HPB Flashcards

Question

Describe the pathogenesis of recurrent pyogenic cholangitis

Answer 1

* Recurrent pyogenic cholangitis is characterized by recurrent cholangitis caused by bile stasis and stone formation proximal to biliary strictures. * The pathogenesis of the stone formation and biliary abnormalities is incompletely understood. Stone formation occurs de novo within the intrahepatic bile ducts in contrast with the more common pattern of stone formation within the gallbladder seen in patients with more common forms of gallstone-related disease. * Transient portal bacteremia is thought to introduce bacteria into the biliary ducts, **_initiating a cycle of infection and secondary stone formation_** which leads to further obstruction and infection. Common organisms cultured from bile include E. coli, Klebsiella, Pseudomonas, and Proteus species and, less frequently, anaerobes, although the culture of multiple organisms is common.

Answer 2

* Gallstones form due to an imbalance of 3 key products in the bile; bile salts, lecithin, and cholesterol. * Cholesterol stones form due to a relative supersaturation of cholesterol in the bile, pigment stones form when there is decreased secretion of biliary acids and an increased secretion of unconjugated bilirubin into the bile. * Stasis and infection also play an important role in the formation of stones. * The formation of stones falls into three phases; supersaturation, nucleation, and stone growth; the imbalanced mixture generates a precipitant which forms a nidus for further stone formation and crystallisation * Once formed the stones persist and enlarge or consolidate over time.

Answer 3

Traditionally the same as HCC

Answer 4

(LaMPS) * Lymphoid aggregates * Mucinous pattern * Poorly differentiated * Signet ring differentiation

Answer 5

Main issues are size (2cm) and presence of vascular invasion.

Answer 6

* often causes abnormal LFTs, eosinophilia * echinococcus serology * initially use indirect haemoglutination antibody * IgG ELISA test for IgG antibodies to hydatid = gold standard * neg serology doesn't r/o echinococcus as high false neg rate in uncomplicated disease; more likely to be neg in non-liver disease, calcified cysts or non-viable cysts (less immunoreactivity) * Ultrasound - WHO classificatoin * CL (cystic lesion) * unilocular, uniformly anechoic cystic lesion w no internal echoes or septations; usu round but may be oval. Can't diagnose on USS alone; if caused by cystic echinococcus is at early stage of development & usu not fertile * CE1 (cystic echinocuccus 1) - active stage * unilocular, simple round/oval cyst w double-layered wall (representing pericyst & laminated cyst membrane), and uniform anechoic content. Snow-flake sign = fine internal echoes due to shifting of brood capsules called hydatid sand * CE2 (cystic echinococcus 2) - active stage * multivesicular, multiseptated cysts; cyst wall usu visible & lesions round or oval. Presence of daughter cysts indicated by rosette-like honeycomb-like structures (collection w a split wall/internal septations & septa, representative of walls of daughter cysts within hydatid cyst itself) * CE3 - transitional stage * unilocular cyst which may contian daughter cysts; anechoic content w detachment of laminated membrane from cyst wall may be visible as floating membrane or 'water-lily sign'. Cyst form may be less round bc of decreased intracystic pressure. Cyst may degenerate further or may give rise to daughter cells * CE3a = daughter cysts have detached - 'water lily sign' * CE3b = daughter cysts sitting within solid matrix * CE4 - inactive/degenerative cyst * cyst characterised by a thick calcified wall that is arch shaped, producing a cone-shaped shadow. Degree of calcificatoin varies from partial to complete. Usu not fertile. Defintiive dx can't be made by US alone * CT & MRI - may show findings similar to above; may also demonstrate external rupture of cyst or wall thickening suggestive of infection * MRI superior for demonstrating cyst wall defects, biliary communication & neural involvement

Answer 7

* benign epithelial tumour - no malignant potential * second commonest benign solid liver tumour after haemangioma * F\>\>\>M (no relation to OCP), 20-40yrs (slightly older than HCA) * **Path** * hyperplastic hepatocellular nodules developing in a noncirrhotic liver * solitary in 80% * peripheral location usu * **macro**: well-circumscribed but not encapsulated, lobular firm tan/yellow-brown mass, with central fibrous scar w radiating septa * **micro**: cords of benign-appearing hepatocytes divided by multiple fibrous septa originating from central scar. Central scar often contains a large artery that branches into multiple smaller arteries in spoke wheel pattern. * **most asymptomatic**; rupture, bleeding, infarction exceedingly rare * **imaging** * **USS** _not imaging of choice_ - iso-echoic, central scar, only subtle difference in echogenicity between FNH & surrounding liver * **CT & T1 MRI** (_MRI preferred_) * non-contrast: homogeneous, hypo or isodense cf normal liver (central scar hypodense cf surrounding liver parenchyma) * arterial phase: strongly enhancing w central scar remaining non-enhanced * venous: isodense again * delayed: hyperattenuation of central scar septae often seen * **T2 MRI**: isointense/mildly hyperintense w hyperintense central scar (central scar high attenuation on T2 whereas low in fibrolamellar HCC) * when no central scar seen, difficult to differentiate from HCA or malignant mass espec fibrolamellar HCC * **routine biopsy not required;** only if dx doubt - some risk of seeding if malignant; alternative interval imaging * leave alone if dx certain and asymptomatic; no indication to stop OCs * **50% spontaneously reduce in size**

Answer 8

* relatively rare monoclonal proliferation of hepatocytes in context of a normal liver * F\>\>M, age 20-40 * associated with steroid hormone use, COC, pregnancy, obesity, T2DM, iron overload * HCAs in men generally smaller but higher risk of developing into malignancy * **Molecular classification - Bordeaux classification** * HNF1-alpha germline-mutated HCAs (30-40%) * low risk of progression to malignancy * inflammatory HCAs (40-50%) * more common in obesity or NAFLD * can also be beta-catenin activated (10%) * beta-catenin-mutated HCAs (10-15%) * much higher incidence of turning into malignancy, much rarer * unclassified HCAs (10%) * ?also Sonic hedgehog HCAs (rare) * **Path** * **micro**: monoclonal proliferation of well-diff, usu bland-looking hepatocytes containing increased glycogen & fat, arranged in sheets & cords that are usu one, or at most two, cells in width (similar to normal liver but no non-parenchymal liver cells, ie no bile ducts, central veins or Kupffer cells) * may transform --\> dysplasia --\> HCC * _4.2% malignant transformation overall but 47% in men_ * risk also increased in beta-catenin activation & \>5cm * **Clinical**: 50% asymptomatic; large (8-15cm) may cause abdo pain/fullness; if \>5cm may present w acute onset abdo pain & shock from intraperitoneal rupture * **Imaging** * **USS**: well-demarcated, hyperechoic (high lipid content), often heterogeneic from haemorrhage, necrosis, fat content * **CT**: often heterogenous due to mixed components of fat, haemorrhage & necrosis * hypodense on unenhanced CT, enhance on arterial phase, isodense or stay hyperdense on PV & delayed phase * peripheral enhancement may be seen on contrast-enhanced CT due to presence of large subcapsular feeding vessels, centripetal pattern * **MRI:** heterogenous * T1: bright * T2: hyperintense predominantly but often heterogenous. Enhance on arterial phase, _remains hyperintense or isointense cf surrounding parenchyma on PV or delayed phase_ * may have peripheral rim corresponding to fibrous capsule * _difference between HCA & HCC: HCC has washout_ - will become hypodense/hypointense on PV imaging rather than staying hyperdense or becoming isodense * PET can differentiate between HCA & FNA well if doubt * biopsy only if doubt though would need core to work out Bordeaux classification so some do * **Management** * spontaneous rupture w acute haemorrhage: hepatic artery embolisation as temporising measure; once stabilised & resuscitated, laparotomy & resection of mass * symptomatic: resect * asymptomatic on OCP: stop OCP & watch for regression, espec if \<5cm; if persistently \>5cm resect * surgery if: male, due to metabolic disorder, haemorrhage, symptomatic, increasing size after stopping OCP or not decreasing if already \>5cm, \>5cm, beta-catenin mutated & inflam HCAs prone to malignant degeneration, diagnostic doubt/increased AFP (some suggest resection prior to planned pregnancy) * **Resection** * don't need wide margin but do need enough FLR * **Alternatives** * RFA or elective transarterial embolisation * liver transplant for exceptional cases * **Follow**-up * usu involute w time, esp if \<4cm and after COC is discontinued * if not resecting then serial imaging & can also monitor AFP as risk of malignant potential = about HCC

Answer 9

* benign mesenchymal tumour * most common benign liver tumour (second most common liver tumour overall after mets) * F\>M, mean age 45 * giant/cavernous haemangiomas = \>10cm * path: * micro = composed of multiple blood vessels lined by single layer of endothelial cells within a thin, fibrous stroma (endothelium-lined, blood-filled spaces separated by thin fibrous septa) * macro = well-circumscribed compressible tumour w dark colour * involution or thrombosis can result in dense fibrotic masses difficult to differentiate from malignant tumours * Clinical * most asymptomatic * vague sx in larger ones * complications include: spontaneous/traumatic rupture (v rare), intratumoural bleeding (rare), consumptive coagulopathy aka Kasabach-Merritt syndrome (thrombocytopenia and hypofibrinogenaemia caused by consumption of coagulation factors), AV shunting wihtin liver leading to cardiac hypertrophy & CHF, rapid growth leading to obstructive jaundice * Imaging * USS: well-defined, lobulated, homogenous hyperechoic masses (+/- heterogenous areas from haemorrhage, fibrosis or calcification) & post-acoustic enhancement, accuracy 70-80%, strongly recommend MRI or CT done to confirm * CT * non-con - well-dermarcated, hypodense * arterial phase: hyperdense peripheral enhancement/peripheral nodular pattern of enhancement (enhanicng rim) w hypodense centre * PV phase: progressive hyperdense peripheral enhancement (enhancement progresses centripetally) * delayed phase: ongoign filling/enhancement of lesion cf surrounding parenchyma * MRI - better if smaller * T1 = hypointense * T2 = hyperintense bc fluid in lesion - lightbulb sign * contrast pattern similar to CT - hypointense on non-con, nodular peripheral enhancement which slowly fills in towards lesion on portal venous phase, ongoing enhancement in delayed phase * overall discontinuous rim unlike in an abscess & must match phase eg PV phase matches portal vein, arterial phase matches artery) * NO BIOPSY * Management * reassure if asymptomatic & \<4cm - most stable over time * indications for invervention * consider if very large, growing (?\>10cm) but risk of rupture pretty negligible * symptmoms * rare things - Kassabach-Merritt, high output CHF, obstructive jaundice * if intervention: enucleation preferred, otherwise complete surgical resection * RFA w or w/o preop arterial embolisation * liver transplant v rarely for complicated, giant haemangiomata * Nat hx: most remain stable for long time. Can increase w pregnancy but no assoc w OCP

