Hepatic encephalopathy US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Hepatic encephalopathy. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Hepatic encephalopathy US Medical PG Question 1: A 38-year-old man presents to his physician with double vision persisting for a week. When he enters the exam room, the physician notes that the patient has a broad-based gait. The man’s wife informs the doctor that he has been an alcoholic for the last 5 years and his consumption of alcohol has increased significantly over the past few months. She also reports that he has become indifferent to his family members over time and is frequently agitated. She also says that his memory has been affected significantly, and when asked about a particular detail, he often recollects it incorrectly, though he insists that his version is the true one. On physical examination, his vital signs are stable, but when the doctor asks him where he is, he seems to be confused. His neurological examination also shows nystagmus. Which of the following options describes the earliest change in the pathophysiology of the central nervous system in this man?
- A. Increased astrocyte lactate
- B. Increased extracellular concentration of glutamate
- C. Increased fragmentation of deoxyribonucleic acid within the neurons
- D. Breakdown of the blood-brain barrier
- E. Decreased α-ketoglutarate dehydrogenase activity in astrocytes (Correct Answer)
Hepatic encephalopathy Explanation: ***Decreased α-ketoglutarate dehydrogenase activity in astrocytes***
- Chronic **alcoholism** leads to **thiamine deficiency**, which impairs the activity of **α-ketoglutarate dehydrogenase** in the **Krebs cycle**.
- This enzyme is crucial for **neuronal energy metabolism** and its deficiency contributes to the earliest **neuropathological changes** observed in Wernicke-Korsakoff syndrome.
*Increased astrocyte lactate*
- While chronic alcoholism and thiamine deficiency can lead to metabolic dysfunction, increased **astrocyte lactate** is typically a response to **hypoxia** or **ischemia**, not the primary initiating event of thiamine deficiency.
- Lactate accumulation can be a downstream effect of impaired glucose metabolism, but not the earliest or most direct consequence of **α-ketoglutarate dehydrogenase** inhibition.
*Increased extracellular concentration of glutamate*
- **Glutamate excitotoxicity** can occur in chronic alcoholism, particularly during withdrawal, leading to neuronal damage.
- However, the primary insult in Wernicke-Korsakoff syndrome, which this patient's symptoms suggest, is **thiamine deficiency**, impacting the **Krebs cycle** before widespread glutamate release.
*Increased fragmentation of deoxyribonucleic acid within the neurons*
- **DNA fragmentation** indicates significant **neuronal damage** and **apoptosis**, which are later consequences of prolonged metabolic stress and oxidative injury.
- It is not the earliest pathophysiological change but rather a result of the progression of metabolic dysfunction caused by **thiamine deficiency**.
*Breakdown of the blood-brain barrier*
- **Blood-brain barrier (BBB) disruption** can occur in various neurological conditions, including chronic alcoholism, leading to inflammation and edema.
- While BBB dysfunction might contribute to the pathology, the initial and most direct effect of thiamine deficiency is on **cellular energy metabolism** within neurons and astrocytes, preceding widespread BBB breakdown.
Hepatic encephalopathy US Medical PG Question 2: A 50-year-old woman presents with esophageal varices, alcoholic cirrhosis, hepatic encephalopathy, portal hypertension, and recent onset confusion. The patient’s husband does not recall her past medical history but knows her current medications and states that she is quite disciplined about taking them. Current medications are spironolactone, labetalol, lactulose, and furosemide. Her temperature is 38.3°C (100.9°F), heart rate is 115/min, blood pressure is 105/62 mm Hg, respiratory rate is 12/min, and oxygen saturation is 96% on room air. On physical examination, the patient is disoriented, lethargic, and poorly responsive to commands. A cardiac examination is unremarkable. Lungs are clear to auscultation. The abdomen is distended, tense, and mildly tender. Mild asterixis is present. Neurologic examination is normal. The digital rectal examination reveals guaiac negative stool. Laboratory findings are significant for the following:
Basic metabolic panel Unremarkable
Platelet count 95,500/µL
Leukocyte count 14,790/µL
Hematocrit 33% (baseline is 30%)
Which of the following would most likely be of diagnostic value in this patient?
