Liver and friends Flashcards

Question

Budd-Chiari syndrome What Presentation

Answer 1

Rare syndrome with obstruction of hepatic veins | Sudden RUQ pain + rapidly developing ascites + hepatomegaly + jaundice + renal involvement (50%)

Answer 2

10% are primary, 90% are secondary cancers (stomach, colon, lung, breast) 90% of primary are HCC, 10% are cholangiocarcinoma (flukes, PSC, biliary cysts, early jaundice) HepC is the leading cause in the UK Worldwide - HBV 8x more common in men Occurs 20 years after initial insult 90-95% of HCC patients have cirrhosis Alcoholism, HH, PBC, metabolic syndrome Anorexia, wt loss, night sweats, RUQ pain + symptoms of liver disease/cirrhosis/failure

Answer 3

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)

Answer 4

Accumulation of fat in the liver. If this is associated with inflammation it is called steatohepatitis (or NASH - non-alcoholic steatohepatitis) Based on alcohol consumption (>2U/day women/ 3U/day men) Metabolic syndrome, PCOS, alcohol excess, starvation, HBV/HCV, metabolic disorders (Wilson’s, glycogen storage disorder...) medications (amiodarone, tamoxifen, glucocorticoids, methotrexate) Steatosis generally is asymptomatic (fatigue/RUQ pain). Advanced disease may have cirrhosis symptoms ascites, oedema, jaundice Hepatomegaly is common

Answer 5

Biopsy: cells swollen with fat - steatosis at zone 3 Abstinence from alcohol (causes reversal in alcoholic fatty liver) and adequate diet (high protein: calorie) Weight loss + regular exercise (increases insulin sensitivity) + control comorbidity - BP, diabetes, lipids Treat cause + prescribe for Delirium tremens

Answer 6

Faeco-oral ``` Food handlers (hand washing), shellfish, travellers 2-6 weeks ``` India, Africa, Far East - Travellers should be vaccinated against hepatitis A with live attenuated vaccine Self limiting, acute, no chronic phase Prodrome - mild flu (VANFAM, vomiting, anorexia, nausea, fever - uncommon, arthralgia, malaise) + lose taste for cigarettes Hepatitis/icteric phase - dark urine, pale stools, jaundice, abdominal pain, itch, hepatomegaly Viral serology: HAV IgM (with onset of symptoms @3W lasts 6 months), HAV IgG (persists years) LFTs up. Supportive (fluids, antiemetics, rest), avoid alcohol, for itch cholestyramine - Recovery may take 6 months

Answer 7

Faeco-oral Heavily associated with pigs, slaughterhouses and vets, contaminated drinking water& 2-9 weeks India, Asia Acute and self-limiting Similar to hepatitis A Viral serology: HEV IgM, HEV IgG ± viral PCR

Answer 8

Parenteral - blood or body fluid Vertical: up to 90% if HBeAg+ve (10% if negative) Horizontal: sexual (more than HCV), IVDU, blood products, dialysis, toothbrush IVDU, health workers, sex workers, prisons *HIGHLY INFECTIOUS & 60 to 90 days SSAfrica, Asia (may be 10% infected)

Answer 9

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: defined as infection lasting longer than 6 months (HBsAg) May lead to fibrosis, cirrhosis and *HCC Fatigue, anorexia, nausea and RUQ pain ?signs of chronic liver disease Viral serollogy: HBsAg found at current infection (may be produced as vaccine) HBsAb indicates immunity post infection/vaccine HBeAg allows assessment of infectivity

Answer 10

vomiting, anorexia, nausea, fever - uncommon, arthralgia, malaise - Common symptoms in Hepatitis

Answer 11

Symptomatic relief, bed rest, antipyretics, fluids, cholestyramine, notification as communicable disease 48 week course of injectable pegylated interferon alpha or second line tenofovir or entecavir oral daily + 6 monthly screen for HCC