Answer 10

* Cyst * Hypovascular, non-enhancing, on MRI T2 bright * FNH * Central scar * Homogenous, hypodense on precontrast; then rapid diffuse enhancement w centrifugal filling w central scar not enhancing; then becomes isodense & fades into rest of liver in venous delayed imaging while hyperattenuation of scar often seen * central scar in fibrolamellar HCC in comparison is low attentuation on T2 MRI * HCA * Hypodense on pre-contrast phase, enhancement on arterial phase, hypo/isointensity on PV & delayed phase * May appear heterogenous depending on how much fat, haemorrhage & necrosis there is * T1: bright * T2 and CT: hyperintense predominantly but often heterogenous. Enhance on arterial phase, _remains hyperintense or isointense cf surrounding parenchyma on PV or delayed phase_ * may have peripheral rim corresponding to subcapsular vessels, centripetal pattern * _difference between HCA & HCC: HCC has washout_ - will become hypodense/hypointense on PV imaging rather than staying hyperdense or becoming isodense * PET can differentiate between HCA & FNA well if doubt * Haemangioma * Often hypointense/hypodense on precontrast; nodular peripheral enhancement on arterial phase, further centripetal filling on PV, usu continued filling on delayed phase * Lightbulb sign on T2 MRI given blood/fluid within it * HCC * Often hypointense/hypodense on precontrast imaging but brisk arterial enhancement & washout meaning darker than surrounding liver parenchyma on PV imaging (bc of 100% hepatic artery blood supply) * Contrast washout = HCC * Cholangiocarcinoma * Often hypodense on original precontrast imaging, may have some rim enhancement; in PV and delayed phases often hypoenhancing. Hard to differentiate from CRC mets * Metastatic cancer * Varies; in general (incl CR) usu hypodense & don’t have a lot of enhancement or just rim enhancement & rapid washout * but can also get hypervascular tumours incl mucinous adenocarcinoma, RCC, melanoma, neuroendocrine tumours

Answer 11

* Definition = cholangiocarcinoma arising from peripheral intrahepatic biliary radicles (exlcudes tumours arising from biliary confluence or first-order branches) * risk factors * traditionally chronic biliary inflammation eg PSC, chronic choledocho, hepatolithiasis, parasitic, Caroli's disease, choledochal cyst * but \>95% dont' have these * newer risk factors: chronic non-alcoholic liver disease, HBV, HCV, diabetes, metabolic syndrome * but 75% have normal livers; 16% chronic hepatitis/liver fibrosis; 9% cirrhosis * Classification * macroscopic findings * mass-forming (most common) * periductal-infiltrating (spreads along ducts) * intraductal-growth type (intraluminal spread) * AJCC staging * Path * 2 precursors to invasive cholangiocarcinoma but seen more freqeuntly in large bile ducts eg hilar tumours * flat or micropap growth of atypical biliary epithelium (biliary dysplasia or biliary intraepithelial neoplasia) * intraductal papillary neoplasm of bile duct - prominent papillary growth of atypical biliary epithelium w distinct fibrovasc cores & frequent mucin overproduction * Clinical: tends to present at advanced stage; though from small ducts, jaundice can be present if tumour compresses or invades biliary confluence * Imaging * fibrous tumour therefore no enhancement on arterial phase & delayed enhancemen t during late phase - on both CT & MRI * MRI - hypointense on T1, mod-markedly hyperintense on T2 * typically large, non-encapsulated, heterogeneous, w narrowing of adjacent portal veins & retraction of liver capsule * satellite nodules form as tumour grows * high propensity for LN invasion * main ddx: other fibrous tumours & in particular CRC mets * Mx * surgical resection = only cure - frequently extensive * no current role for liver transplant

Answer 12

* **cystadenoma** = rare neoplasm generally manifested as large cystic mass; **cystadenocarcinoma** = extremely rare malignant neoplasm * **Incidence**: * cystadenoma almost always in women \>40yrs * cystadenocarcinomas M=F & more aggressive in men * **Path**: * usually multilocular; globular external surface w multiple protruding cysts & locules of various sizes * benign/atypical cuboidal to columnar epithelium & in 95% content is mucin * previously thought all had ovarian-like stroma but 15% don't * epithelium often forms polypoid or papillary projections * cystadenomas grow slowly but precursor to cystadenocarcinoma; 10% of resections for 'cystadenoma' = malignant * **investigations** * **imaging**: cystic structure w varying wall thickness, nodularity, septations, fluid-filled locules * difficult to distinguish the two pre-op; presence of calcs + mixed solid/cystic components, large projections, markedly thickened wall on imaging, mural or septal nodule, nodule diameter \>10mm = assoc w cystadenocarcinoma * **don't biopsy** - limited sensitivity, doesn't change management, risks seeding * **management** * complete tumour excision - both to get definitive histo and to prevent malignant transformation

Answer 13

* resectable metachronous CRLM * data conflicting * potential advantages: facilitating resection of large tumours & assessing tumour response to chemo * potential drawbacks: progression of disease, possible increased risk of post-resection complications & liver insufficiency (but data suggests delaying surgery for chemo won't result in resectable liver mets becoming unresectable & if pts do develop new extrahepatic lesions while on chemo this may have helped identify pts w aggressive tumour biology who surgery wouldn't have been beneficial for) * EORTC 40983 trial - periop FOLFOX decreased non-therapeutic laparotomy bc of extensive disease, higher postop complications but not post-op mortality & increased progression-fre esurvival at 3 and 5yrs but no difference in 5yr OS * FOLFOX, FOLFIRI, XELOX all acceptable * usu 4-6wks chemo & liver resection ≥4wks after finishing chemo * unresectable metachronous CRLM * neoadj chemo may downstage & allow resection * FOLFOXIRI may be best, ?EGFR/VEGFR inhibitors in select pts * resect when mets become clearly resectable but delayed at least 4wks after completion * 40-50% CRLM w complete rad resopnse had viable tumour * synchronous CRLM * neoadj chemo may identify pts w aggressive tumour biology * size of majority of met lesions & primary either decreases or remains stable; widespread progression may be contraindication to subsequent liver resection * if unresectable mets may downstage * options for timing of hepatic resection (no evidence for advantage w any approach, tailored) * simultaneous resection of primary w liver mets * tends to be assoc w shorter total LOS & less morbidity w comparable 5yr survival * relative contraindications: multiple bilateral mets, inadequate FLR or when extensive operations anticipated for either primary or metastatic disease * tho may be able to do first part of 2-stage hepatectomy * resection of primary first & liver mets later * if symptoms related to primary * resection of liver mets first NB neoadj chemo espec oxaliplatin & irinotecan reuslts in liver changes - steatosis, steatohepatitis & sinusoidal dilatation/sinusoidal obstructive syndrome - delay surgery at least 4-6wks after chemo, tolerance of major liver resection may be reduced

Answer 14

Congenital * Simple cysts - contain serous fluid * Polycystic disorder - in assoc. with PCKS Infective * Hydatid cyst * Pyogenic or amoebic abscess Neoplastic * Benign = Cystadenoma - cuboidal epithelium * Malignant = Cystadenocarcinoma, IPMN of bile duct, primary liver ca with cyst degeneration, cystic mets to liver - colorectal, neuroendocrine, GIST, SCC, breast Post-traumatic NB cysts can be: * simple - solitary or polycystic * complex - multilocular/sepated/irregular lining, papillary projections * neoplastic (cystadenoma/cystadenocarcinoma) or echinococcal

Answer 15

Inflammatory fluid collections * Acute peripancreatic fluid collection * Pancreatic pseudocyst * Acute necrotic collection * Walled off pancreatic necrosis Non-neoplastic pancreatic cysts * True cysts/benign epithelial cysts (v rare) * Retention cysts * Mucinous non-neoplastic cysts * Lymphoepithelial cysts Pancreatic cystic neoplasms * Mucinous cystic neoplasm * Serous cystic neoplasm * Intraductal papillary mucinous neoplasm * Solid pseudopapillary neoplasm Cystic degeneration of solid pancreatic tumours eg endocrine, acinar cell carcinoma, ductal carcinoma

Answer 16

* Subjective: platelet count, splenic length (\>13cm), portal vein diameter (\>13mm) * Indirect: gastric varices * Direct: * transjugular hepatic venous pressure gradient (\>10mmHg) * direct portal vein puncture * splenic pulp pressure

Answer 17

**_Asymptomatically_** * Picked up incidentally on USS or CT **_Uncomplicated disease_** * Hepatomegaly * RUQ pain * Nausea/vomiting **_Complicated disease_** * Abscess * Cholangitis * Jaundice * Anaphylaxis * Fistula

Answer 18

* Contusion (likely under-reported) * Perforation (most common) * Avulsion * Traumatic cholecystectomy

