Acute liver failure US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Acute liver failure. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Acute liver failure US Medical PG Question 1: A 63-year-old man comes to the physician for a routine health maintenance examination. He feels well. He has a history of hypertension, atrial fibrillation, bipolar disorder, and osteoarthritis of the knees. Current medications include lisinopril, amiodarone, lamotrigine, and acetaminophen. He started amiodarone 6 months ago and switched from lithium to lamotrigine 4 months ago. The patient does not smoke. He drinks 1–4 beers per week. He does not use illicit drugs. Vital signs are within normal limits. Examination shows no abnormalities. Laboratory studies show:
Serum
Na+ 137 mEq/L
K+ 4.2 mEq/L
Cl- 105 mEq/L
HCO3- 24 mEq/L
Urea nitrogen 14 mg/dL
Creatinine 0.9 mg/dL
Alkaline phosphatase 82 U/L
Aspartate aminotransferase (AST) 110 U/L
Alanine aminotransferase (ALT) 115 U/L
Which of the following is the most appropriate next step in management?
- A. Discontinue amiodarone (Correct Answer)
- B. Discontinue acetaminophen
- C. Follow-up laboratory results in 3 months
- D. Follow-up laboratory results in 6 months
- E. Decrease alcohol consumption
Acute liver failure Explanation: ***Discontinue amiodarone***
* The patient has elevated **AST** and **ALT** levels, suggestive of **drug-induced liver injury**. Amiodarone is a known cause of **hepatotoxicity**, which can occur even with normal baseline liver function.
* **Amiodarone-induced liver injury** can range from asymptomatic transaminase elevation to **fulminant hepatic failure**; therefore, discontinuing the drug is crucial to prevent further liver damage.
*Discontinue acetaminophen*
* Although **acetaminophen** can cause **hepatotoxicity** at high doses, the patient is likely taking it at therapeutic doses for osteoarthritis, as suggested by its use in routine care and the absence of overdose symptoms.
* The chronic nature of amiodarone use (6 months) and its well-established risk of **liver injury** make it a more probable cause of the elevated transaminases than **therapeutic-dose acetaminophen**.
*Follow-up laboratory results in 3 months*
* The current **liver enzyme elevations** (AST 110 U/L, ALT 115 U/L) are significant and indicate acute liver injury. Waiting 3 months for follow-up without intervention significantly risks further liver damage.
* Prompt identification and removal of the offending agent are necessary to prevent potentially irreversible **hepatic injury**.
*Follow-up laboratory results in 6 months*
* Delaying follow-up for 6 months is an inappropriate and potentially harmful approach given the current enzyme elevations. There is an immediate need to identify and address the cause of **liver injury**.
* Such a delay could lead to progression of **liver damage**, especially if the causative agent (e.g., amiodarone) continues to be administered.
*Decrease alcohol consumption*
* While excessive alcohol consumption can cause **elevated liver enzymes**, the patient’s intake of 1–4 beers per week is considered light to moderate and is unlikely to be the sole cause of these significant elevations.
* The presence of a known **hepatotoxic medication** (amiodarone) alongside the elevated enzymes makes the drug a much more probable cause than the patient's modest alcohol intake.
Acute liver failure US Medical PG Question 2: A 60-year-old rock musician presents to the office because he has been feeling increasingly tired for the past 6 months. He has a history of intravenous drug use and alcohol abuse. He states that he feels quite tired, but he otherwise has no complaints. Physical examination is noncontributory. His laboratory values are normal other than moderately elevated liver enzymes. Which of the following additional tests should you order first?
- A. Hepatitis C virus antibodies (Correct Answer)
- B. Hepatitis B surface antigen
- C. Hepatitis E virus-specific IgM antibodies
- D. Hepatitis D virus-specific IgG antibody
- E. Hepatitis A virus-specific IgM antibodies
Acute liver failure Explanation: ***Hepatitis C virus antibodies***
- The patient's history of **intravenous drug use** and **chronic fatigue** with **elevated liver enzymes** strongly suggests chronic viral hepatitis, with hepatitis C being the most common blood-borne infection in persons with IVDU history.
