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FRACS study > Hepatopancreaticobiliary > Flashcards

Hepatopancreaticobiliary Flashcards

1
Q

Embryology of the liver

A

Endodermal origin

Blind tube (hepatic diverticulum) forms from foregut into ventral mesogastrium

Left and right buds form and become lobes

Enclosed within layers of the ventral mesogastrium

Umbilical vein (oxygenated) runs along caudal margin of ventral mesogastrium

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2
Q

Caudal surface anatomy of the liver

A
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3
Q

Anterior surface anatomy of the liver

A
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4
Q

Cuinaud segments

A
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5
Q

Venous supply and drainage of the liver

A

Liver receives 25% of cardiac output

portal vein provides 75% of hepatic inflow

50-70% of the overall oxygen requirement of the liver provided by portal vein

Drainage via the 3 (left, middle,right hepatic veins)

  • caudate drains directly into IVC via several perforators
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6
Q

Relationship of the portal structures

A

Bile duct anterior right

Hepatic artery anterior left

Portal vein posterior

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7
Q

Aberrant anatomy of the hepatic artery

A

Normal is only present 60%

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8
Q

Biliary drainage of the caudate lobe

A

80% left and right

15% left only

5% right only

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9
Q

Variations in the cystic artery

A
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10
Q

Blood supply of the bile duct

A

From sup. pancreaticoduodenal and gastroduodenal arteries

Run on either side at the 3 and 9 o’clock positions

Poor segmental supply until close proximity to the liver where it is well supplied from hepatic supply

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11
Q

Innervation of the liver

A

Sympathetics

  • T7-10
  • through coeliac ganglia

Parasympathetic

  • both vagal nerves
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12
Q

Describe the structure of a liver lobule

A

Central venule surrounded by 4-6 portal triads

Venous sinusoids

3 cell zones with enzymatic/functional differences between hepatocytes- depending on proximity to arterial/portal supply (and nutrients and oxygen)

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13
Q

Role of hepatic stellate cells in cirrhosis

A

Stellate cells located in the space of Disse

  • store Vitamin A
  • synthesise extracellular collagen and other ECM proteins

In acute and chronic injury stellate cells become activated to a myofibroblastic state

  • abnormal deposition of ECM and collagen leads to loss of architecture of liver with fibrosis and ultimately cirrhosis
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14
Q

Substrates for gluconeogenesis

A

Lactate

Pyruvate

Glycerol

Propionate

Alanine

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15
Q

Basic physiologic functions of bile

A
  1. Excretion of waste products of metabolism
  2. Provide enteric bile salts to aid fat absorption
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16
Q

What are major organic solutes in bile

A

Bile acids

Bile pigments

Cholesterol

Phospholipids

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17
Q

Bile volume

A

1500ml/day although some texts also suggest more like 600ml/day

97% Water

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18
Q

Bile solutes and concentrations

A
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19
Q

Bile Salts

A

3 Salts

  • Cholic acid 40%
  • Chenodeoxycholic acid 40%
  • Deoxycholic acid 20%

Produced in liver from cholesterol

Conjugated within hepatocytes with glycine or taurine

Secreted into bile

90% reabsorbed by hepatocytes and resecreted

This cycle constitutes the enterohepatic circulation

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20
Q

Excretion of bilirubin

A
  • Breakdown product of heme
  • Unconjugated binds to albumin
  • Dissociates within space of Disse
  • Uptake by hepatocytes
  • Conjugated with Glucuronic acid
  • Secreted into bile
  • Deconjugated by bacteria to urobilinogens
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21
Q

Substrates for gluconeogenesis

A

Mostly from alanine from muscle breakdown

Some from glycerol from adipose

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22
Q

Ketogenesis

A

From fatty acids from adipose tissue

Beta oxidised in liver to form ketones

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23
Q

Lipid Metabolism

A

Balance of esterification vs oxidisation

Esterification with glycerol yeilds triglycerides for storage in adipocytes

Beta oxidation yeilds ATP and Ketone bodies

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24
Q

Protein metabolism

A
  • Liver metabolises to any of glucose, ketones or lipids or oxidised for energy
    • Oxidation yeilds nitrogenous waste products
      • Nitrogenous waste converted to urea in urea cycle
        • Excreted largely in urine
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25
Q

What pathway is primarily responsible for metabolism of drugs and toxins

A

Cytochrome p450

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26
Q

Histological findings of cirrhosis

A

Regenerating liver nodules surrounded by fibrous septae

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27
Q

Define portal hypertension

A

Portal pressure >5mmHg

Pressures of 8-10mmHg are generally required to cause collateralisation and portosystemic shunting

Pressures are measured by hepatic wedge pressure

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28
Q

Sites of portosystemic shunting

A

Oesophageal Varices

  • flow predominantly from left gastric and coronary veins through distal oesophageal plexus to the azygous

Caput medusae

  • recanalisation of umbilical vein

Retroperitoneal collaterals (of Retzius)

Rectal Varices

  • Superior rectal (IMV) to inf. rectal (int. iliac)

Intrahepatic

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29
Q

Sinestral hypertension

A

Isolated splenic vein thrombosis

High splenic with normal SMV and portal pressures

Usually from mass or pancreatitis

Resultant portoportal collateral flow through gastroepiploic veins

  • Predominantly left gastroepiploic

Isolated gastric varices without oesophageal varices

Curable with splenectomy

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30
Q

Pyogenic liver abscess epidemiology and risks

A

Uncommon (10 per 100000 admissions)

Male 1.5 : 1 female

Cirrhosis

Malignancy

Diabetes

CRF

Sphnicterotomy/hepaticoenterostomy

Biliary sepsis

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31
Q

Caroli disease

A

Rare

Autosomal dominant and recessive form exist (recessive is more severe)

Cystic dilatation of intrahepatic ducts

100 fold risk of cholangiocarcinoma vs gen. pop.