Answer 19

* WSES guidelines 2020 say: best option should be chosen considering balance among risk of complications from ACC, limitations on medication availability depending on trimester, risk of relapse, risk of other specific conditions which may occur during pregnancy & the time until delivery or maturation of the foetus; in general, in absence of contraindications, surgery is suggested as first-line in order to avoid complications and potential drug toxicity for foetus * Retrospective studies say recurrent ACC or pancreatitis can occur in 10% while miscarriage can occur in 10-20% of pts * Non-op mx is alternative option but risk of higher incidence of spont abortion, threatened abortion and premature birth cf pts who underwent cholecystectomy * Within limitations of quality of studies, laparoscopy should be suggested for tx of symptomatic gallstones incl ACC * Vast majority of studies suggest 2^nd trim – first part of 3^rd trimester as best time to do lap chole, as higher risk of miscarriage & toxic effect of anaesthesia in first trimester, while concerns are related to size of uterus in third trimester * British guidlelines 2019 confirm benefits of lap chole over non-op tx, espec in 2^nd trimester * Natural hx * If pt treated non-op (Lu, Am J SUrg 2004) * Relapse rate of biliary disease ~30-40% overall? But trimester dependent * Up to 1^st trim –55-92%, 2^nd – 55-64%, 3^rd – 40-44% (Swisher Am J Surgy 1994, Jelin Surg Endosc 2008) * NB if pt had pancreatitis – 70% risk of recurrence (during pregnancy) * Preterm delivery in up to 17% * Pre-term labour may occur several weeks post-op * periop considerations: * position pt with L lateral tilt, to alleviate impaired venous return via SVC * take care with trocar insertion – supraumbilical Hasson * maintain pressures \<12mmHg * ?give steroids (for foetal lung maturity), in case of preterm delivery * ERCP is an option in pregnancy (with uterus shielded +/- avoid/minimize fluoroscopy, esp in first trim)… but there are risks to foetus (rad risks \* risks from any subsequent pancreatitis) à risk of death 0.2% but risk of prem birth 0.4% (Medscape 2011)

Answer 20

* USS - can be diagnostic; circular area with well-defined border, no vascularity in cyst, posterior acoustic shadowing (nodularity or septations worrying, though thick or nodular wall can also occur in haemorrhage) * CT - hypodense cf surrounding parenchyma, smooth, non-enhancing/no uptake on arterial phase bc avascular, no internal structure * MRI * T1 - low signal intensity (hypointense cf surrounding parenchyma) * T2 - extremely high signal intensity/bright, which doesn't enhance after contrast * Asymptomatic - no treatment (no malignant potential) * symptomatic * perc aspiration considered only to clarify if pain is related to cyst (recur) * perc aspiration + sclerotherapy * consider primary surgical approach if difficult to r/o cystadenoma or malignancy, or if biliary communication * surgical deroofing or fenestration of portion of cyst that is extra-hepatic * if histo of partially removed cyst wall abnormal or suggestive of cystadenoma, need hepatic resection * formal anatomical resection - consider if cyst v large, concern re thick-wall, nodularity or septations, or if intracystic haemorrhage bc suggestive of malignant component

Answer 21

* AFP increased in 50% (may also be increased in cirrhosis) * \<300 = non-specific; \>400 = diagnostic w 95% confidence; v high levels usu indicate aggressive tumour * chronic active hepatitis may increase AFP but almost never \>4000 * 20% HCC non-producers & only 10% small tumours have raised levels * other tumours asso w AFP: non-seminal germinal tumours, hepatoid gastri tuours, neuroendocrine tumours * USS - significant role in screening but need CT or MRI for definitive dx & treatment planning * nodules \<1cm - short interval surveillance period eg q3mo til lesion disappeared, enlarges or displays characteristics of HCC * nodules 1-2cm: do contrast-enhanced triple-phase CT & MRI * CT * early enhancement on arterial phase with washout in delayed phases = presumed HCC (intrahepatic cholangiocarcinoma shows delayed enhancement) * usu hypodense * mosaic appearance w fibrous septa separating areas of variable attenuation, representing internal regions of haemorrhage, necrosis, fatty degeneration & fibrosis * fibrous capsule has low attenuation on unenhanced imagines & enhances on PV phase * MRI * variable appearance on unenhanced T1 (usu hypointense) * typically hyperintense on T2-weighted & DWI but again vary * after gadolinium, characteristic ealry enhancment on artieral phase imaging & washout on delayed images --\> hypointense cf surrounding parenchyma * PET only useful in metastatic HCC * biopsy * not always required if appropriate risk factors & suggestive rad featrues, w or w/o increased AFP * if biopsy required should be transhepatic & preferably in an area for future excision

Answer 22

* transplant gives better 5yr survival (70% vs \>50%) (removes lesion as well as field change/abnormal liver) * but 20% get delisted from waitlist while waiting because progression of disease so sample * option to resect and salvage with a transplant if there is recurrence

Answer 23

* Usu GB should be left undisturbed at the original op as cholecystectomy à ed M+M (in pts who are already often elderly/frail preop) * Intense inflam process in RUQ may complicated the cholecystectomy & duodenal repair * Once the pt has recovered à an elective cholecystectomy can be considered if pt c/o sx (~30%)… and/or if other stones remain in GB * In v fit pts, can consider cholecystectomy at first op (though this is debated); S Connor says more recently a single definitive procedure has been advocated given high reported rates of recurrence & cholangitis, but most recommendations are based on small pt series * S connor says definitive simultaneous or metachronous mx of GB may be determined by symptoms and presence or absence of cholecystolithiasis or choledocholithiasis * In those w a clear CBD & empty GB, spontaneous closure of fistula may occur * If choledocholithiasis only, endoscopic mx of this by stone extraction +/- temporary covered stenting of a patent cystic duct may be appropriate * In pts w persistent cholecystolithiasis the GB is likely to be shrunken & therefore formal dissection of the hepatobiliary triangle may be hazardous – simply opening fundus, extracting stones, performing a cholangiogram (to ensure a clear CBD), closing cystic duct if patent from within then closing duodenal fistula either primarily or w an omental patch would be standard of care * Failure to assess common duct may result in cholangitis once fistula is closed if distal CBD obstruction remains

Answer 24

* Ca19-9, CEA, LFTs * USS not accurate * Cross-sectional imaging ?CT usu ok * EUS not as good as cross-sectional imaging but better than ultrasound * staging CT * PET not routinely used * consider staging laparoscopy if \>pT1b but don't need biopsy if suspected on imaging - can have false negs and may spread tumour into preitoneum * cystic duct, CBD, hepatic artery & portal vein nodes are considered locoregional (paraaortic, paracaval, SMA and celiac LNs considered distant mets) * tumour resectable if no: distant spread (peritoneum, discontiguous liver lesions), tumour involvement of hepatic vasculature or biliary tree that would preclude complete resection, presence of disease in distant LN groups

Answer 25

* depends on cyst stage as classified by WHO - see table, as well as the size, location, complications and overall health of the patient * medical mx * at least 3mo of anti-helminthic drug eg albendazole - 400-600mg BD (trying to kill parasite by impairing its glucose uptake) * surgery * reserved for large (\>5cm), multiple daughter cysts, superficially located or infected, communicating w biliary tree or exerting mass effect on adjacent structures * all pts need pre-op albendazole; ideally 3mo but at least 1mo to try sterilise cyst before surgery - reduces complications if cyst spilt & reduces risk of recurrence * options * resect cyst whenever possible (= cure) * anatomical hepatectomy * peri-cystectomy (removal of whole cyst incl wall) - if close to other structures risks injury; if large may prefer anatomical resection * removing just endocyst within pericyst - not as good * or aspirate cyst at operation, make sure no bile, then inject scolicidal agent; then open & aspirate all daughter cysts w/o spilling them (protect around with hypertonic saline) * scolicidal options include hypertonic saline, ethyl alcohol, betadien, hydrogen peroxide * Principles: eradication of parasite pre-op, adrenaline & steroids available for anaphylaxis, protect peritoneal cavity with hypertonic saline packs, eliminate all viable elements of cyst (suction of contents, inspection of cyst cavity to make sure no communication w biliary tree & if not inject scolicidal agent into cyst), obliteration of residual cavity (can be marsupialised, packed w omentum or plicated) * PAIR - percutaneous aspiration, injection of chemicals and reaspiration * not used as much due to risk of anaphylaxis & risk of sclerosing cholangitis if communication w biliary system * cyst punctured under USS guidance, cyst fluid aspirated, protoscolicidal agent eg hypertonic saline/ethanol injected, fluid re-aspirated * useful for simple cysts in deep location * modification = placement of broad tube to remove solid components of cysts as well as daughter cysts

Answer 26

NETs * liver resection for metastatic NETs improves OS cf supportive care, and R1 & R2 resections give 5yr survival rates of 70% and 60% * cytoreduction aims to reduce tumour volume by ≥90% if R0 not feasible * don't need formal resection with wide margins - enucleation & wedge resection sufficient * aggressive approach, sometimes combining liver resection & other ablative strategies (eg cryoablation & RFA) = warranted * non-surgical tx modalities include RFA, TAE, TACE * systemic treatment options include * somatostatin analogues (symptomatic relief & improvement in PFS) * systemic platinum-based chemo (response rate of 67% in grade 3 but survival benefit limited & signif toxicity) * sunitinib (receptor tyrosine kinase inhibitor), everolimus (mTOR inhibitor), bevacizumab (anti-VEGF) * liver transplant = emerging option but controversial & concerns remain re tumour recurrence in context of immunosuppression Non-CRC, Non-NET mets * general principles to consider re resection = similar to those for metastatic CRC; FLR, poor prognosis if extrahepatic disease, multiple tumours, large tumours or a short disease-free interval * consider in well-selected pts w genitourinary mets * breast, melanoma & sarcoma pts rarely present w isolated liver mets but w a long disease-free interval or long-term stability on chemo, liver resection can be considered * in general, liver resection for metastatic non-CRC, non-NET tumours has to be considered cytoreductive * GISTs: liver mets usu unresectable so imatinib usu first line; if tumour respnods after 6-12mo can consider resection if R0 resection possible * disease rpogression: imatinib dose escalation, then 2nd line (eg sinitinib) & 3rd line agents * if resectable, no good evidence but in retrospective series 5yr survival rates \>70% w combo of surgery & imatinib * can also consider RFA, MWA, TAE, TACE, systemic therapy, immunotherapy

