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Surgery Finals > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

1
Q

What is the epidemiology of gallstones?

A
  • About 8% of the over 40s population
  • Incidence increasing over the last 20 years; western diet
  • Slightly increased incidence in females
  • 90% gallstones are asymptomatic
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2
Q

What are the possible constituents of gallstones?

A
  • Phospholipids: lecithin
  • Bile pigments (broken down Hb)
  • Choelsterol: principle constituent of most
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3
Q

What is the aetiology of gallstones?

A
  • Lithogenic bile: Admirang’s triangle
  • Biliary sepsis
  • Gallbladder hypomotility -> stasis
    • Pregnancy, OCP
    • TPN, fasting
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4
Q

What is the difference in appearance and number between cholesterol gallstones, mixed and pigment stones?

A
  • Cholesterol
    • Large
    • Often solitary
  • Pigment
    • Small, black, gritty, fragile
  • Mixed
    • Often multiple
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5
Q

What % of gallstones are cholesterol, pigment, or mixed?

A
  • Cholesterol - 20%
  • Pigment - 5%
  • Mixed - 75% (but cholesterol is major component)
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6
Q

What determines the formation of cholesterol gallstones?

A

Admirand’s triangle:

  • Low bile salts
  • Low lecithin
  • High cholesterol
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7
Q

What are the risk factors for cholesterol gallstones?

A
  • Female
  • OCP, pregnancy
  • Old
  • High fat diet and obesity
  • Racial e.g. American Indian tribes
  • Loss of terminal ileum (reduced bile salts)
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8
Q

What makes up pigment gallstones and what are they associated with?

A

Calcium bilirubinate; associated with haemolysis

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9
Q

What are the complications of gallstones?

A
  • In the gallbladder:
    • Biliary colic
    • Acute cholecystitis ± empyema
    • Chronic cholecystitis
    • Mucocele
    • Carcinoma
    • Mirizzi’s syndrome (gallstone impacted in cystic duct or neck of gallbladder causing compression of CBD -> obstruction and jaundice)
  • In the CBD
    • Obstructive jaundice
    • Pancreatitis
    • Cholangitis
  • In the gut
    • Gallstone ileus
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10
Q

What is the pathogenesis of biliary colic?

A

Gallbladder spasm against a stone impacted in the neck of the gallbladder (Hartmann’s pouch) or less commonly the CBD

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11
Q

How does biliary colic present?

A
  • RUQ pain radiating to the back (scapular region
  • Associated with sweating, pallor, nausea and vomiting
  • No fever
  • Attacks can be precipitated by fatty food (stimulates release of CCK) and last <6hours or as little as a few minutes but pain is constant for that time
  • May be tenderness in right hypochondrium o/e
  • ± jaundice if stone passes into CBD
  • Settles if stone becomes disimpacted/passess to CBD
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12
Q

What are the differentials for biliary colic?

A
  • Cholecystitis/other gallstone disease
  • Pancreatitis
  • Bowel perforation
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13
Q

How should you investigate suspected biliary colic?

A
  • Same work up as cholecystitis - difficult to distinguish clinically
  • Urine: bilirubin, urobilinogen, Hb
  • Bloods: FBC, U+E, amylase, LFTs, G+S, clotting, CRP
    • Amylase, WCC and CRP usually normal
  • Imaging
    • AXR: 10% stones are radioopaque
    • Erect CXR to look for perf
    • US detects 98% of stones (less reliable if in bile duct)
      • Stones: acoustic shadow
      • Dilated ducts >6mm
      • Inflamed GB: wall oedema
  • If uncertain after US do HIDA cholescintigraphy which shows failure of GB filling (requires functioning liver)
  • If dilated ducts seen on US do MRCP
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14
Q

How is biliary colic managed?

A
  • Conservative
    • Rehydrate and NBM
    • Opioid analgesia: morphine 5-10mg/2h max
    • High recurrence rate therefore surgery favoured
  • Surgical
    • As for conservative with either:
      • Urgent lap chole (same admission)
      • Elective lap chole at 6-12 weeks
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15
Q

What is the pathogenesis in acute cholecystitis?

