HPB Medicine Flashcards
ACTUTE AND CHRONIC HEPATITIS: Describe the morphology and pathological consequences of acute and chronic hepatitis
Morphology:
Acute hepatitis - ‘lobular disarray’
Chronic hepatitis - Fibrosis, characterised by portal inflammation and necroinflammatory activity and fibrosis
Pathological consequences:
- Progression to cirrhosis
- Decompensated liver failure: Hepatitic encephalopathy, ascites, coagulopathy/bleeding (varices), hepatorenal syndrome (hyponatraemia, elevated creatinine)
ACUTE AND CHRONIC HEPATITIS: Describe the features of drug induced liver injury (including paracetamol overdose)
Paracetamol overdose:
- Elevated liver enzymes (hepatocellular injury due to build up of toxic metabolites)
- Deranged clotting screen (if hepatic synthetic function is disrupted) - INR
- Typically, asymptmatic until 24 hrs after ingestion or develop anorexia/nausea/vomiting
- Symptoms/signs start to develop after 24hrs: RUQ pain, metabolic acidosis, hypotension, hypoglycaemia, pancreatitis and arrhythmias
- Liver damage is not detectable on blood tests until 18 hours after ingestion
- Renal failure, due to ATN, may occur
Features of drug induced liver injury:
- Hepatocellular predominant liver injury
- Elevated AST and ALT
- ALT is more specific for hepatocellular injury
ACUTE AND CHRONIC HEPATITIS: Describe the causes of acute and chronic hepatitis
Acute hepatitis
- DILI (drug induced liver injury)
- Infection e.g. viral
- Acute alcoholic hepatitis
- Autoimmune hepatitis
- Ischaemic hepatitis
Chronic hepatitis
- Infection - viral
- Autoimmune
- Alcoholism
- NAFLD
- Drug induced
- Metabolic conditions e.g. Wilson’s disease, haematochromatosis
- Ischaemic hepatitis (secondary to heart failure)
ACUTE AND CHRONIC HEPATITIS: Discuss the diagnosis and investigation of a patient with jaundice
Diagnostic work up:
- FBC:
- Low plts1
- ?anaemia if bleeding suspected
- LFTs:
- Elevated ALP and gGT suggest obstructive jaundice
- PT and INR (plus albumin)
- Checks synthetic function of the liver
- U&Es
- ?hepatorenal syndrome
- Bilirubin levels:
- Conjugated vs unconjugated
- Unconjugated for pre-hepatic and mixed for hepatic
- Virology: May allow cause to be identified
- Abdominal USS
- Look for bile duct dilatation
- Look for possible cause of obstruction
- ?Pancreatic cancer
- CT CAP - if suspected malignancy
Investigation looks to identify whether jaundice is pre-hepatic, hepatic or post-hepatitic in nature
1: Low plts are seen due to reduced production of TPO and destruction of plts by the spleen (portal hypertension → redistribution of blood and platelets to the spleen)
ACUTE AND CHRONIC HEPATITIS: Outline the clinical presentation of acute and chronic hepatitis including relevant features in the medical history
Features in the medical hx:
- Onset: Acute vs chronic as an indication of the cause
- Associated symptoms
- Jaundice, bleeding, ascites, hepatitic encephalopathy
- Pain - Usually present with mechanical obstruction of the cystic duct or CBD e.g. ?cholelithiasis/cholecystitis. Pain is often absent in pancreatic and biliary malignancies
- Fever - ?cholecystitis
- Fatigue, anorexia, pruritis, weight loss, nausea/vomiting, RUQ pain
- Risk factors for different aetiologies:
- Viral hepatitis: IVDU, tattoos, Sexual Hx - unprotected sex, anoreceptive sexual intercours; Alcohol intake
- Features of other infections: Sore throat and lymphadenopathy in EBV and CMV
- Diet (if ?gallstones)
- Medical conditions that may cause liver damage
- Personal or FHx of autoimmune disease
- Previous episodes of hepatic symptoms
ACUTE AND CHRONIC HEPATITIS: Outline the treatment options for hepatitis due to autoimmunity, hepatitis B or C and paracetamol overdose
Autoimmunity
- Corticosteroids +/- immunosuppressant therapy (dependent upon severity)
- Findings: Raised AST and ALT, elevated serum gamma-globulin (IgG) level
Hepatitis C
- Antiviral therapy
Hepatitis B
- Interferon-alpha
- Antivirals may be considered second line
Paracetamol overdose
- Check for complications - renal failure1, hypoglycaemia, metabolic acidosis
