5.1 - Biliary Dysfunction Flashcards

1
Q

What is cholecystitis?

A
  • Obstruction of the gallbladder is caused by gallstones (cholelithiasis) and these are made up of aggregate substances in the bile.
  • Gallstones may stay in the gallbladder or be excreted into the cystic duct along with the bile.
  • Gallstones that become lodged in the cystic duct obstruct the flow of the bile into and out of the gallbladder and can cause inflammation.
  • Inflammation of the gallbladder or cystic duct in termed cholecystitis
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2
Q

What are some risk factors for cholelithiasis (gallstones)?

A
  • Prevalent disorder in developed countries where incidence is 15% in Caucasian adults and 60-70% in Native Americans

Risk factors include:

  • Middle age
  • Female sex
  • Use of oral contraceptives
  • Native American ancestry
  • Genetic predisposition
  • Gallbladder, pancreatic or ileal disease
  • Low high density lipoprotein (HDL) cholesterol level
  • Hypertriglyceridemia
  • Gene-environmental interactions
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3
Q

How do gallstones form?

A

Gallstones are formed from impaired metabolism of cholesterol, bilirubin and bile acids

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4
Q

What are the 3 types of gallstones?

A
  1. Cholesterol: MOST common (70% cholesterol) and makes up 70-80% of ALL stones
  2. Pigmented: (< 30% cholesterol): brown and black
  3. Mixed
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5
Q

How do cholesterol gallstones form?

A
  • Cholesterol gallstones form in bile that is supersaturated with cholesterol produced by the liver and deficient in bile acids and phospholipids
  1. Supersaturation sets the stage for cholesterol crystal formation or the formation of ‘microstones’.
  2. Crystals then aggregate on the microstones, which grow to form ‘macrostones’
  3. Process usually occurs in gallbladder, which may have decreased motility and biliary stasis.
  4. Stones may lie dormant and silent or become lodged in the cystic or common bile duct, causing pain when the gallbladder contracts and cholecystitis.
  5. The stones can accumulate and fill the entire gallbladder.
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6
Q

How do pigmented brown gallstones form?

A

Pigmented brown stones form from calcium bilirubinate and fatty acid soaps that bind with calcium, usually in the common bile duct.

  • Associated with biliary stasis, bacterial infections and biliary parasites
  • More common in East Asia
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7
Q

How do pigmented black stones form?

A
  • Rare; usually form in gallbladder
  • Associated with chronic liver disease and hemolytic disease
  • Composed of calcium bilirubinate with mucin glycoproteins
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8
Q

What are the clinical manifestations of cholelithiasis (gallstones)?

A
  • Epigastric and right hypochondrium pain
  • Intolerance to fatty food
  • Positive Murphy’s Sign: elicited by palpating the right subcostal area while the patient inspires deeply; a positive (+) sign is when the patient feels pain upon this maneuver and may have an associate inspiratory arrest.
    • Provider cannot depend solely on Murphy’s sign
  • Biliary colic – pain that occurs 30 minutes to several hours after eating a fatty meal; and is caused by the lodging of one or more gallstones in the cystic or common bile duct with obstruction and distention
    • Pain can be intermittent or steady; reaches a peak then completely abates over time
    • Usually located in the RUQ and radiates to mid-upper back
    • Jaundice indicates that the stone is lodged in the common bile duct
    • Abdominal tenderness and fever indicate cholecystitis

Vague symptoms, such as:

  • Heartburn
  • Flatulence
  • Epigastric discomfort
  • Pruritus
  • Jaundice
  • Food intolerances (particularly to fats and cabbage)
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9
Q

How do you diagnose a patient with cholelithiasis?

A
  • Diagnosis is based on medical history, PE and imaging evaluation

Imaging techniques include:

  • Abdominal ultrasound: PRIMARY imaging technique to obtain
  • Endoscopic ultrasound
  • Magnetic resonance cholangiopancreatography (MRI)
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10
Q

How do you treat patients with cholelithiasis (gallstones)?

A

Medications:

  • Oral bile sales may dissolve cholesterol stones but they may recur when medication is discontinued
  • Morphine: The administration of Morphine during acute cholecystitis can lead to spasm of the sphincter of Oddi and exacerbate pain symptoms. Therefore, meperidine typically is used for severe pain associated with acute cholecystitis.

