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Gastrointestinal > Liver and Gallbladder Disorders > Flashcards

Liver and Gallbladder Disorders Flashcards

1
Q

Hepatic vein obstruction is also called _____.

A

Budd-Chiari syndrome

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2
Q

What are the most common causes of hepatic vein obstruction?

A
  1. hepatic vein thrombosis (MC)

2. hepatic vein occlusion (ex. by a tumor)

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3
Q

What are the risk factors of hepatic vein obstruction?

A
  1. idiopathic
  2. hyper coagulable states (ex. polycythemia vera, pregnancy, OCPs, Factor V Leiden, malignancy, Protein C and S deficiency)
  3. women in their 20s and 30s
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4
Q

Hepatic vein thrombosis or occlusion causes —>

A

decrease liver drainage and portal HTN and cirrhosis

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5
Q

What is the classic triad for hepatic vein obstruction?

A
  1. ascites
  2. hepatomegaly
  3. RUQ abdominal pain

also have rapid development of jaundice and hepatosplenomegaly

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6
Q

What are the diagnostic tests of choice for hepatic vein obstruction?

A

Ultrasound– shows occlusion of hepatic vein or IVC

Venography

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7
Q

What is the management for mild hepatic vein obstruction?

A

Shunts (ex. TIPS)

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8
Q

What is the management for stenosis of the hepatic vein or obstruction of the IVC?

A

Angioplasty with stent

angioplasty = repair of blood vessel by inserting balloon-tipped catheter to unclog the vessel.

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9
Q

What is the management of ascites?

A

Diuretics
Low sodium diet
Large volume paracentesis (for refractory ascites)

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10
Q

What is cholelithiasis?

A

gallstones in the gall bladder with NO inflammation!

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11
Q

90% of gallstones are _______.

A

cholesterol

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12
Q

What are the risk factors for cholelithiasis?

A

5Fs: fat, fair, female, forty, fertile

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13
Q

What are the clinical manifestations of cholelithiasis?

A
  1. asymptomatic
  2. “biliary colic” —> episodic RUQ pain that begins abruptly and resolves slowly that is often precipitated by fatty foods or large meals
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14
Q

What is the diagnostic test of choice for cholelithiasis?

A

Ultrasound!

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15
Q

What are the management options for cholelithiasis?

A
  1. asymptomatic —> observe

2. symptomatic —> cholecystectomy

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16
Q

What are the complications of cholelithiasis?

A
  1. choledocholithiasis
  2. cholangitis
  3. cholecystitis
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17
Q

What is choledocholithiasis?

A

gallstones in the biliary tree (common bile duct) associated with ductal dilation

As liver produces bile/bilirubin it will push against the stone and the biliary tree with expand until bilirubin overflows into the blood and the patient then gets jaundice!

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18
Q

Choledocholithiasis can lead to _____ and _______.

A
  1. gallstone pancreatitis (so want to check lipase and amylase)
  2. jaundice
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19
Q

What is the clinical manifestation of choledocholithiasis?

A

biliary colic and JAUNDICE (increased bilirubin)

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20
Q

What are the diagnostic tests of choice for choledocholithiasis?

A

Ultrasound and ERCP

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21
Q

What is the management for choledocolithiasis?

A

NPO, IVFs and stone extraction via ERCP

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22
Q

What is cholangitis?

A

biliary tree infxn secondary to obstruction by gallstone

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23
Q

What are the clinical manifestations of cholangitis?

A

Charcot’s triad!

  1. fevers/chills
  2. RUQ pain
  3. jaundice
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24
Q

What is the diagnostic test of choice for cholangitis?

A

ultrasound

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25
Q

What is the management of cholangitis?

A
  1. Emergent ERCP
  2. Abx: penicillin derivaties, ceftazidime (gram -), ampicillin (gram +), and metronidazole (anaerobic coverage)
  3. eventually cholecystectomy
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26
Q

What is acute cholecystitis?