- **Hepatitis C** is the **most prevalent chronic viral hepatitis** in the United States among persons with history of injection drug use, with transmission efficiency via needle sharing being very high.
- Hepatitis C often has a **long asymptomatic phase** (decades) before symptoms like fatigue and liver damage become apparent, making antibody testing the appropriate initial screen.
- While both HBV and HCV should ultimately be screened in this patient, **HCV prevalence is significantly higher** in the IVDU population, making it the priority initial test.
*Hepatitis B surface antigen*
- While **hepatitis B** can also be transmitted via intravenous drug use and cause chronic liver disease, **hepatitis C is more prevalent** in persons with IVDU history in the United States.
- **HBsAg** is used to detect active hepatitis B infection and should also be ordered, but given resource constraints and the clinical context, **anti-HCV is the higher-yield initial test**.
- Many IVDU patients have been vaccinated against HBV, further reducing its likelihood compared to HCV (for which no vaccine exists).
*Hepatitis E virus-specific IgM antibodies*
- **Hepatitis E** is typically transmitted via the **fecal-oral route** (contaminated water) and usually causes **acute, self-limiting hepatitis**, not chronic insidious fatigue and liver enzyme elevation in a Western patient.
- **IgM antibodies** would indicate an acute infection, which is less likely given the 6-month duration of symptoms.
- HEV rarely causes chronic infection except in immunocompromised patients.
*Hepatitis D virus-specific IgG antibody*
- **Hepatitis D** requires an existing **hepatitis B infection** to replicate (it's a satellite virus), meaning you would first need to confirm chronic hepatitis B before testing for HDV.
- While HDV can cause severe liver disease and is transmitted via blood exposure, it's not the initial test to pursue without evidence of HBV co-infection.
*Hepatitis A virus-specific IgM antibodies*
- **Hepatitis A** is transmitted via the **fecal-oral route** and causes an **acute, self-limiting infection** with complete resolution, rarely leading to chronic liver disease or persistent fatigue over 6 months.
- **IgM antibodies** are indicative of acute infection, which contradicts the chronic nature of the patient's symptoms.
- HAV does not cause chronic hepatitis.
Acute liver failure US Medical PG Question 3: A 9-year-old boy presents to the emergency department with a 12-hour history of severe vomiting and increased sleepiness. He experienced high fever and muscle pain about 5 days prior to presentation, and his parents gave him aspirin to control the fever at that time. On presentation, he is found to be afebrile though he is still somnolent and difficult to arouse. Physical exam reveals hepatomegaly and laboratory testing shows the following results:
Alanine aminotransferase: 85 U/L
Aspartate aminotransferase: 78 U/L
Which of the following is the most likely cause of this patient's neurologic changes?
- A. Subarachnoid hemorrhage
- B. Viral meningitis
- C. Reye syndrome
- D. Cerebral edema (Correct Answer)
- E. Bacterial sepsis
Acute liver failure Explanation: ***Cerebral edema***
- The combination of a recent **viral illness** treated with **aspirin** in a child, leading to severe vomiting, increased sleepiness, hepatomegaly, and elevated transaminases, is highly suggestive of **Reye syndrome**.
- **Cerebral edema** is a critical and life-threatening complication of **Reye syndrome**, causing the neurologic symptoms like somnolence, difficulty arousing, and ultimately coma.
*Subarachnoid hemorrhage*
- While subarachnoid hemorrhage can cause acute neurological changes, it typically presents with a **sudden, severe headache** ("thunderclap headache") and signs of meningeal irritation, which are not described here.
- There is no clinical indication such as trauma or ruptured aneurysm to suggest a subarachnoid hemorrhage in this patient.
