Medicine Marrow Pg No 1005-1014 (Hepatology)
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Questions and Answers

How many times a day should Lactulose be administered?

  • 4 times a day (correct)
  • 5 times a day
  • 2 times a day
  • 3 times a day

    • Lactulose is absorbed in the small intestine.

    False

    What is the main mechanism by which Lactulose helps reduce ammonia production?

    It creates H₂ and VFA after fermentation by colonic bacteria.

    NH₃ is incorporated into the ______ as a result of Lactulose treatment.

    <p>stool</p> Signup and view all the answers

    Match the following medications with their indicated dosages:

    <p>Rifaximin = 550mg twice a day Acarbose = Dosage not specified LOLA = Dosage not specified Sodium Benzoate = Dosage not specified</p> Signup and view all the answers

    What is the primary cause of ascites in 90% of cases?

    <p>Portal hypertension</p> Signup and view all the answers

    High SAAG ascites (≥1.1) indicates that the ascites is primarily due to portal hypertension.

    <p>True</p> Signup and view all the answers

    What is the serum ascites albumin gradient (SAAG) formula?

    <p>S. albumin - Ascitic fluid albumin (AFA)</p> Signup and view all the answers

    Ascites without a chronic picture and with high protein levels can be caused by _____ syndrome.

    <p>Budd Chiari</p> Signup and view all the answers

    Match the causes of ascites with their corresponding percentage:

    <p>Portal hypertension = 90% Peritoneal causes = 10% Fulminant Hepatitis = 85% Cirrhosis = Not specified</p> Signup and view all the answers

    What is the primary definitive treatment for Hepatopulmonary Syndrome?

    <p>Liver transplantation</p> Signup and view all the answers

    Orthodeoxia refers to a drop in SpO2 of greater than 3% when standing.

    <p>True</p> Signup and view all the answers

    What are the two main clinical features of Hepatopulmonary Syndrome?

    <p>Platypnea and Orthodeoxia</p> Signup and view all the answers

    The process of _______ leads to intrapulmonary capillary dilatation in Hepatopulmonary Syndrome.

    <p>liver disease</p> Signup and view all the answers

    Match the following treatments with their appropriate indications in Hepatopulmonary Syndrome:

    <p>Terlipressin = Before HPS develops Octreotide = Splanchnic vasodilation prevention Norepinephrine = To manage hypotension Liver transplantation = Definitive management</p> Signup and view all the answers

    What volume of ascitic fluid is generally associated with a fluid thrill?

    <p>1.5 L</p> Signup and view all the answers

    Spontaneous Bacterial Peritonitis (SBP) can be caused by Gram-positive bacteria only.

    <p>False</p> Signup and view all the answers

    What is the primary antibiotic treatment for SBP?

    <p>Inj CEFOTAXIME IV TDS x 5 days</p> Signup and view all the answers

    Ascitic fluid with WBC greater than or equal to ______ cell/ml is a criterion for spontaneous bacterial peritonitis.

    <p>500</p> Signup and view all the answers

    Match the following terms with their descriptions:

    <p>SBP = Spontaneous Bacterial Peritonitis CNNA = Culture Negative Neutrocytic Ascites MNNA = Monobacterial Non Neutrocytic Ascites Prophylaxis = Preventative treatment against SBP</p> Signup and view all the answers

    Which of the following factors can cause acidosis or alkalosis leading to increased ammonia levels?

    <p>Sepsis</p> Signup and view all the answers

    Asterixis is characterized by a continuous tremor of the hand.

    <p>False</p> Signup and view all the answers

    What is the clinical stage characterized by coma and decorticate posture in Hepatic Encephalopathy?

    <p>Grade IV</p> Signup and view all the answers

    The clinical feature of a person with Hepatic Encephalopathy exhibiting personality issues and disorientation is classified as __________.

    <p>Grade II</p> Signup and view all the answers

    Match the following clinical findings with their corresponding Grade of Hepatic Encephalopathy:

    <p>Asterixis = Grade II Rigidity; Clonus; Hyperreflexia = Grade III Coma; Decorticate posture = Grade IV Normal patient, evaluation possible = Covert HE</p> Signup and view all the answers

    What characterizes Diuretic Resistant Ascites?

    <p>No response to full dose diuretics</p> Signup and view all the answers

    Hepato Renal Syndrome can lead to pre-renal failure.

    <p>True</p> Signup and view all the answers

    What is the main management strategy for severe cases of ascites related to liver disease?

    <p>TIPSS</p> Signup and view all the answers

    Diuretic Intractable Ascites involves an inability to administer full dose diuretics due to __________.

