Biliary/Liver Flashcards
Pre-hepatic causes of jaundice (2)
Haemolytic anaemia
Gilberts
Post-hepatic causes of jaundice (2)
Gallstones
Obstructing cancer: head of pancreas, CBD
Hepatic causes of jaundice (5)
Viral hepatitis Alcoholic hepatitis NAFLD AIH Genetic hepatitis
Features of post hepatic jaundice
Pale stools
Dark urine
Features of haemolytic anaemia (4)
HA: low Hb, raised bilirubin, low haptoglobins, raised lactate
Normal urine – unconjugated bilirubin is insoluble in water
Causes of chronic liver disease (5)
Viral hepatitis Alcoholic hepatitis NAFLD AIH Genetic hepatitis
Which hepatic virus’ are chronic
BCD but C is more likely to become chronic
What is the typical population of AIH
Look for fat young women who are cushingoid post tx
Congenital causes of chronic liver disease and what is their inheritance pattern (3)
A1AT, Wilsons, hereditary haemochromatosis
All are autosomal recessive
AI causes of liver disease
AIH, PSC, PBC
Hepatitis A:
Transmission route
Infection length
Symptoms (6)
Oro-anal sex; faeco-oral spread Acute (around 8 weeks) asymptomatic (usually) but can have: Nausea Vomiting (+ Diarrhoea) Fever Jaundice Abdominal pain (particularly RUQ)
Hepatitis B:
Transmission route
Infection length
Symptoms
Blood, Semen, Vertically
Most adults clear it
Hepatitis C:
Transmission route
Only through blood (e.g. drugs or tattoos)
Which hepatic virus can cause HCC
HCV/HBV
Which hepatic virus can only connect with another
D can only co-infect with B
Which hepatic virus is a particular problem for pregnant women
HEV
Which group of patients are particularly at risk of HEV
Pregnant women and immunocompromised
Length of infection of HBV and HCV and difference in adults and children
B adults mostly clear, children stay as carriers
C adults mostly stay as carriers and children clear
Incubation period of HAV
2 weeks
Incubation period of HBV
4-12 weeks
Incubation period of HCV
2 weeks - 6 months
Incubation period of HDV
4-12 weeks
Incubation period of HEV
5-6 weeks
All viral hepatitis’ can cause acute hepatitis with transaminitis in 1000s except…..
Hepatitis B which is mostly cleared by adults
What is the triad for viral hepatitis
(Fever) + Jaundice + Raised AST/ALT (in the 1000’s)
Where is HAV endemic to
Africa/Asia
Where is HBV endemic to
Africa
Where is HCV endemic to
Eastern Mediterranean
Where is HDV endemic to
Africa
Where is HEV endemic to
Poor water supply (India, most third world areas…)
Which is chronic and which is acute IgG and IgM
IgM MAN that’s acute!
IgG Chronic
What does HbsAg mean
HBV is here/around NOW
Negative if been cleared/past vaccine
Positive in acute/chronic infection
What does HbeAg
mean
Infective
What does Anti-HbS
mean
Immune Past clearance (ie got it in past, cleared it, ‘natural immunity’
What does Anti-Hbc
mean
Caught in the past
Positive if natural immunity and cleared
Mx of HAV
A: supportive care
Mx of HBV
B: supportive care for acute, antivirals +peg⍺-interferon for chronic.
Mx of HCV
C: supportive care for acute, direct acting antivirals for chronic.
Elbasvir/glecaprevir
Ritonvair + ribavirin
Which hepatic viruses can have serious complications and what are they
HBV HCV
HCC and cirrhosis
What are causes of transaminitis in the 1000’s (3)
Paracetamol overdose
Acute viral hepatitis (not B)
‘Ischaemic hit’
What does a raised GGT and ALP suggest
Cholestatic/obstructive picture, biliary damage GGT (EtOH)
What does a raised AST:ALT in a 2:1 ratio suggest
alcoholic hepatitis
What does low urea suggest
severe liver disease, (synthesised in liver), malnutrition, pregnancy
What does low albumin suggest
poor synthetic function of liver
What does a raised urea over 10 suggest (2)
UGIB (or large protein meal)
Dehydration/AKI (urea excreted renally)
What LFT pattern suggests:
paracetamol OD
Transaminitis in the 1000s
What LFT pattern suggests:
ischaemic hit
Transaminitis in the 1000s
What LFT pattern suggests:
viral hepatitis
Transaminitis in the 1000s
What LFT pattern suggests:
Cholestatic/obstructive picture
Raised GGT and ALP
What LFT pattern suggests: biliary damage (EtOH)
Raised GGT and ALP
What LFT pattern suggests:
alcoholic hepatitis
AST:ALT 2:1
What LFT pattern suggests:
poor synthetic function of liver
Low albumin
What LFT pattern suggests:
severe liver disease
Low urea
What LFT pattern suggests:
malnutrition
Low urea
What LFT pattern suggests:
pregnancy
Low urea
What LFT pattern suggests:
UGIB (or large protein meal)
Raised urea (>10)
What LFT pattern suggests:
Dehydration/AKI
Raised urea (>10)
Typical NASH patient
Old fat man (metabolic syndrome)
Ix for NASH (4)
Elevated fasting triglycerides, low HDL
High ALT/AST
Incidental liver USS = Steatosis
RF for NAHS (6)
Obesity Type 2 diabetes mellitus Hypertension Hypercholesterolaemia Age > 50 yrs Smoking
Symptoms of NASH (5)
Usually found as an incidental finding Occasional symptoms include: Dull or aching RUQ pain Fatigue Unexplained weight loss Weakness Symptoms of cirrhosis will be experienced in the most advanced stages of NASH
3 main signs of cirrhosis (3)
E.g. jaundice, ascites, pruritus
Mx of NASH (7)
Conservative - controlling risk factors: Blood pressure Diabetes Cholesterol Lose weight Stop smoking Exercise regularly Reduce alcohol consumption (although it is NOT caused by excessive alcohol, drinking can make it worse)
Complications of NASH (6)
Cirrhosis Ascites Oesophageal varices Hepatic encephalopathy Hepatocellular carcinoma End-stage liver failure
3 forms of liver disease caused by alcohol
Alcoholic fatty liver (steatosis)
Alcoholic hepatitis
Chronic cirrhosis
Mild symptoms of alcoholic hepatitis (4)
Nausea
Malaise
Epigastric pain
Right hypochondrial pain Low-grade fever
More severe symptoms of alcoholic hepatitis (4)
Jaundice
Abdominal discomfort or swelling
Swollen ankles
GI bleeding
How long do you need to be drinking to get alcoholic hepatitis
a long history of heavy drinkingis required for the development of alcoholic hepatitis (around 15-20 years)
here may be events that trigger the disease (e.g. aspiration pneumonia, injury)
Signs of alcohol excess (10)
Malnourished Palmar erythema Dupuytren's contracture Facial telangiectasia Parotid enlargement Spider naevi Gynaecomastia Testicular atrophy Hepatomegaly Easy bruising
Signs of severe alcoholic hepatitis (8)
Febrile (in 50% of patients) Tachycardia Jaundice Bruising Encephalopathy (e.g. liver flap, drowsiness, disorientation) Ascites Hepatomegaly Splenomegaly
FBC in alcoholic hepatitis (4)
Low Hb
High MCV
High WCC
Low platelets
LFTs of alcoholic hepatitis (4)
High AST + ALT
High bilirubin
High ALP + GGT
Low albumin
U&E’s in alcoholic hepatitis (2)
Urea and K+ tend to be low
What is a sensitive marker for significant liver damage
Prolonged PT/high INR
What is seen in the main Ix of EtOH related cirrhosis (5)
Low albumin, low platelet, high INR (prothrombin time), USS splenomegaly, ascetic fluid (portal HTN)
Ix for alcoholic hepatitis (8)
FBC LFT U&E's PT/INR US Liver biopsy EEG Upper GI endoscopy
Mx of acute alcoholic hepatitis
Acute
Thiamine
Vitamin C and other multivitamins (can be given asPabrinex)
Monitor and correct K+, Mg2+ and glucose
Ensure adequate urine output
Treat encephalopathy with oral lactulose or phosphate enemas
Ascites - manage with diuretics(spironolactone with/without furosemide) Therapeutic paracentesis
Glypressin and N-acetylcysteine for hepatorenal syndrome
• Nutrition
Via oral or NG feeding is important
Protein restrictionshould be avoided unless the patient is encephalopathic
Nutritional supplementation and vitamins (B group, thiamine and folic acid) should be started parenterally initially, and continued orally
Steroid Therapy - reduce short-term mortality for severe alcoholic hepatitis
How do you treat encephalopathy (2)
oral lactulose or phosphate enemas
Complications of alcoholic hepatitis (3)
Acute liver decompensation
Hepatorenal syndrome
Cirrhosis
What is a very good test for cirrhosis
Albumin and prothrombin time will definitely be abnormal in cirrhosis because these are markers of of the hepatic synthetic function which is less affected by fat build up than fibrosis.
Complications of cirrhosis (4)
portosystemic encephalopathy, hepatorenal and hepatopulmonary syndrome.
Development of hepatocellular carcinoma.
