Podcast
Questions and Answers
What is the most likely diagnosis given the patient's symptoms and examination findings?
What is the most likely diagnosis given the patient's symptoms and examination findings?
Which laboratory finding is most indicative of spontaneous bacterial peritonitis in this patient?
Which laboratory finding is most indicative of spontaneous bacterial peritonitis in this patient?
Which treatment is recommended while awaiting bacterial culture results for spontaneous bacterial peritonitis?
Which treatment is recommended while awaiting bacterial culture results for spontaneous bacterial peritonitis?
What should be done if the patient cannot take lactulose orally due to reduced conscious level?
What should be done if the patient cannot take lactulose orally due to reduced conscious level?
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Which examination should be performed to check for varices in this patient?
Which examination should be performed to check for varices in this patient?
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What complication is associated with the patient’s low ascitic fluid albumin level?
What complication is associated with the patient’s low ascitic fluid albumin level?
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The presence of spider naevi in this patient is indicative of which condition?
The presence of spider naevi in this patient is indicative of which condition?
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Which statement about the patient’s history is significant in assessing his liver condition?
Which statement about the patient’s history is significant in assessing his liver condition?
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What is the primary consequence of the transformation of the normal liver architecture in cirrhosis?
What is the primary consequence of the transformation of the normal liver architecture in cirrhosis?
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Which classification of cirrhosis encompasses both uniform and varied nodular formations?
Which classification of cirrhosis encompasses both uniform and varied nodular formations?
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What is one of the most common causes of cirrhosis due to rising lifestyle factors?
What is one of the most common causes of cirrhosis due to rising lifestyle factors?
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What characterizes micronodular cirrhosis?
What characterizes micronodular cirrhosis?
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Which symptom is NOT typically associated with liver cirrhosis?
Which symptom is NOT typically associated with liver cirrhosis?
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Which statement accurately reflects the process leading to fibrosis in the liver?
Which statement accurately reflects the process leading to fibrosis in the liver?
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What is a consequence of capillarization of the hepatic sinusoids?
What is a consequence of capillarization of the hepatic sinusoids?
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Which factor plays a key role in increasing intrahepatic resistance in liver cirrhosis?
Which factor plays a key role in increasing intrahepatic resistance in liver cirrhosis?
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What is one of the primary features of hepatopulmonary syndrome?
What is one of the primary features of hepatopulmonary syndrome?
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Which gastrointestinal complication can arise due to portal hypertension?
Which gastrointestinal complication can arise due to portal hypertension?
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What is a hematological consequence of liver dysfunction?
What is a hematological consequence of liver dysfunction?
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Which of the following is NOT typically associated with hepatic encephalopathy?
Which of the following is NOT typically associated with hepatic encephalopathy?
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Which symptom is likely a dermatological manifestation of liver disease?
Which symptom is likely a dermatological manifestation of liver disease?
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What is a common endocrine symptom in male patients with liver dysfunction?
What is a common endocrine symptom in male patients with liver dysfunction?
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Which condition is characterized by muscle cramping and reduction in muscle mass?
Which condition is characterized by muscle cramping and reduction in muscle mass?
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What is the 10-year survival rate for compensated cirrhosis?
What is the 10-year survival rate for compensated cirrhosis?
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What defines Type B hepatic encephalopathy?
What defines Type B hepatic encephalopathy?
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Which precipitant is NOT commonly associated with hepatic encephalopathy?
Which precipitant is NOT commonly associated with hepatic encephalopathy?
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What causes an increase in portal pressure in cirrhosis?
What causes an increase in portal pressure in cirrhosis?
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What is the primary pathophysiological trigger in hepatic encephalopathy?
What is the primary pathophysiological trigger in hepatic encephalopathy?
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Which neurohormonal system is activated due to baroreceptors sensing arterial underfilling?
Which neurohormonal system is activated due to baroreceptors sensing arterial underfilling?
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What condition can result from prolonged renal vasoconstriction due to cirrhosis?
What condition can result from prolonged renal vasoconstriction due to cirrhosis?
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Which condition is characterized by minimal hepatic encephalopathy?
Which condition is characterized by minimal hepatic encephalopathy?
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What is a gross examination finding of a liver affected by cirrhosis?
What is a gross examination finding of a liver affected by cirrhosis?
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What is the mainstay of treatment in managing hepatic encephalopathy?
What is the mainstay of treatment in managing hepatic encephalopathy?
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Which clinical feature may indicate the presence of cirrhosis?
Which clinical feature may indicate the presence of cirrhosis?
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Which grading system is used to assess the severity of hepatic encephalopathy?
Which grading system is used to assess the severity of hepatic encephalopathy?
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Which of the following statements about ammonia levels in hepatic encephalopathy is accurate?
Which of the following statements about ammonia levels in hepatic encephalopathy is accurate?
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Which of the following is NOT a complication of decompensated cirrhosis?
Which of the following is NOT a complication of decompensated cirrhosis?
