HPB Flashcards
Gallstone pathophysiology
Bile is formed from cholesterol, phospholipids and bile pigments
Form as a result of supersaturation of bile:
1) Cholesterol stones – excess cholesterol production
2) Pigment stones – excess bile pigment production (commonly seen in those with known haemolytic anaemia)
3) Mixed stones – cholesterol and bile pigments
Gallstone risk factors
Fat
Female
Forty
Fertile
Family history
Pregnancy, oral contraceptives, haemolytic anaemia & malabsorption
Biliary colic
Gallbladder neck is impacted by a gallstone
No inflammatory response, but contraction of the gallbladder against the occluded neck will result in pain
Pain – sudden, dull & colicky, focused in the RUQ but may radiate to the epigastrium/back, may be precipitated by fatty foods
Acute cholecystitis
Constant pain in RUQ or epigastrium, associated with signs of inflammation
Tender in the RUQ & may demonstrate a positive Murphy’s sign
Gallstone and acute cholecystitis investigations
Lab test
* FBC & CRP
* LFTs
* Amylase
Imaging – trans-abdominal ultrasound is first line
* MRCP is gold standard if US scans are inconclusive
Biliary colic management
Should be prescribed analgesia
Patient should be advised about lifestyle factors
Elective laparoscopic cholecystectomy is warranted & should be offered within 6 weeks of first presentation
Acute cholecystitis management
Should be started on appropriate IV abx (co-amoxiclav +/- metronidazole)
Laparoscopic cholecystectomy is indicated within 1 week of presentation, ideally within 72 hours of presentation
For those not fit for surgery & not responding to antibiotics, a percutaneous cholecystostomy can be performed to drain the infection
Mirizzi syndrome
Stone located in Hartmanns pouch/cystic duct itself can cause compression of the adjacent hepatic duct
Results in obstructive jaundice
Diagnosis is confirmed by MRCP & management is usually with laparoscopic cholecystectomy
Gallbladder empyema
Gallbladder becomes filled with pus
Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis
Condition is diagnosed by either US scan/CT scan
Treatment – via laparoscopic cholecystectomy/percutaneous cholecystostomy (if unsuitable for surgery)
Chronic cholecystitis
Typically have a history of recurrent/untreated cholecystitis -> led to persistent inflammation of the gallbladder wall
Patients present with ongoing RUQ/epigastric pain with associated N&V
Diagnosed typically by CT imaging
Management – uncomplicated cases is via elective cholecystectomy
Main complications – gallbladder carcinoma & biliary-enteric fistula
Bouveret’s syndrome and gallstone ileus
Inflammation of the gallbladder can cause a fistula to form (cholecystoduodenal fistula) allowing gallstones to pass directly into the small bowel
Bouveret’s syndrome – stone impacts in the proximal duodenum, causing a gastric outlet obstruction
Gallstone ileus – a stone impacts at the terminal ileum, causing small bowel obstruction
Pre-hepatic jaundice
Excessive red cell breakdown -> overwhelms the liver’s ability to conjugate bilirubin
Causes an unconjugated hyperbilirubinemia (remains in the blood steam to cause jaundice)
E.g. haemolytic anaemia, Gilbert’s syndrome
Hepatocellular jaundice
Dysfunction of the hepatic cells
Loses the ability to conjugate bilirubin & also causes where it may become cirrhotic -> compresses the intra-hepatic portions of the biliary tree to cause a degree of obstruction
Both unconjugated and conjugated bilirubin
e.g. alcoholic liver disease, viral hepatitis, hereditary haemochromatosis
Post-hepatic jaundice
Obstruction of biliary drainage
Conjugated hyperbilirubinemia
e.g. gallstones, cholangiocarcinoma, strictures, pancreatic cancer
Cholangiocarcinoma risk factors
Primary sclerosing cholangitis
Congenital – Caroli’s disease, choledochal cyst
Intraductal gallstone formation
Infective – liver flukes, hepatitis
Toxins – chemicals in rubber & aircraft industry
Liver cirrhosis
Cholangiocarcinoma clinical features
Intrahepatic – generally asymptomatic until a late stage in the disease
Extrahepatic – typically present early
