Liver/Pancreatic/Biliary Disorders Flashcards
A 40-year-old man comes to the emergency department because of increasing upper abdominal pain which began four days ago. He says the pain is constant, with associated nausea and several episodes of vomiting. His temperature is 37.9ºC (100.2˚F), pulse is 105/min, respirations are 18/min, and blood pressure is 115/75 mmHg. The patient appears very pale and his abdomen is extremely tender to palpation. Laboratory studies show:
Serum amylase: 726 IU/L
Serum lipase: 890 U/L
Alanine aminotransferase: 178 U/L
Aspartate aminotransferase: 55 U/L
Which of the following is the most likely diagnosis? and what are the causes? which is the most sensitive test?
How do you manage this?
- Acute pancreatitis (causes can be remembered by IGETSMASHED)
- iatrogenic
- gallstones
- ethanol
- trauma
- steroids
- mumps
- autoimmune condition
- scorpion sting
- hypertriglyceridemia/hypercholesterolaemia
- ERCP
- Drugs like azathioprine/5 ASA
Clinical features
- Epigastric pain radiating to the back, with nausea and vomiting
- Necrotizing pancreatitis-> grey turner’s sign and cullen’s sign due to haemorrhage
Investigations
- Serum lipase (more sensitive than amylase)
- Abdominal ultrasound-> detect gallstones
Management
- Conservative- analgesia (morphine cannot be given) and IV fluids; broad spectrum antibiotics-cefuroxime to prevent necrotizing pancreatitis
What is the pancreatitis glasgow score?
- A score of 3 or more indicates severe pancreatitis and patient needs to be in HDU
What are the pancreatitis complications?
- Fluid collections
- observed; percutaneous drainage is not recommended as it can precipitate infection
- Pseudocyst
- collection held by fibrous/granulation tissue after pancreatitis. Serum amylase/lipase often persistently raised
observed; percutaneous drainage is not recommended as it can precipitate infection
- Pancreatic abscess
- pseudocyst gets infected and produces pus
- requires transgastric drainage
- Necrotising Pancreatitis and Haemorrhage
- best detected by CT scan; present as grey turner’s/cullen’s sign
- surgical necrosectomy/ debridement
A 52-year-old woman presents with sepsis secondary to ascending cholangitis. Blood cultures grew Escherichia coli sensitive to gentamicin. She has received 2 days of treatment with gentamicin. The gentamicin levels have been in normal range. She remains febrile with rigors, a rising white cell count and tenderness in the right upper quadrant.
What is the most likely explanation?
- Deep seated abscess that requires transcutaneous drainage
A 52-year-old woman comes to the urgent care clinic because of abdominal pain. When describing the pain, she points to her epigastric region and shows that it radiates to her back. She said that many years ago, she had the same pain, but it came in episodes of <10 days. Since it always went away by itself, she did not seek medical advice; however, now the pain is more constant and has increased in severity. Her stools are “floating and oily.” Other symptoms include an increased thirst level, as well as the need to urinate more frequently. Her fasting blood glucose concentration is significantly elevated. She has been a chronic alcoholic since she was 20, and has binge drinking tendencies. An abdominal CT scan is obtained and is shown below.
What is this due to? How do you investigate or manage this?
- Chronic pancreatitis (often seen in alcoholics)
Clinical features
- Epigastric pain that radiates to back-> nausea and vomiting
- Exocrine/endocrine function affected-> steatorrhea (pancreatic lipase) and diabetes (insulin)
Investigations
- Faecal elastase reduced
- Abdominal CT scan-> calcifications
Management
- Pancreatic enzyme supplements
- Analgesia
A 71-year-old woman comes to the office because her friends have noticed a slight yellowing of her skin over the past month. She says she has persistent “itching all over”, had a recent weight loss of 6.8-kg (15-lb), and has a mild pain in the middle of her back after she eats a meal. On physical exam, there is round cystic mass in the upper abdomen that is non-tender to palpation. Which of the following specific serum markers is most likely to be abnormally elevated?
What does the imaging show?
How do you investigate/manage this?
- Pancreatic carcinoma
- seen in alcoholics
- chronic pancreatitis
- lynch syndrome
Clinical features
- Head of pancreas/ampulla of vater-> obstruct biliary tree to cause painless jaundice and palpable gallbladder with pruritus (courvoisier’s sign)
- If body/tail affected-> epigastric pain and nausea/vomiting
- Weight loss
- Exocrine/endocrine function affected-> steatorrhea, diabetes
Investigations
- CA 19-9
- CT scan better for pancreatic cancer
-will show double duct sign, “dilatation of CBD and pancreatic duct”
Management
- Whipple’s procedure-> pancreatoduodenectomy
- ERCP and stent can be used for palliative treatment
A 42-year-old man with a history alcohol abuse comes to your practice to discuss his recent diagnosis of chronic pancreatitis. You explain to him that this diagnosis puts him at higher risk of developing diabetes mellitus.
