liver and friends :) Flashcards

Question

rules when managing liver patients

Answer 1

1. THINK SEPSIS blood culture, ascitic fluid taps, fluid resus, prompt abx look for sites of infection - ascites, chest, urine, skin, brain, heart 2. U+E very common to get hypos in kal, natr, magn, phosph, glyc, bicarb (met acid) monitor and CHASE results 3. READ THEIR RECORDS - HBV/HCV? have a label of cirrhosis but no biopsy diuretic intolerance 4. management of ceiling decisions - critical care, transplant, DNAR?

Answer 2

arterial flush, venous washout

Answer 3

``` total protein albumin globulin bilirubin ALT ALP ```

Answer 4

hepatocytes

Answer 5

muscle, heart, kidney

Answer 6

ALP - cells lining the bile duct GGT - endoplasmic reticulum of all cells except muscle. Mainly membrane bound.

Answer 7

bone intestine placenta if elevated with GGT then it will be liver if it was from bone then GGT would stay low raised in bone when things like osteomalacia

Answer 8

``` produced from breakdown of red blood cells bilirubin is water insoluble travels in blood bound to albumin pre-hepatic - haemolysis hepatic - gilberts ```

Answer 9

is what soluable by conjugation with glucuronic acid in the liver excreted from the liver via the biliary tract to the small intestine

Answer 10

paracetamol/analgesics methotrexate amiodarone abx - isoniazid, co-amox, fluclox, erythro statins dietry drugs - herbs CNS drugs - chlorpromazine, carbamazepine, valporate, paroxetine MULTIPLE COMBO?

Answer 11

INR | Prothrombin time

Answer 12

pathophys Bile is secreted by hepatocytes and stored/concentrated in GB. In cholestasis bile cannot flow from the GB to the duodenum. This leads to retention of conjugated bilirubin and regurg to serum, increased serum concentration of unconjugated bilirubin, increased bile salts ``` CAUSES intrahepatic - hepatitis - primary biliary cholangitis - drugs - preg ``` extrahepatic - stones + strictures - ca head of panc - portal hepatic LN mets - sclerosing cholangitis LFTS elevation in ALP GGT +/- bilirubin

Answer 13

chronic alc excess persistent Hep B or C autoimmune inherited metabolic - haemochromatosis, A1AT def, wilsons LFTs hypoalbuminaemia prolonged PT

Answer 14

ALT - not found much else where | L for liver!!

Answer 15

kidneys pancreas heart brain ``` things that make it go up alc - just drinking fatty liver/ insulin resistance/ obesity enzyme inducing drugs - anticonvulsant - CBZ, phenytoin, phenobarb - warfarin - OCP ```

Answer 16

autoimmune anything that raises immunoglobulins so would want to test ANA antibodies, antimitochondrial, anti smooth muscle

Answer 17

95% of primary biliary cholangitis cases | also in RA

Answer 18

hepatic artery from the aorta supplies oxygenated blood. 25% of blood supply it also receives blood from intestines, spleen and stomach that is deoxygenated on their way back to the heart in the portal vein, that is full of nutrients - 75% of blood supply all this blood leaves the liver in the hepatic vein -> IVC

Answer 19

4 lobes - 2 major ones

Answer 20

portal vein bile duct hepatic artery - IN central vein in middle of lobule - OUT

Answer 21

hexagon google it love

Answer 22

1 - ischaemia >25 - alcoholic hepatitis <1 - hepatocellular damage eg paracetamol OD

Answer 23

1. hereditary haemochromatosis - deficiency of iron reg hormone hepcidin 2. wilsons disease - hepatolenticular degeneration - accumulation of copper at tissues 3. alpha-1 antitrypsin deficiency - affects liver and lungs (emphysema)

Answer 24

Hepcidin is produced by hepatocytes in response to high iron levels. It blocks iron absorption by blocking ferroportin at enterocytes and reduces iron exit from liver and macrophages (storage sites) in same way

Answer 25

Binds iron reversibly in blood

Answer 26

Stores iron intracellularly, an acute phase protein

Answer 27

inheritance AR patho Increased intestinal absorption of iron leading to accumulation in tissues: liver (fibrosis, cirrhosis, HCC), heart, skin, joints (arthropathy), pancreas (diabetes) genes HFE gene chromosome 6: most common C282Y (or H63D) epi 40-50 yr old pres Early: fatigue, weakness, arthralgia, erectile dysfunction/amenorrhoea Late: skin bronzing, diabetes, cirrhosis (liver signs), impotence, cardiac arrhythmia, arthropathy 2nd and 3rd metacarpophalangeal joints ix Iron studies - Serum ferritin (high) - lots of iron in cells - low specificity as acute phase protein (so goes up with any inflam) - Transferrin saturation (>45%) - lots of iron in blood specific HFE genetic testing LFTs MRI - iron overloaded liver Liver biopsy with Perl’s stain (blue) *Liver fibroscan/transient elastography ECG/ECHO for cardiomyopathy Tests for other causes of hyperferritinaemia e.g. inflammation (CRP), alcohol, metabolic syndrome (BP, BMI, glucose, triglycerides) ``` mgmt Venesection/phlebotomy 4-500ml weekly desferrioxamine may be used second-line Liver transplant at decompensation of liver Monitor ferritin - <1mg/L = risk of serious liver damage <1% Low iron diet avoid alc genetic counselling ``` ``` comps type 1 diabetes - iron build up in panc liver cirrhosis iron build up in pituitary + gonads = hypogonadism, impotence, amenorrhoea, infert cardiomyopathy hepatocellular carcinoma hypothyroidism chrondocalcinosis/pseudogout ```

Answer 28

ERCP - endoscopic retrograde cholangiopancreatography - uses scope and dye, can intervention at the time, cant see past obstruction, comps = pancreatitis, bleeding, failure MRCP - magnetic resonance cholangiopancreatography

Answer 29

rf - female, fat, fertile , fair + forty + fh, oral contraception, hyperlipidaemia ``` classification CHOLESTEROL (ileum absorbs bile salts): - 80% of stones in UK - large, solitary, radiolucent - admirands triangle (1. Decreased dietary lecithin, 2. Decreased bile salts (impaired flow), 3. Increased cholesterol saturation of bile/loss of bile salts (ileal resection/Crohn’s) ``` PIGMENT stones 10% - black calcium bilirubinate + mucin - glycoproteins - small friable, radiolucent - result of haemo conds - brown calcium bilirubinate + fatty acids - result of stasis and biliary infection e.coli/klebsiella MIXED stones 10% - faceted - calcium salts + pigment + cholesterol pres as biliary colic or acute cholecystitis mgmt gallbladder - lapro cholescystectomy or bile acid dissolution therapy <1/3 success bile duct stones - ERCP with sphincterotomy and: remove, crushing or stent placement. or surgery (large stones)

Answer 30

gallbladder: biliary pain cholecystitis obstructive jaundice - maybe mirizzi ``` bile duct: biliary pain obstructive jaundice cholangitis pancreatitis ```

Answer 31

Mirizzi's syndrome is a rare complication in which a gallstone becomes impacted in the cystic duct or neck of the gallbladder causing compression of the common hepatic duct, resulting in obstruction and jaundice. The obstructive jaundice can be caused by direct extrinsic compression by the stone or from fibrosis caused by chronic cholecystitis (inflammation). A cholecystocholedochal fistula can occur

