Hepatobiliary Flashcards
Presentation of acute pancreatitis
Abdominal pain (epigastric, radiation to back, persists for days, reaches max intensity over 30-60min then remains stable) Nausea, vomiting
Tachycardia Hypotension Tachypnoea Reduced saturations Guarding of the abdomen
Cullen’s and Grey Turners sign may also be present
Cullen’s sign
Superficial oedema and bruising around the umbilicus
Grey Turner’s sign
Bruising on the flanks of the body
- sign of retroperitoneal haemorrhage
- takes 24-48 hours to develop
Causes of chronic liver disease
NASH
Alcoholic SH
Chronic viral hepatitis (hep B/C)
Autoimmune/ Cholestasis (primary biliary cirrhosis, primary sclerosing cholangitis)
Inherited metabolic disorders (haemochromatosis, Wilson’s disease
Hep B serology
HBsAg = active infection (acute or chronic)
Anti-HBs = Immunity (vaccination or cleared infection)
Anti-HBc - infection (past or current)
Management chronic Hep B
No cure
Reduce risk of other liver diseases
Entecavir or tenofovir
Hepatitis C serology
Anti-HCV antibody
HCV RNA qualitative PCR
Management of chronic hep C
Genotype 1: telaprevir/boceprevir + Peg-IFNa + ribavirin
Other genotypes: Peg-IFNa + ribavirin
Management of primary biliary cirrhosis
Ursodeoxycholic acid/UDCA (reduces gallstones)
Liver transplant if severe
Diagnosis of primary biliary cirrhosis
Raised ALP and bilirubin
Antimicrobial antibodies
ANA
Liver biopsy (lymphocytic invasion of ducts)
Diagnosis of primary sclerosing cholangitis
Cholestatic picture in LFTs
+ve pANCA
MRCP/ERCP - multifocal stricturing
Management of primary sclerosing cholangitis
High dose UDCA (ursodeoxycholic acid)
Endoscopic dilatation of dominant structures
Liver transplantation
Symptom relief
Cirrhosis staging
Child-Pugh score: Total bilirubin (34-50) Serum albumin (3.5-2.8) PT INR (1.7-2.3) Ascites Hepatic encephalopathy
Child pugh score and prognosis
5-6 = A 100%1y, 85% 2y 7-9 = B 80% 1y, 60% 2y 10-15 = C 45% 1y, 35% 2y
Complications of cirrhosis
Ascites Oesophageal/gastric varices Spontaneous bacterial peritonitis Hepatic encephalopathy Pulmonary syndromes Hepatocellular cancer Hepatorenal syndrome
Ascitic tap fluid
Serum ascites-to-albumin gradient (SAAG)
- over 11g/L - portal hypertension cause of ascites
- Less than 11g/L - consider infectious or malignant cause
Blood cell count:
- High RBCs - traumatic tap? HCC? Ruptured omental varix?
- High PMNs - infection
Culture
+/- amylase or cytology
Management of ascites
Small:
- dietary sodium restrictions (6-8g/day)
Moderate:
- diuretic therapy (spironolactone +/- frusemide)
Refractory:
- repeated large-volume paracentesis
- transjugular intrahepatic portosystemic shunt
What is hepatic hydrothorax?
