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GI Pathology > 7. Pancreatic disease and surgery > Flashcards

7. Pancreatic disease and surgery Flashcards

1
Q

Define acute pancreatitis.

A

Acute inflammation of the pancreas. Classification:

  • Mild AP: Associated with minimal organ dysfunction and uneventful recovery
  • Severe AP: Associated with organ failure or local complication.
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2
Q

What are the aetiological factors associated with acute pancreatitis?

A
  • Alcohol abuse (60-75%)
  • Gallstones (25-40%)
  • Idiopathic (10%)
  • Trauma (blunt/postoperatively/post-ERCP)
  • Viral infection (Mumps, CMV, HIV)
  • Drugs (steroids, diuretics, azathioprine)
  • Pancreatic carcinoma
  • Metabolic (hypercalcaemia, increased triglycerides, decreased temperature)
  • Autoimmune
  • Anatomical abnormalities
  • scorpion venom
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3
Q

Outline pathogenesis of acute pancreatitis.

A

Primary insult leads to release of activated pancreatic enzymes which starts autodigestion process resulting in inflammatory cytokine release, ROS, oedema, fat necrosis, and haemorrhage etc.
Alcohol: direct injury, increases sensitivity to stimulation
Gallstones: raises pancreatic ductal pressure
ERCP: increases pancreatic ductal pressure

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4
Q

How does acute pancreatitis present?

A

Abdominal pain
Nausea
Vomiting
Collapse

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5
Q

List signs that maybe present in patient with acute pancreatitis?

A

Pyrexia
Dehydration
Abdominal tenderness
Circulatory failure

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6
Q

What are the local complications associated with acute pancreatitis?

A
  1. Acute fluid collections
  2. Pseudocyst (fluid collection without an epithelial lining): present with hyperamylasaemia and/or pain.
  3. Pancreatic abscess
  4. Pancreatic necrosis
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7
Q

What investigations would you carry out if acute pancreatitis suspected?

A

Blood tests: serum amylase (elevated)/lipase, FBC, U&E, glucose, LFTs, Ca2+, arterial blood gases, lipids, coagulation screen.

AXR (ileus), CXR (pleural effusion or to exclude gastroduodenal perforation, which also raises the serum amylase)

Abdominal US (pancreatic oedema, gallstones, pseudocyst)

CT can (contrast enhanced)

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8
Q

Outline general management and monitoring of patients with acute pancreatitis.

A

General management:

  • Analgesia (pethidine, indomethacin)
  • Intravenous fluids
  • Blood transfusion (Hb <10 g/dl)
  • Nasogastric tube (Prevents abdominal distension and vomitus, and hence the risk of aspiration pneumonia).
  • Oxygen
  • May need insulin
  • Rarely require calcium supplements
  • Nutrition (enteral or parenteral) in severe cases

Monitoring:

  • Urine output (via catheter)
  • Pulse, BP
  • CVP
  • Arterial line (arterial blood gases: key predictive factor for severity of an episode and determine the need for continuous oxygen administration).
  • HDU / ITU
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9
Q

Outline management of specific and precipitating factors associated with acute pancreatitis.

A
  • Pancreatic necrosis: CT guided aspiration, antibiotics +/- surgery. If infected necrosis: Necrosectomy (Laparotomy - Minimally invasive)
  • Gallstones (cholelithiasis): ERCP/EUS, cholecystectomy
  • Alcohol: abstinence, counselling
  • Ischaemia: careful support, correct cause
  • Malignancy: resection or bypass
  • Hyperlipidaemia: Diet, lipid lowering drugs
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10
Q

Outline management of complications associated with acute pancreatitis.

A
  1. Abscess: antibiotics + drainage
  2. Pseudocyst: Dx by US or CT scan
    - <6 cm diameter: resolve spontaneously
    - Endoscopic drainage or surgery if persistent pain or complications (such as jaundice, infection, haemorrhage, rupture)
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11
Q

How do you assess severity of acute pancreatitis?

A 
Accurate identification of patients likely to progress to severe pancreatitis permits appropriate monitoring and intensive care to be put in place. Modified Glasgow criteria is used 48hr after the presentation of symptoms. If >3 of the following present then it's severe: 
Glucose > 10 mmol/L
Serum [Ca2+] < 2.00 mmol
WCC > 15000/mm3			
Albumin< 32 g//L
LDH > 700 IU/L
Urea > 16 mmol/L
AST/ALT > 200 IU/L
Arterial pO2 < 60mmHg
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12
Q

How useful is CT scanning when it comes to acute pancreatitis?

