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Junior surgery > GI- HPB > Flashcards

GI- HPB Flashcards

1
Q

Give some of the causes of acute pancreatitis

A
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2
Q

Explain the pathogenesis behind acute pancreatitis

A
  • There is premature and exagggerated activation of the digestive enzymes of the pancreas
  • Causes pancreatic inflammatory response and increased vascular permeability
  • Enzymes are released from the pancreas causing autodigestion which can lead to fat necrosis which causes hypocalcaemia
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3
Q

How do patients with acute pancreatitis present?

A
  • Severe epigastric pain
    • may radiate to the back
  • Nausea and vomting
  • Epigastric tenderness +/- guarding
  • May see Cullen’s or Grey Turner’s sign in severe cases
  • May see tetant due to hypocalcaemia
  • May haemodynamically unstable
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4
Q

How do you make a diganosis of acute pancreatitis?

A
  • Serum amylase - x3 upper limit of normal is main criteria
  • LFTs - assess for any concurrent cholestatic element
    • (acute pancreatitis + ALT >150 is 85% predictive for gallstones as underlying cause)
  • Serum lipase - more accurate than amylase but not routinely done in all hospitals
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5
Q

How do you evaluate the severity of acute pancreatitis? When should this evaluation be done?

A

modifed GLASGOW criteria within the 1st 48hrs of admission

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6
Q

What imaging can be done if suspecting acute pancreatitis?

A
  • Abdominal uss (may be requested if underlying cause is unknown)
  • AXR - not routine but can show sentinal loops
  • CT with contrast - if initial assessment and investigations are inconclusive
    • should only be one 6-10 days after admission
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7
Q

How do you treat acute pancreatitis?

A

Largely conservative + treatment of any underlying cause

  1. NG tube if vomiting
  2. IV fluids crystalloid
  3. O2 therapy
  4. Catheterise and monitor input + output
  5. Opiod pain relief
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8
Q

How do you manage cases of acute severe pancreatitis?

A

Escalate to HDU or ​ITU

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9
Q

What are some of the systemic complications of acute pancreatitis?

A
  • Hypocalcaemia due to fat necrosis
  • Hyperglycaemia due to destruction of islet of Langerhans
  • Acute respiratoyr Distress Syndrome
  • Disseminated Intravascular Coagulation (DIC)
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10
Q

How should pancreatic necrosis be treated?

A
  • Confirm on CT scan
  • Often needs pancreatic necrosectomy
    • typically delayed 3-5 weeks after symptom onset to allow walled off necrosis to develop
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11
Q

What is a pancreatic pseudocyst?

A

A collection of fluid containing pancreatic enzymes, blood and necrotic tissue

Can occur anywhere within or adjacent to the pancreas → usually seen in the lesser sac

Typically form weeks after initial pancreatitis

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12
Q

How do pancreatic pseudocysts present?

A
  • either found incidentally on imaging
  • Or symptoms:
    • biliart obstruction
    • gastric outlet obstruction
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13
Q

How are pancreatic pseudocysts treated?

A
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14
Q

What are the causes of chronic pancreatitis?

A
  1. Chronic alcohol abuse (60%)
  2. Idiopathic (30%)
  3. Metabolic (hyperlipidaemia/ hypercalcaemia)
  4. Infection (HIV, mumps, coxsackie)
  5. Herediary (cystic fibrosis)
  6. Autoimmune
  7. Anatomical - malignancy/ stricure
  8. Congenital abnormalities - pancreas divisum/ annular pancreas
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15
Q

What are the symptoms of chronic pancreatitis?

A
  • Chronic pain
    • typically epigastrum and back
  • Associated N+V
  • Endocrine insufficiency - due to endocrine gland damage → Diabetes mellitus (Type 3c)
  • Exocrine insufficiency - failure to produce digestive enzymes causes malabsorption, weight loss, diarrhoea, steatorrhoea
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16
Q

How do you investigate chronic pancreatitis?

A
  • Urine dip
  • Routine bloods
  • Serum amylase or lipase levels are not raised in chronic disease
  • Check glucose
  • Check LFTs to ensure no concurrent obstructive jaundice
  • Faecal elastase level will be low in most patients
  • CT scan - can show pancreati atrophy, calcification, pseudocysts
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17
Q

How should chronic pancreatitis be managed?

A
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18
Q

What are the types of pancreatic cancer?

A
  • Ductal carcinoma of the pancreas (90%)
  • Exocrine tumours e.g. pancreatic cystic carcinoma
  • Endocrine tumours (derived from islet cells)
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19
Q

Which age group are pancreatic cancers most common in?

A

60-80 years

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20
Q

Which structures are typically affected by direct invasion of pancreatic cancers?

A
  1. Spleen
  2. Transverse colon
  3. Adrenal glands
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21
Q

What are some of the risk factors for developing pancreatic cancer?

A
  • Smoking
  • Chronic pancreatitis
  • Hereditary element (7% have FHx of disease)
  • Late onset diabetes mellitus
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22
Q

How does pancreatic cancer present?

