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Yr3 Surgery: General > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

1
Q

Remind yourself of some pre-, intra- and post-hepatic causes of jaundice

A
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2
Q

State some potential causes of pancreatitis- highlighting the two most common

*HINT: GET SMASHED

A
  • Gallstones
  • Ethanol (alcohol)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune disease e.g. SLE
  • Scorpionn venom (RARE)
  • Hypercalcaemia/hyperlipidaemia
  • ERCP
  • Drugs e.g. azathioprine, NSAIDs, furosemide, thiazides
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3
Q

Discuss the pathophysiology of acute pancreatitis

A
  • Causes stated in previous FC trigger premature & exaggerated activation of pancreatic digestive enzymes
  • Results in inflammatory response in pancreas
  • This increases vascular permeability
  • Leading to both subsequent fluids shifts (3rd spacing) and teh release of pancreatic enzymes into systemic circulation
  • Release into systemic circulation causes autodigestion offats and blood vessels (may lead to haemorrhage)
  • Fat necrosis releases fatty acids which thenr eact with serum calcium to form chalky deposits in fatty tissue resulting in hypocalcaemia
  • Severe end stage pancreatitis will evetnually result in partial or complete necrosis of pancrea
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4
Q

Describe the clinical presentation of acute pancreatitis

A

Acute onset of:

  • Severe epigastric pain
  • Pain radiates to back
  • Associated vomiting
  • Abdo tenderness
  • Systemically unwell (low grade fever, tachycardia)]
  • Cullen’s & Grey Turners sign
  • Tetany due to hypocalcaemia
  • Jaundice (if gallstone pathology causing obstructive jaundice)
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5
Q

Cullen’s and Grey Turner’s are rare signs; what do they represent?

A

Retroperitoneal bleeding

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6
Q

What investigations may you do if you suspect acute pancreatitis?

A

Clinical diagnosis based mainly on presenting features & amylase levels.

Bedside

  • Plasma glucose: quickly get blood glucose
  • ABG: PaO2 and blood glucose (need both for Glasgow score)

Bloods

  • FBC: raised WCC
  • U&Es: raised urea due to fluid loss
  • LFTs: liver enzymes
  • CRP: inflammation
  • Calcium: check for hypocalcaemia
  • Serum amylase
  • Serum lipase: elevated for longer than serum amylase but not routinely available

Imaging

  • Ultrasound:if suspect gallstones
  • Contrast CT abdomen: asses for complications of pancreatitis. Only required if complications suspected
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7
Q

A serum of amylase of ____ x upper limit of normal is diagnostic of acute pancreatitis

A

3x

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8
Q

Serum amylase correlates directly with disease activity in pancreatitis; true or false?

A

FALSE

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9
Q

What score is used to assess severity of acute pancreatitis?

State some factors that are used in the score

**HINT: PANCREAS

A

Glasgow criteria/score

Should be used within first 48hrs of admission and any pt scoring =/>3 should be considered to have severe pancreatitis and HDU care referral is warranted. Factors assessed include:

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10
Q

Discuss the management of acute pancreatitis

A

Pts can become very unwell rapidly so need careful assessment and monitoring. Use Glasgow score to see if pt needs hDU or ICU management.

Treatment is supportive and trying to treat underlying cause if known:

  • IV fluids
  • Analgesia (opiod)
  • Oxygen if required
  • Antiemetic e.g IM ondansetron
  • Encourage to eat & drink if can tolerate. Consider NG tube if cannot eat
  • Catheterisation to allow careful fluid balance monitoring
  • Abx if evidence if confirmed pancreatic necrosis (as prophylaxis) or if evidence of infection
  • Treatment of underlying cause e.g. cholecystectomy or ERCP for gallstone pancreatitis
  • Treatmen of complications
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11
Q

How long does it take for most acute pancreatitis pts to improve?

