Liver & friends Flashcards
list 4 causes of acute pancreatitis
GET SMASHED Gallstones Ethanol (alcohol) Trauma Steroids Mumps/Malignancy Autoimmune Scorpion venom Hyperlipidaemia, hypothermia, hypercalcaemia ERCP and emboli Drugs
describe the pain of acute pancreatitis
gradual or sudden severe epigastric/central abdominal pain, radiates to back, may be relieved by sitting forward.
give 3 symptoms and signs of acute pancreatitis
pain, vomiting. tachycardia, fever, jaundice, shock, ileus, rigid abdomen ± local tenderness. Cullen’s and Grey Turner’s signs.
what are Cullen’s and Grey Turner’s signs? what causes them?
Cullen’s = periumbilical bruising Grey Turner’s = bruising of flanks. due to blood vessel autodigestion and retroperitoneal haemorrhage.
what 2 enzymes would you test for in acute pancreatitis? what would the results be?
serum amylase - raised. serum lipase - raised (more sensitive/specific).
what investigations would you carry out in acute pancreatitis?
serum amylase and lipase. ABG. CT. AXR.
give 3 criteria in the Modified Glasgow criteria for predicting severity of pancreatitis
PANCREAS: PaO2 low Age >55yrs Neutrophilia Calcium - low Renal function Enzymes Albumin Sugar (blood glucose)
how would you medically manage an acute pancreatitis patient?
Nil by mouth / NG tube. pethidine (antispasmodic), tramadol (pain relief). abx (if infective cause eg cholangitis or infected pancreatic necrosis) treat underlying cause.
main stay is supportive:
Iv fluid resus
Catheterisation
O2 (if below 94%)
Opiate analgesia
Early nutritional support
give 2 early and 2 late possible complications of acute pancreatitis
early: shock, ARDS, renal failure, DIC, sepsis, hypocalcaemia. late: pancreatic necrosis, abscesses, bleeding, thrombosis, fistulae.
explain the pathology of chronic pancreatitis
inappropriate activation of enzymes within the pancreas - leads to precipitation of protein plugs within duct lumen - forms a point for calcification - duct blockage - ductal hypertension + pancreatic damage - pancreatic inflammation + impaired function
give 3 causes of chronic pancreatitis
alcohol, tropical chronic pancreatitis, hereditary, autoimmune, cystic fibrosis, haemachromatosis, pancreatic duct obstruction (stones/tumour), hyperparathyroidism, congenital.
give 3 clinical features of chronic pancreatitis
epigastric pain boring through to back - relieved by sitting forward or hot water bottles on epigastrium/back. bloating, steatorrhoea, weight loss, brittle diabetes,
what would you expect serum pancreatic enzymes levels to be in chronic pancreatitis?
amylase and lipase are normal
what investigations would you run in chronic pancreatitis?
ultrasound + CT.
how would you treat a patient with chronic pancreatitis?
NSAIDs and tramdol for abdo pain (amitriptyline for more chronic episodes). lipase + fat-soluble vit supplements. no alcohol, low fat diet. surgery if pain can’t be controlled, or there’s weight loss.
give 2 possible complications of pancreatitis?
pseudocyst, diabetes, biliary obstruction, local arterial aneurysm, splenic vein thrombosis, gastric varices, pancreatic carcinoma
describe the 3 different types of gallstones and their causes
pigment stones - small, friable, irregular - haemolysis. cholesterol stones - large, often solitary - age, obesity, female sex. mixed stones - faceted (calcium salts, pigment and cholesterol).
what are the 2 risk factors for gallstones become symptomatic?
smoking and parity (having given birth).
how does acute cholecystitis develop from an obstruction?
obstruction to gall bladder emptying - increased glandular secretion in gall bladder - distension and inflammatory response to retained bile, leads to infection
what special test would you do on examination to confirm cholecystitis?
