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HPB surgery Flashcards

1
Q

What are the components of bile?

A

Cholesterol, phospholipids, bile salts, water and conjugated bilirubin

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2
Q

What is the action of bile salts?

A

Act to break up and emulsify fats in the gut, and are enterohepatically recycled to be secreted once more into the bile

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3
Q

Where is bile made/stored?

A

Made in the liver

Flows into the gall bladder if the sphincter of Oddi is closed, where it becomes more concentrated as water is absorbed

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4
Q

What does presence of fatty acids in the duodenum lead to?

A

Release of CCK, which causes the gallbladder to contract and bile to be released

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5
Q

What is cholelithiasis?

A

Formation of stones in the gallbladder

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6
Q

What are the risk factors for stone formation?

A 
Female - 90% 
Fair 
Fat 
Forty
Fertile

DM
Ileal disease: disease of the ileum prevents bile salt reabsorption
Liver cirrhosis

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7
Q

What do bile pigment stones contain?

A

Calcium bilirubinate - form independently of cholesterol stones

Black pigment stones = associated with haemolytic conditions

Brown pigment gallstones occur due to biliary stasis / infection, and are a common causes of recurrent bile stones following cholecystectomy

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8
Q

Draw out biliary anatomy

A

Wot r u waiting for, go draw bitch

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9
Q

What is biliary colic?

A

Intermittent right upper quadrant pain caused by gallstones irritating bile ducts

Can lead to mucocoele (stone stuck in Hartman’s pouch) ((and empyema if infected))in obstruction of an empty gallbladder which continues to produce mucin

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10
Q

What is choledocholithiasis?

A

Stone impaction in the common bile duct, which can cause biliary colic if temporary, or painful jaundice if more prolonged

Can predispose to ascending cholangitis/acute pancreatitis

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11
Q

What is Mirizzi’s syndrome?

A

Gallstone impacted in the cystic duct / Hartman’s pouch
(at the neck of the gall bladder) and causes extrinsic compression of the common hepatic duct

This leads to obstructive jaundice without dilation of the cystic/common bile duct

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12
Q

What is Gallstone ileus?

A

uncommon condition where a large gallstone erodes through to the gall bladder lumen to create a fistula into the adjacent duodenum

This can produce an obstruction if it impacts in a narrow segment of bowel

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13
Q

What are the x ray signs of gallstone ileus?

A

Signs of small bowel obstruction

Gallstone may be visible and there will be air in the biliary tree (Aerobilia)

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14
Q

Describe the presentation of biliary colic?

A

Severe constant epigastric / RUQ pain - CRESCENDO characteristic (peaks 2 hours after eating) due to CCK peak at this time

May radiate to back aright shoulder

+/- N+V
Worse with food consumption, especially fatty foods
Worst mid evening
Cessation = spontaneous / opiates

Systemically well

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15
Q

What is cholecystitis?

A

Inflammation of the gallbladder - an obstruction of gall bladder emptying leading to gall bladder distension

Ongoing water reabsorption from retained bile which becomes highly concentrated, leading to secondary inflammatory response in the wall of the gall bladder

30% = superadded infection

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16
Q

What are the features of cholecystitis?

A

Severe localised RUQ pain (as inflamed GB touches peritoneum) with guarding and rigidity

Vomiting and systemic: fever

Murphy’s sign positive - palpable gall bladder
RUQ tenderness exacerbated by deep inspiration
Place hand in RUQ and apply pressure
Ask patient to take deep breath in
Gallbladder will move downwards under your hand and cause pain

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17
Q

What is a rare complication of acute cholecystitis?

A

Gallbladder becomes gangrenous and perforates, leading to generalised peritonitis

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18
Q

What is chronic cholecystitis?

A

Repeated episodes of inflammation due to gallstones leading to fibrosis and thickening of the gall bladder wall

Recurrent bouts of abdominal pain due to mild cholecystitis

Discomfort and flatulence after fatty meals

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19
Q

What is the presentation choledocholithiasis?

A

(gallstones in the common bile duct)

Obstructive jaundice and biliary colic
Attacks last for hours-days, ceasing when the stone passes through the sphincter of Oddi or disimpacts and fallback into the dilated common duct

If obstruction not relieved, the chronic back pressure can lead to secondary biliary cirrhosis and liver failure

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20
Q

What is Courvoisier’s law?

A

If in the presence of jaundice, the gallbladder if palpable, then the jaundice is unlikely to be due to a stone

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21
Q

Why does Courvoisier’s law exist?

A

Because stones lead to fibrosis of the gall bladder meaning it does not fully distend, and obstruction due to stones is rarely complete, so there can be some drainage of the bile and decompression of the gall bladder

More commonly: carcinoma in the head of the pancreas

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22
Q

What is ascending cholangitis?

