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Gastroenterology > Disorders of the Liver > Flashcards

Disorders of the Liver Flashcards

1
Q

What is the percentage of the liver must be destroyed before life is threatened?

A

80%

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2
Q

Yellowish coloration of sclera, skin, mucous membranes due to
hyperbilirubinemia

A

Jaundice

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3
Q

Bilirubin needs to be around what level before you see jaundice?

A

2.5

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4
Q

What are the three main categories of jaundice?

A

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

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5
Q

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

A

Hepatic Encephalopathy

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6
Q

What is the pathophysiology of hepatic encephalopathy?

A

Increased arterial ammonia level is the main cause of symptoms and correlates with severity of the dysfunction?

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7
Q

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

A

Lactulose

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8
Q

Often develops with severe hepatic encephalopathy

Leads to increased ICP 🡪 decreased perfusion of the brain 🡪 cerebral
hypoxia

A major cause

A

Cerebral edema

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9
Q

What is the treatment for cerebral edema?

A

IV Mannitol infusion

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10
Q

Pathologic accumulation of fluid within the peritoneal cavity

An osmotic gradient occurs across the pleura, leads to intraabdominal collection of Na, H20, and protein

A

Ascites

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11
Q

List some causes of ascites

A

Advanced liver disease
Portal HTN
Malignancy
infection

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12
Q

What is a complication of ascites we worry about?

A

spontaneous bacterial peritonitis

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13
Q

This occurs in the absence of an intra-abdominal source (appendicitis, etc)

Bacteria translocates across gut wall to ascitic fluid

A

spontaneous bacterial peritonitis

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14
Q

List some organisms responsible for spontaneous bacterial peritonitis

A

Almost all are monomicrobial infections

Anaerobic bacteria not involved

Gram negative: E. coli, Klebsiella pneumonia

Gram positive: Streptococcus pneumonae, Viridians streptococcus

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15
Q

What are some risk factors for spontaneous bacterial peritonitis?

A

Cirrhosis that is decompensating

Cirrhosis/chronic liver failure on PPI long term

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16
Q

What is an important factor to consider in cases of bacterial peritonitis?

A

Important to distinguish from secondary bacterial peritonitis
from an intra-abdominal source

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17
Q

What are some ways to distinguish the different types of bacterial Peritonitis?

A

spontaneous bacterial peritonitis: Almost all are monomicrobial infections

secondary bacterial peritonitis: for secondary, will see multiple organisms

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18
Q

What is the mortality rate of spontaneous bacterial peritonitis if not caught early?

A

High mortality rate >30% if not caught early

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19
Q

Inflammation and necrosis of liver cells resulting from different types
of injury (viral, toxins, etc)

A

Hepatitis

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20
Q

What type of hepatitis accounts for 80-90% of causes?

A

viral hepatitis

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21
Q

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

A

Chronic viral hepatitis

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22
Q

What are the different types of hepatitis?

A

Viral Hepatitis (most common)
Autoimmune Hepatitis
Alcoholic Hepatitis
Drug-Induced Hepatitis

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23
Q

What is the most common type of hepatitis?

A

viral

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24
Q

What is the only way to diagnose a specific virus responsible for hepatitis?

A

Serological testing

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25
Q

What are the four phases of hepatitis?

A

Acute Phase
Prodromal Phase
Icteric Phase
Convalescent Phase

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26
Q

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

A

Acute Phase

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27
Q

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

A

Prodromal Phase

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28
Q

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)

A

Icteric Phase

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29
Q

What phase of hepatitis is described below?

Increasing sense of well-being

Return of appetite

Resolution of Jaundice, Abdominal pain, Fatigue

A

Convalescent Phase

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30
Q

Which types of viral hepatitis may become chronic?

A

Hepatitis B, C, and D

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31
Q

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

A

Hepatitis A

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32
Q

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

A

Hepatitis B

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33
Q

What are some risk factors for Hepatitis B?

A

Working in a healthcare setting

transfusions

Dialysis

Acupuncture

Tattooing

Extended overseas travel to an endemic area

Residence in an institution (correctional facilities)

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34
Q

How is Hepatitis B transmitted?

A

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

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35
Q

Hepatitis B Panel:

Indicates acute HBV infection

A

HBsAg

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36
Q

Hepatitis B Panel:

Appears during incubation period shortly after detection of HBsAg; represents viral replication and infectivity!

A

HBeAg

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37
Q

Hepatitis B Panel:

Appears shortly after HBsAg is detected

A

IgM Anti-HBc

38
Q

Hepatitis B Panel:

Appears during acute hepatitis, but persists indefinitely – no matter if patient recovers or becomes chronic

A

IgG Anti-HBc

39
Q

Hepatitis B Panel:

Immunized or recovered

A

Anti-HBs/HBeAb

40
Q

What are some complications of Hepatitis B?

A

Can progress to fulminant hepatitis or chronic hepatitis

Risk of cirrhosis and/or hepatocellular Ca (HCC) in chronic cases

41
Q

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

A

Hepatitis C

42
Q

What percentage Hep C infection patients develop
chronic Hepatitis C infection?

A

80%

43
Q

What percentage of chronic Hep C patients develop
cirrhosis?

