Liver and gallbladder Flashcards

1
Q

What has contributed to the increase in chronic liver disorders in the US?

A

A doubling of nonalcoholic fatty liver disease (NAFLD).

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2
Q

What are the etiologies of newly diagnosed chronic liver disease?

A
  • Hepatitis B
  • Hepatitis C
  • Alcohol-related liver disease
  • Nonalcoholic fatty liver disease (NAFLD)
  • Alternative/undetermined etiologies.
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3
Q

What is the most common etiology of chronic liver disease in the US?

A

Hepatitis C.

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4
Q

What defines hepatitis?

A

End organ inflammatory damage to the liver.

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5
Q

What are common causes of hepatitis?

A
  • Viral infection
  • Toxic alcohol exposure
  • Chemical or medication exposure
  • Bacterial, fungal, or parasitic infection
  • Genetic disorders
  • Immune mediated pathology.
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6
Q

Which viruses are known to cause the most significant cases of viral hepatitis?

A
  • Hepatitis A
  • Hepatitis B
  • Hepatitis C
  • Delta viruses.
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7
Q

How is Hepatitis A virus (HAV) primarily transmitted?

A

By the fecal-oral route.

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8
Q

What is the incubation period for hepatitis A?

A

15 to 45 days (typically 30 days).

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9
Q

What is the significance of the hepatitis A vaccine?

A

Approved in the US in 1995, it has contributed to a decrease in reported new cases.

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10
Q

What is the main mode of transmission for Hepatitis B virus (HBV)?

A

Parenteral exposure.

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11
Q

What is the mean interval between exposure and onset of clinical illness for Hepatitis B?

A

120 days.

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12
Q

What percentage of adults and neonates will become asymptomatic chronic carriers of HBsAg?

A
  • 10% of adults
  • 90% of infected neonates.
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13
Q

What does the term ‘non-A, non-B hepatitis’ refer to?

A

Hepatitis C and E.

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14
Q

What is the leading cause of cirrhosis in the US?

A

Hepatitis C infection.

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15
Q

What is the primary risk factor for Hepatitis C virus (HCV) infection?

A

History of intravenous drug use (IVDU).

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16
Q

What percentage of HCV infections progress to chronic hepatitis?

A

Approximately 90%.

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17
Q

What characterizes Hepatitis D virus (HDV)?

A

It can only infect patients who are actively producing HBsAg.

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18
Q

What is the prevalence of Hepatitis D in those with Hepatitis B worldwide?

A

5%.

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19
Q

How is Hepatitis E primarily transmitted?

A

Fecal-oral transmission.

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20
Q

What is the incubation period for Hepatitis E?

A

15 to 60 days.

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21
Q

What is the recent hepatitis virus referred to as?

A

Hepatitis G (HGV) or hepatitis GB virus type C (GBV-C).

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22
Q

True or False: Hepatitis A is associated with a chronic carrier state.

A

False.

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23
Q

Fill in the blank: Hepatitis B surface antigen is abbreviated as _______.

A

HBsAg.

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24
Q

What is the annual estimated number of new HBV infections in the US?

A

22,000.

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25
Q

What is the clinical presentation of viral hepatitis?

A

Highly variable, often asymptomatic, with common findings including malaise, fever, anorexia, nausea, vomiting, abdominal discomfort, diarrhea

Jaundice may be the initial finding prompting further evaluation.

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26
Q

What are the common hepatitis viruses?

A

A, B, C, D, E, G

These viruses are often clinically nondistinct.

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27
Q

What is fulminant hepatitis?

A

An acute onset illness that progresses to hepatic failure and encephalopathy over days

Characterized by altered mentation and spontaneous mucosal bleeding.

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28
Q

What are some physical findings associated with fulminant hepatitis?

A

Fever, scleral icterus, abdominal tenderness, vomiting, dehydration, tachycardia, hypotension, hepatomegaly

Tenderness may be present even without liver enlargement.

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29
Q

What is scleral icterus and when does it occur?

A

Yellowing of the sclera due to elevated bilirubin, occurs when serum bilirubin level is above 2.5 mg/dL

Muddy sclera may obscure this finding.

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30
Q

What are common medications associated with hepatopathy?

A
  • Acetaminophen
  • Antimicrobial drugs (e.g., amoxicillin-clavulanate, isoniazid)
  • Anticonvulsants (e.g., phenytoin)
  • Statins

Acetaminophen is the most common cause of acute liver failure in the US.