Murphy’s sign - 2 fingers over RUQ + ask patient to breathe in - causes pain and arrest of inspiration as inflamed gallbladder hits your fingers
how would you differentiate the pain of biliary colic from cholecystitis?
cholecystitis features an inflammatory component - local peritonism, fever, high WCC
what are the clinical features of acute cholecystitis?
epigastric/RUQ pain, referred to R shoulder. vomiting, fever, local peritonism, possibly a gallbladder mass.
what investigations would you perform in cholecystitis?
ultrasound - thick walled, shrunken gallbladder, pericholecystic fluid, stones, common bile duct dilation. FBC (high WCC).
how would you treat cholecystitis?
nil by mouth, analgesia, IV fluids. IV abx- metronidazole and cefuroxime. laparoscopic cholecystectomy.
describe the clinical features of chronic cholecystitis
chronic inflammation ± colic. flatulent dyspepsia - vague abdo discomfort, distension, nausea, flatulence and fat intolerance.
describe the pain of biliary colic
severe, constant, increasing pain in RUQ, can radiate to right shoulder/scapula.
how would you tell that a gallstone had moved to obstruct the common bile duct?
obstructive jaundice and cholangitis
what is the triad of symptoms for acute cholangitis?
Charcot’s triad - jaundice, fever, biliary colic.
what structure is being obstructed by gallstones if a patient has developed acute cholangitis?
common bile duct
what is the gold standard investigation in cholangitis?
transabdominal ultrasound - measure CBD dilatation.
how would you treat acute cholangitis?
laparoscopic cholecystectomy with IV abx - cefuroxime and metronidazole
list 3 complications of gallstones
in gallbladder and cystic duct: biliary colic, acute and chronic cholecystitis, mucocoele, empyema, carcinoma, Mirizzi’s syndrome. in bile ducts: obstructive jaundice, cholangitis, pancreatitis. in gut: gallstone ileus.
what is jaundice?
yellowing of the skin, sclerae and mucosae due to increased plasma bilirubin
give 3 causes of unconjugated hyperbilirubinaemia (pre-hepatic jaundice)
haemolysis - malaria, DIC. ineffective erythropoiesis. impaired hepatic uptake - drugs (contrast agents, rifampicin), RHF. impaired conjugation - Gilbert’s syndrome, Crigler-Najjar.
what will the urine and faeces look like in conjugated hyperbilirubinaemia (hepatic/post-hepatic jaundice)? why?
urine = dark - conjugated bilirubin is soluble, so excreted in urine. Faeces = pale - less conjugated bilirubin enters gut.
give 3 causes of conjugated hyperbilirubinaemia due to hepatocellular dysfunction
viruses - hep, CMV, EBC. drugs - paracetamol od, isoniazid, rifampicin, pyrazinamide, statins, sodium valproate. alcohol. cirrhosis. liver metastases/abscesses. haemachromatosis. autoimmune hepatitis. septicaemia. syphilis. alpha1-antitrypsin deficiency. Budd-Chiari. Wilson’s disease. Right heart failure.
give 3 causes of conjugated hyperbilirubinaemia due to impaired hepatic excretion (cholestatic / obstructive jaundice)
primary biliary cirrhosis, primary sclerosing cholangitis, drugs, common bile duct gallstones, pancreatic cancer, compression of the bile duct, choledochal cyst
how is hepatitis A spread? what are the risk factors?
faecal-oral route. poor sanitation, overcrowding, contaminated food/water. (fish in sewagey water)
what would you find when looking at viral markers for hepatitis A? what other blood test would you perform?
Anti-HAV IgM (acute) and IgG (raised for life - carrier). LFTs - AST/ALT are raised
how would you treat hepatitis A?
supportive treatment - self-limiting.
how would you prevent hepatitis A?
passive and active immunisation (inactivated protein) and good hygiene
what type of virus is hep A?
RNA
give 3 symptoms of hep A as well as 2 later signs
symptoms: fever, malaise, anorexia, nausea, arthralgia. later signs - jaundice, hepatosplenomegaly, lymphadenopathy.
what type of virus is hep B?
DNA
how is hep B spread?
blood products - vertical transmission, IVDU, found in semen and saliva - sexual/direct contact.
name 3 of the at-risk groups for hep B
IVDUs, their sexual partners/carers, health workers, haemophiliacs, job exposure to blood (morticians), haemodialysis patients, sexual promiscuity, foster carers, staff/residents of institutions/prisons, babies of +ve mothers
what are the clinical features of hep B?
resembles hep A - fever, malaise etc - plus arthralgia and urticaria (hives).
what antiviral agents would you give to treat a chronic HBV infection? what would you monitor?
interferon alpha, lamivudine, adefovir. monitor HBV levels and platelets.
describe how vaccination is used in hep B
passive immunisation is given to non-immune contacts after high-risk exposure. Hep B vaccine given (UK) to children born to +ve mothers, chronic liver patients, haemophilia patients, offered as a travel vaccine, and to healthworkers.
list 2 possible complications of hepatitis B
cirrhosis, HCC, fulminant hepatic failure, cholangiocarcinoma, cryoglobulinaemia
what type of virus is hep C?
