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All the things > Liver, gallbladder n' such > Flashcards

Liver, gallbladder n' such Flashcards

1
Q

Premature activation of what enzyme in particular causes pancreatitis? What does this cause?

A

trypsin–this causes activation of other enzymes

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2
Q

What two types of necrosis ensue d/t pancreatitis?

A
  • Liquefactive

- Saponification / fat necrosis

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3
Q

What are the two most common causes of pancreatitis? How?

A
  • EtOH (contracts sphincter of Oddi)

- Gallstones (blocks drainage)

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4
Q

What cause the saponification seen in pancreatitis?

A

Digestion of fat surrounding pancreas

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5
Q

How does EtOH cause pancreatitis?

A

Contraction of the sphincter of Oddi, causing backup of enzymes and pancreatic juices

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6
Q

How do gallstones cause pancreatitis?

A

Blockage of the duct of Vader

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7
Q

What is the most common traumatic cause of pancreatitis?

A

Seatbelt smashing in car accidents

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8
Q

How does hypercalcemia cause pancreatitis?

A

Activates enzymes

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9
Q

What are the two metabolic disturbances that can lead to pancreatitis?

A
  • Hypercalcemia

- Hyperlipidemia

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10
Q

Which virus can cause pancreatitis?

A

Mumps

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11
Q

Rupture of what part of the duodenum (e.g from an ulcer) ( will lead to acute pancreatitis? anterior or posterior)

A

Posterior

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12
Q

What are the classic s/sx of pancreatitis?

A

Epigastric pain that radiates to the back with n/v

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13
Q

What causes the periumbilical and flank hemorrhage in pancreatitis?

A

Necrosis spread to these two regions as well

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14
Q

What enzymes are elevated in acute pancreatitis? Which is more specific?

A

Lipase

and amylase, but not specific

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15
Q

What is the metabolic disturbance that acute pancreatitis causes? Why?

A

Hypocalcemia d/t saponification (uses up Ca)

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16
Q

What causes shock seen in acute pancreatitis?

A

Damage of the blood vessels

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17
Q

What causes the pancreatic pseudocyst seen in acute pancreatitis? What can this cause if it ruptures?

A

Fibrous tissue surrounds pancreatic necrosis. Amylase within this can cause damage if released

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18
Q

What is the usual bacterial cause of a pancreatic abscess?

A

E.Coli

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19
Q

How can acute pancreatitis cause DIC? ARDS?

A

Amylase can activate coagulation factors and destroy lung tissue.

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20
Q

What is chronic pancreatitis, and what is the most common cause of it in adults? Children?

A
  • Recurrent bouts of acute pancreatitis, resulting in fibrosis
  • Adults = EtOH
  • Children = CF
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21
Q

What should you think if a patient with a recent bout of pancreatitis has persistently high amylase levels, despite resolution of acute phase?

A

pseudocyst

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22
Q

What are the s/sx of chronic pancreatitis?

A
  • Pancreatic insufficiency

- Epigastric pain radiating to the back

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23
Q

What causes the pancreatic insufficiency seen in chronic pancreatitis? How does this manifest itself?

A
  • Fibrosis

- Steatorrhea and malabsorption issues

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24
Q

Are amylase and lipase good indicators for chronic pancreatitis? Why or why not?

A

No, because most of the pancreas has been destroyed

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25
Q

What are the radiological findings of chronic pancreatitis?

A

Dystrophic calcification

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26
Q

What endocrine disorder can result from chronic pancreatitis? How?

A

DM– damage to the beta cells

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27
Q

What CA are patients with chronic pancreatitis at an increased risk for? From what tissue in the pancrease does this usually arise from?

A

-Pancreatic adenocarcinoma– from the ducts

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28
Q

In what age group is adenocarcinoma of the pancreas most common?

A

Elderly

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29
Q

What are the two major risk factors for pancreatic carcinoma?

A

Smoking and chronic pancreatitis

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30
Q

What are the s/sx of pancreatic adenocarcinoma?

A

epigastric pain and weight loss

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31
Q

What are the classic findings of adenocarcinoma in the head of the pancreas?