- A. Therapeutic trial of lactulose
- B. Abdominal paracentesis (Correct Answer)
- C. Noncontrast CT of the head
- D. Serum ammonia level
- E. Esophagogastroduodenoscopy
Hepatic encephalopathy Explanation: ***Abdominal paracentesis***
- The patient presents with **fever, abdominal tenderness, distension, and new-onset confusion** in the setting of **cirrhosis and ascites**, which are highly suggestive of **spontaneous bacterial peritonitis (SBP)**.
- An **abdominal paracentesis** with analysis of ascitic fluid (cell count with differential, culture) is necessary to diagnose SBP and guide appropriate antibiotic treatment.
*Therapeutic trial of lactulose*
- While the patient has **hepatic encephalopathy** and is on lactulose, her current presentation with **fever and abdominal tenderness** suggests an acute infectious process rather than worsening encephalopathy unresponsive to current therapy.
- A therapeutic trial of lactulose alone would delay the diagnosis of a potentially life-threatening infection like SBP.
*Noncontrast CT of the head*
- Although the patient has new-onset confusion, her presentation also includes **fever, abdominal tenderness, and signs of infection** in a patient with cirrhosis.
- A CT head would be more appropriate if there were focal neurological deficits, acute head trauma, or if SBP was ruled out and other causes of altered mental status were suspected.
*Serum ammonia level*
- The patient has known **hepatic encephalopathy**, and her current confusion is likely multifactorial.
- While an elevated ammonia level supports the diagnosis of hepatic encephalopathy, it is not diagnostic for the *cause* of her acute deterioration and would not rule out SBP, which requires urgent diagnosis and treatment.
*Esophagogastroduodenoscopy*
- The patient has a history of esophageal varices, but there is no evidence of active gastrointestinal bleeding (e.g., melena, hematemesis, guaiac positive stool).
- An **EGD** would be indicated for acute variceal bleeding, but it is not the most immediate or relevant diagnostic step for her current acute presentation of fever, abdominal pain, and confusion.
Hepatic encephalopathy US Medical PG Question 3: A 56-year-old woman with a history of alcoholic cirrhosis and recurrent esophageal varices who recently underwent transjugular intrahepatic portosystemic shunt (TIPS) placement is brought to the emergency room by her daughter due to confusion and agitation. Starting this morning, the patient has appeared sleepy, difficult to arouse, and slow to respond to questions. Her temperature is 97.6°F (36.4°C), blood pressure is 122/81 mmHg, pulse is 130/min, respirations are 22/min, and oxygen saturation is 98% on room air. She repeatedly falls asleep and is combative during the exam. Laboratory values are notable for a potassium of 3.0 mEq/L. The patient is given normal saline with potassium. Which of the following is the most appropriate treatment for this patient?
- A. Rifaximin
- B. Lactulose (Correct Answer)
- C. Nadolol
- D. Ciprofloxacin
- E. Protein-restricted diet
Hepatic encephalopathy Explanation: ***Lactulose***
- The patient's symptoms (confusion, agitation, somnolence) following **TIPS placement** and with a history of **cirrhosis** are highly suggestive of **hepatic encephalopathy**. Lactulose is a first-line treatment as it acidifies the colon, converting ammonia (a neurotoxin) to ammonium, which is then trapped and excreted.
- Additionally, this patient has **hypokalemia**, which can exacerbate hepatic encephalopathy by increasing renal ammonia production due to intracellular potassium shifts. Correcting hypokalemia is crucial alongside lactulose therapy.
*Rifaximin*
- Rifaximin is a non-absorbable antibiotic that can be used as an **adjunctive therapy** in hepatic encephalopathy, particularly in patients who do not respond adequately to lactulose or in whom lactulose is contraindicated.
- It works by reducing the number of **ammonia-producing bacteria** in the gut, but it is not the primary or initial treatment of choice for acute hepatic encephalopathy and is typically used after lactulose.