What is the pathology and inheritance behind Wilson’s disease
Impaired excretion of copper from liver via bile through copper transporter, autosomal recessive
Where does Cu accumulate in Wilsons disease and what does that cause (3)
Liver: CLD
Basal ganglia: early onset neuropsychiatric sx/Parkinsonism
Cornea: Keyser Fleischer rings
Mx of Wilson’s disease
penicillamine to chelate Cu
Ix for Wilson’s disease (3)
LOW serum caereuloplasmin
High urinary copper
LOW serum Cu (paradoxical) – not reliable
Age of onset of Wilson’s disease and difference in presentation between children and adults
10-25 years
children present with liver disease, adults present with neurological disease
Symptoms of Wilson’s disease (10)
Liver: Hepatitis, cirrhosis
Neurological: Basal ganglia degeneration,speech and behaviour problems , asterixis, chorea, dementia
Kayser-Fleischer rings
Renal tubular acidosis - fanconi syndrome
Haemolysis
Blue nails
What is the issue with haemochromatosis and pattern of inheritance (2)
dysregulated increased dietary iron absorption and increased iron release from macrophages.
autosomal recessive
Where is iron deposited in haemochromatosis (6)
Deposits in liver, pancreas, skin, joints, heart and pituitary gland
Haematinics of haemochromatosis
Transferrin LOW
High transferrin saturation
Serum Ferritin HIGH (storage)
TIBC LOW
Describe iron metabolism
Iron absorbed in duodenum where it is stored intracellullarly bound to ferritin or transported out of the cells by ferroportin, a transmembrane protein
Ferroportin then binds to transferrin in the blood
Hepcidin is a protein that inhibit ferroportin, thereby regulating the amount of iron entering the blood
Age of onset of haemochromatosis
40-60
Early symptoms of haemochromatosis (6)
Fatigue, arthralgias, weakness, arthropathy, ED, heart problems (vague)
Late symptoms of haemochromatosis (7)
Diabetes, bronzed skin, hepatomegaly, arrhythmias, cardiomyopathy, neuro/psych problems
Cirrhosis
Which Ab are positive in AIH (2)
AIH: anti smooth muscle antibodies, and sometimes anti-liver kidney microsomal antibodies
Common population of AIH
Consider in young fat women on lots of steroid
Clusters with other autoimmune conditions
What does pituitary deposits of Cu cause
loss of libido, sexual dysfunction
Which gallbladder disease has a triad and what is it
Cholangitis
RUQ pain
Fever
Jaundice
What are the main symptoms of biliary colic
RUQ pain
What are the main symptoms of acute cholecystitis
RUQ pain and fever
What are the main symptoms of cholangitis
RUQ pain
Fever
Jaundice
Ix for gallbladder disease (3)
LFT 1st line, Abdo USS (gold-standard, Dx), then consider MRCP
What is Boas signs
Pain radiating to the scapula in cholecystitis (can also be present in gallstones)
Which two signs together strongly indicate acute chollecystitis
Boas and Murphys
Mx of cholelithiasis
Cholecystectomy
Mx of choledocholithiasis
ERCP
Pathology of PBC
Intrahepatic bile duct granulomatous destruction by Abs
Pathology of PSC
Intra- and extrahepatic bile destruction
Biliary obstruction
Backpressure to liver cirrhosis
Typical patient in PBC (3)
Itchy middle aged females (F:M 9:1), fatigue (dry eyes, mouth)
Typical patient in PSC (population and age)
People with IBD – UC
40-50s
Main symptoms of PBC
Fatigue
Weight loss
Pruritis
What does PBC lead to (2)
cholestasis, and, ultimately, cirrhosis
Pathogenesis of PSC (6)
Periductalinflammationwith periductal concentricfibrosis (scarring) Portal oedema Bile duct proliferation Expansion of portal tracts Progressive fibrosis Development of biliary cirrhosis
Ix for PBC (2)
Anti mitochondrial m2 antibodies
Lipids also raised
Ix for PSC
MRCP: beads on a string
Associations in SBA’s of PBC (3)
Hypercholestrolaemia: tendon xanthomata, xanthelasma peri-ocular
Associations in SBA’s of PSC (2)
UC: most PSC patients have UC, most UC patients don’t have PSC
Cholangiocarcinoma (CBD cancer)
Age of pancreatic cancer
Peak incidence 65-75 years old.
Key symptoms of pancreatic cancer (7)
jaundice, non-specific abdo pain, FLAWS.
Also sudden onset DM
Ix for pancreatic cancer (4)
LFTs, Protocol CT scan
If unclear offer PET/CT or EUS
What is Courvoisiers law
a palpable gallbladder in the presence of painless jaundice is unlikely to be due to stones
Associations of HCC (6)
Chronic liver damage (EtOH liver disease, HepB/C, AI), metabolic disease, alpha-1 antitrypsin deficiency
Aflatoxin
Which fungal toxin causes HCC
Aflatoxin
Ix for HCC
urgent direct access ultrasound scan
LFT (marker of liver function: Albumin/Clotting – APPT/PT), alpha-fetoprotein (AFP) – tumour marker, hepatitis serology
Which tumour marker suggests HCC
AFP
What is the marker for pancreatic cancer
CA19-9
What is the marker for cholangiocarcinoma
CA19-9
What associations are with cholangiocarcinoma (2)
Ulcerative colitis + Primary sclerosing cholangitis
Which gender does liver cysts commonly affect
Women