Jaundice, pruritus, steatorrhea, non-specific abdominal pain, dark urine
Courvoisier’s law
In the presence of jaundice and an enlarged/palpable gallbladder, malignancy of the biliary tree/pancreas should be strongly suspected as the cause is unlikely to be gallstones
Cholangiocarcinoma investigations
Bloods – elevated bilirubin, ALP & yGT
Tumour markers – CEA and CA19-9 may also be elevated
MRCP – gold standard imaging modality
CT, ERCP/PTC (obtain tissue brushings for cytological diagnosis)
Triple phase CT imaging/contrast-enhanced MRI of the liver – staging of the disease
Cholangiocarcinoma management
Definitive cure – complete surgical resection (only 10-15% patients are suitable)
Both chemotherapy and radiotherapy may be used in some cases as adjuvant treatments after surgery
Palliative
1) Stenting – relieve obstructive symptoms
2) Surgery – bypass procedures if obstruction cannot be relieved by stenting
3) Medical – palliative radiotherapy/chemotherapy
Cholangitis
Infection of the biliary tract
Caused by a combination of biliary outflow obstruction & biliary infection
During an obstruction, stasis of fluid allows bacterial colonisation of the biliary tree to become pathological
Cholangitis causes
(any condition that causes occlusion of the biliary tree)
Gallstones
ERCP
Cholangiocarcinoma
Most common infective causes – E coli, Klebsiella species & enterococcus
Cholangitis clinical presentation
Charcot’s triad – jaundice, fever, RUQ pain
Reynold’s pentad – jaundice, fever, RUQ pain, hypotension & confusion
Cholangitis investigations
Routine bloods – esp, FBC & LFTs
Blood cultures – should always be taken in suspected cases
Imaging – biliary tract USS, ERCP is gold standard as it is both diagnostic & therapeutic
Cholangitis management
Immediate – IV access, fluid resus, routine bloods, blood cultures, broad spectrum IV abx (co-amoxiclav & metronidazole)
Definitive – endoscopic biliary decompression, ERCP should clear any obstruction (PTC is second line for patients too unwell)
Complications of ERCP
Repeated cholangitis
Pancreatitis
Bleeding
Perforation
Hepatocellular cancer aetiology
Arises as a result of a chronic inflammatory process affecting the liver (80-90% seen with background of established liver cirrhosis)
Mainly due to viral hepatitis, other causes: chronic alcohol excess, hereditary haemochromatosis, PBC
Hepatocellular cancer risk factors
Liver cirrhosis
Aflatoxin exposure
Hepatocellular adenoma
Smoking
Advancing age
Positive family history
Hepatocellular cancer clinical features
Many cases picked up on surveillance imaging
Fatigue, weight loss
Examination – irregular enlarged liver, features of decompensated liver disease (ascites, jaundice or confusion)
Hepatocellular cancer investigations
Routine bloods, AFP
Imaging – USS in screening, MRI/CT are both useful to further assess lesions
Biopsy can be obtained for histological diagnosis by either ultrasound-guided/CT-guided percutaneous biopsy
Hepatocellular cancer management
Decided by discussion by a MDT
Curative options – liver transplantation/liver resection, ablative techniques
Metastatic disease – systemic therapies are indicated
Acute pancreatitis
Inflammation of the pancreas
Distinguished from chronic pancreatitis by its limited damage to the secretory function of the gland
Acute pancreatitis aetiology
Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune disease – SLE/Sjogren’s syndrome
Scorpion venom
Hypercalcaemia
ERCP
Drugs – azathioprine, NSAIDs/diuretics
Acute pancreatitis pathophysiology
Each cause will trigger a premature and exaggerated activation of digestive enzymes in the pancreas
Pancreatic inflammatory response -> increase in vascular permeability & subsequent fluid shifts
Enzymes are released into systemic circulation -> autodigestion of fats & blood vessels
Fat necrosis can cause release of free fatty acids -> react with calcium, resulting in hypocalcaemia
Eventually -> partial/complete necrosis of the pancreas
Acute pancreatitis clinical features
Severe epigastric pain, which can radiate through to the back, with nausea & vomiting
