GI - liver + co. 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
= acute inflammation of pancreas releasing exocrine (secrete via ducts) enzymes causing autodigestion of the organ. activation of proenzymes within duct.
describe the pain of acute pancreatitis
gradual or sudden severe epigastric/central abdominal pain, radiates to back, may be relieved by sitting forward.
presents with this + vomiting
typically presents at around 60yo
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.
shock!
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 causing 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.
FBC, LFT (AST:ALT >3, raised bilirubin)
hypocalcaemia, hypergylcaemia, raised urea.
plain erect AXR - retroperitoneal shadow = bleed, intestinal obstruction, pancreatic calcifications
CT w/ contrast = diagnostic.
USS shows swollen pancreas +/- gallstones
ERCP
explain the Modified Glasgow criteria for predicting severity of pancreatitis
PANCREAS: 3 or more = SEVERE
PaO2 <8kPa
Age >55yrs
Neutrophilia - WCC >15
Calcium - <2mmol/L
Renal function - urea >16mmol/L
Enzymes AST/ALT >200 units
Albumin <32g/L
Sugar >10 mmol/L
how would you medically manage an acute pancreatitis patient?
MILD = Nil by mouth / NG tube, manage on general ward. pain relief = pethidine (antispasmodic) or buprenorphine +/- IV benzodiazepines (morphine causes spasms in ampullar). IV fluids, no need to CT. repeat glasgow scores at 24 and 48h + daily bloods and obs. when symps and blood stabilise can restart fluids/food. refer for Rx of gallstones if relevant.
SEVERE = HDU/ITU + CT for necrosis.
if necrosis - aspirate peritoneal fluid for culture and target IV abx.
enteral nutrition (NG tube), early ERCP for gallstones, give O2.
give 2 early and 2 late possible complications of acute pancreatitis
early: shock, ARDS, renal failure, DIC, sepsis, hypocalcaemia.
late: pancreatic necrosis (raising CRP and dynamic CT), pancreatic abscess, ascities, acute pseudo cyst (4W after attack, needs surgery), pulmonary oedema
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.
typically a 40yo male drinker.
DDX = PANCREATIC CANCER
give 3 clinical features of chronic pancreatitis
epigastric painradiating to back - relieved by sitting forward or hot water bottles on epigastrium/back, made worse by eating.
nausea and vomiting.
exocrine dysfuncton - malabsorption, wt loss, diarrhoea, steatorrhoea.
endocrine dysfunction - DM.
differentiate from pancreatic cancer!!!
what would you expect serum pancreatic enzymes levels to be in chronic pancreatitis?
amylase and lipase are normal - there’s no biochemical markers for chronic pancreatitis, and radiology is frequently nromal.
what investigations would you run in chronic pancreatitis?
bloods - FBC, U&E, LFT, Ca (cause), amylase (normal), glucose/HbA1c (raisesd)
secretin stimulation test - causes pancreas to release bicarb to neutralise stomach acid, will be positive if >60% exocrine function lost.
malabsorption tests - serum trypsinogen/faecal elastase.
imagine - CT (atrophy, duct dilatation or calcification), *MRCP (magnetic retrograde cholangiopancreatography)
how would you treat a patient with chronic pancreatitis?
NSAIDs and tramdol for pain
replace pancreatic enzymes if malabsorption.
alcohol advice
low fat diet
gallstones treatment, diabetes treatment
give 2 possible complications of chronic 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 (10%) - small, friable, radiolucent:
- black = calcium bilirubinate + mucin, glycoproteins. result of haemolytic conditions.
- brown calcium bilirubinate + fatty acids = result of stasis and biliary infection (e. coli/klebsiella)
cholesterol stones - 80% of stones in UK - large, solitary, radiolucent
mixed stones (10%) - faceted (calcium salts, pigment and cholesterol).
who gets gallstones?
fair, fat, fertile, female and forty.
also - FHx, oral contraceptions, hyperlipidaemia.
what are the different outcomes a gallstone can cause, and give some clinical features for each.
biliary colic = RUQ pain
acute cholecystitis = RUQ pain + fever/WCC
ascending cholangitis = RUQ pain + fever/WCC + jaundice - Charcot’s triad.
pancreatitis = jaundice, raised bili, alk phos, GGT - 70% asymptomatic though
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
what is biliary colic? how does it present, how would you investigate it?
most common presentation of gallstones.
due to - temporary obstruction of cystic or common bile duct (jaundice)
pain = 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
Ix = USS is 90-95% sensitive for stones
Urinalysis, CXR, ECG for exclusion
will get =jaundice if stone moves to CBD
what are the clinical features of acute cholecystitis?
second most common presentation of gallstones - 95% due to stones, they get impacted in cystic duct and there’s an inflammatory response to retained bile.
presentation - continuous epigastric/RUQ pain, referred to R shoulder. vomiting, fever, local peritonism, possibly a gallbladder mass. jaundice if stones in CBD. Murphy’s +ve.
what investigations would you perform in acute cholecystitis?
ultrasound - thick walled (>3mm), shrunken gallbladder, fluid or air in GB. dilated CBD >6mm diameter
may do ERCP/MRCP.
management for gallstones/biliary colic/acute cholecystitis - non-surgical v surgical?
