Hepatopancreobiliary Flashcards
173 What is biliary colic?
Biliary colic describes the pain associated with cholelithiasis caused by transient obstruction of the neck of the gallbladder by a gallstone
- *Pathogenesis**
1. Gallbladder contracts due to hormonal or neural stimulation
2. Stone enters GB outlet or cystic duct opening
3. Obstruction → increased intra-gallbladder pressure → stimulation of mechanoreceptors in muscular lumen → pain - *Clinical presentation**
- Severe, dull, constant RUQ/epigastric pain for several hours
- Post-prandial (2-3hrs) or nocturnal (awakening from sleep)
- Radiation to back / R shoulder
- Diaphoresis, N/V
- ABSENCE of fever
- *Complications**
- Acute cholecystitis (inflammation)
- Mucocele or empyema
- Cholecystoduodenal fistula +/- gallstone ileus
- Perforation
Inv: bloods + USS
- *Management:**
- Analgesia and rehydration
- Cholecystectomy
174 What causes cholangitis?
Infection of the biliary tract due to obstruction
- *Aetiology**
- *Cholelithiasis → choledocholithiasis → biliary obstruction**
- Surgical injury → structures
- Sclerosing cholangitis
- Pancreatitis
- Malignancy e.g., biliary, gallbladder, ampullary, pancreatic
Pathophysiology
Obstruction → dilation of the distal CBD → bacteria ascend from the duodenum
Pathogens
E. coli, klebsiella, G +ve enterococcus
- *Clinical presentation**
- Charcot’s triad
- Reynold’s pentad
Investigations:
- Bloods
- USS
- MRCP (but reasonable to proceed to ERCP in presence of Charcot’s triad and LFT derangement)
Treatment:
- Abx
- IV fluids
- Biliary decompression (endoscopic, percutaneous, surgical)
175 What are the clinical features of cholangitis?
Charcot’s triad:
1) Intermittent RUQ pain
2) Swinging fever/rigors
3) Jaundice
Reynold’s pentad:
4) Sepsis/shock
5) Encephalopathy/altered mental status
176 What is cholecystitis?
Inflammation of the gallbadder, most commonly caused by gallstones
Pathogenesis
Cholelithiasis → passage of gallstones into the cystic duct → cystic duct obstruction → distention and inflammation of the gallbladder
Bowel pathogens may infiltrate the bile duct leading to bacterial infection
- *Clinical features**
- RUQ abdominal pain
- *- Fever
- Leukocytosis
- Murphy’s sign**
Complications:
- Gallbladder mucocele/empyema
- Gangrene + perforation
- Fistula
- Mirizzi syndrome - extra-luminal compression of CBD or CHD
Investigation:
- Bloods
- USS
Management:
- IV fluids, analgesia, NBM, group and save, Abx (if toxic)
- Index admission cholecystectomy (lap vs open) - likely to recur and complications can be life-threatening
177 What techniques are available for treating common bile duct stones? Describe the technique briefly.
- *Endoscopically**
- ERCP + papillotomy (s*phincterotomy of sphincter of Oddi to allow the passage of stones)
- *Balloons and baskets** - used to extract stones
- *Biliary stenting**
- *Radiologically**
- *Transhepatic percutaneous drainage**
Operatively
Open or laparoscopic CBD exploration and stone extraction
Cholecystectomy - 72 hours following ERCP to prevent recurrence
178 What are the potential complications of an ERCP?
- *1) Pancreatitis** - either by i) injection of contrast up pancreatic duct, or ii) irritation from instrumentation
- Test amylase post-operatively
2) Bleeding - due to catheter/instrument injury, most commonly sphincterotomy
3) Perforation - due to catheter/instrument injury. Oesophagus, stomach, duodenum, jejunum
4) Cholangitis - due to irritation by catheter/instrument causing inflammatory response, febrile or septic illness, even septic shock
5) Stricture formation in CBD - inflammatory fibrotic response
General: medication reactions, cardiopulmonary accidents, wound infection
179 What are the symptoms of biliary colic? How can it be differentiated from acute cholecystitis clinically?
- *Biliary colic**
- Severe, constant RUQ/epigastric pain (intense/dull, crescendo-decrescendo)
- Commonly occurs 2-3hrs post-prandial or waking patient from sleep
- Radiation to back
- Diaphoresis
- N/V
- *Acute cholecystitis**
- RUQ pain
- Fever and leukocytosis (associated with gallbladder inflammation)
- Murphy’s sign = palpable, tender gallbladder on inhalation, causes patient to stop deep inhalation