A
  • Palpable gallbladder
  • Jaundice
  • Pale stools
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32
Q

Thin elderly pt with new onset DM is suspicious for what?

A

pancreatic adenocarcinoma

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33
Q

What is the tumor marker for pancreatic adenoCA?

A

CA19-9

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34
Q

—-What is the treatment for pancreatic adenoCA? Prognosis?—

A

—–Whipple procedure
(removal of duodenum, head of pancreas, and gallbladder
-Poor prognosis—-

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35
Q

What is biliary atresia?

A

Failure to form, or early destruction of the extrahepatic biliary tree

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36
Q

How does biliary atresia present? What type of bilirubin is elevated in this disorder?

A
  • Jaundice, progressing to cirrhosis early in life

- Direct (conjugated) bili is elevated

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37
Q

What are the three causes of cholelithiasis?

A
  • Supersaturation of cholesterol or bilirubin
  • Decreased phospholipids / bile acids
  • Stasis
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38
Q

How does cholestyramine cause an increased risk for cholelithisasis?

A

Decreased reuptake of bile acids, which is needed for solubility

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39
Q

How does stasis in the bile duct lead to gallstones?

A

Bacteria deconjugate the heme into bili, leading to bili

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40
Q

What is the most common type of gallstones in the west? How do they appear on imaging?

A
  • Cholesterol stones

- Usually radiolucent (don’t appear)

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41
Q

Why is it that estrogen increases the risk for cholelithisais? (2)

A
  1. Increases HMG-CoA reductase and cholesterol synthesis

2. Estrogen also increase cholesterol receptors on liver

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42
Q

How does clofibrate increase the risk for gallstones?

A

It increases the rate of HMG CoA reductase action, leading to increased cholesterol synthesis, and decreases bile acid

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43
Q

What ethnicity has a higher rate of cholelithiasis?

A

Native americans

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44
Q

What is the IBD that increases the risk for cholelithisasis? Why?

A
  • Crohn’s disease

- Ileum is damaged, so there is poor uptake of bile acids and salts, causing precipitation of cholesterol

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45
Q

How does cirrhosis increase the risk for gallstones?

A

Decreased production of bile salts

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46
Q

What are the causes of bilirubin stones? (2) How do they appear grossly?

A
  • extravascular hemolysis
  • Biliary tract infections

-Black or darkly pigmented stones

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47
Q

What are the three infectious agents that increase the risk for the development of a gallstone (hint: 1 bacteria + 2 parasites)?

A
  • E.coli
  • Ascaris lumbricoides
  • Clonorchis sinensis
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48
Q

What are the five key complications that can result from gallstones?

A
  1. Biliary colic
  2. Acute and chronic cholecystitis
  3. Ascending cholangitis
  4. Gallstone ileus
  5. Gallbladder CA
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49
Q

What is biliary colic?

A

Intermittent RUQ abdominal pain caused by contractions of the gallbladder against a stone.

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50
Q

What is acute cholecystitis?

A

Acute inflammation of the gallbladder caused by an impacted stone in cystic duct and bacterial overgrowth

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51
Q

What is the classic presentation of acute cholecystitis? (3)

A
  • RUQ pain with radiation to the right scapula
  • Fever + leukocytosis
  • N/v
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52
Q

What will happen to a gallbladder in acute cholecystitis if left untreated?

A

Rupture

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53
Q

Why is alk phos elevated in gallbladder issues?

A

Alk phos a key component of the endothelial cells of the gallbladder tract

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54
Q

What is chronic cholecystitis?

A

Chronic inflammation of the gallbladder due to longstanding chemical irritation from cholelithiasis

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55
Q

What are Rokitansky-Aschoff sinuses? What disease are these seen in?

A

gallbladder mucosa that dives down into the wall. Classic for chronic cholecystitis

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56
Q

What is the classical s/sx of chronic cholecystitis?

A

Vague RUQ pain after eating

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57
Q

What is the long term complication of chronic cholecystitis?

A

-Porcelain gallbladder–dystrophic calcification of the gallbladder

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58
Q

What is Porcelain gallbladder? What is the risk of leaving this untreated?