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31
Q

What laboratory findings are typically associated with hepatitis?

A

Elevated serum AST and ALT levels (10- to 100-fold), moderately increased bilirubin levels

Hyperbilirubinemia typically emerges days to 1 week after onset of symptoms.

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32
Q

How is acute hepatitis A diagnosed?

A

Presence of immunoglobulin M (IgM) HAV antibody

IgG antibody indicates previous infection.

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33
Q

What characterizes acute hepatitis B?

A

Presence of HBsAg and IgM antibody to HBcAg

HBsAg alone does not establish the diagnosis.

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34
Q

What is the role of serologic testing in hepatitis diagnosis?

A

Provides confirmation of viral causes, impacts prognosis, and may have public health importance

Serologic testing should be initiated as soon as feasible.

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35
Q

What is the recommended management for most patients with viral hepatitis?

A

Supportive management, attention to fluid/electrolyte imbalances, antiemetics, and gradual diet advancement

Most patients have self-limited disease with resolution in 2 to 4 weeks.

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36
Q

What complications can arise from viral hepatitis?

A

Fluid/electrolyte imbalance, refractory emesis, liver failure, hepatic encephalopathy

Severe vomiting can lead to upper gastrointestinal bleeding.

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37
Q

What is the window for effective HBV disease prevention after exposure?

A

About 2 weeks from the time of exposure

Passive immunization with immune globin may prevent disease.

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38
Q

What is the risk of seroconversion after percutaneous exposure to HCV?

A

Approximately 1.8%

No effective vaccine for HCV is currently available.

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39
Q

What is the goal endpoint of chronic hepatitis C treatment?

A

Sustained virologic response (SVR), defined as absence of HCV RNA by PCR testing at 3 to 6 months following treatment

DAA regimens demonstrate SVR rates exceeding 95%.

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40
Q

What should be done for health care workers exposed to potentially infectious materials?

A

Vaccination against HBV and testing within 48 hours for baseline disease presence

Universal precautions are the first and best means of defense.

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41
Q

What should be provided to family members and close contacts of a patient with viral hepatitis?

A

Immuno-prophylaxis if not previously immunized.

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42
Q

What is the recommendation for patients with HAV infection who handle food?

A

They must not return to work while potentially infectious.

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43
Q

When is it advisable for patients with HAV infection to return to work?

A

After the jaundice has cleared.

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44
Q

True or False: Infectivity is greatly diminished by the time jaundice emerges in HAV infection.

A

True.

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45
Q

Serologic Markers in Hepatitis

A
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46
Q

What is alcoholic hepatitis?

A

It is the most extreme manifestation of ongoing alcoholic liver disease, resulting from long-term alcohol consumption and characterized by hepatic decompensation or failure.

It requires specialized medical care.

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47
Q

What factors increase the risk of developing alcoholic hepatitis?

A

Factors include:
* Long-term alcohol consumption
* Gender (women are at higher risk due to estrogen effects)
* Daily ethanol consumption exceeding 80 g in men or 20 g in women
* Obesity
* Dietary factors
* Smoking
* Comorbidities: Viral hepatitis, Hemachromatosis, HIV

Risk fact

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48
Q

What is the most common form of alcohol-induced liver disease?

A

Steatosis

Fatty infiltration of the liver is often reversible upon cessation of alcohol intake.

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49
Q

What percentage of chronic alcoholics may develop hepatocellular carcinoma?

A

Approximately 3% to 10%.

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50
Q

What are common clinical features of alcoholic hepatitis?

A

Features may include:
* Nausea
* Vomiting
* Abdominal pain
* Acute liver failure
* Tachycardia
* Fever
* Hypotension

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51
Q

What laboratory findings are typical in alcoholic hepatitis?

A

Typical findings include:
* Moderate elevations of AST and ALT
* Predominance of AST over ALT
* Leukocytosis
* Hyperbilirubinemia
* Coagulopathy

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52
Q

True or False: A liver biopsy is the diagnostic and prognostic gold standard for alcoholic hepatitis.

A

True

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53
Q

What is the Maddrey discriminant function (MDF) score used for?

A

It assesses disease severity in alcoholic hepatitis and helps determine the need for steroid therapy.

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54
Q

Fill in the blank: The risk of liver injury increases with daily alcohol consumption exceeding _______ in men or _______ in women.