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32
Q

Colorectal cancer and pyogenic abscess

A

4 fold risk of colorectal cancer in liver abscess

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33
Q

Sources of pyogenic liver abscess

A

Portal vein

Biliary tree

Direct extension

Trauma

systemic (arterial)

Most commonly the exact cause is not identified

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34
Q

Distribution of hepatic abscesses

A

Right 75%

left 20%

Caudate 5%

Multiple abscesses are uncommon

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35
Q

Bacteriology of liver abscess

A

Portal/biliary source

  • poly microbial
  • high rate of gram negatives (E.coli, Klebsiella pneumoniae)
  • Assume anaerobes (Bacteroides)
  • Enterococci

Systemic (endocarditis, IVDU etc)

  • Staph. aureaus, Strep. species
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36
Q

What microbial kingdoms may be implicated in liver abscesses

A

Bacterial- most common

Fungal

Mycobacterial

Amoebic

Parasitic (helminthic)

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37
Q

What is a rare complication of Klebsiella liver abscess

A

Endogenous endopthalmitis

esp. in diabetics

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38
Q

CT findings consistent with liver abscess

A

Hypodense central lesion with peripheral enhancement

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39
Q

Differentiating amoebic from pyogenic abscess

A

Entamoeba histolytica serology

Otherwise it can be difficult in an endemic area

Even aspiration unlikely to yeild the answer (may be culture negative)

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40
Q

Entamoeba histolytica and liver abscess

A

Amoebic

  • Endemic in tropics and developing world
  • Exists as cyst or trophozoite
  • faeco-oral transmission
    • Migrates through portal circulation

Causes liquefactive necrosis and subsequent abscess

  • Glissons capsule is resistant to degradation
    • Abscesses classically abut the capsule

Detectable by serology

Treatment is with metronidazole drainage is not needed

  • classic appearance is of anchovy sauce (but odorless) if aspirated
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41
Q

Life cycle of Echinococci

A
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42
Q

Treatment of hydatid disease

A
  • Treatment with Albendazole or albendazole induces cyst regression but resolution in <50%
  • PAIR (puncture, aspiration, injection, reaspiration) is as good as surgery if single cyst with no daughter cysts
    • Treat with Albendazole for 1 month afterward
  • Surgery is still the treatment of choice for multiple cysts
    • technique
      • be prepared for anaphylaxis
      • pack off the rest of the abdomen to reduce contamination
      • expose the cyst, closed aspiration and scolicidal injection (hypertonic saline)
        • leave the cyst open or excise it seem equivalent
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43
Q

Recurrent pyogenic cholangitis

A

Asian peoples, low socioeconomic status

young (age 20-40)

strictures and stones develope in the biliary tree

recurrent segmental cholangitis

Surgical clearance of stones and resection/plasty of strictures is treatment

Probably an increased risk of cholangiocarcinoma

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44
Q

Liver Cell Adenoma epidemiology

A

Rare

Frequently symptomatic (haemorrhage and necrosis)

Female 11 : 1 Male

Age 20-40

Associated with:

  • steroid hormone use- esp OCP (30 fold)
  • Obesity

Usually singular lesion, occasionally multiple (~20%)

Multiple lesions less associate with OCP and female sex

If it’s a man it should probably be resected

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45
Q

Risks of liver cell adenoma

A
  • Rupture and haemorrhage
    • ~ 30% risk
    • All over 5cm when bleeding occurs
    • Can be major haemorrhage with capsular rupture
      • Manage with embolisation, stabilisation then resection
  • Malignant transformation
    • Low risk
    • LCA with beta catenin activation are highest risk for transformation
    • Develop into HCC
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46
Q

Liver cell adenoma imaging

A

CT Peripheral uptake with centripetal filling

MRI- well demarkated mass with fat and haemorhage

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47
Q

What is a liver cell adenoma

A

Benign proliferation of hepatocytes

Loss of normal architecture with no ducts seen on histology

Cords of hepatocytes with increased glycogen and fat

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48
Q

Liver cell adenoma management

A

In a man: probably resect any size

In a woman:

  • If OCP associated- consider stop OCP and observe
  • 5cm is a reasonable guideline
    • <5cm observe
    • >5cm Resect

Balance is of risk of rupture and HCC vs resection

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49
Q

FNH imaging:

CT

A

CT- multiphase is ideal

  • usually hypoattenuating
  • rapid hyperenhancement on arterial phase with central stellate scar
  • isodense on portal and delayed phases with delayed enhancement of the central scar
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50
Q

FNH epidemiology and histology

A

Common (2nd most common benign after haemangioma)

Very strong in F:M preponderance

Benign cellular proliferation with fibrous septa around a central scar, often a large central artery within the central scar

If it’s a man be dubious thats it’s actually an FNH

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51
Q

Haemangioma epidemiology and histology

A

Most common benign liver solid lesion

Female 5 : 1 male

Vascular malformation- enlarge by ectasia rather than proliferation.

