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Pathophysiology - Gastrointestinal > Pathology of the Gallbladder, Extrahepatic Biliary Tract, and Pancreas > Flashcards

Pathology of the Gallbladder, Extrahepatic Biliary Tract, and Pancreas Flashcards

1
Q

What are bile salts and lecithins? Are they water soluble or insoluble?

A
  1. Bile salts - bile acids made from cholesterol, conjugated to glycine or taurine. Water soluble, and the primary component of bile
  2. Lecithins - phosphatylcholine, water-insoluble
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2
Q

Other than bile salts and lecithins, what are the other components of bile?

A

Cholesterol
Proteins - probably acting as the nidus for stone formation
Bilirubin

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3
Q

How does bilirubin get made and transported to the liver?

A

Made in reticuloendothelial system (i.e. spleen)

Heme -> biliverdin = open chain form of heme porphyrin ring

Unconjugated bilirubin made from biliverdin, and transported via albumin in blood (UCB is water insoluble, needs to be conjugated)

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4
Q

What is the fate of bilirubin once it enters the intestine?

A

Bacteria in the gut deconjugate it to urobilinogen.

Urobilinogen can be excreted in stool after being made into stercobilin -> gives the stool its brown color.

Some urobilinogen is reabsorbed -> can be excreted again in bile, or transported to kidneys where it is oxidized to urobilin -> gives the urine its yellow color.

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5
Q

What is the fate of bile salts when they enter the intestines?

A

They are partially deconjugated from glycine / taurine

95% of these will be reabsorbed in the terminal ileum (same site as B12), will return via portal vein, and be used against after conjugation (used 20 times on average)

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6
Q

What is the most common congenital anomaly of the gallbladder?

A

Phrygian cap -> fundus (body, as opposed to neck and cystic duct) of the gallbladder folded inward

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7
Q

What are choledochal cysts and what are the possible complications?

A

Dilatations or outpouchings of the COMMON bile duct (think choledocholithiasis)

possible complications:

  1. choledocholithiasis
  2. cholangitis - infection of pouches
  3. biliary tract obstruction
  4. bile duct carcinoma
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8
Q

What are the causes of biliary atresia?

A

Failure to form (rarer) or early destruction (within 2 mo of birth) of extrahepatic biliary tree (probably due to inflammation from infection leading to stricture and destruction of the bile duct)

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9
Q

What are the consequences of biliary atresia?

A

Bile ducts -> progressive fibrosis may cause extrahepatic to become intrahepatic atresia

Liver - cholestasis causes portal tract infiltration, fibrosis, and bile duct proliferation = secondary biliary cirrhosis

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10
Q

What is the treatment for biliary atresia?

A

Early surgical correction if restricted to extraheptic bile ducts

Liver and bile duct transplant if intrahepatic spread

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11
Q

What are the types of gallstones and which one predominates in the US?

A
  1. Cholesterol - predominates in US

2. Pigment (bilirubin)

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12
Q

What is the pathogenesis of cholesterol stones?

A

Supersaturation of bile with cholesterol due to:
1. Increased biliary secretion of cholesterol
or
2. Decreased secretion of bile salts to solubilize

+ bile stasis in gallbladder = increased cholesterol stone nucleation + excess mucin (produced by epithelium in gallbladder) = stones

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13
Q

What are the risk factors for cholesterol stone formation?

A
  1. Developed countries
  2. Native American ethnicity
  3. Increased secretion of bile - advanced age, estrogen (obesity, women, OCPs, pregnancy)
  4. Gallbladder hypomotility - rapid weightloss, fasting, or neurogenic
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14
Q

How do cholesterol stones appear grossly and are they radio-opaque or translucent?

A

Can be pure cholesterol -> clear to yellow, rarer

Mixed stones -> >50% cholesterol and bile pigments, most common

They are radiolucent, must be detected with ultrasound

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15
Q

What gallbladder pathology is commonly seen with choesterol stones and what is the cause? How does it appear grossly and microscopically?

A

Cholesterolosis - aggregates of foamy macrophages within the subepithelium of gallbladder. Grossly -> little yellow deposits within the mucosa.

Increased bile cholesterol increases cholesterol absorption by gallbladder mucosa -> accumulate in subepithelium

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16
Q

What is the pathogenesis of pigment gallstones?

A

Increased UNconjugated bilirubin in bile which is not water soluble -> aggregation of calcium salts, mucin, and cholesterol

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17
Q

What are the risk factors for pigment gallstones?

