Podcast
Questions and Answers
In a patient status post spinal cord injury, which pathophysiological mechanism most directly contributes to cholesterol gallstone formation?
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?
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?
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?
In a patient with portal hypertension secondary to cirrhosis, which of the following mediators is most directly responsible for the development of esophageal varices?
A patient with chronic hepatitis B develops hepatocellular carcinoma (HCC). Which molecular mechanism is most directly implicated in HBV-related hepatocarcinogenesis?
A patient with chronic hepatitis B develops hepatocellular carcinoma (HCC). Which molecular mechanism is most directly implicated in HBV-related hepatocarcinogenesis?
Which serological marker indicates resolution of acute hepatitis B infection and subsequent immunity?
Which serological marker indicates resolution of acute hepatitis B infection and subsequent immunity?
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?
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?
In alcoholic hepatitis, which pathological change within the liver is most closely associated with disease progression and mortality?
In alcoholic hepatitis, which pathological change within the liver is most closely associated with disease progression and mortality?
Which of the following best describes the pathogenesis of nonalcoholic steatohepatitis (NASH)?
Which of the following best describes the pathogenesis of nonalcoholic steatohepatitis (NASH)?
A patient admitted with acute liver failure exhibits asterixis. Which underlying pathophysiological mechanism is most directly responsible for this clinical sign?
A patient admitted with acute liver failure exhibits asterixis. Which underlying pathophysiological mechanism is most directly responsible for this clinical sign?
What is the underlying mechanism behind the jaundice observed in liver failure?
What is the underlying mechanism behind the jaundice observed in liver failure?
Why is prothrombin time (PT) prolonged in patients with advanced liver disease?
Why is prothrombin time (PT) prolonged in patients with advanced liver disease?
What is the rationale behind advising patients with liver disease to avoid acetaminophen (Tylenol)?
What is the rationale behind advising patients with liver disease to avoid acetaminophen (Tylenol)?
In hepatitis A infection, what does the presence of anti-hepatitis A virus Immunoglobulin G (IgG) indicate?
In hepatitis A infection, what does the presence of anti-hepatitis A virus Immunoglobulin G (IgG) indicate?
Why are patients with ascites often advised to restrict their sodium intake?
Why are patients with ascites often advised to restrict their sodium intake?
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?
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?
In a patient with non-alcoholic steatohepatitis (NASH), which of the following histological findings would be most indicative of disease progression towards cirrhosis?
In a patient with non-alcoholic steatohepatitis (NASH), which of the following histological findings would be most indicative of disease progression towards cirrhosis?
A patient with chronic hepatitis B is being monitored for potential development of hepatocellular carcinoma (HCC). Which surveillance strategy is most appropriate?
A patient with chronic hepatitis B is being monitored for potential development of hepatocellular carcinoma (HCC). Which surveillance strategy is most appropriate?
A patient with advanced cirrhosis develops hepatorenal syndrome. Which pathophysiological mechanism is most directly responsible for the renal dysfunction in this condition?
A patient with advanced cirrhosis develops hepatorenal syndrome. Which pathophysiological mechanism is most directly responsible for the renal dysfunction in this condition?
A patient presents with acute hepatitis E infection contracted during international travel. Which of the following statements regarding hepatitis E is most accurate?
A patient presents with acute hepatitis E infection contracted during international travel. Which of the following statements regarding hepatitis E is most accurate?
Which of the following statements accurately describes the mechanism by which lactulose reduces hepatic encephalopathy?
Which of the following statements accurately describes the mechanism by which lactulose reduces hepatic encephalopathy?
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?
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?
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?
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?
What is the primary rationale for using rifaximin in the treatment of hepatic encephalopathy?
What is the primary rationale for using rifaximin in the treatment of hepatic encephalopathy?
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?
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?
A patient is diagnosed with Budd-Chiari syndrome. Which of the following is the most accurate description of the underlying pathophysiology?
A patient is diagnosed with Budd-Chiari syndrome. Which of the following is the most accurate description of the underlying pathophysiology?
A patient with decompensated cirrhosis and refractory ascites is undergoing large-volume paracentesis. Which complication is most likely to occur following the procedure?
A patient with decompensated cirrhosis and refractory ascites is undergoing large-volume paracentesis. Which complication is most likely to occur following the procedure?
What is the most likely mechanism by which isoniazid causes liver injury?
What is the most likely mechanism by which isoniazid causes liver injury?
A patient presents with RUQ pain, fever, and jaundice. Imaging reveals a choledochal cyst. What is the most appropriate long-term management strategy?
A patient presents with RUQ pain, fever, and jaundice. Imaging reveals a choledochal cyst. What is the most appropriate long-term management strategy?
A patient with hereditary hemochromatosis develops cirrhosis. What is the primary mechanism by which iron overload leads to liver damage?
A patient with hereditary hemochromatosis develops cirrhosis. What is the primary mechanism by which iron overload leads to liver damage?
A patient is suspected of having Wilson's disease. Which diagnostic test is most specific for this condition?
A patient is suspected of having Wilson's disease. Which diagnostic test is most specific for this condition?