A

Typically presents late therefore 80% are unresectable at time of diagnosis.

Specific features depend on site of the tumour

  • Obstructive jaundice - due to compression of common bile duct, typically painless
  • Weight loss - due to metabolic effects of cancer or secondary to endocrine dysfunction
  • Abdominal pain - non specific. Due to invasion of coeliac plexus
  • May present with acute pancreatitis but uncommon
  • Thrombophlebitis migrans (recurrent migratory superficial thrombophlebitis caused by paraneoplastic hypercoagulable state)
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23
Q

What is Courvoisier’s Law?

A

The presence of jaundice and an enlarged/ palpable gallbaldder is a strong indicatory for suspecting malignancy of the biliary tree or pancreas

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24
Q

Which tumour marker is raised in pancreatic cancer?

A

CA19-9

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25
Q

What imaging is done in pancreatic cancer?

A
  • Abdominal ultrasound
  • CT imaging CAP (most prognostic as can give stage disease progression)
  • PET-CT scan
  • Endoscopic ultrasound with fine needle aspiration biopsy for histological evaluation
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26
Q

What treatment is available for pacreatic cancers?

A
  • Pancreaticduodenectomy (Whipple’s procedure) if tumour is in the head of the pancreas
  • Distal pancreatectomy in tumours of the body/tail
  • Adjuvant chemotherapy with 5-fluorouracil is recommened after surgery
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27
Q

What are some of the complications of pancreaticoduodenectomy and pancreatectomy?

A
  • Pancreatic fisutulae
  • Delayed gastric empyting
  • Pancreatic insufficiency
28
Q

Briefly describe the Whipple’s procedure

A

Pancreaticduodenectomy

Removal of the head of pancreas, antrum of stomach, 1st and 2nd parts of duodenum, gallbladder and common bile duct

All are removed due to sharing a common blood supply: gastroduodenal artery

The tail of the pancreas is attached to the jejunum and stomach is anastamosed to the jejunum

29
Q

What is the 5 year survival rate in pancreatic malignancy?

A

<5 %

30
Q

What is multiple endocrine neoplasia 1 syndrome (MEN1)?

A

Typically consists of

  • Hyperparathyroidism
  • Endocrine pancreatic tumours
  • Pituitary tumours
31
Q

What is bile formed from?

A
  • Cholesterol
  • Phospholipids
  • Bile pigments (product of Hb metabolism)
32
Q

What are the 3 main types of gall stone?

A
  • Cholesterol stones formed from excess cholesterol production
  • Pigment stones purely of bile pigments from excess bile production (in known haemolytic aneamis)
  • Mixed stones
33
Q

Give some of the risk factors for developing gall stones

A
  1. Fat
  2. Female
  3. Forty
  4. Fertile
  5. Family Hx
  6. Pregnancy
  7. Oral contraceptives
  8. Haemolytic aenamia
  9. Malabsoprion (previous ileal resection or Crohn’s disease)
34
Q

What is biliary colic?

A

When the gallbladder neck becomes impacted by a gallstone but there is no inflammatory response yet

35
Q

Describe the character of pain felt in biliary colic

A
  • Sudden onset
  • Dull
  • Comes and goes
  • RUQ but can radiate to epigastrum +/- the back
  • May worsen on consumption of fatty food (due to release of CCK)
  • May compain of N+V
36
Q

How does acute cholecystitis present?

A
  • Constant pain inthe RUQ or epigastrum
  • Associated with signs of inflammation e.g. fever, lethargy
  • Murphy’s sign +
37
Q

What is Murphy’s sign?

A
38
Q

Which labarotory tests should be done if suspecting biliary colic/ cholecystitis?

A
  • FBC, CRP - checking for any inflammatory response (in cholecystitis)
  • LFTs
    • show a raised ALP (indicates ductal occlusion)
    • ALT and bilirubin should be normal (unless Mirizzi syndrome)
  • Amylase (or lipase) to check for any evidence of pancreatitis
  • Urinalysis
  • Pregnancy test
39
Q

What 3 features are seen on tran-abdominal ultrasound in gall stone pathology?

A
  1. Presence of gallstones
  2. Gallbladder wall thickness
  3. Bile duct dilatation
40
Q

What imaging can be done if investigating gall stone pathology?

A
  • Transabdominal ultrasound - 1st line
  • MRCP gold standard
  • ERCP is slowly replacing MRCP
41
Q

How should biliary colic be managed?

A
  • Analgesia - regular paracetamol +/- NSAIDs +/- opiates
  • Advise on lifestyle factors: low fat diet, weight loss, increasing exercise
  • Elective laparscopic cholecystectomy - should be offered within 6 weeks of 1st presentation due to high chance of symptom recurrence
42
Q

How sould acute cholecystitis be managed?

A
  • IV antibiotics (co-amoxiclav +/- metronidazole)
  • Analgesia
  • Antiemetics
  • Laparoscopic cholecystectomy within 1 week of presentation but should be done within 72 hours ideally
  • Percutaneous cholecystostomy if not fit for surgery and not responding to abx (drains the infection)
43
Q

What is Mirizzi syndrome?