Examination – often epigastric tenderness, Cullen’s sign (bruising around the umbilicus) & Grey Turner’s sign (bruising in the flanks) – representing retroperitoneal haemorrhage
Tetany (from hypocalcaemia)
Acute pancreatitis investigations
Serum amylase/serum lipase – diagnostic if 3x the upper limit of normal
LFTs – assess for any cholestatic element to the clinical picture
Acute pancreatitis risk scoring
Modified Glasgow criteria – assess the severity of acute pancreatitis within the first 48 hours of admission (> 3 = severe pancreatitis)
PO2 < 8kPa
Age > 55 yrs
Neutrophils > 15 x 10*9L
Calcium < 2mmol/L
Urea > 16mmol/L
LDH > 600U/L or AST > 200U/L
Albumin < 32g/L
Sugar > 10mmol/L
Acute pancreatitis imaging
Abdominal USS
(not routinely performed but AXR can show sentinel loop sign = dilated proximal bowel loops adjacent to pancreas)
Contrast-enhanced CT scan (after 48hrs of initial presentation) – pancreatic oedema, swelling, pancreatic necrosis
Acute pancreatitis management
No curative management, treat any underlying cause
IV fluid resus & oxygen therapy as required
NG tube if patient is vomiting
Catheterisation & fluid balance chart
Opioid analgesia
Broad-spectrum abx should be considered for prophylaxis in cases of confirmed pancreatic necrosis
Acute pancreatitis systemic complications
Disseminated intravascular coagulation
Acute respiratory distress syndrome
Hypocalcaemia
Hyperglycaemia
Acute pancreatitis local complications
Pancreatic necrosis – should be suspected in patients with evidence of persistent systemic inflammation > 7-10 days, confirmed by CT imaging, treatment is pancreatic necrosectomy, prone to infection (can be confirmed by a fine needle aspiration of the necrosis)
Pancreatic pseudocyst – collection of fluid (pancreatic enzymes, blood & necrotic tissue) anywhere within or adjacent to the pancreas (usually seen in lesser sac), may be found incidentally on imaging/present with symptoms of mass effect, surgical debridement/endoscopic drainage if they don’t spontaneous resolve
Chronic pancreatitis
Chronic fibro-inflammatory disease of the pancreas, resulting in progressive & irreversible damage to parenchyma
Male to female 4:1, average onset of 40 years
Chronic pancreatitis aetiology
Chronic alcohol abuse
Idiopathic
Less common – metabolic, infection, hereditary, autoimmune, anatomical or congenital anomalies
Chronic pancreatitis clinical features
Chronic pain – epigastrium and back, often associated with N&V
Endocrine insufficiency – impaired glucose regulation/eventual diabetes mellitus
Exocrine insufficiency – weight loss, diarrhoea, steatorrhoea
Examination – tender in epigastrium, often evidence of significant cachexia
Chronic pancreatitis investigations
Urine dip and routine bloods (amylase/lipase levels are often not raised in established disease), blood glucose, faecal elastase level
Imaging – CT imaging, USS, MRI
Chronic pancreatitis management
Can only be managed definitively by treating any reversible underlying cause, analgesia
Non-surgical – endoscopic management (targetable underlying cause), ERCP, extracorporeal shock wave lithotripsy
Surgical management – Frey’s procedure (large ductal stones), lateral pancreaticojejunostomy, pancreaticoduodenectomy (Whipples procedure) if there is any suspicion of pancreatic head malignancy
Pancreatic cancer
Most common type – ductal carcinoma
Most arise from the head, then the rest from body & tail/diffuse involvement of the pancreas
80% cases occur between 60-80 yrs old
Pancreatic cancer risk factors
Smoking
Chronic pancreatitis
Dietary factors – high red meat, low fruit & veg
Family history
Pancreatic cancer clinical features
Obstructive jaundice – typically painless
Weight loss
Non-specific abdominal pain
Late onset diabetes mellitus
Examination – cachectic, malnourished & jaundiced
Pancreatic cancer investigations
Routine bloods, CA19-9
Imaging – abdominal USS, CT is gold standard for preliminary diagnosis, endoscopic ultrasound is now largely used in staging & biopsy
Pancreatic cancer management
Curative option – radical resection
Non-resectable disease – chemotherapy, symptomatic management