Answer 12

RNA virus (flavivirus) + third largest cause of ESLD in UK (alcohol and NAFLD) - 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%) IVDU, blood transfusion pre 1991, health workers. 6-7 weeks, 9 weeks for seroconversion (may take 9 months) 85% are asymptomatic BUT these are more likely to progress to chronic 15% develop hepatic illness: malaise, nausea, RUQ pain, and jaundice Chronic infection may be malaise, fatigue, intermittent RUQ pain often unrecognised for 20 years (cirrhosis in 20%)

Answer 13

HCV serology (anti HCV Ab, IgM or IgG) +ve at 3 months in 90% but may take 9 months PCR HCV RNA (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+ Prevention: needle exchange, screen blood products, no vaccine, alcohol avoidance Screen for HCC 6 monthly USS and AFP SC pegylated interferon alpha + ribavarin

Answer 14

Chronic disease of unknown cause characterised by hepatocellular inflammation, necrosis and autoantibodies (association with other AI disease) N.b. subclinical so many patients have cirrhosis at symptom onset Generic: Prominent nausea, fatigue, myalgia, anorexia, arthralgias, weight loss Endocrine: Skin rashes, hirsutism, amenorrhoea, oedema, chest pain (pleuritis), Liver: Pruritus and jaundice, URQ discomfort Hepatomegaly, jaundice, splenomegaly, ascites LFT (elevated 10x) Raised IgG +ve auto-antibodies (autoantibody screen) *Liver biopsy = most important diagnostic procedure Interface hepatitis with portal plasma cell infiltrate Prednisolone + azathioprine

Answer 15

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 ABX ± drainage + fluids + pain relief pyogenic - IV third cephalosporin + metronidazole (anaerobes) for ?12 weeks Amoebic - metronidazole (good response 72 hours) + diloxanide furoate to clear intestinal amoebae <5cm = needle aspiration, >5cm = percutaneous catheter drainage

Answer 16

Acute inflammation of pancreas releasing exocrine (secrete via ducts) enzymes causing autodigestion of organ. Activation of proenzymes within duct GETSMASHED gallstones, alcohol, trauma, steroids, mumps, AI, scorpions, hyperlipidaemia/hypothermia/hypercalcaemia, ERCP, drugs Severe sudden onset epigastric pain (LU) + vomiting + radiate to back relieved by sitting forward (retroperitoneal involvement) Cullen’s sign (periumbilical bruising) Grey Turner’s sign (flank bruising) - retroperitoneal haemorrhage Epigastric tenderness + rigidity (fluid shift to gut and peritoneum) Tachycardia, fever, hypoxaemia Jaundice if cause is gallstones/alcohol SHOCK

Answer 17

Serum amylase x3 (also raised in renal failure as renally excreted, DKA, perforated DU), raised serum lipase (more sensitive, pancreas specific) ABG for hypoxaemia FBC (leukocytosis), CRP (>200 = pancreatic necrosis) LFT (AST:ALT > 3), raised bilirubin Hypocalcaemia, hyperglycaemia, raised urea MODIFIED GLASGOW SCORE X-RAY FOR ARDS ``` Plain erect AXR - retroperitoneal shadow = bleed, intestinal obstruction, pancreatic calcif CXR - exclude perforation, shows ARDS CT with contrast is diagnostic USS - swollen pancreas ± gallstones ERCP ``` *Ruptured or dissecting aortic aneurysm

Answer 18

Pain relief pethidine or buprenorphine ± IV benzodiazepines (morphine spasms ampulla) IV fluids - Most important Nil by mouth + NG tube (for severe vomiting) -> stop pancreatic stimulation No need for CT Repeat Glasgow score at 24 and 48 hours + daily bloods and obs Restart food and fluids when symptoms and bloods stabilise + treat gallstones ``` HDU or ITU + CT for necrosis If evidence of pancreatic necrosis - aspirate peritoneal fluid for culture and target IV antibiotics Enteral nutrition via NG tube Early ERCP for gallstones Give oxygen ```

