liver Flashcards
what are the symptoms of primary biliary cholangitis
fatigue
itch without rash
xanthelasma
what is the treatment for PBC
urseodeoxycyclic acid
how is PBC diagnosed
need 2 of 3
positive AMA
cholestatic LFTs
liver biopsy
what happens to patients with PBC
most will not develop symptoms
many developing liver failure will be unfit for transplant
blood flows into the liver via what
liver has dual blood supply
blood flows in from the portal vein and hepatic artery
what is classed as portal hypertension
pressure above the normal range 5-8mmHg
what are the causes of hypertension in the liver
prehepatic-blockage of the portal vein before the liver due to portal vein thrombosis or occlusion secondary to congenital portal venous abnormalities
intrahepatic-due to distortion of the liver architecture
presinusoidal eg, schistomiasis of non-cirrhotic portal hypertension
post sinusoidal eg.cirrhosis causes include cirrhosis, alcoholic hepatitis and congenital hepatic fibrosis
what signs would you see in compensated cirrhosis
spider naevi palmar erythema gynaecomastia clubbing maybe hepatomegaly splenomegaly
what signs would you see in decompensated cirrhosis
jaundice
ascites
encephalopathy
bruising
how would you treat cirrhosis
remove or treat the underlying cause
what are the complications of cirrhosis
variceal bleeding
jaundice
ascites
liver failure
what is the first line drug in treating ascites
spironolactone
where does spironolactone act
in the collecting ducts in the kidneys
what is ammonia normally metabolised to and where
to urea in the liver
what is hepatic encephalopathy
ammonia generated in the intestines form nitrogenous compounds in the diet is taken directly into the systemic circulation rather than being metabolized in the liver
what are oesophageal varices
extremely dilated sub-mucosa veins in the lower third of the oesophagus
what are oesophageal varices usually due to
portal hypertension, commonly due to cirrhosis
how are oesophageal varices treated prophylactically
B blockers non selective eg carvediolol, propanolol
what are the causes of chronic liver disease
alcohol hep B, hep C autoimmune hepatitis primary biliary cholangitis haemochromatosis NAFLD primary sclerosing cholangitis a 1 anti-trypsin budd chiari methotrexate
name 2 diseases that affect the liver chronically but aren’t chronic liver diseases
amyloid and rotor syndrome
what is primary sclerosing cholangitis
an autoimmune disease of large and medium sized bile ducts
how is primary sclerosing cholangitis diagnosed
clinically through cholangitis
diagnosis through imaging of biliary tree
what is haemochromatosis
genetic iron overload syndrome
how is haemochromatosis treated
venesection-patient gives blood
what is Wilson’s disease
lenticulo-hepatic degeneration
how does Wilson’s disease damage the liver
deposition of copper in the liver
Wilson’s disease causes fibrosis
what clinical signs can indicate wilsons disease
Kaiser Fleisher rings
how is wilsons disease treated
copper chelation drugs-pencillamine
what signs can Budd-chiari produce acutely
jaundice, tender hepatomegaly
what symptoms can chronic budd-chiari produce
ascites
what is methotrexate used to treat
rheumatoid arthritis and psoriasis
what does steato mean
relating to fatty matter or tissue
what does sclero mean
hard/hardening
what is pruritis
severe itching of the skin, as a symptom of various ailments
what is anti-microbial antibody used to test for
primary biliary cirrhosis
what is anti-nuclear, smooth muscle (actin), liver/kidney microsomal antibody used to test for
autoimmune hepatitis
what is raised serum IgG a sign of
primary biliary cirrhosis
what is raised serum IgM a sign of
autoimmune hepatitis
what are increased viral markers a test of
Hepatitis A,B,C,D,E
what does a-fetoprotein test for
hepatocellular carcinoma
what does serum iron, transferrin saturation, serum ferritin test for
hereditary haemochromatosis
what does serum and urinary copper, serum caeruloplasmin test for
Wilson’s disease
how would you test for cirrhosis
a1-antitrypsin
what would a1-antitrypsin test for
cirrhosis and emphysema
how would you test for primary sclerosing cholangitis
anti-nuclear cytoplasmic antibodies
what would anti-nuclear cytoplasmic bodies test for
primary sclerosing cholangitis
what would markers of liver fibrosis indicate
non-alcoholic fatty liver disease
hepatitis C
what would genetic analyses test for
HFE gene in hereditary haemochromatosis
what are the true liver function tests
bilirubin
albumin
prothrombin time
what are measured in LFTs
ALT/AST
alkaline phosphatase (ALP)
GGT
Bilirubin
what is acute liver disease
any insult to the liver causing damage
in previously normal liver
acute liver failure defined as causing encephalopathy and prolonged coagulation
how are hep B and C transmitted
blood
what are the causes of acute liver disease
viral A,B,C,D,E, CMV, EBV and toxoplasmosis drugs shock liver cholangitis alcohol malignancy chronic liver disease PARACETAMOL
good questions for probing more into an alcohol history
ask when they last had a drink
what did you drink
what strength
acute liver investigations
LFTS (inc albumin and bilirubin)
