Gallstones and Cholecystitis

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Questions and Answers

In a patient status post spinal cord injury, which pathophysiological mechanism most directly contributes to cholesterol gallstone formation?

  • Bile stasis secondary to decreased gallbladder motility and impaired emptying. (correct)
  • Increased synthesis of bile acids due to altered hepatic enzyme activity.
  • Diminished enterohepatic circulation of bile salts, leading to compensatory cholesterol synthesis.
  • Enhanced intestinal absorption of dietary cholesterol due to neurological dysregulation of enterocytes.

Following a cholecystectomy, a patient reports persistent abdominal bloating and intolerance to fatty foods despite adhering to dietary recommendations. Which of the following best explains this phenomenon?

  • Compensatory up-regulation of pancreatic lipase production leading to fat malabsorption.
  • Increased hepatic synthesis of very-low-density lipoproteins (VLDL) exacerbating postprandial lipemia.
  • Impaired emulsification of fats due to the absence of gallbladder bile reservoir. (correct)
  • Dysbiosis of the gut microbiome altering bile acid metabolism and fat digestion.

A patient with advanced cirrhosis develops spontaneous bacterial peritonitis (SBP). Which pathophysiological mechanism most directly predisposes this patient to SBP?

  • Increased intestinal permeability due to portal hypertension and intestinal edema.
  • Compromised Kupffer cell function leading to impaired clearance of gut-derived bacteria.
  • Reduced opsonization of bacteria due to decreased hepatic synthesis of complement proteins.
  • All of the above. (correct)

In a patient with portal hypertension secondary to cirrhosis, which of the following mediators is most directly responsible for the development of esophageal varices?

<p>Increased portal venous pressure leading to collateral vessel formation and dilation. (C)</p> Signup and view all the answers

A patient with chronic hepatitis B develops hepatocellular carcinoma (HCC). Which molecular mechanism is most directly implicated in HBV-related hepatocarcinogenesis?

<p>All of the above. (D)</p> Signup and view all the answers

Which serological marker indicates resolution of acute hepatitis B infection and subsequent immunity?

<p>Anti-HBs (hepatitis B surface antibody) (D)</p> Signup and view all the answers

A patient with chronic hepatitis C infection is started on direct-acting antiviral (DAA) therapy. What is the primary mechanism of action of DAAs in eradicating HCV?

<p>Inhibition of viral RNA replication by targeting specific HCV enzymes. (B)</p> Signup and view all the answers

In alcoholic hepatitis, which pathological change within the liver is most closely associated with disease progression and mortality?

<p>Neutrophilic infiltration and Mallory-Denk body formation in hepatocytes. (A)</p> Signup and view all the answers

Which of the following best describes the pathogenesis of nonalcoholic steatohepatitis (NASH)?

<p>Insulin resistance and metabolic dysfunction causing hepatic steatosis and inflammation. (A)</p> Signup and view all the answers

A patient admitted with acute liver failure exhibits asterixis. Which underlying pathophysiological mechanism is most directly responsible for this clinical sign?

<p>Accumulation of neurotoxins in the systemic circulation due to impaired hepatic detoxification. (A)</p> Signup and view all the answers

What is the underlying mechanism behind the jaundice observed in liver failure?

<p>Impaired conjugation and excretion of bilirubin by the liver. (B)</p> Signup and view all the answers

Why is prothrombin time (PT) prolonged in patients with advanced liver disease?

<p>Decreased synthesis of clotting factors by the damaged liver. (C)</p> Signup and view all the answers

What is the rationale behind advising patients with liver disease to avoid acetaminophen (Tylenol)?

<p>Acetaminophen is hepatotoxic and its metabolism generates a toxic metabolite that can further damage the liver. (A)</p> Signup and view all the answers

In hepatitis A infection, what does the presence of anti-hepatitis A virus Immunoglobulin G (IgG) indicate?

<p>Past infection with hepatitis A and subsequent immunity. (B)</p> Signup and view all the answers

Why are patients with ascites often advised to restrict their sodium intake?

<p>Sodium promotes fluid retention, worsening ascites. (A)</p> Signup and view all the answers

A patient with chronic hepatitis C develops ascites and hepatic encephalopathy. Which of the following pathophysiological mechanisms contributes most directly to the development of hepatic encephalopathy?

<p>Increased portal hypertension leading to shunting of blood around the liver and systemic hyperammonemia. (B)</p> Signup and view all the answers

In a patient with non-alcoholic steatohepatitis (NASH), which of the following histological findings would be most indicative of disease progression towards cirrhosis?

<p>Pericellular fibrosis ('chicken wire' fibrosis) surrounding individual hepatocytes. (A)</p> Signup and view all the answers

A patient with chronic hepatitis B is being monitored for potential development of hepatocellular carcinoma (HCC). Which surveillance strategy is most appropriate?