Answer 27

* principles of operative management: * control sepsis - drain retroperitoneal/abdominal collections, remove stones, drain biliary tree * repair perforation * wire/basket perfs - usu heal w non-op rx * periampullary perforations: mx controversial * early conservative mx: NBM, NG, abx, frequent rv/repeat CT * +/- consider endoscopic stent placement... or PTC - to divert bile away from injury * perc drainage of any collections which subsequently form * indications for operative mx: * failure of non-op rx * documented perf with retained stones/instruments * large free/retroperitoneal collections or ongoing leakage * increasing peritoneal signs/suspected suppuration/peritonitis * duodenal perfs: generally require operative repair * if early: 1 or 2 layer transverse closure +/- omental patch * if late: consider * Bilroth II and duodenal stump drainage or * repair defect & do a pyloric exclusion (suture from inside via a gastrotomy) with gastroenterostomy

Answer 28

* median survival approaching 3yrs in some trials * chemo * systemic palliative chemo can improve QOL & prolong survival * can use FOLFOX, FOLFIRI or XELOX - relatively similar efficacy * FOLFOXIRI recommended in young pts w severe sx, high tumour burden or contraindications to biologic agents (better RR, PFS, OS) * may add bevacizumab (in some trials increases PFS & OS) * caution if elderly w prev arterial thromboembolic events or pts w recent major surgery * or may add anti-EGFR meds eg cetuximab if inoperable wild-type KRAS metastatic CRC * but bevacizumab preferred if RAS/BRAF mutated tumours, pts w markers of anti-EGFR resistance, right-sided primary tumours * HAI chemo * limited to pts w isolated liver lesions not amenable to resection of ablation but role uncertain * complications: biliary sclerosis, chemical hepatitis, arteiral thrombosis, infection, catheter displacement, gastroduodenal or GB inflammation * other hepatic artery-based strategies: TACE & Y-90 TARE have primising early results * ablation therapy * RFA most common (resection better if possible) * limitations in tumours located close to major blood vessels & other vital structures, tumours \>3cm * so not recommended as first line for unresectable CRLM espec if extrahepatic disease * MWA - same limitations * complications: bleed/haematoma, vascual injury, abscess, biliary fistula * radiation tehrapy * effective antitumour dosage of traditional external beam rad therapy = v toxic to normal liver parenchyma * development of techniques using targeted rad eg sterotactic body radiotherapy has provided new opportunity for local control of CRLM

Answer 29

* pre-op portal vein embolisation * eg embolising R portal vein --\> hypertrophy of left liver lobe & facilitates extended R hepatectomy 6wks later * usually well tolerated bc of dual supply of liver & complications uncommon * can be adapted to enable 2-stage procedure eg if required R hemihepatectomy & multiple resections from L hemiliver * ALPPS (Associating Liver Partition & Portal vein ligation for Staged hepatectomy) * more recent evovlution of principle of 2-stage resection; a short-interval, two-staged liver resection * 1st stage = open right PVL an din situ parenchymal transection in the right trisectionectomy plane (between segment 2/3 and seg 4) * 2nd stage done 1-2wks later and involves right trisectionectomy * ALPPS produces accelerated hypertrophy in FLR in much shorter time interval (growth rate 11x higher) but only done in specialist high-volume centres * advantages = improved hypertrophy rates & higher proportion of pts completing the 2-staged treatment but additional operative risk

Answer 30

**Preneoplastic lesions** * **dysplastic** **foci** = microscopic lesions composed of dysplastic hepatocytes \<1mm in size; occur in chronic liver disease, particularly cirrhosis * **dyplastic** **nodules** = nodular region \<2cm in diameter w dysplasia * _low-grade DNs_ ~1cm diameter - low probability of becoming malignant * _high-grade DNs_ = up to 2cm, less common, often difficult to differentiate from highly differentiated HCC - _become malignant in 1/3 cases_ (remember lesions \<2cm can also represent HCC) **HCC** * **solitary vs multinodular** (doens't affect prognosis); may form * large solitary circumscribed nodule w or w/o adjacent smaller satellite nodules * in cirrhosis may be multinodular within one lobe * or may infiltrate liver diffusely w/o forming circumscribed nodules (ie diffuse, expansive, infiltrative, multifocal etc) * **WHO tumour type classification** - subtypes * fibrolamellar, scirrhous/sclerosing, clear cell type, steatohepatitic, macrotrabecular massive, chromophobe, neutrophil rich, lymphocyte rich etc * **degree of differentiation** (Edmonson-Steiner grading): well, moderately, poorly differentiated or undifferentiated * **molecular pathogenesis** * TERT promoter mutations = most frequent (60%) observed in HCC development & progression - subsequent increase in telomerase expression = a determinant of malignant transformation * **vascularisation** = key parameter in differentiating HCC from regenerating nodules; progression from macroregenerative nodule --\> low grade DN, high grade DN & frank HCC = characterised by loss of portal tracts & development of new non-triadal arterial vessels which become dominant blood supply in overt HCC lesions * _this arterial neoangiogenesis = landmark of HCC diagnosis & rationale for chemoembolisation & anti-angiogenic treatment_ * _HCC derive 100% of bld supply from hepatic a_ * **capsule** - in 80% HCC the tumour nodules are surrounded by a distinct fibrous capsule * **HCC has great tendency to spread locally & invade blood vessels** * rate of portal invasion higher in expansive type, poorly differentiated HCC & large tumours * presence of portal invasion = most important predictive factor assoc w recurrence * once HCC invades portal vein, tumour thrombi grow rapidly in both directions --\> tumour fragments spread throughout liver * once tumour thrombus extended into main portal vein, high risk of complete thrombosis & portal HTN -\> oesophageal varices or liver decompensation * invasion of hepatic veins less frequent but eventually extends into suprahepatic vena cava or RA, assoc w high risk of lung mets * **rarely HCC may invade biliary tract** --\> jaundice or haemobilia; mechanisms of biliary obstruction: * intraductal tumour extension * obstruction by fragment of necrotic tumour debris * haemorrhage of tumour --\> haemobilia * metastatic LN compression of major bile ducts in porta * **extrahepatic mets**: lungs first then adrenals, bones, LNs, meninges, pancreas, brain kidney

Answer 31

* Aetiology of cholecystitis – 4 possible causes * 95% due to stone obstructing neck of GB * loss of mucosal integrity – secondary to immunocompromised or invasive microbial infection * torsion due to gallbladder hanging on mesentery * gallbladder artery ischaemia due to arterial occlusion or hypoperfusion * Pathophysiology of cholecystitis * Prolonged obstruction of cystic duct by gallstones/sludge (impacted in neck) leads to release of prostaglandins/mucus within the GB mucosa resulting in fluid secretion à mucocele +/- triggers =cycle of ed distension & further mucosal damage and inflammation * Days 2-4 get oedematous cholecystitis – increased blood flow, evidence of oedema within the wall, active inflammation/bacterial translocation * Apparently secondary bacterial infection of stagnant pool of bile occurs in ~20% of cases * Enterobacteriaeceae (E coli, Klebsiella, Enterobacter) most common, also enterococcus * May result in empyema * Can go on to get suppurative cholecystitis w at days 7-10 active evidence of repairing inflammation, proliferation of fibrosis, intra-mural abscess * Or days 5-7 necrotising cholecystitis – increased wall pressure à ¯blood flow, venous ischaemia w evidence of vascular thrombosis, patchy mucosal necrosis occurs * If complicated by infection w a gas-forming organism, acute emphysematous cholecystitis * Progressive full-thickness necrosis results in either * Contained pericholecystic abscess, either contained by colon/duodenum or ruptures into liver * Or free perforation of GB due to full-thickness necrosis resulting in biliary peritonitis * If oedematous cholecystitis phase resolves, but you get repeated episodes, end up w chronic cholecystitis – fibrosis, shrunken GB, evidence of chronic inflammation; and can progress to cholecysto fistula to CBD, duo, abdo wall, colon * Pathology of acalculous cholecystitis * Thought to be vascular in origin (ischaemia due to shock/DM vascular disease) --\> small vessel thrombosis / occlusion (cystic artery is end-organ artery w no collateral circulation and can get microvasc occlusion of end arteries within GB wall)then +/- progression to gangrenous cholecystitis +/- secondary bacterial invasion… (E Coli/Clostridia) * SC says not well understood, thought to be due to combo of change in bile salt composition, loss of mucosal integrity & microcirculatory disturbances Rarely, Salmonella typhi may cause acalculous cholecystitis

Answer 32

* bile = 97-98% water, 0.7% bile salts, 0.2% bilirubin, 0.51% fats (cholesterol, fatty acids and lecithin) and inorganic salts * gallstones form due to an imbalance of 3 key products in the bile: bile salts, lecithin and cholesterol * 3 major factors explain most gallstone formation: * supersaturation of secreted bile which causes crystallisation * cholesterol precipitates out into crystal when the amount of cholesterol exceeds the capacity of bile salts & lecithin to contain it in micelles * increased unconjugated bilirubin as a result of increased enterohepatic circulation of bili from excessive breakdown of RBCs --\> increased bilirubin conc in bile --\> precipitation of calcium bilirubinate to form black pigmented stones * crystal formation is further accelerated by pronucleating agents, including glycoprotiens & immunoglobulins/mucin * hypomotility increases stasis in the gallbladder, allowing more time for solutes to precipitate * once formed the stones persist and enlarge or consolidate over time * pts w ileal disease/post resection can get * pigment stones from increased bile salt delivery to the colon (increased enterohepatic cycling) * or cholesterol stones bc of excessive bile salt excretion in faces & diminished bile salt pool so cholesterol precipitates out * brown pigment stones occur due to stasis within the CBD with associated bacterial infection usually * obstruction * Caroli's disease * PSC * biliary infection * mostly seen in south-east asia