A

Cystic duct obstruction by gallstone causing inflammation and infxn

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27
Q

What are the most common bacteria found with cholecystitis and cholangitis?

A
  1. E. coli
  2. Klebsiella
  3. enterococci
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28
Q

What are the clinical manifestations of acute cholecystitis?

A
  1. Biliary colic
  2. Fever, N/V, palpable GB, leukocytosis
    • Murphy’s sign
    • Boas sign

Jaundice is NOT common

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29
Q

What is Boas sign?

A

referred pain to right subscapular area due to phrenic nerve irritation

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30
Q

What are the diagnostic tests of choice for acute cholecystitis and what will they show?

A
  1. Ultrasound—> thickened gallbladder, pericholecystic fluid, and gallstones
  2. Labs—> increased WBCs, bilirubin, ALP, and LFTs
  3. HIDA scan**—> non-visualization of gallbladder is + test
  • = gold standard
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31
Q

What is the management of acute cholecystitis?

A

NPO, IVFs, Abx (3rd gen. ceph + Metronidazole)

Cholecystecomy usually within 72 hours

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32
Q

What is chronic cholecystitis?

A

Associated with gallstones resulting in repeated bouts of acute/subacute cholecystitis

Gallbladder may appear strawberry (interior) or porcelain (pre-malignant condition!)

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33
Q

What is Gilbert’s syndrome?

A

common benign hereditary disorder with mildly reduced activity of UGT enzyme, so you have an increase in indirect bilirubin

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34
Q

What are the clinical manifestations of Gilbert’s syndrome?

A

most are asymptomatic!

may have transient episodes of jaundice during periods of stress, fasting, ETOH or illness

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35
Q

How is Gilbert’s syndrome diagnosed?

A

usually incidental finding when have SLIGHT increase in indirect bilirubin levels with NORMAL liver function values

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36
Q

What is the management of Gilbert’s syndrome?

A

None! Benign disease no associated with sequelae

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37
Q

What causes PHYSIOLOGIC jaundice in newborns?

A

increase indirect bilirubin due to deficiency in UGT and increased breakdown of fetal Hgb.

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38
Q

Physiologic jaundice in newborns usually occurs ____ days after birth.

A

3-5

If jaundice on 1st day is pathologic!! NOT physiologic

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39
Q

What is the management of physiologic jaundice in newborns?

A

observation and phototherapy to make the indirect bilirubin water soluble to enhance renal excretion which then lowers the levels.

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40
Q

What is Crigler Naijar syndrome?

A

autosomal recessive disorder.
Type I —> no UGT activity
Type II —> very little UGT activity

*basically a more severe form of Gilbert’s

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41
Q

What is kernicterus?

A

increased bilirubin in the CNS and basal ganglia

can lead to deafness, lethargy, hypotonia, oculomotor palsy, and death

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42
Q

What are the clinical manifestations of Crigler Naijar syndrome?

A

Type I —> jaundice in 1st week of life with severe progression in 2nd week leading to kernicterus

death in 15 months if not treated!

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43
Q

How is Crigler Naijar syndrome diagnosed?

A

isolated indirect bilirubin hyperbilirubinemia with NORMAL liver functions

Type I —> serum bili 20-50 mg/dL
Type II —> serum bili 7-10 mg/dL (milder form)

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44
Q

What is the management of Crigler Naijar syndrome?

A

phototherapy, liver transplant

plasmapheresis in crisis

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45
Q

What is Dubin-Johnson syndrome?

A

Isolated mild conjugated hyperbilirubinemia due to inability of hepatcytes to secrete conjugated bilirubin (gene mutation)

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46
Q

Patients with Dubin-Johnson syndrome will have a _____ liver.

A

grossly black!

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47
Q

What is the management of Dubin-Johnson syndrome?

A

None!

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48
Q

What is Rotor’s syndrome?

A

a mild form of Dubin-Johnson syndrome (increase conjugated bilirubin)
liver is NOT black

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49
Q

What is the pathophysiology of hemolytic (pre hepatic) jaundice?