<p>Ultrasound of the liver every 6 months, with or without AFP measurement. (A)</p> Signup and view all the answers

A patient with advanced cirrhosis develops hepatorenal syndrome. Which pathophysiological mechanism is most directly responsible for the renal dysfunction in this condition?

<p>Splanchnic vasodilation and reduced effective arterial blood volume leading to renal vasoconstriction. (B)</p> Signup and view all the answers

A patient presents with acute hepatitis E infection contracted during international travel. Which of the following statements regarding hepatitis E is most accurate?

<p>Hepatitis E can cause fulminant hepatic failure, particularly in pregnant women. (A)</p> Signup and view all the answers

Which of the following statements accurately describes the mechanism by which lactulose reduces hepatic encephalopathy?

<p>Lactulose acidifies the colon, promoting the conversion of ammonia to ammonium, which is poorly absorbed. (A)</p> Signup and view all the answers

A patient with cirrhosis develops spontaneous bacterial peritonitis (SBP). Paracentesis reveals a neutrophil count of 300 cells/mm³ in the ascitic fluid. According to current guidelines, what is the most appropriate initial management?

<p>Administer intravenous antibiotics empirically without waiting for culture results. (D)</p> Signup and view all the answers

A patient with jaundice and suspected hepatocellular disease has the following lab results: markedly elevated AST and ALT, moderately elevated alkaline phosphatase, and a normal GGT. Which of the following conditions is LEAST likely?

<p>Biliary obstruction (A)</p> Signup and view all the answers

What is the primary rationale for using rifaximin in the treatment of hepatic encephalopathy?

<p>Rifaximin decreases the number of urease-producing bacteria in the gut, reducing ammonia production. (A)</p> Signup and view all the answers

A patient with long-standing ulcerative colitis is diagnosed with primary sclerosing cholangitis (PSC). Which of the following is the most appropriate next step in management?

<p>Refer the patient for liver transplantation evaluation. (D)</p> Signup and view all the answers

A patient is diagnosed with Budd-Chiari syndrome. Which of the following is the most accurate description of the underlying pathophysiology?

<p>Obstruction of the hepatic venous outflow tract. (B)</p> Signup and view all the answers

A patient with decompensated cirrhosis and refractory ascites is undergoing large-volume paracentesis. Which complication is most likely to occur following the procedure?

<p>Hypotension and renal dysfunction due to decreased effective circulating volume. (A)</p> Signup and view all the answers

What is the most likely mechanism by which isoniazid causes liver injury?

<p>Induction of cytochrome P450 enzymes leading to formation of a toxic metabolite. (D)</p> Signup and view all the answers

A patient presents with RUQ pain, fever, and jaundice. Imaging reveals a choledochal cyst. What is the most appropriate long-term management strategy?

<p>Surgical resection of the cyst with biliary reconstruction. (D)</p> Signup and view all the answers

A patient with hereditary hemochromatosis develops cirrhosis. What is the primary mechanism by which iron overload leads to liver damage?

<p>All of the above. (D)</p> Signup and view all the answers

A patient is suspected of having Wilson's disease. Which diagnostic test is most specific for this condition?

<p>Liver biopsy with copper quantification. (A)</p> Signup and view all the answers

A patient undergoes liver transplantation. What is the primary mechanism of action of calcineurin inhibitors, such as tacrolimus, in preventing graft rejection?

<p>Inhibit T-cell activation by blocking the calcineurin-dependent signaling pathway. (A)</p> Signup and view all the answers

A patient with alpha-1 antitrypsin deficiency develops cirrhosis. What is the underlying mechanism by which the deficiency leads to liver damage?

<p>Accumulation of misfolded alpha-1 antitrypsin protein in hepatocytes, causing cellular stress and apoptosis. (A)</p> Signup and view all the answers

A patient with cirrhosis and esophageal varices is being treated with non-selective beta-blockers. What is the primary rationale for this therapy?

<p>To decrease hepatic venous pressure gradient by reducing portal blood flow. (B)</p> Signup and view all the answers

A patient with decompensated cirrhosis develops hepatopulmonary syndrome. What is the primary abnormality underlying this condition?

<p>Intrapulmonary vasodilation leading to ventilation-perfusion mismatch. (C)</p> Signup and view all the answers

A patient with acute liver failure due to acetaminophen overdose is being considered for liver transplantation. Which prognostic scoring system is most commonly used to assess the severity of liver failure and predict the likelihood of survival?

<p>King's College Criteria (B)</p> Signup and view all the answers

A patient with a history of intravenous drug use presents with symptoms of acute hepatitis. Serological testing reveals a positive anti-HCV antibody but a negative HCV RNA. What is the most likely interpretation of these results?