Answer 33

* extensive calcium encrustation of GB wall * more common in women * aetiology * 95% assoc w gallstones * pathogenesis controversial; ?chronic inflammation due to gallstones leading to scarring, hyalinisation & calcification * or cystic duct obstruction leading to bile stagnation within GB followed by mucosal precipitation of alcium carbonate saltes * classification - by extent of calcification * complete intramural calcification: continuous band of calcium infiltrates & replaces muscular layer of gallbladder wall; accompanied by sloughing of mucosal epithelium & dense fibrosis of entire GB wall * selective mucosal calcification * incidence of malignancy 2-3%; higher with selective mucosal calcification vs complete type * some say do lap chole for all; others say do it if symptomatic or selective mucosal calcification (but if young with complete mural calcification would prob offer it)

Answer 34

* risk 0.1% * routine use of 30 degree scope * cephalad retraction on fundus to 10 o'clock position to reduce redundant infundibulum * lateral traction on GB to place cystic duct perpendicular to CBD * avoid dissection at/below Rouviere's sulcus (a landmark/fissure between R lobe and caudate process which lies at level of porta hepatis where right pedicle enters the liver; visible in 80% of pts * careful use of diathermy * dissect as close to GB as possible * avoid cauterising or clipping arterial bleeding blindly - most bleeding can be controlled w a few mins of direct pressure w a lap forceps compressing Hartmann's pouch onto the bleed point * no division or clipping without identificationobtain critical view: * Calot's triangle cleared of fat and fibrous tissue * lower third of GB separated from liver to expose cystic plate * demonstration of 2 and only 2 structures to be seen entering GB * in severe inflammation, consider * subtotal cholecystectomy

Answer 35

* Aetiology * biliary tree (most common, 38%) * biliary obstruction --\> bile stasis w potential for bacterial colonisation, infection, ascension into liver) * direct extension (1%) * eg cholecystitis, subphrenic abscess, perinephric abscess, perforation of bowel into liver * portal vein bacterial seeding (\<5%) * pyelophlebitits (PV infection) from drainage of GI infection - appendicitis, diverticulitis, pancreatitis, IBD, CRC * arterial haematogenous seeding (\<5%) * any systemic infection - endocarditis, pneumonia, OM * traumatic (5%) * blunt or penetrating trauma -\> intrahepatic hematoma or necrosis -\> abscess (bacteria may be introduced by trauma or seeded from elsewhere * hepatic artery embolisation or thermal ablative procedures * cryptogenic (43%) * no cause found * pathogens: E coli, Klebsiella, Bacteroides, Enterococci eg Step faecalis, anaerobic strep * Risk factors: dibeetes, underlying hepatobiliary/panc disease, chronic renal failure, liver tranpslant, immunosuppression, IBD, goegraphic factors, colorectal neoplasia (monomicrobial klebsiella infections) * Path * 75% right hemiliver * Clinical: remember endogenous endophthalmitis (rare complication specific to Klebsiella) - serious, more common in diabetes, can lose sight * Investigations * send echinococcus serology & antigen testing to r/o * send Entamoeba histolytica specific antigen or PCR testing * stool culture for ova, cyst, parasites * USS - may be hypo or hyperechoic +/- int echoes/septations * CT - gold standard (MRI equally sensitive but not often done) * well-defined lesion w central hypoattenutation & often w IV contrast will have hypernhancement of ring; can be complex w lobulations/subcollections, can have irreg border * complications of abscess eg thrombosis of nearby vessels, rupture of abscess, also looks for causes in rest of abdomen * need to differentiate bc pyogenic mainly tx by abx & drainage, amoebic by abx, echinococcal by surgery * Management * abx after blood cultures; if \>3cm perc drain * surgery if failed perc drainage (more likely if multiloculated) or ruptured abscess or if pts need surgical tx of primary pathologic process

Answer 36

* definition = recurrent bacterial cholangitis caused by cholangiohepatitis or intrahepatic stones * incidence: East Asia, 3-4th decade, M-F * aetiology: * ?underlying susceptibility to cholangiohepatitis or intrahepatic stones from ?helminthic infections (flukes) or ?as a consequence of malnutrition --\> enzyme deficiencies --\> increased unconjugated bili * clinical: * fever, RUQ pain, jaundice * bc the infection, inflammation & stones commonly present in a segmental or lobar pattern, the jaundice tends to be mild * bloods similar to other causes of cholangitis * pathology * biliary pathogens eg Clonorchis sinensis (liver fluke) & Ascaris lumbricoides (round worm) populate biliary tree --\> these and other pathogens secrete an enzyme that hydrolyses water-soluble bilirubin glucuronides to form free bilirubin --\> this then precipitates to form brown pigment stones using a nidus such as small cholesterol crystals, black stones from the GB, parasite eggs & dead worms or flukes * these stones may partially or fully obstruct the biliary tree, causing recurrent episodes of cholangitis (+/- haemobilia) & eventually abscesses or even cirrhosis * resultant patchy/focal dilatation & strictures of intra- and extrahepatic ducts * increased risk of cholangiocarcinoma * unclear whether primary inciting event is infection causing inflammatory stricture or inflammatory stricture w subsequent infection of stagnant bile _Liver flukes (trematodes)_ * Aetiology * Infestation w liver flukes is caused through consuming inadequately cooked, pickled or salted infected fish * immature fluke passes into the biliary tree, where it grows to maturity * ova passed into GI tract & subsequently to water supplies, infecting molluscs & fish * infection w *Clonorchis sinensis* in China, Japan & south-east Asia; *Opisthorchis viverrini* found in parts of Eastern Europe & Siberia * Clinical: asymptomatic or present w acute febrile illness or chronic symptoms * Chronic infestation à hepatolithiasis * Ix: * detection of ova within stool or in duodenal aspirates * eosinophilia may also be present on blood film * ERCP – slender filling defects within bile duct + assoc changes of fibrosis & calculus formation _Ascaris lumbricoides_ * Roundworm *Ascaris lumbricoides* = commonest worm to infect humans * Clinical: rarely, an infected pt can present w obstructive jaundice due to migration of the worm into the biliary tree – difficult to distinguish from stone disease * The more frequent presentation is from cholangitis due to the worm traversing the ampulla * *Ascaris* has also been associated w recurrent pyogenic cholangitis * Ix: * USS sometimes identifies a long, linear filling defect within biliary tree * ID may occur at ERCP where endoscopic extraction may be possible * Mx * Antihelmintics – mebendazole or albendazole; often curative * Prognosis: late complication of papillary stenosis can be treated w endoscpic sphincterotomy

Answer 37

* consider laparoscopy pre-resection in high risk cases (eg v high CEA, indeterminate imaging for peritoneal disease) * one-stage simultaneous multiple adequate hepatic resections, with preservation of adequate FLR = safe & effective if small & favourably positioned bilateral CRLM * if extensive bilobar mets, strategies include * parenchymal-sparing hepatectomy (safe & effective w/o compromising onc outcomes & bc preserves parenchyma, increases potential for salvage repeat hepatectomy for pts w recurrent intrahepatic disease * combo of ablation w repeat PSH * two-stage hepatectomy if inadequate FLR * removal of portion of metastatic disease + occlusion of contralateral PV (by surgical ligation or subsequent perc embolisation); second curative-intent stage of operation done after hypertrophy of contralateral liver * long-term survival comparable to pts w more limited disease treated by single-stage * combo of multimodal therapies when complete resection of all mets not feasible * hepatectomy for main tumour mass * local tumour-ablative therapy to rest

Answer 38

* PSC/UC * congenital cysts - choledochal cysts, Caroli disease * APBD junction * chronic biliary infection: eg typhoid carrier/parasite infestation (liver fluke - Asia) * recurrent pyogenic cholangitis * hepatolithiasis: 5-10% risk * biliary-enteric anastomosis * chemical carcinogens- eg nitrosamines, dioxin, asbestos, smoking * viral hepatitis and cirrhosis

Answer 39

* Prevailing theory focuses on chronic inflammation w subsequent cellular proliferation * Gallstones & chronic cholecystitis (0.5-3% those w stones), espec stones \>3cm * PSC (3%) * Porcelain GB (2-3%) * Choledochal cysts * AJPBD * Cholecystoenteric fistula * Chronic infection – salmonella typhi carriage, Helicobacter colonization of biliary epithelium * Carcinogen exposure - risk in workers in oil, paper, chemical, shoe, textile industries, also smokers * Polyps \>10mm (tend not to occur in pts w GS, chronic inflammation generally absent) * obesity

Answer 40

* \<5mm: ~20% decrease in size, ~5% disappear; some turn out to be stones * polyps \<1cm - 0-5% risk of malignancy * polyps 1-1.5cm - ~10% risk of malignancy * polyps \>1.5cm - 46-70% risk of malignancy

Answer 41

Gallbladder does not have submucosa or muscularis mucosae TX = primary tumour can’t be assessed T0 = no evidence primary tumour Tis = carcinoma in situ T1 = invasion of lamina propria (T1a) or muscular layer (T1b) T2 = invasion of perimuscular fibrous tissue on peritoneal side w/o involvement of serosa (T2a) or on liver side w/o extension into liver (T2b) T3 = invasion of serosa/visceral peritoneum and/or directly invades liver and/or invades one adjacent structure/organ (eg extrahepatic bile duct, stomach, duo, colon, panc, omentum) T4 = involvement of main portal vein or hepatic artery or invasion of ≥2 adjacent structures/organs N1 = 1-3 nodes N2 = ≥4 nodes Stage 1 = T1 Stage 2a = T2aN0, Stage 2b = T2bN0 Stage 3 = T1-3,N0-1 Stage 4a = T4aN0-1, Stage 4b = T4b,anyN or anyT,N2 or M1