*Viral meningitis*
- Viral meningitis would typically present with **fever**, headache, and **nuchal rigidity**, often accompanied by photophobia, which are not the prominent features in this case.
- The elevated liver enzymes and hepatomegaly are not characteristic of viral meningitis.
*Reye syndrome*
- **Reye syndrome** is the underlying diagnosis, characterized by acute **encephalopathy** and hepatic dysfunction following a viral infection treated with salicylates.
- However, the question asks for the **most likely cause of the neurological changes**, which is specifically the brain swelling, or cerebral edema, that occurs as a direct result of Reye syndrome pathophysiology.
*Bacterial sepsis*
- Bacterial sepsis would present with signs of systemic infection, often including **high fever**, tachycardia, and hypotension, which are not present as the patient is afebrile.
- While sepsis can cause encephalopathy, the presence of **hepatomegaly** and the history of **aspirin use** point much more strongly toward Reye syndrome with its associated cerebral edema.
Acute liver failure US Medical PG Question 4: A 32-year-old woman comes to the emergency department for a 2-week history of right upper quadrant abdominal pain. She has also been feeling tired and nauseous for the past 5 weeks. She has a history of depression and suicidal ideation. She is a social worker for an international charity foundation. She used intravenous illicit drugs in the past but quit 4 months ago. Her only medication is sertraline. Her temperature is 37.8°C (100.0°F), pulse is 100/min, and blood pressure is 128/76 mm Hg. She is alert and oriented. Scleral icterus is present. Abdominal examination shows tenderness to palpation in the right upper quadrant. The liver edge is palpated 3 cm below the right costal margin. There is no rebound tenderness or guarding. The abdomen is non-distended and the fluid wave test is negative. She is able to extend her arms with wrists in full extension and hold them steady without flapping. Laboratory studies show:
Hemoglobin 13.8 g/dL
Leukocytes 13,700/mm3
Platelets 165,000/mm3
Prothrombin time 14 seconds
Partial thromboplastin time 35 seconds
Serum:
Total bilirubin 4.8 mg/dL
Direct bilirubin 1.3 mg/dL
Aspartate aminotransferase 1852 U/L
Alanine aminotransferase 2497 U/L
Urea nitrogen 21 mg/dL
Creatinine 1.2 mg/dL
Hepatitis A IgM antibody Negative
Hepatitis B surface antigen Negative
Hepatitis B surface antibody Negative
Hepatitis B core IgM antibody Positive
Hepatitis C antibody Positive
Hepatitis C RNA Negative
Urine beta-hCG Negative
Which of the following is the most appropriate next step in management?
- A. Supportive therapy (Correct Answer)
- B. Vaccination against Hepatitis B
- C. Ribavirin and interferon
- D. Tenofovir
- E. Pegylated interferon-alpha
Acute liver failure Explanation: ***Supportive therapy***
- The patient has **acute hepatitis B** based on positive **hepatitis B core IgM antibody** and highly elevated **ALT** and **AST** (>2000 U/L).
- The serological pattern (**HBsAg negative, HBcore IgM positive, HBsAb negative**) represents the **"window period"** of acute hepatitis B, occurring when HBsAg has cleared but HBsAb has not yet developed.
- Acute hepatitis B in **immunocompetent adults** is typically **self-limiting** (>95% clearance rate), making **supportive care** the appropriate management.
- No signs of **hepatic encephalopathy** (no asterixis), **coagulopathy** (PT normal), or **fulminant hepatic failure** are present, so antiviral therapy is not indicated.
- While she has **Hepatitis C antibody positive**, the **Hepatitis C RNA is negative**, indicating **resolved past infection** (likely from prior IV drug use) and not the cause of her current acute hepatitis.
*Vaccination against Hepatitis B*
- **Vaccination is contraindicated** during active/acute hepatitis B infection, as evidenced by positive **Hepatitis B core IgM antibody**.
- Vaccination is for **prevention**, not treatment, of existing infection.