A

Infection the common bile duct, which usually occurs following obstruction due to choledocholithiasis

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23
Q

What are the symptoms of ascending cholangitis?

A

Charcot’s triad:
Obstructive jaundice
High fever (+/- rigors)
RUQ pain

Duct system is severely inflamed and the liver may be dotted with multiple small abscesses. These patients are very unwell and should be managed aggressively (10% mortality)

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24
Q

What blood tests are used in the diagnosis of gallstones?

A

WBC / inflammatory markers - cholecystitis

LFTs: marginally deranged in cholecystitis, significant derangement and obstructive jaundice type picture in common bile duct obstruction: AST/ALT bit raised, ALP over 330

Amylase: assess for pancreatitis (often mildly elevated in gallstone disease)

Prothrombin time

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25
Q

What is the first line imaging of biliary disease?

A

USS

Acute cholecystitis: thickened gallbladder wall, stones / sludge in gallbladder and fluid around the gallbladder
Gallstones in the gallbladder
Gallstones in the ducts
Bile Duct Dilatation (Upper limit of normal is 6mm plus 1mm for every decade after 60)

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26
Q

What is the second step up after USS for gallbladder disease?

A

MRCP

Indicated if USS doesn’t show ductal stones but the is bile duct dilitation or raised bilirubin
An MRI scan that produces detailed image of the biliary system
Very sensitive and specific for biliary tree diseases (e.g. ductal stones / malignancy)

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27
Q

Stepwise progression for biliary disease ix?

A

USS
MRCP
ERCP
Cholecystectomy

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28
Q

What is the management of asymptomatic gallstones?

A

Cholecystectomy only indicated if the patient is at significant risk of complications due to co-morbidities
e.g. diabetes or chronic renal failure

Young patients may also fit criteria

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29
Q

What is the management of biliary colic?

A

Admit - bed rest, fluid and analgesia (NBM)

Elective laparoscopic cholecystectomy
‘hot’ (within 72 hours) or ‘cold’ - 6 weeks later

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30
Q

What are the complications of cholecystectomy?

A

Bile leakage or jaundice due to ductal injury or missed stones in the common bile duct

Intolerance to fatty meals/chronic diarrhoea

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31
Q

What are the medical treatments instead of lap chole??

A

oral bile salts (chenodeoxycholic acid) for small non-calcified stones

32
Q

What is the management of acute cholecystitis

A

Lap chole + IV cefuroxime

sepsis 6

33
Q

What organisms cause acute cholecystitis?

A

Gut:

E.Coli, Klebsiella, Streptococcus

34
Q

What is the management of chronic cholecystitis?

A

Lap chole + cholangiogram to ensure no stones remain in the common bile duct

35
Q

What is he management of obstructive jaundice due to stones?

A

ERCP for sphincterectomy (making a cut in the sphincter to dilate it and allow stone removal) - as an emergency if high fever

Stone removal: a basket can be inserted and pulled through the CBD to remove stones
Balloon dilatation: a balloon can be inserted and inflated to treat strictures

Elective lap chole

36
Q

Why is jaundice relief important pre-operatively (ERCP)

A

Higher risk of infection, venous thrombosis, bleeding and hepatic/renal failure

If the stones are impacted then a stent can be placed beside it to allow drainage

37
Q

What is ascending cholangitis management?

A

Sepsis six bundle, with IV cefuroxime + metronidazole and emergency ERCP

38
Q

Who gets carcinoma of the gall bladder?

A

elderly - associated with long-standing gallstones

39
Q

What are the symptoms of gall bladder carcinoma?

A

resemble acute cholecystitis:
RUQ pain
Nausea + vomiting
weight loss

Finally obstructive jaundice and a palpable mass

40
Q

What is the treatment of gall bladder carcinoma?

A

Surgical, with radical cholecystectomy +/- liver resection if caught incidentally, although most tumours present too late for surgical therapy (survival is short)

41
Q

What is cholangiocarcinoma?

A

Adenocarcinoma arising from the epithelium of the bile duct/ampulla

42
Q

Where are the common sites of cholangiocarcinoma?

A

Common sites are at the confluence the ducts in the biliary tree

43
Q

What is the presentation of cholangiocarcinoma?

A

Painless, progressive jaundice
As with cancer of head of pancreas

Can also arise from intrahepatic ducts - present more like HCC

44
Q

What conditions might predispose to cholangiocarcinoma?

A

Primary sclerosis cholangitis

and IBD

45
Q

What is the prognosis/management for cholangiocarcinoma?