*Nadolol*
- Nadolol is a **non-selective beta-blocker** primarily used to prevent rebleeding from esophageal varices by reducing portal pressure.
- It does not directly treat or improve the symptoms of **hepatic encephalopathy** and is not indicated for the acute management of this condition.
*Ciprofloxacin*
- Ciprofloxacin is an antibiotic sometimes used to prevent **spontaneous bacterial peritonitis (SBP)** in patients with cirrhosis and ascites, or for the treatment of **bacterial infections**.
- While infections can precipitate hepatic encephalopathy, ciprofloxacin is not a direct treatment for encephalopathy itself, nor is there evidence of active infection here (e.g., fever, leukocytosis) that would necessitate its use over lactulose.
*Protein-restricted diet*
- In the past, protein restriction was a common recommendation for hepatic encephalopathy to reduce ammonia production from protein catabolism. However, severe protein restriction can lead to **malnutrition and sarcopenia**, which are detrimental in cirrhotic patients.
- Current guidelines recommend maintaining adequate protein intake and only briefly restricting protein (if at all) in severe, refractory cases, as it is generally not helpful for acute management and can worsen patient outcomes in the long term.
Hepatic encephalopathy US Medical PG Question 4: A 2-day-old male infant is brought to the emergency department by ambulance after his parents noticed that he was convulsing and unresponsive. He was born at home and appeared well initially; however, within 24 hours he became increasingly irritable and lethargic. Furthermore, he stopped feeding and began to experience worsening tachypnea. This continued for about 6 hours, at which point his parents noticed the convulsions and called for an ambulance. Laboratories are obtained with the following results:
Orotic acid: 9.2 mmol/mol creatinine (normal: 1.4-5.3 mmol/mol creatinine)
Ammonia: 135 µmol/L (normal: < 50 µmol/L)
Citrulline: 2 µmol/L (normal: 10-45 µmol/L)
Which of the following treatments would most likely be beneficial to this patient?
- A. Galactose avoidance
- B. Aspartame avoidance
- C. Benzoate administration (Correct Answer)
- D. Uridine administration
- E. Fructose avoidance
Hepatic encephalopathy Explanation: ***Benzoate administration***
- This patient presents with hyperammonemia (135 µmol/L), elevated orotic acid (9.2 mmol/mol creatinine), and **low citrulline (2 µmol/L)**, which is the classic triad for **ornithine transcarbamylase (OTC) deficiency**.
- The low citrulline distinguishes OTC deficiency from other urea cycle defects, while elevated orotic acid results from accumulation of carbamoyl phosphate that gets shunted into pyrimidine synthesis.
- **Sodium benzoate** is a nitrogen scavenger that conjugates with glycine to form hippurate, which is excreted renally, providing an alternative pathway for nitrogen disposal and reducing toxic ammonia levels.
- This is a life-saving acute treatment for hyperammonemia in urea cycle disorders.
*Galactose avoidance*
- This is the treatment for **galactosemia**, a disorder of galactose metabolism caused by galactose-1-phosphate uridyltransferase deficiency.
- Galactosemia presents with hepatomegaly, jaundice, cataracts, intellectual disability, and hypoglycemia after milk feeding.
- The patient's hyperammonemia and elevated orotic acid pattern is incompatible with galactosemia.
*Aspartame avoidance*
- This is relevant for **phenylketonuria (PKU)** dietary management, as aspartame contains phenylalanine.
- PKU presents with developmental delay, intellectual disability, musty odor, and eczema, with elevated phenylalanine levels.
- Ammonia and orotic acid are normal in PKU, making this diagnosis inconsistent with the lab findings.
*Uridine administration*
- **Uridine** treats **hereditary orotic aciduria** (UMP synthase deficiency), which presents with megaloblastic anemia, growth retardation, and developmental delays.
- While orotic acid is elevated in both conditions, hereditary orotic aciduria has **normal ammonia** and the primary pathology is impaired pyrimidine synthesis, not ammonia disposal.