Consist of endothelially lined cavernous blood filled spaces

Can bleed

No malignant potential

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52
Q

Kasabach Merritt syndrome

A

Rare complication of giant liver haemangiomas

Thrombocytopaenia and consumptive coagulopathy

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53
Q

Haemangioma imaging

A

Look at the blood pool, haemangiomas are an extension of this

  • Non contrast- density of blood- (lower than liver)
  • Arterial phase- density of aorta
    • peripheral nodular enhancement pattern.
  • Portal phase- density of portal vein
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54
Q

Liver haemangiomas in children

A

Large haemangiomas can cause massive haemodynamic demand and CHF from shunting.

High mortality if left untreated

Small lesions can still be observed

Consider embolisation of large lesions

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55
Q

name rare benign solid liver lesions

A

Most are haemangiomas, adenomas or FNH.

Others:

  • Macroregenerative nodules (in cirrhotics, have malignant potential)
  • Nodular regenerative hyperplasia
  • Mesenchymal hamartomas (paeds)
  • Lipomas
  • AML
  • Myelolipomas
  • Angiolipomas
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56
Q

HCC risk factors

A

Chronic hepatitis

  • Hepatitis B
  • Hepatitis C

Metabolic liver diseases

  • Haemochromatosis
  • Apha 1 antitrypsin defiency
  • Wilson’s disease

Cirrhosis

  • Alcoholic
  • PBC
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57
Q

HCC characteristics on CT

A

Blood supply is prodominantly from the hepatic artery

  • Rapid contrast enhancement in late arterial phase
  • Early washout of contrast
  • May leave a capsule like area of enhancement on portal venous phasing
  • Occasionally have central scar (which does not then have late enhancement as for FNH)
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58
Q

HCC pathology and variants

A

Metastasises to lung, bone and peritoneum

Classically aggressive

Path/histo variants include:

  • hanging (pedunculated)
  • pushing type
  • infiltrative type
  • multifocal type
  • fibrolamellar type
    • young patients without cirrhosis- better prognosis
  • mixed HCC/cholangiocarcinoma
  • clear cell
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59
Q

Treatment options in HCC

A

Patients have 2 diseases

  • balance of malignancy vs liver function/reserve
    • Resection
      • many scoring systems but Childs Pugh is important
        • A- ok
        • B- maybe- individualise
        • C- No
    • Transplant
    • Ablation
    • TACE
    • Radiotherapy
    • Systemic
      • TKI
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60
Q

Prognostic factors in HCC

A

Tumour size

Cirrhosis

infiltrative pattern

Lack of capsule

Mets

Multifocal tumours/intrahepatic mets

Margin <1cm

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61
Q

Transplant criteria for HCC and cirrhosis

A

Milan criteria

  • single tumour <5cm, or
  • up to three tumours, each smaller than 3cm, and
  • no gross vascular invasion

UCSF (Uni of Cali, San Fran.)

  • used by Transplant society of Aus and NZ
  • Single tumour <6.5cm, or
  • up to three tumours with
    • largest lesion <4.5cm, and
    • sum of tumour diameters <8cm
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62
Q

Intrahepatic cholangiocarcinoma imaging

A

Dilated ducts peripheral to tumour

hypoattenuating on non contrast

low peripheral enhancement on arterial

gradual centripetal filling on delayed

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63
Q

Intrahepatic cholangiocarcinoma risks

A

viral

  • Hep a,b
  • HIV
  • EBV

PSC

Caroli’s

Cholangitis

  • recurrent pyogenic
  • choledocholithiasis
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64
Q

Name rare liver solid primary malignancies

A

Sarcomas

Lymphomas

Hepatoblastomas

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65
Q

Hepatic mets on imaging

A

hypoattentuating on non contrast

Enhancing less than surrounding liver on contrast

washout on delayed phase

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66
Q

Poor predictors of prognosis in liver metastectomy

A

CEA >200

size >5cm

recurrence <1 year from resection of primary

Multiple tumours

LN positive primary

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67
Q

Solid liver lesion malignant differential

A

Metastasis

  • Colorectal
  • Neuroendocrine (esp PNETs)
  • melanoma, breast, urological, gynaecological, lung

Primary

  • HCC
  • IHCC
68
Q

Cystic liver lesions

A

Degenerative

  • Simple cysts

Congenital

  • Polycystic liver disease
    • manifestation of PKD
  • Carolis disease

Neoplastic

  • Cystadenoma
    • Mucin filled cyst
    • Malignant potential to progress to cystadenocarcinoma

Infectious

  • Hydatid
  • Abscess

Trauma

  • Biloma
69
Q

Variations of the biliopancreatic ductal confluence

70
Q

Anatomy of the gallbladder

A

Fibromuscular sac lined by simple columnar epithelium

  • 50ml

Three parts

  • fundus, body, neck
    • mucus glands in the neck only

Undersurface of liver, between segments 4b and 5.