A

3-7 days

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12
Q

State some potential complications of acute pancreatitis

A

Systemic complications

  • DIC
  • ARDS
  • Hypocalcaemia
  • Hyperglycaemia

Local complications

  • Necrosis of pancreas +/- infection of necrotic area
  • Abscess formation
  • Pseudocysts
  • Chronic pancreatitis
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13
Q

When should you suspect pancreatic necrosis as a complication of acute pancreatitis?

What investigations would you do?

How would you mange this?

A
  • Pt with persistent systemic inflammation for more than7-10 days after onset
  • Confirm pancreatic necrosis by CT. Fine needle aspiration of necrosis can give definitive diagnosis of infected pancreatic necrosis
  • Pancreatic necrosectomy (generally do this 3-5 weeks after diagnosis to allow walled-off necrosis to develop)
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14
Q

What is a pancreatic pseudocyst?

How do they present?

What are they prone to?

Discuss the managment

A
  • Collection of flid containing pancreatic enzymes, blod & necrotis tissue; can occur anywhere within or adjacent to pancreas. Commonly in lesser sac
  • May be found incidentally or present with symptoms of mass effect e.g. biliary obstruction, gastric outlet obstruction
  • Haemorrhage & infection
  • 50% resolve spontaenously. If not resolved in 6 weeks unlikely to hence do surgical debridement or endoscopic drainage
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15
Q

What is chronic pancreatitis?

State some risk factors

A
  • Chronic inflammation of pancreas leading to fibrosis and reduced function of pancreatic tissue. Damage is irreversible.
  • Most common causes:
    • Chronic alcohol abuse (60%)
    • Idipathic (30%)
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16
Q

Discuss the presentation of chronic pancreatitis

A
  • Chronic pain
    • Epigastric
    • Radiate to back
  • Associated nausea & vomiting
  • Endocrine insufficiency
    • Impaired gluose regulation
    • DM
  • Exocrine insufficiency leading to malabsorption
    • Weight loss
    • Steatorrhoea
    • Diarrhoea
  • Signs of cachexia & malabsorption
  • Biliary obstruction or gastric outlet obstruction due to pseudocysts (often present)
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17
Q

What investigations should you do if you supect chronic pancreatitis?

A

Bedside

  • Plasma glucose
  • Faecal elastase test

Bloods

  • FBC
  • U&Es
  • LFTs
  • Serum amylase: not often raised
  • Serum lipase: not often raised

Imaging

  • CT abdomen & pelvis: can show atrophy, calcification and if any pseudocysts present
  • Ultrasound: anatomy of biliary tree & pancreas
  • MRCP: anatomy of biliary tree & pancreas

*Reduced faecal elastase & CT are used to confirm diagnosis

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18
Q

Discuss the management of chronic pancreatitis

A
  • Treat any reversible underlying cause
    • E.g. abstinence from alcohol
    • E.g. statin for hyperlipidaemia
  • Anaglesia
    • WHO pain ladder
    • In long term may replace opiods with neuropathhic analgesia instead
  • Pancreatic enzyme replacement
    • E.g. Creon
  • Fat soluble vitamine supplements
  • Insulin if diabetic
  • ERCP (endoscopic retrograde cholangiopancreatography) for stone removal, stent insertion etc to treat obstruction to biliary system & pancreatic duct
  • Surgery (RARE due to high morbidity & mortality); may be done if:
    • Abscesses
    • Pseudocyts
    • Obstruction of biliary system & pancreatic duct
    • Sever chronic pain (drain ducts & remove inflammed tissue)
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19
Q

If a pt has had chronic pancreatitis for 20yrs or more what are they at risk of?

A

Pancreatic malignancy

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20
Q

Remind yourself of components of bile

A

*bile salts= products of Hb metabolism

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21
Q

Remind yourself of the anatomy of the biliary tree

A

The right hepatic duct and left hepatic duct leave the liver and join together to become the common hepatic duct. The cystic duct from the gallbladder joins the common hepatic duct halfway along. The pancreatic duct from the pancreas joins with the common hepatic duct further along. When the common bile duct and the pancreatic duct join they become the ampulla of Vater, which then opens into the duodenum. The sphincter of Oddi is a ring of muscle surrounding the ampulla of Vater that controls the flow of bile and pancreatic secretions into the duodenum.