A

80 g; 20 g

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55
Q

What is the recommended treatment for patients with a MDF score greater than 32?

A

Corticosteroids (oral prednisolone or parenteral methylprednisolone)

This is recommended in the absence of GI bleeding, hepatorenal syndrome, or sepsis.

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56
Q

What dietary considerations should be made for patients with alcoholic hepatitis?

A

A high-calorie, vitamin-supplemented diet should be administered, with possible protein restriction if cirrhosis and encephalopathy are present.

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57
Q

What complications can arise from alcoholic hepatitis?

A

Complications may include:
* Variceal bleeding
* Hepatorenal syndrome
* Ascites

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58
Q

What is the role of magnesium in the management of alcoholic hepatitis?

A

Magnesium replacement is often necessary due to ethanol-induced magnesium wasting.

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59
Q

What are the characteristic physical signs of cirrhosis?

A

Signs may include:
* Gynecomastia
* Spider angiomata
* Muscle wasting
* Ascites
* Palmar erythema

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60
Q

What is the typical progression of liver disease in chronic alcohol users?

A

Progression typically goes from steatosis to fibrosis, cirrhosis, and potentially hepatocellular carcinoma.

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61
Q

What is the mortality rate associated with variceal bleeding within 5 years?

A

65%

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62
Q

What should be assessed in patients with clinical signs of alcoholic hepatitis?

A

Patients should be assessed for symptoms of gastritis or GI bleeding.

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63
Q

What is the potential effect of short-term abstinence from alcohol in patients with alcoholic hepatitis?

A

It may increase the risk for withdrawal.

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64
Q

What are the common causes of differential diagnosis for alcoholic hepatitis?

A

Common causes include:
* Gastritis
* Pancreatitis
* Other alcohol-related GI maladies

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65
Q

What is the expected AST to ALT ratio in alcoholic hepatitis compared to viral hepatitis?

A

A relative predominance of AST to ALT is expected in alcoholic hepatitis.

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66
Q

What is the recommended treatment for close personal contact exposure to Hepatitis A?

A

ISG, 0.1 mL/kg IM

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67
Q

What is the treatment for daycare center employees or attendees exposed to Hepatitis A?

A

ISG, 0.1 mL/kg IM

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68
Q

What is the treatment for school contacts exposed to Hepatitis A?

A

None

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69
Q

What is the treatment for hospital contacts exposed to Hepatitis A?

A

None

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70
Q

What is the treatment for workplace contacts exposed to Hepatitis A?

A

None

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71
Q

What is the treatment for food-borne source exposure to Hepatitis A within 2 weeks?

A

ISG, 0.2 mL/kg IM

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72
Q

What is the treatment for food-borne source exposure to Hepatitis A after 2 weeks?

A

None

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73
Q

What is the recommended treatment for percutaneous or mucosal exposure to Hepatitis B from an HBsAg (+) source?

A
  1. HBIG ×1
  2. Hepatitis B vaccination booster
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74
Q

What should be done if the anti-HBs titer is adequate after exposure to Hepatitis B?

A

No treatment

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75
Q

What is the treatment for an unvaccinated individual exposed to an HBsAg (−) source of Hepatitis B?

A

Initiate hepatitis B vaccination series

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76
Q

What is the treatment for a vaccinated individual exposed to an HBsAg (−) source of Hepatitis B?

A

No treatment

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77
Q

What is the treatment for exposure to an unknown source of Hepatitis B?

A
  1. HBIG ×1
  2. Initiate hepatitis B vaccination series
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78
Q

What is the treatment for intimate sexual exposure to an HBsAg (+) source of Hepatitis B?

A
  1. HBIG ×1
  2. Initiate hepatitis B vaccination series
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79
Q

What is the recommended treatment for Hepatitis C prophylaxis?

A

ISG, 0.06 mL/kg IM can be considered for parenteral exposures

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80
Q

What is the treatment for Hepatitis Delta exposure?

A

Same as for hepatitis B

81
Q

What is autoimmune hepatitis (AIH)?

A

AIH results from antibodies targeted to hepatospecific antigens

82
Q

What are the common age peaks for autoimmune hepatitis?

A

Second, fifth, and sixth decades

83
Q

Is autoimmune hepatitis more common in males or females?

84
Q

What are the two diagnostic types of autoimmune hepatitis based on?