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What should be the focus of laboratory evaluation in diagnosing hepatic encephalopathy?
What should be the focus of laboratory evaluation in diagnosing hepatic encephalopathy?
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What type of examination is crucial for determining the presence and cause of cirrhosis?
What type of examination is crucial for determining the presence and cause of cirrhosis?
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What change in laboratory results may signify hepatic synthetic dysfunction in cirrhosis?
What change in laboratory results may signify hepatic synthetic dysfunction in cirrhosis?
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What percentage of patients typically develop varices annually in decompensated cirrhosis?
What percentage of patients typically develop varices annually in decompensated cirrhosis?
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Which of the following is a feature of portal hypertension?
Which of the following is a feature of portal hypertension?
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What is the significance of an AST/ALT ratio greater than 1 in patients with chronic hepatitis progressing to cirrhosis?
What is the significance of an AST/ALT ratio greater than 1 in patients with chronic hepatitis progressing to cirrhosis?
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Which diagnostic test for hepatocellular injury is characterized by elevated prothrombin time?
Which diagnostic test for hepatocellular injury is characterized by elevated prothrombin time?
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Which imaging modality is most reliable for assessing hepatic vasculature without using nephrotoxic contrast?
Which imaging modality is most reliable for assessing hepatic vasculature without using nephrotoxic contrast?
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Which of the following tests is specifically used as a tumor marker for hepatocellular carcinoma (HCC)?
Which of the following tests is specifically used as a tumor marker for hepatocellular carcinoma (HCC)?
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What percentage of patients with decompensated cirrhosis are likely to develop ascites within five years?
What percentage of patients with decompensated cirrhosis are likely to develop ascites within five years?
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What radiological investigation is often used to confirm a diagnosis of hepatocellular carcinoma?
What radiological investigation is often used to confirm a diagnosis of hepatocellular carcinoma?
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Study Notes
Liver Cirrhosis
- A diffuse process characterized by fibrosis and the conversion of normal liver architecture into abnormal nodules
- Results in impairment of hepatic function manifesting as jaundice, portal hypertension, varices, ascites, and spontaneous bacterial peritonitis
- Associated with hepato-renal syndrome, hepatic encephalopathy, and progressive hepatic failure
Case Presentation
- A 50-year-old male was admitted with a 4-week history of increasing abdominal distension, anorexia, and 2 weeks of jaundice
- No change in bowel habits or vomiting, denies weight loss
- His wife noticed confusion over the previous 24 hours
- Used intravenous drugs at age 20
- 5-6 spider naevi on upper chest wall
- Asterixis (flapping tremor) observed
- Firm, sharp-bordered, non-tender liver palpable 6 cm below right costal margin at midclavicular line
- Ascites confirmed by abdominal examination (shifting dullness)
Clinical Signs
- Jaundice: Yellowing of the eyes and skin
- Ascites: Fluid buildup in the abdomen
- Spider naevi: Vascular birthmark on the skin
- Bilateral pitting oedema LL: Swelling of the legs
Investigations
-
Initial Investigations:
- Sodium: 130 mmol/L
- Potassium: 3.8 mmol/L
- Urea: 0.9 mmol/L
- Creatinine: 89 µmol/L
- Albumin: 25 g/L
- Bilirubin: 90 µmol/L
- Alkaline phosphatase: 400 U/L
- ALT: 150 U/L
- AST: 180 U/L
- Hemoglobin: 110 g/dL
- WCC: 8x109/L
- Platelets: 70x109/L
- Prothrombin time: 20 s
- Ultrasound Examination: Enlarged liver with coarse texture, enlarged spleen, no intrahepatic/common bile duct dilatation, main portal vein patent and dilated (16mm), and moderate ascites
- Virology screening: Positive for Hepatitis C antibody
- PCR for HCV RNA viral load: 2654000 iu/ml
- Ascitic fluid analysis: WBC count 1500/cmm, 90% neutrophils, ascitic fluid albumin 0.4 g/dl
Treatment
- Spontaneous Bacterial Peritonitis (SBP) diagnosed
- Intravenous cephalosporins or oral quinolones
- Secondary prophylaxis needed to reduce risk of further infections
- Lactulose given orally, if reduced conscious level, then phosphate enemas
- Beta-blocker prophylaxis to reduce risk of bleeding from asymptomatic varices
- Hepatitis C treatment to be considered when liver function improves
Liver Cirrhosis Definition/Pathology
- A diffuse process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules
- Leads to impaired hepatic function
- Gross examination often shows irregular surface with multiple yellowish nodules; enlarged liver may shrink in later stages