Answer 32

hepatocellular cholestatic mixed

Answer 33

progression from normal to liver decompensation

Answer 34

``` reasons: impaired reticulo-endothelial function reduced opsonic activity leucocyte function permeable gut wall ``` ``` sites: spont bacterial peritonitis septicaemia pneumonia skin urinary tract ```

Answer 35

what is it intra-abdo sepsis ``` pres - vague symps fever mild abdo pain vom triad of peritonism: gaurding, rebound tenderness, pain on palpation ``` ``` ix diagnostic paracentesis - culture + amylase - neuts in ascitic fluid >250 cells/ul - gram stain ascitic fluid often gram neg (e.coli, enterococcus)- use blood culture bottles FBC - leukocytosis LFTs U+E imaging? ``` mx abx proph - IV 3rd gen cephalosporins eg cefotaxime liver transplant prog 50% chance of death in 1 year - liver transplant asap

Answer 36

drugs - diuretics, NSAIDs, ACEi, aminoglycosides infection GI bleeds myoglobinuria renal tract obstruction

Answer 37

subtract 7 from 100 and continue WORLD backwards how many animals can you count in a minute draw 5 point start number connection test (dot to dot basically)

Answer 38

malnutrition - NG tube coagulopathy - impaired coagulation factor synthesis, vit k deficiency (cholestasis), thrombocytopenia variceal bleeding - endoscopic banding, propanolol, terlipressin endocrine - gynaecomastia, impotence, amenorrhoea hyperglycaemia (+/-) encephalopathy - lactulose ascites/oedema - salt/fluid restriction, diuretics, paracentesis infections - proph abx

Answer 39

pmh - alc probs, biliary surgery, autoimmune disease, blood products social - alc, sex, contacts, travel, IVDU DH - all review

Answer 40

viral - A,B,C, CMV, EBV drug-induced autoimmune alcoholic

Answer 41

``` AIH IgG antinuclear, anti sm, liver-kidney microsome 41% have other AI - various 4:1 familial - 5x risk HLA DRB1 0301/0401 response to IS - good ``` ``` PBC IgM antimitochondrial 33% various 10:1 10x HLA D8 limited ``` ``` PSC variable antineutrophil cytoplasmic (ANCA) 70% - mainly colitis 0.6:1 9-39 x HLA class I (b) response to IS therapy - little ```

Answer 42

liver biopsy

Answer 43

mayo clinic | uses bilirubin, albumin, PT time

Answer 44

Ursodeoxycholic Acid - antihistamines (little help) cholestyramine - 50% helps rifampicin is effective - occasionally damages liver :/ opioid antagonists UV light, plasmapheresis, liver transplant FATIGUE - check for any other causes and correct modafinil

Answer 45

inheritance AR mech A1AT is a glycoprotein produced in the liver. It is a serine protease inhibitor and controls inflammatory cascades and balances the action of neutrophil elastase in the lung (cigs/inflammation). NE will break down elastin leading to alveolar destruction. In A1ATd an abnormal protein is produced which cannot leave, congests in liver cells and causes destruction. genes SERPINA1 gene chromosome 14. M alleles are normal variant. MS or MZ are carriers. onset lung disease in 30/40s pres jaundice baby young person with COPD - dyspnoea, wheeze, cough, emphysema typically in lower lobes hepatits, cirrhosis (HCC), fibrosis ix serum A1AT low -> phenotyping CXR + spirometry - obstructive LFT + biopsy liver - shows cirrhosis + acid-Schiff-positive staining globules in hepatocytes ``` mgmt asymp - smoking and alc advise lung symps - as COPD liver - reg LFTs, rx cirrhosis, screen for HCC transplants ``` comps hepatocellular carcinoma

Answer 46

``` causes thrombosis (budd-chiari) membrane obstruction veno-occlusive disease (irradiation, antineoplastic drugs) congestion causes acute + chronic ``` pres abnormal liver tests, ascites, acute liver failure mgmt anticoag transjugular intrahepatic portosystemic shunt liver transplant

Answer 47

acute <12w | chronic >12w

Answer 48

O-Gradey jaundice to enceph time hyperacute - <7 days (best prog) - paracetamol, drugs, ?viral acute 8-28 days - viral, ischaemic sub acute: 29 days - 12 weeks (worst prog) - seroneg hepatitis (aka unknown), autoimmune

Answer 49

UK - paracetamol | develop - viral hep (most common worldwide E)

Answer 50

``` staggered alc malnutrition HIV, cancer chronic liver disease takes liver enzyme inducers (antiepileptic, rifampicin, spironolactone) ```

Answer 51

IV NAC - check above treatment line in curve graph in BNF IV crystalloids 100-250mls/hr IV broad spec abx/antifungals (INR>2.5) - as at high risk of infections call liver transplant centre - each day post overdose there is criteria for referral you can check

Answer 52

the surface antigen takes 3 months to get back !! | send for HBV C IgM in acute setting or HBV DNA test

Answer 53

``` bile = bile acids + phospholipids + cholesterol bile acids = cholic acid + chenodeoxycholic acid form by cholesterol liver metabolism secondary bile acids = bacterial metabolites of bile acid formed in colon function = fat digestion. absorption of fat, cholesterol and fat soluable vitamins - A,E,D,K. bole forms micelles - binds to fat/cholesterol and aids absorption through micellar transport system ```

Answer 54

stone eg cholelithiasis = gall stones choledocal-lithiasis = bile duct stone

Answer 55

``` jaundice itch - resistant to antihistamines RUQ pain - intermittent colic or painless acute or chronic dark urine pale/white stool that floats as not absorbing fats weight loss lethargy anorexia ```

Answer 56

laproscopic cholecystectomy if not suitable for surg - - ursodeoxycholic acid - dissolve over 2 years <50%

Answer 57

inflammation of gallbladder due to retained bile gallstones obstruction trauma pres biliary pain thats progressive -> right shoulder sepsis signs - fever, vom, local peritonism GB mass history of prev attacks MURPHYS sign = acute cholecystitis (2 fingers, breathe in, halts inspiration, negative on other side), NO? = biliary colic ``` ix raised WCC + CRP bil and alk phos could be high USS - thick walled tender GB (>3mm) with stones + fluid or air in gall bladder CBD dilatation - ?MRI (>6mm) ?ERCP/MRCP ``` mx lap cholecystectomy conservative = abx comps gangrene - perf, abscess empyema chronic cholecystitis - repeat attacks of cholecystitis, more likely to be fat intolerant cholangitis hydrops porcelain gall bladder - increased risk of ca

