Liver, gallbladder n' such Flashcards
(183 cards)
1
Q
Premature activation of what enzyme in particular causes pancreatitis? What does this cause?
A
trypsin–this causes activation of other enzymes
2
Q
What two types of necrosis ensue d/t pancreatitis?
A
- Liquefactive
- Saponification / fat necrosis
3
Q
What are the two most common causes of pancreatitis? How?
A
- EtOH (contracts sphincter of Oddi)
- Gallstones (blocks drainage)
4
Q
What cause the saponification seen in pancreatitis?
A
Digestion of fat surrounding pancreas
5
Q
How does EtOH cause pancreatitis?
A
Contraction of the sphincter of Oddi, causing backup of enzymes and pancreatic juices
6
Q
How do gallstones cause pancreatitis?
A
Blockage of the duct of Vader
7
Q
What is the most common traumatic cause of pancreatitis?
A
Seatbelt smashing in car accidents
8
Q
How does hypercalcemia cause pancreatitis?
A
Activates enzymes
9
Q
What are the two metabolic disturbances that can lead to pancreatitis?
A
- Hypercalcemia
- Hyperlipidemia
10
Q
Which virus can cause pancreatitis?
A
Mumps
11
Q
Rupture of what part of the duodenum (e.g from an ulcer) ( will lead to acute pancreatitis? anterior or posterior)
A
Posterior
12
Q
What are the classic s/sx of pancreatitis?
A
Epigastric pain that radiates to the back with n/v
13
Q
What causes the periumbilical and flank hemorrhage in pancreatitis?
A
Necrosis spread to these two regions as well
14
Q
What enzymes are elevated in acute pancreatitis? Which is more specific?
A
Lipase
and amylase, but not specific
15
Q
What is the metabolic disturbance that acute pancreatitis causes? Why?
A
Hypocalcemia d/t saponification (uses up Ca)
16
Q
What causes shock seen in acute pancreatitis?
A
Damage of the blood vessels
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
18
Q
What is the usual bacterial cause of a pancreatic abscess?
A
E.Coli
19
Q
How can acute pancreatitis cause DIC? ARDS?
A
Amylase can activate coagulation factors and destroy lung tissue.
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
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
22
Q
What are the s/sx of chronic pancreatitis?
A
- Pancreatic insufficiency
- Epigastric pain radiating to the back
23
Q
What causes the pancreatic insufficiency seen in chronic pancreatitis? How does this manifest itself?
A
- Fibrosis
- Steatorrhea and malabsorption issues
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
25
What are the radiological findings of chronic pancreatitis?
Dystrophic calcification
26
What endocrine disorder can result from chronic pancreatitis? How?
DM-- damage to the beta cells
27
What CA are patients with chronic pancreatitis at an increased risk for? From what tissue in the pancrease does this usually arise from?
-Pancreatic adenocarcinoma-- from the ducts
28
In what age group is adenocarcinoma of the pancreas most common?
Elderly
29
What are the two major risk factors for pancreatic carcinoma?
Smoking and chronic pancreatitis
30
What are the s/sx of pancreatic adenocarcinoma?
epigastric pain and weight loss
31
What are the classic findings of adenocarcinoma in the head of the pancreas?
- Palpable gallbladder
- Jaundice
- Pale stools
32
Thin elderly pt with new onset DM is suspicious for what?
pancreatic adenocarcinoma
33
What is the tumor marker for pancreatic adenoCA?
CA19-9
34
----What is the treatment for pancreatic adenoCA? Prognosis?---
-----Whipple procedure
(removal of duodenum, head of pancreas, and gallbladder
-Poor prognosis----
35
What is biliary atresia?
Failure to form, or early destruction of the extrahepatic biliary tree
36
How does biliary atresia present? What type of bilirubin is elevated in this disorder?
- Jaundice, progressing to cirrhosis early in life
| - Direct (conjugated) bili is elevated
37
What are the three causes of cholelithiasis?
- Supersaturation of cholesterol or bilirubin
- Decreased phospholipids / bile acids
- Stasis
38
How does cholestyramine cause an increased risk for cholelithisasis?
Decreased reuptake of bile acids, which is needed for solubility
39
How does stasis in the bile duct lead to gallstones?
