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Flashcards in HPB Surgery Deck (42)
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1

What is Mirizzi syndrome? 

  • A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct.
  • Causes obstructive jaundice

2

How is Mirizzi's syndrome diagnosed and managed? 

Diagnosis: MRCP

Laparoscopic cholecystectomy

3

What tests/ investigations would you do for jaundice?

  • Bloods: FBC, UE, CRP  clotting, film, reticulocyte count, Coombs’ test and haptoglobins for haemolysis, malaria parasites, u&e, LFT, γ‎-gt, total protein, albumin. Paracetamol levels. Hep A,B,C
  • USS
  • ERCP: If bile ducts are dilated and lft not improving
  • MRCP:  Or endoscopic ultrasound (eus) if conventional ultrasound shows gallstones but no definite common bile duct stones.
  • Liver biopsy
  • CT/ MRI

4

Why does jaundice result in dark urine? 

  • As conjugated bilirubin is water-soluble, it is excreted in urine, making it dark.
  • Less conjugated bilirubin enters the gut and the faeces become pale.

5

Briefly describe the process of bilirubin metabolism? 

  • Bilirubin is conjugated with glucuronic acid by hepatocytes, making it water-soluble.
  • Conjugated bilirubin is secreted in bile and passes into the gut.
  • Some is taken up again by the liver (via the enterohepatic circulation) and the rest is converted to urobilinogen by gut bacteria.
  • Urobilinogen is either reabsorbed and excreted by the kidneys, or converted to stercobilin, which colours faeces brown

6

How would pre hepatic, hepatic and post hepatic jaundice appear? 

  • Pre hepatic - no changes to stool or to urine 
  • Hepatic - dark urine, no stool changes 
  • Post hepatic - pale stools, dark urine 

7

What are some of the causes of jaundice? 

  • Pre hepatic: 
    • Haemolysis
    • Drugs/ contrast
    • Rifampacin
    • Gilbert's syndrome
    • Malaria
  • Hepatic: cholangiocarcinoma, hepatitis ABC, EBV, budd chiaria, haemachromatosis, cirrhosis, A1 anti trypsin deficiency
    • ​Drugs: anti malarials, RIP of TB, paracetemol, alcohol
  • Post hepatic: PBC, PSC, gallstones, acute cholesytitis, ascending cholangitis, mirrizzi syndrome, pancreatic cancer 
    • Drugs: flucloxacillin, prochloperazine, steroids, fusidic acid, steroids, sulphonylurea 

8

What drugs can induce jaundice? 

  • Haemolysis: antimalarials
  • Hepatitis: Paracetemol, Isoniazid, rifamipicin, pyrazinamide, monoamine oxidase inhibitors, sodium valproate, statins
  • Cholestasis: flucloxacillin, fusidic acid, co amox, nitrofuranton, steroids, sulphonylureas, chlorapromazine

9

What are some of the signs of chronic liver disease? 

  •  Hepatic encephalopathy
  • Lymphadenopathy
  • Hepatomegaly
  • Splenomegaly
  • Ascites
  • Palpable gallbladder

10

What is biliary colic?

  • Biliary colic occurs when the gallbladder neck becomes impacted by a gallstone. Gallbladder contracts against the stone → pain

11

How does Biliary Colic present? 

  • RUQ pain (radiates → back): sudden, dull, colicky
  • ± Jaundice
  • +/- Nausea or vomiting 
  • Pain is usually worse on eating fatty foods

12

How would you manage BC?

  • Conservative: lifestyle, diet, lose weight
  • Pharmacological 
    • IV fluids
    • Analgesia: morphine
    • Anti emetic: ondansetron
  • Sugery: 
    • Elective lap. cholecystectomy within 6 weeks of first presentation 

13

How does acute cholecystitis arise? 

How does it present? 

  • Follows stone or sludge impaction in the neck of the gallbladder
  • May cause continuous epigastric or RUQ pain (referred to the right shoulder)
  • Vomiting, fever, local peritonism, or a GB mass.
  • Inflammatory component: local peritonism, fever, wcc↑
  • Positive Murphy’s sign

14

How would you investigate acute cholecystitis? 

  • Bedside: urinalysis and pregnancy test 
  • Bloods: FBC (↑WCC),UE, CRP, amylase, lipase, LFT, gamma GT
  • US: a thick-walled, shrunken gb (also seen in chronic disease), pericholecystic fluid, stones, cbd (dilated if >6mm).
  • MRCP: use if US has not detected common bile duct stones but the bile duct is dilated and/or

    LFTs are abnormal.

  • Plain AXR: shows ~10% of gallstones; it may identify a ‘porcelain’ gb (associated risk of cancer).

15

What is murpheys sign?