A

Massive RBC lysis! (hemolytic anemia)

increased indirect bilirubin production —> overwhelms liver’s ability to conjugate it

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50
Q

Hemolytic (prehepatic) jaundice results in ________ hyperbilirubinemia.

A

increased indirect/unconjugated

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51
Q

Hemolytic (prehepatic) jaundice results in _____ urine color.

A

normal

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52
Q

What is the pathophysiology of obstructive (post-hepatic) jaundice?

A

Cholestasis = bile duct blockage!

So conjugated bilirubin is prevented from passing into the intestine and refluxes back into the blood so get increased CONJUGATED bilirubin

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53
Q

Obstructive (post-hepatic) jaundice results in _____ hyperbilirubinemia.

A

increased direct/conjugated

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54
Q

What LFTs are markedly elevated with biliary obstruction or intrahepatic cholestasis?

A

ALP and GGT! —> GGT more sensitive indicator

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55
Q

Dark urine = increased _____ bilirubin

A

Direct/conjugated

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56
Q

What is the pathophysiology of hepatocellular (intra-hepatic) jaundice?

A

Liver damage (hepatitis)

  1. decreases conjugation
  2. direct bilirubin not efficiently secreted into bile
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57
Q

Hepatocellular (intra-hepatic) jaundice results in increased _____ bilirubin.

A

BOTH indirect and direct

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58
Q

What LFTs are markedly elevated with hepatocellular (intra-hepatic) jaundice?

A

ALT and AST

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59
Q

How does ETOH hepatitis effect AST and ALT?

A

increased AST:ALT >2:1 (AST usually ETOH causes direct mitochondrial injury —> increased AST

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60
Q

How does Acute hepatitis effect AST and ALT?

A

increased ALT and AST >1,000

ALT > AST usually

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61
Q

How does Chronic hepatitis effect AST and ALT?

A

increased ALT:AST but

62
Q

What are the lab tests of TRUE liver function?

A
  1. Prothrombin time (PT)

2. Albumin

63
Q

Prothrombin time depends on the synthesis of coagulation factors, so it is ______ dependent.

A

vitamin K

64
Q

Which “actual” liver function test is an earlier indicator of severe liver injury?

A

PT

65
Q

Albumin is a marker for overall liver….

A

protein synthesis

66
Q

Which indicators point towards autoimmune hepatitis?

A
  1. increased ALT > 1,000
  2. +ANA
    • smooth muscle antibodies
  4. increased IgG
  5. Responds to corticosteroids!
67
Q

Autoimmune hepatitis will respond to ______.

A

corticosteroids

68
Q

Acute hepatic failure is defined as….

A

rapid liver failure + hepatic encephalopathy often with coagulopathy

is within 8 wks after onset of liver injury in a previously healthy patient

69
Q

Reye’s syndrome is most commonly seen in who?

A

children and associated with aspirin use during viral infxn

70
Q

What is Reye’s syndrome?

A

fulminant hepatitis (acute hepatic failure) most commonly seen in children after aspirin use during viral infxn

71
Q

Children with Reye’s syndrome will most commonly present with?

A
  1. rash (hands and feet)
  2. intractable vomiting
  3. liver damage
  4. encephalopathy
  5. dilated pupils
  6. multi-organ failure
72
Q

What are the most common causes of acute hepatic failure (fulminant hepatitis)?

A
  1. Acetaminophen overuse or overdose
  2. drug runs
  3. viral hepatitis
  4. Reye’s syndrome
  5. Budd-Chiari syndrome (hepatic vein obstruction)
  6. autoimmune hepatitis
73
Q

What is asterixis?

A

flapping tremor of the hand with wrist extension

associated with hepatic encephalopathy

74
Q

What are the main diagnostic indicators of fulminant hepatitis (acute hepatic failure)?

A
  1. increased ammonia!**
  2. increased PT/INR —> decreased liver production of clotting factor proteins
  3. increased LFTs
  4. hypoglycemia
75
Q

How does hepatic encephalopathy present?