- This patient's life-threatening hyperammonemia requires immediate nitrogen scavenging, which uridine does not provide.
*Fructose avoidance*
- This treats **hereditary fructose intolerance** (aldolase B deficiency), which causes hypoglycemia, vomiting, hepatomegaly, and jaundice after fructose ingestion.
- The presentation is triggered by dietary fructose exposure and does not cause hyperammonemia or elevated orotic acid.
- The patient's metabolic profile is inconsistent with a fructose metabolism disorder.
Hepatic encephalopathy US Medical PG Question 5: A 36-year-old man is brought to the emergency department by his girlfriend because of increasing confusion for the past 6 hours. He drinks large amounts of alcohol daily and occasionally uses illicit drugs. He is lethargic and oriented only to person. Physical examination shows jaundice, hepatomegaly, and scattered petechiae over the trunk and back. Neurologic examination shows normal, reactive pupils and a flapping tremor when the wrists are extended. A drug with which of the following mechanism of action would be most appropriate for this patient's condition?
- A. Production of NH3
- B. Activation of GABA receptors
- C. Excretion of free iron
- D. Inhibition of D2 receptors
- E. Excretion of NH4 (Correct Answer)
Hepatic encephalopathy Explanation: ***Excretion of NH4***
- The patient presents with **hepatic encephalopathy**, characterized by **confusion**, **jaundice**, **hepatomegaly**, **petechiae**, and a **flapping tremor (asterixis)**, stemming from chronic alcohol abuse and liver damage. The main pathophysiology in hepatic encephalopathy is the accumulation of **ammonia (NH3)**, which is neurotoxic.
- Excretion of **NH4** (ammonium) through drug mechanisms such as **lactulose** (which acidifies the colon, trapping ammonia as ammonium for excretion) is the primary therapeutic target to reduce ammonia levels and improve neurological symptoms.
*Production of NH3*
- This mechanism would exacerbate the patient's condition by increasing the toxic load of **ammonia (NH3)**, which is already elevated in hepatic encephalopathy.
- Therapeutic interventions aim to decrease, not increase, ammonia production or absorption.
*Activation of GABA receptors*
- While **GABA receptor activation** is involved in the neurological effects of some substances that contribute to confusion, it is not the primary target for treating the underlying pathophysiology of **hepatic encephalopathy**.
- Medications that activate GABA receptors (e.g., benzodiazepines) can worsen encephalopathy by further depressing CNS function.
*Excretion of free iron*
- **Iron overload** can cause liver damage, but the acute confusion and flapping tremor are more indicative of **hepatic encephalopathy** due to ammonia toxicity, not primarily iron accumulation.
- Excreting free iron (e.g., with chelation therapy) is for conditions like hemochromatosis and would not address the immediate, life-threatening neurological symptoms in this patient.
*Inhibition of D2 receptors*
- This mechanism is characteristic of some **antipsychotic medications**. While dopamine imbalances can play a role in some neurological disorders, inhibiting D2 receptors is not a primary therapeutic target for **hepatic encephalopathy**.
- Such medications could have side effects that might complicate the clinical picture in a patient with acute liver failure.
Hepatic encephalopathy US Medical PG Question 6: A 56-year-old woman is brought to the emergency department by her family with altered mental status. Her husband says that she complained of fever, vomiting, and abdominal pain 2 days ago. She has a history of long-standing alcoholism and previous episodes of hepatic encephalopathy. Current vital signs include a temperature of 38.3°C (101°F), blood pressure of 85/60 mm Hg, pulse of 95/min, and a respiratory rate 30/min. On physical examination, the patient appears ill and obtunded. She is noted to have jaundice, a palpable firm liver, and massive abdominal distension with shifting dullness. Which of the following is the best initial step in management of this patient's condition?
- A. Empiric antibiotics (Correct Answer)
- B. Diagnostic paracentesis
- C. Large volume paracentesis
- D. Intravenous albumin
- E. Non-selective beta-blockers
Hepatic encephalopathy Explanation: ***Empiric antibiotics***
- This patient presents with **altered mental status**, **fever**, **hypotension (85/60 mm Hg)**, **tachypnea**, and **massive ascites** in the setting of **cirrhosis**, indicating **suspected spontaneous bacterial peritonitis (SBP) with septic shock**.