Flow of ascitic fluid into the thoracix cavity due to a tear in the diaphragm
More common on the right side
Prognosis following onset of ascites in chronic liver disease
Poor. Less than 50% will survive 2y after onset of ascites
Definition of spontaneous bacterial peritonitis
A common and severe complications of ascites characterised by spontaneous infection of the ascitic fluid without an intraabdominal source
Most common organisms implicated in spontaneous bacterial peritonitis
E. coli Other gut bacteria S. viridans S. aureus Enterococcus
If more than 2 organisms identified ?perforated viscus
Management of spontaenous bacterial peritonitis
Cefotaxime or another 2nd generation cephalosporin
Definition of hepatic encephalopathy
AKA portosystemic encephalopathy, an alteration in mental status and cognitive function in the presence of liver failure due to vascular shunting allowing nitrogenous metabolites to bypass hepatic filtration, thus reaching the brain and causing damage to neurons
Clinical features of hepatic encephalopathy
Confusion
Change in personality (violent, difficult to manage)
Sleepy, difficult to rouse
Asterixis/hepatic flap
Management of hepatic encephalopathy
management of precipitating factors (hydration and correction of electrolytes may be all the treatment required)
Lactulose (elimination of nitrogenous products in the gut via cathartis)
Investigations in HCC
Alpha fetoprotein (only increased in 50%)
AFP-L3 is more specific
Imaging: USS liver, triphasic CT abdo/pelvis
Core liver biopsy
- allows distinction between HCC and adenocarcinoma
- higher bleeding risk compared to other cancers
Staging of HCC
Based on tumour number and extent
Child-Pugh score
AFP level
Portal vein thrombosis
Management options of HCC
Presence of cirrhosis usually restricts surgical resection, ablative therapies and CTx
Resection
Transplant
Local injection therapy (ethanol - max tumour size 3cm)
TACE (transcatheter arterial chemoembolisation)
New agents (sorafenib, bevacizumab + erlotinib)
Radiation therapy (if less than 2cm)
Stats regarding HCC site
75% portal vein invasion
75% bilobar
65% have 3 or more distinct tumours present
Causes of HCC
Hepatitis
- Chronic HBV (only 50% have cirrhossi)
- Chronic HCV (only after cirrhosis)
Cirrhosis of any cause (less so for PBC or haemochromatosis)
Alfatoxin B1 (product of aspergillus) found in stored grains/rice/peanuts in humid conditions
Average survival for HCC
6 months
Less than 5% 2 year survival if unresectable HCC
High recurrence regardless of treatment
Definition of biliary colic
Pain associated with the temporary obstruction of the cystic or common bile duct by a stone migrating from the gall bladder
Types of biliary stones
Black pigment gallstones:
- calcium bilirubinate + mucin glycoproteins + salts e.g. calcium carbonate
- range in colour from deep black to very dark brown
- glass-like cross-sectional surface on fracturing
Brown stones:
- muddy hue
- alternating brown/tan layers on cross-section
- calcium salts of fatty acids + calcium bilirubinate
- almost always found in presence of stasis and/or infection
- most common cause of recurrent bile duct stones following cholecystectomy
Clinical features of biliary colic
Abdominal pain:
- epigastric
- radiation to R shoulder tip
- severe
- constant with cresecendo characteristic
- often following over indulgence with food (esp. high fat content)
Nausea/vomiting
Spontaneous cessation of attack after a number of hours or terminated by opiate analgesia
more protracted pain, esp with fevers and rigors, suggests secondary complications such as cholecystitis, cholangitis or gallstone-related pancreatitis
Management of biliary colic
Opiate analgesia
Stone extraction via ERCP
OR
Laparoscopic cholecystectomy with bile duct exploration
Cholecystectomy to prevent recurrence in surgical candidates
Complications of biliary colic
Gallstone pancreatitis
Acute cholangitis
Presentation of acute/ascending cholangitis
Charcot’s triad:
- fever
- jaundice
- abdominal pain
Management of acute cholangitis
Antibiotics (ampicillin or tazocin)
Causes of acute cholecystitis
Gallstones (95%) Ischaemia in critically ill patient Infection, especially in AIDs (CMV, cryptosporidium) Bile duct strictures Neoplasms