A
  1. vomiting
  2. coma
  3. seizures
  4. asterixis (flapping tremor of hand with wrist extension)
  5. hyperreflexia
  6. increased ICP
76
Q

Why is there increased serum ammonia levels with fulminant hepatitis?

A

failure of liver to excrete ammonia and reduced ability of converting ammonia to urea. Protein breakdown also leads to increased ammonia

77
Q

Why is there coagulopathy with fulminant hepatitis?

A

decreases production of coagulation factors

78
Q

What is the management of hepatic encephalopahty?

A
  1. Lactulose —> neutralizes the ammonia
  2. Neomycin—> abx that decreases the bacteria producing ammonia in GI tract
  3. Protein restriction—> reduces breakdown of protein into ammonia
79
Q

What is the definitive tx of fulminant hepatitis?

A

Liver transplant!

80
Q

What are the 2 phases of viral hepatitis?

A
  1. Prodromal phase

2. Icteric phase (most don’t develop this phase)

81
Q

The prodromal phase of viral hepatitis is associated with….

A 
malaise
arthralgia
fatigue
URI sx
N/V
82
Q

Hepatitis ___ is the only one associated with spiking fevers during the prodromal phase.

A

A

83
Q

What is the main clinical manifestation during the icteric phase of viral hepatitis?

A

jaundice! (usually after the patient’s fever breaks)

84
Q

Chronic hepatitis is defined as the disease lasting for…

A

more than 6 months

85
Q

Which viral hepatitis’s are associated with chronic liver disease?

A

B, C, and D.

86
Q

What % of HCV patients develop chronic disease?

A

80%

87
Q

What is the transmission of HAV?

A

feco-oral

Outbreaks with contaminated water/food during international travel
Day-care workers
Homosexuals

88
Q

What is the most common source of HAV in adults?

A

asymptomatic children

89
Q

Acute HAV is diagnosed by having a positive..

A

IgM HAV Ab

IgM = acute!

90
Q

Past exposure of HAV is diagnosed by having a positive…

A

IgG HAV Ab with a negative IgM

91
Q

What is the management of HAV?

A

symptomatic tx. It is self-limiting

**HAV immune globulin is available for close contacts.

92
Q

What is the transmission of HCV?

A

parental (ex. IV drug use)
sexual
increased risk if blood transfusion before 1992

93
Q

Which test implies recovery of HCV?

A

HCV-RNA

*anti-HCV may become negative after recovery!

94
Q

Acute HCV titers will show..

A
  1. (+) HCV RNA

2. (+/-) anti-HCV (becomes + in 6 weeks)

95
Q

Resolved HCV titers will show…

A
  1. (-) HCV RNA

2. (+/-) anti-HCV

96
Q

Chronic HCV titers will show…

A
  1. (+) HCV RNA

2. (+) anti-HCV

97
Q

What is the management of chronic HCV?

A

interferon AND ribavirin

98
Q

Screenings for hepatocellular carcinoma (HCC) for patients with HCV is done via…

A

serum alpha-fetoprotein and ultrasound

99
Q

How is HBV typically transmitted?

A
  1. Perinatal
  2. Per cutaneous
  3. Sexual
  4. Parenteral
100
Q

If HBsAg is positive for more than 6 months it means –>

A

Chronic infection is established

101
Q

What does HBsAg mean?

A

surface antigen

1st evidence of HBV infection (before symptoms)

102
Q

What does HBsAb or anti-HBs mean?

A

surface antibody

Means distant resolved infection OR vaccination

103
Q

If patient does NOT develop anti-HBs in 6 months —->

A

the patient has chronic infection

104
Q

What are the HBcAb’s?

A

Core antibodies

IgM –> indicates acute infection (1st Ab to appear)
IgG –> indicates chronic infection OR distant resolved infection

105
Q

What does HBeAg mean?

A

envelope antigen

increased viral replication and increased infectivity

106
Q

If a patient has a positive HBeAg for more than 3 months they have increased likelihood of…

A

developing chronic HBV

107
Q

What does HBeAb mean?