Answer 58

``` pancreatitis appendicitis peptic ulcer disease liver abscess pneumonia MI perf bowel - DU ```

Answer 59

ddx cancer ?painless/low grade - panc, bile duct, gall bladder, metastatic liver disease mx ERCP - remove stone Lap - chole +/- intraoperative cholangiogram IV abx - e.coli - co-amox

Answer 60

chronic diffuse inflam + fibrosis of intra + extrahepatic bile ducts leading to multifocal biliary strictures small epi men>w assoc risks - UC in 80%, increased risk of colon cancer - yrly colonoscopy HCC ``` pres Asymptomatic + abnormal LFT hepatomegaly Jaundice/pruritus RUQ pain Fever, wt loss, fatigue, sweats ``` severity childs-pugh - BRAIN ix difficult differential - MRCP (shows beaded appearance), liver biopsy - perductal onion skin fibrosis, Degeneration of ducts + ductal + periportal triad inflammatory cell infiltrate and scarring leading to disappearance of bile ducts and periportal cholestasis Bloods - LFTs (elevated alk phos, ggt, raised trans) raised immunos - IgG, IgM, hypergammaglobulnaemia, autoantibodies: p-ANCA ``` mgmt acute bact - ?cipro chronic - dominant stricture = balloon dilate or ?resect - cholangio urso reduce CRC yearly surveillance pruritic? cholestyramine if cholestatic - supplement diet with DEAK fat soluble vits avoid alc liver transplant if cirrhotic ``` comps cholangiocarcinoma, gallstones, GB polyps/cancer colorectal cancer cirrhotic liver prog 12-17 ``` poor outcome factors: age bilirubin albumin varices dom stricture extra hepatic changes ```

Answer 61

``` surgery/injury panc gallstone intervention cholangitis mx ERCP - dilation or removable metal or plastic stents ```

Answer 62

``` like biliary colic but without any gallstones chronic acalculus cholecystitis women >50 RUQ after fatty foods HIDA scan helpful ``` treat with lap chole (85% cure) path chronic cholecystitis

Answer 63

1. projection - standard is AP with patient supine 2. patient details + date of film 3. technical adequacy - entire abdomen? includes hemidiaphragms to symphysis pubis/hernial orifices 4. obvious abnormalities 5. systematic review A - assess the bowel: large bowel - diameter <6cm large bowel <9cm caecum + wall thickness small - diameter <3cm + wall thickness (should be hard to see if theyre normal) B - check for pneumoperitoneum - riglers, subdiaphragmatic, visible falciform ligament, triangular lucent areas, hyperlucency of the liver, football sign C - obvious abnormality of liver, gallbladder, spleen eg radio-opaque gallstones D - assess renal tract - ?calculi E - vascular structures - aorta, iliac vessels - vascular calcification, aneurysm F - assesses imaged skeleton G - comment on iatrogenic abnormalities - surgical clips, stents summary - present findings, review previous imaging, provides differentials, suggest further approp ix or mgmt

Answer 64

bowel obstruction, perf, exclusion of toxic megacolon much higher amounts of radiation than CXR and really cant see a lot

Answer 65

patho inflam process with cascade release of inflam cytokines (TNF alpha, IL2, IL4) and pancreatic enzymes (trypsin/lipase etc) causing autodigestion of organ. gallstones block bile duct, back log in panc duct, periductal necrosis ``` causes -GET SMASHED Gallstones - most likely in women Ethanol - most likely in men Trauma Steroids Mumps Autoimmune Scorpion sting - trindiad hyperlipidaemia, hypotherm, hypercalc ERCP Drugs - azathiprine, diuretics, NSAIDs ``` pres severe epigastric pain radiating to back relieved by sitting anorexia n + v fever, dehydration, hypotension, tachy - SEPTIC SHOCK abdominal guarding 1-3% have haemorrhagic panc - grey-turners sign - left flank ecchymosis, cullens sign periumbilical ecchymosis abdo rigidity classification 1. oedematous -70% - phlegmon formation + multiple transient fluid collections 2. severe/necrotising - 25% - sterile or infected, pseudocyst formation (periductal or perilobular) 3. haemorrhagic 5% diagnosis 2/3 hx (pain), amylase x3 of normal (+raised lipase, more panc specific), imaging (CT) pathology (loss of fat planes/panc oedema and swelling +/- fluid loculations) ``` ix ABG FBC - leukocytosis CRP >200 = necrosis LFT AST:ALT >3, raised bili hypocalc hyperglyc U+E - raised urea plain erect AXR - panc calcification CXR - exclude perf, ?ARDS CT with contrast - diagnostic USS - swollen pan + glasstones ERCP? ``` ``` severity three main scoring tools: abbreviated glasgow scoring system >3 = ITU/anaesthetic review: PANCREAS P=pa02 <8kpa Age = >55 yrs Neutrophils >15x10-9 calc <2mmol/l raised urea >15mmol/l elevated enzymes LDH >200IU/l or AST>600IU/l albumin <32g/l sugar - serum glucose >15mmol/l ``` ranson criteria balthazar score - CT severity index score mgmt pain control - pethidine or buprenorphine ± IV benzodiazepines (morphine spasms ampulla) ABCDE IV fluids, catheterise severe - insulin, calcium correct, no abx unless culture postive/cholangitis (usually cef/met if +) TP nutrition - NBM + NG tube >48hrs for gut rest + antiemetics observes for internal necrosis (pancreas dissolving gallstones out <2w after discharge - 18% remission ``` comps SIRS - systemic inflam response syndrome Pro-inflammatory state that does not include a documented source of infection. two or more of: temp <36 or >38 hr >90 rr >20 WCC >12x10-9 MODS - Multiple Organ Dysfunction Syndrome (MODS) Sequalae of above causing loss of body homeostatic mechanisms panc necrosis panc abscess ascites pulm oedema shock death ```

Answer 66

irreversible fibrosis following necrosis of panc paranchyma - calc + dilation of ducts abnormal bicarb excretion ``` causes alc!!! can cause chronic panc directly smoking meds - aza, tetracy, oestrogens idiopathic/tropical AD CF autoimmune (IgG4) - japan (may also have raised ANA, RF) - reversible + steroid responsive hypercalc - PTH ``` ddx carcinoma of panc types large duct = dilatation and dysfunction of large ducts + diffuse calc + steatorrhoea - men small = no calc or steat, women pres episodes of exacerbation or cont pain still epigastric radiating to back relieved by sitting forward n +v anorexia exocrine dysfunction - malabsorption with weight loss, diarrhoea, steatorrhoea and protein deficiency endocrine dysfunction - diabetes ix Bloods: FBC, U+E, Cr, LFT, Ca (cause), amylase (normal), glucose, HBa1C (raised) Secretin stimulation test: causes pancreas to release bicarb to neutralise stomach acid -> +ve result if over 60% exocrine function lost Malabsorption tests: serum trypsinogen/faecal elastase Imaging: CT for atrophy, duct dilatation or calcification MRCP (magnetic retrograde cholangiopancreatography) ?Endoscopic ultrasound mgmt Manage pain and malabsorption Pain - simple + opiate (normally tramadol) - risks opioid dependence and gastroparesis Malabsorption - replace pancreatic enzymes + Alcohol advice + low fat diet/gallstones treatment/diabetes treatment ``` comps pain - local inflam/duct obstruction with stones bile duct stricture nutrition endocrine - diabetes cancer ``` autoimmune pancreatitis - IgG4

Answer 67

5 year survival 3%

Answer 68

panc cancer | it gets missed cos people have USS and cant see panc well on USS cos of stuff in the way eg stomach that has gas in it.

Answer 69

AR mech disorder of biliary excretion of copper Wilson’s ATP-ase normally moves copper across cell membranes in hepatocytes leading to incorporation into caeruloplasmin. This is deficient in Wilson’s leading to copper retention in liver and basal ganglia. genes ATP7B gene on chromosome 13 onset - young adult with liver abnormalities or movement disorders features LIVER - acute liver failure, chronic hepatitis + cirrhosis @ younger PSYCH - severe dep 50% NEURO - asymmetrical tremor, ataxia, mask-like faces, clumsiness, excess salivation, dysarthria (speech probs), choreiform movement - parkinsonian @older OPTHALMOLOGICAL - kayser-fleischer ring 95% + sunflower cataracts OTHER - haemolytic anaemia, renal tubular acidosis, oesteopenia, blue nails ``` ix copper-studies - low serum caeruloplasmin, high 24 hour urine copper excretion, high free copper slit-lamp - opth liver biopsy - copper MRI head - density at basal gang ``` mgmt chelation agents - penicillamine (oral) or trientine - binds to copper for excretion in urine zinc compounds - stop absorption of copper avoid - mushrooms, liver, choco, nuts monitor hepatic + renal fucntions, FBC + clotting avoid alc + hepatotoxic drugs

Answer 70

when This occurs when liver loses the ability to regenerate. 4 characteristics + why: 1. hepatic encephalopathy - In liver failure ammonia builds up in circulation and crosses BBB. Astrocytes clear this turning glutamate to glutamine. Glutamine excess causes fluid shift to cells -> cerebral oedema. Altered mood, drowsiness, restless, coma 2. jaundice - build up of unconjugated bilirubin 3. abnormal bleeding - factor 1972 (10, 9, 7, 2 with vit k) fibrinogen (factor 1) 4. ascites - shifting dullness, fluid thrill, hypoalbuminaemia ``` ix FBC - thrombocytopenia LFTs bilirubin ammonia glucose - low copper studies paracetamol/tox creatinine PT/INR blood cultures - susceptible to infection - sepssi leading cause of death viral serology - ABCE, EBV, CMV doppler USS -ascites, occluded hepatic vein ?budd chiari ?CT/MRI ?CT head ``` ``` gen mgmt consider transplant early - scores - MELD / UK MELD child-pugh - BRAIN B = bilirubin high R = refractory ascites A = albumin low <28 INR = >1.7 eNcephalopathy A = <7, B = 7-9, C = >9 specific management for cause: paracet = NAC ammonia = lactulose + neomycin raised ICP = IV mannitol AKI - haemodialysis bleeding - FFP, platelets, IV vit K ``` comps infection/sepsis - spont bact peritonitis, pneumonia cerebral oedema haemorrhage from oesophageal varices

Answer 71

when 50% of patients with cirrhosis feature of decompensated cirrhosis ``` precipitants AKI infection constipation sedatives diuretics GI bleed TIPPS ``` features confusion, altered GCS (see below) asterix: 'liver flap', arrhythmic negative myoclonus with a frequency of 3-5 Hz constructional apraxia: inability to draw a 5-pointed star grading 0 - minimal changes in memory/intelligence 1 - irritable, change in mood 2 - confusion, drowsiness, gross deficits in mental ability, inappropriate behaviour 3 - somnolent but rousable, unable to perform mental tasks, marked confusion, occasional fits 4 - coma ix arterial/serum ammonia EEG - triphasic waves MRI/CT for other causes of encephalopathy mgmt avoid sedatives + diagnose early decrease nitrogen load - lactulose removes nitrogen from gut neomycin - abx lowers nitrogen forming gut bacteria rifaximin - given as secondary prophylaxis of hepatic encephalopathy

Answer 72

what is it A complication of end-stage liver disease (40%) e.g. cirrhosis with ascites and acute liver failure Impaired renal function often precipitated by events lowering BP spotted by juxtaglomerular apparatus e.g. spontaneous bacterial peritonitis, GI bleed, pneumonia. Splanchnic vasodilation drops BP, activates SNS and RAAS, which causes renal vasoconstriction but not enough to counterbalance effects of splanchnic vasodilation criteria - diagnosis of exclusion Cirrhosis with ascites, Cr > 133 micromol, no shock, no hypovolaemia, no nephrotoxics mgmt General: Admit to HDU + monitor fluids (urine output), treat infections + stop nephrotoxics/diuretics Specific: Splanchnic vasoconstrictors e.g. terlipressin with albumin - increases blood pressure and GFR + TIPS (transjugular intrahepatic shunt) - reduces ascites in portal HTN

Answer 73

