Pathoma Chapter 11(Gall Bladder, Pancreas And Liver)

Front 1

Acute pancreatitis

Back 1

Premature activation of trypsin activate other enzymes leading to autodigestion of pancreatic parenchyma.

Causes both liquefactive(pancreatic parenchyma) and fat necrosis(peripancreatic fat)

Front 2

Most common cause of pancreatitis

Back 2

Alcohol and gallstones
Rupture of a posterior duodenal ulcer
Mumps virus

Front 3

Lab findings for pancreatitis(acute)

Back 3

lipase and amylase.
lipase more specific

Hypocalcemia due to fat necrosis

Front 4

Complications of acute pancreatitis

Back 4

Shock due to peripancreatic hemorrhage

Pancreatic PSEUDOcyst - just lined by fibrous tissue surrounding the liquefactive necrosis and enzymes.(Causes persistent elevation of amylase)
DIC and ARDS(enzymes can activate coagulation, can also destroy lung tissue if they get into blood)

Front 5

Common cause of pancreatic abscess? presentation?

Back 5

E. coli; presents with abdominal pain, fever and persistently elevated amylase(normally would reduce after bout of acute pancreatitis)

Front 6

Common causes of chronic pancreatitis

Back 6

Alcohol(adults) and cystic fibrosis(children). Can also be idiopathic.

CF - slows the ability of the pancreas to drain

Front 7

Clinical features of chronic pancreatitis

Back 7

--Epigastric abdominal pain that radiates to the back.
--Pancreatic Insufficiency leading to fat malabsorption, steatorrhea, poor absorption of Vitamins DAKE
--ABSENCE of amylase/lipase in chronic pancreatitis
--dystrophic calcification of pancreas
--damage to islets leading to secondary Diabetes Type II
--Risk for pancreatic carcinoma

Front 8

Pancreatic Carcinoma demographic and risk factors

Back 8

elderly(>70)
Smokers and chronic pancreatitis

Front 9

Clinical features of pancreatic cancer(head)

Back 9

--Tumor in the head of pancreas blocks the flow of bile which allows whatevers in bile to leak into blood. As such, conjugated bilirubin leaks into blood(jaundice).
--Since bile can't get to GI tract, you get pale stool.
--Since duct is blocked, bile swells up making it palpable.

obstructive jaundice, pale stool, palpable bladder

Front 10

Clinical features of pancreatic cancer(tail)

Back 10

Secondary diabetes if they knock out islet cells.

Front 11

Serum tumor marker for pancreatic cancer?

Back 11

CA 19-9

Front 12

Classic sign for pancreatic cancer?

Back 12

Trousseau sign -- presents as swelling erythema and tenderness in the extremities

Front 13

Biliary obstruction within first 3 months of life?

Back 13

Biliary atresia

Front 14

Biliary atresia presentation

Back 14

Presents within first 3 months, CONJUGATED bilirubin can leak into blood causing jaundice and can lead to cirrhosis due to back pressure to the liver

Front 15

Cholelithiasis(Gallstones)

Back 15

Precipitation of cholesterol or bilirubin in bile(both components of bile)
Can occur due to supersaturation OR decreased phospholipids/bile acids which help solubilize cholesterol.
OR stasis which can lead to infection where bacteria can unconjuage bilirubin causing stones

Front 16

Cholestyramine

Back 16

lipid lowering agent which binds bile acids which prevents ileum from recycling bile acids. Thus decreased bile acids increase risk of cholesterol stones

Front 17

Cholesterol Stones description/risk factors

Back 17

usually radioLUCENT, YELLOW stones

Age(40ish),
estrogen-- which increase activity of HMG-CoA reductase which increases cholesterol and increase Lipoprotein receptors on hepatocytes increasing cholesterol uptake(female, obese)
--clofibrate(lipid lowering agent increasing HMG-Coa reductase activity causing increased cholesterol and decreases conversion of cholesterol to bile acids which decreases solubility
--Crohn's Disease(terminal ileum) which damages ability to reuptake bile salts/acids which is necessary for solubility in bile
--Cirrhosis leads to decreased production of bile salts