What is Mirizzi syndroem
Mild jaundice in acute cholecystitis caused by external compression of the common bile duct by a stone within the gallbladder or cystic duct
USS findings of cholecystitis
Shadowing of stones
Dilated gallbladder with thickened wall
Surrounding oedema
Management of cholecystitis
nil by mouth IV fluids Opiate analgesia IV antibiotics (local policy) - extended-spectrum cephalosporins - fluoroquinolones - tazocin
Cholecystectomy delayed for a few days to allow symptoms and inflammation to settle
Complications of acute cholecystitis
Empyema or gangrene
failure to respond to conservative management (especially if increased pain and fever)
URGENT IMAGING
Surgical intervention required
Risk factors for acute pancreatitis
Gallbladder disease
Chronic alcohol consumption
Autoimmune disease (E.g. SLE)
Congenital anomalies
Causes of acute pancreatitis
Gallstones (70-80%) Chronic alcohol binges Other drugs/toxins Metabolic (hyperlipidaemia, hypercalcaemia) Trauma (most commonly post-ERCP) Non-gallstone obstruction of pancreatic duct (stricture, neoplasm, sphincter of Oddi dysfunction) Infections (CMV, mumps, rubella) Genetics (CF) Autoimmune Idiopathic
Investigations in acute pancreatitis
Amylase and lipase- 3x upper limit of normal
Blood urea nitrogen
CBE (raised haematocrit and WCC)
Liver enzymes (ALT ?gallstones)
CT abdo - pancreatic necrosis best seen approx 3 days after presentation
MRCP if gallstones suspected
grading severity of acute pancreatitis
APACHE II Takes into account 12 continuous variables 1. body temp 2. mean arterial pressure 3. heart rate 4. respiratory rate 5. oxygenation 6. sodium 7. potassium 8. phosphate 9. creatinine 10. haematocrit 11. WCC 12. GCS
Management of acute pancreatitis
General supportive care - Nil by mouth until bowel sounds and appetite return - Parenteral opioids - IV fluid repletion - anti-emetics (IV promethazine) Treatment of complications
Complications of chronic pancreatitis
Pancreatic pseudocyst
Ascites, pleural effusions
Pancreatic cancer
Definition of pancreatic pseudocyst
Fluid collection in the pancreas surrounded by granulation tissue occurring in a period of enhanced inflammatory activity with abdominal pain
Most common type of pancreatic cancer
Adenocarcinoma (96%)
mostly of ductal origin
Most commonly in the head of the pancreas
Hereditary pancreatic cancer syndromes
BRCA2
Familial atypical multiple mole melanoma
Peutz-Jeghers syndrome
Hereditary pancreatitis
What is Courvoisier’s law
In the presence of an enlarged, non-tender gallbladder + mild jaundice, the diagnosis is unlikely to be gallstones and more likely to be malignancy of the head of the pancreas
Presentation of carcinoma of head of pancreas or ampulla of vater
Painless
Jaundice
Scratch marks/pruritus
palpable gall bladder
thromboembolic phenomena
Polyarthritis
Skin nodules
Complications of carcinoma of the head of the pancreas
Episodes of acute pancreatitis
Pancreatic damage - abnormal glucose homeostasis
Presentation of carcinoma of the body or tail of the pancreas
Abdominal pain (dull, radiating to back, partial relief by sitting forward) Non-specific (anorexia, weight loss)
thromboembolic phenomena
Polyarthritis
Skin nodules
investigations in pancreatic cancer
Transabdominal ultrasound - less reliable in picking up tumours in body and tail due to overlying bowel
Contrast CT
Laparoscopy
ERCP (restricted to palliative treatment usually, provide source of cytology if unclear)
Percutaneous needle biopsy (discouraged in operable cases, essential prior to palliative chemotherapy)
Tumour marker CA19-9
Associated with CA19-9
Pancreatic cancer
Which tumour marker is associated with pancreatic cancer
CA19-9
Red flags of chronic diarrhoea/abdominal pain (i.e. not IBS)
Weight loss Rectal bleeding Onset after 55y Nocturnal pain Family history of malignancy or IBD Abnormal examination (mass, enlarged LN, muscle wasting, +ve FOBT etc.) Abnormal laboratory investigations
Management of IBS
Low FODMAP diet
High-fibre intake
Avoid aggravating foods, caffeine, dairy, fatty foods
CBT (if psychosocial stressors are important triggers)
Regular exercise, adequate fluid intake
Sedatives of SSRIs (esp in patients who appear anxious)