``` def diffuse hepatic process characterised by fibrosis + conversion of normal liver architecture to nodules. final histological pathway for wide variety of liver pathology. can cause increased resistance in vessels = portal HTN ``` patho Cytokines activate stellate cells at space of disse Normal matrix replaced by collagen and fibronectin Loss of fenestration/sinusoid and impaired function causes Common: alcohol, hep B/C, NAFLD and NASH - non-alcoholic fatty liver/steatohepatitis rf Alcohol, hepatitis, older age, obesity, T2DM pres occurs when 80% of parenchyma destroyed so may be asymp (40%) vague - fatigue, anorexia, nausea, weight loss if decompensated - oedema, ascites, brusing, poor mem, bleeding, SBP clinical signs - FLAPS - finger clubbing, leukonychia, asterixis, palmar erythema, spider naevi, scratch, + jaundice, dupuytren's contracture OTHERS - hepatomeg, gynaecomastia (increased production androstenedione by adrenals and conversion to oestrogen), hypogonadism (toxicity of alcohol/iron) ix LFT albumin - low FBC - ?anaemia ?low platelets (hypersplenism), macrocytosis (alc) U+E - hepatorenal syndrome coag screen ferritin viral screen - B/C NASH - Fasting glucose, insulin, triglycerides and uric acid levels met - A1AT level, caeruloplasmin, urinary copper, fasting transferrin saturation AAb screen - AMa image - USS, CXR GOLD STANDARD - biopsy - histology - loss of hepatic archiecture, bridging fibrosis, nodular regeneration or Fibroscan - transient elastography and acoustic radiation force impulse imaging - measures stiffness of liver classification child-pugh for cirrhosis - BRAIN = 5-6 A, 15-20 yr life expectancy, 7-9 B 4-14 yr, 10-15 C 1-3 yrs MELD ``` mgmt delay progression, treat cause + comps adequate nutrition no alc review meds vaccinate for hep A, flu, penumococcal transplant ``` ``` monitoring oesophageal varices + HCC alpha-fetoprotein - tumour marker for hepatocellular carcinoma and should be checked every 6 months as screening with USS. high protein low sodium diet MELD every 6 months consider liver transplant ``` comps Malnutrition Portal Hypertension, Varices and Variceal Bleeding Ascites and Spontaneous Bacterial Peritonitis (SBP) Hepato-renal Syndrome Hepatic Encephalopathy Hepatocellular Carcinoma

Answer 74

what is it Abnormally high pressure in hepatic portal vein (significant if hepatic venous pressure gradient >10mmHg) causes PREHEP - Portal vein thrombosis, splenic vein thrombosis, extrinsic compression e.g. tumour HEP - Cirrhosis, hepatitis, schistosomiasis, granuloma (sarcoid) POSTHEPATIC - Budd-Chiari, RHF/CHF, constrictive pericarditis pathophys PHTN from increased vascular resistance/increased blood flow Raised pressure opens venous collaterals connecting portal to systemic system: - Gastro-oesophago junction - Anterior abdominal wall via umbilical vein (caput medusae) - Anorectal junction - Retroperitoneum - ileocaecal junction Portosystemic shunts may cause encephalopathy due to toxins bypassing liver effect on circ PHTN and cirrhosis produce hyperdynamic circulation (bounding pulse, low BP): splanchnic vasodilatation, increased cardiac output, arterial hypotension and hypervolaemia There is salt and water retention, ascites and hyponatraemia signs Ascites, splenomegaly, dilated umbilical veins *Haematemesis/melaena -> bleeding varices Signs of cirrhosis/liver failure ``` ix AUSS for liver/spleen/ascites Doppler ultrasound - blood flows Spiral CT for portal vasculature Endoscopy for oesophageal varices Portal pressure by hepatic venous pressure gradient (normal < 5, varices > 10) ``` mgmt Treat cause ± liver transplantation Reduce portal venous pressure (beta blockers ± nitrates or shunts TIPS) Non specific beta blockers e.g. carvedilol TIPS for ascites, or refractory oesophageal varices or gastric varices comps Varices bleeding Ascites complications (SBP, hepatorenal) Pulmonary complications (portopulmonary hypertension, hepatopulmonary syndrome: hepatic dysfunction, hypoxaemia and extreme vasodilation)