Answer 19

Chronic inflammation/fibrosis and calcification of pancreas resulting in irreversible damage, impaired endocrine and impaired exocrine function Large duct: dilatation and dysfunction of large ducts + diffuse calcification + steatorrhoea. Occurs more in men. Small duct: not associated with calcification, steatorrhoea. Occurs more in women Epigastric pain radiating to back relieved by sitting forward - exacerbated by eating Nausea and vomiting Exocrine dysfunction: malabsorption, wt loss, diarrhoea, steatorrhoea (pale/loose/offense) Endocrine dysfunction: diabetes mellitus

Answer 20

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 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

Answer 21

Endocrine or exocrine (Most) 95% are adenocarcinoma 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 22

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 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 (Use Prokinetic antiemetics - metoclopramide) Advanced disease: rapid wt loss, persistent back pain, ascites, epigastric mass, Virchow’s node 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 Abdominal CT for diagnosis and staging

Answer 23

Insulinoma: confusion, sweating, dizziness, weakness, hypoglycaemia Gastrinoma: severe peptic ulceration/diarrhoea - Zollinger-Ellison (excess gastrin -> HCl) VIPoma - profuse watery diarrhoea with hypokalaemia and achlorhydria (no HCl) Glucagonoma - DM, weight loss, necrolytic migratory erythema Non-functional (MEN1 - Most) - mass effect e.g. jaundice

Answer 24

Cholesterol, bile pigments (from Hb), phospholipids Cholesterol stones (n.b. Ileum absorbs bile salts) -80% of stones at UK -Large, solitary, radiolucent Admirands triangle Pigment stones 10% - Small, friable, radiolucent - Result of haemolytic conditions Mixed stones 10% faceted - calcium salts + pigment + cholesterol

Answer 25

Decreased dietary lecithin Decreased bile salts (impaired flow) Increased cholesterol saturation of bile/loss of bile salts (ileal resection/Crohn’s)

Answer 26

RUQ pain RUQ pain + fever/WCC RUQ pain + fever/WCC + jaundice - Charcot’s triad Jaundice - raised bilirubin, alk phos, GGT Nb. Most are asymptomatic

Answer 27

Temporary obstruction of cystic or common bile duct (jaundice) Sudden onset, epigastric/RUQ, radiation to interscapular region, constant lasting 15 minutes- 24 hours, relieved spontaneously or with analgesia With nausea and vomiting due to GB distension USS is 90-95% sensitive for stones Urinalysis, CXR, ECG for exclusion

Answer 28

Second most common presentation of gallstones (95%) or trauma. Continuous epigastric pain - right shoulder, vomiting, fever, local peritonism (main differences), GB mass Jaundice if stone moves to common bile duct Murphy’s +ve - 2 fingers, breathe in, halts inspiration, negative on other side Raised WCC, abnormal LFT *USS - *thickened GB wall (>3mm) + fluid or air in the GB, CBD diameter >6mm ERCP/MRCP

Answer 29

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) Laparoscopic cholecystectomy for removal of GB Complications: fat intolerance, injury to bile duct

Answer 30

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%) - This is a medical emergency E.coli, klebsiella, enterococci Obstruction of gallbladder (stones), ERCP, tumours (ca panc, cholangiocarcinoma), bile duct stricture RUQ + fever/chills + jaundice