Bacteria deconjugate the heme into bili, leading to bili
40
What is the most common type of gallstones in the west? How do they appear on imaging?
- Cholesterol stones
| - Usually radiolucent (don't appear)
41
Why is it that estrogen increases the risk for cholelithisais? (2)
1. Increases HMG-CoA reductase and cholesterol synthesis
| 2. Estrogen also increase cholesterol receptors on liver
42
How does clofibrate increase the risk for gallstones?
It increases the rate of HMG CoA reductase action, leading to increased cholesterol synthesis, and decreases bile acid
43
What ethnicity has a higher rate of cholelithiasis?
Native americans
44
What is the IBD that increases the risk for cholelithisasis? Why?
- Crohn's disease
| - Ileum is damaged, so there is poor uptake of bile acids and salts, causing precipitation of cholesterol
45
How does cirrhosis increase the risk for gallstones?
Decreased production of bile salts
46
What are the causes of bilirubin stones? (2) How do they appear grossly?
- extravascular hemolysis
- Biliary tract infections
-Black or darkly pigmented stones
47
What are the three infectious agents that increase the risk for the development of a gallstone (hint: 1 bacteria + 2 parasites)?
- E.coli
- Ascaris lumbricoides
- Clonorchis sinensis
48
What are the five key complications that can result from gallstones?
1. Biliary colic
2. Acute and chronic cholecystitis
3. Ascending cholangitis
4. Gallstone ileus
5. Gallbladder CA
49
What is biliary colic?
Intermittent RUQ abdominal pain caused by contractions of the gallbladder against a stone.
50
What is acute cholecystitis?
Acute inflammation of the gallbladder caused by an impacted stone in cystic duct and bacterial overgrowth
51
What is the classic presentation of acute cholecystitis? (3)
- RUQ pain with radiation to the right scapula
- Fever + leukocytosis
- N/v
52
What will happen to a gallbladder in acute cholecystitis if left untreated?
Rupture
53
Why is alk phos elevated in gallbladder issues?
Alk phos a key component of the endothelial cells of the gallbladder tract
54
What is chronic cholecystitis?
Chronic inflammation of the gallbladder due to longstanding chemical irritation from cholelithiasis
55
What are Rokitansky-Aschoff sinuses? What disease are these seen in?
gallbladder mucosa that dives down into the wall. Classic for chronic cholecystitis
56
What is the classical s/sx of chronic cholecystitis?
Vague RUQ pain after eating
57
What is the long term complication of chronic cholecystitis?
-Porcelain gallbladder--dystrophic calcification of the gallbladder
58
What is Porcelain gallbladder? What is the risk of leaving this untreated?
- Dystrophic calcification of the gall bladder secondary to chronic cholecystitis
- Predisposes to gallbladder cancer
59
What is the treatment for chronic cholecystitis?
Cholecystectomy
60
What is ascending cholangitis?
Bacterial infection of the bile ducts
61
How does ascending cholangitis present?
Sepsis, jaundice, and abdominal pain
62
What type of bacteria usually cause ascending cholangitis?
Enteric, Gram negative
63
What poses an increased risk of developing ascending cholangitis? How?
Choledocholithiasis-- decreased flow of bile allows bacteria to grow upwards in the bile duct
64
What is a gallstone ileus? How do these occur?
-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
65
What cancer is associated with cholecystitis?
Adenocarcinoma from the gland cells of the gallbladder
66
What is the major risk factor for the development of gallbladder adenoCA
Gallstones
67
----What is the classical presentation of gallbladder carcinoma?----
----Cholecystitis in an *elderly* women----
68
Jaundice occurs when serum bilirubin rises above what level?
>2.5 mg/dL
69
What is the transporter for the heme component of Hb when it is broken down in the blood? Where does this go?
Albumin, goes to the liver
70
What causes the brown coloration of stool? Yellow urine?
Urobilinogen
71
What changes bili to urobilinogen?
Intestinal bacteria
72
What causes the increased risk of pigmented gallstones in hemolysis of ineffective erythropoiesis?
Increase in bili being poured out of the liver
73
What causes the dark urine in hemolysis/ineffective erythropoiesis?
increase in urine urobilinogen,. NOT due to the increased unconjugated bili
74
Can unconjugated bili be excreted through the urine?