A
  • Stone or sludge impaction in Hartmann’s pouch
  • Leads to chemical and/or bacterial inflammation
  • 5% are acalculous due to sepsis, burns, DM
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16
Q

What are the possible sequelae of acute cholecystitis?

A
  • Resolution ± recurrence
  • Gangrene and rarely perforation
  • Chronic cholecystitis
  • Empyema
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17
Q

How does acute cholecystitis present?

A
  • Similar to biliary colic but pain is more severe and persistent
  • Severe RUQ pain that radiates to the right scapula and epigastrium
  • Fever
  • Vomiting
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18
Q

What are the examination findings in acute cholecystitis?

A
  • Local peritonism in RUQ
  • Tachycardia with shallow breathing
  • ± jaundice
  • Murphy’s sign
    • 2 fingers over the gallbladder and ask the patient to breath in
    • Causes pain and breath catch - must be negative on the left
  • Phlegmon may be palpable (mass of adherent omentum and bowel)
  • Boas’ sign - hyperaesthesia below the right scapula (ribs 9-11 posteriorly)
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19
Q

How should you investigate suspected acute cholecystitis?

A
  • Urine: bilirubin, urobilinogen, Hb
  • Bloods: FBC (raised WCC), U+E (dehydration from vomiting), amylase (raised but not as much as pancreatitis), LFTs (may be raised), G+S, clotting, CRP
  • Imaging
    • AXR: gallstone, porcelain gallbladder
    • Erect CXR to look for perf
    • US
      • Stones: acoustic shadow
      • Dilated ducts >6mm
      • Inflamed GB: wall oedema
  • If uncertain after US do HIDA cholescintigraphy which shows failure of GB filling (requires functioning liver)
  • If dilated ducts seen on US do MRCP
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20
Q

How is acute cholecystitis managed?

A
  • Conservative
    • NBM
    • Fluid resus
    • Analgesia: paracetamol, diclofenac, codeine
    • Antibiotics: cefuroxime and metronidazole
    • 80-90% settle over 24-48 hours
    • Deterioration: perforation, empyema
  • Surgical:
    • Used to do lots of interval surgery after 6 weeks; less common now because doesn’t have an advantage
    • Lap chole especially if mucocoele
  • Empyema (high fever and RUQ mass)
    • Percutaneous drainage: cholecystostomy
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21
Q

How does chronic cholecystitis present?

A
  • Flatulent dyspepsia
  • Vague upper abdominal discomfort
  • Distension, bloating
  • Nausea
  • Flatulence, burping
  • Symptoms exacerbated by fatty foods (CCK release stimulates gallbladder)
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22
Q

What are the differentials for chronic cholecystitis?

A
  • PUD
  • IBS
  • Hiatus hernia
  • Chronic pancreatitis
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23
Q

What investigations should you do in suspected chronic cholecystitis?

A
  • AXR: porcelain gallbladder
  • US: stones, fibrotic, shrunken gallbladder
  • MRCP
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24
Q

How do you manage chronic cholecystitis?

A
  • Medical
    • Bile salts
    • Not very effective
  • Surgical
    • Elective cholecystectomy
    • ERCP first if US shows dilated ducts and stones
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25
Q

What is a gallbladder mucocoele and what is the concern with it?

A

Where the neck of the gallbladder gets blocked by a stone but its contents remain sterile; can be very large and create a palpable mass. Can become infected (empyema)

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26
Q

How common is gallbladder carcinoma and what is it associated with?

A
  • Rare - incidentally found in 0.5-1% of lap choles
  • Associated with gallstones and gallbladder polyps
  • Calcification of gallbladder -> porcelain gallbladder
  • Adenoma or cholangiocarcinoma
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27
Q

What is Mirizzi’s syndrome?

A
  • Rare
  • Large stone in the gallbladder presses on the common hepatic duct leading to obstructive jaundice
  • Stone may erode through into the ducts
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28
Q

What is a gallstone ileus?

A

Where a large stone (>2.5cm) erodes from the gallbladder into the duodenum through a cholecysto-duodenal fistula secondary to chronic inflammation. May impact in the distal ileum leading to obstruction

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29
Q

Which triad is seen in gallstone ileus?

