if not caught early?
High mortality rate >30% if not caught early
Inflammation and necrosis of liver cells resulting from different types
of injury (viral, toxins, etc)
Hepatitis
What type of hepatitis accounts for 80-90% of causes?
viral hepatitis
continued disease activity > 6 months
Occurs more frequently in acute Hepatitis C (75% of cases)
Inflammation is confined to portal triads without destruction of normal liver tissue
Chronic viral hepatitis
What are the different types of hepatitis?
Viral Hepatitis (most common)
Autoimmune Hepatitis
Alcoholic Hepatitis
Drug-Induced Hepatitis
What is the most common type of hepatitis?
viral
What is the only way to diagnose a specific virus responsible for hepatitis?
Serological testing
What are the four phases of hepatitis?
Acute Phase
Prodromal Phase
Icteric Phase
Convalescent Phase
What phase of hepatitis is described below?
Usually lasts a few weeks with complete clinical and laboratory
recovery
<1% will have an acute fulminant course
This phase is often unnoticed
Acute Phase
What phase of hepatitis is described below?
Symptomatic:
Low grade fever
Nausea
Vomiting
RUQ or epigastric abdominal pain
Anorexia
Malaise
Myalgias/arthralgias
Fatigue
Aversion to smoking
Prodromal Phase
What phase of hepatitis is described below?
Jaundice (in some patients) - Bilirubin needs to be around 2.5
before you see jaundice
Icteris of sclera
Worsening of the prodromal symptoms
Ask if their urine is dark or if their stool is clay colored (bilirubin)
Icteric Phase
What phase of hepatitis is described below?
Increasing sense of well-being
Return of appetite
Resolution of Jaundice, Abdominal pain, Fatigue
Convalescent Phase
Which types of viral hepatitis may become chronic?
Hepatitis B, C, and D
An acute, short-lived illness with a very low mortality rate and no long term sequela
65% of causes of hepatitis in the US
Generally self-limited, will never be chronic
Fecal-oral transmission
Low mortality
Hepatitis A
Longer and more insidious onset
Longer course of the disease, slower recovery
Clinical outcome depends on host defense
Incubation period is 6 weeks to 6 months
Insidious onset: urticaria, rash, arthralgia
Chronic carrier (US) – 5-10%
Risk of chronicity related to age – 90% infants, immune status
90% of patients recover completely
Hepatitis B
What are some risk factors for Hepatitis B?
Working in a healthcare setting
transfusions
Dialysis
Acupuncture
Tattooing
Extended overseas travel to an endemic area
Residence in an institution (correctional facilities)
How is Hepatitis B transmitted?
Parenteral (IV drug use) – 35%
Sexual contact – 19% (Easier to transmit HBV sexually than HCV)
Transfusion – 5%
Needlestick – 1%
Present in blood, saliva, semen, and vaginal secretions
Mother may transmit HBV to neonate: 90% risk of chronic infection, a major route in developing countries
Hepatitis B Panel:
Indicates acute HBV infection
HBsAg
Hepatitis B Panel:
Appears during incubation period shortly after detection of HBsAg; represents viral replication and infectivity!
HBeAg
Hepatitis B Panel:
Appears shortly after HBsAg is detected
IgM Anti-HBc
Hepatitis B Panel:
Appears during acute hepatitis, but persists indefinitely – no matter if patient recovers or becomes chronic
IgG Anti-HBc
Hepatitis B Panel:
Immunized or recovered
Anti-HBs/HBeAb
What are some complications of Hepatitis B?
Can progress to fulminant hepatitis or chronic hepatitis
Risk of cirrhosis and/or hepatocellular Ca (HCC) in chronic cases
Most common blood-borne infection
Leading cause of chronic liver failure
Most common indication for transplant
High rate of chronic hepatitis (>80%)
In the past >90% of cases were from blood transfusions
Up to 50% of cases are from IV drug use
~3.2 million people are chronically infected
Hepatitis C
What percentage Hep C infection patients develop
chronic Hepatitis C infection?
80%
What percentage of chronic Hep C patients develop
cirrhosis?
20%
What percentage of chronic Hep C carriers develop
hepatocellular carcinoma?
1-5% of chronic carriers
How is Hepatitis C transmitted?
