HPB Flashcards
What are the screening questionnaires for alcohol consumption?
CAGE
AUDIT
What are the signs of alcoholic liver disease?
Jaundice + scleral jaundice Palmar erythema Hepatomegaly Spider naevi Caput medusa Flapping tremor (asterixis) Ascites Gynaecomastia Unexplained bruising
How is alcoholic liver disease diagnosed?
Careful history taking and examination
LFTs: Raised AST/ALT, normal/mild raised ALP, raised gamma gt, low albumin, raised bilirubin
Clotting: prolonged PT
USS abdo: may show enlarged/fatty liver in acute inflammation or small, sclerotic liver
CT abdomen
Liver biopsy
OGD can be done to look for varices
What is the management of alcoholic liver disease?
- Stop drinking / detox programme
- Calorie and nutrition support- incl thiamine
- Consider suitability for transplant
- Symptomatic treatment
What are the stages of alcohol withdrawal?
- 6-12 hrs: tremors, sweating, headache, cravings and anxiety
- 12-24 hrs: hallucinations and tactile disturbance - characteristically insects crawling
- 24-48hrs: seizures
- 48-36 hrs: delirium tremens
What is delirium tremens?
Alcohol withdrawal syndrome - 48-36hr into withdrawal
Downregulation of GABA, up regulation of glutamate -> brain excitability and adrenergic overactivity
Sx: confusion, agitation, delusions and hallucinations
tremor, ataxia, tachycardia, hyperthermia, arrhythmia
What classification system is used in alcohol withdrawal?
CIWA-AR tool
How should you manage acute alcohol withdrawal?
Benzodiazepine e.g. chlordiazepoxide (librium) titrated regimen
Thiamine: IV pabrinex followed by oral thiamine
Manage any seizures/other symptoms
What are the 3 features of Wernicke’s encephalopathy?
Confusion
Ataxia
Occulomotor disturbance
What are the three features of Korsakoff’s syndrome?
- Amnesia- anterograde and retrograde
- Confabulation
- Behavioural change: lack of insight, apathy
What are the causes of liver cirrhosis?
Common:
- Alcoholic liver disease
- Non-alcoholic steatohepatitis
- Chronic viral hepatitis
- Drug causes
Less common
- a1-antitripsin deficiency
- Wilson’s disease
- Haemochromatosis
- Primary biliary cirrhosis
- Autoimmune hepatitis
- Cystic fibrosis
Which drugs most commonly cause liver cirrhosis?
- Methotrexate
- Amiodarone
- Sodium valproate
- Chemotherapy agents
TPN is also associated with liver injury and fibrosis.
What are the signs of liver cirrhosis?
Palmar erythema Asterixis Jaundice Spider naevi, caput medusa Ascites and oedema Bruising and bleeding Pale stool and dark urine Splenomegaly Gynaecomastia
What investigations should be done in liver cirrhosis?
- LFTs: raised AST/ALT, raised ALP, low albumin, high bilirubin, ?gamma gt
- Coagulation: prolong PT
- AFP: marker for HCC
- U&E: can cause deranged urea and creatinine, hyponatraemia due to dilution
- Hepatitis viral screen and autoantibody testing
- USS abdomen and Fibroscan
- CT scan and biopsy
- Endoscopy looking for varies
Enhanced liver fibrosis blood test= new test, not available in all centres
What are the scoring systems for liver cirrhosis?
Child-Pugh score - indicated severity
MELD score- done 6 monthly in those with compensated cirrhosis to estimate mortality and need for transplant
How should patients with liver cirrhosis be managed?
Avoid alcohol!
- Vitamin and nutrition replacement - high protein, low sodium, vitamin supplements
- Coagulopathy management
- Diuretics for ascites
- BP control for hepatorenal syndrome
- Consideration for transplant
What are the complications of cirrhosis?
Ascites + SBP Portal hypertension Varices + variceal bleeding Hepatorenal syndrome Encephalopathy Bleeding/bruising Malnutrition HCC
What is the blood marker for HCC?