A

Individual’s expression of autoantibodies

85
Q

What is the primary treatment modality for autoimmune hepatitis?

A

Immunosuppression with corticosteroids

86
Q

What is defined as remission in autoimmune hepatitis treatment?

A

Normalization of aminotransferases, serum bilirubin, and IgG levels and absence of clinical symptoms

87
Q

What is the 5-year survival rate for untreated autoimmune hepatitis?

A

Approximately 32%

88
Q

What is the 10-year survival rate with treatment for autoimmune hepatitis?

A

Approximately 90%

89
Q

What second-line therapy is widely supported for autoimmune hepatitis?

A

Mycophenolate mofetil

90
Q

What is cirrhosis?

A

End-stage chronic liver disease characterized by destruction of hepatocytes and fibrotic tissue

91
Q

What type of cirrhosis is characterized by a diffuse process involving the entire lobule?

A

Laënnec cirrhosis

92
Q

What is a common cause of postnecrotic cirrhosis?

A

Chronic hepatitis of various causes

93
Q

What is biliary cirrhosis a consequence of?

A

Chronic extrahepatic biliary obstruction or autoimmune-mediated intrahepatic duct inflammation

94
Q

What are common clinical features of cirrhosis?

A

Chronic fatigue, poor appetite, GI bleeding, ascites, hepatic encephalopathy

95
Q

What physical examination findings may be present in cirrhosis?

A

Muscle wasting, spider angiomata, palmar erythema, gynecomastia

96
Q

What is the most common complication of cirrhosis?

97
Q

What laboratory findings are suggestive of biliary cirrhosis?

A

Elevation of alkaline phosphatase out of proportion to other liver enzyme levels

98
Q

What is the MELD score used for?

A

Predicting 3-month mortality in patients with end-stage liver disease

99
Q

What is the primary treatment for ascites?

A

Therapeutic paracentesis

100
Q

What is the recommended IV dosing of albumin after large-volume paracentesis?

A

8 g/L removed

101
Q

What should be avoided in patients with ascites without peripheral edema?

A

Exceeding 500 mL of fluid removal/day

102
Q

What dietary recommendation is suggested for chronic management of ascites?

A

A low-sodium diet of less than 2000 mg of sodium

103
Q

What medications should be avoided in patients with cirrhosis?

A

ACEIs, ARBs, NSAIDs

104
Q

What is the mortality rate associated with acute upper GI bleeding in patients with cirrhosis?

A

10% to 15%

This statistic highlights the seriousness of GI bleeding in cirrhotic patients.

105
Q

What are common causes of GI bleeding in cirrhosis patients?

A

Esophageal or gastric varices and other sources such as gastritis and duodenal ulcer

Over half of the cases result from sources other than varices.

106
Q

What is the target platelet count for transfusion in active bleeding with coagulopathy in cirrhosis?

A

Greater than 50,000/mm3

This target helps manage bleeding risks effectively.

107
Q

What is the role of fresh-frozen plasma in treating asymptomatic abnormalities in PT and INR?

A

There is little support for its use

Fresh-frozen plasma is not recommended for asymptomatic cases.

108
Q

What is the recommended dose of cryoprecipitate for active bleeding?

A

1 unit/10 kg body weight

This treatment aims to achieve a fibrinogen level of more than 100 mg/dL.

109
Q

What treatment may be used for uncomplicated prolongation of PT or INR in individuals with nutritional or gastrointestinal losses?

A

Oral vitamin K supplementation (10–20 mEq PO every 6 to 12 hours)

This approach helps manage clotting issues.

110
Q

What is the significance of mean arterial pressure (MAP) in patients with cirrhosis?

A

MAP is an independent predictor of mortality

Lowering MAP may adversely affect survival.

111
Q

Which medications should be used with caution in patients with cirrhosis?

A

ACEIs, ARBs, and beta blockers such as propranolol

These medications can impact blood pressure and survival.

112
Q

What is hepatorenal syndrome (HRS)?

A

Renal dysfunction occurring in the setting of cirrhosis without obvious renal pathology

HRS is a serious complication that requires careful management.

113
Q

What serum creatinine level is associated with type I hepatorenal syndrome?

A

Exceeding 2.5 mg/dL

Type I HRS is the more severe form of this syndrome.

114
Q

What treatments are typically used for hepatorenal syndrome?