    <p>medical complications</p> Signup and view all the answers

    Match the following conditions with their corresponding characteristics:

    <p>Diuretic Resistant Ascites = No response to full dose diuretics Diuretic Intractable Ascites = Unable to use full dose due to complications Hepato Renal Syndrome = Pre renal failure from renal vasoconstriction Acute Kidney Injury = 100% mortality without transplant</p> Signup and view all the answers

    Which of the following is NOT a presentation of Wilson's Disease?

    <p>Elevated ALP levels</p> Signup and view all the answers

    Wilson's Disease is characterized by high ALP levels due to zinc and copper interactions.

    <p>False</p> Signup and view all the answers

    What is a common laboratory finding in Wilson's Disease related to liver enzymes?

    <p>Elevated ALT</p> Signup and view all the answers

    Wilson's Disease can lead to _____ hepatic failure.

    <p>fulminant</p> Signup and view all the answers

    Match the following conditions with their corresponding laboratory findings in Wilson's Disease:

    <p>Fulminant hepatic failure = Characteristic presentation Coombs-negative hemolytic anemia = Laboratory finding Low ALP = Due to Zn²⁺ and Cu²⁺ competition Elevated ALT = Common enzyme abnormality</p> Signup and view all the answers

    What is the most common type of hepatic encephalopathy?

    <p>Type C</p> Signup and view all the answers

    Type A hepatic encephalopathy is associated with increased cerebral edema.

    <p>True</p> Signup and view all the answers

    Name one major complication of portal hypertension.

    <p>Hepatic encephalopathy</p> Signup and view all the answers

    NH3 is the most common cause of hepatic encephalopathy related to _______.

    <p>liver dysfunction</p> Signup and view all the answers

    Match the following substances with their roles in hepatic encephalopathy:

    <p>NH3 = Primary toxic substance implicated Glutamate = Decreased in blood Glutamine = Increased in CSF Bacteria in Colon = Source of toxic metabolites</p> Signup and view all the answers

    What is the cause of chylous ascites?

    <p>Trauma</p> Signup and view all the answers

    Pseudochylous ascites has a gradual onset.

    <p>True</p> Signup and view all the answers

    What is the appearance of chylous ascites?

    <p>Milky-white or yellow to bloody</p> Signup and view all the answers

    Chylous ascites contains chylomicrons, while pseudochylous ascites contains _______ crystals.

    <p>cholesterol</p> Signup and view all the answers

    Match the features of chylous and pseudochylous ascites:

    <p>Onset = Sudden Cause = Rheumatoid Arthritis/TB Appearance = Milky or greenish, metallic sheen Microscopic Examination = Lymphocytosis &gt;110 mg/dL</p> Signup and view all the answers

    What is the primary molecular defect in Wilson's disease?

    <p>Copper not being incorporated into ceruloplasmin</p> Signup and view all the answers

    Wilson's disease is inherited in an autosomal dominant manner.

    <p>False</p> Signup and view all the answers

    What is the function of ceruloplasmin in relation to copper?

    <p>Copper transport</p> Signup and view all the answers

    Wilson's disease is linked to a defect in the ATP7B gene located on chromosome ______.

    <p>13q</p> Signup and view all the answers

    Match the following copper-rich foods with their descriptions:

    <p>Chocolates = Rich in copper and often consumed as a treat Nuts = Commonly eaten as a snack with high nutritional value Shellfish = Seafood that is a significant source of copper Seeds = Snack food that can provide healthy fats and copper</p> Signup and view all the answers

    Study Notes

    Hepato Pulmonary Syndrome (HPS)

    • Treatment:
      • Pre-HPS:
        • Terlipressin: 1 mg IV every 4-6 hours, max 12 mg/day
        • Octreotide + Midodrine: s/c Octreotide + oral α agonist (midodrine)
        • Norepinephrine: IV infusion
      • Definitive: Liver transplantation
    • Pathogenesis:
      • Liver disease leads to increased nitric oxide (NO) production.
      • NO causes intrapulmonary capillary dilatation (from 8-15 μm to 50-500 μm).
      • This leads to a decrease in oxygenation, causing hypoxia and hypoxemia due to a ventilation/perfusion (V/Q) mismatch.
      • Arteriovenous (AV) shunts develop.
    • Clinical Features:
      • Platypnea: Dyspnea (shortness of breath) on standing due to increased AV shunt activation.
      • Orthodeoxia: Drop in SpO2 (oxygen saturation) >3% on standing.
    • Investigations:
      • Echocardiography: Bubble or Contrast Transthoracic echocardiography.