AFP
How are stable varices managed?
- Stop drinking if alcohol-related / abstain either way
- Propranolol to reduce BP
- Elective banding procedure
- TIPS procedure
How are unstable varices managed?
A-E
Bloods: FBC, U&E, LFT, CRP, coagulation, group and save
Resuscitation if necessary
Correct any coagulopathy
IV terlipressin + IV Abx
if stable enough for endoscopy- endoscopic banding
Sengstaken-Blakemore tube / balloon tamponade in less stable patients
How does ascites form?
Less albumin produced by the liver -> lower osmotic pull of the bloodstream
Fluid loss into extracellular space
Reduced blood volume -> reduced renal perfusion -> activation of RAAS
Fluid and sodium retention
How should ascites be managed?
- Low sodium diet
- Spironolactone
- Ascitic tap / drain
- > Sample should always be sent for analysis
- > for every litre of fluid drained, a certain amount of albumin should be given to the patient to prevent immediate recurrence.
What are the most common organisms causing SBP?
Ecoli
Klebsiella
Gram positive cocci
What are the symptoms of SBP?
May be asymptomatic Ascites Abdominal pain Fever Sepsis Ileus
How is SBP diagnosed?
Record all vital signs
Bloods: FBC, CRP, U&E, LFT, coagulation
Ascitic tap: send for MC&S, pH, glucose, protein, LDH
Full infection work-up
How is SBP managed?
IV antibiotics - usually cefotaxime
Ascitic drain - albumin replacement for each L of fluid drained
What is hepatorenal syndrome?
In portal hypertension, due to the increased blood volume in the portal system there is dilation of the vessels to cope with the increased pressure and pooling of blood.
This leads to reduced blood supply to the kidneys, activation of the RAAS as a result and renal vasoconstriction as a result.
This constriction with the addition of blood pooling elsewhere leads to reduced renal blood supply and reduced function as a result.
This is a fatal complication of cirrhosis if liver transplant is not obtained ASAP.
What is the cause of hepatic encephalopathy?
Increased ammonia in circulation due to reduced hepatic metabolism and increased collateral blood flow bypassing the liver. This ammonia is produced by intestinal bacteria and absorbed into circulation, crosses BBB to cause encephalopathy.
What are the symptoms of hepatic encephalopathy?
Flapping tremor
Reduced GCS
Confusion, change in behaviour/personality
How do you manage hepatic encephalopathy?
Laxatives to increase excretion of intestinal ammonia
Enemas
Oral rifampicin to kill bacteria and reduce ammonia production
Nutritional support
What can precipitate hepatic encephalopathy?
- Constipation
- Renal impairment
- Infection
- GI bleed
- Excess protein
How is non-alcoholic fatty liver disease diagnosed?
Often incidental
LFT derangement
Non-invasive liver screen: USS, hep B&C serology, autoantibodies, immunoglobulins, coeruloplasmin, a1 antitrypsin, ferritin + transferrin
-> rules out other causes of hepatic disease
Liver USS
Enhanced liver fibrosis test / NAFLD fibrosis score / fibroscan
What is the management for non-alcoholic fatty liver disease?
Weight loss and nutrition support
Stop smoking, control other RFs e.g. diabetes, BP, cholesterol
Alcohol avoidance
Vitamin E or pioglitazone for anti-oxidant/anti-fibrotic action
What is the inheritance pattern for a1-antitrypsin deficiency?
Autosomal recessive
How is hepatitis A diagnosed?
Symptom profile= N&V, anorexia, jaundice, cholestasis, hepatomegaly, fever
HAV IgM
What percentage of HBV and HCV become chronic infections?
HBV: 10%
HCV: 75%
What do each of the serology factors mean in HBV?
HBsAg, HBeAg, Anti-HBc, Anti-HBs, HBV DNA
HBsAG= presence of infection HBeAg= indication of viral replication and infectivity Anti-HBc= Current or past infection Anti-HBs= resolution of infection
What would you expect to see on serology in acute HBV infection?