*Ribavirin and interferon*
- This combination therapy was historically used for **chronic hepatitis C infection**, which this patient does not have (negative HCV RNA indicates resolved infection).
- It is **not indicated for acute hepatitis B** treatment.
*Tenofovir*
- **Tenofovir** is an antiviral agent used to treat **chronic hepatitis B** or **severe/fulminant acute hepatitis B** with signs of liver failure.
- Given the patient's **immunocompetent status**, absence of hepatic decompensation, and the typically **self-limiting nature of acute HBV** in adults, antiviral therapy is **not indicated**.
- Treatment would only be considered if signs of **fulminant hepatic failure** develop (encephalopathy, severe coagulopathy, rapidly rising bilirubin).
*Pegylated interferon-alpha*
- **Pegylated interferon-alpha** is used in some cases of **chronic hepatitis B and C**, but it is **not indicated for acute hepatitis B** in immunocompetent adults.
- The infection is expected to resolve spontaneously with supportive care in >95% of immunocompetent adults.
- Side effects are significant, and its use is reserved for chronic cases, not acute self-limiting presentations.
Acute liver failure US Medical PG Question 5: 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
Acute liver failure 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.
Acute liver failure US Medical PG Question 6: A 57-year-old man presents to the emergency department with fatigue. He states that his symptoms started yesterday and have been worsening steadily. The patient endorses a recent weight loss of 7 pounds this past week and states that he feels diffusely itchy. The patient has a past medical history of alcohol abuse, obesity, asthma, and IV drug use. His current medications include metformin, atorvastatin, albuterol, and fluticasone. In addition, the patient admits to smoking and drinking more than usual lately due to the stress he has experienced. His temperature is 98.7°F (37.1°C), blood pressure is 130/75 mmHg, pulse is 90/min, respirations are 15/min, and oxygen saturation is 98% on room air. Physical exam is notable for an ill-appearing man. The patient's skin appears yellow. Abdominal exam is notable for right upper quadrant tenderness. Cardiac and pulmonary exams are within normal limits. Laboratory values are ordered as seen below:
Hemoglobin: 14 g/dL
Hematocrit: 42%
Leukocyte count: 5,500 cells/mm^3 with normal differential
Platelet count: 70,000/mm^3
Partial thromboplastin time: 92 seconds
Prothrombin time: 42 seconds
AST: 1110 U/L
ALT: 990 U/L
Which of the following is most likely to be found in this patient's history?
- A. Recent antibiotic treatment with gentamicin
- B. Appropriate acute management of a deep vein thrombosis
- C. Decreased UDP-glucuronosyltransferase activity at birth
- D. Prosthetic valve with appropriate post-operative care
- E. Severe migraine headaches treated with acetaminophen (Correct Answer)
Acute liver failure Explanation: ***Severe migraine headaches treated with acetaminophen***
- The patient's presentation with **acute liver failure** (elevated AST/ALT, coagulopathy, jaundice) in the context of increased stress and likely increased medication use, strongly suggests **acetaminophen overdose** as the cause. Given his past medical history of alcohol abuse further increases his risk of liver injury with acetaminophen.
- While other etiologies such as acute viral hepatitis or ischemic hepatitis should be considered, acetaminophen overdose is the most common cause of acute liver failure.
*Recent antibiotic treatment with gentamicin*
- **Gentamicin** is an **aminoglycoside antibiotic** primarily associated with **nephrotoxicity** and **ototoxicity**, not acute liver failure.
- Liver dysfunction is not a typical adverse effect of gentamicin, making it an unlikely cause of the patient's symptoms.
*Appropriate acute management of a deep vein thrombosis*
- Treatment for deep vein thrombosis typically involves **anticoagulants** such as heparin or warfarin. While these medications can rarely cause liver injury, the severe and acute elevation in liver enzymes and coagulopathy seen here points away from a standard anticoagulant side effect.
- The clinical picture aligns much more closely with a direct hepatotoxic injury rather than an idiosyncratic reaction to anticoagulation.