Answer 42

* includes extent of disease & extent of cirrhosis work-up (mos tpts w HCC have 2 diseases & survival as much related to tumour as it is cirrhosis * dx lap & lap USS = useful - lap USS better than preop staging CT * TNM criticised as doesn't accurately predict survival (doesn't take liver function into account) & also relies on pathology that is frequently unavailable pre-op * but fibrosis score of underlying liver, AFP level, presence/absence of cirrhosis & MELD score = included as clinically significant prognostic factors * Okuda, Barcelona, CLIP systems more useful for predicting outcomes in pts w poor liver function who have advanced HCC & are undergoing nonsurgical therapy * CLIP (Italian): combines tumour-related features (macroscopic tumour morphology, serum AFP levels, presence/absence of portal vein thrombosis) + index of severity of cirrhosis to give prognostic score these systems variably incorporate 4 features recognised as being important determinants of survival: severity of underlying liver disease, size of tumour, extension of tumour into adjacent strucutres, presence of mets +/- performance status

Answer 43

* early (T1a)/incidental Ca which is limited to mucosa --\> cholecystectomy alone * nodal disease \<3% * T1b and above - extended cholecystectomy and lymph node dissection * extended cholecystectomy = involves en bloc removal of GB with a rim of liver of at least 2cm adjacent to the gallbldder bed; a formal central liver resection (segments IVb and V) may be appropriate depending on location of tumour * when gross tumour extends into CBD, or a negative cystic duct margin can't be obtained, extrahepatic bile duct resection should be done w Roux-en-Y hepaticojejunostomy * regional lymph node dissection = nodes in porta hepatis and along hepatoduodenal ligaments, including those of the cystic duct, common bile duct, hepatic artery and portal vein * T1b - 15% nodes * T2 - up to 50% nodes * T3 - extended cholecystectomy en bloc w involved adjacent organ may be done but hasn't been assoc w improved survival * in many cases need division of left hepatic duct and excision of biliary confluence + extended right hepatectomy * T4 - generally locally unresectable due to vasc invasion of main PV or hepatic artery or involvement of multiple adjacent extrahepatic organs or structures, but curative resection may be possible in selected stage IVa disease * consider adjuvant therapy for T4, positive LNs, R1 resection * unresectable disease: 5FU based chemo or supportive care * may include endoscopic orr perc biliary drainage, enteric stenting or intestinal bypass

Answer 44

* Bismuth I & II - en bloc resection of extrahepatic bile ducts & GB with 5-10mm bile duct margins and a regional lymphadenectomy with Roux-en-Y hepaticojejunostomy; resection of caudate lobe en bloc for hilar or intrahepatic cholangio now standard of care * clinically often difficult to distinguish between tyeps I and II and most recommend treating uncelar causes as type II * Bismuth III&IV - in addition to above, usu requires hepatic lobectomy or trisectionectomy * may involve complex resection and recon of portal vein, hepatic artery or both Criteria for unresectability: * patient factors * medically unfit or otherwise unable to tolerate major operation * hepatic cirrhosis * tumour factors * tumour extension to secondary biliary radicles bilaterally * encasement or occlusion of main portal vein prox to its bifurcation or bilat portal vein involvement * bilateral hepatic arterial involvement * atrophy of one hepatic lboe w contralateral portal vein branch encasement or occlusion * atrophy of one hepatic lobe w contralateral tumour extension to secondary biliary radicles * unilateral tumour extension to secondary biliary radicles w contralateral portal vein branch encasement or occlusion * need for portal vein resection not contraindication to resection but role of arterial resection & recon more controversial - signif increased M&M w/o long-term survival benefit * intraop frozen section should be done *

Answer 45

The European Colorectal Metastases Treatment Group have proposed a staging system for CRC liver metastases: * IVa - easily resectable at detection * IVb - borderline resectable at detection * IVc - potentially resectable after NAC * IVd - little or no hope of being rendered curable * Va - resectable extra-hepatic disease * Vb - unresectable extrahepatic disease

Answer 46

* wire-guided cannulation cf contrast-guided cannulation * balloon dilatation of biliary sphincter is a risk but incidence can be reduced by longer duration of dilatation rather than shorter one * prophylactic panc stent placement * rectal NSAIDs * aggressive periprocedure hydration with lactated Ringers - reduces incidence and severity

Answer 47

* curative: transplant, resection, ablation * when underlying liver disease present, only transplantation is curative by simultaneously treating aetiology of HCC & preneoplastic lesions; recurrence virtually constant w all other treatments * resection * in pts w/o cirrhosis, liver resection ideal * in pts w cirrhosis, mx depends on tumour extension, status of non-tumoural liver & general condition of pt * pts w CPC or CPC cirrhosis or portal HTN don't tolerate resection * in pts w CPA, volume of FLR important: consider PVE * mx of underlying chronic liver disease reduces likelihood of recurrence * both anatomical resections (cf tumourecetomies) & wide (cf limited) margins may improve long-term survival w/o increasing risk - aim for \>1-2cm margins to ensure potential satellite nodules/spread through microvasc invasion are also resected * lymphadenectomy recommended * adjuvant chemo not recommended * transarterial - embolisation, chemoembolisation * TACE = 1 of 2 noncurative options that can improv survival * HCC receives almost 100% of blood supply from artery; obstruction of feeding vessel -\> necrosis * can use iodised oil to target cytotoxic drugs - gets retained in malignant tumours * ablative - ethanol injection- acetic acid injectoin- thermal ablation (cryotherapy, RFA, micrwave) * RFA most effective; initially done in pts unsuitable for resectional surgery; now for neoadj tx in liver transplant candidates & for tx of recurrence after liver resection * only likely to be successful for tumours \<5cm & presence of \>3 tumours is limitation * systemic * chemotherapy - no role * hormonal ?? * immunotherapy - Sorafenib (targets angiogenesis & EGF receptor pathways) - improves OS, first line if not eligible for resection, transplant, perc ablation or TACE, if still have preserved liver function * radiotherapy * external beam limited value * radioembolisation comparable to chemoembolisation - inject radioisotopes directly into hepatic artery * transplant * if partial liver resection precluded by anatomical factors or need to preserve sufficient FLR, or as a rescue treatment for intrahepatic tumour recurrence * most effective strategy to prevent HCC recurrence * criteria in cirrhosis pts: * if HCC confined to liver, no extrahepatic disease icnl LN, no vasc extension, limited tumour burden * initially Milan criteria: single tumour \<5cm or presence of 2 or 3 tumours \<3cm * now expanded UCSF criteria: single tumour \<6.5cm or ≤3 tumours, largets \<4.5cm w sum of tumour diameters \<8cm

Answer 48

CLIP combines tumor-related features (macroscopic tumor morphology, serum AFP levels, and the presence or absence of portal vein thrombosis) with an index of the severity of cirrhosis to determine a prognostic score ranging from 0 to 6

Answer 49

* NORMAL: arises from RHA on right side of RHD in Calot's and passes lateral to GB in 70% of cases * usu divides into ant and post branches; latter goes between GB & liver * ABERRANT: * 20% arises from CHA, its bifurcation or from LHA * 10% from accessory RHA * 2.5% from GDA * also SMA * in 25% arises to left of duct system & usu crosses in front of ducts to reach GB * cystic artery can be v short with RHA in close proximity or even adherent to CD/HP * in 2-5%, artery divides early into multiple small branches and a significant cystic artery is never discovered "may arise from common hepatic, proper hepatic, from left hepatic, from GDA or SMA and in either case may pass in front of cystic and bile ducts"

Answer 50

* usu 2-8cm * entry into CHD variable: angular 70%, parallel 20%, spiral 10% (ant or post) * may have short CD, long CD or accessory CD * 1-2% join RHD or RPSD * may cross anomalous low-lying RHD in 1 in 1000

Answer 51

**_For_** * Increased recognition of CBD injury * Helps identification of abnormal ductal anatomy * If requisite skills for trans-cystic or CBD exploration are present then reduced number of procedures for patients with stones * Allows for placement of a stent at time of IOC which improves success of subsequent IOC and relieves obstruction * Detects previously unexpected CBD stones * Keeps skills up/good for training **_Against_** * Occult CBD stone found in ~5%; many pass spontaneously so ~150 IOCs with 8 unnecessary CBD explorations done to clear 1 stone that would have caused symptoms (ie small unexpected stones likely clinically insignificant anyway) * Doesn't eliminate/reduce risk of CBD injury * False positives expose patients to more risk * Increased theatre time

Answer 52

* Congestive * Cirrhosis * Heart failure * Venous thrombosis (Portal, Hepatic, IVC) * Benign haematological * Haemolytic anaemias. * Neoplastic * Myeloproliferative * ALL/CLL/AML/ALL * Polycythaemia rubra vera * Metastases * Primary splenic tumour * Multiple myeloma * Infective * EBV, CMV * Parasitic; malaria, echinococcus * Abscesses; SBE, diverticular * Fungal * Infiltrative * Gaucher's disease * Amyloidosis * Niemann-Pick * Sarcoid * Inflammatory * Lupus * Felty's syndrome

Answer 53

The DeMeester score is derived from data collected during a 24-hour ambulatory pH study, often combined with impedance testing. It generates a score from variables including: * Total number of reflux events * Longest episode of reflux * Number of episodes of reflux greater than 5 minutes * Time spent in reflux supine and standing A normal value is \<14.72