- Episodes of pain continue for longer than 24 hours
180 What are the common causes of painless obstructive jaundice in a 65 yoa person?
HALLMARK PRESENTATION FOR PANCREATIC CANCER - may also be characterised by weight loss, dark urine (conj. bilirubin excess), pale stools (no conversion of urobilinogen to stercobilin), palpably enlarged gallbladder
Other:
- Biliary stricture (often secondary to chronic alcoholism, surgical damage or stones)
- Biliary stenosis
- Cholangiocarcinoma
- Ampulla of Vater carcinoma
181 How might a person with pancreatic cancer present to their GP?
Common:
- Weight loss, anorexia (80%)
- Vague abdominal pain (60%)
- Obstructive jaundice, often painless (50%)
- Aged 65-75
- Presence of risk factors (smoking, fx, hereditary cancer syndromes, DM, obesity)
Less common presenting features:
- Steatorrhoea/malabsorption - exocrine dysfunction due to impeded bile/pancreatic enzyme flow
- New-onset diabetes - endocrine dysfunction due to auto-digestion
- Acute pancreatitis (N/V/A, epigastric pain) - rare
- Courvoisier’s sign = painless, palpable gallbladder
- Trousseau’s sign = venous thrombosis or migratory thrombophlebitis
- Hepatomegaly (advanced/metastatic disease)
182 Why does a tumour of the head of pancreas cause jaundice? What are the haematological consequence of biliary obstruction?
1) Extra-hepatic biliary obstruction by compression of CBD as it passes through head of pancreas
2) Metastasis to porta hepatis lymph nodes, which then cause extra-luminal compression of the biliary duct
Haematological consequences:
- LFT derangement (obstructive picture) = elevated ALP (also associated with calcification of bone), elevated GGT (sharpest rise with biliary obstruction)
- Elevated conjugated bilirubin, decreased urobilinogen (conjugated in liver but unable to pass into duodenum in bile so not converted to urobilinogen)
183 Why or how do gallstones cause pancreatitis?
Gallstones → pancreatic duct obstruction at the ampulla of Vater → backflow of pancreatic secretions → zymogen activation → trypsin activation → activation of lipases, amylases, nucleases etc., → pancreatic self-digestion
184 What are the common causes of pancreatitis?
I GET SMASHED
Idiopathic (10-15%) or Iatrogenic (steroids, ERCP, drugs)
Gallstones (30-70%)
EtOH (30-70%)
Trauma
Steroids
Mumps/malignancy
Autoimmune (e.g. SLE)
Scorpion (Trinidad)/snake bite
Hypercalcaemia/hyperlipidaemia
ERCP
Drugs (#1 azathioprine, frusemide, metronidazole)
185 How do you assess the severity of an episode of pancreatitis when the patient is first being admitted to the hospital?
Glasgow Imrie criteria
At least 3 within 48 hours of admission = severe attack
- *P**aO2 < 60
- *A**ge > 55
- *N**eutrophils (WCC) > 15
- *C**alcium < 2mmol/L
- *R**aised urea > 16mmol/L
- *E**nzymes AST > 200, LDH > 600
- *A**lbumin <32g/L
- *S**ugar > 10mmol/L
Mortality:
0-2 = 2%
3-4 = 15%
5-6 = 40%
7-8 = ~100%
186 What is the initial management of pancreatitis?
- 2 large bore IV cannulas and aggressive rehydation
- Nil by mouth. Begin enteral feeding once pain subsides
- Analgesia (IV opioids)
- Catheterise and put on fluid balance chart
187 What are the potential late complications of severe, acute pancreatitis, late being 2 or 3 weeks after the start of the episode?
Long-term:
- Pancreatic insufficiency → malabsorption, DM
- Chronic pancreatitis
- Pancreatic pseudocyst (encapsulated collection of pancreatic enzymes, inflammatory fluid, and necrotic debris, with a well-defined inflammatory wall)
- Portal vein/splenic thombosis
- Enteric fistulas
- Intestinal obstruction
- Walled-off pancreatic necrosis
- Pancreatic ascites (due to chronic leakage of a pseudocyst or duct disruption)
Variable:
- Infected pancreatic necrosis (typically after 10 days)
- ARDS (due to production and excretion of inflammatory mediators)
- DIC (due to cytokines and SIRS)
- Gastrointestinal/retroperitoneal/intraperitoneal bleeding