Answer 75

what is it rare syndrome with obstruction of hepatic veins association genetic myeloproliferative disorders (+hypercoagulable state, TB, tumour) pres sudden RUQ pain + rapidly developing ascites + hepatomegaly + jaundice + renal involvement (50%) ix doppler USS mgmt treat cause if associated with chronic inferior vena cava thrombosis begin warfarin, treat ascites e.g. TIPS

Answer 76

types 10% are primary, 90% are secondary cancers (stomach, colon, lung, breast) 80% of primary are HCC, 20% are cholangiocarcinoma (flukes, PSC, biliary cysts, early jaundice) 70-90% have chronic liver disease causes 90-95% of HCC patients have cirrhosis Worldwide - HBV, Europe - HCV (5% annual risk) Alcoholism, HH, PBC, metabolic syndrome pres Anorexia, wt loss, night sweats, RUQ pain + symptoms of liver disease/cirrhosis/failure cholangiocarcinoma - presents with painless jaundice - similar to panc cancer screening Screen high risk i.e. HBV ± cirrhosis and HCV/alcoholic cirrhosis 6-12 monthly USS + AFP (alpha fetoprotein levels >400 n.b. If <4cm may be normal) diagnosis Focal liver lesion in someone with cirrhosis >2cm mass on USS + Alpha FetoProtein raised in HCC, CA19-9 in cholangiocarcinoma CT/MRI for staging ix LFT consistent cirrhosis, clotting abnormalities, low albumin, CXR for raised right hemidiaphragm/lung mets For cholangiocarcinoma - GB biopsy with ERCP mgmt Treat complications of cirrhosis or liver failure Surgical resection (appropriate if no cirrhosis), ablation (e.g. alcohol injection, radiofrequency ablation), systemic chemotherapy (HCC relatively chemo resistant), liver transplant (sometimes), kinase inhibitors - sorafenib prognosis Median survival is 6 months, if early stage then 5 year survival can be 50% Death from cachexia, variceal bleeding prevention HBV vaccine, reduced alcohol, screen those with cirrhosis

Answer 77

alcohol converted to acetaldehyde by alcohol dehydrogrenase. this increases NADH and causes lipid peroxidation. NADH increase causes oxidative stress and lipogenesis. lipogenesis inhibits gluconeogensis and causes fatty liver. Oxidative stress and lipid peroxidation lead to hepatocyte injury and impair carb and protein metabolism Increasing NADH:NAD ratio leads to increased hepatic fatty acid synthesis with decreased oxidation

Answer 78

``` def Accumulation of fat in the liver. If this is associated with inflammation it is called steatohepatitis (or NASH - non-alcoholic steatohepatitis) ``` categories alcohol-related fatty liver disease and non-alcoholic fatty liver disease. its alcohol when their consumption is more than >2U/day w and >3U/day men pathophys Accumulation of triglycerides and lipids in hepatocytes Result of defective fatty acid metabolism, excess intake, mitochondrial damage (alcohol) ``` RF obesity poor diet/low activity levels T2DM high cholesterol middle age smoking high blood pressure ``` ``` causes metabolic syndrome PCOS alcohol excess starvation HBV/HCV metabolic disorders - wilsons medication - amiodarone, tamoxifen, glucocorticoids, methotrexate ``` epi NAFLD - 20% NASH - 5% fatty liver in 90% of heavy alcohol users pres steatosis - asymp (some potentially hav fatigue/RUQ pain) advanced - symps of cirrhosis - ascites, oedema, jaundice hepatomeg diagnosis biopsy - cells swollen with fat - steatosis at zone 3, in steatohepatitis + inflammation ie mononuclear cell infiltrate, centrilobular hepatocyte necrosis and mallory bodies (dense eosinophilic cytoplasmic inclusions) initial ix USS - echogenic liver ELF - enhanced liver fibrosis blood test - not always available bloods for cause (baso non-invasive liver screen): - LFTs - ALT>AST, rasied GGT if alc, 50% normal FBC - macrocytosis in alc fasting lipids, fasting glucose - metabolic syndrome viral serology caeruloplasmin + iron studies autoimmune- ANA, ASMA raised in NASH NALFD fibrosis score fibroscan ``` mgmt abstinence from alc diet - high protein weight loss reg exercise + control co-morb eg BP, diabetes, lipids treat cause refer hepatologist if failure/cirrhotic ``` comps progression to cirrhosis, liver failure, HCC AST:ALT Ratios In steatosis ratio is <1 In alcoholic liver disease ratio is >2 (but ALT > 500IU/L -> other cause)

Answer 79

haemangioma | focal nodular hyperplasia

Answer 80

fever mallory bodies steatosis

Answer 81

group of chronic health conditions relating to processing and storing energy that increase risk of heart disease, stroke and diabetes. features obesity abnormal glucose tolerance dyslipidaemia associations NAFLD

Answer 82

1. Non-alcoholic Fatty Liver Disease 2. Non-Alcoholic Steatohepatitis (NASH) 3. Fibrosis 4. Cirrhosis

Answer 83

``` Antinuclear antibodies (ANA) Smooth muscle antibodies (SMA) Antimitochondrial antibodies (AMA) Antibodies to liver kidney microsome type-1 (LKM-1) ```

Answer 84

stepwise alcohol related fatty liver alcoholic hepatitis cirrhosis unit 14 units/w m + w - spread evenly over 3 or more days and not more than 5 units in a day. volume x percent of alc / 1000 screening qs CAGE C – CUT DOWN? Ever thought you should? A – ANNOYED? Do you get annoyed at others commenting on your drinking? G – GUILTY? Ever feel guilty about drinking? E – EYE OPENER? Ever drink in the morning to help your hangover/nerves? AUDIT - alcohol use disorders identification test ``` comps Alcoholic Liver Disease Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma Alcohol Dependence and Withdrawal Wernicke-Korsakoff Syndrome (WKS) Pancreatitis Alcoholic Cardiomyopathy ``` ``` signs Jaundice Hepatomegaly Spider Naevi Palmar Erythema Gynaecomastia Bruising – due to abnormal clotting Ascites Caput Medusae – engorged superficial epigastric veins Asterixis – “flapping tremor” in decompensated liver disease ``` ``` ix FBC LFTs - gamma GT specifically, ADT:ALT >3 strongly suggestive of acute alc hepatitis clotting U+E USS - echogenicity CT/MRI **liver biopsy - gold standard ``` gen mgmt stop drinking alc permanently detox regime nut support - vitamins, espesh thiamine + high protein steroids (pred) - improve short term outcomes treat comps - PHTN, varices, ascites, hep enceph referral for transplant - must abstain from alc for 3 months prior to referral