- HBsAg +ve
- HBeAg +ve
- Anti-HbC IgM
- HBV DNA +ve
Raised ALT
What would you expect to see on serology in chronic HBV infection?
- HBsAg +ve
- HBeAg +ve or -ve
- Anti-HbC IgG
- HBV DNA +ve
Elevated ALT
What would you expect to see on serology in somebody who has recovered from HBV infection?
Anti-HBs
Anti-HBc IgG
Normal ALT
No Antigens or DNA
What would you expect to see on serology for somebody who has been vaccinated against HBV?
Anti-HBs
Normal ALT
No antigens or DNA
How is HBV managed?
- Testing for other BBVs, informing public health
- Reduce risk factors: stop smoking, alcohol abstinence
- Monitoring for complications: Fibroscan, USS
- Antivirals to slow progression (no cure)
- Transplant
How is HCV diagnosed?
Anti-HCV Ab = screening test
HCV RNA= diagnostic confirmation, viral load
How is HCV managed?
Direct-acting antivirals- 8-12 week course, curative in 90%
Screen for other BBVs, inform PHE
Reduce risk factors: stop smoking, drinking etc
Monitoring for complications: Fibroscan, USS
Transplant
What is the main complication of chronic hepatitis?
Hepatocellular carcinoma
When should you worry about HEV?
In pregnant women or immunocompromised -> can cause chronic hepatitis and liver failure in these populations
What are the two types of autoimmune hepatitis?
Type 1: most common affects women in 40-50s (around menopause) with fatigue and liver dysfunction
Associated with ANA, anti-smooth muscle and anti-soluble liver antigen
Type 2: most commonly affects teenagers/early 20s, causes acute hepatitis, raised enzymes & jaundice
Associated with anti-liver antibodies
How is autoimmune hepatitis diagnosed and managed?
- Liver biopsy + antibody testing
2. Managed using high-dose prednisolone (tapering), azathioprine and transplant in end-stage disease
What are the symptoms of haemochromatosis?
Fatigue, Joint pain, Hair loss
Bronze/grey pigmentation
Mood/memory disturbance
Amenorrhoea, erectile dysfunction
What is the inheritance pattern of haemochromatosis?
Autosomal recessive
How is haemochromatosis diagnosed?
Serum ferritin ^ Serum transferrin saturation ^ Genetic testing Liver biopsy with PERL'S STAIN- show's parenchymal iron concentration CT abdomen
What is the treatment for haemochromatosis?
- Weekly venesection and serum iron monitoring
- Genetic counselling
- Monitor for complication e.g. liver cirrhosis and avoid alcohol
What are the complications of haemochromatosis?
Liver cirrhosis T1DM Endocrine disturbance e.g. DI HCC Cardiomyopathy Hypothyroidism
What is the inheritance pattern for Wilson’s disease?
Autosomal recessive
What are the features of Wilson’s disease?
Chronic hepatitis and liver cirrhosis
Neurological: dysarthria, dystonia, Parkinsonism
Psych: depression -> psychosis (wide spectrum)
Haemolytic anaemia
Renal tubular acidosis
Osteopenia
Kayser-Fleischer rings in the eyes
How is Wilson’s disease diagnosed?
Liver biopsy for copper content= gold standard
Serum caeruloplasmin = low (protein carrying copper)
Serum copper
Genetic testing
How is Wilson’s disease managed?
Copper chelation: penicillamine
What is primary biliary cirrhosis?
Where the immune system attacks the small bile ducts, leading to cholestasis, fibrosis and cirrhosis of the ductal system. This leads to build-up of bile acids and cholesterol in the blood -> jaundice + xanthelasma
This is associated with other autoimmune and rheumatological conditions
What are the symptoms of primary biliary cirrhosis?