  • Fundus touches abdominal wall at tip of 9th costal cartilage

Cystic duct 2-3cm in length

  • contains spiral valves of Heister

Blood supply from cystic artery

Venous drainage though cholecystic plate to liver parenchyma

Lymphatic to cystic node (of Lund) then coeliac

71
Q

CHD/CBD normal size and length

A

CHD 4cm

CBD 8cm

Diameter 5mm until age 50 then 1mm extra per decade thereafter

72
Q

Variations in cystic duct anatomy

73
Q

Pathogenesis of gallstones

A

Four phases

  • super saturation
  • concentration
  • crystal nucleation
  • GB dysmotility

70% cholesterol and calcium

  • Gallbladder actively resorbs Na
  • Water follows
  • Increased cholesterol concentration
  • Also increased calcium concentration
  • Calcium destabilises phospholipid and cholesterol vesicles
  • Cholesterol and calcium precipitates form

10% pure cholesterol

Bile pigment stones more rare

74
Q

What factors stimulate gallbladder contraction

A

CCK

vagal tone

75
Q

Bacteriology of the biliary tree

A

E.coli

Klebsiella

Enterobacter

Enterococci

76
Q

Bismuth Strassbourg classification

A

Bismuth-Strasberg classification of bile duct injury.

  • (A) Bile leak from cystic duct or liver bed;
  • (B) occlusion of the right segmental duct;
  • (C) bile leak from divided right segmental duct;
  • (D) lateral injury to the common hepatic duct;
  • (E1) main bile duct injury,>2 cm from the confluence;
  • (E2) main bile duct injury,<2 cm from the confluence;
  • (E3) hilar injury with intact confluence;
  • E4) confluence involved, right and left hepatic ducts are separated;
  • (E5) injury of aberrant right sectoral duct with concomitant injury of main bile duct
77
Q

Reynolds Pentad

A

Charcots triad

  • Fever
  • Jaundice
  • RUQ pain

Plus:

  • Mental status changes
  • Hypotension
78
Q

Pathophysiology of recurrent pyogenic cholangitis

A

colononisation of biliary tree by Clonorchis and Ascaris species

hydrolyse congugated bilirubin to free bilirubin

Brown pigment stones form

Unclear if this is primary or secondary to benign biliary strictures

79
Q

PSC salient points

A

Associated with IBD esp UC

  • Not affected by resection of IBD

Prognosis

  • Ultimately fatal due to cirrhosis
  • Increased risk of cholangiocarcinoma

Treatment

  • no medical treatment options
  • Transplant may be necessary but strictures may develop in transplanted liver also
80
Q

Mirizzi Classification

A

Type I (11%)

  • External compression, no fistula

Type II (41%)

  • Fistula <1/3 of CBD circumference

Type III

  • Fistula 1/3-2/3 CBD circumference

Type IV

  • > 2/3 (complete destruction) of CBD
81
Q

Classification of choledochal cysts

A

The Todani classification

82
Q

Choledochal cyst complications

A

Obstruction

Fibrosis

Cirrhosis

Cyst rupture

Malignancy (10-30% risk) (choledochgal cysts should be considered a premalignant condition)

83
Q

GB Cancer risks

A

Female sex (3:1)

porcelain GB

Stones esp. large stones >3cm

GB polyp >1cm

APBJ

Choledochal cysts

PSC

84
Q

Distrbution of cholangiocarcinoma

A

2/3 perihilar (Klatskin)

Remainder are usually intrahepatic or periampullary

85
Q

Cholangiocarcinoma risks

A

recurrent pyogenic cholangitis

Asian liver flukes (Clonorchis and Opistorchis sp.)

PSC

Choledochal cysts

86
Q

How many AJCC staging systems are there for are cholangiocarcinoma

A

Differs by anatomic location

AJCC has 3 separate staging systems

  • Intrahepatic
  • Perihilar
  • Periampullary
87
Q

Pancreas

gross anatomy

A

~15cm in length

Divisions

  • Head- right of portal vein
  • Neck- Anterior to portal and SMV
  • Body- to left renal hilum
  • Tail- to splenic hilum

Blood supply

  • Arterial
    • Splenic artery to neck, body, tail
    • Superior and inferior pancreaticoduodenals to head
  • Venous
    • Head- SPDV to portal and IPDV to SMV
    • Neck, body and tail to splenic vein

Nerve

  • Parasympathetic mainly post. vagus, coeliac plexus
  • Sympathetic T6-10 (pain fibres also)
88
Q

Pancreas microscopic structure

A

Composed of exocrine serous acinii spotted with endocrine islet of Langerhan

beta cells produce insulin

alpha cells produce glucagon

delta cells produce somatostatin

89
Q

Pancreatic development

A

Endodermal origin

Develops as separate dorsal and ventral buds

Ventral bud arises as a diverticulum from lower bile duct in ventral mesogastrium

  • becomes uncinate process

Dorsal bud arises separately from gut tube

Ventral and dorsal ducts fuse and drainage

  • Major papilla eventually primarily drains upper head, neck, body, tail and biliary tree
  • Accessory duct papilla is found proximal and anterior to the main papilla
    • primarily drains the uncinate process
90
Q

Name the main pancreatic proteases.