A
  • Dystrophic calcification of the gall bladder secondary to chronic cholecystitis
  • Predisposes to gallbladder cancer
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59
Q

What is the treatment for chronic cholecystitis?

A

Cholecystectomy

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60
Q

What is ascending cholangitis?

A

Bacterial infection of the bile ducts

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61
Q

How does ascending cholangitis present?

A

Sepsis, jaundice, and abdominal pain

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62
Q

What type of bacteria usually cause ascending cholangitis?

A

Enteric, Gram negative

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63
Q

What poses an increased risk of developing ascending cholangitis? How?

A

Choledocholithiasis– decreased flow of bile allows bacteria to grow upwards in the bile duct

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64
Q

What is a gallstone ileus? How do these occur?

A

-Gallstone that enters and obstructs the small bowel–usually the result of a fistula development between the gallbladder and the duodenum, which allows for a large stone to pass through and obstruct the ileocecal junction

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65
Q

What cancer is associated with cholecystitis?

A

Adenocarcinoma from the gland cells of the gallbladder

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66
Q

What is the major risk factor for the development of gallbladder adenoCA

A

Gallstones

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67
Q

—-What is the classical presentation of gallbladder carcinoma?—-

A

—-Cholecystitis in an elderly women—-

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68
Q

Jaundice occurs when serum bilirubin rises above what level?

A

> 2.5 mg/dL

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69
Q

What is the transporter for the heme component of Hb when it is broken down in the blood? Where does this go?

A

Albumin, goes to the liver

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70
Q

What causes the brown coloration of stool? Yellow urine?

A

Urobilinogen

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71
Q

What changes bili to urobilinogen?

A

Intestinal bacteria

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72
Q

What causes the increased risk of pigmented gallstones in hemolysis of ineffective erythropoiesis?

A

Increase in bili being poured out of the liver

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73
Q

What causes the dark urine in hemolysis/ineffective erythropoiesis?

A

increase in urine urobilinogen,. NOT due to the increased unconjugated bili

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74
Q

Can unconjugated bili be excreted through the urine?

A

NO–not water soluble

75
Q

What is the enzyme that conjugates bili?

76
Q

What causes physiological jaundice of the newborn?

A

Newborn liver has transiently low UGT

77
Q

What type of bili is increased in physiological jaundice of the newborn?

A

Indirect (unconjugated)

78
Q

Where in an infant does unconjugated bilirubin go in physiological jaundice of the newborn? Why here?

A

Basal ganglia, since these are fatty, and unconjugated bili is fat soluble

79
Q

What is the MOA of bili light?

A

Makes unconjugated bili water soluble–does NOT conjugate it

80
Q

What is the cause of Gilbert syndrome?

A

Genetically, mildly low UGT activity, leading to jaundice when exposed to stress. Benign condition

81
Q

What is Crigler-Najjar syndrome (type I)? Does it respond to phenobarbital?

A
  • Absence of UGT, causing kernicterus and death of infants

- Does not respond to phenobarbital

82
Q

What is Dubin-Johnson syndrome? What type of bili builds up?

A

Defective transport protein from the hepatocytes into the biliary tree, causing a build up of CONJUGATED bili

83
Q

What are the liver findings of Dubin-Johnson syndrome?

A

Black liver

84
Q

What is the prognosis for Dubin-johnson syndrome?

A

not clinically significant

85
Q

What is Rotor syndrome?

A

Defective transport protein from the hepatocytes into the biliary tree, causing a build up of CONJUGATED bili, but does NOT have the black liver

86
Q

What are the s/sx of biliary tract obstruction?

A
  • Increased conjugated bili
  • Dark urine d/t bilirubinemia
  • Xanthomas
  • Pruritus/jaundice
87
Q

—-What causes the dark urine in viral hepatitis?—-

A

—-Increase in both CB and UB, causing increased urine bili—

88
Q

What is hepatitis?

A

Inflammation of the liver parenchyma

89
Q

What are the virus that usually cause hepatitis? (3)

A
  • EBV
  • CMV
  • Hepatitis viruses
90
Q

Which bilirubin is elevated in acute viral hepatitis? Why?