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22
Q

Remind yourself of the following definitions:

  • Cholestasis
  • Cholelithiasis
  • Choledocholithiasis
  • Biliary colic
  • Cholecystitis
  • Cholangitis
  • Gallbladder empyema
  • Cholecystectomy
  • Cholecystostomy
A
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23
Q

What are gallstones?

What are most gallstones made from?

State some potential complications of gallstones

A
  • Stones that form within the gallbladder as a result of supersation of bile
  • Most= cholesterol
  • Gallstones can be/cause:
    • Asymptomatic
    • Biliary colic
    • Acute cholecystitis
    • Ascedning cholangitis
    • Pancreatitis
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24
Q

State the 3 different possible compositions of gallstones

A

All formed from supersaturation of bile:

  • Cholesterol stones
  • Pigment stones (commonly seen in those with haemolytic anaemia)
  • Mixed stones
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25
Q

State some risk factors for gallstones

*HINT: 5 F’s

A
  • Fat
  • Female
  • Fertile
  • Forty
  • Family history
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26
Q

For biliary colic, ,discuss:

  • What it is
  • Presentation
  • Why pts advised to avoid fatty foods
A
  • Stones temporarily obstructing the drainage of gallbladder; may be lodged in neck of gallbladder or in cystic duct. When it falls back into gallbladder symptoms resolve. Pain occurs when get contraction of gallbladder.
  • Presentation:
    • Severe, sudden, dull & colikcy epigastric or RUQ pain
    • May radiate to back
    • Triggerd by consumptoinof meals (particularly fatty ones)
    • Last between 30mins-8hrs
    • Associated nausea & vomiting
  • Fatty acids stimulate CCK secretion from dodenum; CCK triggers contraction of gallballder leading to biliary colic
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27
Q

For acute cholecystitis, discuss:

  • What it is including pathophysiology
  • Presentation
A
  • Inflammation of gallbladder due to blockage of cystic duct preventing gallbladder from emptying. 95% caused by gallstones being permanently lodged in either gallbladder neck or cystic duct
  • Presentation:
    • RUQ pain
    • Pain may radiate to R shoulder
    • Fever
    • Nausea & vomiting
    • Tachycardia
    • Tachypnoea
    • RUQ tenderness
    • Murphy’s sign positive
    • Raised CRP & WCC
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28
Q

If cholecystitis is caused by gallstones what can it be termed?

A

Calculous cholecystitis

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29
Q

What is acalculous cholecystitis?

A

Inflammation of gallbladder in which the dysfunction in gallbladder emptying is caused by something other than gallstones e.g.

  • TPN or long periods of fasting- gallbladder not stimulated by food to regularly empty so pressure builds up
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30
Q

What is Murphy’s sign?

A
  • Place hand in RUQ and apply pressure
  • Ask pt to take deep breath in
  • Gallbladder will move downwards and come into contact with hand
  • If inflamed gallbladder touches hand pt will be in acute pain and stop inspiration
  • Murphy’s sign positive is when there is a halt in inspiration due to pain

*Sonographic Murphy sign= doing Murphy’s test under USS- more accurate

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31
Q

What investigations would you do if you suspect biliary colic or acute cholecystitis?

*For each of the blood tests state what you would expect results to be in a.) biliary colic b.) acute cholecystitis

A

Bedside

  • Urine dipstick: rule out renal pathology
  • Pregnancy test: abdo pain any woman child bearing

Bloods

  • FBC: raised WCC in cholecystitis
  • LFTs: both biliary colic and acute cholecystitis likely to show raised ALP but ALT and bilirubin should stay in normal range
  • Amylase: rule out pancreatitis
  • CRP: raised in cholecystitis

Imaging

  • Ultrasound biliary tree: first line. Do MRCP if inconclusive
  • MRCP (magnetic resonance cholangiopancreatography)= GOLD STANDARD
  • ERCP: largely replaced by MRCP for diagnostic purposes. Main indication is to clear stones.
  • CT scan abdomen pelvis: used to look for complications e.g. abscesses or perforation
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32
Q

What might you find on USS of biliary tree if there is gallstone pathology?