How are they synthesised and activated?

A

Trypsin

Chymotrypsin

Carboxypeptidase

Elastase

Synthesised as inactive proenzymes (trypsinogen and chymotrypsinogen, procarboxypeptidase and proelastase)

Stored as zymogen granules in acinar cells

Activated by duodenal Enterokinase

91
Q

Mechanisms for maintaining inactivation of pancreatic enzymes

A

pH <7 (ideal is 8-9 for proteases and lipase)

Pancreatic secretory trypsin inhibitor (encoded by SPINK1)

Storage within zymogen granules as inactive precursors

92
Q

Phases of pancreatic secretion

A

Cephalic

  • vagus mediated
  • 20-25% or secretion

Gastric

  • vagovagal reflex
  • 10%

Intestinal phase

  • Secretin (S cells) in response to low pH
    • fluid and bicarb secretion
  • CCK (I cells) in response to nutrient load
    • enzyme secretion
  • 65-70%
93
Q

Pathophysiology of pancreatitis

A

Pancreatic acinar cell injury

Colocation of lysosome and zymogen granules

  • Mediated by Calcium influx whish is increased by
    • NFkB
    • Duct HTN
    • Ethanol
    • Low pH

Activation of pancreatic enzymes

Tissue injury

Inflammatory cascade induced

  • TNFa, IL-1
  • IL-2, IL-6, IL-8, IL-10, bradykinin, PAF

SIRS

MODS

Death

94
Q

Functions of the interleukins

A

IL-1

  • Fever

IL-2

  • Activation of NK and cytoxic T-cells

IL-4

  • B cell antibody production (plasma cell differentiation)

IL-6

  • Hepatic acute phase proteins

IL-8

  • Neutrophil chemattractant
  • Angiogenesis

IL-10

  • Suppression of inflamatory pathway
95
Q

Immunosuppressants used in transplant

A

Usually triple pathway

  • Calcineurin inhibitors
    • Tacrolimus
    • Inhibit calcineurin-calmodulin pathway
      • Prevent nuclear factor of activated T cells
  • Antimetabolites
    • Mycophenolate mofetil
    • Interruption of purine synthesis
  • Steroid
    • prevents nuclear translocation of NFkB
      • prevents T- cell activation
      • reduces antigen presentation
96
Q

Somatostatin

Cell, location, functions

A

Released from D cells in panceatic islets and GI mucosa

Downregulates GI hormones

Antigrowth hormone

97
Q

Pancreatic pseudocyst definition

A

Wall is composed of collagen and granulation tissue

Not epithelialised

At least 4-8 weeks to develop

98
Q

Genes in congenital pancreatitis

A

CFTR

  • regulation of fluid, chloride and bicarb,
  • increases enzyme concentration in ducts

PRSS1

  • Encode trypsinogen-
  • defects lead to unstable and easily activated trypsin

SPINK1

  • Encodes serine proteas inhibitory protein
99
Q

Autoimmune chronic pancreatitis

A

Type 1

  • IgG4 Mediated
  • Dense infiltration with plasma cells

Type 2

  • Idiopathic duct centric pancreatitis
  • Associated with IBD
100
Q

Chronic pancreatitis

A

Probably a spectrum of disease with acute pancreatitis

Various aetiologies

Often an underlying genetic factor also (SPINK1, CFTR, PRSS1)

Varies in that predominant manifestation is glandular fibrosis

Progression of fibrosis leads to ductal strictures, calcifications and loss of acinar and islet cells

Often culminates in endocrine and exocrine insuffiency

Pain!

101
Q

Peustow procedure

A

Simple longitudinal pancreaticojejunostomy

Useful if a dilated panc duct present

102
Q

Freys Procedure

A

Longitudinal pancreaticojejunostomy with resection of the anterior head

103
Q

Name the cystic neoplasms of the pancreas

A

MCN

  • Mucinous cystic neoplasm

SCN

  • Serous cystic neoplasm

IPMN

  • Intraductal papillary mucinous neoplasm
    • Main duct
    • Side branch

SPN

  • Solid pseudopapillary neoplasms

pNET

  • Neuroendocrine tumours will occasionally appear cystic
104
Q

Characteristics increasing suspicion for malignancy in pancreatic cysts

A

Symptoms

Cyst size >3 cm (OR 3.0)

Solid component within the cyst (mural nodule) (OR 7.7)

Main pancreatic duct dilated (OR 2.4)

Type of cystic neoplasm

  • Serous cystic- very low
  • Solid pseudopapillary, mucinous cystic neoplasms, side branch IPMNs- Moderate
  • Main duct IPMN- up to 70%
105
Q

Algorythm for cystic pancreatic neoplasms:

Fukuoka guidelines (2017)