A

Both CB and UCB

  • Increased CB d/t bile duct destruction
  • Increased UCB d/t hepatocyte destruction
91
Q

What happens to the urine with acute viral hepatitis?

A

Dark d/t increased CB in the blood

92
Q

What happens to the LFTs in viral hepatitis, and how do they relate to one another? How does this compare to hepatitis caused by EtOH?

A
  • Elevated with ALT > AST

- EtOH has AST:ALT in 2:1 ratio

93
Q

How long do symptoms last for in acute viral hepatitis?

A

Less than 6 months

94
Q

What are the histological characteristics of acute viral hepatitis?

A

Inflammation between the hepatocytes, and within the portal tracts

95
Q

What is the MOA of hepatocellular destruction in acute viral hepatitis?

A

CTL via MHC class I upregulation

96
Q

What is the definition of chronic hepatitis? What is the risk of chronic hepatitis?

A
  • Symptoms that last greater than 6 months

- There is a risk of progression to cirrhosis

97
Q

What are the histological characteristics of chronic hepatitis?

A

Portal tract inflammation WITHOUT hepatocyte inflammation (like you see in acute)

98
Q

What is the route of transmission for Hepatitis A-E?

A

A and E = fecal oral

BCD = Parenteral

99
Q

Which of the Hepatitis viruses cause acute hepatitis, but no chronic state?

100
Q

What does the presence of IgM indicate in a hepatitis infection? IgG?

A 
IgM = Active infection
IgG = prior infx or immunization
101
Q

HEV infection is worrisome in whom? Why?

A

Pregnant women since it has a high risk of progression to fulminant hepatitis

102
Q

What percent of HBV infections will progress to a chronic disease state? What is the serological marker of this, and how long must it be elevated for?

A
  • 20%

- HBsAg for more than 6 months

103
Q

What does HBsAg indicate?

A

Active infection (either acute or chronic)

104
Q

What happens to HBsAg through the course of HBV infection?

A

Starts high, then resolves, or goes through a window period if progression to a chronic state

105
Q

What is the first marker to rise in the acute phase of HBV infection?

106
Q

What is the major marker for the initial immune response toward HBV?

A

IgM of HBcAb

107
Q

What is the only marker that is present during the window phase of HBV infection?

A

IgM of HBcAb

108
Q

What is the IgM in HBV infection specific for (what part of the virus)? What about IgG?

A 
IgM = Core (HBcAb)
IgG = core and surface ag
109
Q

What is the “sign of victory” against HBV infection?

A

IgG against

110
Q

What is the only serological marker that will be seen in an immunized individual for HBV?

111
Q

What is the serological marker in HBV infection that indicates that the virus is still transmissible?

112
Q

What is the serological test used to confirm HCV infection? How is this used to monitor patients with HCV?

A

HCV RNA

Will go down with resolution

113
Q

Which hepatitis virus needs another hepatitis’s surface antigen?

A

D requires B’s surface antigen

114
Q

—-What is hepatitis coinfection? Superinfection?—-

A
  • ——Coinfection = getting B and D at the same time

- Superinfection = getting D with chronic B infection—-

115
Q

What is cirrhosis? What are the histological characteristics? When does it occur?

A

End stage liver damage characterized by broad bands of fibrosis and regenerative nodules of hepatocytes

116
Q

What is the cell that mediates fibrosis of the liver in cirrhosis? What cytokine does this cell secrete? Where do these cells lie in the liver?

A
  • Stellate cells that secrete TGF-beta

- These lie beneath the endothelial cells that line the sinusoids

117
Q

What are the four consequences of portal HTN caused by cirrhosis?

A
  • Ascites
  • Congestive splenomegaly
  • Portosystemic shunts
  • Hepatorenal syndrome
118
Q

What are the s/sx of decreased detoxification of the liver secondary to cirrhotic liver? (3)

A
  • AMS (asterixis and coma)
  • Gynecomastia
  • Jaundice
119
Q

What causes the CNS s/sx of cirrhosis?

A

Decreased breakdown of NH4, causes cerebral edema

120
Q

What causes the gynecomastia, spider angiomas, and palmar erythema seen in cirrhosis?