A

Slow growing and mets late - often advanced at presentation with low long-term survival

Extra-hepatic or periampullary tumours may be treated by curative resection (Whipple’s procedure)

Palliative stenting (ERCP) may be used in advanced disease

46
Q

What are the symptoms of acute pancreatitis?

A

Gradual/sudden onset severe epigastric pain
Classically radiates to the back, may be removed by sitting forwards
Nausea / vomiting is prominent

47
Q

What are the signs of pancreatitis?

A

Tachycardia / shock
Fever
Ileus
Jaundice (30%)
Rigid abdomen
Cullen’s sign - periumbilical discolouration due to haemorrhage in the peritoneal space
Grey-Turner’s sign: discolouration in the flanks

48
Q

What are the causes of acute pancreatitis?

A 
I GET SMASHED 
Idiopathic 
Gallstones 
Ethanol
Trauma
Steroids
Mumps 
Autoimmune (SLE etc) 
Scorpion bite
Hyper/hypo hyperlipidaemia, hypercalcaemia, hypothermia 
ERCP 
Drugs: thiazides, sulphonamides, ACEis, NSAIDs
49
Q

How does pancreatitis occur?

A

An initial insult to the pancreas leads to leakage of activated pancreatic enzymes into the pancreatic and peripancreatic tissue, causing an acute inflammatory reaction

e.g. gallstones - damage ampulla of V, allowing gastric contents up the pancreatic duct where they can activate the pro-enzymes

Liberation of digestive enzymes results in extensive local tissue necrosis (esp fat)

Fluids collect in gut, peritoneum and retroperitoneum

50
Q

What is periductal necrosis?

A

Necrosis of the acinal cells adjacent to the ducts

Generally due to duct obstruction (e.g. gallstones)

51
Q

What is pan lobular necrosis?

A

Necrosis of the whole acinar lobule
Generally due to drugs/toxins/viruses/metabolic insults that cause direct damage

Can also spread from periductal necrosis

52
Q

What is perilobular necrosis?

A

Necrosis of the peripheries of lobules

Generally due to poor vascular perfusion (shock/hypothermia)

53
Q

What is the acute management of pancreatitis?

A

ABCDE

Aggressive IV fluid resuscitation, catheterise and consider CVP monitoring 
Hourly pulse, BP, urine output and daily bloods (FBC, U+E, Ca2+ glucose, ABG)
Analgesia
NBM until pain free 
NG tubs suction if ileus / emesis 
PPI
anticoagulation
ITU??

Laparotomy and debridement if abscess / pancreatic necrosis on CT
Urgent ERCP (if due to gallstones)
Find and treat causative

54
Q

What are the early complications of pancreatitis?

A 
Shock (hypovolaemic, septic
ARDS
Renal failure 
DIC
Hypocalcaemia 
Hyperglycaemia
55
Q

What are the late complications of pancreatitis?

A

Pancreatic pseudocyst
Abscess
Bleeding from elastase eroding a major vessel
thrombosis of the splenic / gasproduodenal arteries causing bowel necrosis
fistulae

56
Q

What bloods are done for acute pancreatitis?

A

Baseline FBC, CRP, U+E, LFT, glucose and calcium (if low, bad) to assess progression
ALT >3x normal = gallstone disease

Serum amylase: very sensitive if within 24 hours and >3x normal
Lipase is the most specific if the presentation is delayed <24 hours). Also has a longer half life than amylase and doesn’t go up and down as much

Will also be raised in cholecystitis, GI perforation and mesenteric infarction
Raised serum lipase is more sensitive and specific
ABG - monitor oxidation and acid-base status
LDH

57
Q

What imaging is done for pancreatitis?

A

AXR: sentinel loop/small bowel ileus
microcalcification

Erect CXR: assess for perforations

CT: show enlarged pancreas with stranding, abscess, collections, necrosis or pseudocyst (USS not diagnostic)

MRCP: Better visualisation of collections and ductal systemic

58
Q

What are the components of the modified Glasgow criteria?

A 
P – Pa02 < 60
A – Age > 55
N – Neutrophils (WBC > 15)
C – Calcium < 2
R – uRea >16
E – Enzymes (LDH > 600 or AST/ALT >200)
A – Albumin < 32
S – Sugar (Glucose >10)
1-3 = mild
4-6 = moderate to severe pancreatitis 
3+ = prompt transfer to ITU
59
Q

What are the other scoring systems for acute pancreatitis?

A

APACHE II allocates points for assessment of clinical parameters (A) age (B) and co-morbid disease (C)
Scores >9 indicate acute severe pancreatitis and mortality is very high if this score increases after admission

Ranson: age and lab scores on admission, then clinical findings at 48 hours to give a mortality risk figure

60
Q

What are the metabolic complications of acute pancreatitis?