A
  1. Chronic hemolysis -> increased biliary excretion of conjugated bilirubin, and a small percentage always becomes unconjugated
  2. Biliary tract infections -> microbial deconjugation of bile acids
  3. Gallbladder hypomotility -> thickens bile
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18
Q

What are the two morphological types of pigment stones? What causes them? Are they radio-opaque or translucent?

A

Black - occur in chronic hemolysis -> majority are radio-opaque from complexing with calcium. Multiple and smooth.

Brown - occur in biliary tract infections -> soft and soapy, radiotranslucent

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19
Q

What are the four F’s of cholelithiasis risk factors?

A

Female
Fat
Fertile (pregnant)
Forty

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20
Q

What are the possible complications of cholelithiasis?

A
  1. *Acute cholecystitis
  2. Hydrops of gallbladder due to chronic obstruction
  3. Choledocholithiasis -Obstruction of the common bile duct
  4. Chronic cholecystitis
  5. Gallstone ileus
  6. Carcinoma of the gallbladder
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21
Q

What are some severe variants of acute cholecystitis? Include also one complication of an ulcer forming during this time.

A
  1. Empyema of gallbladder - bag of pus
  2. Gangrene and perforation - if ischemia is very severe, hemorrhagic necrosis of gallbladder wall

Ulceration:
3. Fistula tracts -> ulceration forms in wall which allows attachment to nearby loop of duodenum

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22
Q

What are the possible complications of choledocholithiasis?

A
  1. Cholestasis with secondary biliary cirrhosis
  2. Ascending cholangitis with possible liver abscess formation
  3. Pancreatitis - if stone is wedged right before ampulla of Vater
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23
Q

What is a gallstone ileus and how does it occur?

A

Large stone plugging the lumen of the duodenum
-> occurs due to formation of a fistula tract thru gall bladder, allowing stones to leak into duodenum and obstruct lumen

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24
Q

What is the most common type of cholecystitis and its pathogenesis?

A

Calculous cholecystitis - obstruction of neck of gallbladder via a stone = retention of bile, gallbladder distention, and vascular compression in the wall (venous congestion, causing hemorrhagic infarct overtime)

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25
Q

What are the risk factors for the less common type of cholecystitis (acalculous)?

A

Critically ill patients - occurs without stone, due to hypomotility or hypoperfusion

  • > Cystic duct obstruction by concentrated bile with excessive reabsorption due to dehydration and hypomotility
  • > poor vascular perfusion (during shock)
  • > bacterial infection
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26
Q

How will acute cholecystitis appear grossly? Microscopically?

A

Enlarged, erythematous gallbladder with thick edematous wall due to inflammation / hyperemia.

Dull serosal opacities, appearing whitish-yellow (pus), maroonish (blood), and greenish-black (bile)

Microscopically - acute inflammatory infitlrate with ulceration and necrosis

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27
Q

What are the clinical signs and symptoms of acute cholecystitis?

A

RUQ pain, fever with increased WBC count w/neutrophilia, nausea / vomiting, loss of appetite (causes gallbladder contraction)

28
Q

What are the potential complications of acute cholecystitis?

A
  1. Gallbladder perforation -> peritonitis. Especially in gangrenous type.
  2. Secondary bacterial infection with abscess formation
  3. Fistula tracts
29
Q

What are the predisposing factors to chronic cholecystitis, and what are the characteristic microscopic features?

A

Chronic cholelithiasis and bacterial contamination

Chronic inflammation - lymphocytes, macrophages, plasma cells, and fibrosis

Rokitansky-Aschoff sinuses - mucosal diverticula seen in gallbladder wall due to contraction against thick gallbladder wall

30
Q

What is the most well-described variant of chronic cholecystitis, how should it be treated, and why?

A

Porcelain gallbladder - shrunken gallbladder with marked dystrophic calcification seen on Xray -> treatment is cholecystectomy to prevent transformation to adenocarcinoma of gallbladder

31
Q

What is it called when you have chronic cholecystitis marked by a small, chronically obstructed gallbladder filled with clear, mucinous secretions?

A

Hydrops of the gallbladder

32
Q

What are the clinical features of chronic cholecystitis?

A

Biliary colic-like symptoms - nausea/vomiting and dull RUQ exacerbated by eating fatty foods (stimulates CCK-mediated gallbladder contraction)

33
Q

Who tends to get carcinoma of the gallbladder? What IS it?

