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Flashcards in Tombazzi - Gallbladder Deck (56)
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What is going on here?

Acute emphysematous cholecystitis: invasion of gas-forming organisms, notably clostridia and coliforms, can cause this

- Not hemorrhage in bottom right, but congestion; not fat in the wall, but air  


What happened here?

Gangrenous cholecystitis: severe cases where gallbladder is transformed to green-black necrotic organ, with small-to-large perforations (before this, wall is thickened, edematous, and hyperemic)

- Inflammation is predominantly neutrophilic


What do you see here?

Chronic cholecystitis: serosa usually smooth and glistening, but may be dulled by subserosal fibrosis 

- MICRO: scattered lymphos, plasma cells, macros

1. Mostly looking for diving down of glands into sinuses

- Reactive proliferation of mucosa and fusion of the mucosal folds may give rise to buried crypts of epithelium within the gallbladder wall = Rokitansky-Aschoff sinuses (*)

- Presence of acute inflam = acute on chronic 


What is this?

Cholesterolosis: strawberry gallbladder

- Can see this if fatty meal eaten: epi and sub-epi accumulation of cholesterol 

- NOTE: not tied to cholelithiasis or cholecystitis


What is going on here?

- Xanthogranulomatous cholecystitis: triggered by rupture of Rokitansky-Aschoff sinuses into wall of gallbladder followed by accumulation of macros that have ingested biliary phospholipids 

- Lipid-containing cells with foamy cytoplasm called xanthoma cells (bubbly, fat, stuffed up macros full of lipid)

- FRONT IMAGE: thickened, fibrotic gallbladder wall with a centrally located xanthogranulomatous cholecystitis lesion (arrows) containing chronic inflammatory cells, bile pigment, and foamy pigment-laden macrophages 


What is cholestasis? 2 types? How can you distinguish these clinically?

- Condition where bile can't flow from liver to the duodenum, leading to conjugated hyper-bilirubinemia and high alkaline phosphatase

- Types: 

1. OBSTRUCTIVE: mechanical blockage in duct system (extrahepatic) -> flow

2. METABOLIC: disturbances in bile formation (intrahepatic) -> making it

- Can distinguish these clinically by:

1. Medical history

2. PE

3. Abdominal US looking for intrahepatic biliary ductal dilation (indicating obstruction) 


What are some of the causes of extrahepatic and intrahepatic cholestasis?

- EXTRAHEPATIC (mechanical): stones, malignancy, large ducts primary sclerosing cholangitis, post-surgical complications, chronic pancreatitis, other

- INTRAHEPATIC (metabolic): primary biliary cirrhosis, medication, malignant infiltration, small ducts primary sclerosing cholangitis, other

- PSC: Crohn's, UC


What findings lead you to suspect extrahepatic cholestasis? Diagnostic techniques?


1. Cholestatic pattern of liver enzymes: alk phos, GGT, and bilirubin all elevated  

2. Biliary ductal dilatation by US


1. Clinical findings

2. MRCP (magnetic resonance cholangial pancreatography) and/or ERCP (endoscopic retrograde cholangio pancreatography)

3. EUS

- NOTE: attached images are of MRCP (left) and ERCP (right) 


What is this?

Cholestasis: impaired bile formation and bile flow that gives rise to accumulation of bile pigment in the hepatic parenchyma

- Can be caused by extrahepatic or intrahepatic obstruction of bile channels, or by defects in hepatocyte bile secretion 

- Can have bile plugs, which are more green than hemosiderin (brown) or lipofuscion


What do you see here?

- Hepatocytes and Kupffer cells full of granular brown deposits of hemosiderin from accumulation of excess iron in the liver


Describe what you see here.

- Normal bile duct travelling just above portal system

- Look for portal vein on US: if nothing above it of similar size, this is normal 


What do you see here? Unlabeled arrows?

- Biliary ductal dilatation (top left arrow)

- Hyper-echoic structure sitting inside CBD and shadow behind what is there that is typical for stones (top right arrow)


What malignancy most commonly causes biliary obstruction? How does it present?

- Pancreatic malignancy: when tumor is located at the head of the pancreas

- Note in the attached image that the bile duct must go through the pancreas

- As with most of the pancreatobiliary malignancies, pancreatic cancer presents clinically w/progressive painless jaundice and weight loss 


Female with complete colonectomy due to genetic disease that predisposes to colon cancer. Now, she has this ulcerated mass in her ampulla.

What genetic disease does she have? What is this mass? Tx?

- FAP: pts with FAP can develop adenomas in the second portion of the duodenum, and can develop duodenal and ampullary adenocarcinoma

- Not frequent, and slow growth

- TX: surgery and/or stent placement

- NOTE: image of normal apulla attached here


What is primary sclerosing cholangitis? Associations? Presentation? Tx?