    Lactulose Bowel Wash Treatment

    • Administration: 4 times a day.
    • Other Medications:
      • Rifaximin: 400 mg three times a day or 550 mg twice a day.
      • Acarbose: Oral medication.
      • LOLA (Branched Chain AA): Oral medication.
      • Sodium Benzoate: Oral medication.
    • Mechanism of Action (MOA):
      • Lactulose is fermented by colonic bacteria producing Hydrogen gas (H₂) and Volatile Fatty Acids (VFAs).
      • Bacteria use VFAs as a substrate, reducing ammonia production.
      • Ammonia (NH₃) is incorporated into the stool.
      • NH₃ excretion: secondary to laxative effect.
      • Decreased pH: Ammonia (NH₃) + H+ → Ammonium (NH₄⁺)
      • Volatile fatty acid formation: Stimulates bowel movement.
      • Laxative effect: Promotes stool passage.

    Ascites

    • Definition: Free fluid in the peritoneal cavity.
    • First sign of decompensation: Indicates worsening liver disease.
    • Onset:
      • Portal hypertension (PHTN): 90% of cases.
        • Cirrhosis: Most common underlying cause.
      • Peritoneal causes: 10% of cases.
        • Fulminant Hepatitis: Ascites without a prior history of PHTN or cirrhosis.
          • Causes: Paracetamol poisoning, alcohol abuse, mushroom poisoning, rat killer poisoning.
    • SAAG (Serum Ascites Albumin Gradient):
      • SAAG: Serum albumin - Ascitic fluid albumin (AFA).
      • High SAAG ascites (≥1.1): 90% of cases, indicates PHTN as the primary cause.
        • High SAAG, high protein: Indicates decreased AFA and increased protein in the ascitic fluid (e.g., Budd-Chiari syndrome).
        • High SAAG, low protein: Indicates decreased AFA and decreased protein in the ascitic fluid.
    • Ascitic Fluid Detection:
      • < 100 ml: Ultrasound (USG).
      • 500 ml: Shifting dullness on percussion of the abdomen.
      • 1.5 L: Fluid thrill (vibration felt when tapping the abdomen).
    • Refractory Ascites: No response to maximum doses of diuretics.
      • Large volume paracentesis: Should be followed by albumin replacement (expensive).

    Spontaneous Bacterial Peritonitis (SBP)

    • Cause: Gram-negative bacteria (e.g., E. coli).
    • Criteria:
      • Ascitic fluid white blood cell count (WBC) ≥ 500 cells/ml OR polymorphonuclear neutrophils (PMNs) ≥ 250 cells/ml.
      • Positive ascitic fluid culture.
      • No surgically treatable source of infection.
    • Differentials:
      • CNNA (Culture Negative Neutrocytic Ascites): Only criterion 1 and 3 present, criterion 2 absent.
      • MNNA (Monobacterial Non Neutrocytic Ascites): Only criterion 2 and 3 present, criterion 1 absent. (Gram-positive organisms are more common than Gram-negative organisms).
    • Surgical peritonitis:
      • Protein > 1 g/dl.
      • Sugar < 50 mg/dl.
      • Increased lactate dehydrogenase (LDH).
    • Treatment: Inj Ceftriaxone IV three times a day for 5 days.
    • Prophylaxis:
      • Prior SBP, Child's score 29, Ascitic fluid protein < 1.5 g/dl (cirrhosis).
      • Upper gastrointestinal (UGI) bleed: Tab Norfloxacin 400 mg twice a day for 7 days.
      • Tab Norfloxacin 400 mg once a day for life.

    Hepatic Encephalopathy (HE)

    • Precipitating Factors:
      • NH3 (Ammonia) increasing factors:
        • Alkalosis
        • Acidosis
      • Factors causing Acidosis and Alkalosis:
        • Dietary protein overload
        • Constipation
        • GI hemorrhage
        • Sepsis
        • Blood transfusion
        • Hypokalemia
        • Hypovolemia
        • Hyponatremia
        • Dehydration
    • TIPSS (Transjugular Intrahepatic Portosystemic Shunt): Can cause HE.
    • Uremia: Renal symptoms can contribute to HE.
    • Clinical Features:
      • West Haven Criteria:
        • Covert HE: Normal patient (tests for evaluation: Psychometric test or Number connection test).
        • Grade I HE: Anxious, altered sleep pattern, short attention span.
        • Grade II HE: Personality changes, behavioral abnormalities, disorientation, impaired speech, Asterixis (hand tremor).
        • Grade III HE: Semi-stupor, gross disorientation, bizarre behavior, responsive only to painful stimuli.
        • Grade IV HE: Coma, decorticate posture, triphasic waves on EEG.
    • Number connection test: A test used for early detection of HE. The patient is asked to connect numbers in a particular order.
    • Asterixis: Hand tremor, a characteristic sign of HE.
    • EEG: EEG tracing with triphasic waves is a characteristic finding in HE.