What testing should you offer this patient in regards to this risk?
- Annual HbA1c test
- chronic pancreatitis patients are at risk of developing DM due to insulin production being affected
A 34-year-old male is admitted with central abdominal pain radiating through to the back and vomiting. The following results are obtained:
Amylase1,245 u/dl
Which one of the following medications is most likely to be responsible?
- phenytoin
- sodium valproate
- metoclopramide
- sumatriptan
- pizotifen
Sodium valproate
- other drugs that cause pancreatitis-azathiprine, mesalazine, furosemide, bendroflumethiazide, sodium valproate
A 44-year-old woman presents to her GP with right upper quadrant pain. She had a cholecystectomy 4 weeks ago for acute cholecystitis and describes the pain now similar to how it was when she was in hospital and it has been present for the past 2 weeks. She reports being clinically well in the interval 2 weeks.
On examination she is mildly jaundiced and very tender in the right upper quadrant, although no masses are palpable. She is apyrexial and tachycardic.
What is the most likely cause of this lady’s symptoms?
- Common Bile Duct Gallstones
- may be present in CBD after cholecystectomy, causing jaundice and pain
A 43-year-old woman comes to her primary care physician because of right upper quadrant pain. The pain occurs only after eating a fatty meal. She denies any sick contacts, fever, and chills. Her temperature is 37.6°C (99.5°F), pulse is 92/min, respirations are 18/min, and blood pressure is 125/80 mm Hg. LFTs shows raised ALP, GGT and raised bilirubin. Which of the following is the most likely diagnosis? What is the pathophysiology?
How do you investigate this?
How do you manage this?
- Gallstone
- cholesterol/bilirubin
Risk factors:
- female
- fertile: pregnancy
- forty
- fat
Clinical features
- Colicky right upper quadrant pain that radiate to right shoulder/scapular region-> often precipitated by fatty meal
- Nausea and vomiting
Investigations
- LFTs-> obstructive/cholestatic picture-> ALP, GGT, raised bilirubin
- Abdominal ultrasound
- If stone in CBD suspected-> ERCP (enterograde)
Management
-often if asymptomatic manged conservatively, however if stone is in CBD and patient is at risk of pancreatitis/cholangitis-> ERCP can be done to rule out. Cholecystectomy.
Describe the complications of gallstones as it travels in biliary tree
Impacts the cystic duct; how can you get acalculous cholecystitis
Chronic cholecystitis
Ascending cholangitis
Acute pancreatitis
Gallstone ileus
Acute cholecystitis
- occurs when gallstone impacts the cystic duct. This causes damage to the mucosa and causes inflammation. This causes symptoms like fever, RUQ pain radiating to scapula/back, tenderness and guarding (murphy’s sign especially on deep inspiration)
- acalculous cholecystitis stems from ischemia of the cystic artery (hypotension, multi-organ failure in sepsis, burns etc). Can cause gangrene of gallbladder
Chronic cholecystitis
-repeated episodes of cholecystitis causes fibrosis of gallbladder (porcelain GB on ultrasound) that causes gallbladder to shrink in size
Ascending cholangitis
- gallstone is trapped in CBD (choledocholithiasis) causing bile stasis. Bacteria like Ecoli multiply causing inflammation of biliary tree-charcot’s triad: fever, RUQ pain, jaundice.
- If left untreated can cause abscess in liver.
Acute pancreatitis
-gallstone gets trapped in ampulla of vater and causes pancreatitis: epigastric pain radiating to back , nausea and vomiting
Gallstone ileus
-causes a SBO due to fistula formation between small bowel and inflamed gallbladder: causing diffuse abdominal pain and distention, bilious vomiting and absolute constipation/flatus.
A 36-year-old woman was admitted to our hospital due to appetite loss, nausea, and back pain. A physical examination disclosed right hypochondriac tenderness and obvious jaundice and fever. Laboratory studies showed elevated levels of total bilirubin (9.7 mg/dl), direct reacting bilirubin (6.0 mg/dl), aminotransferase (AST 281 U/l, ALT 362 U/l), alkaline phosphatase (1945 U/l,) and γ-glutamyltransferase (1769 U/l); however, her white blood cell count and C-reactive protein level were within the normal ranges. Magnetic resonance cholangiography revealed that the intrahepatic and common hepatic bile ducts were dilated, revealing a stone compressing common hepatic duct.
What is your likely diagnosis/management?