prothrombin time
treatment of liver disease
rest, up to 3 months for recovery may be up tp 6
fluids, no alcohol
increase calories, high fat foods poorly tolerated
for itch-sodium bicarbonate bath, cholestryamine or uresodeoxycholic acid
what metabolic considerations are needed for acute liver disease
monitor and supplement K, PO4 and Mg, hypoglycaemia is a very serious clinical sign
why is paracetamol toxic in high quantities
when paracetamol is metabolised a toxin called NAPQI is made, this can be mopped up by glutathione but at high overdoses the glutathione can be all used up
what is the name of the dangerous toxin made by the metabolism of paracetamol
NAPQI
what drugs can cause liver disease
co-amoxiclav
flucloxacillin
NSAID
fulminant hepatic failure has what symptoms
jaundice and encephalopathy in a patient with a previously normal liver
what are the common causes of fulminant hepatic failure
paracetamol fulminant viral drugs HBV Non A-E rare but Wilsons, Budd Chiari, malignancy
fulminant hepatic failure treatment
supportive
inotropes and fluids
renal replacement
transplantation
categories for super-urgent transplantation for acute liver failure due to paracetamol
ph 100 (inr 6.5) + creatinine 300 or anuria + grade 3 or 4 encephalopathy
lactate >3.5 )3.0 after resus >24 hr after ingestion
any 2 of 3 from category 2 plus life-threatening deterioration without sepsis
how is hep A transmitted
faecal oral-route
can you get acute or chronic Hep A
just acute hepatitis A, no chronic infection
what is hep A associated with
poor hygiene/overcrowding
some cases in gay men and injecting drug users
how is Hep E transmitted
faecal oral route
which is more common in Uk Hep A or E
Hep E
which Hep is there no available vaccination
hep E
does hep E produce acute or chronic hepatitis
acute but can be chronic in immunocompromised patients
how is hep E spread in the UK
zoonose from pigs, rabbit or deer
how do you get Hep D
only get Hep D after getting hep B
what is co-infection of Hep D
co-infection where you get hep B and D at the same time
what is it called when you get hep D after getting hep B
superinfection
what is superinfection (in relation to hep)
get hep D after getting hep B
who is at higher risk of hep B
people born in areas of intermediate/high prevalence
multiple sex partners
inject drug users
children to infected mothers
what is HBsAg
hep B surface antigen
when is HBsAg present
in the blood of all infectious individuals
what is also USUALLY present in highly infectious individuals with hep B
HBeAg
what is ALWAYS present in high titre in highly infectious individuals with hep B
Hep B virus DNA
what are present in immunity with Hep b
anti-HBs
what is likely to be present in recently infected cases
Hep B igM
how is Hep B prevented/controlled
safe blood transfusions safe sex needle exchange prevention of needle stick injuries screening of pregnant women
if you have been exposed to Hep B what do you do for post-exposure prophylaxis
can give vaccine plus HBIG (hyperimmune HepB immunoglobulin)
is there a vaccine available for hep C
no
if patient at risk of hep C or with signs of chronic liver disease
test for antibody to Hep C virus
if test for antibody to hep C virus and positive what does this indicate
past or active infection
how would you differentiate between past or active infection in hep C
test for Hep C virus RNA by PCR
what does a test for Hep C virus RNA by PCR negative indicate
past infection
which two tests would have to be positive to indicate a active infection of hep C
positive antibody to Hep C virus and positive test for hep C virus RNA by PCR
can you get acute or chronic hepatitis with hep B and C
both
how long is infection of hepatitis before it is chronic
6 months or less=acute more than that =chronic
does chronic hep C usually resolve
no once chronic infection is established, spontaneous cure IS NOT seen
pattern of infected children at birth in hep B is similar to what
hep C in that high levels of chronic infection is seen
how is acute viral hepatitis treated
symptomatic treatment no antivirals given monitor for encephalopathy monitor for resolution-hep B, C or Hep E notify public health vaccinate against other infections if at risk
how is the drug used to treat HCV chosen
depending on genotype of HCV
what are some of the side effects to inferon alpha
flu like symptoms
autoimmune disease eg SLE
psychosis
what can ribavirin cause
anaemia (made worse by telaprevir and boceprevir)
what can telepravir and boceprevir
rash which can be very severe
anaemia
what are the options for treatment of chronic hep B
1-peginterferon alone
2-suppressive antiviral drug eg.entecavir, tenofovir
what is the advantage of suppressive antivirals such as entecavir and tenofovir
they are safer less side effects than peginterferon
what is the disadvantage to suppressive antiviral drugs like entecavir, tenofavir
they are suppression not cure and resistance can develop
what are the aims/benefits of hep B therapy
reduction in HBV DNA (suppression)
loss of HBeAg
loss of HBsAg (cure)
what new therapies are being used in hepatitis C
new antivirals simeprevir, ledipasvir, daclatasvir