    Refractory Ascites

    • Types: - Diuretic-resistant ascites: No response to full dose diuretics (40 mg spironolactone + 160 mg furosemide). Progresses to Hepato Renal Syndrome (HRS). - Diuretic-intractable ascites: Unable to administer full dose diuretics due to other medical complications (e.g., electrolyte imbalances (hypo/hyperkalemia), renal failure).

    Hepato Renal Syndrome (HRS)

    • Pathogenesis:
      • Splanchnic vasodilation (stimulated by ADH) which stimulates the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS), resulting in renal vasoconstriction over time.
      • Leads to pre-renal failure.
    • Diagnosis:
      • Diagnosis of exclusion in a patient with:
        • Cirrhosis
        • Portal hypertension
        • Ascites
      • Rule out:
        • Pre-renal: Diuretic excess, low serum albumin, UGI bleed.
        • Intra-renal: Proteinuria, hematuria.
        • Diagnostic imaging (USG): Rule out structural abnormalities.
    • HRS-AKI (Acute Kidney Injury): Serious complication with poor prognosis. 100% mortality without transplantation.
    • Management:
      • TIPSS

    Chylous vs Pseudochylous Ascites

    Feature Chylous Pseudochylous
    Onset Sudden Gradual
    Cause Trauma Rheumatoid Arthritis/TB
    Appearance Milky-white, yellow to bloody Milky or greenish, metallic sheen
    Microscopic Exam Lymphocytosis >110 mg/dl Mixed cellular reaction
    Triglycerides Chylomicrons present Cholesterol crystals

    Hepatic Encephalopathy (HE)

    • AKA: Porto systemic encephalopathy.
    • Major complication of: Portal hypertension or advanced liver failure.
    • Reversible encephalopathy: Abnormal brain function.
    • Types:
      • Type A HE: Fulminant hepatic failure- producing HE. Increased cerebral edema (most common cause of death).
      • Type B HE: TIPSS-associated HE.
      • Type C HE (most common): Cirrhosis with portal hypertension, producing HE.
    • Etiology:
      • Ammonia (NH3) (most common), mercaptan, phenol, aromatic amino acids, manganese (Mn), gamma-aminobutyric acid (GABA), octopamine, free fatty acids, bacteria in the colon, increased protein intake (high-protein diet).
    • Pathophysiology:
      • Urea cycle dysfunction: Due to liver damage.
      • Portosystemic shunting: Blood bypasses the liver.
      • Glutamine accumulation: Due to increased glutaminase activity.
    • Astrocytes: Alzheimer's type-α astrocytes:
      • NH3 + Glutamate → Glutamine (Toxic)
      • Glutamine is absorbed by non-ionic diffusion, damaging astrocytes.
      • Glutamine: Increased in cerebrospinal fluid (CSF).
    • Note:
      • Glutamate: Decreased in blood, increased in CSF.
      • Alzheimer's type-1 cells: Aggressive multifocal leukoencephalopathy (PMLE).

    Wilson'sDisease

    • Inheritance: Autosomal recessive disease.
    • Gene: ATP7B (Wilson ATPase) on chromosome 13q.
    • Pathophysiology:
      • Copper (Cu²⁺): Absorbed mainly in the duodenum, daily intake is 2-5 mg, high copper foods include chocolates and nuts.
      • Molecular Defect: Copper is not incorporated into ceruloplasmin.
      • Decreased Ceruloplasmin degradation: Screening test: Decreased Serum Ceruloplasmin (normal range is 20-35 mg/dl).
      • Presentation:
        • Fulminant hepatic failure: Coombs-negative hemolytic anemia, and low alkaline phosphatase (ALP) (due to Zn²⁺ and Cu²⁺ competing for ALP)
        • Chronic presentation: Fatigue and elevated liver enzymes (ALT > AST).
    • Signs and symptoms:
      • Hemoatocrit:
        • Decreased hematocrit can be a sign of anemia in advanced stages.
      • Copper Levels:
        • Liver biopsy: Demonstrates increased copper levels.
        • Serum: Elevated serum copper levels.
        • Urine: Elevated urinary copper levels (24-hour urine test).
      • Brain:
        • Neurological signs: Dystonia, tremor, rigidity, ataxia, dysarthria, psychiatric problems.
        • MRI/CT scan: Imaging may reveal basal ganglia lesions.
      • Kayser-Fleischer rings: Characteristic brown-green rings around the cornea.
    • Treatment:
      • Chelation therapy: Penicillamine, Trientine, Tetrathiomolybdate.
      • Zinc: Increases copper absorption and reduces copper levels.
      • Liver transplantation: In severe cases.

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    This quiz covers the key aspects of Hepato Pulmonary Syndrome (HPS), including its pathogenesis, clinical features, treatment options, and necessary investigations. Test your understanding of how liver disease leads to respiratory complications and the management strategies involved.

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