- In a **hemodynamically unstable patient** with suspected SBP, **empiric antibiotics** (typically a third-generation cephalosporin like ceftriaxone or cefotaxime) should be initiated **immediately** without waiting for diagnostic paracentesis results.
- Current **AASLD and EASL guidelines** emphasize that antibiotic therapy should not be delayed in critically ill patients, as early treatment significantly reduces mortality in SBP.
- Diagnostic paracentesis should still be performed urgently but should **not delay antibiotic administration** in this unstable patient.
*Diagnostic paracentesis*
- While **diagnostic paracentesis** is the gold standard for confirming SBP and should be performed promptly, it is not the **best initial step** in a hemodynamically unstable patient.
- In this critically ill patient with septic shock, obtaining ascitic fluid can be done **simultaneously with** or **immediately after** starting antibiotics, but antibiotics take priority.
- If the patient were stable, diagnostic paracentesis before antibiotics would be appropriate to guide therapy.
*Large volume paracentesis*
- **Large volume paracentesis** is indicated for symptomatic relief of tense ascites causing respiratory compromise, not as an initial step in suspected infection.
- In the setting of suspected SBP, only diagnostic paracentesis (50-100 mL) is needed initially, not large volume removal.
*Intravenous albumin*
- **Intravenous albumin** is given as adjunctive therapy in SBP patients with **renal dysfunction** (creatinine >1 mg/dL, BUN >30 mg/dL) or **hypotension** to prevent hepatorenal syndrome.
- While this patient may benefit from albumin, it is not the **initial step**—antibiotics and fluid resuscitation take priority.
- Albumin is typically given at 1.5 g/kg within 6 hours and 1 g/kg on day 3.
*Non-selective beta-blockers*
- **Non-selective beta-blockers** (propranolol, nadolol) are used for **primary and secondary prophylaxis of variceal bleeding** in portal hypertension.
- They are **contraindicated** in patients with **hypotension** (BP 85/60 mm Hg), **sepsis**, or **SBP**, as they can worsen hemodynamic instability.
- Recent studies suggest beta-blockers may be harmful in patients with refractory ascites or SBP.
Hepatic encephalopathy US Medical PG Question 7: A 55-year-old man comes to the physician for a follow-up examination. During the past month, he has had mild itching. He has alcoholic cirrhosis, hypertension, and gastroesophageal reflux disease. He used to drink a pint of vodka and multiple beers daily but quit 4 months ago. Current medications include ramipril, esomeprazole, and vitamin B supplements. He appears thin. His temperature is 36.8°C (98.2°F), pulse is 68/min, and blood pressure is 115/72 mm Hg. Examination shows reddening of the palms bilaterally and several telangiectasias over the chest, abdomen, and back. There is symmetrical enlargement of the breast tissue bilaterally. His testes are small and firm on palpation. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 10.1 g/dL
Leukocyte count 4300/mm3
Platelet count 89,000/mm3
Prothrombin time 11 sec (INR = 1)
Serum
Albumin 3 g/dL
Bilirubin
Total 2.0 mg/dL
Direct 0.2 mg/dL
Alkaline phosphatase 43 U/L
AST 55 U/L
ALT 40 U/L
α-Fetoprotein 8 ng/mL (N < 10)
Anti-HAV IgG antibody positive
Anti-HBs antibody negative
Abdominal ultrasonography shows a nodular liver surface with atrophy of the right lobe of the liver. An upper endoscopy shows no abnormalities. Which of the following is the most appropriate next step in management?
