Gallbladder and Pancreas Flashcards

1
Q

Causes of Gallstone (cholelithiasis) (3)

A
  1. Inc. cholesterol and/or bilirubin
  2. Dec. phospholipids (e.g., lecithin) or bile salts (normally inc. solubility)
  3. Gallbladder stasis (inc. growth of bacteria)
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2
Q

Cholelithiasis risk factors (4 F’s)

A

Female, Fat, Fertile (pregnant), Forty

Factors combine to create a high-cholesterol, low-gallbladder motility environment

Progesterone specifically inhibits gallbladder motility… in same manner that it inhibits uterine smooth muscle contraction during pregnancy

Estrogen inc. HMG CoA reductase activity (synthesis of cholesterol) and also inc. expression of LDL-R (inc. cholesterol uptake)

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3
Q

2 types of gallstones

A
  1. Cholesterol stones (80% of stones)
    1. Radiolucent with 10-20% opaque due to calcifications
    2. Associated with:
      1. Obesity
      2. Crohn disease
      3. Advanced age
      4. Estrogen therapy
      5. Multiparity
      6. Rapid weight loss
      7. Native American origin
  2. Bilirubin (Pigment) stones
    1. Black = radiopaque, Ca2+ bilirubinate, hemolysis
    2. Brown = radiolucent, infection
    3. Seen in pts with:
      1. Crohn disease
      2. Chronic extravascular hemolysis (inc. bilirubin in bile)
      3. Alcoholic cirrhosis
      4. Advanced age
      5. Biliary tract infections (E. coli, Ascaris lumbricoides, Clonorchis sinensis)
        1. ​Ascaris lumbricoides = common roundworm that infects 25% of world’s population, especially in areas w poor sanitation (fecal-oral transmission) –> infects biliary tract
        2. Clonorchis sinensis = endemic in China, Korea, Vietnam (Chinese liver fluke)
      6. Total parenteral nutrition (TPN) - form of nutrition that bypasses GI
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4
Q

How does uncomplicated disease manifest?

A

Biliary colic

(neurohormonal activation… eg, by CCK after fatty meal) triggers contraction of gallbladder, forcing a stone into cystic duct

May present without pain (e.g., in diabetics)

No Murphy sign (in contrast to cholecystitis)

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5
Q

How to diagnose gallstones?

Treatment?

A

Ultrasound

Tx: cholecystectomy if symptomatic

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6
Q

Most common complication of gallstones

A

Cholecystitis

Also: acute pancreatitis, ascending cholangitis, biliary colic, gallstone ileus, gallbladder cancer

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7
Q

Charcot triad of cholangitis

A

Jaundice

Fever

RUQ

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8
Q

Pneumobilia

A

Air in biliary tree which can be caused by fistula between gallbladder and GI tract

Result: passage of gallstones into GI tract –> obstruct ileocecal valve (gallstone ileus)

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9
Q

Cholecystitis

Presentation

Labs

How to diagnose?

A

Acute or chronic inflammation of gallbladder usually from cholelithiasis (stone at neck of gallbladder)

2ndary infection often occurs (esp w E. coli, Enterococcus, Klebsiella)

Positive Murphy sign: inspiratory arrest on RUQ palpation due to pain

Labs: inc AP if bile duct becomes damaged (e.g., ascending cholangitis)

Diagnose with U/S or cholescintigraphy (HIDA, or hepatobiliary iminodiacetic acid scan)

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10
Q

Porcelain gallbladder

What is found on imaging?

What is found on histology?

Treatment?

A

Late complication of chronic cholecystitis

Calcified gallbladder; usually found incidentally on imaging

Histology:

Herniation of gallbladder mucosa into muscular wall (Rokitansky-Aschoff sinus)

Tx: prophylactic cholecystectomy due to high rates of gallbladder cancer (mostly adenocarcinoma)

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11
Q

Acute pancreatitis

A

Usually caused by gallstones present in ampulla causing reflux of pancreatic enzymes –>

  • Autodigestion and inflammation of pancreas by pancreatic enzymes (pre-mature activation of trypsin leads to activation of other pancreatic enzymes)
  • SPINK1 (specific trypsin inhibitor serine protease inhibitor Kazal type 1) inhibitor of autoactivation [mechanism gets messed up]
  • High Ca2+ (hypercalcemic state is no good as well)
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12
Q

Causes of acute pancreatitis

I GET SMASHED

A

Idiopathic

Gallstones

Ethanol

Trauma

Steroids

Mumps

Autoimmune disease

Scorpion sting

Hypercalcemia/Hypertriglyceridemia (>1000 mg/dL)

ERCP (Endoscopic retrograde cholangiopancreatography)