A

Albumin and vasoactive medications such as norepinephrine

These treatments aim to increase MAP.

115
Q

What is the mortality risk associated with hepatorenal syndrome?

A

High mortality

Hepatorenal syndrome is a critical condition with poor outcomes.

116
Q

Common underlying causes of hepatic encephalopathy in patients with known liver disease

117
Q

How does ammonia affect the brain in hepatic encephalopathy?

A

It disrupts GABA receptors

118
Q

What is the grading scale for the severity of hepatic encephalopathy?

A

Grade I to IV

119
Q

What are the symptoms of Grade I hepatic encephalopathy?

A

Mild confusion and slurred speech

120
Q

What is asterixis?

A

Low-amplitude, alternating flexion and extension of the wrist

121
Q

What is fetor hepaticus?

A

Musty breath odor from mercaptans

122
Q

What physical signs may be present in patients with hepatic encephalopathy?

A
  • Spider angiomata
  • Testicular atrophy
  • Muscle wasting
  • Superficial bruising
  • Gynecomastia
  • Ascites
123
Q

What can be included in the differential diagnosis for hepatic encephalopathy?

A

All causes of altered sensorium

124
Q

What tests are recommended for diagnosing hepatic encephalopathy?

A

Liver function tests, serum ammonia levels, serum chemistry tests

125
Q

What is the principal treatment for hepatic encephalopathy?

A

Nonabsorbable disaccharides such as lactulose

126
Q

What is the usual dose of lactulose for hepatic encephalopathy?

A

30 to 60 g orally or 200 g rectally daily

127
Q

What is the main adverse effect of lactulose?

A

Excessive diarrhea

128
Q

Which oral antibiotic is preferred in treating hepatic encephalopathy?

129
Q

What dietary recommendations are made for patients with hepatic encephalopathy?

A

Small frequent meals with complex carbohydrates

130
Q

What is spontaneous bacterial peritonitis (SBP)?

A

An acute bacterial infection of ascitic fluid in liver disease

131
Q

What is the primary organism associated with SBP?

A

Escherichia coli

132
Q

What is a key laboratory finding for diagnosing SBP?

A

Elevated PMN leukocytes (>250 cells/mm3) in peritoneal fluid

133
Q

What is the first-line treatment for SBP?

A

IV antibiotics, specifically third-generation cephalosporins like cefotaxime

134
Q

What is the significance of a serum-ascites albumin fluid gradient greater than 1.1 g/dL?

A

It is an early indicator of SBP

135
Q

What should be done if a patient with SBP has a PMN count greater than 250 cells/mm3?

A

Empiric antibiotics should be initiated

136
Q

What is the typical duration of antibiotic treatment for SBP?

137
Q

What are common symptoms of peritonitis in patients undergoing peritoneal dialysis?

A
  • Abdominal pain
  • Cloudy peritoneal effluent
138
Q

What is the typical management for bacterial peritonitis in peritoneal dialysis patients?

A

Intraperitoneal antimicrobial administration

139
Q

What prophylactic measure can reduce the risk of infection at the catheter exit site in peritoneal dialysis?

A

Topical application of mupirocin or aminoglycosides

140
Q

What is the role of prophylaxis at the catheter exit site?

A

Reduces the risk for infection through topical application of mupirocin or aminoglycosides.

141
Q

What increases the risk for the development of SBP in patients with ascites?

A

Ascitic fluid protein levels less than 1 g/dL.

142
Q

What are other important risk factors for SBP?

A
  • Serum bilirubin level greater than 3.2 mg/dL
  • Platelet count less than 98,000/mm3
  • Previous history of SBP
143
Q

How can management with diuretics affect SBP risk?

A

It helps decrease the risk of developing SBP.

144
Q

What is the controversy surrounding proton pump inhibitors (PPIs) in relation to SBP?

A

Some studies found an increased risk of SBP with PPIs, while a recent study showed no increased incidence.

145
Q

How might beta blockers affect SBP risk?

A

They may increase risk secondary to resultant systemic hypotension.

146
Q

What is the effect of antibiotic prophylaxis in high-risk patients for SBP?

A

It can reduce SBP incidence by 60% to 80% and can be cost-effective.

147
Q

What is a common daily prophylaxis regimen for high-risk patients?