A
  • Stones or sludge in gallbladder
  • Increased thickness of gallbladder wall (IF INFLAMMATION therefore not in biliary colic but would see in acute cholecystitis)
  • Bile duct dilation
  • Fluid around gallbladder
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33
Q

Discuss the managment of biliary colic

A
  • Analgesia
    • Paracetamol
    • +/- NSAIDs
    • +/- opiods
    • +/- antispasmodic e.g. hyoscine
  • Lifestyle:
    • Low fat diet
    • Weight loss
    • Increase exercise
  • High chance of reccurence & development of complications hence elective laparoscopic cholecystectomy within 6 weeks of first presentation
34
Q

Discuss the management of acute cholecystitis

A
  • Analgesia
    • Paracetamol
    • +/- NSAIDs
    • +/- opioids
  • Antiemetics
  • IV abx (e.g. co-amoxiclav +/- metronidazole)
  • IV fluids if required
  • Laparoscopic cholecystectomy within 1 week (NICE- but ideally in 72hrs)
  • Percutaneous cholecystotomy if unsuitable for surgery or do not improve after initial treatment
35
Q

If cholecystectomy is done open rather than laparoscopically what incision is made?

A
  • Kocher incision
  • Right subcostal
36
Q

If a pt having a cholecystectomy has stones in bile duct, what can we do?

A
  • Remove before via ERCP
  • Or remove during surgery
37
Q

State some potential complications of cholecystectomy

A

Generic

  • Bleeding
  • Infection
  • Pain
  • Scar
  • VTE
  • Anaestheti risks

Surgery specific

  • Stones left in bile duct
  • Damage to bile duct leading to leakage or stricutres
  • Damage to surroudning organs e.g. bowel
  • Post-cholectomy syndrome
38
Q

What is post-cholectomy syndrome?

A

Group of non-specific symptoms that can occur after cholecystectomy; may be due to change in bile flow after gall bladder removal. Symptoms improve with time but can include:

  • Diarrhoea
  • Indigestion
  • Epigastric or RUQ pain or discomfort
  • Nausea
  • Intolerance of fatty foods
  • Flatulence
39
Q

State some potential complications of acute cholecystitis

A
  • Mirizzi syndrome
  • Gallbladder empyema
  • Chronic cholecystitis
  • Bouveret’s syndrome
  • Gallstone ileus
  • Perforation
  • Sepsis
  • Gangrenous gallbladder
40
Q

What is Mirizzi syndrome?

How do you diagnose?

Management?

A
  • A stone is impacted in Hartmann’s pouch (outpouching of gallbladder wall at junction with cystic duct). Can cause compressionof common hepatic bile duct leading to obstructive jaundice (even though stones not in bile duct)
  • MRCP
  • Laparascopic cholecstectomy
41
Q

What is gallbladder empyema?

How do you diagnose?

Management

A
  • Gallbladder filled with pus. Pts very unwell often septic. High morbidity & mortality.
  • US or CT scan
  • Laparscopic cholecystectomy +/- intra-operative drainage. May have to do open. If can’t do surgery do percutaneous cholecystestomy
42
Q

Explain the pathophysiology of:

  • Bouveret’s syndrome
  • Gallstone ileus
A

Inflammation of gallbladder can cause fistula formation between gallbladder & small bowel- a cholecystoduodenal fistula. Allows gallstones to pass directly into smal bowel typically at duodenum.