Answer 85

``` Lobular disarray Inflammatory cell infiltrate Zone 3 necrosis Bile duct proliferation @chronic = lymphoid follicles at portal tract - classical ```

Answer 86

Replication of virus at hepatocytes and secretion into bile | Liver inflammation and necrosis caused by immune response

Answer 87

virus type small RNA - picoRNAvirus spread via faeco-oral culprits food handlers shellfish travellers incubation 2-6 weeks where? india africa far-east - related to socio-economic indicators course of illness self limiting, acute, no chronic phase pres prodrome - mild flu (VANFAM - vomiting, anorexia, nausea, fever, arthralgia, malaise) + lose taste for cigs hepatitis phase - dark urine, pale stools, jaundice, abdo pain, itch, hepatomeg (this when its causes cholestasis) recovery = 6 months ix viral serology - HAV IgM @3w from onset, HAV IgG - persists yrs LFT - AST + ALT rise to >1000 (AST:ALT <1), rise in ALP + bilirubin mgmt supportive - fluids, antiemetics, rest avoid alc itch? cholestyramine travellers should have live attenuated vaccine

Answer 88

``` virus type RNA virus (calcivirus) ``` spread faeco-oral route ``` culprit pigs slaughterhouses vets contaminated drinking water ``` incubation 2-9 weeks where india asia course acute self-limiting pres similar to hep A ix viral serology - HEV IgM + IgG +/- viral PCR mgmt supportive prevention no vaccine good hygiene + sanitation

Answer 89

virus DNA most common worldwide spread parenteral - blood or bodily fluid vertical - up to 90% if HBeAg+ve (10% if negative) Horizontal: sexual (more than HCV), IVDU, blood products, dialysis, toothbrush at risk IVDU, health workers, sex workers, prisons *HIGHLY INFECTIOUS incubation 60 to 90 days where SSAfrica Asia (10% may be infected) course acute may go chronic if it persists after 6 months what do these indicate: HBsAg - surfce antigen, current infection (may be produced at vaccine) HBsAb - surface antibody, immunity post infection/vaccine HBcAg - core antigen, diagnostic purpose HBcAb - core antibody, indicates exposure but doesnt differentiate acute, chronic or cleared (however IgM = recent infection, IgG = recovered or chronic infection) HBeAg - when virus is actively replicating, indicates someone is infectious HBeAb - evidences immune response to above HBcAg (IgG) + HBsAb = past HBV infection HBcAg (IgG) + HBsAg = chronic HBV infection pres ACUTE Prodromal: VANFAM + disinclination to smoke Hepatic: RUQ pain + hepatomegaly + jaundice (50%) - darkening urine and lightening stools Occasionally may lead to fulminant hepatic necrosis - marker is increasing INR and requires transplant CHRONIC >6m active infection (HBsAg) May lead to fibrosis, cirrhosis and *HCC Fatigue, anorexia, nausea and RUQ pain ?signs of chronic liver disease ix PCR HBV (for response to therapy and viral replication) Viral serology including HDV serology (5% HBV have HDV) FBC, LFT, clotting, ferritin, AA screen, caeruloplasmin Screen for liver cancer (USS, AFP) + Hep C/A + HIV immune tolerant = normal ALT, HBeAg +ve, HBV DNA high clearance = ALT high, HBeAg +/-, HBV DNA low surveillance = ALT normal/slightly raised, HBeAg mostly -ve, HBV DNA low reactivation = ALT high, HBeAg -ve, HBV DNA high ``` prevention blood screening safe sex vaccinate (partners + at risk groups) educate -transmission ``` mgmt - ACUTE symptomatic relief bed rest stop smoke + alc antipyretics fluids cholestyramine notify PHE refer to gastro, hepatology, ID for specialist mgmt test for potential comps - fibroscan + USS CHRONIC 48 week course of injected pegylared interferon alpha second line = tenofovir or entecavir oral daily, + 6m screen for HCC ``` comps Fulminant hepatic failure Relapse - chronic hep = ground glass hepatocytes on light micro Cirrhosis HCC Concurrent HCV/HIV (increases progression to cirrhosis) glomerulohephritis polyarteritis nodosa cryoglobulinaemia ```

Answer 90

``` acute HBcAb IgM HBcAb IgG HBsAg HBeAg HBV DNA - high/low ``` ``` chronic HBcAb IgG HBsAg HBeAg +/- Anti-HBe +/- HBV DNA - low/high ``` cleared/recovery HBcAb IgG Anti-HBs Anti-HBe +/- vaccination Anti-HBs

Answer 91

Polyarteritis nodosa (PAN): found in 10-30%. Systemic vasculitis of medium and small vessels. Characterised by small aneurysm formation that can rupture. Multi-system disease affecting skin, joints, GI tract, kidneys and more. Glomerulonephritis: More common in children. Causes a range of glomerulonephritides including membranous, mesangiocapillary and focal proliferative. For more information see notes on glomerulopathies. Mixed cryoglobulinaemia: systemic inflammation due to cryoglobulins in the serum, which are immunoglobulins that precipitant at low temperature. Associated with digital ulcers, Raynaud’s, purpura and peripheral neuropathy. More common in hepatitis C. Papular acrodermatitis: seen in young children. Typically presents with an eruption of a erythematous, symmetrical, maculopapular rash on the thighs, buttocks, outer arms and face. Non-itchy

Answer 92

immune clearance and immune escape (reactivation) as that is when ALT is high aim = control viral replication and reduce inflammation to decrease cirrhosis and HCC

Answer 93

HBsAg | 3 doses at different intervals

Answer 94

virus RNA (flavivirus) - 3rd largest cause of ESLD in UK following alc + NAFLD spread 6 genotypes, in UK HCV1 (50%) or HCV2/3 (50%) Parenteral - blood or body fluid, IV drug use, tattoos, *sexual transfer is much less common as is vertical (6%), blood, transfusion, needlestick (3%) ``` at risk IVDU blood transfusion pre 1991 health workers male >40, co-infected with HBV/HIV, alc ``` incubation 6-7 weeks 9 weeks for seroconversion where UK middle east course acute or chronic - often asymp so found on routine blood tests pres 85% asymp BUT more likely to progress to chronic 15% develop hepatic illness: malaise, nausea, RUQ pain + jaundice chronic infection often not recognised for 20 yrs ``` extra-hep AI thyroid disease membranoproliferative glomerulonephritis sjorgrens cryoglobulinaemia ``` chance of ESLD 1/3 25 yrs 1/3 after 1/3 never ix HCV serology - (anti HCV Ab, IgM or IgG) +ve at 3 months in 90% but may take 9 months PCR HCV RNA to confirm diagnosis (for ongoing/chronic infection) treat if detectable > 2 months LFT (AST:ALT < 1) will fluctuate in chronic infection HIV, HBV testing Biopsy for degree of inflammation and fibrosis if HCV-PCR+ (*may measure fibrosis non-invasively with *FibroScan) *HCV genotype + calc viral load mgmt Prevention: needle exchange, screen blood products, no vaccine, alcohol avoidance Screen for HCC 6 monthly USS and AFP, also for cirrhosis - fibroscan Treatment aims to prevent cirrhosis and HCC ACUTE - self-limiting, wont know got it, no mgmt CHRONIC Specific treatment depends on serotype and degree of fibrosis: aims to negative HCV RNA PCR 6 months after treatment (95%) i.e. a sustained virological response currently a combination of protease inhibitors (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir) with or without ribavirin direct acting antivirals are curative prog 20% cirrhosis at 20 yrs

Answer 95