RNA flavivirus
how is hep C transmitted and can the spread be prevented?
blood products, mainly IVDU (also transfusions, sexual etc) Can’t prevent spread - vaccination impossible due to rapid change of proteins.
what haematological disorder is associated with hep C?
Non-Hodgkin’s lymphoma
give 3 risk factors for progression of hepatitis C to cirrhosis
male, older, higher viral load, alcohol use, HIV, HBV
what viral markers would you look for in hepatitis C at 8 weeks?
HCV RNA at 8weeks.
if you took a liver biopsy of a hepatitis C patient, what might you see?
lymphoid follicles in portal tracts and fatty change
how would you treat a chronic infection with hepatitis C? what major problem should be noted about one of the drugs?
serine protease inhibitors (boceprevir, telaprevir) - directly acting antivirals against genotype 1 HCV. combine with: interferon alpha. ribavirin - very teratogenic.
give 3 possible complications of hepatitis C
glomerulonephritis, cryoglobulinaemia, thyroiditis, autoimmune hepatitis, PAN, polymyositis, porphyria cutanea tarda
what other virus is needed for hep D to infect someone? why?
hep B. hep D is an incomplete RNA that needs hep B for assembly.
how can hepatitis D be prevented?
hep B vaccine
how can you test for hepatitis D?
test for anti-HDV antibody
what can hep D cause?
acute liver failure/cirrhosis
how can you treat a hep D infection?
may need liver transplant as interferon alpha has limited success.
what type of virus is hep E? what infection is it similar to?
RNA. hep A.
how is hep E transmitted?
enterally - contaminated water.
what can you detect in blood and stools to confirm a diagnosis of hep E?
hep E RNA
what collagen type is deposited in the liver in cirrhosis?
type 1 and 3
what is the difference between macro and micronodular cirrhosis?
macronodular - variable nodule size, normal acini within, tends to follow hepatitis. micronodular - uniform involvement of liver and regenerating nodules
if there was alpha-fetoprotein present in the serum of a cirrhosis patient, what would you suspect to be the cause of their cirrhosis?
hepatocellular carcinoma
what medications should be avoided when treating cirrhosis?
NSAIDs, opiates, sedatives
list 3 causes of cirrhosis
*chronic alcohol abuse. *HBV or HCV infection haemachromatosis alpha1-antitrypsin deficiency Budd-Chiari non-alcoholic steatohepatitis autoimmune - primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis. drugs - amiodarone, methyldopa, methotrexate.
give 3 clinical features of cirrhosis
pruritus jaundice raised LFTs leuconchyia Terry’s nails clubbing palmar erythema hyperdynamic circulation Dupuytren’s circulation spider naevia xanthelasma gynaecomastia atrophic testes loss of body hair parotid enlargement hepatomegaly
list 3 possible complications of cirrhosis
hepatic failure - coagulopathy, encephalopathy, hypoalbuminaemia, sepsis, SBP, hypogylcaemia. portal hypertension - ascites, splenomegaly, portosystemic shunt + oesophageal varices. increased risk of HCC.
what investigations would you carry out in cirrhosis? what would you find?
bloods - raised bilirubin/AST/ALT/alk phos, low albumin. liver ultrasound and duplex - small liver or hepatomegaly, focal liver lesions, ascites. MRI - big caudate lobe, small islands of regenerating nodules, right posterior hepatic notch. transient elastography scan. ascitic tap for urgent MC&S. liver biopsy - confirms diagnosis.
if a cirrhosis patient presented with ascites, how would you treat this?
bed rest, fluid and salt restriction, spironolactone ± furosemide.
how would cirrhosis be treated?
nutrition, alcohol abstinence, avoid certain drugs. colestyramine for pruritus. treat underlying cause.SBP-abx. Acites- fluid and salt restrict and spironolactone. Encephalopathy - prophylactic lactulose and rifaximin. At risk hep a and b vaccine. Liver transplant.
what are the indications for liver transplant?
advanced cirrhosis secondary to - alcoholic liver disease, hepatitis (B, C, autoimmune), primary biliary cirrhosis, Wilson’s disease, alpha1-atintrypsin deficiency, primary sclerosing cholangitis. hepatocellular cancer.
what are the contraindications for liver transplant?