<p>The patient has cleared the hepatitis C virus spontaneously but remains antibody positive. (C)</p> Signup and view all the answers

A patient develops significant ascites despite maximal medical therapy, including sodium restriction and high-dose diuretics. What intervention should be considered next?

<p>Perform transjugular intrahepatic portosystemic shunt (TIPS) to reduce portal pressure. (D)</p> Signup and view all the answers

A patient with alcoholic cirrhosis presents with sudden onset of hematemesis. After initial resuscitation, what is the most important next step in management?

<p>Perform upper endoscopy to identify and treat the source of bleeding. (A)</p> Signup and view all the answers

A patient with chronic liver disease develops hepatic hydrothorax. What is the underlying mechanism leading to fluid accumulation in the pleural space?

<p>Direct passage of ascitic fluid through diaphragmatic defects into the pleural space. (C)</p> Signup and view all the answers

A patient with chronic hepatitis C infection is being considered for treatment with direct-acting antiviral agents (DAAs). What baseline laboratory test is essential prior to initiating therapy?

<p>Hepatitis B surface antigen (HBsAg) to rule out HBV co-infection. (C)</p> Signup and view all the answers

A patient with cirrhosis develops spontaneous bacterial peritonitis (SBP). Besides antibiotics, what additional treatment has been shown to improve survival in these patients?

<p>Intravenous albumin infusion. (C)</p> Signup and view all the answers

Flashcards

Cholelithiasis Pathophysiology

Cholesterol crystals aggregate, bile becomes saturated, bile stasis occurs leading to stone formation.

Cholelithiasis Manifestations

Severe RUQ pain, fever, biliary colic (after fatty foods).

Cholelithiasis Lab Results

Leukocytosis, increased bilirubin, elevated ALT.

Cholelithiasis Treatment

ERCP and lithotripsy.

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Cholecystitis Pathophysiology

Inflammation of the gallbladder wall, acute or chronic.

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Acute Cholecystitis Symptoms

Elevated temp, severe RUQ pain, leukocytosis.

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Cholecystitis Diagnosis

MRI, CT, Ultrasound.

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Cholecystitis Diet

Low fat, increased protein, avoid gas-forming food, no alcohol.

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ERCP Complication

Fever.

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Cholecystectomy Post-op

Call surgeon if febrile, no fatty foods for 4-6 weeks, walk to relieve gas pain.

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Portal Hypertension Patho

GI congestion, enlarged portal vein.

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Portal Hypertension Risk

Advanced liver disease.

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Portal HTN Manifestations

Ascites, esophageal varices.

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Liver Failure Signs

Jaundice, hypoalbuminemia, splenomegaly.

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Liver Disease Care

Mild soaps, monitor PT, avoid alcohol, Tylenol, hepatotoxic substances.

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Hepatitis A (HAV)

RNA virus from unsafe water, poor sanitation. Incubation 2-7 weeks.

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Hep A Labs IgG

Anti-hepatitis virus A Immunoglobulin G (IgG).

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Hepatitis B (HBV)

Double-stranded DNA virus. Incubation 2-6 months. Transmission by blood and body fluids.

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Hep B Risk Factors

IV drug use.

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Hepatitis B (HBV) Symptoms

Anorexia, fever, jaundice, serum sickness.

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Hepatitis B Surface antigen (HBsAg)

Surface antigen (HBsAg): early/active and chronic infection.

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Hepatitis B Surface antibody (HbsAb)

Surface antibody (HbsAb): resolution and immunity.

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Hepatitis B Core antigen (HBcAg)

Core antigen (HBcAg): appears first in active infection.

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Hepatitis B (HBV) Treatment

Avoid hepatotoxic substances, no alcohol, high carb/low fat diet.

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Hepatitis B (HBV) Education

Avoid sexual activity until HVB testing is negative.

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Hepatitis C (HCV)

Single-stranded RNA virus.

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Chronic Hep C Symptoms

Peripheral edema, ascites, mental status changes.

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Hepatitis C Labs

HCV RNA, anti-HCV (antibodies to the virus are present).

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Hepatitis C Treatment

Antiviral treatment, take as prescribed.

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Hepatitis E (HVE)

Fecal oral virus from contaminated food/water, contracted by international travel.

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Hepatitis E Education

Avoid drinking or Tylenol, wash hands.

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Non-Viral Hepatitis Types

Alcoholic Hepatitis and Nonalcoholic Steatohepatitis (NASH).

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NASH Risk Factors

Diabetes type 1, high cholesterol.

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Alcoholic Hepatitis

Inflammation of the centrilobular region of the liver causes necrosis of the liver cells because of chronic alcohol abuse.

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Non-Viral Hepatitis Symptoms

Portal HTN, Encephalopathy, Fever, Hepatomegaly.

