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GI II Exam 2 EH > Lecture 11: Diseases of the Liver > Flashcards

Lecture 11: Diseases of the Liver Flashcards

1
Q

Anorexia, nausea, vomiting, malaise, and aversion to smoking are characteristic early symptoms of which viral infections?

A

HAV and HBV

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2
Q

What is the #1 risk factor for contracting HAV?

A

International travel

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3
Q

Detection of what antibody is an excellent test for diagnosing ACUTE HAV?

A

IgM anti-HAV

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4
Q

Glomerulonephritis, serum sickness, and polyarteritis nodosa are symptoms that may arise with what type of hepatitis viral infection?

A

HBV

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5
Q

Which labs may be elevated in HAV infection?

A
  • Markedly elevated AST/ALT
  • Elvated bilirubin and alkaline phosphatase = Cholestasis
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6
Q

Which antibody indicates immunity/clearance of HBV?

A

Anti-HBs Ab

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7
Q

Persistence of what in the serum for >6 months after acute illness w/ HBV signifies a chronic HBV infection?

A

HBsAg

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8
Q

Which antibody appears during acute HBV infection and persists indefinetely?

A

IgG anti-HBc

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9
Q

Which subset of patients have shown chronic infections due to HEV with progression to cirrhosis?

A

Transplant pts treated w/ tacrolimus

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10
Q

If an unvaccinated person is exposed to HBV (i.e., during sex or at birth) what is the recommended therapy?

A
  • Give hepatitis B immunoglobulin (HBIG) immediately up to 14 days post-exposure
  • Also give them the vaccine (3 doses)
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11
Q

What is the most sensitive indicator of HCV infection?

A

HCV RNA

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12
Q

If a patient is found to have anti-HCV in serum, without HCV RNA in the serum what does this indicate?

A

Recovery from prior HCV infection

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13
Q

What is the effect of chronic HCV infection on serum cholesterol levels?

A

Decreased

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14
Q

What is the only marker found in the serum during the “window period” of HBV infection?

A

IgM anti-HBc Ab

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15
Q

Which hepatitis viruses can become chronic?

A
  • HBV
  • HCV
  • HDV (w/ HBV)
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16
Q

Mixed cryiglobulinemia is an extraintestinal manifestation associated with chronic infection by which virus?

A

HCV

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17
Q

Which 2 tests can ID presence or absence of fibrosis (cirrhosis) in chronic hepatitis?

A
  • Serum FibroSure and/or
  • US elastography
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18
Q

What are 2 drugs associated with idiosyncratic drug induced liver injury?

A
  • Isoniazid
  • Sulfonamides
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19
Q

What are 2 common dose-depent causes of drug/toxin induced liver injury?

A
  • Mushroom poisoning
  • Acetaminophen
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20
Q

What is the specific therapy used in treating acetaminophen OD’s?

Important to check acetaminophen at what time period?

A
  • Treat w/ sulfhydryl compounds (N-acetylcysteine aka NAC)
  • Important to get a 4 hour acetaminophen level
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21
Q

How soon should therapy be administered for somone who ingests a toxic dose of acetaminophen?

A

Within 8 hours, but may be effective if given as late as 24-36 hrs after OD

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22
Q

Which tool is used during the assessment/treatment of someone with a suspected Acetaminophen OD?

A

Rumack-Matthew Nomogram

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23
Q

Massive hepatic necrosis with impaired consciousness occuring within 8 weeks of the onset of illness is known as?

A

Fulminant Hepatitis

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24
Q

What are the findings that when summed together equal hepatic failure with encephalopathy?

What is occuring to levels of aminotransferases?

A
  • Rapidly shrinking liver + Rapidly rising bilirubin + marked prolongation of the PT + clinical signs of confusion, disorientation, somnolence, ascites, and edema
  • Even as aminotransferase levels fall!
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25
Q

The intake of what should be restricted in a patient with hepatic failure + encephalopathy?

A

Protein

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26
Q

Which drugs should be administered in someone suffering from hepatic failure w/ encephalopathy?

A

Lactulose or Neomycin

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27
Q

Meticulous intensive care + _____________ = one factor that improves survival in patients with hepatic failure + encephalopathy?