A

Decreased breakdown of estrogen

121
Q

What are the two liver synthesis functions that are decreased with cirrhosis?

A
  • Hypoalbuminemia

- Coagulopathy

122
Q

What is the consequence of hypoalbuminemia secondary to liver cirrhosis?

A

Decreased oncotic pressure ion the blood, leading to ascites

123
Q

What is the lab the is used to follow the coagulopathy seen with liver damage?

A

PT (same as warfarin), although both are increased

124
Q

True or false: fatty liver disease cause by EtOH can resolve with abstinence from EtOH

125
Q

What is the cause of alcoholic hepatitis?

A

Direct chemical injury to hepatocytes due to increased acetaldehyde damage

126
Q

What are the histological characteristics of alcohol mediate hepatitis?

A

Swelling and inflammation of hepatocytes with mallory bodies

127
Q

What are mallory bodies? What causes it?

A

Damaged intermediate filaments in hepatocytes caused by EtOH damage

128
Q

What is the usual presentation of alcoholic hepatitis?

A

Painful hepatomegaly

129
Q

What is the classic finding of LFTs with alcoholic hepatitis?

A

AST:ALT in a 2:1 ratio (and elevated of course)

130
Q

Why is AST preferentially elevated in EtOH mediate liver hepatitis?

A

EtOH damages mitochondria, which contain lots of AST

131
Q

What is nonalcoholic fatty liver disease? What is this associated with? What are the characteristic LFTs findings with this?

A
  • Fatty change of the liver without EtOH exposure
  • Associated with obesity
  • ALT>AST
132
Q

What is hemosiderosis? Hemochromatosis?

A
  • Hemosiderosis is deposition of Fe in tissue

- Hemochromatosis is when this causes damage to the tissues

133
Q

What mediates the damage seen in hemochromatosis?

A

ROS generation by Fe

134
Q

What is the key regulatory step in the human body for Fe absorption? What protein is involved in this step?

A

Enterocytes take up Fe via ferroportin

135
Q

What is the genetic mutation that causes primary hemochromatosis?

A

HFE gene mutation caused by C282Y

136
Q

What are the secondary causes of hemochromatosis?

A

Transfusions

137
Q

When and how does hemochromatosis present? (3)

A
  • 30-40s
  • Cirrhosis
  • Secondary DM
  • Bronze skin
138
Q

What are the Fe studies like in hemochromatosis:

  • Ferritin
  • TIBC
  • Serum Fe
  • Percent saturation
A
  • Increased Ferritin
  • Lower TIBC
  • Increased Serum Fe
  • Increase % sat
139
Q

How does hemochromatosis cause secondary DM (“bronze DM”)?

A

Destruction of beta cells through Fe deposition and ROS generation

140
Q

What is the relationship between ferritin and TIBC? Why?

A

Ferritin measures how much Fe is bound to transferrin, and TIBC measures the open spaces for new Fe.

141
Q

What is the diagnostic test for hemochromatosis? What is the stain used to identify Fe in a histological sample?

A

Liver biopsy with prussian blue stain

142
Q

What are the two pigments that can cause hepatocytes to turn brown? How do you differentiate them?

A
  • Lipofuscin
  • Fe

(prussian blue to highlight only Fe)

143
Q

What is lipofuscin? What is the significance of this?

A

Brown pigment from the breakdown of lipids. Benign.

144
Q

What is the treatment for hemochromatosis?

A

Phlebotomy to draw off Fe

145
Q

The risk of what cancer is increased with hemochromatosis? Why?

A

Hepatocellular CA d/t ROS generation by Fe

146
Q

What is the genetic defect caused by Wilson’s disease? Inheritance pattern? What does this do?

A

AR defect in ATP7B gene, causing defective ATP-mediated Cu transport

147
Q

What is the pathophysiology of Wilson’s disease?

A

Lack of Cu transport into the bile, and a lack of Cu incorporation into ceruloplasmin. This causes a buildup of Cu in tissues

148
Q

What is the role of ceruloplasmin?

A

Cu transporter in the blood

149
Q

What is the MOA of Cu mediated tissue damage?

