Liver & Biliary System Flashcards
what is delireum tremens, how is it treated and what do you do first when they present
acute confusional state when someone who drinks daily suddenly stops drinking
benzodiazapenes
ABCDE
what is biliary colic and how is it treated
RUQ pain, due to gallstones blocking cystic or CB duct which goes away when stone moves into SI
colic = pain occuring after eating a fatty meal which causes gall bladder contraction
surgical removal of gallbladder
what is painless jaundice
obstructive cause of jaundice but with the absence of abdominal pain
risk factors for liver and pancreatic diseases
alcohol intake drugs, both prescription and non blood transfusions tattoos travel unprotected sex (hep)
what are the 5 f’s (risk factors) for gall stones
female, fat, fair (american), forty, fertile (pregnant or on combined pill)
what is the most common cancer of the GI system
carcinoma of pancreas head, excluded via imaging tests in patients over 40 who have painless, obstructive jaundice
what marker do you use to test for liver cancer
AFP - alpha fetoprotein
what is the hormone used to contract the gallbladder
cholecystikinin
what does conjugation mean and where does it happen
making bilirubin water soluble by adding glucoronic acid, in hepatocytes in liver
where is bilirubin made from
breakdown of Hb by biliverdin
when would you get high levels of unconjugated bilirubin
in high breakdown of RBC, haemolysis or gilbert syndrome
may be physiological or pathological but is toxic
when would you get high levels of conjugated bilirubin and why (conjugated hyperbilrubinaemia)
causes are obstructive jaundice, aka post–hepatic jaundice
non toxic but ALWAYS pathological
why do you get pale stools and dark urine
because bilirubin doesn’t get into bowel, isn’t metabolised –> low levels of uro and sterobilinogen = makes stool brown
get dark urine cos conjugated BR = water soluble and goes into kidneys and hence into urine
what is jaundice?
yellowing of skin, sclera and mucous membranes due to high levels of bilirubin in the body
becomes clinically apparent at >50uM/L
what are the other symtpoms of jaundice
scratches from pruritus, evidence of weight loss and troisier’s node (left supraclavicular node enlargement)
what are the tests when someone presents with jaundice?
- transabdominal USS - check for dilated bile ducts and look at liver
- CT, contrast and non-contrast: look at pancreatic ducts
- ERCP - look for gallstones (in bile ducts)
what is haemolytic jaundice / pre-hepatic and what are the causes
abnormal RBC, due to sickle cell, drug reactions, hypersplenism or incompatible blood transfusion
what is the pathophys of haemolytic jaundice
liver compensates by increasing conjugated bilirubin output
= stools are NOT pale
there is excess unconjugated bile in plasma but LFT’s are normal
uncojugated bilirubin cannot be excreted in urine and hence no bilirubin in urine
what is hepatocellular jaundice
compromised liver not excreting bilirubin even though it is formed at a normal rate
high levels of unconjugated bilirubin, but hepatic injury may also prevent conjugated bilirubin from reaching the gut
what are the causes of HC jaundice
common: alcoholic liver cirrohosis or hepatitis, drug induced (paracetamol, co-amoxiclav, methotrexate), viral hep
autoimmune liver disease, wilsons disease, haemachromatosis
what is neonatal jaundice
common condition in newborns, usually resolved in 2 weeks. happens bc RBC constantly broken down and liver not fully formed to get rid of bilirubin
what is kernicterus
clinical features of untreated hyperbilirubinaemia
unconjugated bilirubin can cross the blood-brain barrier and is toxic to neural tissue - may be treated with phototherapy or exchange transfusion
what is obstructive or post hepatic jaundice
blockage of flow of bile through bile ducts or intra and extrahepatic ducts
what are the causes of obstructive jaundice
gallstones, cholecystitis (inflammation of gall bladder), carcinoma of pancreatic head, chronic pancreatitis
PBC, PSC, cholangiocarcinoma
what are the symptoms or signs of obstructive jaundice
dark urine, pale stools and an itch
what is PBC
primary biliary cholangitis - auto-immune disease in which interlobular ducts in liver are destroyed
diagnosed with high ALP, often asymptomatic
treatments: UDCA, symptomatic treatment
what is PSC
primary scleorising cholangitis
affects larger ducts within and outside the liver
causes hardening and narrowing of bile ducts
comparing the 3 types of jaundice
LOOK AT TABLE in notes
what are the steps to investigating jaundice
ultrasound, if ducts dilated = CT
if ducts not dilated = prehpatic or hepatocellular
what are the transaminases
ALT and AST
enzymes that convert protein to energy
what is ALP
alkaline phosphatase
prothrombin time and liver?
increased if liver damage
what is found, LFT wise, in hepatocellular damage?
rise in ALT, and rise in AST more than a rise in ALP
what is found, LFT wise, in obstructive damage?
rise in ALT, and rise in ALP more than in AST
what are the reasons why ALP is higher in obstructive
ALP found in hepatic bile duct cells so damage involving biliary tract causes ALP containing cells to be damaged = raised
AST and ALT are found in normal hepatic cells not bile duct cells
what is hepatitis
inflammation of the liver
what are the symptoms of alcoholic hepatitis and what are the consequences
jaundice, swollen and tender liver
vomiting
- possible to go back to a normal liver with abstinence
can result in acute, chronic or fulminant hepatitis
repeated attacks = cirrhosis
what is chronic hep
inflammation persisting for more than 6 months, but low grade
symptoms of chronic hepatitis
fatigue, often none
presents with cirrhosis
what are the investigations for chronic hepatitis?
what are the symptoms that come on in the later stages?