A

Prophylactic antibiotic coverage

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28
Q

Which 2 values are used to calculate a Maddrey’s discriminant function?

Used in which patients to assess what?

A
  • PT and serum bilirubin
  • Used to assess risk of mortality in pts with alcoholic hepatitis
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29
Q

Which calculated value associated w/ a Maddrey’s discriminant function indicates a poor prognosis in pts with alcoholic hepatitis?

A

≥32

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30
Q

A score of what calculated using the Model for End-Stage Liver Disease (MELD) is associated w/ significant mortality in alcoholic hepatitis?

A

>21

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31
Q

Glasgow Alcoholic Hepatitis Score predicts mortality using which 5 factors?

Patients receiving which drug and a score of ≥9 have higher survival rates than those who didn’t?

A
  • Age, Serum bilirubin, BUN, PT, and peripheral WBC count
  • ≥9 who received glucocorticoids
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32
Q

In patients with alcoholic steatosis what may be the only laboratory abnormality?

A

Mild liver enzyme elevations

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33
Q

Leukocytosis with a shift to the left is common in patients in which stage of alcohol related liver damage?

A

Severe alcoholic hepatitis

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34
Q

A liver biopsy of a patient with alcoholic hepatitis will often have identical findings of what other disorder?

A

Nonalcoholic steatohepatitis

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35
Q

What are the serum levels of AlkPhos, GGT, and bilirubin like in a patient with alcoholic hepatitis?

A

Typically elevated

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36
Q

If glucose is administered during the treatment of somone with alcoholic hepatitis what must be added?

A

Thiamine –> can precipitate Wernicke-Korsakoff if not given

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37
Q

A patient with alcoholic hepatitis should be given what supplements during treatment?

A
  • Thiamine
  • Daily MV
  • Folic acid
  • Zinc
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38
Q

Wernicke Encephalopathy vs. Korsakoff Syndrome?

A

Wernicke = confusion, ataxia, and involuntary eye movements

Korsakoff = severe memory issues, confabulation/making up stories

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39
Q

With severe alcoholic hepatitis (discriminant function ≥32 or MELD >20) what therapy should be considered?

What is an alternative to this therapy and has demonstrated improved survival (decreased hepatorenal syndrome)?

A
  • Steroids
  • Pentoxifylline = has demonstrated improved survivial (decreased hepatorenal syndrome)
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40
Q

What is absolutely critical for a patient with severe alcoholic hepatitis to do if they are to be considered for a liver transplant?

A

Abstain from alcohol for 6 months

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41
Q

Which ethnic group are at increased risk for NAFLD?

A

Hispanics

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42
Q

What are 2 factors that protect against the development of NAFLD?

A

1) Coffee
2) Exercise

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43
Q

Which toxin is associated with fatty liver change?

A

Vinyl chloride

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44
Q

What is the histological characteristic of NAFLD?

A

Focal infiltration by PMN’s and Mallory hyaline

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45
Q

Cirrhosis caused by NASH appears to be uncommon in which ethnic group?

A

African Americans

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46
Q

Lab values in person with NAFLD?

A
  • Mildly elevated Aminotransferase and AlkPhos
  • 80% of patients with hepatic steatosis will have normal labs!
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47
Q

Most common signs and symptoms of PBC?

A
  • Pruritus
  • Fatigue
  • Progressive jaundice
  • Xanthelasma
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48
Q

What are 4 relevant pieces of someones hx that are risk factors for PBC?

A

1) UTI’s (caused by E. coli or L. delbrueckii)
2) Smoking
3) Use of Hormone Replacement Therapy
4) Hair dye

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49
Q

Autoimmune hepatitis is associated with an increased risk for what cancer?

A

Heptaocellular CA

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50
Q

Which drug is used for the treatment of Autoimmune Hepatitis?

A

Glucocorticoids

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51
Q

Hemochromatosis typically manifests when?

A

After the age of 50

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52
Q

Major clinical manifestations of Hemochromatosis?

A
  • Hepatic abnormalities –> Cirrhosis
  • Heart failure
  • Hypogonadism
  • Arthritis
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53
Q

Patients with Hemochromatosis are at an increased risk for infection by what 3 organisms?

A
  1. Vibrio vulnificus
  2. Listeria monocytogenes
  3. Yersinia enterocolitica
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54
Q

What are the major lab findings associated with Hemochromatosis?