A
  • Norfloxacin 400 mg PO daily
  • Ciprofloxacin 500 mg PO daily
  • Trimethoprim-sulfamethoxazole (TMP-SMX) 800/160 mg PO daily
148
Q

What prophylactic antibiotic is recommended for patients with cirrhosis admitted for GI bleeding?

A

Ceftriaxone (1 g IV daily) until the patient can take food orally.

149
Q

What should be done when a patient starts eating after receiving ceftriaxone for GI bleeding?

A

Switch to oral TMP-SMX.

150
Q

What is recommended for long-term outpatient prophylaxis in cirrhosis patients?

A
  • Norfloxacin
  • Ciprofloxacin
  • TMP-SMX
151
Q

What are high-risk features that warrant long-term outpatient prophylaxis?

A
  • Ascitic fluid protein less than 1.5 g/dL
  • Serum BUN level greater than 25 mg/dL
  • Serum creatinine greater than 1.2 mg/dL
  • Serum sodium level less than 130 mmol/L
152
Q

In what situations might repeat paracentesis be helpful?

A

Inconsistent symptoms, abnormal treatment response, atypical organisms, or recent beta-lactam exposure.

153
Q

Runyon criteria for SBP

154
Q

What are the two broad categories of hepatic abscesses?

A

Pyogenic and amebic.

155
Q

What are some conditions that may lead to pyogenic hepatic abscess?

A
  • Biliary tract obstruction
  • Cholangitis
  • Diverticulitis
  • Pancreatic abscess
  • Omphalitis
  • Appendicitis
  • Inflammatory bowel disease
  • Pneumonia
156
Q

What is a common causative organism of pyogenic hepatic abscess?

A
  • E. coli
  • Klebsiella
  • Pseudomonas
  • Enterococcus spp.
  • Anaerobic streptococci
  • Various Bacteroides spp.
157
Q

What are the typical clinical features of a pyogenic hepatic abscess?

A
  • High fever
  • Chills
  • RUQ pain
  • Nausea
  • Vomiting
158
Q

What laboratory findings are common in pyogenic hepatic abscess?

A
  • Leukocytosis (70-80% of cases)
  • Elevated alkaline phosphatase (up to 90%)
  • Bilirubin > 2 mg/dL (50% of patients)
  • Elevated serum aminotransferase levels (2-4 times normal)
159
Q

What is the initial treatment for a pyogenic hepatic abscess?

A
  • Hemodynamic stabilization
  • IV antibiotics
  • Pain control
160
Q

True or False: Abscesses less than 5 cm are often treated with drainage.

161
Q

What is the recommended antibiotic regimen for pyogenic hepatic abscess?

A
  • Cefotaxime 2 g IV every 8 hours
  • Ceftriaxone 2 g IV daily plus metronidazole 500 mg IV every 8 hours
  • Ampicillin 2 g IV every 6 hours plus gentamycin and metronidazole
  • Piperacillin-tazobactam 3.375 IV every 6 hours
  • Imipenem 500 mg every 6 hours
  • Meropenem 1 gm every 8 hours
162
Q

What is the typical management for amebic abscess?

A
  • Supportive therapy
  • Initiation of amebicidal therapy
  • Metronidazole for tissue infection
  • Paromomycin for luminal cysts
163
Q

What protozoan is responsible for amebic liver abscess?

A

Entamoeba histolytica.

164
Q

What are the common symptoms of amebic abscess?

A
  • Fever
  • Chills
  • Nausea
  • Vomiting
  • Abdominal pain
165
Q

What are the laboratory findings in amebic abscess?

A
  • Neutrophilic leukocytosis
  • Elevated alkaline phosphatase (75% of cases)
  • Elevated aminotransferase levels (50%)
166
Q

What is the incidence of liver disease in pregnancy?

A

Less than 1%.

167
Q

What are the two primary hepatic disorders associated with pregnancy?

A
  • Benign cholestasis
  • Acute fatty liver
168
Q

What is a key symptom of benign cholestasis during pregnancy?

A

Progressive pruritus.

169
Q

What is the treatment for benign cholestasis in pregnancy?

A

Ursodeoxycholic acid (UDCA) 300 mg PO every 8 hours until delivery.

170
Q

What is Budd-Chiari syndrome caused by?

A

Hepatic venous outflow obstruction.

171
Q

What are the two types of Budd-Chiari syndrome?