A 
Occasionally helpful in diagnosis
Useful in severe disease
Days 4-10 to identify necrosis
Useful for complications
  - Acute fluid collections
  - Abscess
  - Necrosis
  - Monitoring progress of disease
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13
Q
  1. How useful are antibiotics when it comes to acute pancreatitis?
  2. How useful is ERCP and EUS when it comes to acute pancreatitis?
A
  1. Controversial

2. Still controversial: Reduces complications in severe gallstone AP but associated with high mortality.

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14
Q

Define chronic pancreatitis.

A

Continuing inflammatory disease of the pancreas characterised by irreversible glandular destruction and typically causing pain and/or permanent loss of function.

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15
Q

What are the causes of chronic pancreatitis?

A

O-A-TIGER

  • Obstruction of main pancreatic duct due to tumour, trauma, pancreas divisum, fibrosis
  • Autoimmune
  • Toxin: alcohol, smoking, drugs
  • Idiopathic
  • Genetic: CFTR mutations. PRSS1, SPINK1 genes. Hereditary pancreatitis (rare, auto dominant)
  • Environmental: tropical chronic pancreatitis
  • Recurrent injuries: hypercalcaemia, hyperlipidaemia
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16
Q

Outline pathogenesis of chronic pancreatitis.

A
  1. Duct obstruction due to stones (calculi) leads to inflammation and protein plugs.
  2. ?Abnormal sphincter of Oddi function: spasm: increases intrapancreatic pressure. Relaxation: reflux of duodenal contents.
  3. Genetic polymorphisms: Abnormal trypsin activation
17
Q

Outline pathology of chronic pancreatitis.

A
  • Glandular atrophy & replacement by fibrous tissue
  • Ducts become dilated, tortuous & strictured
  • Inspissated (thickened) secretions may calcify
  • ‘Exposed’ nerves due to loss of perineural cells
  • Splenic , superior mesenteric & portal veins may thrombose leading to portal hypertension
18
Q

What are the clinical features of chronic pancreatitis?

A
  • Early disease is asymptomatic
  • Abdominal pain: exacerbated by food & alcohol; severity decreases with time
  • Weight loss (pain, anorexia, malabsorption)
  • Exocrine insufficiency (late manifestation)
    > fat malabsorption leads to steatorrhea and decrease in fat soluble vitamins (A,D,E,K), and Ca2+/Mg2+
    > protein malabsorption leads to weight loss, and decrease in vit B12.
  • Endocrine insufficiency leads to Diabetes in 30%
  • Misc.: jaundice, portal hypertension, GI haemorrhage, pseudocysts, ?pancreatic carcinoma
19
Q

What investigations would you carry out if chronic pancreatitis suspected?

A
  • Plain AXR (30% have calcification of pancreas)
  • Ultrasound: pancreatic size, cysts, duct diameter, tumours
  • EUS
  • CT scan
  • Pancreatic exocrine function (used infrequently):
    > faecal / serum enzymes (elastase)
    > Pancreolauryl test (enzyme response to a stimulus)
  • Blood tests:
    > Serum amylase increased in acute exacerbations
    > decrease in albumin, Ca2+/Mg2+, vit B12
    > increase in LFTs, Prothrombin time (vit K), glucose
20
Q

How is pain managed in chronic pancreatitis patients?

A
  • avoid alcohol
  • pancreatic enzyme supplements
  • opiate analgesia (dihydrocodeine, pethidine)
  • Coeliac plexus block (CT/EUS or Fluoroscopy guided)
  • referral to pain clinic/psychologist
  • Endoscopic treatment of pancreatic duct stones and strictures
  • Surgery in selected cases
21
Q

How are exocrine/endocrine symptoms managed in chronic pancreatitis patients?

A
  • Low-fat diet (30-40 g/day)
  • Pancreatic enzyme supplements (eg. Creon, Pancrex); may need acid suppression to prevent hydrolysis in stomach
  • Vitamin supplements usually not required
  • Insulin for diabetes mellitus (oral hypoglycaemics usually ineffective)
22
Q

When and type of surgery performed in chronic pancreatitis patients?