Non-Surgical:
- NBM (stops CCK release)
- parenteral opioids (pethidine) or **PR diclofenac
- if >24hrs admit, rehydrate IV fluids, consider IV abx (3rd gen cephalosporin)
Surgical:
- lap chole to remove gallbladder
- comps - fat intolerance, injury to bile duct
describe the clinical features of chronic cholecystitis
chronic inflammation ± colic. flatulent dyspepsia - vague abdo discomfort, distension, nausea, flatulence and fat intolerance (fat stimulates CCK).
can occur if repeated attacks of acute cholecystitis.
USS shows shrunken gallbladder
describe the pain of biliary colic
severe, constant, increasing pain in RUQ, can radiate to right shoulder/scapula.
what is the triad of symptoms for ascending cholangitis?
Charcot’s triad (70%) - RUQ pain + fever/chills + jaundice.
also Reynold’s pentad (20%) - RUQ pain + fever/chills + jaundice + altered mental state + hypotension/tachycardia.
what structure is being obstructed by gallstones if a patient has developed ascending cholangitis? what’s the mechanism? what organisms are involved?
common bile duct
bile normally sterile, if CBD is obstructed then flow of bile is reduced –> biliary stasis and infection. infection can also be due to acute cholecystis or ERCP (1%).
organisms = E coli, klebsiella, enterococci
*medical emergency*
what is the gold standard investigation in ascending cholangitis? other Ix?
transabdominal ultrasound - measure CBD dilatation.
also - WCC/ESR/CRP/LFT
?sepsis 6
imaging - KUB XR + AUSS + contrast CT (best method), MRCP
how would you treat ascending cholangitis?
fluid resus, broad spec abx, correct any coagulopathy,
Rx as sepsis if shocked.
if AKI, shock, DIC etc - emergency endoscopic biliary drainage.
might do 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 is liver cirrhosis
- diffuse hepatic process with fibrosis and conversion of normal liver architecture to ndoles - final pathway for most liver disease.
- cytokines activate stellate cells at space of disse. normal matrix replaced by collagen (types 1 and 3) and fibronectin. loss of fenestration/sinusoids –> impaired function
complications:
- distortion of hepatic vessels –> increased intrahepatic resistance + portal hypertension (causes oesophageal varices, hypoperfused kidneys, increase CO)
- hepatocyte damage –> impaired liver function and decreased synthesis of clotting factors
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
jaundice
hyperdynamic circulation
Dupuytren’s contracture
xanthelasma
gynaecomastia
atrophic testes
loss of body hair
parotid enlargement
hepatomegaly
cutaneous signs = FLAPS = Finger clubbing, Leukonychia, Asterixis (liver flap) Palmar erythema, Spider naevi, Scratch (pruritus)
arise when 80% of parenchyma destroyed so often asymptomatic.
Vauge - fatigue, malaise, anorexia, nausea, wt loss
decompensated - oedema, ascites, bruising, poor memory, bleeding varices, SBP
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?
- LFT = AST+ ALT raised w/hepatocyte damage, GGT raised if alcohol
- Albumin = low if advanced cirrhosis
- FBC = bleeding (anaemia), low pltls (hypersplenism), macrocytosis (alcohol)
- U+E = hepatorenal synd.
- Red cell folat = low if alcohol
- Coag screen = increased PT if advanced
- Ferritin = raised in hereditary haemachromatosis, low in IDA/blood loss
- Viral screen = hep B/C
- Non-alcoholic fatty liver disease = fasting glucose, insulin, triglycerides and uric acid levels
- Metabolic = A1AT level, caeruloplasmin, urinary copper, fasting transferrin saturation
- Imaging = USS (complications of cirrhosis/fatty change), CXR (elevated diaphragm and pleural effusions - passage of ascites across diaphragm)
**Biopsy = Gold standard for histology - 1) loss of hepatic architecture, 2) bridging fibrosis, 3) nodular regeration
how would cirrhosis be treated?
aim to delay progression + treat cause + avoid complications
general - nutrition, alcohol abstinence, exercise (muscle wasting)
avoid certain drugs - beware those hepatically metabolised.
colestyramine/antihistamines for pruritus.
treat underlying cause.
monnitor for oesophageal varices and HCC.
proph. abx (ciprofloxacin if protein <15g/l), vaccinate against hep A, flu, pneumococcus.
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.
try and learn the divisions of abdo aorta (to gut)
blood supply to spleen etc