Lay 2 fingers over the RUQ; ask patient to breathe in. This causes pain & arrest of inspiration as an inflamed GB impinges on your fingers.

It is only +ve if the same test in the LUQ does not cause pain.

16

What are the complications of gall stones? 

17

How would you treat manage acute cholecystitis? 

  • Medical:
    • NBM, IVI
    • Pain relief (opioids): morphine
    • Abx (based on local guidelines), eg co-amoxiclav 625mg/8h iv
    • Anti emetic: ondansetron
  • Surgery:
    • Laparoscopic cholecystectomy: within 1 week of presentation, ideally within 72hrs of presentation
    •  
    • Percutaneous cholescystecomy: if not fit for surgery and not responding to antibiotics
    • Open surgery: if there is GB perforation.

 

18

When looking at gallstones, what things are usually visualised on USS? 

  • The presence of gallstones or sludge (the start of gallstone formation)
  • Gallbladder wall thickness (if thick walled, then inflammation is likely)
  • Bile duct dilatation (indicates a possible stone in the distal bile ducts)

19

What are the sx of chronic cholescystitis? 

  • Chronic inflammation ± colic.
  • Ongoing RUQ or epigastric pain
  • Nausea and vomiting
  • ‘Flatulent dyspepsia’: vague abdominal discomfort, distension, nausea, flatulence, and fat intolerance (fat stimulates CCK release and GB contraction)

20

How would you treat obstructive jaundice with CBD stones? 

  • ERCP with sphincterotomy ± biliary trawl
  • Then cholecystectomy may be needed, or open surgery with CBD exploration

21

What is ascending cholangitis? 

  • Infection of the biliary tract
  • It is caused by a combination of biliary outflow obstruction* and biliary infection. 

22

How does cholangitis present? 

  • Charcot's triad: RUQ pain, fever and jaundice 
  • Reynold’s Pentad: Jaundice, Fever, and RUQ Pain, Hypotension, and Confusion
  • Other Signs: pale stool with dark urine, pruritus, rigors

23

What organisms are most commonly implicated in cholangitis? 

  • Escherichia Coli (27%)
  • Klebsiella species (16%)
  • Enterococcus (15%).

24

What is Gallstone Ileus? 

What would you see on imaging? 

  • A stone erodes through the GB into the duodenum; it may then obstruct the terminal ileum. 
  • AXR shows: air in CBD (= pneumobilia), small bowel fluid levels, and a stone
  • Duodenal obstruction is rarer (Bouveret’s syndrome).

25

What are some of the causes of acute pancreatitis? 

‘get smashed‘. Gallstones (~35%), Ethanol (~35%), Trauma (~1.5%), Steroids, Mumps, Autoimmune (pan), Scorpion venom, Hyperlipidaemia, hypothermia, hypercalcaemia, Ercp (~5%) and emboli, Drugs

26

What are some of the signs of acute pancreatitis? 

  • Hypocalcaemia: tetany, chvosek and trousseau sign 
  • Cullen's and grey turner sign: bruising around the umbilicus and the flanks; second to retroperitoneal haemorrhage

27

What is the pathogenesis behind acute pancreatitis? 

  • Premature and exaggerated activity of digestive enzymes in pancreas
  • Enzyme release -> autodigestion of fat -> fat necrosis -> free fatty acid release + hypocalcaemia 
  • End stage pancreatitis is necrosis of the pancreas

28

What are the symptoms of acute pancreatitis? 

  • Gradual or sudden severe epigastric or central abdominal pain (radiates to back, sitting forward may relieve)
  • Nausea and vomiting prominent
  • Epigastric tenderness and guarding
  • Signs of hypovolaemia: tachycardia, hypotension, tachypnoea

29

What are the signs of acute pancreatitis? 

  • Fever
  • Jaundice
  • Shock: ↑HR, tachypnoea, hypotensive
  • Ileus
  • Rigid abdomen ± local/general tenderness,
  • Periumbilical bruising (Cullen’s sign) or flanks (Grey Turner’s sign) -  blood vessel autodigestion and retroperitoneal haemorrhage
  • Signs of hypocalcaemia 

30

How would we investigate acute pancreatitis? 

  • Bloods: FBC, UE, LFT, CRP, serum amylase + lipase (diagnostic of acute pancreatitis if 3x the upper limit of normal*), Ca2+
  • Imaging: 
    • Abdo USS if cause is unknown
    • AXR: not usually performed routinely: can show a ‘sentinal loop sign’ - dilated proximal bowel loop adjacent to the pancreas, which occurs secondary to localised inflammation
    • Contrast-enhanced CT scan: If performed after 48hrs from initial presentation, it will often show areas of pancreatic oedema and swelling
    • MRCP