A

envelope antibody

indicates waning viral replication and infectivity

108
Q

What is the management of acute HBV?

A

supportive care

109
Q

When is the HBV vaccination given?

A

at 0, 1, and 6 months

110
Q

What is the management of chronic HBV?

A

alpha-interferon 2b, lamivudine, adefovir

111
Q

How is HDV transmitted?

A

It is a defective virus! Requires HBV (HbsAg) to cause coinfection or superimposed infection

112
Q

How is HEV typically transmitted?

A

feco-oral

associated with waterborne outbreaks

113
Q

How is HEV diagnosed?

A

+ IgM anti-HEV

114
Q

What is the management of HEV?

A

it is a self-limiting virus

115
Q

Which hepatitis has the highest mortality during pregnancy? especially the 3rd trimester?

A

HEV!

116
Q 
Window period for HBV:
HBsAg -->
anti-HBs -->
anti-HBc -->
HBeAg -->
anti-Hbe -->
A 
HBsAg (-)
anti-HBs (-)
anti-HBc (IgM)
HBcAg (-)
anti-Hbe (-)
117
Q 
Acute HBV:
HBsAg -->
anti-HBs -->
anti-HBc -->
HBeAg -->
anti-Hbe -->
A 
HBsAg (+)
anti-HBs (-)
anti-HBc (IgM)
HBeAg (+/-) 
anti-Hbe (+/-)
118
Q 
Recovery HBV:
HBsAg -->
anti-HBs -->
anti-HBc -->
HBeAg -->
anti-Hbe -->
A 
HBsAg (-)
anti-HBs (+)
anti-HBc (IgG)
HBeAg (-)
anti-Hbe (-)
119
Q 
Immunization against HBV:
HBsAg -->
anti-HBs -->
anti-HBc -->
HBeAg -->
anti-Hbe -->
A 
HBsAg (-)
anti-HBs (+)
anti-HBc (-)
HBeAg (-)
anti-Hbe (-)
120
Q 
Chronic HBV replicative:
HBsAg -->
anti-HBs -->
anti-HBc -->
HBeAg -->
anti-Hbe -->
A 
HBsAg (+)
anti-HBs (-)
anti-HBc (IgG)
HBeAg (+)
anti-Hbe (-)
121
Q 
Chronic HBV non-replicative:
HBsAg -->
anti-HBs -->
anti-HBc -->
HBeAg -->
anti-Hbe -->
A 
HBsAg (+)
anti-HBs (-)
anti-HBc (IgG)
HBeAg (-)
anti-Hbe (+)
122
Q

What is the pathophysiology of cirrhosis?

A

irreversible liver fibrosis with nodular regeneration secondary to chronic liver disease. Nodules cause increased portal pressure!

123
Q

What is the most common cause of cirrhosis of the liver in the U.S.?

A

ETOH

124
Q

What are other causes of cirrhosis besides ETOH?

A
  1. chronic viral hepatitis (esp. HCV*, HBV, HDV)
  2. non-alcohol fatty liver disease
  3. hemochromatosis
  4. primary sclerosing cholangitis
125
Q

What are the skin manifestations as a result of cirrhosis?

A
  1. spider angioma
  2. caput medusa (distended and engorged superficial epigastric veins, which are seen radiating from the umbilicus across the abdomen)
  3. jaundice
  4. Dupuytren’s contractures
  5. pruritus
126
Q

What are the diagnostic studies of choice for cirrhosis?

A

Ultrasound and liver bx

127
Q

What are the screening tests for hepatocellular carcinoma?

A

Ultrasound + increased alpha fetoprotein + biopsy for definitive dx

128
Q

What are the additional clinical manifestation of cirrhosis (not including skin)?

A
  1. hepatic encephalopathy–> confusion and lethargy, increased ammonia levels
  2. esophageal varices–> due to portal HTN
  3. ascites
  4. hepatosplenomegaly
  5. gynecomastia–> liver can’t metabolize estrogen
129
Q

What are the most common causes of hepatocellular carcinoma?