extrahepatic malignancy, multiple tumours, severe cardiorespiratory disease, systemic sepsis, HIV infection, non-compliance (drug therapy or alcohol abstinence)
what immunosuppression would a liver transplant patient be put on?
ciclosporin or tacrolimus + azathioprine.
what’s the difference between hyperacute and acute transplant rejection?
hyperacute - due to ABO incompatibility. acute - T cell mediated, 5-10d post-op, patient feels unwell with pyrexia and tender hepatomegaly - managed by altering immunosuppressives.
describe the underlying pathogenesis of primary biliary cirrhosis?
serum antimitochondrial antibodies (AMA) cause chronic autoimmune granulomatous inflammation damages interlobular bile ducts causing cholestasis, cirrhosis and portal hypertension.
give 2 risk factors for primary biliary cirrhosis
family history, frequent UTIs, smoking, past pregnancy, other autoimmune diseases, hair dye/nail polish
give 2 signs found in a patient with biliary cirrhosis
jaundice, skin pigmentation, xanthelasma, hepatomegaly, splenomegaly
what blood test results would you find in a patient with primary biliary cirrhosis?
**very high alkaline phosphate - unique to PBC **AMA ab +ve. raised AST/ALT increased Igs.
what other investigation, apart from blood tests, might you perform in primary biliary cirrhosis?
ultrasound
how would you treat primary biliary cirrhosis?
ursodeoxycholic acid. vitamin supplements for malabsorption. bisphosphonates for osteoporosis, colestyramine/rifampicin for pruritus.
give 3 diseases associated with primary biliary cirrhosis
scleroderma, thyroid disease, keratoconjunctivitis sicca, renal tubular acidosis, membranous glomerulonephritis, coeliac disease, interstitial pneumonitis
explain secondary biliary cirrhosis
destruction of biliary tracts due to prolonged large duct biliary obstruction, caused by gall stones, bile duct stones, sclerosing cholangitis.
how would you investigate secondary biliary cirrhosis?
US followed by ERCP.
what are the CAGE questions?
ever felt you should Cut down on your drinking? have people Annoyed you by criticising your drinking? ever felt Guilty about your drinking? ever had an Eye opener to help you get up in the morning?
what changes would you see on a liver biopsy of an alcoholic hepatitis patient?
fatty change and infiltration by polymorphonuclear leucocytes and hepatocytes in zone 3. Mallory bodies - dense cytoplasm and giant mitochondria.
what is “fatty change”?
first change in the alcoholic liver - hepatocytes contain microvesicular droplets of triglycerides. reversible, but will progress if alcohol isn’t stopped.
what is the path of damage the alcoholic liver follows?
fatty change - alcoholic heptatitis - fibrosis - micronodular cirrhosis
what are the clinical features of alcoholic hepatitis?
SPIDER NAEVI. rapid onset jaundice, nausea, anorexia, RUQ pain, encephalopathy, fever, ascites, tender hepatomegaly
how would you manage an alcoholic hepatitis patient?
supportive - poss. NG tube. alcohol cessation - IV thiamine and diazepam if needed.
what causes hereditary haemachromatosis?
autosomal recessive inheritance with a mutation in the HFE gene (chromosome 6). mostly affects middle aged men.
what is the defining feature of hereditary haemachromatosis?
increased intestinal iron absorption leading to excess iron deposition in organs.
list 3 clinical features of hereditary haemochromatosis
erectile dysfunction, slate grey skin pigmentation, hepatomegaly, cirrhosis, dilated cardiomyopathy, osteoporosis, diabetes mellitus, hypogonadism
what would be the blood test results (iron, ferritin, total iron binding capacity) in hereditary haemachromatosis? what disease is this the same as?
increased iron and ferritin, low total iron binding capacity. the same as sideroblastic anaemia.
what staining would you use on liver biopsy in hereditary haemachromatosis?
Perl’s staining
how would you treat hereditary haemachromatosis?
venesection - once a week, then a few times a year. desferrioxamine (iron chelator) if can’t venesect. testosterone replacement. low iron diet, screen family members.
what is alpha1-antitrypsin?
glycoprotein that controls the inflammatory cascade. synthesised in the liver and protects lung tissue from damage by elastase.
what diseases does deficiency of alpha1-antitrypsin causes?
emphysema, COPD, chronic liver disease and HCC
what are the different genotypes you can inherit for alpha1-antitrypsin? which one brings about symptomatic disease?
