Disorders of the Liver Flashcards

(90 cards)

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
What are the four phases of hepatitis?
Acute Phase Prodromal Phase Icteric Phase Convalescent Phase
26
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
27
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
28
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
29
What phase of hepatitis is described below? Increasing sense of well-being Return of appetite Resolution of Jaundice, Abdominal pain, Fatigue
Convalescent Phase
30
Which types of viral hepatitis may become chronic?
Hepatitis B, C, and D
31
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
32
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
33
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)
34
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
35
Hepatitis B Panel: Indicates acute HBV infection
HBsAg
36
Hepatitis B Panel: Appears during incubation period shortly after detection of HBsAg; represents viral replication and infectivity!
HBeAg
37
Hepatitis B Panel: Appears shortly after HBsAg is detected
IgM Anti-HBc
38
Hepatitis B Panel: Appears during acute hepatitis, but persists indefinitely – no matter if patient recovers or becomes chronic
IgG Anti-HBc
39
Hepatitis B Panel: Immunized or recovered
Anti-HBs/HBeAb
40
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
41
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
42
What percentage Hep C infection patients develop chronic Hepatitis C infection?
80%
43
What percentage of chronic Hep C patients develop cirrhosis?
20%
44
What percentage of chronic Hep C carriers develop hepatocellular carcinoma?
1-5% of chronic carriers
45
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%
46
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)
47
List some treatment options for Hepatitis C?
Peginterferon Alfa-2a IM q weekly for months Ribavirin tablets PO Protease inhibitors Polymerase inhibitors
48
What are some contraindications of Hepatitis C treatment?
Psychiatric illness (can make someone suicidal) Autoimmune disease Malignancy history
49
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
50
How is Hepatitis D transmitted?
Parenteral – drug addicts, hemophiliacs Intimate personal contact
51
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
52
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
53
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)
54
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
55
How to confirm the diagnosis of alcoholic liver disease?
Liver biopsy – confirms diagnosis
56
Fatty Liver Disease is also called what?
AKA alcoholic hepatitis and Steatohepatitis
57
Fat deposition in liver cells Usually found incidentally – usually mild or asymptomatic Associated with obesity, insulin resistance, diabetes, and dyslipidemia
Fatty Liver Disease
58
What is a hallmark of insulin resistance?
Steatosis
59
What is the most common cause of cirrhosis?
Alcoholic Hepatitis
60
What finding in fatty liver disease indicates a poor prognosis?
Prolonged PT/low albumin
61
Which liver enzyme is the higher enzyme in alcoholic hepatitis?
AST > ALT
62
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
63
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
64
How is the diagnosis of cirrhosis confirmed?
Diagnosis confirmed by biopsy
65
List some causes of cirrhosis
Chronic viral hepatitis Drug toxicity Alcoholism Other uncommon disorders
66
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
67
What are some complications of cirrhosis?
Portal hypertension Esophageal varices Ascites Spontaneous bacterial peritonitis Wernicke’s encephalopathy
68
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
69
What is the hallmark lab finding in Hereditary Hemochromatosis?
Transferrin sat >50% - hallmark
70
Hemochromatosis is susceptible to what organisms?
Listeria monocytogenes Yersinia enterocolitica Vibrio vulnificus
71
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
72
This disease is essentially copper poisoning
Wilson’s Disease
73
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)
74
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)
75
Brown rings at corneal margins
Kayser-Fleischer rings
76
What is a characteristic finding in Wilson's disease?
Kayser-Fleischer rings
77
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
78
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
79
Most frequently identified hepatic mass
Hepatic Cysts
80
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
81
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
82
You should suspect this condition in a patient with previously stable cirrhosis who presents with rapid and dramatic change
Hepatocellular Carcinoma
83
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
84
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
85
What is the treatment for Hepatocellular Carcinoma?
Surgical resection if tumors are small when found Very resistant to chemotherapy
86
What is the prognosis for Hepatocellular Carcinoma?
Frequently fatal within months Tumor typically found late
87
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
88
What is the most common liver tumors?
Metastatic Liver Tumors Metastatic liver tumors are more common than primary liver tumors
89
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
90
What is the treatment for metastatic liver tumors?
Resection Find and treat primary site Transplant (rare)