Answer 54

* Haemangioma * Centripetal filling on arterial contrast * FNH * Central feeding arteriole * Homogenous arterial enhancement with iso-enhancement of delayed phases * Hepatic Adenoma * Blood and fat (heterogenous) components * Homogenous arterial enhancement with iso-enhancement of delayed phases * Young female on OCP * HCC * Arterial enhancement with washout on later phases * Cirrhotic liver * DWI - restricts diffusion * Cholangiocarcinoma * Heterogeneous minor peripheral enhancement with gradual centripetal enhancement * Often "absence of a mass" present; i.e IH duct dilatation without clear mass * DWI - restricts diffusion * Metastases * Hypo-attenuating cannon-ball lesions * Most commonly gastrointestinal origin * Hyper-attenuating metastases from C.T.M.R.PnET tumours

Answer 55

1. Fat metabolism 2. Carb/glucose metabolism 3. Protein metabolism and Nitrogen homeostasis 4. Immune function 5. Bile synthesis and secretion 6. Coagulation 7. Metabolism of drugs and toxins 8. Vitamin metabolism

Answer 56

* Haematologic disorders; * Hereditary anaemias * Primary hypersplenism * ITP * Autoimmune haemolytic anaemia * Selected cases of myelofibrosis, CLL, and lymphoma * Primary splenic tumour * Splenic abscess * Splenic cysts * Gastric varices due to splenic vein thrombosis * Infilitrative diseases; * Gaucher's and Niemann-Pick * Felty's and Fanconi's anaemia * Amyloidosis, sarcoidosis

Answer 57

1. Howell-Jolly bodies (nuclear fragments) 2. Heinz bodies (Hb deposits) 3. Pappenheimer bodies (Fe deposits) 4. Target cells (increased surface membrane to cell volume ratio) 5. Siderocytes (iron not bound to Hb) 6. Acanthocytes 7. Transient leukocytosis 8. Transient thrombocytosis 9. Persistent lymphocytosis and monocytosis

Answer 58

* 95% are adenocarcinoma (other histo variants 5%) * 3 pathologic subtypes * sclerosing - tends to occur in prox bile ducts, causing periductal fibrosis in concentric pattern & circumferential duct occlusion * nodular - tends to occur in distal cholangios, firm mass based in duct wall, can be seen growing into duct lumen * papillary - tends to occur in distal cholangio, more common, polypoid lesion that is soft with less periductal fibrosis, though can grow to signif size often arise from well-defined stalk w bulk of tumour mobile within ductal lumen, more often resectable, better prognosis

Answer 59

According to the Atlanta Classification: * **Interstitial oedematous pancreatitis** - Acute inflammation of the pancreatic parenchyma and peripancreatic tissues, but without recognizable tissue necrosis * No findings of peripancreatic necrosis * Pancreatic parenchyma enhancement by intravenous contrast agent * **Necrotizing pancreatitis** - Inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis * Lack of pancreatic parenchymal enhancement by intravenous contrast agent, and/or * Presence of findings of peripancreatic necrosis

Answer 60

BE-CCALM-PT JEM Worrisome 1. BD-IPMN \>3cm 2. Enhancing mural nodule \<5mm 3. CA19-9 elevated 4. Cyst growth \>5mm in 3yrs 5. Abrupt cut-off of main duct w proximal atrophy 6. Lymphadenopathy 7. Main duct 5-9mm 8. Pancreatitis 9. Thickened and enhancing cyst wall High-risk 1. Jaundice 2. Enhancing mural nodule \>5mm 3. Main duct ≥10mm

Answer 61

Liver or kidney failure, inflammatory bowel disease, atrophic gastritis or chronic use of proton-pump inhibitors

Answer 62

**Resectable** * localised to pancreas * no evidence of SMV or portal vein involvement (ie no abutment, distortion, thrombus or encasement) * preserved fat plane surrounding the SMA & celiac artery branches, incl the hepatic artery **Borderline** * solid tumour contact with SMV or PV of \>180degrees or contact of ≤180degrees w contour irregularity of vein or thrombosis of vein, but suitable vessel prox & distal to site of involvement, allowing for safe & complete resection and vein reconstruction * solid tumour contact w CHA (abutment or encasement) w/o extension to celiac axis or hepatic artery bifurcation allowing for safe & complete resection & recon * solid tumour contact w SMA of ≤180 degrees **Unresectable** * mets including LN mets outside field of resection * ascites * solid tumour contact with SMA \>180° * solid tumour contact with Coeliac Axis \>180° * solid tumour contact with primary jejunal artery or vein * un-reconstructable SMV/PV

Answer 63

1. General condition of the patient 2. Number, size and location of the stones 3. Anatomy of biliary tree – size of cystic duct & common duct (espec relative to size of stones) and whether contrast flows freely into duo 4. Size of the stone 5. Accessibility of the ducts * Small stones (\<4mm) may flush w Buscopan 20mg IV or Glucagon 1mg IV and saline * Can place additional clip or endoloop on cystic duct, place large adjacent drain & subsequent ERCP * Small stones are amenable to spiral basketing under a fluoroscopic approach * Long or tortuous or inflamed cystic ducts will hamper a trans-cystic approach * Medium stones (4-10mm) unlikely to be dealt w via fluoroscopy alone so use a trans-cystic 5mm scope; may need to dilate cystic duct up to 8mm * Large stones (\>10mm) should be treated w a trans-CBD approach, open if I am doing it * Alternatively, passing an antegrade transcystic stent through and post-op ERCP is a safe bail out

Answer 64

The hallmark of HCC on CT and MRI is strong arterial enhancement and washout of contrast in the delayed phase, often with rim enhancement. Intra-hepatic cholangiocarcinoma shows delayed enhancement.

Answer 65

* Chronic pancreatitis is a fibro-inflammatory condition characterised by structural changes to pancreatic parenchyma which lead to endocrine and exocrine dysfunction * The causes are varied; * Toxins * EtOH * Hyperclacaemia / Hyperlipidaemia * Idiopathic * Genetic * CFTR mutations (cystic fibrosis) * SPINK1 mutations * Autoimmune * In isolation * In conjunction with Sjögren's, IBD, PBC * Recurrent acute pancreatitis * Obstructive causes * Pancreatic divisum * Sphincter of Oddi disorders * Stricture due to ERCP, stone disease.

Answer 66

* rare variant of HCC w remarkably different clinical features * occurs at 20-35yrs, generally w/o hx of cirrhosis, F:M * path: usu well demarcated & encapsulated and may have cenral fibrotic ara; central scar can make it difficult to distinguish from FNH * doesn't produce AFP but assoc w elevated neurotensin levels * LN invasion within hepatic pedicle frequent * usu 8-10cm (large) at time of dx & symptomatic * imaging: large solitary hypervascular heterogeneous liver mass w central hypodense region due to central necrosis or fibrosis, well defined margins, calcification in 68% * MRI - central scar has low attenuation on T2, whereas cenral scar of FNH has high attenuation * management: * if resection considered, simultaneous lymphadenectomy recommended * if recurs, repeat surgery reasonable due to rel indolent disease course & relative inefficacy of non-surgical tx * transplant may be alternative option in select cases * outcome: better than HCC, prob related to high-resectability rates, lack of chronic liver disease & more indolent course * long term survival in 50-75% but recurrence common ≥80%

Answer 67

* a rare idiopathic chronic disease, likely involving an autoimmune process, characterised by non-infective progressive obliterative fibrosis of the intra and extrahepatic bile ducts * M\>F, 20-50yrs * 60-80% of cases occur in UC pts; PSC occurs in 5-11% of UC pts * routinely evaluate PSC pts for IBD but don't routinely screen pts w IBD for PSC unless abnormal liver tests * less common associations: Crohn's, Riedel's thyroiditis, retroperitoneal fibrosis * entire biliary tree affected by inflammation --\> causes irregular partial obliteration of the duct lumen; intra- and/or extrahepatic ducts affected (most commonly both) * inflammation, fibrosis, cholestasis * progressive chronic cholestasis and advances at unpredictable rate to biliary cirrhosis & eventually death from liver failure * complications: * ESLF * fat soluble vitamin deficiencies * metabolic bone disease espec osteoporosis * dominant biliary strictures * cholangitis & cholelithiasis (cholesterol and/or pigment stones) * cholangiocarcinoma 10-15% lifetime risk - often heralded by rapid clinical deterioration w jaundice, weight loss & abdo discomfort * dx can be v challenging in PSC - tests include biliary brush cytology, endobiliary biopsy, CT or MRCP and tumour markers * GB ca in 3-4% * NB 40-60% of GB polyps in pts w PSC are malignant * HCC (in pts w cirrhosis) * colon ca (in pts w concomitant UC) * diagnostic approach * suspect if cholestatic liver tests espec if IBD * dx by cholangiographic evidence of characteristic bile duct changes (chain of lakes) & excluding secondary causes of sclerosing cholangitis, primary biliary cholangitis & IgG4-assoc cholangitis/autoimmune pancreatitis * liver biopsy may support dx but rarely diagnostic * antimitochondrial antibody - present in primary biliray cholangitis but not PSC * IgG4 * exclude secondary causes of PSC: chronic bacterial cholangitis, infectious or ischaemic cholangiopathy, cholangiocarcinoma, choledocholithiasis, diffuse intrahepatic mets, eosinophilic cholangitis, intra-arterial chemo, mast cell cholangiopathy, portal hypertensive biliopathy, recurrent pancreatitis, recurrent pyogenic cholangitis, surgical biliary trauma * ix: * pANCA positive in 30-80% * LFTs may fluctuate * cholangiogram w MRCP, ERCP or PTC or CT cholangio - beaded appearance or chain of lakes (long strictures concerning for cholangiocarcinoma) * benefit of MRCP = non-invasive & avoids introduction of bacteria * liver boipsy: pericholangitis, bile stasis, fibrous obliteration of small bile ducts w concentric replacement by connective tissue in 'onion skin' pattern * mx * abx for cholangitis * cholestyramine for itch * no therapy that slows progression of disease * observation early in disease w mild sx reasonable * if symptomatic, ERCP/PTC/endoscopic therapies to stent/balloon dilate dominant strictures may help alleviate pruritis and reduce likelihood of cholangitis * exclude cholangiocarcinoma - may appear as dominant stricture; serum Ca19-9, brush cytology of biliary tree, endobiliary biopsy & FISH all used in assessment of dominant biliary stricture * perc or EUS-guided needle biopsies shouldn't be done - precludes transplant * resection of extrahepatic biliary tree and HJ - may improve symptoms and postpone need for transplant * transplant superior to biliary surgical procedure - indicated for advanced disease w cirrhosis * cholecystectomy in PSC pts w GB polyps * outlook * progression to cirrhosis after several years * median survival w/o liver transplant 10-12yrs * adenoCA espec in UC pts - in 10-30% - cholangio or GB * not affected by proctocolectomy * after liver transplant 80-90% 5yr survival * surveillance * screen for fat soluble vitamin deficiencies (PR, vits A, D, E) * bone density exam at dx & q2-3yrs after * studies failed to show benefit of screening for cholangioca but given high incidence many screen annually & USS or MRCP + serum CA19-9 * if PSC & cirrhosis, screen for HCC * if UC & PSC, colonoscopy screening