NO--not water soluble
75
What is the enzyme that conjugates bili?
UGT
76
What causes physiological jaundice of the newborn?
Newborn liver has transiently low UGT
77
What type of bili is increased in physiological jaundice of the newborn?
Indirect (unconjugated)
78
Where in an infant does unconjugated bilirubin go in physiological jaundice of the newborn? Why here?
Basal ganglia, since these are fatty, and unconjugated bili is fat soluble
79
What is the MOA of bili light?
Makes unconjugated bili water soluble--does NOT conjugate it
80
What is the cause of Gilbert syndrome?
Genetically, mildly low UGT activity, leading to jaundice when exposed to stress. Benign condition
81
What is Crigler-Najjar syndrome (type I)? Does it respond to phenobarbital?
- Absence of UGT, causing kernicterus and death of infants
| - Does not respond to phenobarbital
82
What is Dubin-Johnson syndrome? What type of bili builds up?
Defective transport protein from the hepatocytes into the biliary tree, causing a build up of CONJUGATED bili
83
What are the liver findings of Dubin-Johnson syndrome?
Black liver
84
What is the prognosis for Dubin-johnson syndrome?
not clinically significant
85
What is Rotor syndrome?
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
What are the s/sx of biliary tract obstruction?
- Increased conjugated bili
- Dark urine d/t bilirubinemia
- Xanthomas
- Pruritus/jaundice
87
----What causes the dark urine in viral hepatitis?----
----Increase in both CB and UB, causing increased urine bili---
88
What is hepatitis?
Inflammation of the liver parenchyma
89
What are the virus that usually cause hepatitis? (3)
- EBV
- CMV
- Hepatitis viruses
90
Which bilirubin is elevated in acute viral hepatitis? Why?
Both CB and UCB
- Increased CB d/t bile duct destruction
- Increased UCB d/t hepatocyte destruction
91
What happens to the urine with acute viral hepatitis?
Dark d/t increased CB in the blood
92
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?
- Elevated with ALT > AST
| - EtOH has AST:ALT in 2:1 ratio
93
How long do symptoms last for in acute viral hepatitis?
Less than 6 months
94
What are the histological characteristics of acute viral hepatitis?
Inflammation between the hepatocytes, and within the portal tracts
95
What is the MOA of hepatocellular destruction in acute viral hepatitis?
CTL via MHC class I upregulation
96
What is the definition of chronic hepatitis? What is the risk of chronic hepatitis?
- Symptoms that last greater than 6 months
| - There is a risk of progression to cirrhosis
97
What are the histological characteristics of chronic hepatitis?
Portal tract inflammation WITHOUT hepatocyte inflammation (like you see in acute)
98
What is the route of transmission for Hepatitis A-E?
A and E = fecal oral
| BCD = Parenteral
99
Which of the Hepatitis viruses cause acute hepatitis, but no chronic state?
A and E
100
What does the presence of IgM indicate in a hepatitis infection? IgG?
```
IgM = Active infection
IgG = prior infx or immunization
```
101
HEV infection is worrisome in whom? Why?
Pregnant women since it has a high risk of progression to fulminant hepatitis
102
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?
- 20%
| - HBsAg for more than 6 months
103
What does HBsAg indicate?
Active infection (either acute or chronic)
104
What happens to HBsAg through the course of HBV infection?
Starts high, then resolves, or goes through a window period if progression to a chronic state
105
What is the first marker to rise in the acute phase of HBV infection?
HBsAg
106
What is the major marker for the initial immune response toward HBV?
IgM of HBcAb
107
What is the only marker that is present during the window phase of HBV infection?
IgM of HBcAb
108
What is the IgM in HBV infection specific for (what part of the virus)? What about IgG?
```
IgM = Core (HBcAb)
IgG = core and surface ag
```
109
What is the "sign of victory" against HBV infection?
IgG against
110
What is the only serological marker that will be seen in an immunized individual for HBV?
IgG
111
What is the serological marker in HBV infection that indicates that the virus is still transmissible?
HBeAg
112
What is the serological test used to confirm HCV infection? How is this used to monitor patients with HCV?
HCV *RNA*
Will go down with resolution
113
Which hepatitis virus needs another hepatitis's surface antigen?