Chronic cholestatic disease of intra- and extra-hepatic bile ducts -> nobody really knows how this happens, and there is no real treatment

1. Reaction to something in bile duct (maybe coming from colon; toxin): leads to scar tissue, and segmental narrowing of bile ducts

2. Severe ITCHING as part of cholestasis

- More common in AA, M

- Present with cholestatic pattern of liver enzymes: elevated GGT, alk phos, and bilirubin 

- Association with IBD: 70% of these people also have UC; less frequently Crohn’s 

1. 20-30% chance for cholangiocarcinoma

- TX: liver transplantation

- NOTE: HIV cholangiopathy presents similar radiologic findings


What do you see here?

Primary sclerosing cholangitis

1. LARGE DUCT inflam: acute, neutrophilic infiltration of epithelium superimposed on a chronic inflammation

2. SMALL DUCTS have little inflammation and show striking circumferential “onion skin” fibrosis around atrophic duct lumen, with eventual obliteration 

- Culminates in biliary cirrhosis (attached image), much like that seen with chronic obstruction and primary biliary cirrhosis -> irregular, puzzle-piece appearance

1. When we talk about hepatitis and cirrhosis of liver, the pattern is a little different: more nodular, regular, and even

- Biliary intraepithelial neoplasia may devo and cholangiocarcinoma -> usually w/fatal outcomes


What is going on here?

PSC: degenerating bile duct with "ONION SKIN" fibrosis (compare to attached normal image) 

- Cholestasis: gold pigment  

- Biliary cirrhosis: pretty far advanced because pt already has some cirrhosis


What is this? What neoplasm might you be worried about? Describe it.

- Stricture due to PSC -> can lead to devo of cholangiocarcinoma

- RISK FACTORS: most freq in 50-70-y/o M

1. PSC, Hep C-related cirrhosis, toxin exposure, infection w/liver flukes (clonorchis)

- Commonly present w/biliary obstruction causing painless jaundice

1. Labs suggest biliary obstruction: elevated total bilirubin, alk phos, 5’-nucleotidase, GGT

2. May have high tumor markers, like Ca 19-9


- TX: surgery, endoscopic palliation -> need to get early dx in order to offer some kind of tx

1. Not good for transplant because cancers come back -> very selective pts can be presented for this, but only some centers, incl Memphis, and protocol very detailed 

2. Mostly fatal in a few months 


How does cholangiocarcinoma advance?

- Progressively: starts with an in situ lesion

1. Note the Rokitansky-Aschoff sinus in the chronic inflammatory lesion

- Do NOT memorize all of these; images are what is important here


What do you see here?

Infiltrating cholangiocarcinoma (of gallbladder): more common; usually appears as a poorly defined area of diffuse mural thickening and induration 

- Deep ulceration can cause direct penetration into the liver or fistula formation to adjacent viscera into which the neoplasm has grown 

- Need to look at wall to see if thickened: may be from edema, but if solid, tan-white, then area of tumor 

- Note the attached histo image 

- Other gross pattern: exophytic (both types are adenocarcinomas) 


What is this?

- Exophytic cholangiocarcinoma (of gallbladder): grows into lumen as an irregular, cauliflower mass, but at the same time invades the underlying wall 

- This type is much more rare 

- Note the attached histo image 

- Other gross pattern: infiltrative -> both types are adenocarcinomas


What do you see in these 3 images?

- Normal gallbladder (left) vs. carcinoma (right two images) 

- Invasive adenocarcinoma

- Dysplasia at top, and atypical glands going down

- Can be tough b/t Rokitansky-Aschoff and cancer sometimes: R-A will never go horizontal

1. Cytology should also give it away -> loss of polarity, hyperchromasia, ugly, elongated cells in cancer  


What is this?

- Porcelain gallbladder: rare, caused by extensive dystrophic calcification in the gallbladder wall  

- Notable for a markedly INC incidence of assoc cancer 


How are chronic pancreatitis and biliary obstruction related? Tx?

- 20% of pts w/chronic pancreatitis will present with biliary obstruction 

1. Clinical presentation: cholestatic pattern of liver enzymes + chronic pancreatitis

- Compression as CBD enters pancreas due to chronic pancreatitis + inflammation: compressed from outside, OR: 

1. Stone inside pancreatic duct: different than biliary -> hard Ca stone from chronic pancreatitis

- TX: biliary stent placement (to decompress the obstruction) and/or surgery


What do you see here (post-liver transplantation)?

- 2 cystic ducts: one from patient and one from donor -> anastamosis can get narrow and get strictures

- Can tx with balloon dilatation through scope (most do well after this)

- Biliary complications in 5% of pts after liver transplantation -> present with a cholestatic pattern of liver enzymes


2. TX: endoscopic mgmt successful in many pts; complex complications require surgery 


What is hemobilia? Signs? Presentation? Tx?

- 3 SIGNS: 1) jaundice, 2) melena, 3) abdominal pain

1. Only thing that will give you this combo

- Blood from biliary treee: can happen as a cx of gallbladder surgery, trauma, etc.

- Tx: radiologic procedures with embolization or surgery