A
  • Mildly abnormal liver tests (ALT, AlkPhos)
  • Elevated plasma iron w/ GREATER than 45% transferrin saturation
  • Elevated serum ferritin
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55
Q

What are 3 risk factors for advanced fibrosis in a patient w/ Hemochromatosis?

A
  1. Male sex
  2. Excess alcohol consumption
  3. Diabetes
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56
Q

Iron studies and HFE testing should be done in whom?

A

ALL first-degree family members

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57
Q

What should patients with Hemochromatosis avoid in their diet?

A
  • Foods rich in iron (i.e., red meat) + iron supplements
  • Alcohol
  • Vitamin C
  • Raw shellfish
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58
Q

Which treatment is indicated for all symptomatic patients w/ Hemochromatosis?

A

Weekly phlebotomies of 1 or 2 units of blood

59
Q

What can be given to patients that have hemochromatosis + anemia or w/ secondary iron overload due to thalassemia who cannot tolerate phlebotomies?

A

Deferoxamine

60
Q

Wilson disease is associated with excess copper deposition in the tissue, especially in which 4 places?

A
  • Liver
  • Brain
  • Cornea
  • Kidney
61
Q

Low serum _______ levels can be useful in the diagnosis of Wilson Disease

A

Ceruloplasmin

62
Q

Budd-Chiari Syndrome is associated with __________ (painful/painless) hepatomegaly, jaundice, splenomegaly, and ascites

A

Budd-Chiari Syndrome is associated with painful hepatomegaly, jaundice, splenomegaly, and ascites

63
Q

Caval webs and right-sided heart failure lead to what characteristic liver finding in Budd-Chiari Syndrome?

A

Nutmeg liver = centrilobular congestion

64
Q

What is the screening test of choice for Budd-Chiari syndrome?

Which lobe of the liver will be most prominent?

A
  • Contrast-enhanced US (CEUS) —-> Color or pulsed-Doppler US
  • Prominent CAUDATE liver lobe
65
Q

Treatments of choice fo alpha-1 anti-trypsin deficiency?

A
  • Smoking abstinence/cessation
  • Liver transplant
66
Q

Which therapy given prior to admission of someone with heart failure may protect against ischemic hepatitis?

A

Statin therapy

67
Q

What are the hallmark lab findings associated with ischemic hepatitis due to heart failure?

A
  • Elevation of serum aminotrasnferase levels, often >5000 units/L
  • Early rapid rise in the serum LDH level
68
Q

In right heart failure and patients with passive congestion of the liver (“nutmeg liver”) which reflux is present?

With tricuspid regurgitation what may be seen at the liver?

A
  • Hepatojugular reflux is present
  • With tricuspid regurgiation the liver may be pulsatile
69
Q

What are the 3 major causes of non-cirrhotic portal HTN?

A
  1. Portal vein thrombosis
  2. Splenic vein obstruction = gastric varices w/o esophageal varices
  3. Schistosomiasis
70
Q

Treatment of thrombocytopenia with eltrombopag has been shown to be a risk factor for what?

A

Noncirrhotic Portal HTN

71
Q

Symptoms/signs of noncirrhotic portal HTN?

Especially if due to acute portal vein thrombosis?

A
  • Acute portal vein thrombosis usually causes abdominal pain
  • Splenomegaly
  • GI bleeding
72
Q

If splenic vein thrombosis is the cause of variceal bleeding, which procedure is curative?

A

Splenectomy

73
Q

What is the most common identifiable cause of hepatic abscess in the US?

Some cases (10%) due to what other causes?

A
  • Ascending cholangitis = most common
  • Appendicitis or Diverticulitis = 10% of cases
74
Q

What are the most frequently encountered organisms responsible for Hepatic Abscesses/Ascending Cholangitis?

A
  • E. coli
  • Klebsiella pneumoniae
  • Enterobacter aerogenes
  • Proteus vulgaris
75
Q

Pyogenic liver abscess has been observed ti be associated with an increased risk of?

A

GI malignancy

76
Q

What is the most common benign neoplasm of the liver?

How is most often discovered?

A
  • Cavernous hemangioma
  • Often incidental finding on US or CT
77
Q

Cavernous hemangiomas are known to enlarge in whom?