RUQ pain Jaundice Fatigue Steatorrhoea + dark urine, itching Xanthelasma, xanthomata Signs of cirrhosis
How is primary biliary cirrhosis diagnosed?
LFTs: ALP raises first due to obstruction, followed by ALT/AST due to liver fibrosis + bilirubin due to reduced liver function.
Autoantibody tests: anti-mitochondrial antibodies, ANA in some
ESR + IgM
Liver biopsy for diagnosis and staging
What is the antibody most associated with primary biliary cirrhosis?
Anti-mitochondrial antibody
How is primary biliary cirrhosis managed?
- Ursedoxycholic acid to decrease intestinal cholesterol absorption
- Cholestyramine to prevent bile acid absorption
- Transplant in end-stage disease
- Steroids used in some
What are the indications for liver transplant?
- Acute liver failure - most commonly paracetamol OD
- Chronic liver failure and cirrhosis
- Hepatocellular carcinoma
Contraindications:
Alcohol, significant comorbidity, malnutrition, active infection, end-stage HIV
What condition is most commonly associated with primary sclerosing cholangitis?
Ulcerative colitis
What is primary sclerosing cholangitis?
Stricturing and fibrosis of the intra/extrahepatic ducts -> obstruction of bile flow
Chronic obstruction -> hepatitis, fibrosis, cirrhosis
What is the triad of symptoms for primary sclerosing cholangitis?
RUQ pain
Jaundice
Pruritus
How is primary sclerosing cholangitis diagnosed?
- LFTs: Cholestatic pictire
- Autoantibodies: p-ANCA and ANA
- MRCP - gold standard test
How is primary sclerosing cholangitis managed?
ERCP to dilate and stent ducts
Cholestyramine to reduce bile acid absorption
Vitamin supplementation
Monitor complications - key = cholangiocarcinoma
Transplant can be curative
What are the risk factors for HCC?
Alcoholic Liver Disease
Chronic hepatitis
Non-alcoholic fatty liver disease
Liver cirrhosis of different aetiology
What are the symptoms of HCC?
Often asymptomatic / normal symptoms of liver disease
RUQ pain, jaundice, ascites, nausea, pruritus
Weight loss, malaise
How is HCC diagnosed?
AFP = serum marker
LFTs
USS liver
CT scan and liver biopsy
How is HCC treated?
Resection if extremely localised
Liver transplant if confined to liver
Chemo/radiotherapy
Kinase inhibitor can prolong survival
What is the main risk factor for cholangiocarcinoma?
Primary sclerosing cholangitis
What are the symptoms of cholangiocarcinoma?
Often asymptomatic until quite advanced
Painless jaundice- like pancreatic cancer
Weight loss, fatigue, night sweats
How is cholangiocarcinoma diagnosed?
CA19-9 = blood marker LFTs USS CT scan ERCP to take brushings/biopsy
How is cholangiocarcinoma managed?
Surgical resection if small and localised
Chemo/radiotherapy - resistant disease, poor prognosis
ERCP stenting of the bile ducts
What are the key risk factors for gallstones?
Female
Fat
Fair
Forty
What are the symptoms of gallstones?
May be asymptomatic and incidentally found
Biliary colic if temporary obstruction - RUQ/epigastric pain, triggered by meals (esp fatty ones)
May be associated with nausea and vomiting
How are gallstones diagnosed?
LFT derangement
USS abdo- first line: may see individual stones / dilation of ducts or gallbladder
MRCP if suggestive sx but not seen on USS
ERCP can be used in both diagnosis and management
How are gallstones managed?
- If asymptomatic, no management required
- ERCP removal of stones
- Cholecystectomy
What is post-cholecystectomy syndrome?
Syndrome of diarrhoea, indigestion, abdominal pain, nausea, flatulence and intolerance of fatty food
Occurs after cholecystectomy due to changes in bile flow
Settles with time, no treatment needed- only symptomatic help
What are the symptoms of acute cholecystitis?