  • Bouveret’s syndrome: stone impacts in proximal duodenum causing gastric outlet obstruction
  • Gallstone ileus: stone impacts in terminal ileum (narrowest part of small bowel) causing smal bowel obstruction
43
Q

For ERCP state:

  • Main indication
  • What it entails
  • Complications
A
  • Main indication= clear stones in bile ducts
    • Others include: injecting contrast to visualise, sphincterotomy of sphincter of Oddi, inserting stents, biopsies of tumours
  • Insert endoscope down oesophagus into duodenum then through sphincter of Oddi and into Ampulla of Vater; gives access to biliary system.
  • Complications:
    • Excessive bleeding
    • Cholangitis (infection of bile ducts)
    • Pancreatitis
44
Q

What is acute cholangitis?

Is is serious?

A
  • Acute cholangitis (also known as ascending cholangitis)= infection & inflammation of bile ducts
  • Surgial emergency as has a high mortality due to risk of sepsis
45
Q

State two main causes of acute/ascending cholangitis

A
  • Obstruction in bile ducts (e.g. gallstones in common bile duct or cholangiocaricinoma. Causes stasis of fluid & increased intraluminal pressure allowing bacterial colonisation to become pathological)
  • Infection introduced by ERCP
46
Q

State the 3 most common causative organisms of acute/ascending cholangitis

A
  • Escherichia coli (27%)
  • Klebsiella species (16%)
  • Enterococcus (15%)
47
Q

Describe the clinical presentation of acute/ascending cholangitis

A
  • Charcots triad
    • RUQ pain
    • Fever
    • Jaundice (raised bilirubin)
  • Reynold’s pentad
    • RUQ pain
    • Jaundice
    • Fever
    • Hypotension
    • Confusion
  • Itching
  • Pale stools
  • Dark urine
  • PMH of gallstones, cholangiocarcinoma, cholangitis, ERCP
48
Q

Remind yourself of Charcot’s triad

Remind yourself of Reynold’s pentad

A
49
Q

What investigations are required if you suspect acute/ascending cholangitis?

A

Bedside

Bloods

  • FBC: leucocytosis
  • LFTs: raised ALP +/- gamma GT, raised conjugated bilirubin)
  • U&Es
  • CRP: raised
  • Blood cultures: ALWAYS TAKE. 20% are positive
  • Clotting: surgery
  • Serum amylase: rule out pancreatitis

Imaging

  • USS biliary tree: duct dilation >6mm
  • ERCP: gold standard. Both diagnostic & therapeutic
  • MRCP: may be required prior to ERCP to obtain detailed images of tree before scoping
50
Q

Discuss the management of acute/ascending cholangitis, include:

  • Immediate
  • Defintive
A

Immediate

  • A-E
  • Sepsis 6 if septic
  • Broad spectrum abx (e.g. co-amoxiclav & metronidazole)
  • Analgesia

Definitive

  • ERCP to decompress biliary tree
  • Percutanesous transhepatic cholangiograpy (PTC) and percutaneous transhepatic biliary drainage (PTBD) if pt not suitable for ERCP or if ERCP unsucessful
51
Q

What is PTC and PTBD?

A

PTC allows placement of a biliary drain (PTBD) to decompress the biliary tree from above. This is performed by passing a needle through the skin and into the bile ducts. It is more likely to be successful when the intrahepatic bile ducts are sufficiently dilated. Contrast material is injected and the anatomy of the biliary tree is defined. A drain (the PTBD) can then be inserted and fixed to the skin. Stent may also be inserted

52
Q

State the mortality of acute/ascending cholangitis

A

5-10%

53
Q

Many procedures can be performed during ERCP; state some

A
54
Q

For cholangiocarcinoma, discuss:

  • What it is
  • Where it most commonly occurs
  • Most common type of cancer
  • Slow or fast growing
A
  • Cancer of the biliary tree
  • Can affect intra- and extra-hepatic ducts but most common site is the perihilar region where the R and L hepatic duct join to form the common bile duct (termed Klatskin tumour)
  • Adenocarcinoma (95%) arising from cholangiocytes in biliary tree
  • Slow growing
55
Q