PiMM - normal (M = medium) PiZZ - homozymgous, symptomatic (Z = very slow) PiMZ - heterozygous (slow)
give the clinical features of alpha1-antitrypsin deficiency
dyspnoea (emphysema), cirrhosis, cholestatic jaundice.
how would you diagnose alpha1-antitrypsin deficiency?
serum alpha1-AT levels. genotyping. liver biopsy.
what stain would you use on a liver biopsy in alpha1-antitrypsin defiency? what would you see?
Periodic Acid Schiff - PAS +ve globules.
what is the curative treatment of alpha1-antitrypsin deficiency?
liver transplant
what is Wilson’s disease?
autosomal recessive disorder resulting in impaired excretion of copper in bile and faeces, leading to toxic accumulation of copper.
what system, apart from the liver, is affected by Wilson’s disease? how does this present?
CNS - basal ganglia degeneration, depression, labile emotions, decreased libido, personality changes, tremor, dysarthria, dementia, decreased memory/IQ, delusions
what is a Kayser-Fleischer ring?
copper deposition in cornea - see in eyes of Wilson’s disease patients
what investigations would you carry out in Wilson’s disease? what would they show?
slit lamp eye exam. 24h urine copper - excretion high. liver biopsy - increased hepatic copper, hepatitis, cirrhosis. + genetic testing, serum copper/caeruloplasmin.
how would you treat Wilson’s disease?
lifetime copper chelation - penicillamine. screen siblings (treatment whilst asymptomatic prevents liver damage).
name an infective cause of liver failure
EBV, hep B and C, yellow fever
name a drug cause of liver failure
paracetamol OD, halothane, isoniazid
name a toxin cause of liver failure
carbon tetrachloride, mushrooms
name a vascular cause of liver failure
Budd-Chiari, venous thrombosis
name an inherited cause of liver failure
primary biliary cirrhosis, haemachromatosis, autoimmune hepatitis, antitrypsin deficiency, Wilson’s disease
name some other causes of liver failure
alcohol, fatty liver of pregnancy, malignancy
give 4 signs of fulminant hepatic failure
hepatomegaly, jaundice, splenomegaly, ‘pear drop’ smell, asterixis (flapping tremor) palmar erythema, clubbing, ascites, pruritus, portal hypertension
what is hepatic encephalopathy? explain it
a major complication of liver failure: liver fails - nitrogenous waste (ammonia) builds up in circulation - passes to brain - astrocytes clear it by converting glutamate to glutamine - excess glutamine causes an osmotic imbalance - cerebral oedema
what might you find on investigating the blood of a patient with liver failure?
high bilirubin and aminotransferases. low sodium, albumin, prothrombin, factor V
how would you manage a liver failure patient?
treat cause. treat complications: seizures - lorazepman. bleeding - vit K. ascites - diuretics. infection - blind abx = ceftriaxone. hypoglycaemia - IV glucose.
what tests would you run on ascitic fluid once aspirated?
cell count, MC&S, protein/albumin, cytology for malignancy, amylase to exclude pancreatitis.
give 3 causes of transudate ascites
portal hypertension (cirrhosis). hepatic outflow obstruction. Budd-Chiari syndrome. cardiac failure. tricuspid regurgitation. constrictive pericarditis. Meig’s syndrome.
give 3 causes of exudate ascites
peritoneal carcinomatosis peritoneal TB pancreatitis nephrotic syndrome lymphatic obstruction
what would you find on abdo examination of a patient with ascites?
SHIFTING DULLNESS. fullness in flanks.
how would you manage a patient with ascites?
aspirate for testing. sodium restriction + oral spironolactone ± furosemide.
what would you seen on a liver biopsy of a patient with cirrhosis?
irregular nodules of fibrous tissues.
how would you investigate ascites?
paracentesis - investigation and intervention.
what would you see on biopsy in primary biliary cirrhosis?
bile duct granuloma
explain why gynaecomastia can be a feature of liver failure in males
failure of liver to eliminate steroid hormones
what would you find in the blood of a patient that would indicate they have carrier status for HBV?
HBsAg - surface antigen. present 1-6 months after exposure. present for >6 months = carrier status.
what would you find in the blood of a patient that has recently (last couple of months) been infected with HBV? what does this mean?
HBeAg (e antigen) - present 1.5-3 months after exposure. implies high infectivity.
what might you find in the blood of a patient that indicates they have immunity to HBV through having previously been infected?
anti-HBc antibody
what might you find in the blood of a patient that indicates they have immunity to HBV through having been vaccinated?
anti-HBs antibody
what blood test would you do on an HBV patient to monitor progress?