D requires B's surface antigen
114
----What is hepatitis coinfection? Superinfection?----
- ------Coinfection = getting B and D at the same time
| - Superinfection = getting D with chronic B infection----
115
What is cirrhosis? What are the histological characteristics? When does it occur?
End stage liver damage characterized by broad bands of fibrosis and regenerative nodules of hepatocytes
116
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?
- Stellate cells that secrete TGF-beta
| - These lie beneath the endothelial cells that line the sinusoids
117
What are the four consequences of portal HTN caused by cirrhosis?
- Ascites
- Congestive splenomegaly
- Portosystemic shunts
- Hepatorenal syndrome
118
What are the s/sx of decreased detoxification of the liver secondary to cirrhotic liver? (3)
- AMS (asterixis and coma)
- Gynecomastia
- Jaundice
119
What causes the CNS s/sx of cirrhosis?
Decreased breakdown of NH4, causes cerebral edema
120
What causes the gynecomastia, spider angiomas, and palmar erythema seen in cirrhosis?
Decreased breakdown of estrogen
121
What are the two liver synthesis functions that are decreased with cirrhosis?
- Hypoalbuminemia
| - Coagulopathy
122
What is the consequence of hypoalbuminemia secondary to liver cirrhosis?
Decreased oncotic pressure ion the blood, leading to ascites
123
What is the lab the is used to follow the coagulopathy seen with liver damage?
PT (same as warfarin), although both are increased
124
True or false: fatty liver disease cause by EtOH can resolve with abstinence from EtOH
True
125
What is the cause of alcoholic hepatitis?
Direct chemical injury to hepatocytes due to increased acetaldehyde damage
126
What are the histological characteristics of alcohol mediate hepatitis?
Swelling and inflammation of hepatocytes with *mallory bodies*
127
What are mallory bodies? What causes it?
Damaged intermediate filaments in hepatocytes caused by EtOH damage
128
What is the usual presentation of alcoholic hepatitis?
Painful hepatomegaly
129
What is the classic finding of LFTs with alcoholic hepatitis?
AST:ALT in a 2:1 ratio (and elevated of course)
130
Why is AST preferentially elevated in EtOH mediate liver hepatitis?
EtOH damages mitochondria, which contain lots of AST
131
What is nonalcoholic fatty liver disease? What is this associated with? What are the characteristic LFTs findings with this?
- Fatty change of the liver without EtOH exposure
- Associated with obesity
- ALT>AST
132
What is hemosiderosis? Hemochromatosis?
- Hemosiderosis is deposition of Fe in tissue
| - Hemochromatosis is when this causes damage to the tissues
133
What mediates the damage seen in hemochromatosis?
ROS generation by Fe
134
What is the key regulatory step in the human body for Fe absorption? What protein is involved in this step?
Enterocytes take up Fe via ferroportin
135
What is the genetic mutation that causes primary hemochromatosis?
HFE gene mutation caused by C282Y
136
What are the secondary causes of hemochromatosis?
Transfusions
137
When and how does hemochromatosis present? (3)
- 30-40s
- Cirrhosis
- Secondary DM
- Bronze skin
138
What are the Fe studies like in hemochromatosis:
- Ferritin
- TIBC
- Serum Fe
- Percent saturation
- Increased Ferritin
- Lower TIBC
- Increased Serum Fe
- Increase % sat
139
How does hemochromatosis cause secondary DM ("bronze DM")?
Destruction of beta cells through Fe deposition and ROS generation
140
What is the relationship between ferritin and TIBC? Why?
Ferritin measures how much Fe is bound to transferrin, and TIBC measures the open spaces for new Fe.
141
What is the diagnostic test for hemochromatosis? What is the stain used to identify Fe in a histological sample?
Liver biopsy with prussian blue stain
142
What are the two pigments that can cause hepatocytes to turn brown? How do you differentiate them?
- Lipofuscin
- Fe
(prussian blue to highlight only Fe)
143
What is lipofuscin? What is the significance of this?
Brown pigment from the breakdown of lipids. Benign.
144
What is the treatment for hemochromatosis?
Phlebotomy to draw off Fe
145
The risk of what cancer is increased with hemochromatosis? Why?