- Mirizzi syndrome
- gallstone compresses the common hepatic duct
Clinical features
- Fever, jaundice, RUQ pain due to inflammation in the common hepatic duct
Investigations
- ultrasound
- MRCP (most sensitive) before ERCP
Management
- ERCP to remove the stone
A 75-year-old woman comes to the emergency department because of abdominal pain and distention. The abdominal pain is colicky, and associated with nausea and vomiting. For three days she has not been able to pass flatus or stool. Her temperature is 37.0oC (98.6oF), pulse is 99/min, respirations are 15/min, and blood pressure is 125/75 mm Hg. Abdominal examination shows high-pitched bowel sounds. Abdomen CT is done. Which of the following is the most likely diagnosis?
What are the other complications?
- Gallstone ileus (due to gallstone obstructing small bowel)
Other complications of gallstones:
- Cholecystitis
- Pancreatitis
- Gallstone cancer
A 42-year-old woman comes to the emergency department because of abdominal pain. The pain began five hours ago, is postprandial, steadily increasing in intensity, and associated with nausea and vomiting. Her temperature is 37.0°C (98.6°F), pulse is 80/min, respirations are 16/min, and blood pressure is 125/85 mm Hg. Examination shows an overweight middle-aged woman in mild distress. She has no signs of jaundice. Her abdomen is exquisitely tender in the right upper quadrant. Ultrasound shows several gallstones, an edematous gallbladder wall, and a positive sonographic Murphy sign.
What is this due to?
How do you investigate/manage this?
- Acute cholecystitis (inflammation of the gallbladder)
- due to impaction of gallstone
Clinical features
- RUQ pain that radiates to right shoulder/interscapular region often after fatty meal (boas sign)
- Systemic upset like fever; tenderness and guarding of RUQ on examination. Murphy’s sign is +ve (arrest on inspiration)
Investigation
- FBC-leucocytosis
- LFTs-cholestatic picture (ALP, GGT may be raised)
- Abdominal ultrasound-may show gallstone; if not cholescintigraphy (w radioactive tracer may be used)
Management
- Analgesia and IV fluids with IV broad spectrum antibiotics like cefotaxime
- laparoscopic Cholecystectomy is performed within 1 week-> minimise complication s like perforation or empyema
A 50-year-old woman comes to the emergency department because of severe abdominal pain that started the day before and is getting progressively worse. She states that she has not experienced this pain before and rates it as an 8 on a 10 point scale. She also has light-colored foul-smelling diarrhea. Physical examination shows mild jaundice and a fever of 39°C (102.2°F). Abdominal examination shows tenderness in the right upper quadrant but no palpable masses. Laboratory studies show the following:
WBC: 15,000 with 10% bands
Hgb: 13.3
Platelets: 230,000
Alk phos: 300
Total bilirubin: 7.4
Direct bilirubin: 6.3
Based on the patient’s presentation, which of the following is the most likely diagnosis? What is it due to?
What is Charcot’s triad/ reynold’s pentad?
How do you investigate/manage this?
- Acute cholangitis (inflammation of biliary tree often due choledocholithiasis-gallstone in CBD that causes stasis-> Ecoli accumulates)
Clinical features
- Charcot’s triad-Fever, jaundice, RUQ pain
- Jaundice- urine dark and stools are pale (post-hepatic)
- Reynold’s pentad- hypotension, confusion
Investigations
- FBC-leucocytosis
- Blood culture-E coli.
- LFTs-cholestatic picture; bilirubin, ALP and GGT raised
- Ultrasound-dilated CBD
- ERCP/MRCP-more sensitive
Management
- IV antibiotics like cefurotaxime
- ERCP to remove gallstone in CBD
A 74-year-old woman comes to the clinic because of stomach pain for the past 6 months. It used to only occur after meals, but has gotten progressively more frequent and wakes her up at night. She also notes that she has lost 20-lb (9.1kg) in the past 3 months, and attributes this to a decreased appetite. Her current medications include atorvastatin and metformin. Her temperature is 38.1°C (100.6°F), pulse is 84/min, respirations are 12/min, and blood pressure is 136/84 mm Hg. Physical examination shows a cachectic appearing woman with yellow-colored skin. A non-tender mass is palpated in the right upper quadrant of the abdomen. Laboratory studies show a direct bilirubin of 3.5 mg/dL. Abdominal ultrasound is shown below. A cholecystectomy is performed and histologic examination shows a primary malignancy.
What is your likely diagnosis? What are the risk factors?
How do you manage this?