- A. Perform liver biopsy now
- B. Obtain CT scan of the abdomen now
- C. Repeat abdominal ultrasound in 6 months (Correct Answer)
- D. Measure serum α-fetoprotein levels in 3 months
- E. Administer hepatitis A vaccine now
Hepatic encephalopathy Explanation: ***Repeat abdominal ultrasound in 6 months***
- This patient has **alcoholic cirrhosis** and is at high risk for developing **hepatocellular carcinoma (HCC)**
- **Current AASLD/ACR guidelines** recommend surveillance with **ultrasound (with or without AFP) every 6 months** for all cirrhotic patients
- The patient just had an ultrasound showing cirrhotic changes but **no focal lesions**, and AFP is normal (8 ng/mL)
- The **most appropriate next step** is to continue routine HCC surveillance with **ultrasound in 6 months**
- Ultrasound is the **primary surveillance modality** due to its non-invasive nature, wide availability, and reasonable sensitivity for detecting early HCC
*Measure serum α-fetoprotein levels in 3 months*
- AFP alone is **not recommended** as a standalone surveillance tool for HCC
- The surveillance interval for cirrhotic patients is **6 months, not 3 months**
- While AFP can be checked alongside ultrasound during surveillance, it has **limited sensitivity** (approximately 60%) and is not sufficient by itself
- Checking AFP in 3 months without imaging does not follow standard surveillance protocols
*Perform liver biopsy now*
- Liver biopsy is indicated when there is a **discrete liver lesion** that needs tissue diagnosis for staging or treatment planning
- The current ultrasound shows only **diffuse cirrhotic changes** with no focal lesion identified
- Biopsy is **not indicated** for routine HCC surveillance in the absence of a suspicious mass
*Administer hepatitis A vaccine now*
- The patient has a **positive anti-HAV IgG antibody**, indicating **prior exposure and immunity** to Hepatitis A
- Vaccination is **not needed** as the patient is already immune
- Hepatitis A vaccine would only be indicated in cirrhotic patients who are **anti-HAV IgG negative**
*Obtain CT scan of the abdomen now*
- CT or MRI is indicated when ultrasound identifies a **suspicious lesion** requiring further characterization
- CT would also be considered if ultrasound quality is inadequate or if there is high clinical suspicion for HCC despite negative ultrasound
- In this case, the ultrasound was adequate and showed **no focal lesions**, so advanced imaging is not currently indicated
- Routine surveillance uses ultrasound, not CT, due to cost-effectiveness and lack of radiation exposure
Hepatic encephalopathy US Medical PG Question 8: A 47-year-old woman comes to the physician because of a 3-week history of generalized fatigue, mild fever, abdominal pain, and nausea. She attended the state fair over a month ago, where she tried a number of regional foods, and wonders if it might have been caused by something she ate. She has also noticed darkening of her urine, which she attributes to not drinking enough water recently. She has type 2 diabetes mellitus. She drinks 1–2 beers daily. She works as nursing assistant in a rehabilitation facility. Current medications include glyburide, sitagliptin, and a multivitamin. She appears tired. Her temperature is 38.1°C (100.6°F), pulse is 99/min, and blood pressure is 110/74 mm Hg. Examination shows mild scleral icterus. The liver is palpated 2–3 cm below the right costal margin and is tender. Laboratory studies show:
Hemoglobin 10.6 g/dL
Leukocyte count 11600/mm3
Platelet count 221,000/mm3
Serum
Urea nitrogen 26 mg/dL
Glucose 122 mg/dL
Creatinine 1.3 mg/dL
Bilirubin 3.6 mg/dL
Total 3.6 mg/dL
Direct 2.4 mg/dL
Alkaline phosphatase 72 U/L
AST 488 U/L
ALT 798 U/L
Hepatitis A IgG antibody (HAV-IgG) positive
Hepatitis B surface antigen (HBsAg) positive
Hepatitis B core IgG antibody (anti-HBc) positive
Hepatitis B envelope antigen (HBeAg) positive
Hepatitis C antibody (anti-HCV) negative
Which of the following is the most likely diagnosis?
- A. Acute hepatitis B infection
- B. Resolved acute hepatitis B infection
- C. Active chronic hepatitis B infection (Correct Answer)
- D. Alcoholic hepatitis
- E. Inactive chronic hepatitis B infection
Hepatic encephalopathy Explanation: ***Active chronic hepatitis B infection***
- The presence of **HBsAg positive**, **anti-HBc IgG positive** (not IgM), and **HBeAg positive** indicates chronic hepatitis B infection with active viral replication.