- Microscopic examination reveals nodularity (regenerative nodules), fibrosis, abnormal hepatic architecture, and abnormal hepatocytes
- Importance of histologic examination for establishment of cirrhosis, grading histologic activity, degree of liver fibrosis, and cause of cirrhosis in some cases
Clinical Features
- General: Fatigue, anorexia, malaise, sleep-wake reversal, weight loss, muscle wasting
- Gastrointestinal: Parotitid gland enlargement, diarrhea, cholelithiasis, gastrointestinal bleeding (due to ruptured esophageal, gastric, duodenal, rectal, and/or stomal varices)
- Hematological: Anemia, thrombocytopenia, leukopenia, impaired coagulation, disseminated intravascular coagulation, portal vein thrombosis
- Pulmonary: Hepatopulmonary syndrome
- Cardiac: Hyperdynamic circulation, diastolic dysfunction
- Renal: Secondary hyperaldosteronism
Clinical Features -Continued
- Endocrinological: Hypogonadism, Feminization, diabetes mellitus
- Neurological: Hepatic encephalopathy, peripheral neuropathy, asterixis
- Musculoskeletal: Reduction in muscle mass, hepatic osteodystrophy, muscle cramping, umbilical herniation
- Dermatological: Spider naevi, palmar erythema, jaundice, pruritus, Dupuytren contractures, clubbing, paper-money skin, caput medusa, easy bruising
- Infections: Spontaneous bacterial peritonitis, urinary tract infection, respiratory tract infection, bacteremia, cellulitis
- Cirrhotic features on physical exam: Spider naevi, palmar erythema, Dupuytren contractures, gynecomastia, testicular atrophy, ascites, splenomegaly, caput medusa, resting tachycardia, water hammer pulse, venous hum, hepatic encephalopathy, jaundice, parotid gland enlargement, scanty suprapubic and axillary hair
Diagnosis
- Clinical exam: Presence of stigmata of cirrhosis, features of portal hypertension (ascites, splenomegaly, caput medusa, etc.), and features of hepatic encephalopathy
-
Lab evaluation:
- Tests of hepatocellular injury (AST, ALT)
- Tests of cholestasis (bilirubin, ALP, GGT)
- Tests of synthetic function (albumin, prothrombin time)
- Tests for cause (e.g., viral markers, autoimmune antibodies)
- Tumor markers
- Radiological investigations: Abdominlal ultrasonography (assessing liver echotexture, border irregularities, size, detecting ascites, biliary dilatation, Doppler ultrasonography assess hepatic and portal vein patency, diameter, and blood flow), Computed tomography (CT, more expensive, requires administration of potentially nephrotoxic contrast to confirm HCC diagnosis), Magnetic resonance imaging (MRI, hepatic masses, hepatic vasculature), Magnetic resonance cholangio-pancreaticography (MRCP, biliary tract imaging)
- Endoscopic investigations: Esophagogastroduodenoscopy (EGD, for gastro-esophageal varices screening)
- Noninvasive markers of fibrosis/cirrhosis: APRI score, FIB-4 score, transient elastography (Fibroscan)
- Liver biopsy: Useful in rare cases to diagnose cause of cirrhosis (e.g., Wilson's disease, autoimmune hepatitis, hemochromatosis). Usually performed percutaneously, sometimes transjugular or during laparoscopy.
Prognostic Scores
- Child-Turcotte-Pugh (CTP) score and class: Classifies severity of cirrhosis based on clinical and lab criteria (encephalopathy, ascites, bilirubin, albumin, prothrombin time).
- Model for End-stage Liver Disease (MELD) score: Predicts 90-day mortality and guides organ allocation policies. Scores can range from 6-40; higher number indicates more severe liver impairment. Formula: MELD = 9.57 × loge (creatinine) + 3.78 × Loge (total bilirubin) + 11.2 × Loge (INR) + 6.43
Hepatic Encephalopathy
- A neuropsychiatric disorder associated with severe liver disease
- Classified according to the condition during which manifestations appear and graded by the West Haven criteria
- Types include acute (type A), bypass (type B) and cirrhotic (type C)
- Common precipitating factors include gastrointestinal bleeding, post-transjugular intrahepatic portosystemic shunts (TIPS), constipation, spontaneous bacterial peritonitis, narcotics, benzodiazepines, hepatocellular carcinoma
Treatment
- Treatment of cirrhosis aims at addressing the underlying cause:
- Lifestyle modifications: Avoiding alcohol, weight management
- Medications: Antivirals for chronic hepatitis C or B, glucocorticoids/azathioprine for autoimmune hepatitis, D-penicillamine/trientine for Wilson disease, Ursodeoxycholic acid and/or obeticholic acid for primary biliary cholangitis (PBC)
- Treatment for complications: Hemorrhage, hepatic encephalopathy, ascites, spontaneous bacterial peritonitis, cirrhosis surveillance for HCC (ultrasound, AFP)
- Vaccination: Against hepatitis A and B
- Avoiding hepatotoxins: alcohol and other hepatotoxins
- Liver transplantation: indicated in end-stage cirrhosis (CTP class B/C or MELD score ≥15)
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Description
This quiz evaluates your understanding of key aspects related to liver disease, including diagnoses, laboratory findings, treatments, and complications. Questions will focus on spontaneous bacterial peritonitis, liver examination techniques, and significant historical factors impacting liver conditions.