- Gallbladder cancer
- risk factors:
- chronic cholecystitis (causing porcelain gallbladder-> calcification)
- gallbladder adenoma
- gallstone
- primary sclerosing cholangitis
- environmental factors: obesity/smoking
Clinical features
- Palpable mass in RUQ
- May present like cholithiasis-> RUQ pain, nausea and vomiting
- Weight loss
- Post hepatic jaundice-> urine dark, stools are light-coloured
Investigation
- CA 19-9, CEA raised
- LFTs-> obstructive picture (ALP, GGT)
- Abdominal ultrasound
- CT/MRI scan-> for staging
- Endoscopic ultrasound and FNA (gold standard)
Management
- Surgical removal
- Endoscopic stent for obstructive jaundice can be done
A 45-year-old woman comes to the outpatient clinic because of fatigue, abdominal swelling, and bloating. She has hypertension and type 2 diabetes mellitus. She denies any sick contacts, fever, or chills. Physical examination shows tanned skin, scleral icterus, palmar erythema, and a prominent abdominal distention with a fluid wave. Liver biopsy reveals hemosiderosis.
Explain your most likely diagnosis and investigations?
How would you manage this?
- Haemochromatosis
- iron overload due to autosomal recessive mutation in HFE mutation
Clinical features
- Skin tanned-> iron deposits
- Fatigue, arthralgia
- Pituitary gland-> hypogonadism
- Heart-> restrictive cardiomegaly and heart failure
- Pancreas-> T2DM
- Liver-> liver cirrhosis
Investigations
- LFTs-> ALT deranged due to hepatic inflammation
- Iron increased; ferritin stores increased; transferrin decreased (TIBC decreased)
- Gene mutation shows HFE mutation
- Liver biopsy-> cirrhosis
Management
- Venesection
A 10-year-old boy comes to his pediatrician because of difficulty articulating his speech. His parents have noticed that he was previously very talkative but now appears taciturn and moody. When he does speak, he has difficulty forming his words correctly. Physical examination of the patient shows a well-developed male with mild tenderness to palpation in his right upper quadrant and hepatomegaly. Closer examination of his eyes shows yellow-brown deposits in the corneoscleral junction.
What is your likely diagnosis? How do you investigate/manage this?
- Wilson’s disease
- autosomal recessive due to deposition of copper in organs
Clinical features
- CNS-> deposition in basal ganglia causing movement disorders, asterixis, parkinsonism and psychiatric problems
- Eyes-> Kayser Fleischer rings
- Liver-> cirrhosis
- Renal tubular acidosis
- Haemolytic anaemia-> anaemia, hepatosplenomegaly, jaundice
- Blue nails
Investigations
- Serum ceruloplasmin reduced
- Decreased serum copper because of increased urinary excretion
Management
- Chelating agent like penicillamine
A 35-year-old man with a history of ulcerative colitis comes to the office because of jaundice, itching, and right upper quadrant pain for the past week. Physical exam shows icteric sclera, excoriations on the upper shoulder, and pain of the right upper quadrant upon palpation. Liver function tests are ordered and laboratory studies show:
Total bilirubin: 5.3 mg/dL (raised)
Direct bilirubin: 4.1 mg/dL
AST: 45 U/L
ALT: 50 U/L
Phosphatase (alkaline): 150 U/L (raised)
Endoscopic retrograde cholangiopancreataography is performed and shows alternating strictures and dilated portions of the ducts. Which of the following antibodies is most commonly associated with these findings?
What is this due to/investigations/management?
- Primary sclerosing cholangitis
- inflammation of intra and extra hepatic ducts. May be due to p-ANCA (against myeloperoxidase). Associated with ulcerative colitis
Clinical features
- Cholangitis-> Charcot’s traid of RUQ pain, fever and jaundice (urine dark and pale stools)
- Jaundice (post hepative)
- Fatigue
Investigations
- LFTs-> obstructive/cholestatic picture (ALP, GGT, bilirubin raised)
- ERCP/MRCP (sensitive)-> will show strictures
- pANCA +ve in some cases
Management
- Ursodeoxycholic acid (bile acid) for fat digestion)
- ERCP with stenting
A 25-year-old Afro-Brazilian woman was hospitalized in a public hospital with the following complaints:sudden right upper quadrant pain, ascites and the development of veins and edema in the abdominal wall and swelling in the legs. Yellowing of the sclera was also noticed. She has a PMHx of polycythaemic vera.
What is your likely diagnosis? How do you investigate/manage this?
- Budd Chiari syndrome
- hepatic vein occlusion with a clot. This causes liver congestion and hepatocyte necrosis.
Risk factors:
- Polycythaemia vera
- Thrombophilia->Antithrombin III deficiency, Resistance to proteinase C
- OCP
Clinical features
- Sudden RUQ pain, hepatomegaly
- Liver fails-> ascites and jaundice (hepatic-> urine dark and stools normal.