- The key distinguishing feature is **anti-HBc IgG** rather than anti-HBc IgM. In acute hepatitis B, **anti-HBc IgM** would be positive, whereas **anti-HBc IgG** indicates infection that occurred more than 6 months ago (chronic infection).
- The **HBeAg positivity** indicates active viral replication and high infectivity, making this an "active" chronic infection rather than an inactive carrier state.
- The markedly elevated **AST (488 U/L)** and **ALT (798 U/L)** levels indicate significant hepatocellular damage with active inflammation.
- Clinical features of **scleral icterus**, **dark urine** (conjugated hyperbilirubinemia), **fever**, **fatigue**, and **abdominal pain** are consistent with active hepatitis.
*Acute hepatitis B infection*
- This is ruled out by the presence of **anti-HBc IgG** rather than **anti-HBc IgM**.
- In acute hepatitis B infection, **anti-HBc IgM** (the IgM class antibody to core antigen) would be positive, indicating recent infection.
- The presence of IgG class antibody indicates the infection occurred more than 6 months ago, establishing chronicity.
*Resolved acute hepatitis B infection*
- In resolved infection, **HBsAg** would be negative, and **anti-HBs** (Hepatitis B surface antibody) would be positive, indicating immunity.
- This patient is **HBsAg positive**, ruling out resolved infection.
- Resolved infection would not cause the current hepatocellular injury.
*Alcoholic hepatitis*
- Although the patient drinks 1-2 beers daily (modest consumption), the **AST:ALT ratio** (488:798 = 0.61) is less than 2:1.
- In alcoholic hepatitis, the AST:ALT ratio is typically **>2:1** due to alcohol-induced pyridoxine deficiency affecting ALT more than AST.
- The specific **viral serology markers** (positive HBsAg, HBeAg, and anti-HBc IgG) definitively establish hepatitis B as the cause of liver inflammation.
*Inactive chronic hepatitis B infection*
- In inactive chronic hepatitis B (also called inactive carrier state), **HBsAg** would be positive, but **HBeAg** would be negative with positive **anti-HBe** antibody.
- **ALT levels** are typically normal or minimally elevated (<40-50 U/L) in inactive carriers, not markedly elevated as in this case (ALT 798 U/L).
- The positive **HBeAg** and significantly elevated transaminases indicate active viral replication and inflammation, not an inactive state.
Hepatic encephalopathy US Medical PG Question 9: A 32-year-old man with a history of chronic alcoholism presents to the emergency department with vomiting and diarrhea for 1 week. He states he feels weak and has had poor oral intake during this time. The patient is a current smoker and has presented many times to the emergency department for alcohol intoxication. His temperature is 97.5°F (36.4°C), blood pressure is 102/62 mmHg, pulse is 135/min, respirations are 25/min, and oxygen saturation is 99% on room air. On physical exam, he is found to have orthostatic hypotension and dry mucus membranes. Laboratory studies are ordered as seen below.
Serum:
Na+: 139 mEq/L
Cl-: 101 mEq/L
K+: 3.9 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 9.8 mg/dL
The patient is given normal saline, oral potassium, dextrose, thiamine, and folic acid. The following day, the patient seems confused and complains of diffuse weakness and muscle/bone pain. An ECG and head CT are performed and are unremarkable. Which of the following is the most likely explanation for this patient's new symptoms?
- A. Hypomagnesemia
- B. Hyponatremia
- C. Hypoglycemia
- D. Hypophosphatemia (Correct Answer)
- E. Hypocalcemia
Hepatic encephalopathy Explanation: **Hypophosphatemia**
- **Hypophosphatemia** is common in **alcoholics**, often exacerbated by refeeding (administration of glucose and fluids). The patient's initial symptoms of weakness and muscle/bone pain after treatment suggest this condition.