RUQ pain -> may be referred to R shoulder
Fever, tachycardia, tachypnoea
Nausea and vomiting
What are the signs of acute cholecystitis on examination?
^ RR, HR, temp
RUQ tenderness and guarding
Murphy’s sign +ve - pain on inspiration
Peritonism in severe disease
How would you investigate acute cholecystitis?
A-E assessment
Bloods: FBC, U&E, LFT, CRP, lipase,
USS abdo: thickened wall, stones / sludge in the gallbladder, fluid around the gallbladder
MRCP
How to manage acute cholecystitis?
A-E Make NBM and get IV access NG tube if vomiting IV fluids, analgesia and antibiotics ERCP to remove stones Cholecystectomy: performed within 72 hours or may be delayed until inflammation resolves (6-8 w)
What are the main causes of ascending cholangitis?
Gallstones
ERCP
What are the most common causative organisms in ascending cholangitis?
E-coli
Klebsiella
Enterococci
What are the symptoms of ascending cholangitis?
Charcot’s triad:
Fever, RUQ pain, Jaundice
How is ascending cholangitis diagnosed?
Symptom profile
Bloods: Raised WCC and CRP, obstructive liver picture
Blood cultures
USS -> CT -> MRCP
ERCP actually most sensitive but also most invasive
How is ascending cholangitis managed?
A-E Make NBM and get IV access NG tube if vomiting IV fluids, analgesia, antibiotics ERCP to remove any stones / stent ducts
What are the causes of pancreatitis?
Idiopathic Gallstones Ethanol Trauma Steroids Mumps Autoimmune Scorpion sting Hypercalcaemia, hyperlipidaemia ERCP Drugs
What are the common drugs causing pancreatitis?
Thiazide diuretics Furosemide Amiodarone Propofol Azathioprine
What are the symptoms of pancreatitis?
Epigastric pain radiating to the back, better when leant forwards
Nausea and vomiting
Fever, ^HR, RR
Epigastric tenderness and guarding
What is the severity scoring for pancreatitis?
GLASGOW score- PANCREAS PaO2 Age Nutrophils Calcium levels R uRea Enzymes: LDH, liver enzymes, lipase Albumin Sugar
0-1= mild
2=moderate
3+= severe
How is pancreatitis diagnosed?
- Raised WBC, CRP, serum lipase/amylase
ABG, LFT, calcium, U&E, blood cultures - USS
- CT abdomen
How is pancreatitis managed?
A-E
IV access: fluids, antibiotics, analgesia
NBM if vomiting, feed asap to prevent malnutrition (may need enteral feed)
Manage cause e.g. ERCP for stones, stop causative medication
Most Improve in 3-7 days
What are the complications of acute pancreatitis?
Pseudocyst formation Abscess formation Perforation Sepsis Chronic pancreatitis Pancreatic necrosis
What are the complications of acute pancreatitis?
Pseudocyst formation Abscess formation Perforation Sepsis Chronic pancreatitis Pancreatic necrosis
What is the most common cause of chronic pancreatitis?
Alcohol excess
What are the symptoms of chronic pancreatitis?
Chronic epigastric pain Steatorrhoea Diabetes features Malnutrition Recurrent episodes of acute pancreatitis
How is chronic pancreatitis managed?
Stop alcohol and smoking Pancreatic enzyme supplements + nutrition support Analgesia ERCP and stunting of ducts Surgical removal of necrotic pancreas
What are the symptoms of pancreatic cancer?
Painless jaundice
Dark urine, pale stool, itch
Nausea and vomiting
Weight loss, night sweats, fatigue
How is pancreatic cancer diagnosed?
CA 19-9
USS/MRCP
ERCP and biopsy
CT scan staging
How is pancreatic cancer managed?
MDT discussion
Surgical removal of tumour if small/localised
-> Whipple’s procedure for pancreatic head tumour: removal of head, bile ducts, duodenum, pylorus, gallbladder, lymph nodes,
Chemo/radiotherapy
Palliative stenting