Surgery:

  • Laparoscopic cholecystectomy is PREFERRED treated for gallstones that cause obstruction and inflammation
  • Endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy with stone retrieval- used for treatment of bile duct stones.
  • Lithotripsy or open cholecystectomy – reserved for larger or intrahepatic stones.
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11
Q

What is/causes cholecystitis?

A
  • An acute/chronic obstruction of the gallbladder almost exclusively being caused by the lodging of gallstones within the cystic duct, leading to gallbladder distention and inflammation.
  • Pressure against the distended wall of the gallbladder caused by stones decreases blood flow and can result in ischemia, necrosis and perforation of the gallbladder
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12
Q

What are the symptoms associated with cholecystitis?

A
  • Pain is similar to that caused by gallstones
  • Fever, leukocytosis, rebound tenderness, and abdominal muscle guarding are common findings
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13
Q

How do you diagnose cholecystitis?

A
  • Cholescintigraphy (Nuclear medicine test) is the MOST SENSITIVE imaging for cholecystitis
  • Serum bilirubin and alkaline phosphatase levels may be elevated​
  • Ultrasound and MRI have a substantial margin of error but can demonstrate some nonspecific changes
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14
Q

How do you treat cholecystitis?

A
  • Pain control
  • Replacement of fluid and electrolytes
  • Fasting
  • Antibiotics- if bacterial infection is present in severe cases
  • Laparoscopic gallbladder resection – cholecystectomy – is usually required in acute attacks.
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15
Q

What are some risk factors for pancreatitis?

A
  • Obstructive biliary tract disease (particularly cholelithiasis)
  • Alcoholism
  • Peptic ulcers
  • Abdominal trauma
  • Hyperlipidemia
  • Smoking
  • Certain medications
  • Genetic factors (hereditary pancreatitis and cystic fibrosis)
  • Cause unknown in 15-25% of cases
  • May be acute or chronic
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16
Q

Describe the pathophysiology associated with how acute pancreatitis develops

A

1. In obstructive disease, the backup of pancreatic secretions or duodenal contents or both triggers activation and release of enzymes (activated trypsin activates chymotrypsin, lipase and elastase) within the pancreatic acinar cells

  • The activated enzymes cause auto digestion (i.e. proteolysis, lipolysis) of pancreatic cells and tissues, resulting in inflammation and release of inflammatory cytokines
  • Auto digestion causes vascular damage, coagulative necrosis, fat necrosis and formation of pseudocysts (walled off collection of pancreatic secretions)
  • Edema within pancreatic capsule leads to ischemia and can contribute to necrosis

2. In alcohol abuse, the pancreatic acinar cell metabolizes ethanol with the generation of toxic metabolites that injure pancreatic acinar cells, causing release of activated enzymes

  • Chronic alcohol use may also cause formation of protein plugs in pancreatic ducts and spasm of the sphincter of Oddi, resulting in obstruction
  • The obstruction leads to intrapancreatic release of activated enzymes, auto digestion, inflammation and pancreatitis.
17
Q

What are the complications associated with acute pancreatitis?

A
  • Acute respiratory syndrome (ARDS)
  • Heart failure
  • Renal failure
  • Coagulopathies
  • Intra-abdominal hypertension
  • Systemic inflammatory response syndrome (SIRS)
  • Paralytic ileus
  • Intra-abdominal or retroperitoneal hemorrhage- Worsening prognosis if Hematocrit decreases > 10% from baseline
  • Peritonitis or sepsis (due to translocation of intestinal bacteria to bloodstream)
  • Pancreatic fibrosis, strictures and duct obstruction (leading to chronic pancreatitis)
  • Infected necrotizing pancreatitis- associated with the HIGHEST mortality rate.
18
Q

What are the subjective manifestations of acute pancreatitis?

A
  • Epigastric or mid-abdominal constant pain ranging from mild abdominal discomfort to severe, incapacitation pain – MAIN MANIFESTATION
  • Pain may radiate to the back due to the retroperitoneal location of the pancreas
  • Pain is caused by:
    • Edema (which distends the pancreatic ducts and capsule)
    • Chemical irritation and inflammation of the peritoneum
    • Irritation and obstruction of biliary tract
    • Inflammation of the nerves
  • Nausea and vomiting are caused by paralytic ileus secondary to pancreatitis or peritonitis
  • Fever
19
Q

What are the physical exam findings associated with pancreatitis?