Answer 68

A constellation of symptoms and signs resulting from too small a 'functional mass' of liver for that individual recipient; leads to * prolonged cholestasis (raised bili) * coagulopathy (raised PT) * portal HTN * ascites * GI bleeding * death at 4-6wks from sepsis

Answer 69

* term SOD has been used to describe a clinical syndrome of biliary or pancreatic obstruction related to mechanical or functional abnormalities of the sphincter of Oddi. The literature regarding SOD is often difficult to interpret because of differences in nomenclature * 2 separate pathologic entities are recognized based on their distinct pathogenic mechanisms: SO stenosis and SO dyskinesia; term SOD encompasses both * has been assoc w 2 clinical syndromes: biliary SOD and idiopathic recurrent pancreatitis * clinical criteria for FUNCTIONAL GB & SO disorders have been proposed on basis of expert consensus; Rome IV criteria specify 3 subsets of functional GB & SO disorders * functional GB disorder * functional biliary sphincter disorder * functional pancreatic sphincter disorder * Rome IV criteria for biliary pain (need all of them) * Pain in epigastrium and/or RUQ * Episodes lasting ≥30mins * Recurrent sx occurring at diff intervals (not daily) * Pain builds up to steady level * Pain severe enough to interrupt daily activities or lead to ED visit * Pain not significantly (\<20%) related to BM * Pain not significantly (\<20%) relieved by postural change or acid suppression * Supportive criteria include: pain assoc w N&V, pain radiating to back and/or right infrascapular region, pain awakening pt from sleep * Rome IV criteria for functional biliary SOD * Criteria for biliary pain fulfilled * Absence of bile duct stones or other structural abnormalities * Elevated liver enzymes (ALT, AST, bilirubin or ALP \>2x normal that normalize between attacks) or dilated bile duct (\>8mm) but not both (that would be more likely to be stenosis/type I) * Rome IV criteria for functional pancreatic SOD * Documented recurrent episodes of pancreatitis (≥2) * Other aetiologies of pancreatitis excluded * Negative EUS * Abnormal sphincter manometry * (not part of Rome criteria but liver transaminases & bilirubin may also be elevated & may have dilation of panc duct) * criteria for likely mechanical biliary SOD (type I): biliary-type pain AND abnormal LFTs AND duct dilatation (with bile duct stones/other structural abnormalities excluded)

Answer 70

HIDA = radiolabelled iminodiacetic acid is given and will collect in GB; then pt given IV dose of CCK and %ejection of GB in response to CCK is calculated EF 40% at 20mins after CCK or fatty meal administration in pts w/o stones = considered diagnostic of dyskinesia cholecystectomy may be justifiable if typical biliary pain & absence of other disease processes - 50% likelihood of pain resolution

Answer 71

Theoretically, early ERCP in gallstone pancreatitis could remove impacted stones in the distal CBD, thereby alleviating the initiating stimulus and reducing pancreatic inflammation. **_Three randomised trials_** assessing early ERCP have been published with **_mixed results_**. Overall there is a suggestion that early ERCP may be beneficial in patients with **_prognostically severe pancreatitis_** with evidence of cholangitis or obstructive pattern LFTs.

Answer 72

1. Canine (dog/dingoe) hosts harbour adult Echinococcus granulosus tapeworms in their jejunum - definitive, asymptomatic host 2. Ova are passed in faeces; ingested by intermediate hosts; usually sheep. * ***(humans are inadvertant intermediate hosts)*** 3. In intermediate host, ova hatch to release larva due to interaction w bile salts & trypsin --\> larva penetrate lamina propria in jejunum & are transported by portal system into liver (75%) or via lymphatics to lung 4. Larvae develop into hydatid cysts; mature cysts have 3 layers (cyst wall itself 2 layers) * innermost layer = endocyst - inner germinal layer which produces hydatid fluid, has absorbative function for nutrition & is where daughter cysts (endocysts) are formed * has brood capsules = small, intracystic cellular masses in which future worm heads evelop into scoleces (ie contain protoscolices) * in a definitive host, the scoleces develop into adult tapeworm, but in intermediate host can only differentiate into a new hydatid cyst * freed brood capsules & scoleces are found in the hydatid fluid & form the so-called hydatid sand * daughter cysts = true replicas of the mother cyst * exocyst = external, laminated, gelatinous acellular hilar membrane around germinal layer * ectocyst/pericyst = host-derived external fibrous capsule 5. Sheep offal is consumed by dogs (definitive host) so larvae re-infect the primary host * when a cyst-containing organ is ingested, the protoscolices evaginate then scolices attach to intestines of definitive host & develop into adult tapeworms which completes the lifecycle

Answer 73

1. Ingested as cysts via the fecal to oral route 2. Incubation for 2-4 weeks (may be longer) 3. Excystation in the small bowel 4. Trophozoites colonize large bowel 5. Invade colon - amoebic dysentery 6. Invade porto-venous system - abscess

Answer 74

* Babbitt’s theory = based on an abnormal biliopancreatic junction, where the main ducts join abnormally proximal to the ampulla of Vater * Postulates that the long common channel allows mixing of the panc & biliary juices, which then activates pancreatic enzymes * These active enzymes cause inflammation & deterioration of the biliary duct wall, leading to dilation * Furthermore, greater pressures in the panc duct can further dilate weak-walled cysts * Competing theories suggest choledochal cysts are purely congenital in nature, resulting from aganglionosis similar to Hirchsprung’s disease

Answer 75

1. No matter what the inciting event, there is abnormal activation of proteolytic enzymes within the pancreatic acinar cell. There is abnormal co-localization of lysozymes and zymogen granules allowing cathepsin-B to hydrolyse trypsinogen. 2. Acinar cell injury allows trypsin to be released into the pancreatic parenchyma where it activates more trypsinogen. These overwhelm the natural anti-proteases. 3. Local inflammation causes monocytes and neutrophils to release cytokines including IL-1, IL-6, TNF, and PAF leading to SIRS. 4. Hypoperfusion and erosion into vessels leads to necrosis.

Answer 76

Patients with resectable colorectal hepatic metastases can look forward to a 5-year-survival of 40-50% and a 10 year survival of 24%, with age being no barrier to resection if fit.

Answer 77

**_Cysts_** * Congenital * Simple cysts * Polycystic disorder * Infective * Pyogenic or amoebic abscess * Hydatid cyst * Neoplastic * Benign = Cystadenoma * Malignant * Cystadenocarcinoma * IPMN of bile duct * Primary liver ca with cyst degeneration * Cystic mets to liver - colorectal, neuroendocrine, GIST, SCC, breast * Post-traumatic **_Pseudotumours_** * Foetal lobulatons or focal fatty sparing **_Solid tumours_** * Mesenchymal * benign - haemangioma, lipoma, angiolipoma * malignant - haemangiosarcoma * Benign Epithelial * FNH * Hepatocellular adenoma * Bile duct adenoma/biliary hamartoma/von Meyenburg complexes * Intermediate/benign epithelial * Dysplastic nodules * Malignant Epithelial * Primary * Hepatoblastoma * HCC (incl fibrolamellar variant) * Cholangiocarcinoma * Secondary (mets) * Lymphoma

Answer 78

Bacteria with a polysacharide capsule are removed by the spleen, so loss of the spleen puts patients at increased risk of infection from; Pseudomonas, Strep. pneumoniae, Haemophilus influenzae, Neisseria meningitidis, E. coli, Salmonella, Klebsiella, group-B Streptococci, and Bordatella pertussis (**P**lease **SHiNE** my **SK**i**S** and bordatella) Deliver vaccines pre-operatively by at least two weeks where possible. 14 days post op following emergent splenectomy. Hiberix, Pneumovax-23, Prevenar-13, Menactra, Influenza, DTaP.

Answer 79

Progression of a stricture on serial cholangiograms marked biliary dilation above a dominant stricture polypoid ductal mass ≥1cm diameter

Answer 80

* Stercobilin results from breakdown of the heme moiety of hemoglobin found in erythrocytes. * Macrophages break down senescent erythrocytes and break the heme down into **_biliverdin_** (green pigment), which rapidly reduces to free **_bilirubin_**. * Bilirubin binds tightly to plasma proteins (especially albumin) in the blood stream and is transported to the liver, where it is **_conjugated_** with one or two glucuronic acid residues into **_bilirubin diglucuronide_**, and secreted into the small intestine as bile. * In the small intestine, some **_bilirubin glucuronide is converted back to bilirubin_** via bacterial enzymes in the terminal ileum. This bilirubin is further converted to **_colorless urobilinogen_**. * Urobilinogen that remains in the colon can either be **_reduced to stercobilinogen_** and finally oxidized to stercobilin, or it can be directly **_reduced to stercobilin_**. * Stercobilin is responsible for the brown color of human feces. Stercobilin is then excreted in the feces.