A

Rigler’s triad:

  • Pneumobilia
  • Small bowel obstruction
  • Gallstone in RLQ
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30
Q

What is the treatment for gallstone ileus?

A

Stone removal via enterotomy

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31
Q

What is Bouveret’s syndrome?

A

Like gallstone ileus but duodenal obstruction

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32
Q

What are the causes of obstructive jaundice?

A
  • 30% stones
  • 30% Ca head of pancreas
  • 30% other:
    • LNs at porta hepatis: TB, cancer
    • Inflammatory: PBC, PSC
    • Drugs: OCP, sulfonylureas, fluclox
    • Neoplastic: cholangiocarcinoma
    • Mirizzi’s syndrome
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33
Q

What are the clinical features of obstructive jaundice?

A
  • Jaundice
    • Noticeable at 50mM
    • Seen at tongue frenulum first
  • Dark urine
  • Pale stools
  • Itch (bile salts) - specific to obstructive jaundice
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34
Q

What investigations should be done in obstructive jaundice?

A
  • Urine
    • Dark
    • High bilirubin, low urobilinogen
  • Bloods
    • FBC: raised WCC in cholangitis
    • U+E: hepatorenal syndrome
    • LFT: raised cBR, very high ALP, high AST/ALT
    • Clotting: low vitamin K -> high INR
    • G+S as may need ERCP
    • Immune: AMA, ANCA, ANA
  • Imaging:
    • AXR: may visualise stone, pneumobilia suggests gas forming infection
    • US:
      • Dilated ducts >6mm
      • Stones (95% accurate)
      • Tumour
    • MRCP or ERCP
    • Percutaneous transhepatic cholangiography
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35
Q

How should obstructive jaundice from stones be managed?

A
  • Conservative
    • Monitor LFTs: passage of stone may lead to resolution
    • Vitamins ADEK
    • Analgesia
    • Cholestyramine
  • Interventional
    • If: no resolution, worsening LFTs or cholangitis
    • ERCP with sphincterotomy and stone extraction
  • Surgical:
    • Open/lap stone removal with T tube placement
      • T tube cholangiogram 8 days later to confirm stone removal
    • Delayed cholecystectomy to prevent recurrence
36
Q

What are the features of ascending cholangitis/its associated triad and pentad?

A
  • May complicate CBD obstruction
  • Charcot’s triad: fever/rigors, RUQ pain, jaundice
  • Reynolds pentad: Charcot’s triad + shock + confusion
37
Q

How is ascending cholangitis managed?

A
  • Cef and met
  • 1st: ERCP
  • 2nd: open or lap stone removal with T tube drain
38
Q

What are the risk factors for pancreatic carcinoma?

A
  • Smoking
  • Inflammation: chronic pancreatitis
  • Nutrition (high fat diet/Western)
  • EtOH
  • Diabetes
  • Family history
39
Q

What is the pathology in pancreatic carcinoma?

A
  • 95% ductal adenocarcinomas
  • Present late and metastasise early
    • Direct extension to local structures
    • Lymphatics
    • Blood -> liver and lungs
    • Within peritoneum: transcoelomic spread
  • 70% head, then body, then tail
40
Q

How does pancreatic carcinoma present?

A
  • Typically males >60
  • Painless obstructive jaundice: dark urine, pale stools, itching
  • Epigastric pain which radiates to the back, relieved by sitting forward
  • Anorexia, weight loss and malabsorption
  • Acute pancreatitis
  • Sudden onset DM in the elderly
41
Q

What are the signs associated with pancreatic carcinoma?

A
  • Palpable gallbladder
  • Jaundice
  • Epigastric mass (occasionally)
  • Thrombophlebitis migrans (Trousseau sign)
  • Splenomegaly: PV thrombosis -> portal hypertension
  • Ascites
  • Virchow’s node (L supraclavicular)
42
Q

What is Courvoisier’s law?

A

In the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to stones

43
Q

What investigations should be done in suspected pancreatic carcinoma?