A
  • Primary BCS (thrombosis or phlebitis)
  • Secondary BCS (external compression)
172
Q

What imaging modality is the choice for diagnosing Budd-Chiari syndrome?

A

Doppler ultrasound imaging of the hepatic vein.

173
Q

What is the significance of the Swansea criteria in pregnancy?

A

High sensitivity for diagnosing acute fatty liver disease.

174
Q

Fill in the blank: Acute fatty liver of pregnancy can progress rapidly to _______.

A

[maternal or fetal demise]

175
Q

What complication can occur with rupture of an amebic liver abscess?

A
  • Involvement of the lung
  • Abdominal pain with peritonitis
  • Involvement of the pericardium
176
Q

What factors are associated with primary Budd-Chiari syndrome?

A
  • Hypercoagulable states
  • Factor V Leiden
  • Protein S or C deficiency
  • Thrombophilia
  • Antithrombin III deficiency
177
Q

What is the clinical distinction between acute hepatic necrosis secondary to viral infection and BCS?

A

It is clinically indistinguishable from acute hepatic necrosis but treatment options differ significantly.

178
Q

What is the sensitivity of Doppler ultrasound imaging of the hepatic vein for diagnosing BCS?

A

85% to 95%

179
Q

What is the most sensitive diagnostic modality for BCS?

A

Venography with access through internal jugular, cephalic, or femoral veins.

180
Q

What may ascitic fluid analysis help distinguish in BCS?

A

It helps distinguish among etiologies of ascites due to high portal pressure.

181
Q

What serum-to-ascites protein gradient is associated with elevated portal pressure in BCS?

A

Greater than 1.1 g/dL.

182
Q

What does the management of BCS focus on?

A

Relieving underlying disorders such as hypercoagulopathy and managing complications of portal hypertension.

183
Q

What interventions are considered for newly diagnosed BCS with acute decompensation?

A
  • TIPS placement
  • Percutaneous angioplasty
  • Thrombolytic therapy
184
Q

How can previously diagnosed BCS with worsening ascites be managed?

A
  • Modification of diuretics
  • Therapeutic paracentesis
  • Referral to a primary care physician or gastroenterologist
185
Q

What treatment is used to prevent clot propagation in primary BCS?

A

Anticoagulation.

186
Q

What are the treatment options for disease refractory to medical or percutaneous interventions in BCS?

A
  • Portacaval surgical shunting
  • Liver transplantation
187
Q

What is the 5-year survival rate for patients undergoing human orthotopic liver transplantation?

A

Approximately 80%.

188
Q

What are common early complications of liver transplantation?

A
  • Bleeding
  • Acute rejection
  • Vascular or biliary tract issues
  • Infection
189
Q

What are delayed complications that may occur after liver transplantation?

A
  • Recurrence of underlying disease
  • Malignancy
  • Infection
  • Chronic rejection
  • Medication toxicity
  • Biliary complications
  • Renal failure
190
Q

What is a common regimen of immunosuppressive agents used after liver transplantation?

A
  • Glucocorticoid (e.g., prednisone)
  • Calcineurin inhibitor (e.g., cyclosporine or tacrolimus)
  • Either sirolimus, mycophenolate, or azathioprine
191
Q

What is a potential side effect of corticosteroid toxicity?

A
  • Glucose intolerance
  • Diabetes
  • Osteoporosis
  • Gastric ulceration
  • Muscle wasting
192
Q

What is the most common dose-limiting effect of cyclosporine and tacrolimus?

A

Renal impairment.

193
Q

What complications are associated with azathioprine?

A
  • Hepatotoxicity
  • Bone marrow suppression
194
Q

What remains the leading cause of mortality in liver transplant recipients?

A

Infections.

195
Q

What are the signs of chronic rejection in liver transplant recipients?

A
  • Low-grade temperature elevation
  • Fatigue
  • Jaundice
196
Q

What laboratory abnormalities are expected in rejection of a transplanted liver?

A
  • Elevated bilirubin
  • Elevated transaminase levels
  • Prolonged PT or INR
  • Low serum albumin level
197
Q

What is the best means of early identification of evolving renal dysfunction post-transplant?

A

Routine serum creatinine level measurement.

198
Q

What assessments may be included in the management of liver transplant complications?

A
  • CBC
  • Glucose
  • BUN
  • Creatinine
  • Serum electrolytes
  • Transaminase
  • Bilirubin
  • Albumin levels
  • Coagulation studies