``` def Chronic disease of unknown cause characterised by hepatocellular inflammation, necrosis and autoantibodies (association with other AI disease) ``` patho Hepatocyte expression of HLA antigens (B8/14,DR3,4,DW3) becomes focus of T-cell mediated AI attack. Lymphoid infiltration of portal tract and necrosis. types 75% Type 1: ANA (anti-nuclear Ab), ASMA (anti-smooth muscle Ab) Adults 25% Type 2: ALKM-1 (anti-liver-kidney-microsomal), anti-LC-1 (anti-liver-cystolic) children course acute, severe (fulminant), asymp, or chronic pres subclinical - many present with cirrhosis generic symps - prominent nausea, fatigue, myalgia, anorexia, arthralgia, wt loss endo - skin rashes, amenorrhoea, oedema, chest pain liver - pruritis, jaundice, RUQ discomfort potentially - hepatomeg, juandice, spleno, ascites ix non-invasive liver screen diagnostic - liver biopsy - Interface hepatitis with portal plasma cell infiltrate raised IgG +ve autoantibodies Serum protein electrophoresis and quantitive immunoglobulins (IgG polyclonal hypergammaglobulinaemia) Raised alk phos, low albumin FBC and blood film - leukopenia, normochromic anaemia associated with IBD, coeliac, proliferative glomerulonephritis, Grave’s, AI thyroiditis, T1DM mgmt immunosuppression (if AST > 5x, serum globulins > 2x or symptoms, established cirrhosis) Prednisolone + azathioprine (good response at 80%) AZT - BM suppression Monitor: 6M USS + AFP, liver biopsies, Hep A/B vaccination, liver transplant if end stage comp hyperviscosity syndrome IgG, HCC

Answer 96

pres normally asymp if large RUQ pain + bloating causes Mainly congenital, biliary epithelium, fluid continuously secreted therefore reaccumulate post aspiration ix USS/CT/MRI mgmt wait for spontaneous resolution or aspirate/sclerotherapy (injection of irritant salt soln causing collapse) if symptomatic

Answer 97

Mainly congenital, associated AD PKD - kidney cysts often present before liver - similar management to simple

Answer 98

simple polycystic liver disease neoplastic hydatid - tapeworm - echinococcus granulosus

Answer 99

causes bacteria parasite fungus epi developed world = pyogenic (Single or multiple following abdominal infection (cholangitis, malignancy, diverticulitis, Crohn’s) developing = amoebic RF immunocomp liver surg liver cirrhosis organisms amoebic - Entamoeba histolytica (12% of world pop Cx infected) R lobe 80% may present months after travel pyogenic - staph aureus, e.coli infection route Faeco-oral, amoeba invade intestinal mucosa and pass to portal system pres RUQ pain (prominent in amoebic), tenderness, hepatomegaly *Swinging fever (pyogenic may be pyrexia of unknown origin) + night sweats + wt loss Nausea, vomiting, anorexia Pain referred to R shoulder, *cough due to diaphragmatic irritation + reactive pleural effusion, jaundice amoebic dysentery ix FBC - raised WCC, mild anaemia Raised ESR Abnormal LFT Blood cultures - 50% Stool microscopy and cultures - cysts or trophozoites of E.histolytica CXR - right reactive pleural effusion, raised hemidiaphragm USS/CT liver - show abscess and guide aspiration Aspiration + culture mgmt ABX ± drainage + fluids + pain relief pyogenic - IV third cephalosporin (or cipro + amox) + metronidazole (anaerobes) for ?12 weeks Amoebic - metronidazole (good response 72 hours) + diloxanide furoate to clear intestinal amoebae <5cm = needle aspiration, >5cm = percutaneous catheter drainage comps sepsis rupture into pleural , peritoneal or pericardial space.

Answer 100

``` SADPUCKER Suprarenal Aorta/IVC Duodenum (2+3) Pancreas Ureter Colon Kidney Esophagus Rectum ```

Answer 101

types endo or exo 95% adenocarcinoma most common exo 90% of cancers are infiltrating ductal adenocarcinoma @head/neck/uncinate 90% of periampullary malignancies are pancreatic (10% distal common bile, ampulla, duod *these have a better prognosis as they present early with obstructive jaundice) why worry High mortality, early metastasis (liver/peritoneum/lung) late presentation - 11th cancer but 5th death RF Main: Smoking, alcohol, obesity + diet (low fruit veg), diabetes Precursor: chronic pancreatitis Family history pancreatic cancer + familial cancer syndromes (BRCA1/2, FAP, Lynch, MEN)

Answer 102

pres Early: vague - epigastric discomfort/dull backache *painless, progressive, obstructive jaundice (⅔ are in the head of the pancreas) Pancreatic pain (body/tail) Obstructive jaundice (dark urine, pale stools, pruritus) Weight loss, anorexia, steatorrhoea (loss of exocrine) Palpable gallbladder (from retrograde flow) - Courvoisier’s sign *if it is painless it is unlikely to be gallstones Stomach/duodenum compression -> gastric outlet obstruction -> nausea/vom Advanced disease: rapid wt loss, persistent back pain, ascites, epigastric mass, Virchow’s node Tousseau sign - migratory thrombophlebitis ddx Gallstones, PUD, hepatitis, liver abscess, pancreatitis (bile duct stricture) ``` assocs increasing age smoking diabetes chronic pancreatitis (alcohol does not appear an independent risk factor though) hereditary non-polyposis colorectal carcinoma multiple endocrine neoplasia BRCA2 gene KRAS gene mutation ``` ix non-invasive liver screen FBC - anaemia of Ca, LFT - for jaundice (bilirubin + ALP + GGT raised), serum glucose - hyperglycaemia Tumour marker - CA19-9 Imaging: USS liver, bile duct, pancreas -> tumour mass + dilated bile ducts (double duct sign - simultaneous dilation of common bile duct and panc duct) Abdominal CT (multiphase spiral/helical) for diagnosis and staging ERCP visualises common bile duct and pancreatic duct (contrast) T1 - limited to pancreas < 2cm T2 - limited to pancreas > 2cm T3 - beyond pancreas not to coeliac axis or SMA T4 - to coeliac axis or SMA tumour types Solid - 90% ductal adenocarcinoma etc… Cystic - serous cystic/mucinous cystic etc… mgmt Only 10-20% are resectable (often metastatic) 1. Whipple’s procedure - proximal pancreaticoduodenectomy 2. Distal pancreatectomy for body/tail Adjuvant chemotherapy 5-FU (flourouracil) Unresectable: (IIB - 4 locally advanced to metastatic) Bile duct stent (ERCP) for pruritus/jaundice, palliative chemo (suctal adenocarcinoma resistant)/radio

Answer 103