Front 18

Bilirubin Stone description/risk factors

Back 18

RadioOPAQUE, BLACK in color

Risk factors:
--Extravascular Hemolysis(increases bilirubin in bile.) Hb --> Heme and Globin
Heme --> Iron and Protoporphyrin
Protophorphyrin --> Unconjugated Bilirubin
This bilirubin is eventually put in gall bladder, so if theres a lot of extravascular hemolysis, there's a lot of conjugated bilirubin in the gall bladder when the liver eventually works through it.
-- Biliary tract infection(bacteria can deconjugate increasing risk of precipitation)

Front 19

Complications associated with gallstones

Back 19

Biliary colic, acute/chronic cholecystitis, ascending cholangitis, gallstone ileus and gallbladder cancer

Front 20

Biliary colic presents where?

Back 20

Right upper quadrant pane

Waxing and waning pain as gall bladder contracts against stone

Front 21

Acute Cholecystitis Etiology

Back 21

A stone blocking duct will cause dilatation of gall bladder leading to pressure ischemia and bacterial overgrowth of E.Coli

Front 22

Right upper quadrant pain radiating to the right scapula

Back 22

Acute cholecystitis

Front 23

Acute cholecystitis lab findings

Back 23

increased serum alk phosp, increased WBC

Front 24

What key sign is associated with Chronic Cholecystitis

Back 24

Rokitansky-Aschoff sinus -- herniation of gallbladder mucosa into the muscular wall(PICTURE)

Front 25

Chronic Cholecystitis long term complication...

Back 25

Porcelain gall bladder
Shrunk hard gallbladder due to chronic inflammation, fibrosis and dystrophic calcification

Front 26

Gallstone ileus etiology

Back 26

fistula formed between gallbladder wall and small bowel allowing a huge ass stone to block GI tract

Front 27

cholecystitis in an elderly woman(80 year old)

Back 27

Gall bladder carcinoma

Front 28

What binds unconjugated bilirubin to allow it to travel in blood?

Back 28

Albumin

Front 29

What enzyme conjugates bilirubin?

Back 29

Uridine Glucuronyl Transferase(UGT) in hepatocytes.

Front 30

Describe what happens to conjugated bilirubin?

Back 30

It is released in the small bowel to aid in digestion. The intestinal flora then convert conjugated bilirubin into urobilinogen

Front 31

Extravascular Hemolysis

Back 31

Overpowers livers ability to conjugate, leads to an increase in unconjugated bilirubin in the blood.
EVENTUALLY, this will lead to high concentration bilirubin in bile that enters small bowel. Turns to urobilinogen in GI tract and turns urine and stool dark.(Urine dark due to UROBILINOGEN)

Front 32

Physiologic Jaundice of the Newborn

Back 32

Newborn has transiently low UGT activity. UCB can deposit in brain and lead to neurologic deficits and death(kernicterus). UCB cannot leave in urine because it is not water soluble, but Phototherapy simply makes UCB water soluble.

Front 33

Gilbert Syndrome

Back 33

mildly low UGT, leading to an increase in UCB

Front 34

Crigler-Najjar Syndrome

Back 34

Absence of UGT, leads to kernicterus. It is a genetic disorder thats usually fatal.

Front 35

Pitch dark liver incidental finding

Back 35

Dubin Johnson Syndrome -
Deficiency of bilirubin canalicular TRANSPORT(after it has been conjugated). Not clinically significant, but will have a conjugated bilirubinemia(CB in blood).

Can have this deficiency without discoloration(Rotor syndrome)

Front 36

Liver fluke

Back 36

Clonorchis Sinensis

Front 37

Biliary tract obstruction(obstructive jaundice)

Back 37

anything that blocks bile duct.

--dark urine(water soluble CB in blood gets filtered
--DECREASED Urobilinogen
--pale stools(CB doesn't get to GI)
--Lots of cholesterol in bile leaks into blood leading to hypercholesterolemia with xanthomas
--steatorrhea with malabsorption of fat soluble vitamins

Front 38

Viral hepatitis

Back 38

Inflammation disrupts hepatocytes and small bile ducts leading to an increase in increased CB and UCB

Dark urine due to increase CONJUGATED bilirubin. Urine urobilinogen is normal or decreased due to the hepatocyte +bile ductules dysfunction

Front 39

Acute Hepatitis lab tests

Back 39

ALT >> AST

Front 40

Chronic Hepatitis predominantly involves...?