A
  • Jaundice may occur from obstruction of bile duct (i.e. gallstone) or from pancreatic edema compressing the duct
  • Abdominal distention with bowel hypo-motility or paralytic ileus
  • Ascites
  • Abdominal compartment syndrome- a potential emergent complication
  • Grey Turner’s Sign: bruising of the flanks; a sign of retroperitoneal hemorrhage or bleeding behind the peritoneum, which is the lining of the abdominal cavity
  • Cullen’s sign: abdominal distention with peri-umbilical ecchymosis; sign of intra-abdominal bleeding.
  • Both Grey-Turner’s and Cullen’s signs are not specific, but are associated with severe acute pancreatitis and a high mortality.
20
Q

What are some lab/diagnostic tests used to diagnose pancreatitis?

A

Diagnosis is based on clinical findings, identification of associated disorders, laboratory studies and imaging results (CT with contrast, endoscopic ultrasound, MR cholangiopancreatography)

  • Elevated serum amylase – characteristic but NOT diagnostic of severity or specificity of disease
  • Elevated serum lipase – PRIMARY DIAGNOSTIC MARKER
    • Both lipase and amylase may be elevated to at least three (3) times their normal value
  • Elevated C-reactive protein – SUGGESTIVE OF SEVERE DISEASE
21
Q

What is the goal of treatment for patients with acute pancreatitis?

A

Stop the process of auto digestion and prevent system complications

22
Q

How do you treat patients with pancreatitis?

A
  • Narcotics, NSAIDs, acetaminophen – for pain control
  • Hemodynamic monitoring
  • Parenteral fluids – to restore blood volume and prevent hypotension and shock; particularly in first 24 hours
  • Nasogastric suction – may or may not be necessary in mild cases, but may relieve pain and prevent paralytic ileus in individuals who have n/v
  • If NO ileus, may feed in 24-48 hours
  • In severe acute pancreatitis- enteral nutrition with use of jejunal tube feeding may be tolerated and may decrease pancreatic enzyme secretion, prevent bacterial gut overgrowth and maintain gut barrier function
  • Parenteral hyper alimentation – use ONLY if enteral feeding is not tolerated
  • H2 receptor antagonists: decrease gastric acid (hydrochloric acid) production and can decrease stimulation of pancreas by secretin
  • Antibiotics – in infection only
  • Necrotizing pancreatitis – can be sterile or infected; requires surgical debridement if patient stable
23
Q

What is and what causes chronic pancreatitis?

A
  • It is a progressive fibrotic destruction of the pancreas
  • Toxic metabolites and chronic release of inflammatory cytokines contribute to the destruction of acinar cells and islets of Langerhans, fibrosis, strictures, calcification, ductal obstruction, ischemia and pancreatic cysts
24
Q

What are the 3 types of chronic pancreatitis?

A

1. Chronic calcifying – MOST COMMON

  • Chronic alcohol abuse and smoking (nicotine induces oxidative stress in the pancreatic acinar cells) are the MOST COMMON causes of chronic calcifying pancreatitis

2. Chronic obstructive – associated with fibrosis and stricture from trauma endoscopic procedures, abdominal blunt trauma, gallstones or tumors

3. Steroid responsive is associated with autoimmune pancreatitis; has 2 subtypes which are both responsive to steroids and immunomodulators

25
Q

What are pancreatic pseudocysts?

A
  • Walled-off areas or pockets of pancreatic juice, necrotic debris, or blood within or adjacent to the pancreas
  • May appear up to 1 month post pancreatitis
26
Q

What are the symptoms associated with chronic pancreatitis?

A

Pain is CLASSIC symptom of all forms of chronic pancreatitis and is due to intraductal pressure, increased tissue pressure, ischemia, neuritis, ongoing injury and changes in central pain perception

  • Weight loss
  • Steatorrhea –less common
  • Malnutrition
  • Fat-soluble vitamin deficiency
  • Diabetes mellitus (known as type 3C to differentiate it from type 1 or 2)
27
Q

How do you manage patients with chronic pancreatitis?

A
  • Low fat diet
  • Oral lipase
  • Insulin
  • Prevention of disease progression includes lifestyle modification- stop alcohol use, tobacco.
  • Pain management - complex- use of analgesics, endoscopic therapy, nerve block and surgical drainage of cysts or partial resection of pancreas
  • Chronic pancreatitis is a risk factor for pancreatic cancer.