A

Classically, elderly women with a history of cholelithiasis, especially causing chronic cholecystitis with porcelain gallbladder

It is cancer of the glandular epithelium of the gallbladder wall

34
Q

How is diagnosis of gallbladder carcinoma usually made and what’s the prognosis?

A

Made incidentally after cholecystectomy (think of Bosch’s story) with poorly delineated mass seen in gallbladder

Prognosis is poor as metastasis to liver / adjacent structures happens before presentation

35
Q

What is a Klatskin tumor and what are its risk factors?

A

A type of carcinoma of the extrahepatic bile ducts, which is located at the origin of the common hepatic duct (before it merges with cystic duct)

Risk factors for all adenocarcinomas of extrahepatic bile ducts:
Older males, biliary tract infections, PSC, choledochal cysts

36
Q

What is released from the duct cells and acinar cells in the pancreas?

A

Duct cells -> bicarbonate

Serous acini -> zymogen granules with digestive proteins

37
Q

What stimulates the release of the contents from duct cells and acinar cells?

A

Vagus nerve - acetylcholine

Duct cells are stimulated by -> secretin, produced by S cells in duodenum

Acinar cells are stimulated by -> cholecystokinin, released by I cells

38
Q

What enzymes are present in the zymogen granules of the acinar cells, and what activates the digestion cascade?

A

Trypsin, chymotrypsin, elastase, amylase, lipase, phospholipase

Trypsin activated by membrane-bound enterokinase in the duodenum

39
Q

What do the two buds of the pancreas form?

A

Ventral bud - forms off of the hepatic diverticulum (off the biliary tree endoderm which will induce formation of liver) -> will form the caudal portion of the head of the pancreas as well as the uncinate process

Dorsal bud - comes off of duodenum dorsally - forms the rostral portion of head of pancreas plus budy and tail

40
Q

How does the pancreatic / bile duct system develop in most people / why?

A

The dorsal pancreatic bud communicates with the duodenum via the accessory pancreatic duct (of Santorini). This will merge with the duct in the ventral pancreatic bud in most people.

The large portion of the pancreas drains into the main pancreatic duct which connects with the main duct from the ventral bud, merging both the common bile duct and pancreatic duct just before emptying into the duodenum at the ampulla of Vater.

41
Q

What occurs if the ventral pancreatic bud doesn’t know how to rotate in embryonic development?

A

Annular pancreas - It will rotate in both directions, around the duodenum

Risk is duodenal obstruction

42
Q

What is pancreas divisum and what is the risk?

A

Incomplete fusion of the dorsal and ventral pancreatic buds, including incomplete ductal fusion

  • > since accessory duct of dorsal bud will be smaller than main duct, some secretions will be trapped in body of pancreas
  • > risk of recurrent pancreatitis
43
Q

What is it called when you have histologically normal pancreatic tissue outside of the pancreas? Where does it usually appear?

A

Ectopic pancreas, a type of choristoma

Appears on wall of stomach or small intestine

44
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED

Idiopathic, Ischemia

**Gallstones
**Ethanol
Trauma - i.e. MVA in children, stabbings

Steroids
Mumps infection
Autoimmune disease
Scorpion stings
Hypercalcemia / hypertriglyceridemia (>1000 mg/dL)
ERCP - to clear stone
Drugs
45
Q

Why do mumps, hypercalcemia, and genetic abnormalities in trypsin cause acute pancreatitis?

A

Mumps - cytotoxic T cells mediate release of activated enzymes (mumps invades glandular epithelium)

Hypercalcemia - calcium is an activator of enzymes

Trypsin - can cleave C3 and greatly worsen enzyme activation if constitutively active

46
Q

What is the pathogenesis of acute pancreatitis?

A

Inappropriately activated acinar enzymes and indirect activation of clotting and complement pathways via:

  1. Duct obstruction (i.e. stones / alcohol) -> increased intraductal pressure
  2. Acinar cell injury - > release and activation of enzymes
47
Q

How is alcohol thought to cause pancreatitis?

A

Directly injures acinar cells

Causes thick, viscous excretions blocking the ducts

Messes up intracellular transport of pancreatic proenzymes -> causes fusion with lysosome and activation within the cell

48
Q

In what patients will ductal obstruction cause pancreatitis? What damage does this cause?

A

Patients who have a normal main pancreatic duct merging with common bile duct before emptying into ampulla of Vater -> both can be blocked by a single stone

Causes fat necrosis with secondary acute inflammation with edema, compromising local blood flow

49
Q

How does acute pancreatitis appear grossly?