Investigations
- Doppler ultrasound–> blood flow reduced
Management
- Transjugular intrahepatic portosystemic shunt
An 80-year-old man comes to the office because of worsening swelling in both his legs. He complains of fatigue, decreased appetite, recent weight loss, and abdominal pain. A CT scan is obtained and shows a large mass on the liver. Which of the following tumor markers would be elevated in this patient to support the most likely diagnosis? What are the risk factors
What investigations/management would you do?
- Hepatocellular carcinoma
Risk factors:
- Hepatitis B/C
- Alcohol
- Haemochromatosis
- Drugs-OCP/anabolic steroids; aflatoxin
Clinical features
- Weight loss, anorexia
- Liver decompensation-RUQ pain, hepatomegaly, ascites and jaundice (hepatic-urine dark, stools normal)
Investigations
- Alpha feto-protein raised
- LFTs-ALT raised; bilirubin high and albumin low due to decompensation
- US/CT/MRI scan and biopsy
Management
- Surgical management and resection
- Liver transplant if severe
A 65-year-old man comes to the clinic because he has been feeling unwell for the past few weeks. He says that it hurts to lie down on his stomach, which is his preferred way to sleep. He feels hungry only once a day, and has noticed that his skin looks yellow under certain lights. He states that he drinks approximately six alcoholic drinks per day because he has been unemployed over the last 10 years. Blood tests reveal a serum aspartate aminotransferase activity of 200 U/L, serum alanine aminotransferase activity of 105 U/L, and anemia. Liver biopsy demonstrates the histology below:
What is your likely diagnosis and investigations you would carry out?
What is the Maddrey’s discriminant function?
- Alcoholic hepatitis
- inflammation due to alcohol which causes steatosis (fat deposition) and mallory bodies in hepatocytes (eosinophilic damaged filaments)
Clinical features
- Liver decompensation-> RUQ pain, hepatomegaly, ascites, jaundice (hepatic), hepatic encephalopathy
Investigations
- FBC-> leucocytosis; non-megaloblastic anaemia (MCV raised); thrombocytopenia (due to hypersplenism from hepatic portal hypertension)
- Us and Es-> hyponatraemia
- LFTs-> AST/ALT >2:1, both elevated. Bilirubin raised; albumin is low and prothrombin time elevated
- CT/MRI/US and biopsy
Management
- If Maddrey discriminant function is 32 or more-> prednisolone can be given to reduce inflammation
An overweight woman (BMI 30.1) aged 52 complained to her GP of vague feelings of malaise. On examination, she had hepatomegaly. A fasting blood sample was collected with the following results:
What is this due to and what is it associated with?
How do you investigate/manage this?
- Non-alcoholic fatty liver disease
- often associated with metabolic syndrome (obesity, T2DM, hypertension, hyperlipidemia)
Clinical features
- Hepatomegaly
- Asymptomatic
Investigations
- LFTs- ALT higher than AST
- ELF test (enhanced liver fibrosis test)-hyaluronidase + procollagen III + metalloproteinase I
- Or Fibroscan (ultrasound will be hyperechoic) +FIB4 (fibrosis 4)/NAFLD fibrosis score
Management
- Weight loss
A 66-year-old man comes to the emergency department because of right upper quadrant pain. Physical examination shows scleral icterus, asterixis, abdominal striae, a reduced liver span, and spiral-shaped angiomas. Serum electrophoresis shows incorporation of beta and gamma peaks, with elevated gamma globulin and decreased levels of albumin and pre-albumin. Serum assays for hepatitis are all negative and there is no family history of liver disease is available. Liver biopsy is postponed due to the risk of bleeding and the patient passes away overnight from a massive hemorrhage. Autopsy shows a ptosed liver with extensive fibrosis. Which of the following is the most likely psychiatric diagnosis?
LFT shows raised liver enzymes.
What is this due to (asterixis)? investigations?
How do you manage?
Liver cirrhosis due to:
- hepatitis B/C
- alcohol
- non-alcoholic liver disease
Clinical features (when decompensated):
- portal hypertension (varices/haemorrhoids)
- ascites
- coagulopathy
- hepatorenal/hepatopulmonary syndrome
- jaundice
- portosytemic encephalopathy (due to build up of ammonia in brain): confusion at first, slurred speech, fetor hepaticus (due to ammonia), asterixis, constructional apraxia (cannot draw 5 pointed star)
Investigations
- LFTs-deranged liver enzymes (alt/ast/alp)
- Liver function test-prothrombin raised, albumin low
- Urea and electrolytes-raised in hepatorenal syndrome, low urinary sodium
- FBC-thrombocytopenia, anemia and leucopenia due to reduction of TPO
Management
- lactulose to stop ammonia absorption and stop diuretics to prevent ammonia accumulation
A 50-year-old alcoholic man comes to the emergency department because of an episode of hematemesis. The patient looks disheveled and is disoriented to time and place. Past medical history includes hepatitis C infection. Abdominal examination shows abdominal distension with a fluid wave and caput medusae. Examination of the extremities shows a bilateral “flapping” tremor, red palms, and bilateral 2+ lower extremity edema. Which of the following is the most likely cause of the patient’s palmar erythema?