Parenteral (IV sticks):
IV drug use – 40%
Transfusion – 5-10%
Healthcare workers – 5%
Maternal-neonatal transmission (small)
Sexual (small) - 10%
What are risk factors for acquiring Hepatitis C?
IV drug use
Tattoo/body piercing (particularly prison systems)
HIV infection
Healthcare workers
Received clotting factor before 1987
H/O organ transplant before 7/92
Persistently increased ALT
Sharing personal hygiene tools with infected individuals (razors, toothbrush, etc)
List some treatment options for Hepatitis C?
Peginterferon Alfa-2a IM q weekly for months
Ribavirin tablets PO
Protease inhibitors
Polymerase inhibitors
What are some contraindications of Hepatitis C treatment?
Psychiatric illness (can make someone suicidal)
Autoimmune disease
Malignancy history
Non-pathogenic by itself – can only replicate if HepBsAg is present
Must be in conjunction with HBV to be pathologic
Tends to accelerate the progress of liver disease associated with HBV
infection
Hepatitis D
How is Hepatitis D transmitted?
Parenteral – drug addicts, hemophiliacs
Intimate personal contact
Enterically transmitted
Associated with large water-borne epidemics in many developing
countries
Usually causes a benign self-limiting illness
High mortality in pregnant patients
Hepatitis E
Occurs in children and adults (all ages)
Etiology is unknown
Presentation ranges from asymptomatic to fulminant liver failure
Can exist with Hepatitis C
May lead to primary HCC
Autoimmune Hepatitis
What are the two types of autoimmune hepatitis?
Type 1 (classic) - Characterized by circulating antibodies to nuclei (ANA) and/or smooth muscle (ASMA)
Type 2 - Defined by the presence of antibodies to liver/kidney microsomes (anti-LKM1)
Manifested by one or more of the following: Hepatitis, Cirrhosis, Fatty liver (steatosis)
Acute inflammation and necrosis of hepatocytes
Occurs when chronic alcoholics binge drink and drink higher quantities
than usual
Chronic EtOH > 80g/day in men and 30-40g/day in women
Symptoms range from mild to severe
Alcoholic Liver Disease
How to confirm the diagnosis of alcoholic liver disease?
Liver biopsy – confirms diagnosis
Fatty Liver Disease is also called what?
AKA alcoholic hepatitis and Steatohepatitis
Fat deposition in liver cells
Usually found incidentally – usually mild or asymptomatic
Associated with obesity, insulin resistance, diabetes, and dyslipidemia
Fatty Liver Disease
What is a hallmark of insulin resistance?
Steatosis
What is the most common cause of cirrhosis?
Alcoholic Hepatitis
What finding in fatty liver disease indicates a poor prognosis?
Prolonged PT/low albumin
Which liver enzyme is the higher enzyme in alcoholic hepatitis?
AST > ALT
The irreversible end stage of hepatic injury
Characterized by diffuse hepatic fibrosis and regenerating nodules 🡪
permanent changes in hepatic blood flow and liver function
12th leading cause of death in US
Most patients are asymptomatic for years
Cirrhosis
What are the three stages of cirrhosis?
1) compensated
2) compensated with varices
3) decompensated – patient has ascites, hx of variceal bleeding, encephalopathy, underlying jaundice
How is the diagnosis of cirrhosis confirmed?
Diagnosis confirmed by biopsy
List some causes of cirrhosis
Chronic viral hepatitis
Drug toxicity
Alcoholism
Other uncommon disorders
What is the most important in management of cirrhosis?
Abstinence from alcohol is the most important
ZERO tolerance – you cannot drink at all, there is no safe amount
What are some complications of cirrhosis?
Portal hypertension
Esophageal varices
Ascites
Spontaneous bacterial peritonitis
Wernicke’s encephalopathy
What toxic liver disease is described below?
Increased level of iron absorption and excessive accumulation in vital organs
Excessive iron loading of tissue caused by primary genetic defect of HFE gene on chromosome 6
Usually presents after age 50
Pattern of disease correlates with level of iron accumulation
Up to 25% of patients develop hepatocellular carcinoma
Hereditary Hemochromatosis
What is the hallmark lab finding in Hereditary Hemochromatosis?
Transferrin sat >50% - hallmark
Hemochromatosis is susceptible to what organisms?
Listeria monocytogenes
Yersinia enterocolitica
Vibrio vulnificus
What toxic liver disease is described below?