A
  • Bloods: cholestatic LFTs, raised CA19-9 (90% sensitivity), raised calcium, PT prolonged with obstructive jaundice
  • Imaging:
    • US: pancreatic mass, dilated ducts, hepatic mets, guide biopsy
    • EUS: better than CT/MRI for staging
    • CXR: mets
    • Laparoscopy: mets, staging
  • ERCP
    • Shows anatomy
    • Allows stenting
    • Biopsy of peri-ampullary lesions
44
Q

How is pancreatic carcinoma managed?

A
  • Surgery
    • Fit, no mets, tumour ≤3cm (≤20% patients)
    • Whipple’s pancreaticoduodenectomy
    • Distal pancreatectomy
    • Post op chemo delays progression
    • 5 year survival 5-14%
  • Palliation
    • Endoscopic/percutaneous stenting of CBD
    • Palliative bypass surgery: cholecystojejunostomy and gastrojejunostomy
    • Pain relief: may need coeliac plexus block
45
Q

What is the prognosis in pancreatic carcinoma?

A

Mean survival is <6 months, and 5 year survival is <2%

46
Q

What is the pathophysiology in acute pancreatitis?

A

Pancreatic enzymes are released and activated in a vicious circle; multi stage process:

  1. Oedema + fluid shift + vomiting -> hypovolaemic shock while enzymes -> autodigestion and fat necrosis
  2. Vessel autodigestion -> retroperitoneal haemorrhage
  3. Inflammation -> pancreatic necrosis
  4. Superadded infection: 50% of patients with necrosis
47
Q

How common is pancreatitis, what is the mortality and what age group gets it?

A

4th and 5th decades. 1% of surgical admissions with a 10% mortality

48
Q

What are the causes of pancreatitis?

A
  • Gallstones (45%)
  • Ethanol (25%)
  • Idiopathic (20%) - maybe microstones
  • Trauma
  • Steroids
  • Mumps and other infections e.g. coxsackie B
  • Autoimmune e.g. PAN
  • Scorpion (Trinidadian)
  • Hyperlipidaemia (I and V), hypercalcaemia, hypothermia
  • ERCP: 5% Risk
  • Drugs e.g. thiazides, azathioprine
49
Q

What are the clinical features of acute pancreatitis?

A
  • Symptoms:
    • Severe epigastric pain radiating to the back and relieved by sitting forward in some cases
    • Vomiting
  • Signs
    • Acutely unwell with circulatory insufficiency
    • High HR and RR
    • Fever
    • Hypovolaemia -> shock
    • Epigastric tenderness
    • Jaundice
    • Ileus -> absent bowel sounds
    • Ecchymoses
      • Grey Turners: flank
      • Cullens: periumbilical (tracks up falciform)
50
Q

What are the differentials for acute pancreatitis?

A
  • Perforated DU
  • Mesenteric infarction
  • MI
51
Q

What is the scoring system for acute pancreatitis that allows you to assess severity and predict mortality that is valid for EtOH and gallstones?

A

Modified Glasgow Criteria: PANCREAS

  • PaO2 <8kPa
  • Age >55 years
  • Neutrophils >15x109/L
  • Ca2+ <2mM
  • Renal function U>16mM
  • Enzymes: LDH >600iu/L, AST >200iu/L
  • Albumin <32g/L
  • Sugar >10mM
  • 1 = mild, 2 = moderate, 3 = severe
52
Q

What are Ranson’s criteria?

A

Scoring system for acute pancreatitis that is only applicable to EtOH and can only be fully applied after 48h

53
Q

What investigations should be done in suspected acute pancreatitis?

A
  • Bloods:
    • FBC (raised WCC)
    • Amylase >1000/3xULN but don’t rely on this; rised in 80% and returns to normal in 5-7 days
    • Elevated lipase (elevation lasts longer than amylase
    • Cholestatic LFTs with raised AST and LDH
    • Low calcium
    • High glucose
    • CRP to monitor progress: severe if >150 after 48 hours
    • ABG: low O2 suggests ARDS
  • Urine: glucose, raised cBR, low urobilinogen
  • Imaging:
    • CXR: ARDS, exclude perfed DU
    • AXR: sentinel loop, pancreatic calcification
    • US: gallstone and dilated ducts, inflammation
    • Contrast CT: Balthazar severity score
54
Q