What is the management for oesophageal varices?
Liver cirrhosis due to:
- hepatitis B/C
- alcohol
- non-alcoholic liver disease
Clinical features (when decompensated):
- portal hypertension (varices/haemorrhoids)
- ascites
- coagulopathy
- hepatorenal/hepatopulmonary syndrome
- jaundice
- portosytemic encephalopathy (due to build up of ammonia in brain): confusion at first, slurred speech, fetor hepaticus (due to ammonia), asterixis, constructional apraxia (cannot draw 5 pointed star)
Investigations
LFTs-deranged liver enzymes (alt/ast/alp)
Liver function test-prothrombin raised, albumin low
Urea and electrolytes-raised in hepatorenal syndrome, low urinary sodium
FBC-thrombocytopenia, anemia and leucopenia due to reduction of TPO
Management
- terlipressin(reduce PHTN) and endoscopic band ligation
- sengaksten-blakemore tube at GOJ junction
- Repeat endoscopic intervention
- Transjugular intrahepatic portosystemic shunt
A 54-year-old man comes to the clinic because of breathlessness. He describes worsening dyspnea, particularly when upright, over the past 3 months. He denies any peripheral swelling or other respiratory symptoms. His medical history includes liver failure and hypertension. Vital signs show pulse is 86/min, blood pressure is 108/72mmHg, RR is 18/min, and oxygen saturations are 91% on room air. Physical examination shows spider nevi, jaundice, clubbing, and peripheral cyanosis. Arterial blood gas taken on room air shows PaO2 of 64mmHg (8.5kPa). CXR shows no focal consolidation or evidence of failure. Lung function testing excludes obstructive lung disease. Which of the following tests could confirm the diagnosis?
Liver cirrhosis due to:
- hepatitis B/C
- alcohol
- non-alcoholic liver disease
Clinical features (when decompensated):
- portal hypertension (varices/haemorrhoids)
- ascites
- coagulopathy
- hepatorenal/hepatopulmonary syndrome(hypoxaemia)
- jaundice
- portosytemic encephalopathy (due to build up of ammonia in brain): confusion at first, slurred speech, fetor hepaticus (due to ammonia), asterixis, constructional apraxia (cannot draw 5 pointed star)
Investigations
LFTs-deranged liver enzymes (alt/ast/alp)
Liver function test-prothrombin raised, albumin low
Urea and electrolytes-raised in hepatorenal syndrome, low urinary sodium
FBC-thrombocytopenia, anemia and leucopenia due to reduction of TPO
Contrast echocardiogram for hepatopulmonary syndrome to check for pulmonary blood flow
A 65-year-old man with a history of cirrhosis and hepatocellular carcinoma (HCC) comes to the emergency department because of 3 weeks of mild but increasing abdominal pain. He has a history of ascites refractory to salt restriction and diuretic therapy. He endorses intermittent chills, but no nausea or diarrhea. The patient denies constipation and black stools, but endorses a notable decrease in how much urine he has produced in the past week. Physical exam shows the patient’s temperature is 37.8°C (100°F), with otherwise normal vital signs. Examination of his abdomen shows shifting dullness by percussion. An abdominal ultrasound shows ascites and no signs of hydronephrosis. Laboratory studies are shown below:
Serum
WBC 7,000/μL
Creatinine 3.56 mg/dL, today
1.50 mg/dL, at an outpatient provider visit 1 month ago
Urinalysis
Negative for nitrites and leukocyte esterase
0-2 RBCs per high powered field
0-1 WBC per high powered field
No evidence of casts or proteinuria
What is this likely due to and how do you investigate/manage this?