Hepatocellular CA d/t ROS generation by Fe
146
What is the genetic defect caused by Wilson's disease? Inheritance pattern? What does this do?
AR defect in ATP7B gene, causing defective ATP-mediated Cu transport
147
What is the pathophysiology of Wilson's disease?
Lack of Cu transport into the bile, and a lack of Cu incorporation into ceruloplasmin. This causes a buildup of Cu in tissues
148
What is the role of ceruloplasmin?
Cu transporter in the blood
149
What is the MOA of Cu mediated tissue damage?
Production of Hydroxyl free radiacls
150
What are the classic s/sx of Wilson's disease?
- Cirrhosis
- Neurological manifestations
- Kayser-Fleisher rings in cornea
151
There is an increased risk for which cancer with Wilson's disease?
hepatocellular CA
152
What is the treatment for Wilson's disease?
D-Penicillamine (Cu chelating agent)
153
What are the three lab findings with Wilson's disease?
1. Increased urinary Cu
2. Decreased serum ceruloplasmin
3. Increased Cu on liver biopsy
154
What is primary biliary cirrhosis?
Autoimmune granulomatous destruction of intrahepatic bile ducts
155
Who usually gets primary biliary cirrhosis?
Women in their 40s
156
What is primary biliary cirrhosis associated with?
Other autoimmune diseases
157
What is the antibody that is elevated with Primary biliary cirrhosis?
AMA
158
What is the usual presentation of primary biliary cirrhosis?
Obstructive jaundice with cirrhosis as a late complication
159
What is primary sclerosing cholangitis?
Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts
160
What are the gross findings of primary sclerosing cholangitis? Histological?
Periductal fibrosis with an "onion skin" appearance
161
What is the classical radiological finding of primary sclerosing cholangitis?
Beaded bile duct
162
What biliary disease is associated with Ulcerative colitis?
Primary sclerosing cholangitis
163
What is the antibody that is elevated with primary sclerosing cholangitis?
pANCA (just like UC has)
164
What is the classic histological finding of ulcerative colitis? Crohn's disease?
```
UC = inflammation of the duct
CD = granuloma formation
```
165
How does a patient with primary sclerosing cholangitis present?
Cirrhosis and obstructive jaundice
166
Patients with primary sclerosing cholangitis have an increased risk for developing what CA?
Cholangiocarcinoma
167
What is Reye syndrome?
Fulminant hepatitis and encephalopathy when a child takes ASA during an infection. MOA unknown.
168
What is the likely (but not proven) cause of Reye syndrome?
Mitochondrial damage of hepatocytes
169
What are the classical ssx of Reye syndrome?
- Hypoglycemia
- Elevated LFTs
- N/v
170
What are the severe consequences of Reye syndrome?
Coma and death
171
What is the ONLY disease where a child should be given ASA?
Kawasaki syndrome (systemic vasculitis that usually presents with macroglossia and coronary problems)
172
What are hepatic adenomas associated with?
Oral contraceptive use
173
What are the risk factors for hepatic adenomas? When are these particularly concerning in women?
Rupture and intraperitoneal hemorrhage, especially during pregnancy
174
What are the risk factors for developing hepatocarcinoma? Which infectious toxin cause?
- Chronic hepatitis
- Cirrhosis
- Aflatoxins from aspergillus
175
What is the MOA of aflatoxins produced by aspergillus?
Induce p53 mutations, causing hepatocellular carcinomas
176
What is Budd-Chiari syndrome?
Liver infarction secondary to hepatic vein obstruction
177
What are the s/sx of Budd-Chiari syndrome?
Painful hepatomegaly and ascites
178
Why is Budd-Chiari syndrome more common in hepatocellular CA?
moving of CA into the hepatic vein
179
Why is there a poor prognosis for hepatocellular CA?
Found late d/t masking of symptoms by cirrhosis
180
What is the serum marker that is used for following hepatocellular CA?
Alpha-fetoprotein
181
What is the most common cause of hepatic carcinomas (in general)?
Mets from other organs
182
Where do the mets that go to the liver usually come from?
- Colon
- Breast
- Lung
- Pancreas
183
How are mets to the liver detected clinically?
Large liver with nodular free-edge of the liver