Describe the medical/conservative management of acute pancreatitis

A
  • Manage at appropriate level e.g. ITU, constant reassessment with hourly TPR and UO and daily FBC, U+E, calcium, glucose, amylase and ABG
  • Fluid resus: aggressive to keep UO >30ml/hour, catheter ±CVP
  • Pancreatic rest: NBM, NGT if vomiting, TPN may be needed if severe to prevent catabolism
  • Analgesia: pethidine via PCA or morphine 5-10mg/2h max ± epidural
  • Antibiotics: not routinely given if mild, but use if suspicion of infection or before ERCP; penems often used e.g. meropenem, imipenem
  • Manage complications: ARDS (O2, ventilation), high glucose (insulin sliding scale), high/low calcium, EtOH (chlordiazepoxide), renal support
55
Q

Describe the interventional management of acute pancreatitis

A
  • ERCP
  • If pancreatitis with dilated ducts secondary to gallstones
  • ERCP + Sphincterotomy - decreases complications
56
Q

Describe the surgical management of acute pancreatitis

A
  • Indications:
    • Infected pancreatic necrosis
    • Pseudocyst or abscess
    • Unsure diagnosis
  • Operations
    • Laparotomy + necrosectomy (pancreatic debridement)
    • Laparotomy + peritoneal lavage
    • Laparostomy: abdomen left open with sterile packs in ITU
57
Q

What are the early complications of acute pancreatitis?

A
  • Respiratory: ARDS, pleural effusion
  • Shock: hypovolaemic or septic
  • Renal failure
  • DIC
  • Metabolic
    • Low calcium
    • High glucose
    • Metabolic acidosis
58
Q

What are the late complications of acute pancreatitis (>1 week)?

A
  • Pancreatic necrosis
  • Pancreatic infection
  • Pancreatic abscess
    • May form in pseudocyst or in pancreas
    • Open or percutaneous drainage
  • Bleeding e.g. from splenic artery (may need embolisation)
  • Thrombosis
    • Splenic artery, GDA or colic branches of SMA
      • May lead to bowel necrosis
    • Portal vein -> portal hypertension
  • Fistula formation
    • Pancreato-cutaneous - skin breakdown
59
Q

What is a pancreatic pseudocyst and how common are they?

A

Collection of pancreatic fluid in the lesser sac surrounded by granulation tissue that occur in 20%, especially EtOH pancreatitis

60
Q

How does a pancreatic pseudocyst present?

A
  • 4-6 weeks after the acute attack
  • Persisting abdominal pain
  • Epigastric mass -> early satiety
61
Q

What are the complications of a pancreatic pseudocyst?

A

Infection -> abscess, obstruction of duodenum or CBD

62
Q

What investigations should you do in a suspected pancreatic pseudocyst?

A

Persistently raised amylase ± LFTs

US/CT

63
Q

How do you treat a pancreatic pseudocyst?

A
  • <6cm: spontaneous resolution
  • >6cm:
    • Endoscopic cyst-gastrostomy
    • Percutaneous drainage under US/CT
64
Q

What are the causes of chronic pancreatitis?

A
  • Alcohol (70%)
  • Genetic (CF)
  • Immune (lymphoplasmacytic sclerosing pancreatitis - raised IgG4)
  • Raised triglycerides
  • Structural
    • Obstruction by tumour
    • Pancreas divisum
65
Q

How does chronic pancreatitis present?

A
  • Epigastric pain
    • Bores through to back
    • Relieved by sitting back or hot water bottle -> erythema ab igne
    • Exacerbated by fatty food or EtOH
  • Steatorrhoea and weight loss
  • DM: polyuria, polydipsia
  • Epigastic mass: pseudocyst
66
Q

What investigations should you do in suspected chronic pancreatitis?

A
  • Hyperglycaemia
  • Low faecal elastase: decreased exocrine function
  • US: pseudocyst
  • AXR: speckled pancreatic calcifications
  • CT: pancreatic calcifications
67
Q

How do you treat chronic pancreatitis?