A 
chronic hepatitis (MC)
aflatoxin exposure (from Aspergillus infxn)
130
Q

What is primary biliary cirrhosis (PBC)?

A

idiopathic autoimmune disorder of the intrahepatic small bile ducts causing decreased bile duct excretion, cirrhosis and ESLD.

131
Q

Who does primary biliary cirrhosis commonly effect?

A

Middle-aged women (40-60 yrs)

132
Q

What is the clinical manifestation of primary biliary cirrhosis (PBC)?

A

Most asymptomatic! –> incidental finding of high ALP

May have fatigue, pruritus, jaundice, RUQ discomfort, or hepatomegaly

133
Q

What is the hallmark diagnostic for primary biliary cirrhosis (PBC)?

A

+ anti-mitochondrial antibody!!

134
Q

What liver enzymes will be elevated with PBC?

A

ALP with GGT

GGT often strikingly elevated –> reflects cholestasis

ALT, AST, and bilirubin will also be elevated

135
Q

What is the first line management for PBC?

A

Ursodeoxycholic acid –> protects cholangiocytes from toxic effects of bile acids and stabilizes hepatic inflammation

136
Q

What is the management of pruritus for patients with PBC, PSC, or cirrhosis?

A

Cholestyramine and UV light

binds bile acids in gut, reducing bile salts’ irritant effect on skin

137
Q

What is primary sclerosing cholangitis (PSC)?

A

autoimmune, progressive cholestasis with diffuse fibrosis of intrahepatic and extra hepatic ducts
Is RARE

138
Q

Primary sclerosing cholangitis (PSC) is most commonly associated with what disease?

A

inflammatory bowel disease

139
Q

90% of people with primary sclerosing cholangitis also have _____

A

ulcerative colitis

140
Q

What are the clinical manifestations of primary sclerosing cholangitis (PSC)?

A
  1. progressive jaundice
  2. pruritus
  3. RUQ pain
  4. hepatosplenomegaly
141
Q

What is the definitive management of primary sclerosing cholangitis (PSC)?

A

Liver transplant

Meds like steroids and immune meds have no significant benefit

142
Q

What is the diagnostic test of choice for primary sclerosing cholangitis (PSC)?

A

ERCP

143
Q

What liver enzymes will be significantly elevated with primary sclerosing cholangitis (PSC)?

A 
Increased ALP (3-5x) + GGT
\+ P-ANCA*
144
Q

What is Wilson’s disease?

A

free copper accumulation in liver, brain, kidney, and cornea

145
Q

What is the pathophysiology of Wilson’s disease?

A

autosomal recessive disorder with inadequate bile excretion of copper with increased small intestine absorption of copper –> copper deposition in tissues causing cellular damage

146
Q

What are the clinical manifestations of Wilson’s disease?

A
  1. Basal ganglia deposition –> Parkinson-like sx (bradykinesia, tremor, rigidity, dementia)
  2. Liver disease –> hepatitis, hepatosplenomegaly, cirrhosis, hemolytic anemia
  3. Corneal copper deposits –> Kayser-Fleischer rings
147
Q

How does Wilson’s disease affect the corneas?

A

Kayser-Fleischer rings –> brown or green pigment in cornea

148
Q

How is Wilson’s disease diagnosed?

A

increased urinary copper excretion

decreased ceruloplasmin

149
Q

What is the serum carrier molecule for copper?

A

ceruloplasmin

150
Q

What is the management for Wilson’s disease?

A

Ammonium tetrathiomolybdate –> increases urinary copper excretion

Pencillamine –> chelates copper

Zinc –> enhances urinary copper excretion and blocks intestinal copper absorption

151
Q

What must also be given in addition to Pencillamine for the treatment of Wilson’s disease?

A

Pyridoxine/vitamin B6 to prevent depletion

Gastrointestinal (8 decks)

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