106
Q

Serous cystic neoplasms of the pancreas

A

Female > male

Negligible malignant potential

CT shows cystic lesion with “honeycomb” or “bunch of grapes” appearance

  • central scar or sunburst calcification is pathognomonic
107
Q

Mucinous Cystic Neoplasms (MCN) of the pancreas

A

Almost exclusively female

CEA >192

Classically septated cyst with peripheral calcifications

  • occasionally unilocular
  • Usually occur in body and tail

Moderate malignant potential >4cm

Low risk <3cm

108
Q

IPMNs

A

Female = male

Cystic lesion associated with:

  • Main duct diatation (>5mm) in MD IPMN
    • high malignant potential
  • Side duct dilatation in SB IPMN
    • Low malignant potential

solid component suggests malignancy

CEA >200

109
Q

Solid pseudopapillary tumour of the pancreas

A

Females > males

young age

mixed solid and cystic lesions on imaging

CEA not helpful

Moderate to high malignant potential

Should be resected

110
Q

Genetic syndromes associated with pancreatic adenocarcinoma

A

CFTR

  • Delta F508

Peutz-Jeghers

  • STK11

Hereditary pancreatitis

  • SPINK1
  • PRSS1

Familial atypical mole and multiple melanoma syndrone

  • CDKN2A

Hereditary breast and ovarian cancer

  • BRCA2

Lynch syndrome

  • MMR mutations
    • MLH1, MSH2, MSH6

FAP

  • APC

Familial pancreatic cancer

  • No known gene

Li-Fraumeni

  • TP53
111
Q

Tumour suppressor and oncogenes of PDAC

A

PDX1

KRAS2 oncogene

  • Activated in 95% of pancreatic cancers

p53 tumour suppressor

  • occurs late in progression to invasive cancer, seen in 90% of PDAC

DPC4 (SMAD4) tumour suppressor

  • occurs late in progression to invasive cancer, seen in 80% of PDAC

CDKN2A/p16 tumour suppressor

112
Q

Oncogenetic progression in pancreatic intraepithelial neoplasia to PDAC

113
Q

Signs to assess in advanced or deseminated pancreatic cancer

A

Courvoisier

Blummer Shelf

Sister Mary Joseph

Virchow Node

114
Q

Laboratory investigations in pancreatic cancer

A

LFT’s

Albumin and prealbumin

CEA

CA 19-9 (most useful)

  • Caution as elevated in biliary obstruction anyway
  • 10-15% of PDAC do not produce.

Alpha fetoprotein

115
Q

Definition of post operative pancreatic fistula?

A

Any measurable volume output from an operative or percutaneous drain with amylase >3x serum

116
Q

Splenic ligaments and their contents

A

4 Ligaments

  • Splenocolic
    • Largely avascular
  • Splenophrenic
    • Largely avascular
  • Splenorenal
    • Carries the splenic artery and vein and the tail of the pancreas
  • Gastro splenic
    • Carries the short gastrics
117
Q

Splenic gross anatomy

A

Arises from dorsal mesogastrium

Mesodermal not endodermal origin

1,3,5,7,9,11

  • 1x3x5 inches (2.5x7.5x12.5cm)
  • 7 Ounces (200g)
  • 9th to 11th ribs

Blood supply from splenic artery

Splenic Vein

Lymphatics follow the artery to coeliac via retropancreatic and hilar nodes

4 ligaments

118
Q

relationships of the spleen

A

Diaphragm

9-11th ribs

upper pole of left kidney

tail of pancreas

greater omentum, short gastrics, stomach

119
Q

The substance and function of the spleen

A

Substance comprised of:

  • Capsule
  • Red pulp
    • Sinusoids
      • Removal of sinescent erythrocytes
  • White pulp
    • Periarteriolar lymphatic sheath (PALS)
      • T cells
    • Folicles
      • B cells
        • Antibody production
          • Opsonisation of encapsulated organisms

Primary site of haematopoesis until 5th month of gestation

  • Afterwards just filters and assists humoral immunity
120
Q

OPSI pathogens

A

Overwhelming Post Splenectomy Infection

  • Pneumococcus
  • Strep. pneumoniae
  • Haemophillus influenzae B
  • Nisseria meningitidis

OPSI risk most significant in kids and for haematologic disorders

121
Q

Indications for splenectomy

A

Haematologic disorders

  • ITP (platelet antibodies)
    • Failure of steroid or IVIg
  • Haemoglobinopathies
    • Heriditary spherocytosis

Trauma

Abscess or cyst

Primary or metastatic disease

  • Lymphoma
  • Leukemia
    • CLL, CML

Sinestral hypertension

122
Q

OPSI pathophysiology

A

Asplenia

Infection with polysaccharide-encapsulated organism

Decreased production of properdin and tuftsin

  • Properdin activates alternative compliment cascade
  • Tuftsin enhances phagocytosis

Decreased cleavage of tuftsin to functional form

Decreased opsonisation of bacteria

Reduced phagocytosis by splenic macrophages

Overwhelming infection

123
Q

Post splenectomy complications

A

Pancreatic leak

OPSI

Thrombocytosis causing thrombosis (esp portal)

124
Q

Vaccination in splenectomy

125
Q

Algorythm for cystic pancreatic neoplasms:

European guidelines (2018)

126
Q

European guidelines on pancreatic cystic neoplasms:

Absolute indications for surgery

A
  • Positive cytology
  • Solid mass
  • Jaundice
  • Enhancing mural nodule >5mm
  • MPD dilated 10mm or more
127
Q

European guidelines on pancreatic cystic neoplasms:

Relative indications for surgery

A
  • Growth >5mm/12 months
  • Elevated serum CA 19-9
  • MPD 5-10mm
  • Diameter 40mm or more
  • New DM
  • Pancreatitis
  • Enhancing mural nodule <5mm
128
Q

Variations in intrahepatic bile duct anatomy

129
Q

Define the critical view of safety in cholecystectomy

A
  • The hepatocystic triangle is cleared of fat and fibrous tissue.
    • The hepatocystic triangle is defined as the triangle formed by:
      • the cystic duct
      • the common hepatic duct
      • inferior edge of the liver.
  • The lower one third of the cystic plate.
  • Two and only two structures should be seen entering the gallbladder.
130
Q

CT imaging of acute pancreatitis

A

CT Severity Index (CTSI)

  • Graded 0-10
    • 2 Subscores
      • Balthezar
        • 0- Normal
        • 1- Enlarged
        • 2- Inflamatory changes in pancreas and peripancreatic fat
        • 3- single peripancreatic collection
        • 4- two or more peripancreatic collections
      • Pancreatic necrosis score
        • 0- None
        • 2- <30%
        • 4- 30-50%
        • 6- >50%​​

NB “Severe” pancreatitis on imaging is defined by the presence of necrosis and in imaging the terms are synonymous

131
Q

Post cholecystostomy management and decision making

A
  • Leave it for 6 weeks
  • Perform a check cholecystostogram
    • If the duct is obliterated spiggott for 2/52
      • If fine remove and no further management
    • If duct patent
      • Consider either risk reducing ERCP or cholecystectomy
132
Q

What guidelines can be used for diagnosis and severity scoring in cholangitis?

What are the parameters

A

The Tokyo guidelines 2018

  • Provides
    • diagnostic criteria
      • (suspected vs definite)
    • severity grading
      • (mild, moderate, severe)

Parameters

  • SIRS
    • Temp, WCC/CRP
  • Cholestasis
    • Jaundice, LFT’s
  • Imaging
    • biliary dilatation, etiology seen
  • Grading
    • cardio, neuro, resp, renal, hepatic (INR), haematological dysfunction
    • WCC>12, Temp >39
    • age
    • bili >5, hypoalbuminaemia
133
Q

Define cholangitis

A

Jaundice with stasis leading to bacterial infection and sepsis either suspected or established

134
Q

What is the Atlanta classification

A

An international, web-based consensus which provides clear definitions to classify acute pancreatitis using easily identified clinical and radiologic criteria.

135
Q

What is the Atlanta criteria definition of acute pancreatitis

A

The diagnosis of acute pancreatitis requires two of the following three features:

(1) abdominal pain consistent with acute pancreatitis
* (acute onset of a persistent, severe, epigastric pain often radiating to the back)
(2) serum lipase activity
* (or amylase activity) at least three times greater than the upper limit of normal
(3) characteristic findings on imaging

  • Preferably contrast-enhanced computed tomography (CECT)
    • less commonly MRI or USS
136
Q

What two subtypes of pancreatitis does the Atlanta criteria define.

With what relative frequency does each occur

A

Interstitial oedematous pancreatitis (90-95%)

Necrotizing pancreatitis (5-10%)

137
Q

What are the limitations of amylase when compared to lipase in detecting acute pancreatitis

A

Shorter half life

Amylase may be falsely normal in hypertriglygeridaemia

138
Q

Pathophysiology of pancreatitis:

Secondary enzyme activations after trypsin activation

139
Q

Complications of pancreatitis:

Local complications

A

Pancreas

  • peripancreatic fluid collections
  • necrosis
  • infection

Luminal

  • GOO
  • colonic stricture
  • colonic perforation
  • biliary obstruction

Vascular

  • venous thrombosis
  • arterial pseudoaneurysm
  • haemorrhage
    • direct or DIC

Compartment

  • pseudoobstruction/ileus
  • abdominal compartment syndrome
140
Q

How does the Atlanta criteria define collections associated with pancreatitis

A

Fluid alone

  • Acute peripancreatic fluid collection
    • <4 weeks
  • Pancreatic pseudocyst
    • >4 weeks

With a solid component (and variable fluid content)

  • Acute necrotic collection
    • <4 weeks
  • Walled off necrosis
    • >4 weeks
141
Q

How is organ dysfunction defined in the Atlanta criteria

A

By the Marshall criteria

  • Graded score 0-4 in 3 organ categories
    • Resp by Pa02/FiO2
    • Renal by creat
    • Cardio by BP
  • Score of 2 or more in a system defines organ dysfunction
142
Q

Severity in pancreatitis by Atlanta criteria

Outside Atlanta criteria what is an additional category proposed

A

Mild

  • No organ failure
  • No local complications

Moderate

  • Transient organ failure <48H
  • and/or
  • Local or systemic complications without persistent organ failure