A patient undergoes liver transplantation. What is the primary mechanism of action of calcineurin inhibitors, such as tacrolimus, in preventing graft rejection?
A patient undergoes liver transplantation. What is the primary mechanism of action of calcineurin inhibitors, such as tacrolimus, in preventing graft rejection?
A patient with alpha-1 antitrypsin deficiency develops cirrhosis. What is the underlying mechanism by which the deficiency leads to liver damage?
A patient with alpha-1 antitrypsin deficiency develops cirrhosis. What is the underlying mechanism by which the deficiency leads to liver damage?
A patient with cirrhosis and esophageal varices is being treated with non-selective beta-blockers. What is the primary rationale for this therapy?
A patient with cirrhosis and esophageal varices is being treated with non-selective beta-blockers. What is the primary rationale for this therapy?
A patient with decompensated cirrhosis develops hepatopulmonary syndrome. What is the primary abnormality underlying this condition?
A patient with decompensated cirrhosis develops hepatopulmonary syndrome. What is the primary abnormality underlying this condition?
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?
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?
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?
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?
A patient develops significant ascites despite maximal medical therapy, including sodium restriction and high-dose diuretics. What intervention should be considered next?
A patient develops significant ascites despite maximal medical therapy, including sodium restriction and high-dose diuretics. What intervention should be considered next?
A patient with alcoholic cirrhosis presents with sudden onset of hematemesis. After initial resuscitation, what is the most important next step in management?
A patient with alcoholic cirrhosis presents with sudden onset of hematemesis. After initial resuscitation, what is the most important next step in management?
A patient with chronic liver disease develops hepatic hydrothorax. What is the underlying mechanism leading to fluid accumulation in the pleural space?
A patient with chronic liver disease develops hepatic hydrothorax. What is the underlying mechanism leading to fluid accumulation in the pleural space?
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?
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?
A patient with cirrhosis develops spontaneous bacterial peritonitis (SBP). Besides antibiotics, what additional treatment has been shown to improve survival in these patients?
A patient with cirrhosis develops spontaneous bacterial peritonitis (SBP). Besides antibiotics, what additional treatment has been shown to improve survival in these patients?
Flashcards
Cholelithiasis Pathophysiology
Cholelithiasis Pathophysiology
Cholesterol crystals aggregate, bile becomes saturated, bile stasis occurs leading to stone formation.
Cholelithiasis Manifestations
Cholelithiasis Manifestations
Severe RUQ pain, fever, biliary colic (after fatty foods).
Cholelithiasis Lab Results
Cholelithiasis Lab Results
Leukocytosis, increased bilirubin, elevated ALT.
Cholelithiasis Treatment
Cholelithiasis Treatment
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Cholecystitis Pathophysiology
Cholecystitis Pathophysiology
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Acute Cholecystitis Symptoms
Acute Cholecystitis Symptoms
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Cholecystitis Diagnosis
Cholecystitis Diagnosis
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Cholecystitis Diet
Cholecystitis Diet
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ERCP Complication
ERCP Complication
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Cholecystectomy Post-op
Cholecystectomy Post-op
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Portal Hypertension Patho
Portal Hypertension Patho
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Portal Hypertension Risk
Portal Hypertension Risk
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Portal HTN Manifestations
Portal HTN Manifestations
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Liver Failure Signs
Liver Failure Signs
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Liver Disease Care
Liver Disease Care
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Hepatitis A (HAV)
Hepatitis A (HAV)
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Hep A Labs IgG
Hep A Labs IgG
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Hepatitis B (HBV)
Hepatitis B (HBV)
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Hep B Risk Factors
Hep B Risk Factors
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Hepatitis B (HBV) Symptoms
Hepatitis B (HBV) Symptoms
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Hepatitis B Surface antigen (HBsAg)
Hepatitis B Surface antigen (HBsAg)
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Hepatitis B Surface antibody (HbsAb)
Hepatitis B Surface antibody (HbsAb)
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Hepatitis B Core antigen (HBcAg)
Hepatitis B Core antigen (HBcAg)
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Hepatitis B (HBV) Treatment
Hepatitis B (HBV) Treatment
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Hepatitis B (HBV) Education
Hepatitis B (HBV) Education
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Hepatitis C (HCV)
Hepatitis C (HCV)
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Chronic Hep C Symptoms
Chronic Hep C Symptoms
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Hepatitis C Labs
Hepatitis C Labs
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Hepatitis C Treatment
Hepatitis C Treatment
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Hepatitis E (HVE)
Hepatitis E (HVE)
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Hepatitis E Education
Hepatitis E Education
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Non-Viral Hepatitis Types
Non-Viral Hepatitis Types
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NASH Risk Factors
NASH Risk Factors
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Alcoholic Hepatitis
Alcoholic Hepatitis
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Non-Viral Hepatitis Symptoms
Non-Viral Hepatitis Symptoms
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Non-Viral Hepatitis Treatment
Non-Viral Hepatitis Treatment
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Alcoholic Hepatitis Patho
Alcoholic Hepatitis Patho
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Medication Liver Toxic
Medication Liver Toxic
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Symptom Treatment
Symptom Treatment
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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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