A

Hyperglycaemia
Hypocalcaemia
Raised serum albumin
Malabsorption leading to reduced vitamin levels

61
Q

What is a pancreatic pseudocyst?

A

Localised fluid collection rich in pancreatic enzymes, with a non-epithelialized wall containing fibrous/granulation tissue

Commonly occur in pancreatitis from day 10 onwards
form due to disruptions of the pancreatic duct, lading to extravasation of enzymes

62
Q

What is the presentation of pseudocyst?

A 
'Deep' persistent abdominal pain
Abdominal mass
Anorexia (due to pressure on adjacent bowel) 
Jaundice
Sepsis (if infected) 
Pleural effusion

Amylase/lipase may or may not be elevated, and LFTs may be abnormal if the biliary tree is involved

63
Q

What are the outcomes for pseudocyst?

A

Most resolve without intervention, however, outcomes are worse if the cyst is >6cm or there is evidence of pancreatic necrosis

Complications: bleeding (erosion into a vessel), infection, GI obstruciton, rupture of cyst

64
Q

What are the treatment options for pseudocyst?

A

Abdominal CT = gold standard if pseudocyst suspected

MRI may better differentiate pseudocyst from necrosis

ERCP/endoscopic USS can be useful to plan therapy if endoscopic drainage is being considered

65
Q

What are the indications for drainage of pseudocyst?

A

Complications (bleeding/infection)
Relief of symptoms
Concern about malignancy (cytology and cystic fluid analysis)

66
Q

What is the typical patient with pancreatic carcinoma?

ADENOCARCINOMA

A 
>60
smoking 
alcohol
diabetes
chronic pancreatitis 
Genetic
67
Q

What is the presentation of carcinoma of the head of the pancreas?

A

Painless jaundice (obstructive) but pain may develop as the disease progresses

On examination - signs related to obstructive jaundice, Courvoisier’s sign or palpable abdominal mass

Hepatosplenomegaly/ascites also common

68
Q

What is the presentation of carcinoma of the body/tail of the pancreas?

A

Late - dull abdominal pain radiating through to the back, partially relieved on sitting fowards

Non specific B symptoms common, often no physical signs on examination

either can also present as acute pancreatitis or diabetes

69
Q

What is Trousseau’s syndrome?

A

Thrombosis of the superficial / deep leg veins (thrombophlebitis migrans) related to pancreatic carcinoma

70
Q

What investigations are done for pancreatic cancer?

A

Bloods: FBC, U+E, LFTS (obstructive jaundice)
Ca 19-9 or CEA
Amylase (rarely elevated)

USS - confirms obstruction and duct dilation

CT - pancreatic mass +/- dilated biliary tree +/- hepatic metastases

Endoscopic USS (EUS +/- biopsy) 
Detailed information about the location of the tumour, its local spread and involvement of local lymph nodes + allows biopsy
71
Q

Where are pancreatic carcinomas found?

A

DUCTAL ADENOCARCINOMA
60% in the head
25% in the body
15% in the tail of the pancreas

72
Q

What other types of pancreatic cancers are there?

A

Islet cell tumours:
Insulinoma - symptomatic hypoglycaemic events + weight gain (usually benign)

Glucagonoma - often asymptomatic, secondary diabetes may develop

Gastrinoma - Zollinger-Ellison syndrome, with oesophagitis, GI ulcers and diarrhoea

Somatostainoma - Diabetes, achlorrydia (gastrin release inhibited) and gallstones (CCK release inhibited)

VIPoma - vasoctive intestinal peptide release causes profound diarrhoea

73
Q

What are the pt requirements for surgery for pancreatic cancer?

A

Tumour <3cm with no mets,

patient fit

74
Q

What procedure is done for pancreatic cancer?

A

Wipple’s procedure

Involves removing head of pancreas, gallbladder, duodenum and pylorus

Modified Whipple’s involves leaving the pylorus, and has equal success rates to traditional Whipples

Remaining organs are re-attached to restore digestive function

Post operative mortality stands at 5% , morbidity high

75
Q

What are the other management options for pancreatic cancer?

A

Distal pancreatectomy for tumour of body/tail of pancreas
Adjuvant chemotherapy

Palliative:
Palliative chemotherapy may be offered if fit to attempt to extend life
Palliative stenting of bile ducts to relive obstruction
Palliative care

76
Q

What is the prognosis of pancreatic cancer?

A

Mean survival <6 months
5 year survival <2% rising to 5-15% following wipple’s

Ampullary and islet cell tumours = better prognosis as they often present relatively early

CP3 Surgery (12 decks)

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