A

20%

44
Q

What percentage of chronic Hep C carriers develop
hepatocellular carcinoma?

A

1-5% of chronic carriers

45
Q

How is Hepatitis C transmitted?

A

Parenteral (IV sticks):
IV drug use – 40%
Transfusion – 5-10%
Healthcare workers – 5%

Maternal-neonatal transmission (small)

Sexual (small) - 10%

46
Q

What are risk factors for acquiring Hepatitis C?

A

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)

47
Q

List some treatment options for Hepatitis C?

A

Peginterferon Alfa-2a IM q weekly for months

Ribavirin tablets PO

Protease inhibitors

Polymerase inhibitors

48
Q

What are some contraindications of Hepatitis C treatment?

A

Psychiatric illness (can make someone suicidal)

Autoimmune disease

Malignancy history

49
Q

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

A

Hepatitis D

50
Q

How is Hepatitis D transmitted?

A

Parenteral – drug addicts, hemophiliacs

Intimate personal contact

51
Q

Enterically transmitted

Associated with large water-borne epidemics in many developing
countries

Usually causes a benign self-limiting illness

High mortality in pregnant patients

A

Hepatitis E

52
Q

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

A

Autoimmune Hepatitis

53
Q

What are the two types of autoimmune hepatitis?

A

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)

54
Q

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

A

Alcoholic Liver Disease

55
Q

How to confirm the diagnosis of alcoholic liver disease?

A

Liver biopsy – confirms diagnosis

56
Q

Fatty Liver Disease is also called what?

A

AKA alcoholic hepatitis and Steatohepatitis

57
Q

Fat deposition in liver cells

Usually found incidentally – usually mild or asymptomatic

Associated with obesity, insulin resistance, diabetes, and dyslipidemia

A

Fatty Liver Disease

58
Q

What is a hallmark of insulin resistance?

A

Steatosis

59
Q

What is the most common cause of cirrhosis?

A

Alcoholic Hepatitis

60
Q

What finding in fatty liver disease indicates a poor prognosis?

A

Prolonged PT/low albumin

61
Q

Which liver enzyme is the higher enzyme in alcoholic hepatitis?

A

AST > ALT

62
Q

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

A

Cirrhosis

63
Q

What are the three stages of cirrhosis?

A

1) compensated

2) compensated with varices

3) decompensated – patient has ascites, hx of variceal bleeding, encephalopathy, underlying jaundice

64
Q

How is the diagnosis of cirrhosis confirmed?

A

Diagnosis confirmed by biopsy

65
Q

List some causes of cirrhosis

A

Chronic viral hepatitis

Drug toxicity

Alcoholism

Other uncommon disorders

66
Q

What is the most important in management of cirrhosis?

A

Abstinence from alcohol is the most important

ZERO tolerance – you cannot drink at all, there is no safe amount

67
Q

What are some complications of cirrhosis?

A

Portal hypertension
Esophageal varices
Ascites
Spontaneous bacterial peritonitis
Wernicke’s encephalopathy

68
Q

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

A

Hereditary Hemochromatosis

69
Q

What is the hallmark lab finding in Hereditary Hemochromatosis?

A

Transferrin sat >50% - hallmark

70
Q

Hemochromatosis is susceptible to what organisms?

A

Listeria monocytogenes
Yersinia enterocolitica
Vibrio vulnificus

71
Q

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

A

Wilson’s Disease

72
Q

This disease is essentially copper poisoning

A

Wilson’s Disease

73
Q

What is the pathophysiology of Wilson’s Disease?

A

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)

74
Q

How does Wilson’s disease typically present?

A

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)

75
Q

Brown rings at corneal margins

A

Kayser-Fleischer rings

76
Q

What is a characteristic finding in Wilson’s disease?

A

Kayser-Fleischer rings

77
Q

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

A

Acetaminophen Toxicity

78
Q

What is the treatment for Acetaminophen Toxicity?

A

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

79
Q

Most frequently identified hepatic mass

A

Hepatic Cysts

80
Q

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

A

Hepatic Cysts

81
Q

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)

A

Hepatocellular Carcinoma

82
Q

You should suspect this condition in a patient with previously stable cirrhosis who presents with rapid and dramatic change

A

Hepatocellular Carcinoma

83
Q

What is the pathophysiology of Hepatocellular Carcinoma (four steps)?

A

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

84
Q

List some causes of Hepatocellular Carcinoma

A

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

85
Q

What is the treatment for Hepatocellular Carcinoma?

A

Surgical resection if tumors are small when found

Very resistant to chemotherapy

86
Q

What is the prognosis for Hepatocellular Carcinoma?

A

Frequently fatal within months

Tumor typically found late

87
Q

What lab can be important in assessing for Hepatocellular Carcinoma?

A

Alpha fetoprotein (AFP)

AFP is increased in 70-90% of patients – AFT can be increased with active hepatocellular necrosis and metastases to liver

88
Q

What is the most common liver tumors?

A

Metastatic Liver Tumors

Metastatic liver tumors are more common than primary liver tumors

89
Q

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

A

Metastatic Liver Tumors

90
Q

What is the treatment for metastatic liver tumors?

A

Resection

Find and treat primary site

Transplant (rare)

Gastroenterology (9 decks)

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