HBV PCR
are most liver tumours primary or secondary?
90% are secondary.
list some common origins of secondary liver tumours
men - stomach, lung, colon. women - breast, colon, stomach, uterus.
what are the 5 types of primary malignant liver tumours?
hepatocellular carcinoma (HCC). cholangiocarcinoma angiosarcoma hepatoblastoma fibrosarcoma and hepatic GIST
list the 5 types of primary benign liver tumours
cysts, haemangioma, focal nodular hyperplasia, fibroma, benign GIST
list 3 symptoms of liver tumours
fever, malaise, anorexia, weight loss, RUQ pain. jaundice - late, apart from in cholangiocarcinoma.
list 3 signs of liver tumours
hepatomegaly - smooth, or hard and irregular (mets, cirrhosis, HCC). signs of chronic liver disease. jaundice/ascites. abdo mass. bruit over liver = HCC.
how would you investigate liver cancer?
bloods. US guided biopsy / MRI.
what protein is raised in serum in HCC?
alpha fetoprotein
how would you treat liver metastases? what is the prognosis?
mostly palliative treatment - prognosis is often less than 6/12
list 3 causes of HCC
*HBV. HCV, autoimmune hepatitis, cirrhosis, non-alcoholic fatty liver, aflatoxin, clonorchis sinesis, anabolic steroids.
how would you diagnose HCC?
4 phase liver CT. MRI. biopsy.
how might HCC be treated?
resect solitary tumours. liver transplant. percutaneous ablation, tumour embolisation and sorafenib.
give 3 causes of cholangiocarcinoma
flukes, primary sclerosing cholangitis, HBV, HCV, diabetes mellitus.
what breakdown product is raised in the serum of those with cholangiocarcinoma?
bilirubin
how might cholangiocarcinoma be managed?
precutaneous (or via ERCP) stenting of obstruction. surgery not an option.
what is the usual prognosis of cholangiocarcinoma?
5 months
what is the most common benign liver tumour? should it be biopsied?
haemangiomas. incidental finding on US/CT - DON’T biopsy.
what are hepatic adenomas associated with? when is surgical resection indicated?
oral contraceptives, anabolic steroids. only if symptomatic.
list some risk factors for pancreatic carcinoma
male >60yo smoking alcohol carcinogens diabetes mellitus chronic pancreatitis central adiposity diet high in fat + red/processed meat
what is the genetic association seen in pancreatic carcinoma?
95% have mutations in KRA52
what are the clinical features of carcinoma of the head of pancreas?
painless obstructive jaundice (pain late on, radiates to back). pruritus, Courvoisier’s sign (enlarged, palpable gallbladder), central abdo mass, hepatomegaly
what are the clinical features of carcinoma of the body/tail of pancreas?
abdo pain, weight loss, anorexia, dull ache radiating to back, relieved when sitting forward. polyarthritis, skin nodules
what investigations would you carry out in pancreatic carcinoma?
transabdominal ultrasound. CT. bloods - Ca19-9 antigen - not specific, but good marker for monitoring progress.
how would you manage a patient with pancreatic carcinoma? what is their prognosis like?
surgical resection with post-op chemo or palliative endoscopic stents. opiates/radiotherapy for pain. mean survival less than 6/12.
what are the 3 types of liver abscess?
pyogenic, amoebic or hyatid
give 3 causes of pyogenic liver abscess
*idiopathic. biliary sepsis portal pyaemia from intra-abdominal sepsis trauma bacteraemia direct extension from e.g. perinephric abscess
list the most common causative organisms in liver abscesses
E coli, Strep milleri. anaerobes e.g. bacterioides
what causes an amoebic liver abscess?
spread of entamoeba histolytica from bowel to liver via portal system
what is the main GI feature of amoebic liver abscess?
bloody diarrhoea
what would you see on performing blood investigations on a patient with a pyogenic liver abscess?
raised serum bilirubin, normocytic anaemia, raised alkaline phosphatase, ESR, serum B12
if you took a stool culture and liver aspiration of an amoebic abscess patient, what would you see?
faeces - pus and amoeba trophozoites. liver aspiration - ‘anchovy sauce’ pus
how would you manage an amoebic liver abscess?
metronidazole. no need to aspirate.
how would you manage a pyogenic abscess?
percutaneous aspiration under radiological (e.g. US) control. pig tail catheter for continuous drainage. IV metronidazole and cefuroxime.