State some risk factors for cholangiocarcinoma- highlight main 2

A
  • PSC
  • UC (they have increased risk of PSC)
  • Liver flukes
  • HIV
  • Hepatitis
  • Alcohol excess
  • Diabetes
56
Q

Cholangiocarcinoma is generally asymptomatic until late stage in disease; what symptoms & signs would pts get when they do get symptoms

A
  • Features of obstructive jaundice
    • Pale stools
    • Dark urine
    • Generalised itching
  • Non-specific:
    • Unexplained weight loss
    • Early satiety
    • Anorexia
    • RUQ pain
    • Palpable gallbladder
    • Hehpatomegaly
57
Q

What is Courvoisier’s law and what is it’s relevance in cholangiocarcinoma?

A

In the presence of jaundice and an enlarged or palpable gallbladder, malignancy of the biliary tree or pancreas should be suspected as the cause is unlikely to be gallstones.

58
Q

What two conditions should painless jaundice make you think of?

A
  • Cholangiocarcinoma
  • Cancer of head of pancreas (more common so more likely to be MCQ answer)
59
Q

What invesigations should be done if you suspect cholangiocarcinoma?

A

Bedside

Bloods

  • LFTs:elevated ALP, gamma GT
  • CA19-9: tumour marker both cholangio & pancreatic cancer
  • CEA: tumour marker pancreatic cancer
  • Other usual blood tests

Imaging

  • US biliary tree: may be used to initially find obstructive cause but most likley know this from clinical picture
  • MRCP: best imaging for cholangiocarcinoma
  • ERCP to get biopsy for histology
  • Staging CT scan/CT TAP
60
Q

Discuss the management of cholangiocarcinoma

A

As with all cancers, MDT meeting.

If early stages curative surgery with complete surgical resection +/- neoadjuvant and/or adjuvant radiotherapy

  • Intrahepatic or Klatsin: partial hepatectomy & reconstruction of biliary tree
  • Distal common duct: Whipple’s procedure (pancreaticoduodenectomy)

MOST pts have inoperalbe disease at time of presentation hence palliative treatment:

  • Stenting: releive obstructive symptoms
  • Surgical bypass procedure: if can’t stent
  • Palliative chemotherapy
  • Palliative radiotherapy
  • Other palliative care measures
61
Q

What % of pts who undergo resection for curative intent for cholangiocarcinoma have recurrence in 5yrs?

A

50%

*survival tends to be better for distal tumours

62
Q

State 2 potential complications of cholangiocarcinoma

A
  • Biliary tract sepsis (due to obstruction, stasis, increased risk of infection etc..)
  • Secondary biliary cirrhosis
63
Q

What type of pancreatic cancer most common?

Where abouts in pancreas- head, body or tail- do pancreatic cancers most commonly occur?

A
  • 90% are ductal adenocarcinomas of pancreas.
    • Rest can be divided into exocrine and endocrine tumours
  • Head
64
Q

Pancreatic cancer tends to spread and metastasise late; true or false?

A

FALSE; spread & metastasises early to

  • Liver
  • Peritoneum
  • Lungs
  • Bones
65
Q

What is the average survival when diagnosed with advanced pancreatic cancer?

A

6 months

66
Q

State some risk factors for pancreatic cancer

A
  • Smoking
  • Chronic pancreatitis
  • Late onset diabetes mellitus
  • FH
  • Excessive alcohol
  • Increasing age
67
Q

Describe the clinical presentation of pancreatic cancer

A
  • Painless obstructive jaundice
    • Yellow skin
    • Scleral icterus
    • Pale stools
    • Dark urine
    • Generalised itching
  • Weight loss
  • Non-specific abdo or back pain
  • Palpable mass in epigastrium
  • Change in bowel habit
  • Nausea & vomiting
  • New onset diabetes or worsening of T2DM
  • Acute pancreatitis
  • Thrombophlebitis migrans
68
Q

If a pt has worsening glycaemic control despite good lifestyle measures and medication or has new onset diabetes you must make sure you have considered pancreatic cancer as a differential; true or false?