*Decreased UDP-glucuronosyltransferase activity at birth*
- **Decreased UDP-glucuronosyltransferase (UGT) activity** at birth is characteristic of **Crigler-Najjar syndrome** or **Gilbert's syndrome**, which cause **unconjugated hyperbilirubinemia**.
- These are typically chronic conditions that present earlier in life and do not cause acute, severe hepatocellular injury with massively elevated AST/ALT and coagulopathy.
*Prosthetic valve with appropriate post-operative care*
- A prosthetic heart valve, even with appropriate post-operative care, is not directly linked to acute liver failure.
- While complications like endocarditis or hemolysis could cause some liver involvement, they would not typically present with this constellation of severe acute symptoms and laboratory findings.
Acute liver failure US Medical PG Question 7: A boy with diabetic ketoacidosis is admitted to the pediatric intensive care unit for closer monitoring. Peripheral venous access is established. He is treated with IV isotonic saline and started on an insulin infusion. This patient is at the highest risk for which of the following conditions in the next 24 hours?
- A. Cerebral edema (Correct Answer)
- B. Intrinsic kidney injury
- C. Cognitive impairment
- D. Hyperkalemia
- E. Deep venous thrombosis
Acute liver failure Explanation: ***Cerebral edema***
- **Cerebral edema** is a severe and potentially fatal complication of **diabetic ketoacidosis (DKA)** treatment, particularly in children.
- It results from a rapid decrease in serum osmolality during treatment, causing water to shift into brain cells.
*Intrinsic kidney injury*
- While dehydration in DKA can lead to **prerenal acute kidney injury**, **intrinsic kidney injury** is less common as an acute risk directly from DKA treatment in the first 24 hours.
- Initial fluid resuscitation often improves renal perfusion, reducing the risk of intrinsic damage unless other predisposing factors are present.
*Cognitive impairment*
- Cognitive impairment after DKA is more commonly observed in the long term, potentially due to recurrent episodes or severe DKA with cerebral edema.
- It is not the most immediate and highest risk acute complication in the short-term (next 24 hours).
*Hyperkalemia*
- Patients with DKA typically present with **hyperkalemia** due to acidosis and insulin deficiency, which resolves with insulin therapy as potassium shifts back into cells.
- The more immediate risk during treatment, especially after initial fluid resuscitation and insulin, is **hypokalemia**, not hyperkalemia, due to the intracellular shift of potassium.
*Deep venous thrombosis*
- **Dehydration** and **hyperviscosity** associated with DKA can increase the risk of **thrombosis**, but **deep venous thrombosis** is not the highest or most immediate acute risk in the next 24 hours.
- **Cerebral edema** is a more specific and life-threatening complication directly related to the treatment of DKA in children.
Acute liver failure US Medical PG Question 8: A 78-year-old man dies suddenly from complications of acute kidney failure. An autopsy is performed and microscopic evaluation of the kidneys shows pale, swollen cells in the proximal convoluted tubules. Microscopic evaluation of the liver shows similar findings. Which of the following is the most likely underlying mechanism of these findings?
- A. Double-stranded DNA breakage
- B. Impaired Na+/K+-ATPase pump activity (Correct Answer)
- C. Free radical formation
- D. Cytochrome C release
- E. Cytoplasmic triglyceride accumulation
Acute liver failure Explanation: ***Impaired Na+/K+-ATPase pump activity***
- **Acute kidney failure** leads to **hypoxia** and ATP depletion, which impairs the function of the **Na+/K+-ATPase pump** on the cell membrane.
- Failure of this pump results in **intracellular accumulation of sodium** and water, causing **cellular swelling** and pallor as seen in the kidneys and liver.
*Double-stranded DNA breakage*
- This is primarily associated with **apoptosis** or **radiation injury**, which would lead to nuclear fragmentation and cellular death rather than simple cellular swelling.