A
  • If suspicion of malignancy, intractable pain or any complications (e.g. pancreatic duct stenosis)
  • Surgery: drainage vs resection
    > Drainage: Pancreatic duct sphincteroplasty, Puestow (Rochelle modification)
    > Resection: Frey procedure (longitudinal pancreato-jejunostomy with local pancreatic resection) etc.
23
Q

List cancers of the pancreas.

A 
Majority = duct cell mucinous adenocarcinoma (mostly head of the pancreas).
Other pathological types:
- carcinosarcoma
- cystadenocarcinoma (better prognosis)
- Acinar cell
24
Q

List aetiological and risk factors associated with pancreatic cancer.

A

Aetiology = unknown
Risk factors:
- cigarette smoking: 25–30%
- chronic pancreatitis: 5–15 fold
- Adult onset DM of less than two years’ duration
- Hereditary pancreatitis
- Inherited predisposition: Periampullary cancer is a feature of FAP

25
Q

What are the clinical features of carcinoma of pancreas?

A
  • Upper abdominal pain - Ca body & tail
  • Painless obstructive jaundice - Ca head
  • Weight loss
  • Anorexia, fatigue, diarrhoea/steatorrhea, nausea, vomiting
  • Tender subcutaneous fat nodules (like erythema nodosum) due to metastatic fat necrosis
  • Thrombophlebitis migrans
  • Ascites, portal hypertension
26
Q

What physical signs you may see in a patient with pancreatic cancer?

A
  1. Unresectable tumour if following signs present:
    - Hepatomegaly
    - Jaundice
    - Abdominal mass
    - Abdominal tenderness
    - Ascites, splenomegaly
    - Supraclavicular lymphadenopathy
  2. Palpable gallbladder (with ampullary carcinoma)
27
Q

What investigations would you carry out if pancreatic cancer suspected?

A
  1. General investigations: Blood tests, CXR
  2. Tumour markers: CA19-9
  3. Imaging: Abdominal US +/- CT +/- EUS. If mass without jaundice then do EUS/percutaneous needle biopsy. If carcinoma identified then perform CT scan/EUS/Laparoscopy/Laparotomy and see if the tumour is resectable or not.
    If jaundice +/- mass then perform ERCP +/- stent.
28
Q

How is pancreatic cancer managed?

A
  • Majority have advanced disease at presentation and <10% are operable.
  • If tumour operable: pancreatoduodenectomy (Kausch- Whipple procedure), PPPD
  • Obstructive jaundice: Palliative bypass vs. ERCP or PTC stenting
  • Duodenal obstruction: Palliative bypass vs. Duodenal stent
  • Pain control (opiates, coeliac plexus block, radiotherapy)
29
Q
  1. Define Intraductal papillary mucinous neoplasm (IPMN).

2. T/F: Mucinous Cystic Neoplasia of the pancreas has potential for malignancy.

A
  1. IPMN is a pancreatic cystic neoplasm that can arise in either the main pancreatic duct (main duct IPMN) or its side branches (branch duct IPMN).
  2. True
30
Q

What are the worrisome features of main duct IPMN?

A
  • MPD 5-9 mm,
  • non-enhanced mural nodule,
  • abrupt change in MPD
  • LN’s.
31
Q

What are the worrisome features of Mucinous Cystic Neoplasia (MCN)?

A

> 3 cm
Enhanced cyst wall
Non-enhanced nodules

32
Q

When is resection indicated for IPMN?

A
  • Indicated for MD-IPMN
  • BD-IPMN: In elderly >3 cm without high risk stigmata (mural nodules, positive cytology): can be observed
    > In younger patients: >2 cm may be considered depending on location
33
Q

When is resection indicated for MCN?

A

Indicated in all fit patients: <4cm without mural nodules: lap. Spleen preservation

34
Q

What are the methods of resection?

A 
Pancreatectomy + LN’s 
Focal and LN or spleen sparing:
- Laparoscopic
- Robotic
- Multifocal BD-IPMN: total pancreatectomy
35
Q

Compare high stigmata of MD-IPMN and MCN.

A

MD-IPMN: high risk stigmata: MPD > 10 mm, Enhanced solid component
MCN:
High risk stigmata: > 1cm with enhanced solid component, MPD > 1cm

GI Pathology (20 decks)

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