Severe acute pancreatitis

  • Persistent organ failure >48H

Critically severe

  • severe pancreatitis with bacterial infection of local complications
143
Q

Fluid resuscitation in pancreatitis

A

—Fluid resuscitation has to be balanced

  • Enough to maintain organ perfusion
  • Avoid overload and resultant organ dysfunction from intra abdominal hypertension
  • Lactated ringers is preferred crystalloid
  • About 2500ml to 4000 ml usually is enough in first 24hours
    • IAP/APA suggests 5-10ml/kg/h for initial resuscitation with switch to goal directed therapy as able
  • Aim for
    • UO >0.5
    • MAP 65-85
    • HCT 35-44%.
    • Pulse <120
    • Advanced/Invasive measures (central venous oxygenation, Echo, serial lactate can all be used also)
144
Q

In what ways does cirrhosis affect perioperative and operative care

A

Protein synthesis dysfunction

  • poor wound healing

Portal HTN

  • Bleeding risk
    • Splenic sequestration = peripheral thrombocytopenia
    • Abnormal secondary haemostasis
      • coagulation + fibrinolysis

Abnormal drug metabolism

Poor renal function

145
Q

Contraindications to elective surgery in patients with liver disease

A

Acute hepatitis

Childs-Pugh C cirrhosis

Fulminant hepatic failure

severe chronic hepatitis

severe coagulopathy

severe extrahepatic complicaations

  • ARF
  • Cardiomyopathy, CHF
  • Hypoxaemia
146
Q

What parameters are included in the Child-Turcott-Pugh score

A

ABCDE

Albumin

Bilirubin

Coagulation

Distension (ascites)

Encephalopathy

147
Q

FNH imaging:

MRI

A

T2 hyperintense

T1 hypo

Rapid peripheral, nodular enhancement

Progressive, centripetal filling

Central scar

148
Q

Overview of MRI findings in benign liver lesions

149
Q

What is the role and significance of CEA measurements on pancreatic cyst aspirates by EUS

A

CEA is a sentitive and specific differentiator for mucinous vs non mucinous neoplasia at a cut off of 192ng/ml

Values >800ng/ml are seen in malignancy

150
Q

What is an IPMN

A

A mucin producing epithelial neoplasm of the pancreas which results in dilatation of pancreatic ducts either side branch or main duct

151
Q

lymphoepithelial pancreatic cysts

A

M>F

Very rare

Entirely benign

“zero” malignant risk but:

CEA>800

May be difficult to differentiate from MCN

May require resection to achieve diagnosis

152
Q

How much liver can be resected

A

Measured in functional liver remnant

Marathon runner level of fitness 20%

Normal fitness 30%

Cirrhosis 40%

153
Q
A

Strawberry gallbladder

  • Gallbladder cholesterolosis
  • Typical stippled appearance of the mucosal surface on gross examination

Results from abnormal deposits of cholesterol esters in macrophages within the lamina propria (foam cells) and in mucosal epithelium.

Benign

  • Not closely associated with cholelithiasis or cholecystitis
154
Q

What classification system can be used for post ERCP perforations

A

Stapfer classification.

  • Type I: Free bowel wall perforation
  • Type II: Retroperitoneal duodenal perforation secondary to periampullary injury
  • Type III: Perforation of the pancreatic or bile duct
  • Type IV: Retroperitoneal air alone
155
Q

What is a rare complication of giant liver haemangiomas

resulting in thrombocytopaenia and consumptive coagulopathy

A

Kasabach Merritt syndrome

156
Q

what is the classic ERCP appearance of PSC

A

Chain of beads

157
Q

Familial hepatic adenomas

A

Gene: HNF1A

Liver adenomatosis is a rare disease defined by the presence of multiple adenomas within an otherwise normal hepatic parenchyma

  • bi-allelic inactivation of TCF1/HNF-1alpha identified in hepatocellular adenomas
    • heterozygous germline mutations of TCF1/HNF1a have been linked to the occurrence of MODY3 in humans.
      • MODY3 is a rare dominantly inherited subtype of non-insulin-dependent diabetes mellitus characterized by early onset, usually before the age of 25, and a primary defect in insulin secretion.
158
Q

Insulinoma clinical features

A

Whipples triad

  • Symptoms of hypoglycaemia
  • Hypoglycaemia
  • Symptoms relieved by glucose
159
Q

Insulinoma tumour location

A

Pancreas (>99%)

160
Q

Zollinger-Ellison syndrome clinical manifestations

A

Peptic ulceration

Diarrhoea

161
Q

Gastronoma location

A

The gastrinoma triangle

  • Junction of cystic/CBD
  • D2/D3 junction
  • Junction of body/neck of pancreas
162
Q

VIPoma clinical syndrome

A

Diarrhoea

Hypokalaemia

Dehydration

163
Q

Glucagonoma clinical syndrome

A

Rash

Glucose intolerance

Necrolytic migratory erythema

Weight loss

164
Q

Somatostatinoma clinical syndrome

A

DM

Cholelithiasis

Diarrhoea

165
Q

What criteria can be used to classify suspected sphincter of oddi dysfunction

A

The Milwaulkee criteria

166
Q

What are the subtypes of IPMN

A

Main duct

Mixed

Side branch IPMN

FRACS study (13 decks)

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