A

TRUE

69
Q

What are the NICE guidelines in regards to pancreatic cancer referrals?

A
  • 2 week wait referral= >40yrs with jaundice
  • Direct access CT abdomen to assess for pancreatic caner if over 60yrs with weight loss PLUS any of:
    • Diarrhoea
    • Back pain
    • Abdominal pain
    • Nausea
    • Vomiting
    • Constipation
    • New onset diabetes

*Pancreatic cancer is teh only scenario where GPs can directly refer for a CT scan

70
Q

What is Trosseau’s sign of malignancy?

A

Migratory thrombophlebitis as a sign of malignancy- particularly pancreatic adenocarcionma.

71
Q

What investigations are required if you suspect pancreatic cancer?

A

Bedside

Bloods

  • FBC: anaemia, thrombocytopenia
  • LFTs: raised ALP, gamma GT, bilirubin
  • CA19-9: tumour marker
  • CEA: tumour marker
  • Other routine blood tests…

Imaging

  • CT abdomen: visualise cancer **MOST important in terms of diagnosis
  • Staging CT TAP
  • Biopsy via ERCP or percutaneously under US or CT guidance
72
Q

Discuss the management of pancreatic cancer

A

As with all cancer, MDT meeting.

Only curative option= radical resection with adjuvant chemotherapy. Surgical options depend on location of tumour & include:

  • Whipples procedure/pancreaticoduodenectomy
  • Modified Whipples procedure/pylorus presevering pancreaticoduodenectomy
  • Total pancreatectomy
  • Partial pancreatectomy

In most pts surgery is not posible so palliative treatment involves:

  • Stents to relieve obstruction
  • Bypass surgery to relieve obstruction
  • Palliative chemotherapy
  • Palliative radiotherapy
  • Enzyme replacements e.g. Creon
  • Other usual palliative care measures

In pts with good performance status but metastatic disease use of FOLFRIOX regime

73
Q

What is a Whipple’s procedure?

A

Also called pancreaticodudenectomy; removal of:

  • Head of pancreas
  • Antrum of stomach
  • Duodenum
  • Gallbladder
  • Common bile duct
  • Relevant lymph nodes

All viscera are removed due to common blood supply from gastroduodenal artery.

Tail of pancres and hepatic duct are then attached to jejenum and stomach is anastomed with jejenum

74
Q

What is a modified Whipple’s procedure?

A

Same as Whipple’s but don’t remove antrum & pylorus of stomach

75
Q

What is the 5yr survival rate of pancreatic cancer?

A

5%

76
Q
A
77
Q

We have said that 90% of pancreatic cancers are adenocarcinomas of the ducts. The remainig tumours can be divided into exocrine or endocrine tumous. What syndrome are endocrine tumours of pancreas associated with?

A
  • MEN 1
  • MEN1 typically consists of:
    • Hyperparathyroidism
    • Endocrine pancreatic tumours
    • Pituitary tumours (most commonly prolacintoma)
78
Q

Endocrine tumours of pancrease can be functional or non-functional. For each of the endocrine cells (G, alpha and beta cells) in the pancreas state:

  • The hormone it secretes
  • Physiological function
  • Features of a functional tumour
A
79
Q

Endocrine tumours of pancrease can be functional or non-functional. For each of the endocrine cells (delta and non-islet cells) in the pancreas state:

  • The hormone it secretes
  • Physiological function
  • Features of a functional tumour
A
80
Q

Briefly discuss management of pancreatic endocrine cancers

A
  • Small non-functioning= observe
  • Larger or functioning= resection of tumour & any metastases
81
Q

Summary of non-invasive liver screeen (see med block for more)

A

Yr3 Surgery: General (13 decks)

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