Liver cirrhosis due to:
- hepatitis B/C
- alcohol
- non-alcoholic liver disease
Clinical features (when decompensated):
- portal hypertension (varices/haemorrhoids)
- ascites
- coagulopathy
-hepatorenal (lack of BF causing AKI-> rise in urea/creatinine; decrease in urinary Na+)
- jaundice
- portosytemic encephalopathy (due to build up of ammonia in brain): confusion at first, slurred speech, fetor hepaticus (due to ammonia), asterixis, constructional apraxia (cannot draw 5 pointed star)
Investigations
LFTs-deranged liver enzymes (alt/ast/alp)
Liver function test-prothrombin raised, albumin low
Urea and electrolytes-raised in hepatorenal syndrome, low urinary sodium
FBC-thrombocytopenia, anemia and leucopenia due to reduction of TPO
Management
- Fluid rescuscitation with 0.9%NaCl solution
What are the causes of a high Serum albumin-ascitic albumin gradient? (1.1mg/dl)
>1.1mg/dl (portal hypertension causes due to high pressure causing everything except for albumin to leak from BV-TRANSUDATIVE)
- liver cirrhosis
- alcoholic hepatitis
- congestive heart failure
- budd-chiari syndrome
- fatty liver of pregnancy
<1.1mg/dl (EXUDATIVE cause which causes inflammation in endothelial cells causing leakage of albumin)
- peritonitis
- nephrotic syndrome
- Bowel obstruction or mesenteric infarct
A 64-year-old woman comes to the emergency department because of abdominal distension and fever. She has a history of alcohol abuse and was recently diagnosed with cirrhosis. Her temperature is 39.1°C (102.4°F) and blood pressure is 173/95 mm Hg. Physical examination shows significant abdominal distension with rebound, guarding, and shifting dullness with fluid wave. Blood cultures are found to be positive for enterococcus, and a diagnosis of spontaneous bacterial peritonitis is made.
What are the investigations for ascites/SBP? How do you manage them?
Liver cirrhosis due to:
- hepatitis B/C
- alcohol
- non-alcoholic liver disease
Clinical features (when decompensated):
- portal hypertension (varices/haemorrhoids)
- ascites
- coagulopathy
- hepatorenal (lack of BF causing AKI-> rise in urea/creatinine; decrease in urinary Na+)
- jaundice
- portosytemic encephalopathy (due to build up of ammonia in brain): confusion at first, slurred speech, fetor hepaticus (due to ammonia), asterixis, constructional apraxia (cannot draw 5 pointed star)
Investigations
LFTs-deranged liver enzymes (alt/ast/alp)
Liver function test-prothrombin raised, albumin low
Urea and electrolytes-raised in hepatorenal syndrome, low urinary sodium
FBC-thrombocytopenia, anemia and leucopenia due to reduction of TPO
Paracentesis-albumin in ascites>1.1g/dl (due to portal hypertension like liver cirrhosis) vs <1.1g/dl
Neutrophils to rule out SBP; culture/biochem/cytology
Management
- For ascites-> diuretics like spironolactone; do total paracentesis if that does not work out; prophylactic antibiotics
- For SBP-> IV co-amoxiclav or IV ciprofloxacin
A 33 year-old female comes to the office because of increasing fatigue and joint pain for the past 3 months. She has also noticed a decreased appetite and a 4-kg (8.8-lb) weight loss. She does not complain of abdominal pain, neurologic symptoms, and she has not noticed any new rashes. She has always had irregular periods, but her last “regular” period was 8 weeks ago. Her medical history is noncontributory and she takes no medications. She has been sexually active with her boyfriend for the past 4 months. Her temperature is 37.8°C (100°F), pulse is 77/min, and blood pressure is 132/88 mm Hg. Examination shows scleral icterus, spider telangiectasias on the trunk, and mild hepatosplenomegaly. Urine pregnancy test is negative. Laboratory studies show:*
What is your most likely diagnosis (which type)?
How would you investigate/manage this?
- Autoimmune hepatitis (often associated with other autoimmune diseases like hypergammaglobulinemia)
There are 3 different types:
Clinical features
- Fatigue, weight loss, malaise
- Acute onset-> fever, jaundice
- Chronic liver disease symptoms-> hepatosplenomegaly, jaundice, ascites etc.
Investigations
- Antinuclear antibodies/anti smooth muscle antibodies (type 1-adults and children); anti liver-kidney microsomal antibodies (type 2-children); soluble liver-kidney antigen-type 3 in adults
- IgG will be high
- LFTs-bilirubin and ALT/AST will be deranged
- Liver biopsy (sensitive)-piecemeal necrosis
Management
- Prenisolone
- Liver transplantation
A 32-year-old actot comes to the office for a routine check up. He has been feeling flu-like symptoms and malaise. He shared that he has been using IV drugs since he was 17 On examination, her sclera is yellow and she has mild hepatosplenomegaly. Her temperature is 36.8°C (98°F), pulse is 87/min, respirations are 18/min, and blood pressure is 117/78 mm Hg. Examination is noncontributory. Laboratory investigations shows abnormal liver function tests (LFTs).
Interpret these tests and describe the graph.
Describe the structure of the virus and risk factors.
How would you manage this?