LFT’s - abnormal, but mild elevation ALT’s
later symptoms include encephalopathy, jaundice etc
only really picked up through screening
what is acute hepatitis and how is it caused
not associated with any liver damage
due to viruses or drug overdose
symptoms of acute hep
generally unwell
jaundice
RUQ pain
severe: coagulopathy, renal impairment
blood test results of acute hep
raised ALT and AST >1000
high bilirubin
what is fulminant hepatitis
hepatitis leading to very acute liver failure (happens quickly and even if you’ve never had liver problems before)
necrosis of liver cells
causes of fulminant hep
usually hep A, drug-induced or toxic agents
symptoms of fulminant hepatitis
jaundice, pain etc
encephalopathy within 28 days
poor prognosis = needs transplant urgently
what is steatohepatitis
inflammation of liver in association with a fatty liver
what are the signs of decompensated liver in steatohepatitis?
variceal bleeding and ascites, jaundice
what other virus can cause viral hepatitis
EBV/ glandular fever
where is hep A found and how is it spread
faceo-oral spread
endemic in the developing world
common in childhood and lasts around 12 weeks
what are the markers of hepatitis
IgM in acute infection, IgG goes up later
how is hep B spread and where is it found
mother to child
IVDU
unprotected sex
africa and asia
what are the consequences of hep B and why
liver cancer bc causes changes in DNA
liver cirrhosis
what hepatitis viruses are we vaccinated against
hep A - everyone
hep B - at risk groups
what is the serology of hep B
IgM = core
surface antigen HBsAG - goes up quickly and then decreases after 24 weeks
hence if surface antigen negative but antibody positive = immunised or prev exposure
what is chronic hep B
Presence of surface antigen for greater than 6 months
Immunotolerant phase: E antigen positive
• High viral levels = infectious
• Normal LFTs
• Few liver problems
Immunoreactant phase: E antigen negative
• Low viral levels = less infectious
• ALT raised
• Often fibrotic/cirrhotic
what is the treatment for hep B
acute - not necessary
chronic - uncurable but treatable
anti-virals: nucleotide analogues which directly inhibit viral replication - tenofovir etc
interferon - immune stimulation. 48 week course; stimulates IS to develop long-term immune response for hepb
given to E antigen positive patients
how is hep c spread and where is it found
locally in NW england
blood borne - medical equipment, IVDU, no RF
90% of acute hepC - asymptomatic but increases risk of cirrohosis
how do you test and treat hep C
antibodies
PCR - if antibody positive, look for RNA of virus, and if not present they have recovered
treatment - interferon - ribavarin
protease inhibitors
what is hep E
identical to hep A
may cause severe disease in pregnancy
test for IgM and IgG
what is hep delta
requires co-infection with hepB, cannot replicate itself but worsens prognosis of hep b
Just treat hep b
what is liver cirrhosis and what are the 4 main causes
fibrosis of the liver with nodule formation
alcoholic liver disease, non-alcoholic fatty liver disease, hep B and hep C
what is the 1st way cirrhosis can cause problems and what are the symptoms
portal hypertension - venous blood supply: increased back-flow or pressure
- varices: oesophageal
- piles
- ascites - salt and water retention due to HT
- encephalopathy - toxins not removed by liver
- renal failure
*EASIER TO TREAT by managing HT
what is the 2nd way cirrhosis can cause problems and what are the symptoms
loss of function
- jaundice
- coagulopathy - loss of ability to form clotting factors
- decreased drug metabolism - decreased hormone metabolism = increased levels of oestrogen can lead to gynacomastea but can also present with spider naevi, palmar erythemia etc
- increased sepsis level bc liver manages immune system
what is the staging for liver cirrhosis
child-pugh (score out of 15 for severity)
MELD: 3 month prognosis %
what is the management for liver cirrhosis
sympomatic high protein, low sodium diet spironolactone prophylactic AB propanolol vasopressin analogues, vit k and FFP
what are the complications of liver cirrhosis and why
hepatorenal - HT in portal system = dilation of portal BV = less blood to kidney = hypotension in kidney = renin-angiotensin system = vasoconstriction so starvation of blood
hepatic encephalopathy - ammonia build up in blood
what is taken into consideration for liver transplant referral
decompensated liver disease after best management and 3 months alcohol abstinence
when to offer corticosteroid treatment for alcohol-hep
severe, discriminant function of 32, after treating bleeding and renal problems
what are the risks with corticosteroid treatment for alcohol-related hepatitis
improves survival short term -1 month
not long term >3 months
increases risk of infection
what is the CAGE questionnaire
have you ever felt….
- you need to CUT down drinking
- ANNOYED by people critisicing your drinking
- felt GUILTY about drinking
- EYE-OPENER (need to drink when you wake up to cure a hangover)