A

When a gallstone located in Hartmanns pouch or the cystic duct can compress with adjacent common hepatic duct

Causes an obstructive jaundice without any stones present in the lumen of the common hepatic/ bile duct

confirmd by MRCP, managed by lap chole

44
Q

What is a gallbladder empyema?

A

When the gallbladder fills with pus

Patients often unwell, often septic, significant morbidity and mortality

45
Q

What is chronic cholecystitis?

A
  • Hx of recurrent or untreated cholecystitis leading to persistant inflammation of the gallbladder wall
  • Ongoing RUQ/ epigastric pain +/- N+V
46
Q

What is Bouveret’s syndrome?

A

Condition where a stone impacts in the proximal duodenum causing gastric outlet obstruction

Happens due to reccurrent gallbladder inflammation causing cholecystoduodenal fistula​ allowing gallstoneto pass directly to small bowel

47
Q

What is gallstone ileus?

A

Condition where a gallstone impacts at the terminal ileum (narrowest part of small bowel) causing obstruction

Happens due to reccurrent gallbladder inflammation causing cholecystoduodenal fistula​ allowing gallstones to pass directly to small bowel

48
Q

What is Charcot’s triad?

A
49
Q

What is Reynold’s pentad?

A
50
Q

What are the common causes of cholangitis?

A

Anything that causes occlusion of the biliary tree

Commonly:

  1. Gallstones
  2. ERCP
  3. Cholangiocarcinoma
51
Q

Which organisms are most common involved in cholangitis?

A
  1. E. Coli - gram -ve rods
  2. Klebsiella - gram -ve rods
  3. Entercoccus - gram +ve diploccoci
52
Q

What are the clinical features of cholangitis?

A
  • RUQ pain
  • Fever
  • Jaundice (bilirubin >50 micromol/L)
  • Pruritis (due to bile accumulation)
  • Pale stools
  • Dark urine
53
Q

Which laboratory investigations can be done for cholangitis?

A
  • FBC - leukocytosis seen in most patients
  • LFTs - show a riased ALP, +/-raised GGT, raised bilirubin
  • Always take blood cultures incase pateints is septic
54
Q

What imaging can be done if patients are susepected to have acute ascending cholangitis?

A
  • USS of biliary tract - will show bile duct dilation ( >6cmm)
  • ERCP gold standard but mainy require MRCP before intervention
55
Q

How should acute ascending cholangitis be managed prior to definitive management?

A
  • IV access
  • IV fluids
  • Broad spectrum IV antibiotics
  • Monitor for sepsis and implement sepsis 6
56
Q

What is the definitive management for acute cholangitis?

A
  • Endoscopic biliary decompression (removes cause of blocked biliary tree)
  • If too sick to tolerate ERCP, percutaneous transhepatic cholangiography is 2nd line intervention
  • May require cholecystectomy long term if gallstones are the underlying cause
57
Q

What are some of the complications of ERCP?

A
  • Repeat cholangitis
  • Pancreatitis
  • Bleeding
  • Perforation
58
Q

What is cholangiocarcinoma?

A

Cancer of the biliary system

59
Q

What is the most common site for a cholangiocarcinoma to occur?

A

At the bifurcation of the right and left hepatic ducts (Klatskin tumours)

60
Q

Histologically, what are the most common types of cholangiocarcinomas?

A
  • 95% are adenocarcinomas (arising from cholangiocytes in biliary tree)
  • Remaining majority are squamous cell carcinomas
  • Rarer types: sarcomas, lymphomas, small cell cancers
61
Q

What are some of the risk factors for developing cholangiocarcinoma?

A
  • Primary sclerosing cholangitis (life time risk 10-20%)
  • Ulcerative colitis
  • Infection (Liver flukes, HIV, hepatitis)
  • Toxins (rubber and aircraft industry chemicals)
  • Congenital (Caroli’s disease, choledochal cyst)
  • Alcohol excess
  • Diabetes Mellitus
62
Q

What are the clinical features of cholangiocarcinoma?

A
  • Often asymptomatic until late stage of disease
  • Post hepatic jaundice
  • Pruritis
  • Pale stools
  • Dark urine
  • RUQ less common
  • Early satiety
  • Weight loss
  • Anorexia
  • Malaise
  • Jaundice
  • Anorexia
63
Q

Which tumour markers will be elevated in cholangiocarcinoma?

A

CEA and CA19-9

64
Q

How is cholangiocarcinoma managed?

A
  • Definitive cure: complete surgical resection
    • however most patientsare inoperable by time of presentation
  • Intrahepatic or Klatskin tumours require partial hepatectomy and reconstruction of the biliary tree
  • Radiotherapy (adjunct or neoadjunct)
65
Q

What are the palliative options for cholangiocarcinoma?

A
  • Stenting - ERCP to stent bile duct and relieve obstruction
  • Surgery - surgical bypass if obstruction cannot be relieved by stenting
  • Medical - palliative radiotherapy (cisplatin and gemcitabine)

Junior surgery (8 decks)

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