- While cell death can occur in acute kidney failure, the initial changes described (pale, swollen cells) are characteristic of **reversible cell injury** before extensive DNA damage.
*Free radical formation*
- **Free radical formation** (oxidative stress) can cause cellular injury, but it primarily leads to **lipid peroxidation of membranes** and damage to proteins and DNA, not directly to the widespread intracellular water accumulation described.
- While part of the injury cascade, it's not the most direct mechanism for the initial gross and microscopic findings of swelling.
*Cytochrome C release*
- **Cytochrome C release** from mitochondria is a critical step in the **intrinsic pathway of apoptosis**, leading to programmed cell death.
- The findings described (pale, swollen cells) are more indicative of **reversible cellular injury** or early necrosis, prior to the widespread activation of apoptosis.
*Cytoplasmic triglyceride accumulation*
- **Cytoplasmic triglyceride accumulation** (steatosis or fatty change) is often seen in conditions like **alcoholic liver disease** or **metabolic syndrome**.
- While it can be a sign of cellular injury, it does not directly explain the generalized "pale, swollen cells" observed in both the kidneys and liver following acute kidney failure, which points to water influx.
Acute liver failure US Medical PG Question 9: A 25-year-old male is brought to the emergency department by his friends after a camping trip. He and his friends were in the woods camping when the patient started experiencing severe right upper quadrant abdominal pain after foraging and ingesting some wild mushrooms about 3 hours earlier. The patient is lethargic on exam and appears jaundiced. He has scleral icterus and is severely tender to palpation in the right upper quadrant. He has scattered petechiae on his extremities. Liver function tests are:
Serum:
Na+: 134 mEq/L
Cl-: 100 mEq/L
K+: 4.2 mEq/L
HCO3-: 24 mEq/L
Urea nitrogen: 50 mg/dL
Glucose: 100 mg/dL
Creatinine: 1.4 mg/dL
Alkaline phosphatase: 400 U/L
Aspartate aminotransferase (AST, GOT): 3278 U/L
Alanine aminotransferase (ALT, GPT): 3045 U/L
gamma-Glutamyltransferase (GGT): 100 U/L
The most likely cause of this patient’s clinical presentation acts by inhibiting which of the following molecules?
- A. RNA polymerase II (Correct Answer)
- B. RNA polymerase III
- C. Topoisomerase
- D. RNA polymerase I
- E. Prokaryote RNA polymerase
Acute liver failure Explanation: ***RNA polymerase II***
- The clinical presentation with severe hepatotoxicity (jaundice, elevated AST/ALT, RUQ pain, petechiae, lethargy) following wild mushroom ingestion is highly suggestive of poisoning by **Amanita phalloides** (death cap mushroom).
- The primary toxin in *Amanita phalloides* is **alpha-amanitin**, which specifically inhibits **RNA polymerase II**, thereby halting mRNA synthesis and leading to cellular death, particularly in rapidly dividing cells and hepatocytes.
*RNA polymerase III*
- **RNA polymerase III** is responsible for synthesizing **tRNA** and **5S ribosomal RNA**.
- While essential for cell function, it is not the primary target of amanitin toxins, and its inhibition would not directly cause the severe hepatotoxicity observed.
*Topoisomerase*
- **Topoisomerases** are enzymes that regulate the supercoiling of **DNA** during replication, transcription, and repair.
- While critical for cell survival, they are not the target of the toxins found in *Amanita phalloides* mushrooms.
*RNA polymerase I*
- **RNA polymerase I** is responsible for synthesizing most **ribosomal RNA (rRNA)**.
- While also essential, it is less sensitive to **alpha-amanitin** than RNA polymerase II, requiring much higher concentrations for inhibition.
*Prokaryote RNA polymerase*
- **Prokaryote RNA polymerase** is fundamentally different in structure and function from eukaryotic RNA polymerases.
- **Alpha-amanitin** specifically targets eukaryotic RNA polymerases and has no significant inhibitory effect on prokaryotic RNA polymerase.