A
  • Diet
    • No alcohol
    • Low fat, high carb
  • Drugs:
    • Analgesia: opiates, may need coeliac plexus block
    • Enzyme supplements: pancreatin (Creon)
    • ADEK vitamins
    • DM treatment - insulin requirements are often greater than idiopathic diabetes because of a lack of glucagon (?)
  • Surgery
    • Distal pancreatectomy, Whipple’s
    • Pancreaticojejunostomy: drainage
    • Endoscopic stenting
68
Q

What are the indications for surgery in chronic pancreatitis?

A
  • Unremitting pain
  • Obstructive jaundice
  • Duct blockage
  • Malignancy
  • Correctable anatomical complications
69
Q

What are the possible complications of chronic pancreatitis?

A
  • Pseudocyst
  • DM
  • Pancreatic cancer
  • Pancreatic swelling -> biliary obstruction
  • Splenic vein thrombosis -> splenomegaly
  • Ascites (rare): usually due to alcoholic pancreatitis with communication between the pancreatic duct and peritoneal cavity
70
Q

What is the epidemiology of pancreatic endocrine neoplasias?

A

30-60 years, ~15% associated with MEN1

71
Q

What are the features of insulinoma?

A
  • Fasting/exercise-induced hypoglycaemia
  • Confusion, stupor, LOC
  • High insulin and C-peptide, low glucose
72
Q

What is the pathophysiology of gastinoma/Zollinger-Ellison?

A

Hypergastrinaemia -> hyperchlorhydria -> PUD and chronic diarrhoea (inactivation of pancreatic enzymes)

73
Q

What are the features of a glucagonoma?

A
  • Rise in glucagon -> mild DM
  • Characteristic blistering rash - necrolytic migratory erythema
74
Q

What are the features of VIPoma/Verner-Morrison?

A
  • Watery diarrhoea
  • Hypokalaemia
  • Achlorhydria
  • Acidosis
  • (also called WDHA syndrome)
75
Q

What are the features of a somatostatinoma and why?

A
  • Somatostatin inhibits glucagon and insulin release, and inhibits pancreatic enzyme secretion
  • Features:
    • DM
    • Steatorrhoea
    • Gallstones
    • Usually very malignant with a poor prognosis
76
Q

Where are the 2 commonest sites for an ectopic pancreas?

A

Meckel’s, small bowel

77
Q

What is a pancreas divisum and is it significant?

A
  • Failure of fusion of the dorsal and ventral buds
  • Bulk of pancreas then drains through a smaller accessory duct
  • Usually asymptomatic but can lead to chronic pancreatitis
78
Q

What is an annular pancreas and how may it present?

A
  • Fusion of dorsal and ventral buds around duodenum
  • May present with infantile duodenal obstruction
79
Q

What is the pathology seen in cholangiocarcinoma?

A

Rare bile duct tumour - adenocarcinoma. Typically occurs at the confluence of the right and left hepatic ducts (‘Klatskin’ tumour)

80
Q

What are the risk factors for cholangiocarcinoma?

A
  • PSC
  • Ulcerative colitis
  • Choledocholithiasis
  • Hep B/C
  • Choledochal cysts
  • Lynch 2
  • Flukes
81
Q

How does cholangiocarcinoma present?

A
  • Progressive painless obstructive jaundice
    • Gallbladder not palpable
  • Steatorrhoea
  • Weight loss
82
Q

What investigations are key in cholangiocarcinoma?

A

CA 19-9 and cholestatic LFTs

83
Q

How is cholangiocarcinoma managed?

A
  • Poor prognosis so no curative treatment
  • Palliative stenting by ERCP
84
Q

What is the pathophysiology of a hydatid cyst?

A
  • Zoonotic infection by Echinococcus granulosus
  • Occurs in sheep-rearing communities
  • Parasite penetrates the portal system and infects the liver -> calcified cyst
85
Q

How does a hydatid cyst present?

A
  • Mostly asymptomatic
  • Pressure effects
    • Non specific pain
    • Abdominal fullness
    • Obstructive jaundice
  • Rupture
    • Biliary colic
    • Jaundice
    • Urticaria
    • Anaphylaxis
  • Secondary infection
86
Q

What investigations are key in a hydatid cyst?

A

CT and eosinophilia

87
Q

How is a hydatid cyst treated?

A
  • Medical: albendazole
  • Surgical cystectomy - indicated for large cysts

Surgery Finals (12 decks)

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