- If < 8 hours since ingestion - activated charcoal
- NAC
- Nausea/vomiting is common following adminsitration. Antiemetic should be considered
- Fluids
1: Renal failure may manifest as loin pain, haematuria or proteinuria. Serum creatinine may also be elevated. ?cause - may be ‘acute’ hepatorenal syndrome
ACUTE AND CHRONIC HEPATITIS: Outline the indications for and dicuss contraindications of liver biopsy in hepatitis
Indications:
- Clinical picture suggestive of hepatitis/fibrosis/cirrhosis without an immediate cause identified
- Viral
- Autoimmune
- AFLD or NAFLD
- Suspected malignancy
- Diagnostic and evaluation of severity
Contraindications for percutaneous liver biopsy:
- Coagulopathy
- INR < 1.5
- Low platelet count
- If so, transjugular biopsy may instead be performed (with FFP)
- Complications include bleeding, bowel perforation and pneumothorax
ACUTE AND CHRONIC HEPATITIS: Be aware of other investigations
- Fibroscan
- Ultrasound
- Blood tests: Clotting, albumin, U&Es (sodium, creatinine), LFTs, platelet count (splenic sequesting)
LIVER NEOPLASMS, ABSCESS AND CYSTS: Compare and contrast the pathology and natural histories of liver neoplasia, abscesses and cysts
LIVER NEOPLASMS, ABSCESS AND CYSTS: Describe the symptoms and signs associated with liver abscess
- RFs for liver abscess present e.g. possible route of infection
- Biliary tract disease, hepatic/biliary intervention, sepsis, DM, malignancy
- RUQ pain
- Fever/chills (swinging fever)
- Hepatomegaly
- Nausea and vomiting
- Non-specific symptoms: Weight loss, fatigue, abdo pain
LIVER NEOPLASMS, ABSCESS AND CYSTS: List the investigations that differentiate neoplasia, abscesses and cysts - outlining their treatment options
LIVER NEOPLASMS, ABSCESS AND CYSTS: Outline the aetiology and pathology of primary and secondary liver neoplasms
Primary Liver Neoplasms
Aetiology:
- Secondary to chronic liver disease/cirrhosis e.g. hepatitis, NAFLD, AFLD, autoimmune, metabolic
- Often remains asymptomatic for long periods, presenting with non-specific symptoms of fatigue, weight loss, anorexia, nasuea and abdo pain. Jaundice and pruritis often develop later on.
Pathology:
- Hepatocellular carcinoma (90%) (AFP)
- Cholangiocarcinoma (10%) - associated with PSC (CA19-9)
- Benign neoplasms include haemangiomas and focal nodular hyperplasia (often related to oestrogen, hence more common in women and those on the COCP)
Secondary Liver Neoplasms
Aetiology:
- 90% of liver neoplasms are metastases
- Commonly from the lung, stomach, colon, breast and uterus
Pathology:
CHRONIC LIVER DISEASE: Define cirrhosis in pathological terms
Cirrhosis: An irreversible pathological result of chronic liver inflammation, which leads to fibrosis and the formation of nodules. There is destruction of hepatocytes.
CHRONIC LIVER DISEASE: Describe the morphology and pathological consequences of cirrhosis
Morphology
- Distortion of the hepatic architecture and dense bands of fibrosis, leading to nodules of hepatocytes
Pathological consequences
- Decompensated Liver failure
- Hepatic encephalopathy, ascites (→SBP), bleeding (sythetic function disruption and varices), hepatorenal syndrome and hepatocellular carcinoma
- Jaundice
- Loss of hepatic synthetic function → bleeding, hypoalbuminaemia
- Hyponatraemia
- Elevated urea and creatinine (due to hepatorenal syndrome)
*
CHRONIC LIVER DISEASE: Describe the investigation of a patient with suspected cirrhosis
Bloods
- Clotting: PT/INR, PTT
- Platelet count: Thrombocytopenia is highly sensitive and specific1
- Albumin levels
- LFTs: Reranged LFTs
- U&Es: Hyponatraemia, elevated urea and creatinine may be seen due to hepatorenal syndrome
- AFP: Elevated in malignancy
Imaging
USS: Nodularity, ‘corkscrew’ appearance to the arteries, enlarged portal vein with reduced flow, ascites, splenomegaly
Fibroscan reveals reduced elastisticy
Endoscopy: Diagnostic and therapeutic potential for varices
CT and MRI: Check for neoplasms
Liver biopsy: Confirms diagnosis. Architectural disruption with formation of regenerative nodules.