Acute liver failure US Medical PG Question 10: A 67-year-old man presents to the emergency department with increased fatigue. He states that he has been feeling very tired lately but today lost consciousness while walking up the stairs. He reports mild abdominal distension/discomfort, weight loss, a persistent cough, and multiple episodes of waking up drenched in sweat in the middle of the night. The patient does not see a primary care physician but admits to smoking 2 to 3 packs of cigarettes per day and drinking 1 to 3 alcoholic beverages per day. He recently traveled to Taiwan and Nicaragua. His temperature is 99.5°F (37.5°C), blood pressure is 177/98 mmHg, pulse is 100/min, respirations are 17/min, and oxygen saturation is 98% on room air. On physical exam, you note a fatigued appearing elderly man who is well-groomed. Cardiopulmonary exam reveals mild expiratory wheezes. Abdominal exam is notable for a non-pulsatile mass in the left upper quadrant. Laboratory values are ordered as seen below.
Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 105,500/mm^3
Platelet count: 197,000/mm^3
Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 92 mg/dL
Creatinine: 1.4 mg/dL
Ca2+: 10.2 mg/dL
Leukocyte alkaline phosphatase score: 25 (range 20 - 100)
AST: 12 U/L
ALT: 17 U/L
Which of the following is the most likely diagnosis?
- A. Tuberculosis
- B. Leukemoid reaction
- C. Acute myelogenous leukemia
- D. Acute lymphoblastic leukemia
- E. Chronic myeloid leukemia (Correct Answer)
Acute liver failure Explanation: ***Chronic myeloid leukemia***
- The patient presents with **fatigue, weight loss, night sweats, and a persistent cough**, which are common symptoms of CML. The **extreme leukocytosis (105,500/mm^3)**, **non-pulsatile LUQ mass (splenomegaly)**, and a **low-normal leukocyte alkaline phosphatase (LAP) score of 25** are highly indicative of CML.
- CML characteristically shows a **low LAP score (typically <20)**, which distinguishes it from a leukemoid reaction. This patient's LAP of 25, while technically within the normal range (20-100), is at the lower end and consistent with CML.
- CML is a myeloproliferative disorder characterized by the **Philadelphia chromosome (BCR-ABL fusion gene)**, leading to uncontrolled proliferation of myeloid cells.
*Tuberculosis*
- While **fatigue, weight loss, night sweats, and cough** can be present in tuberculosis, the **dramatically elevated leukocyte count** and **splenomegaly** are not characteristic findings of TB.
- Tuberculosis would typically show a more prominent respiratory symptomology (e.g., hemoptysis) and imaging findings consistent with lung involvement, and its diagnosis would be confirmed by microbiologic studies.
*Leukemoid reaction*
- A leukemoid reaction is a **reactive leukocytosis (>50,000/mm^3)** often triggered by severe infection or inflammation, but it would present with an **elevated leukocyte alkaline phosphatase (LAP) score (typically >100)**, which contradicts the patient's low-normal LAP score of 25.
- Unlike CML, a leukemoid reaction does not typically cause **splenomegaly** to the extent that it forms a palpable mass.
*Acute myelogenous leukemia*
- AML typically presents with **malignant myeloid blasts** in the peripheral blood (often >20%) and bone marrow, and patients are usually more acutely ill with symptoms related to **pancytopenia** (e.g., severe anemia, thrombocytopenia with bleeding), which are not present in this case.
- While AML can cause leukocytosis, it is characterized by a **predominance of immature blast cells** rather than the mature granulocytes seen in CML.
*Acute lymphoblastic leukemia*
- ALL is primarily a disease of **lymphoid progenitor cells** and is more common in children, though it can occur in adults. It is characterized by the presence of **lymphoblasts** in the blood and bone marrow.
- While it can cause fatigue and weight loss, the **extremely high leukocyte count composed primarily of mature myeloid cells** and **prominent splenomegaly** are inconsistent with ALL.
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