A

Scattered chalky white foci within pancreatic and abdominal fat -> fat necrosis with saponification

Can be liquified tissue and hemorrhage if very severe

50
Q

How does acute pancreatitis appear microscopically?

A

Edema and acute inflammation, with proteolytic digestion of things

  • > fat necrosis (appears like coagulative necrosis of adipocytes with a slightly blue hue due to saponification of fatty acids via calcium deposition)
  • > hemorrhage due to proteolytic destruction of blood vessels
51
Q

What are the clinical manifestions of acute pancreatitis?

A

Acute abdominal pain, often radiating to the back

Increased serum amylase or lipase (more specific marker)

52
Q

What are the systemic complications of acute pancreatitis and why?

A

DIC - circulating amylase and lipase damage endothelium

ARDS - damage to pulmonary membranes

Shock - bleeding and loss of edema fluid -> progress to renal failure

Metabolic effects

Extrapancreatic fat necrosis - circulating lipases

53
Q

What are the metabolic effects seen in acute pancreatitis and why?

A

Hypocalcemia - due to saponification of fat necrosis

Hypoalbuminemia - loss of fluid

Hyperglycemia - failure of islets to produce insulin

Acidosis - due to shock with lactic acid production

54
Q

What are the localized complications of acute pancreatitis?

A

Pseudocyst - necrotic cyst lined by fibrotic granulation tissue, not epithelium

Abscess - infected pseudocyst

Biliary obstruction / jaundice

55
Q

What is chronic pancreatitis and what are the causes?

A

Relapsing acute pancreatitis -> progressive injury

Often idiopathic, but:

Adults - alcoholism

Children - Cystic fibrosis

May also be autoimmune, secondary to hyperlipidemia/hypercalcemia, or due to pancreas divisum

56
Q

How does chronic pancreatitis appear grossly and what is the general underlying process which causes it?

A

Grossly - Sclerotic gland with calcifications and pseudocysts

Caused by ductal obstruction leading to necrosis which slowly progresses to fibrosis

57
Q

How does chronic pancreatitis appear microscopically?

A

Fibrosis with acinar atrophy, relative sparing of islets -> acini go first because of spilling of proteolytic enzymes

Proteinaceous material within dilated ducts, which often have squamous metaplasia due to epithelial alterations

Chronic inflammatory infiltrate

58
Q

What are the clinical manifestations of chronic pancreatitis?

A

Abdominal pain, fat malabsorption, followed later by diabetes

Jaundice and duodenal obstruction may occur with chronic fibrosis / scarring

59
Q

What diseases cause true cysts in the pancreas?

A

ADPKD, von Hippel-Lindau

-> cysts are lined with epithelium (vs pseudocysts)

60
Q

What cells of the pancreas does pancreatic adenocarcinoma arise from? How is this differentiated from chronic pancreatitis?

A

Ductal cells of pancreas (acinar is insanely rare)

-> differentiated from chronic pancreatitis by loss of normal lobular architecture in adenocarcinoma

61
Q

What are the major risk factors for pancreatic adenocarcinoma?

A

Smoking and chronic pancreatitis

Diabetes, being black, male, and old age also play a role

62
Q

Does pancreatic cancer have a normal progression? Where does it tend to arise?

A

Yes -> sequential genetic and epigenetic alterations including early KRAS mutations to late p53 mutations

Tends to arise in head of pancreas more often (where the ducts are most concentrated)

63
Q

What are the gross and microscopic appearance of pancreatic adenocarcinoma?

A

Gross - infiltrative, firm, tan tissue due to desmoplasia

Microscopic - loss of normal lobular architecture with haphazard, irregularly glandular structure, desmoplasia, and perineural invasion -> can be painful

64
Q

Where does pancreatic adenocarcinoma spread locally if in the head vs the body/tail? Distant metastases?

A

Head -> duodenum and common bile duct

Body/tail -> vertebrae, retroperitoneum

Distant metastases -> regional lymph nodes, liver

65
Q

What are the clinical manifestations of pancreatic adenocarcinoma?

A

Nonspecific - weight loss, nausea/vomiting, pain

Obstructive jaundice -> especially if in pancreatic head

Trousseau syndrome -> best characterized in this adenocarcinoma

66
Q

What is Trousseau syndrome?

A

Migratory thrombophlebitis - redness and tenderness on palpation of extremities -> thrombosis of arms and legs due to hypercoagulability. The adenocarcinoma produces a procoagulant (probs mucin)

Pathophysiology - Gastrointestinal (24 decks)

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