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Non-Viral Hepatitis Treatment

Avoid ETOH and hepatotoxic meds, prednisolone, N-acetyl cysteine, statins.

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Alcoholic Hepatitis Patho

Inflammation of the centrilobular region of the liver causes necrosis of the liver cells.

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Medication Liver Toxic

Isoniazid.

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Symptom Treatment

Zofran, Toradol, docusate.

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Study Notes

  • Gallstones/Cholelithiasis patho involves cholesterol crystals aggregating to form a stone, caused by bile secretions becoming saturated with cholesterol and bile stasis due to slow secretion.
  • Cholesterol gallstone formation can occur with spinal cord injuries, TPN, rapid weight loss, and pregnancy.
  • Clinical manifestations include severe RUQ pain, fever, and biliary colic, especially after eating high-fat foods.
  • Labs will show leukocytosis, increased bilirubin, and elevated ALT.
  • Diagnosis is via ultrasound and risk factors include the four F's: forty, fat, female, and fertile.
  • Treatment includes ERCP and lithotripsy.

Cholecystitis

  • Cholecystitis patho is inflammation of the gallbladder wall, which can be acute or chronic.
  • Acute cholecystitis clinical manifestations include elevated temperature, severe RUQ pain, and leukocytosis.
  • Chronic cholecystitis clinical manifestation is often asymptomatic.
  • Diagnosis tests are MRI, CT, and ultrasound.
  • Patients should follow a diet low in fat, increased protein, avoid gas-forming foods, and no alcohol.
  • With ERCP, monitor for complications like fever and with cholecystectomy, conduct post-op monitoring and teach patients to call the surgeon if febrile and avoid fatty foods for 4-6 weeks, and walk to relieve gas pain from the surgery.

Portal Hypertension

  • Portal Hypertension patho involves GI congestion and enlargement of the portal vein.
  • A complication is advanced liver disease.
  • Clinical manifestations are ascites and esophageal varices.
  • Clinical manifestations for liver failure are jaundice, hypoalbuminemia, and splenomegaly.
  • Treatment/interventions for liver disease include using mild soaps for bathing, monitoring prothrombin time (which will be elevated), and avoiding alcohol, Tylenol, and hepatotoxic substances.

Viral Hepatitis A (HAV)

  • Hepatitis A is an RNA virus due to lack of safe water and poor sanitation with an incubation period of 2-7 weeks.
  • Lab results showing Anti-hepatitis virus A IgG indicate immunity to HAV.

Viral Hepatitis B (HBV)

  • Hepatitis B is a double-stranded DNA virus with an incubation period of 2 to 6 months.
  • Risk factors include IV drug use and transmission by blood and body fluids.
  • Clinical manifestations include anorexia, fever, jaundice, and serum sickness.
  • Labs findings inlcude:
    • Surface antigen (HBsAg) indicates early/active and chronic infection
    • Surface antibody (HbsAb) indicates resolution and immunity
    • Core antigen (HBcAg) appears first in active infection
    • Core antibody (HBcAb) indicates seroconversion
    • Hepatitis B e antigen (HBeAg) indicates viral replication and infectivity.
  • Treatment/interventions involve avoiding hepatotoxic substances, no alcohol, a diet high in carbs and low in fat, and avoiding sexual activity until HBV testing comes back negative.

Viral Hepatitis C (HCV)

  • Hepatitis C is a single-stranded RNA virus.
  • Clinical manifestations are the same as Hepatitis B.
  • Chronic Hepatitis C presents with peripheral edema, ascites, and changes to mental status.
  • Labs: HCV RNA and anti-HCV indicate antibodies to the virus are present.
  • Treatment involves antiviral medications, as prescribed.

Viral Hepatitis E (HVE)

  • Hepatitis E is a fecal-oral virus contracted from contaminated food/water, often by international travelers.
  • Clinical manifestations are the same as Hepatitis A.
  • Patient education includes no drinking or Tylenol and hand washing to prevent spread.

Non Viral Hepatitis

  • Non-viral hepatitis includes alcoholic hepatitis and nonalcoholic steatohepatitis (NASH).

Nonalcoholic Steatohepatitis (NASH)

  • Risk factors include diabetes type 1 and high cholesterol.

Alcoholic Hepatitis

  • Alcoholic hepatitis is inflammation of the centrilobular region of the liver that causes necrosis of liver cells.
  • Clinical manifestations for both include portal hypertension, encephalopathy, fever, and hepatomegaly.
  • Treatment is AVOID ETOH and hepatotoxic medications, take prednisolone, N-acetyl cysteine, statin meds for cholesterol.
  • Isoniazid is liver toxic, treat symptoms with Zofran, Toradol, docusate.

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