Drugs (e.g., sulfa drugs, NRTIs, protease inhibitors)

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13
Q

Acute pancreatitis:

Diagnosis

A

2 of 3 criteria:

acute epigastric pain often radiating to the back

inc. serum amylase or lipase (more specific) to 3x upper limit of normal

Characteristic imaging findings (pancreas surrounded by edema)

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14
Q

Complications of acute pancreatitis

A
  • Pseudocyst (formed by fibrous tissue surrounding liquefactive necrosis… lined by granulation tissue, not epithelium)
  • Necrosis
  • Hemorrhage
  • Infection (E. coli… abdominal pain, high fever, persistently elevated amylase)
  • Organ failure (ARDS, shock, renal failure)
    • ARDS: enzymes can chew on alveolar-capillary interface
  • Hypocalcemia (calcium is consumed during saponification in fat necrosis)
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15
Q

Chronic pancreatitis

A
  • Chronic inflammation
  • Atrophy
  • Calcification of pancreas (CT reveals a ‘chain of lakes’ pattern due to dilatation of pancreatic ducts)
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16
Q

Chronic pancreatitis: major causes

A
  • Adults = Alcohol abuse (ethanol can alter zymogen activation)
  • Children = Cystic fibrosis
  • Idiopathic
17
Q

Chronic pancreatitis: presentation

A
  • Epigastric abdominal pain that radiates to the back
  • Pancreatic insufficiency:
    • Exocrine insufficiency (malabsorption) - deficiency of fat-soluble vitamins (A, D, E, K) –> steatorrhea
    • Endocrine insufficiency (diabetes)
  • Labs: amylase/lipase typically normal
    • (normal serum enzyme levels because of significant fibrosis of the pancreas, resulting in decreased concentrations of these enzymes within the pancreas)
  • Mutations in CFTR (cystic fibrosis) –> chronic pancreatic insufficiency (malabsorption due to thickened pancreatic secretions)
18
Q

Chronic pancreatitis: association with gallstones?

A

No

19
Q

Pancreatic adenocarcinoma

A

Very aggressive tumor arising from pancreatic ducts (disorganized glandular structure w cellular infiltration)

Often metastatic at presentation, with average survival ~1 yr after diagnosis (tumor in head of pancreas more common and higher prognosis b/c more likely to obstruct early –> can be detected earlier): obstructive jaundice

Associated with CA 19-9 tumor marker (also CEA, less specific)

20
Q

Pancreatic adenocarcinoma: presentation

A
  • Weight loss (due to malabsorption and anorexia)
  • Early satiety
  • Abdominal pain radiating to back
  • Painless jaundice (obstructive with palpable, nontender gallbladder - Courvoisier sign)
  • Migratory thrombophlebitis (venous blood clot) - redness and tenderness on palpation of extremities (Trousseau syndrome) - seen in 10% of pts
  • Diabetes (late development b/c cancer knocks out islet cells)
21
Q

Pancreatic adenocarcinoma: Risk factors

A
  • Tobacco use
  • Chronic pancreatitis (especially > 20 years)
  • Diabetes
  • Age > 50 yrs
  • Jewish and AA males
22
Q

Pancreatic adenocarcinoma: Treatment

A
  • Whipple procedure (remove head/neck of pancreas, proximal duodenum, gallbladder)
  • Chemo
  • Radiation therapy
23
Q

Biliary colic:

presentation and cause

What can common bile duct obstruction result in?

A

Waxing and waning RUQ pain

Due to gallbladder contracting against stone lodged in cystic duct

Symptoms relieved if stone passes

Common bile duct obstruction may result in acute pancreatitis or obstructive jaundice

24
Q

3 places gallstones can get lodged + associated symptoms

A
  1. Cystic bile duct
    1. Painful gallbladder contractions
  2. Common bile duct
    1. Pain and nausea
    2. Lack of bile release
    3. Failure to excrete bilirubin –> jaundice
  3. Duodenal papilla (where common bile duct and pancreatic duct meet)
    1. Jaundice
    2. Inappropriate activation of pancreatic zymogens
    3. Acute pancreatitis
25
Q

Genetic Pancreatitis (rare) (3)

A

Mutations in three genes associated with disease:

  • PRSS1 - Encodes trypsinogen –> dominant mutations cause “super” trypsins
  • SPINK1 - Encodes trypsin inhibitor –> lack of effective inhibition allows premature activation of trypsinogen
  • CFTR - Encodes chloride channel associated with CF –> thick secretions
26
Q

Four genes most commonly mutated or inactivated in pancreatic cancer

A
  • KRAS
  • p16/CDKN2A (tumor-suppressor genes)
  • p53
  • SMAD4