Back 40

Portal tract

Front 41

Fecal-oral transmission?

Back 41

Hep A and E
No Chronic state

Front 42

Pregnant women with fulminant hepatitis(liver failure and massive liver necrosis)

Back 42

Hepatitis E

Front 43

Immunization is available for what heps? What antibody signifies immunity?

Back 43

Hepatitis A, IgG

Front 44

Commonly acquired by travelers

Back 44

Hep A

Front 45

Commonly acquired from contaminated water or undercooked seafood

Back 45

Hep E

Front 46

How is hepatitis B transmitted?

Back 46

parenteral tranmission(childbirth, intercourse, IV drugs)

Front 47

Hep B Serology

Back 47

1.) HBsAG is KEY MARKER for infection. First marker that arises during infection. If it stays for longer than 6 months, then you're chronic.
2.) IgM vs core in the beginning. Transition to IgG when you level up. If you WIN then HBsAG goes away. If you don't it stays
3.) IgG vs HBsAB means VICTORY.(or immunization)
4.) HBeAG indicates infectivity. "need an envelope to mail to friend, etc."

Front 48

How is Hepatitis C transmitted?

Back 48

Parenterally.
HCV-RNA test confirms infection. Decreased RNA indicates recovery while persistence indicates disease.

Front 49

What virus more commonly progresses to chronic hepatitis?

Back 49

Hepatitis C OFTEN progresses to chronic disease vs Hep B which rarely progresses.

Front 50

Which is worse? coinfection or superinfection of Hep D?

Back 50

superinfection

Front 51

Decreased detox in liver failure can lead to what symptoms?

Back 51

Excess estrogen(gynecomastia, spider angiomata, palmar erythema)
Jaundice, mental status changes

Front 52

What lab test gauges coagulopathy in liver disease?

Back 52

PT - loss of epoxide reductase

Front 53

Enzyme elevation in Alcoholic hepatitis. Why?

Back 53

AST>>ALT

AST is mitochondrial, and alcohol is a mitochondrial poison

Front 54

What distinctive histologic feature presents in alcoholic hepatitis?

Back 54

Mallory bodies which are damaged cytokeratin filaments(IMF)

Front 55

The protein coded for by the gene involved in primary hemochromatosis is most similar to what other protein?

Back 55

Mutations in the HFE gene

Similar to MHC Class I. HFE also associated with Beta 2 microglobulin. Regulates interaction of transferrin receptor with transferrin

Front 56

What is the triad for hemochromatosis?

Back 56

cirrhosis, secondary diabetes mellitus, and bronze skin.

Also find cardac arrhythmias and gonadal dysfunction.

Front 57

What labs do you find with hemochromatosis?

Back 57

Increased ferritin, decreased TIBC, inreased serum Iron and increased Saturation.

Front 58

What stain, stains for iron?

Back 58

Prussian Blue, will distinguish between iron and lipofuscin which is commonly present in hepatocytes.

Front 59

Wilson disease

Back 59

Autosomal recessive defect(APT7B) in ATP mediated hepatocyte copper transport. Can't transport copper into bile or ceruloplasmin.

Front 60

Lab findings in Wilson disease

Back 60

increased urinary copper, decreased serum ceruloplasmin(can't transport copper into this transport protein), and increased copper on liver biopsy.

Front 61

Primary Biliary Cirrhosis demographic

Back 61

40 yr old women

Front 62

What classic lab finding do you see in Primary Biliary Cirrhosis?

Back 62

antimitochondrial antibody

Front 63

Primary Sclerosing Cholangitis

Back 63

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts that presents with obstructive jaundice

Front 64

Primary Sclerosing Cholangitis associated with?

Back 64

Ulcerative Colitis(p-ANCA positive)

Front 65

What one disease do you give aspirin to children for?

Back 65

Kawasaki Disease

Front 66

What microbe is a risk factor for hepatocellular carcinoma?

Back 66

Aspergillus that releases aflatoxins. These toxins induce p53 mutations.

Front 67

Serum tumor marker for Hepatocellular Carcinoma?

Back 67

alpha-fetoprotein