move is towards all oral, interferon free courses of a few moths with high SVRs (sustained virological response)
what plasma proteins does the liver produce
all main plasma proteins except gamma (y) globulins
what does albumin transport
fatty acids, bilirubin and drugs
what do alpha globulins transport
lipoproteins, lipids, hormones and bilirubin
what does retinol binding protein transport
transports vitamin A
give two examples of b globulins
transferrin and fibrinogen
what does LDL transport
cholesterol transport to peripheral tissues
what do chylomicrons transport
transport of exogenous fat to liver
how does HDL reverse cholesterol transport
cholesterol is esterified with fatty acids and transported back to liver where it is excreted as bile salts via biliary system or faeces
where can cholesterol be metabolised and excreted
ONLY THE LIVER
what vitamins does the liver store
vitamin A, D, B12 and iron
where is cholesterol located in a lipoprotein
in the core
what causes prehepatic jaundice
excess production of bilirubin after haemolysis
what causes post hepatic jaundice
from a blocked bile duct (gallstone)
increased conjugated bilirubin in plasma
pale coloured stools due to reduction of faecal bile pigments
dark urine due to excretion of water soluble bilirubin conjugates
what are the three types of benign liver masses
Haemangioma
Focal Nodular hyperplasia
Adenoma
also liver cysts
what are the types of malignant tumours in the liver
primary liver cancers-hepatocellular carcinoma
cholangiocarcinoma
or metastases
which is the commonest benign liver tumour
haemangioma
what are the clinical features of a haemangioma
commonest liver tumour hypervascualr tumour usually single small wel demarcated capsule asymptomatic
do you need to biopsy a haemangioma
no diagnosis is made based on imaging-ultrasound and CT
what is focal nodular hyperplasia
benign nodule formation of normal liver disease
what is focal nodular hyperplasia associated with
congenital vascular anomaly associated with osler weber rendu and liver haemangioma
classically-central scar containing a large artery, radiating branches to the periphery (hub and spoke)
what cells are present on histology of focal nodular hyperplasia
sinusoids, bile ductules and kupffer cells
is focal nodular hyperplasia symptomatic
no
when is focal nodular hyperplasia more common
in young and middle aged women
what does a focal nodular hyperplasia look like on imaging
us-nodule with varying echogenicity
ct-hypervascular mass with a central scar
how is focal nodular hyperplasia treated
no treatment necessary
what are the features of a hepatic adenoma
benign neoplasm composed of normal hepatocytes no portal tract, central veins or bile ducts
what are hepatic adenomas associated with
contraceptive hormones
what are the symptoms or hepatic adenoma
usually asymptomatic but may have RUQ pain
how can hepatic adenomas change over time
may present with rupture, haemorrhage or malignant transformation(v rare)
what is contained in hepatic adenoma
most are solitary fat containing lesions
which lobe are hepatic adenomas usually present in
the right lobe
what are the symptoms of hepatic adenoma
symptoms (pain bleeding) are size related
what are multiple adenomas associated with
glycogen storage diseases
what does hepatic adenoma look like on imaging
us-filing defect
ct-diffuse arterial enhancement
MRI-hypo or hyper intesnse lesion
how do you treat adenomas
stop hormones if that is what is causing them
observe
if no regression then surgical excision
what are the differences in adenoma and focal nodular hyperplasia
adenoma-purely a hepatocyte tumour but FNH-contains all the liver ultrastructure including RES and bile ductules
malignant degeneration in adenoma but no malignant risk in FNH
adenoma may cause pain and bleed
FNH-ay cause pain but minima bleeding risk
what are the 5 types of cystic lesions
simple, hydatid, atypical, polycystic lesion, pyogenic or amoebic abscess
simple cyst appears how
liquid collection lined by an epithelium
no biliary tree communication
how do simple cysts present
generally no symptoms but symptoms can be related to intracystic haemorrhage, infection, rupture, compression
is a simple cyst connected to biliary tree
no biiary tree communication, liquid collection of pus lined by an epithelium, solitary and unilocualted
how are simple cysts managed
no follow up necessary-if symptomatic or uncertain diagnosis then consider surgery
what is a hydatid cyst
echinoccocus granulosus
how can a hydatid cyst present
patients may present with disseminated disease or erosion of cysts into adjacent structure and vessels
how is a diagnosis of a hydatid cyst made
clinical diagnosis based on history appearance and serologic testing detection of anti-echinococcus antibodies
what is the most common form of treatment for a hydatid cyst
surgery or with albendazole or percutaneous drainage-PAIR but surgery is the most common
what is polycystic liver disease
numerous cysts throughout liver parenchyma due to embryonic ductal plate malformation of the intrahepatic biliary tree
what are the tHree types of PLD
von meyenburg complexes (VMC)
polycystic liver disease
autosomal dominant PLD