A

Woman who take hormonal therapy

78
Q

Which hypervascular mass found in the liver is not a true neoplasm, but instead a proliferation of hepatocytes in reponse to altered blood flow?

A

Focal nodular hyperplasia

79
Q

Are oral contraceptives a risk factor for focal nodular hyperplasia of the liver?

A

Probably NOT

80
Q

Which benign neoplasm of the liver occurs most commonly in women in the the 3rd-4th decades of life?

Major risk factor?

A
  • Hepatocellular adenoma
  • Usually caused by oral contraceptives
81
Q

Which benign neoplasm of the liver is hypervascular and which is hypovascular?

A
  • Focal nodular hyperplasia = HYPERvascular
  • Hepatocellular adenoma = HYPOvascular
82
Q

The only physical finding in focal nodular hyperplasia or hepatocellular adenoma is what in a minority of cases?

A

Palpable abdominal mass

83
Q

Which 2 imaging techniques can distinguish an hepatocellular adenoma from focal nodular hyperplasia in 80-90% of cases?

A
  • Arterial phase helical CT, and
  • Multiphase dynamic MRI w/ contrast
84
Q

What is the treatment for focal nodular hyperplasia?

Discountinuation of OC’s?

A
  • OC’s should not necessarily be discontinued
  • Affected women should undero annual US for 2-3 yrs to ensure lesion is not enlarging
85
Q

What is the treatment for Hepatocellular Adenomas?

Discountinuation of OC’s?

A
  • Resection is advised in all affected men/women in whom the tumor causes sx’s or is 5cm or > in diameter, even in absence of sx’s
  • Regression may follow cessation of OC’s
86
Q

What is the initial treatment for a Hepatocellular Adenoma that is complicated by hemorrhage?

A

Transarterial embolization

87
Q

What are the 3 types of Cirrhosis which can be present?

A
  1. Compensated
  2. Compensated w/ varices
  3. Decompensated (ascites, variceal bleeding, encephalopathy, or jaundice)
88
Q

Which dermatologic manifestations may be present with Cirrhosis?

A
  • Palmar erythema
  • Spinger telangiectasias
  • Jaundice
  • Glossitis and Cheilosis –> related to vitamin deficiencies
89
Q

A CBC of someone with Cirrhosis will characteristically show what?

PT time?

A
  • Anemia (microcytic due to blood loss, macrocytic due to folate deficiency; hemolytic)
  • Pancytopenia (hypersplenism)
  • Prolonged PT
90
Q

What are the characteristic chemistry labs (Na+, K+, glucose, and albumin) associated with Cirrhosis?

A
  • Hyponatremia
  • Hypokalemic alkalosis
  • Glucose disturbances
  • Hypoalbunimemia
91
Q

Higher consumption of what has been reported to reduce risk of cirrhosis?

A
  • Coffee
  • Tea
92
Q

Which GI malabsorption syndromes have been implicated in the development of Cirrhosis?

A
  • Celiac disease
  • Cystic Fibrosis
93
Q

4 most common causes of Cirrhosis?

A
  1. Alcohol
  2. Chronic HCV infection
  3. NAFLD
  4. HBV infection
94
Q

Definitive diagnosis of Cirrhosis often depends on?

A

Liver biopsy –> percutaneous, jugular, or open

95
Q

Which scoring system can be used to predict the severity of cirrhosis and risk of complications?

A

Child-Pugh scoring system

96
Q

What findings/labs are necessary to use the Child-Pugh scoring system for cirrhosis?

A
  • Order: CMP or Hepatic function panel (serum bilirubin, albumin), PT/INR
  • PE for: ascites and encephalopathy
97
Q

Patients with Cirrhosis are at increased risk for what metabolic sydrome?

What vitamin deficiency is often present?

A
  • Diabetes mellitus
  • Vitamin D deficiency
98
Q

Elevation of the hepatic venous pressure gradient with portal HTN is associated with an increase in which pressure (Starling)?

A

Increased hydrostatic pressure

99
Q

Portal vein thrombosis, Splenic vein thrombosis, and Massive Splenomegaly are _____-hepatic causes of portal HTN

A

Portal vein thrombosis, Splenic vein thrombosis, and Massive Splenomegaly are pre-hepatic causes of portal HTN

100
Q

What are 2 sinusoidal causes of portal HTN?