- Hepatitis B infection
- often due to blood transmission: men who have sex with men, IV drug use, blood transfusions are risk factors
- only virus that is double stranded DNA ; rest are single stranded RNA
Clinical features
- Prodromal phase-fever, malaise, weight loss
- Hepatosplenomegaly and jaundice may develop
Investigations(Hepatitis B serology)
Graph explains:
- HBsAg is released first (symptoms); followed by HBeAg (important for viral replication)
- IgMHBcAg is released in response; followed by IgGHBcAg. Window period occurs when immune response against core antigen is so high surface antigen disappears
- at 6 months, IgG HBsAg develops and you are cured!
-HBsAg-> currently have infection
- acute infection: HBsAg +ve, IgM/IgG HBcAg +ve, IgG HBsAg-ve
- chronic infection: HBsAg +ve, IgMHBcAg-ve, IgGHBcAg +ve, IgGHBsAg-ve
-IgGHBsAg-> you have won battle (cured/vaccinated)
- +IgGHBcAg-> most likely to be cured in prior infection as there is immunity to core antigen
- -IgGHBcAg-> vaccinated as vaccination only has surface antigen
Management is via pegylated interferon alfa. Can get it with HIV co-infection
What are the complications of chronic hepatitis C infection (and definition)?
Chronic hepatitis C
- HCV RNA present for 6 months or more
Clinical features
- hepatocellular carcinoma
- mesangioproliferative glomerulonephritis
- rheumatological conditions-arthralgia, sjogren’s condition
- porphyria cutanea tarda (PCT)-vampire’s disease affecting the skin. Skin becomes v photosensitive, person starts to develop blisters and hyperpigmentation
A 43-year-old woman comes to the emergency department because of palpitations for the past hour after consuming a lot of aspirin in a suicide attempt. An arterial blood gas is drawn and shows the following results:
PaO2 98 mmHg (13.1 kPa)
pH 7.64
PaCO2 20 mmHg (2.71 kPa)
HCO3- 23 mmol/L
Which of the following is most consistent with her results?
How do you treat this?
- Aspirin overdose- causing overstimulation of RO causing respiratory alkalosis
Management
- Oral charcoal to reduce absorption
- Gastric lavage to remove toxic products from stomach
What are the 3 causes of jaundice?
How do you investigate this?
Jaundice is hyperbilirubinemia typically becoming symptomatic when it is more than 50 micromol/l
Types:
- Pre-hepatic jaundice
- due to haemolytic anaemias causing increase in unconjugated bilirubin
- urine and stool is normal colour
- Congenital jaundice
- Gilbert’s syndrome where there is dysfunction in UDP glucoronyl transferase; or Crigler Najar syndrome when there is no UDP glucoronyl transferase
- urine and stool is normal colour
- Hepatic jaundice
- alcoholic hepatitis; viral hepatitis; liver cirrhosis; hepatocellular carcinoma; haemchromatosis/wilson’s; medication
- urine dark and stool is normal
- Post hepatic jaundice
- intraluminal: gallstones
- mural: primary biliary cirrhosis/primary sclerosing cholangitis, cholangiocarcinoma
- extramural: pancreatic cancer, pancreatic pseudocyst etc.
Investigation
- LFTs
- coagulation-prothrombin increased
- liver screen-hepatitis screen and autoimmune markers
- ultrasound-if they suspect gallstone
- MRCP
A 63-year-old man has lost 10kg in weight and become increasingly jaundiced over the last 4 weeks. He has no abdominal discomfort but his urine has become very dark and his stools pale in colour. He drinks
15 units of alcohol per week. An ultrasound scan of the liver shows a dilated common bile duct. Which single set of liver function test results would confirm the most likely diagnosis?
- Cholestatic picture (C)-Bilirubin, ALP, GGT raised.
The scenario suggests a diagnosis of cholestatic jaundice, compatible with
biliary obstruction due to a pancreatic mass.
A Raised ALP (normal GGT) suggests a bone source for the ALP.
B This indicates Gilbert’s syndrome.
D This is a mixed hepatitic–cholestatic picture.
E This indicates hepatitis.
A man consumes between 100 and 150 units of alcohol per week. He has slight ascites but no evidence of encephalopathy.
Prothrombin time: 3s > normal.
The doctor who sees him uses the Child–Pugh grading system to assess his risk of variceal bleeding. Which single pair of additional variables should be used to grade his risk?
A Age + urea
B Alanine transferase + amylase
C Bilirubin + albumin
D Creatinine + sodium
E Platelet count + ferritin
What causes grade A, B,C?
- Child-Pugh grading system measures the extent of liver cirrhosis and risk of variceal bleeding. It consists of these variables
- bilirubin (high)
- albumin (low)
- prothrombin time (elevated due to lack of anticoagulants)
- hepatic encephalopathy
- ascites
- Grade A-7
- Grade B-7-9
- Grade C->9