Answer 31

``` Systemic inflammation (A) -Fever/chills/ T>38 -Lab data - elevated WCC or CRP Cholestasis (B) -Jaundice -Abnormal LFT: raised ALP, ALT/AST, GGT Imaging (C) -Biliary dilatation -Evidence of aetiology: stricture, stone, stent (KUB XR + AUSS + contrast CT (best method). ``` Definite diagnosis if one in A + B + C, suspect if A + B/C

Answer 32

Fluid resuscitation, correct coagulopathy, broad-spec abx If septic shock O2 + IV fluids + BC + IVABX ?metronidazole + ceftriaxone Emergency biliary drainage if AKI, shock, DIC etc Endoscopic biliary drainage ``` Severe may cause Septic shock AKI All other system dysfunction Liver abscess Liver failure ```

Answer 33

Chronic inflammation + fibrosis of intra + extrahepatic bile ducts leading to multifocal biliary strictures Asymptomatic + abnormal LFT/hepatomegaly Jaundice/pruritus RUQ pain Fever, wt loss, fatigue, sweats Bloods: LFT (elevated alk phos/GGT, raised transaminase) Raised immunoglobulins: IgG, IgM, hypergammaglobulinaemia Autoantibodies: p-ANCA Imaging: USS may show bile duct dilatation but MRCP is standard Biopsy for staging ERCP - Beaded appearance

Answer 34

Used to assess the prognosis of chronic liver disease, mainly cirrhosis Scored 1-3 for each criteria ``` Total bilirubin Serum albumin Prothrombin time, prolongation (s) OR INR Ascites Hepatic encephalopathy ```

Answer 35

Symptomwise + treat strictures with balloon dilatation Pruritus - Colestyramine Nutrition - With cholestatic disorders supplement fat soluble vitamins DEAK Prevent progression - Avoid alcohol (risk for cholangiocarcinoma) + ursodeoxycholic acid (secondary bile acid) *little response to immunosuppression

Answer 36

Slowly progressive AI disease causing destuction of small interlobular bile ducts (canals of Hering) AMA - antimitochondrial antibody Biochemical evidence of cholestasis (raised alk phos) AMA Hist evidence of destruction interlobular bile ducts Heavy association with Sjogren’s (dry eye, dry mouth) + other AI disease e.g. thyroid

Answer 37

Alleviate symptoms + slow disease + only transplant is curative Pruritus Sedating antihistamines or colestyramine Ursodeoxycholic acid slows disease progression Immunosuppression: methotrexate, steroids N.b. oestrogens promote cholestasis so avoid COCP

Answer 38

Both involve primary sclerosis of bile ducts PSC affects intrahepatic and extrahepatic bile ducts PBC affects small interlobular bile ducts PSC occurs more in men, PBC occurs x10 in women Both have x10 familial association PSC is an autoimmune condition with pANCA antibodies PBC is an autoimmune condition with AMA antibodies The cause of PSC is unclear, but it is associated with UC and colon cancer PBC is associated with Sjogren’s and thyroid disease

Answer 39

Carcinoma arising in any part of the biliary tree (may be intrahepatic) 90% ductal adenocarcinoma, 10% squamous cell carcinoma Jaundice early in perihilar tumours, URQ abdo pain + jaundice + cholestasis + pruritus + hepatomegaly + wt loss LFT: cholestatic picture Tumour marker CA19-9 and CEA but not AFP USS/CT, MRI is optimal 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 40

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. Jaundice - elevated serum conjugated bilirubin Pale stools and dark urine - no bilirubin to GI tract, reflux of conj bili into blood - excreted in urine Pruritus - bile salts irritation note this is not histamine mediated and so antihistamines will have no effect therefore use *colestyramine Cholestasis characterised by elevated serum bilirubin, elevated alkaline phosphatase (>3x), raised GGT compared to transaminase. Serum concentration of conjugated bilirubin and bile salts Elevated AST/ALT suggest a hepatocellular picture Low serum albumin in chronic disease Hyperlipidaemia if ability to break down cholesterol

Answer 41

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

Answer 42

``` Oesphageal varacies Encephalopathy Ascites Asterixis Hepato renal syndrome (NO build up causes vasoconstriction in kindeys) ```

Answer 43

Viral hepatits Drugs Alcholic hepatits Autoimmune cholangitis Gall stones Ca bile duct/head of pancreas/ampulla Biliary stricture Pancreas pseudocyst

Answer 44

Cardio - Directly toxic = Cardiomyopathy and arrythmias Neuro - Polyneuropathy, myopathy, cerebellar degeneration, dementia, Wernicke's/Korsakoff GI - Liver damage, pancreatits, oesophagitis, oesophageal ca Haem - Thrombocytopenia, raised MCV, anaemia Psych - Depression, self harm, dependance

Answer 45

Terliipressin - Restricts portal inflow (CI in IHD - Use Somatostatin) Somatostatin - Lowers portal pressure Endoscopy - Band ligation B Blockers Band ligation TIPS