- Symptoms such as **confusion**, **diffuse weakness**, and **muscle/bone pain** are classic manifestations of severe hypophosphatemia as phosphorus is vital for muscle and nerve function, and bone health.
*Hypomagnesemia*
- While common in alcoholics and capable of causing weakness, **hypomagnesemia** typically presents with symptoms like **tremors**, **seizures**, and **cardiac arrhythmias**.
- The patient's primary symptoms of confusion and diffuse muscle/bone pain are less characteristic of magnesium deficiency compared to phosphorus deficiency.
*Hyponatremia*
- The patient's initial sodium level was 139 mEq/L, which is within the normal range, making **hyponatremia** unlikely to be the cause of new symptoms.
- While severe hyponatremia can cause confusion, it typically presents with other neurological symptoms like **headache** and **seizures**, which are not reported here.
*Hypoglycemia*
- The initial glucose level of 99 mg/dL was normal, and the patient received dextrose, making **hypoglycemia** an unlikely cause of the new symptoms.
- Symptoms of hypoglycemia usually include **sweating**, **tremors**, and **palpitations**, in addition to confusion.
*Hypocalcemia*
- The patient's initial calcium level was 9.8 mg/dL, which is within the normal range, making **hypocalcemia** an unlikely cause of the new symptoms.
- Symptoms of hypocalcemia typically include **tetany**, **paresthesias**, and a **prolonged QT interval** on EKG, none of which are described.
Hepatic encephalopathy US Medical PG Question 10: An 18-year-old Caucasian female presents to your clinic because of a recent increase in thirst and hunger. Urinalysis demonstrates elevated glucose. The patient's BMI is 20. Which of the following is the most common cause of death in persons suffering from this patient's illness?
- A. Coma
- B. Peripheral neuropathy
- C. Infection
- D. Renal failure
- E. Myocardial infarction (Correct Answer)
Hepatic encephalopathy Explanation: ***Myocardial infarction***
- **Cardiovascular disease, particularly myocardial infarction, is the leading cause of death in Type 1 Diabetes Mellitus**, accounting for approximately 40% of mortality.
- Patients with Type 1 diabetes develop **accelerated atherosclerosis** due to chronic hyperglycemia, dyslipidemia, endothelial dysfunction, and increased oxidative stress.
- Even young patients with T1DM have significantly elevated cardiovascular risk compared to age-matched controls, with risk increasing proportionally with disease duration and glycemic control.
- While acute complications like DKA are immediately life-threatening, modern medical management has reduced DKA mortality to <1%, making chronic cardiovascular complications the predominant cause of death.
*Coma*
- **Diabetic ketoacidosis (DKA)** leading to coma is indeed a serious acute complication of Type 1 diabetes.
- However, with contemporary medical care and improved access to insulin, DKA mortality is less than 1% in developed countries.
- While DKA may be the presenting feature or an immediate threat, it is not the most common cause of death over the lifetime of T1DM patients.
*Peripheral neuropathy*
- Diabetic peripheral neuropathy is a common chronic complication affecting up to 50% of long-standing diabetics.
- While it significantly impacts quality of life and can lead to foot ulcers, infections, and amputations, it is not a direct cause of death.
- Autonomic neuropathy can contribute to sudden cardiac death, but this is still categorized under cardiovascular mortality.
*Infection*
- Diabetes does increase susceptibility to certain infections due to impaired neutrophil function, reduced chemotaxis, and hyperglycemia promoting bacterial growth.
- While infections can be serious (e.g., necrotizing fasciitis, mucormycosis), they are not the leading cause of mortality in T1DM.
- Infection-related deaths are far less common than cardiovascular deaths.
*Renal failure*
- **Diabetic nephropathy** is the second most common cause of death in Type 1 diabetes, affecting approximately 20-30% of patients.
- End-stage renal disease develops over many years and contributes significantly to mortality.
- However, cardiovascular disease remains more common, and many patients with diabetic nephropathy ultimately die from cardiovascular events rather than renal failure alone.
More Hepatic encephalopathy US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