Excessive amounts of copper accumulate in the brain, liver, kidneys and cornea due to low levels of ceruloplasmin (protein that carries copper)
Linked to ATP7B gene which causes the retention of copper in the liver and impaired incorporation of copper into ceruloplasmin
Hepatocyte degeneration
Rare, autosomal recessive disorder
People under 40
Wilson’s Disease
This disease is essentially copper poisoning
Wilson’s Disease
What is the pathophysiology of Wilson’s Disease?
Copper doesn’t pass through the liver and accumulates
Damaged liver allows copper into bloodstream 🡪 circulates and is deposited in kidneys primarily, but also brain, nervous system, and eyes
(Normal: Copper is processed in the liver 🡪 gallbladder 🡪 duodenum 🡪 through intestine 🡪 excreted in stool)
How does Wilson’s disease typically present?
Usually presents before age 50 in one of the three following ways:
Intravascular hemolytic anemia
Hepatic dysfunction in children (Begins as hepatomegaly, fatty liver, and LFT elevation)
Neuropsychiatric illness (Seen as a movement disorder or rigid dystonia or as psychiatric symptoms)
Brown rings at corneal margins
Kayser-Fleischer rings
What is a characteristic finding in Wilson’s disease?
Kayser-Fleischer rings
What toxic liver disease is described below?
Causes severe hepatic necrosis when ingested in large amounts (accidental by children, Suicide attempt)
Fatal fulminant disease is associated with > 25g
Serum levels correlate with level of injury - Hepatic injury is thought to occur when protective levels of glutathione are low or depleted and detoxicification cannot occur
Acetaminophen Toxicity
What is the treatment for Acetaminophen Toxicity?
Airway, breathing, circulation
Activated charcoal 50g if within 4 hours of ingestion
Sulfhydryl compounds (N-acetylcysteine) reduce severity of necrosis – either bind toxic metabolites or stimulate synthesis and repletion of glutathione
Most frequently identified hepatic mass
Hepatic Cysts
What type of liver neoplasm is described below?
Most frequently identified hepatic mass
Incidental finding – benign
Ultrasound shows clearly demarcated lesion
CT may no identify cysts < 2cm
Hepatic Cysts
What type of liver neoplasm is described below?
Arise from liver parenchyma
History of hepatitis B, hepatitis C, and cirrhosis
Tumors are frequently large and multiple on presentation
Account for 90-95% of tumors
Males > females (6 to 1)
Hepatocellular Carcinoma
You should suspect this condition in a patient with previously stable cirrhosis who presents with rapid and dramatic change
Hepatocellular Carcinoma
What is the pathophysiology of Hepatocellular Carcinoma (four steps)?
Initiation: infection/chemical exposure leads to fixed genetic change, cell is responsive to promotion
Promotion: necrosis, inflammation, or specific chemicals 🡪 liver regeneration and active or inactive cirrhosis
Progression: malignant cells reproduce clones
Cancer: macroscopic foci of HCC 🡪 clinical cancer
List some causes of Hepatocellular Carcinoma
Ionizing radiation
Chemicals (Aflatoxin mold (Aspergillus flavus), Vinyl chloride monomer (PVCs))
Viral agents (Hep B and C)
Trematodes (liver flukes) - Schistosomiasis
Cirrhosis
Drugs and alcohol
Genetic
What is the treatment for Hepatocellular Carcinoma?
Surgical resection if tumors are small when found
Very resistant to chemotherapy
What is the prognosis for Hepatocellular Carcinoma?
Frequently fatal within months
Tumor typically found late
What lab can be important in assessing for Hepatocellular Carcinoma?
Alpha fetoprotein (AFP)
AFP is increased in 70-90% of patients – AFT can be increased with active hepatocellular necrosis and metastases to liver
What is the most common liver tumors?
Metastatic Liver Tumors
Metastatic liver tumors are more common than primary liver tumors
Most common liver tumors
Metastatic liver disease is frequently the first sign of a tumor
Major site of blood-borne metastases from within the abdomen
Common site of metastases from tumors above the diaphragm
Colon, bile duct, pancreas, ovary, breast, lung, prostate
These are more common than primary liver tumors
Metastatic Liver Tumors
What is the treatment for metastatic liver tumors?
Resection
Find and treat primary site
Transplant (rare)