A

Production of Hydroxyl free radiacls

150
Q

What are the classic s/sx of Wilson’s disease?

A
  • Cirrhosis
  • Neurological manifestations
  • Kayser-Fleisher rings in cornea
151
Q

There is an increased risk for which cancer with Wilson’s disease?

A

hepatocellular CA

152
Q

What is the treatment for Wilson’s disease?

A

D-Penicillamine (Cu chelating agent)

153
Q

What are the three lab findings with Wilson’s disease?

A
  1. Increased urinary Cu
  2. Decreased serum ceruloplasmin
  3. Increased Cu on liver biopsy
154
Q

What is primary biliary cirrhosis?

A

Autoimmune granulomatous destruction of intrahepatic bile ducts

155
Q

Who usually gets primary biliary cirrhosis?

A

Women in their 40s

156
Q

What is primary biliary cirrhosis associated with?

A

Other autoimmune diseases

157
Q

What is the antibody that is elevated with Primary biliary cirrhosis?

158
Q

What is the usual presentation of primary biliary cirrhosis?

A

Obstructive jaundice with cirrhosis as a late complication

159
Q

What is primary sclerosing cholangitis?

A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts

160
Q

What are the gross findings of primary sclerosing cholangitis? Histological?

A

Periductal fibrosis with an “onion skin” appearance

161
Q

What is the classical radiological finding of primary sclerosing cholangitis?

A

Beaded bile duct

162
Q

What biliary disease is associated with Ulcerative colitis?

A

Primary sclerosing cholangitis

163
Q

What is the antibody that is elevated with primary sclerosing cholangitis?

A

pANCA (just like UC has)

164
Q

What is the classic histological finding of ulcerative colitis? Crohn’s disease?

A 
UC = inflammation of the duct
CD = granuloma formation
165
Q

How does a patient with primary sclerosing cholangitis present?

A

Cirrhosis and obstructive jaundice

166
Q

Patients with primary sclerosing cholangitis have an increased risk for developing what CA?

A

Cholangiocarcinoma

167
Q

What is Reye syndrome?

A

Fulminant hepatitis and encephalopathy when a child takes ASA during an infection. MOA unknown.

168
Q

What is the likely (but not proven) cause of Reye syndrome?

A

Mitochondrial damage of hepatocytes

169
Q

What are the classical ssx of Reye syndrome?

A
  • Hypoglycemia
  • Elevated LFTs
  • N/v
170
Q

What are the severe consequences of Reye syndrome?

A

Coma and death

171
Q

What is the ONLY disease where a child should be given ASA?

A

Kawasaki syndrome (systemic vasculitis that usually presents with macroglossia and coronary problems)

172
Q

What are hepatic adenomas associated with?

A

Oral contraceptive use

173
Q

What are the risk factors for hepatic adenomas? When are these particularly concerning in women?

A

Rupture and intraperitoneal hemorrhage, especially during pregnancy

174
Q

What are the risk factors for developing hepatocarcinoma? Which infectious toxin cause?

A
  • Chronic hepatitis
  • Cirrhosis
  • Aflatoxins from aspergillus
175
Q

What is the MOA of aflatoxins produced by aspergillus?

A

Induce p53 mutations, causing hepatocellular carcinomas

176
Q

What is Budd-Chiari syndrome?

A

Liver infarction secondary to hepatic vein obstruction

177
Q

What are the s/sx of Budd-Chiari syndrome?

A

Painful hepatomegaly and ascites

178
Q

Why is Budd-Chiari syndrome more common in hepatocellular CA?

A

moving of CA into the hepatic vein

179
Q

Why is there a poor prognosis for hepatocellular CA?

A

Found late d/t masking of symptoms by cirrhosis

180
Q

What is the serum marker that is used for following hepatocellular CA?

A

Alpha-fetoprotein

181
Q

What is the most common cause of hepatic carcinomas (in general)?

A

Mets from other organs

182
Q

Where do the mets that go to the liver usually come from?

A
  • Colon
  • Breast
  • Lung
  • Pancreas
183
Q

How are mets to the liver detected clinically?

A

Large liver with nodular free-edge of the liver

All the things (36 decks)

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