A

1) Cirrhosis
2) Alcoholic hepatitis

101
Q

Hepatic sinusoidal obstruction (venoocclusive syndrome) is classified as being a __________ cause of portal HTN

A

Hepatic sinusoidal obstruction (venoocclusive syndrome) is classified as being a postsinusoidal cause of portal HTN

102
Q

Which class of drugs recommended to reduce the risk of 1st variceal hemorrhage in pts with medium/large varices or pts with small varices that have variceal red wale marks or advanced cirrhosis?

A

Nonselective beta-adrenergic blockers

103
Q

Which 2 diagnostic modalities can be utilized to determine whether varices are present in a pt?

A
  • EGD
  • Capsule endoscopy
104
Q

Encephalopathy may complicate an episode of GIB in patients with severe liver disease, which drug can be given to combat this and is the mainstay of treatment?

105
Q

What are the 4 stages of overt encephalopathy associated with severe liver disease?

A
  1. Mild confusion
  2. Drowsiness
  3. Stupor
  4. Coma
106
Q

Most common cause of ascites is __________ secondary to ________.

A

Most common cause of ascites is portal HTN secondary to chronic liver disease.

107
Q

Which imaging modality reliably establishes the presence of fluid in ascites?

A

Abdominal ultrasound

108
Q

Which technique is performed on all patients with new onset ascites, patients admitted to hospital w/ cirrhosis + ascites, and when pts with known ascites deteriorate clinically?

A

Abdominal paracentesis

109
Q

What is the most important test/study performed on ascitic fluid?

A

WBC count w/ differential

110
Q

Which finding on examination of Ascitic Fluid is highly suggestive of spontaneous bacterial peritonitis (SBP)?

A

PMN count greater than 250/mcL (neutrocytic ascites)

111
Q

Which study performed on Ascitic Fluid is the single best test for classification of ascites?

A

Serum-ascites albumin gradient (SAAG)

112
Q

What does an SAAG of 1.1 g/dL or more vs. SAAG of less than 1.1 g/dL tell you about the classification of the ascites?

A
  • Portal HTN = SAAG of 1.1 g/dL or more
  • Nonportal HTN = SAAG of less than 1.1 g/dL
113
Q

How is the serum-ascites albumin gradient (SAAG) calculated?

*One of the LO’s!*

A

Ascitic fluid albumin - serum albumin

114
Q

Abdominal US + Doppler allows for vascular evaluation and to detect which cause of hepatic dysfunction?

A

Budd-Chiari syndrome

115
Q

What is the SAAG value associated with Hypoalbuminemia and its associated causes i.e., Nephrotic Syndrome, Protein-losing enteropahty, and Severe malnutrition w/ anasarca?

A

SAAG = < 1.1 g/dL

116
Q

Myxedema (aka severe hypothyroidism) is associated with an SAAG value of?

A

SAAG = >1.1 g/DL

117
Q

A diseased peritoneum associated w/ infections, malignant conditions, and others (i.e., familial meditteranean fever, vasculitis, granulomatous peritonitis, and eosiniphilic peritonitis) is associated with what SAAG value?

A

SAAG = <1.1 g/dL

118
Q

Spontaneous (primary) bacterial peritonitis (SBP) occurs in the absence of?

A

Absence of an apparent intra-abdominal source of infection

119
Q

Which type of bacteria are not assocated with spontaneous bacterial peritonitis?

A

Anaerobic bacteria

120
Q

Spontaneous bacterial peritonitis is caused by a (mono/polymicrobial) infection?

A
  • Monomicrobial
  • Most common = E. coli, Klebsiella, S. pneumonia, V. streptococci, Enterococcus
121
Q

What is the most important diagnostic test for Spontaneous (primary) Bacterial Peritonitis?

A

Abdominal paracentesis —> WBC count w/ differential

122
Q

How is the cause of secondary bacterial peritonitis different from spontaneous bacterial peritonitis?

How can they be distinguished?

A
  • Secondary is due to ascitic fluid becoming secondarily infected by an intra-abdominal cause
  • Presence of multiple organisms on ascitic fluid gram stain or culture is diagnostic of seondary peritonitis
123
Q

Since 70% of people who survive an episode of SBP will have another episode within 1 year, what is done clinically as prevention?