``` classified as neuroendocrine tumours (PNET) which can be functional (hormone hypersecretion) or non-functional (majority eg MEN1) low grade, med or high ``` types insulinomas (beta islet, 90% benign) and gastrinomas (>50%) VIPoma (1/8th) - vasoactive intestinal polypeptide glucagonoma (alpha islet) assoc 75%of MEN1 (AD famililal cancer syndrome) pres insulinoma = confusion, sweating, dizziness, weakness, hypoglycaemia gastrinoma = severe peptic ulceration/diarrhoea - zollinger-ellison (excess gastrin -> HCl) VIPoma - profuse watery diarrhoea and hypokalaemia + achlorhydria (no HCl) glucagonoma - DM, weight loss, necrolytic migratory erythema non-functional - mass effect eg jaundice

Answer 104

biliary colic - RUQ pain acute cholecystitis - RUQ pain + fever/WCC ascending cholangitis - RUQ pain + fever/WCC + jaundice - charcot's triad pancreatitis - jaundice - raised biirubin, alk phos, GGT NOTE - 70% are asymp

Answer 105

due to temp obstruction of cystic or common bile duct pres sudden onset epi/RUQ pain radiation to intrascapular region, constant lasting 15mins-24 hours, relieved spont or with analgesia jaundice - if stone moves to common bile duct n+v due to GB distension ``` ix USS - 95% sensitice urinalysis CXR ECG for exclusion if unsure ``` mgmt NON SURG Note the patient is probably vomiting NBM (stop CCK release) Good response of pain to parenteral opioids (pethidine) or ******PR diclofenac >24 hours admit Rehydrate IVI Consider antibiotics IV (3rd gen ceph) SURG Laparoscopic cholecystectomy for removal of GB Complications: fat intolerance, injury to bile duct

Answer 106

what is it infection of bile duct This is a medical emergency pres charcots triad 70% - RUQ +fever/chills + jaundice reynolds pentad 20% - RUQ +fever/chlls + jaundice + altered mental state + hypotension/tachycardia patho Bile normally sterile. If CBD is obstructed, flow of bile is reduced leading to biliary stasis and infection. Infection may also be retrograde flow due to acute cholecystitis or ERCP (1%) organisms ecoli klebsiella enterococci ``` causes Obstruction of gallbladder (stones), ERCP, tumours (ca panc, cholangiocarcinoma), bile duct stricture ``` criteria have one of each of: (or suspect if have 2) 1. systemic inflammation - fever >38 - lab - high WCC/CRP 2. cholestasis - jaundice/ abnormal LFTs (alk phos/gamma gt) 3. imaging - biliary dilatation, evidence of aetiology (stricture, stone, stent) ix as above WCC/ESR/CRP, LFT worry about sepsis, pancreas, AKI - U+E, amylase, blood cultures imaging - KUB XR + AUSS + contrast CT (best method) MRCP (non-calc biliary stone) mgmt fluid resus correct coagulopathy broad spec abx if septic - o2 + fluids + BC + IVAbx ?metro + ceftriaxone emergency biliary drainage via ERCP 24-48 hrs ``` comps Severe may cause: Septic shock AKI All other system dysfunction Liver abscess Liver failure ```

Answer 107

``` def Slowly progressive AI disease causing destuction of small interlobular bile ducts (canals of Hering) ``` typical patient 50 yr old woman, sister had it aswell 90% women ``` pres asymp 25% suspect in causes of chronic cholestasis fatigue pruritis RUQ pain cholestatic jaundice O/E - may have hepatomeg, jaund, hyperpigmentation ``` assoc sjorgrens other AI - thyroid AI ab high cholesterol - xanthelasma AMA - antimito ab ``` ix AMA FBC - ESR raised LFT - raised alk phos + gamma gt late rise in bili raised IgM TFT - strong assoc USS - rule out obstruction MRCP - rule out PSC fibroscan for cirrhosis liver biopsy - stage - non suppurative cholangitis of interlobular and septal bile ducts + granulomatous lymphocytic infiltration of portal triad ``` dx criteria 2 of: - Biochemical evidence of cholestasis (raised alk phos) - AMA - Hist evidence of destruction interlobular bile ducts mgmt allievate symps + slow disease + only transplant is curative prurits - cholestyramine or antihist ursodeoxycholic acid slows disease prog immunosuppression - methotrexate, steroids oestrogens promote cholestasis so avoid OCP comp 50% renal tubular necrosis 20% hypothyroidism malabsorption of fats + steatorrhoea

Answer 108

Both involve primary sclerosis of bile ducts: - PSC affects intrahepatic and extrahepatic bile ducts - PBC affects small interlobular bile ducts Sex - PSC occurs more in men, - PBC occurs x10 in women Both have x10 familial association AAb - PBC is an autoimmune condition with AMA antibodies - PSC is an autoimmune condition with pANCA antibodies Associations - PSC is associated with UC and colon cancer - PBC is associated with Sjogren’s and thyroid disease Liver transplant is curable for both but there is significant recurrence

Answer 109

aka klatskins tumour ``` def carcinoma arising in any part of the biliary tree (may be intrahep) ``` where/type 90% ductal adenocarcinoma, 10% squamous cell carcinoma Normally at bifurcation of right and left hepatic duct = perihilar region Next near to ampulla of Vater epi v rare SE asia due to liver flukes RFs Liver flukes, chronic UC with PSC pres Jaundice early in perihilar tumours, RUQ abdo pain (biliary colic) + jaundice + cholestasis + pruritus + hepatomegaly + wt loss + anorexia - a palpable mass in the right upper quadrant (Courvoisier sign) - periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen ix LFT: cholestatic picture Tumour marker CA19-9 and CEA but not AFP USS/CT, MRI is optimal mgmt To treat it needs removal but only 33% are resectable at presentation Aggressive surgical resection including liver resection ± liver transplantation Symptom relief with stents and ERCP Intrahepatic tumours have worst prognosis

Answer 110

ix non-invasive liver screen Cholestasis characterised by elevated serum bilirubin, elevated alkaline phosphatase (>3x), raised GGT compared to transaminase. Serum concentration of conjugated bilirubin and bile salts Low serum albumin in chronic disease Hyperlipidaemia if ability to break down cholesterol FBC Anaemia suggests malignancy Raised WCC suggests infection e.g. ascending cholangitis Reticulocytosis suggests prehepatic jaundice ddx Obstructive cholestasis - Gallstones + carcinoma head of pancreas (most common) - Obstruct lumen: gallstones, parasite, post ERCP - Obstruct within wall: sclerosing cholangitis, cholangiocarcinoma, congenital stricture (biliary atresia) - Obstruct outside wall: pancreatitis, Ca HoP Hepatocellular cholestasis - Commonly cirrhosis and drug reactions (erythromycin, gold, anabolic steroids) - Viral/alcoholic hepatitis - Sclerosing cholangitis, primary biliary cirrhosis, A1AT q1 *Unconjugated hyperbilirubinaemia (pre-hepatic) q2 Haematuria Dehydration q3 Atopic disease Drugs Lymphoma mgmt manage cause Biliary drainages, colestyramine, rifampicin, UDCA (ursodeoxycholic acid) Involve dietician for fat soluble vitamins comps Retention of bile salts -> injury to cell membrane e.g. hepatic fibrosis/cirrhosis Chronic cholestasis -> metabolic bone disease = hepatic osteodystrophy Chronic cholestasis -> asthmatic wheeze unresponsive to normal treatment

Answer 111

Haemolysis - antimalarials Cholestasis - Gold salts, nitrofurantoin, statins, erythromycin, anabolic steroids, oestrogen COCP Hepatitis - paracetamol, rifampicin, statins

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