Investigations to establish possible cause
- Autoantibodies: PBS
- Viral serology
- Serum ceruloplasmin (reduced in Wilson’s disease - excess Cu2+)
- Haemochromatosis: Elevated total iron, transferrin saturation and ferritin with reduced TIBC
1: Thrombocytopenia is resultant of platelet sequestration by the liver
CHRONIC LIVER DISEASE: Discuss how to establish the diagnosis of the cause of cirrhosis
Assessing Severity
- Child-Pugh Score for Cirrhosis
- Uses bilirubin, albumin, INR, ascites ans encephalopathy to assess the severity and prognosis of cirrhosis
- MELD score
- Used every 6/12 to assess patients with cirrhosis
Possible causes and associated investigations
- NAFLD
- Biopsy
- Enhanced Liver Fibrosis (ELF) blood test
- AFLD
- Autoimmune causes
- ANA and anti-smooth muscle Igs raised in autoimmune hepatitis
- PBS - Elevated AMA (anti-mitochondrial antibody)
- Metabolic disease
- Wilson’s disease - Serum ceruloplasmin
- Alpha-1 antitypsin deficiency
- Haemachromatosis - Total iron, TIBC, transferrin saturation and ferritin
- Hepatitis
- HCV IgG = chronic HCV infection
- HBV surface antigen = infection
CHRONIC LIVER DISEASE: Outline the pathophysiology underlying the clinical features of cirrhosis
Hepatic encephalopathy: Due to retention of urea, crosses the BBB
Ascites: Due to hypoalbuminaemia and fluid retention
Asterixis: Due to retention of urea
Hepatorenal syndrome: Reduced renal blood flow leads to RAAS activation, eventually renal perfusion is permanently reduced and AKI results
Thrombocytopenia: Splenic sequestration
Splenomegaly: Due to venous congestion
Bleeding (varices): Reduced synthetic function of the liver and portal hypertension
Jaundice – caused by raised bilirubin
Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
Splenomegaly – due to portal hypertension
Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
Palmar Erythema – caused by hyperdynamic cirulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising – due to abnormal clotting
Ascites
Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease
CHRONIC LIVER DISEASE: Describe the clinical features of complications of cirrhosis and portal hypertension. Outline their management
Clinical features and management
Malnutrition: Regular meals, low sodium with high protein and calorie content
Hepatic encephalopathy:
- Pathophysiology: Ammonia is produced by the breakdown of proteins by intestinal bacteria, it is then absorbed by the gut
- Laxatives - promote ammonia excretion
- Abx - reduced the number of ammonia producing intestinal bacteria
- Nutritional support - low protein diet. May require NG feeding
Portal hypertension
- Beta-blocker - propranolol to reduce portal hypertension
- Varices: Endoscopy +/- banding if required. Haemodynamic stabilisation, terlipressin and abx in acute bleeding
- TIPS (transjugular intra-hepatic portosystemic shunt): Used if medical and endoscopic treatment fails
Hepatorenal syndrome:
- Liver transplant
Ascites:
- Anti-aldosterone diuretics (spironolactone): To reduce Renin driven fluid reabsorption and sodium retention
- Paracentesis (ascitic tap or drain)
- Low sodium diet
- Prophylactic abx to prevent SBP
- TIPs or transplantation for refractory peritonitis
PORTAL HYPERTENSION: Describe portal venous anatomy
Portal venous system: Venous drainage for the alimentary system, carrying nutrient rich blood to the liver.
The portal vein is formed by the union of the splenic vein and the SMV.
Upon entering the liver the portal vein divides into right and left branches.
PORTAL HYPERTENSION: Define portal hypertension and classify its causes
Portal hypertension: Increased back-pressure within the portal system.
Causes:
Pre-hepatic: Portal vein thrombosis or obstruction
Hepatic: Cirrhosis; acute hepatitis; schistomiasis; congenital hepatic fibrosis
Post-hepatic: Compression (e.g. malignancy); Budd-Chiari syndrome- constrictive pericarditis; R sided heart failure
PORTAL HYPERTENSION: Describe the clinical manifestations of portal hypertension
Varices, +/- bleeding
- Oesophageal, periumbilical, rectal
Clinical signs
- Caput medusa
- Splenomegaly
- Haemorrhoids
- Ascites
- Hepatic encephalopathy (toxins bypass the liver via shunt due to increased pressure)
PORTAL HYPERTENSION: Outline the treatment methods available for bleeding oesophageal varices
General management of varices
- Beta-blockers
- Banding
Bleeding varices
- A-E approach, fluid resuscitation
- Pharmacological: Beta-blockers, terlipressin and abx
- Banding
- Balloon tamponade (can be used as a bridge to more definitive treatments)
- TIPS (transjugular intrahepatic portosystemic shunt)
ACUTE AND CHRONIC GALLBLADDER DISEASE AND CARCINOMA OF THE BILIARY TRACT: Define the following: Murphy’s sign, Courvoisier’s sign, T-tube and gallstone ileus
Murphy’s sign: Apply pressure in the RUQ, ask the pt to breathe in. If inspiration is hindered by pain then inflammation is likely e.g. cholecystitis.
Courvoisier’s sign: Painless jaundice, in the presence of a palpable gallbladder is unlikely to be due to gallstones. It is likely to be due to an obstructing pancreatic or biliary neoplasm.
T tube: A drainage tube placed in the common bile duct following CBD exploration, cholecystectomy or liver transplant.
Gallstone ileus: Fistula between the biliary tree and dueodenum allows passage of a gallstone into the duodenum, causing small bowel functional obstruction
DIAGNOSTIC STUDIES IN BILIARY TRACT DISEASE: Contrast changes in liver function tests in obstructive and hepatocellular jaundice
Obstructive jaundice:
Elevated conjugated bilirubin, ALP and gammaGT
Hepatocellular jaundice:
Elevated unconjugated bilirubin, AST and ALT