A

Oral once-daily prophylactic therapy

124
Q

What is the emperic therapy for SBP?

A
  • Third-generation cephalosporin IV (Cefotaxime or Ceftriaxone), OR
  • Combo beta-lactam/beta-lactamase agent (Ampicillin/Sulbactam)
125
Q

Due to a high risk of nephrotoxicity in patients with chronic liver disease which antibiotic class should not be used to treat SBP?

A

Aminoglycosides

126
Q

What type of injury develops in 40% of patients with SBP and is a major cause of death?

How can this be dealt with clinically?

A
  • Kidney injury
  • Give IV albumin
127
Q

What is the most effective treatment for reccurent SBP?

A

Liver transplant

128
Q

Malignant ascites is associated with which value of SAAG?

Most common causes are primary adenocarcinomas arising from where?

A
  • SAAG = < 1.1 g/dL
  • Ovary, uterus, pancreas, stomach, colon, lung, or breast
129
Q

Symptoms presenting in a patient younger than 20 with episodic bouts of acute peritonitis that may be associated with serositis involving the joints and pleura is associated with what disorder?

A

Familial Mediterranean Fever

130
Q

Familial Mediterranean Fever is characterized by peritoneal attacks w/ sudden onset of fever, severe abdominal pain, and tenderness, what occurs if these attacks are left untreated?

A

Resolve witin 24-48 hours

131
Q

Which medication has been shown to decrease the frequency and severity of the peritoneal attacks associated with Familial Mediterranean Fever?

A

Colchicine

132
Q

What is the ascitic fluid and cytology like in Mesothelioma?

A
  • Ascitic fluid often hemorrhagic
  • Cytology is often negative
133
Q

Which type of ascites is characterized by the accumulation of milky, lipid-rich lymph in the peritoneal cavity w/ triglyceride levels >1000 mg/dL?

Most common cause(s)?

A
  • Chylous Ascites
  • Lymphoma, post-op trauma, cirrhosis, tuberculosis, pancreatitis, and filariasis
134
Q

Is pain associated with Pancreatic Ascites?

A

NO, since pancreatic enzymes are not acitvated

135
Q

What will paracentesis of Bile Ascites reveal?

Ratio of ascites bilirubin to serum bilirubin?

A
  • Yellow fluid on paracentesis
  • Ascites bilirubin:serum bilirubin = >1.0
136
Q

Most important treatment measure for Cirrhosis?

Which vaccines should be given?

A
  • Abstinence from alcohol = most important
  • HAV, HBV, pneumococcal, and yearly influenza should be given
137
Q

Which drug is contraindicated in cirrhosis?

Which 2 drug classes should be avoided?

A
  • NSAIDs = CONTRAINDICATED
  • ACE inhibitors and Angiotensin II antagonists = should be avoided
138
Q

Which procedure has shown benefit in the treatment of severe refractory ascites, and is an effective tx of variceal bleeding refractory to standard treatment (i.e., endoscopic band ligation)?

A

Transjugular Intraheptic Portosystemic Shunt (TIPS)

139
Q

What has been associated with mortality after TIPS procedure?

A
  • Chronic kideny disease
  • Diastolic cardiac dysfunction
  • Refractory encephalopathy
  • Hyperbilirubinemia
140
Q

What is often the precipitating even of Hepatorenal Syndrome and how do the kidneys appear histologically?

A
  • Acute decrease in cardiac output = precipitating event
  • Kidneys appear normal
141
Q

Treatment of choice for Hepatorenal Syndrome?

A

Liver transplant

142
Q

What are the 2 prognostic scoring systems for Cirrhosis?

A

1) Child-pugh score –> CMP or HFP (serum bilirubin, albumin), PT/INR and PE for ascites and encephalopathy
2) MELD score —> CMP (serum bilirubin and creatinine), PT/INR

143
Q

What tests must be ordered to calculate a MELD score?

*NEED TO KNOW*

A
  • CMP —> serum bilirubin and creatinine levels
  • PT/INR
144
Q

Which MELD score is required for liver transplant listing?

A

MELD score >14

GI II Exam 2 EH (15 decks)

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