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Hepato-pancreato-biliary Flashcards

1
Q

ALCOHOLIC LIVER DISEASE

What is the natural course of alcoholic liver disease?

A
  • Alcoholic fatty liver = build-up of fat in liver, reversible
  • Alcoholic hepatitis = longer-term alcohol or binge drinking leads to inflammation in liver, if mild reversible
  • Cirrhosis = liver replaced by scar tissue, irreversible but stopping prevents more
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2
Q

ALCOHOLIC LIVER DISEASE

What is the clinical presentation of alcoholic liver disease?

A
  • Jaundice + hepatomegaly
  • Spider naevi
  • Palmar erythema
  • Gynaecomastia
  • Bruising
  • Ascites
  • Caput medusae
  • Asterixis
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3
Q

ALCOHOLIC LIVER DISEASE

What investigations would you do in alcohol liver disease?

A
  • FBC (raised MCV), deranged clotting
  • LFTs
  • USS liver = fatty changes early (increased echogenicity)
  • Transient elastography (FibroScan) can check elasticity of liver to assess degree of cirrhosis
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4
Q

ALCOHOLIC LIVER DISEASE

What would the LFTs show in alcoholic liver disease?

A
  • AST/ALT ratio >2 (>3 suggestive of acute alcoholic hepatitis)
  • GGT elevated
  • Low albumin (reduced synthetic function)
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5
Q

ALCOHOLIC LIVER DISEASE

What is the management of alcoholic liver disease?

A
  • Stop drinking with ?detox regime, thiamine
  • Pred often used during acute episodes of alcoholic hepatitis
  • Referral for liver transplant in severe disease but abstain 3m before referral
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6
Q

LIVER CIRRHOSIS

What is liver cirrhosis?

A
  • Diffuse fibrosis + structural abnormality of the liver secondary to chronic inflammation
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7
Q

LIVER CIRRHOSIS

What are the common and rarer causes of liver cirrhosis?

A
  • Common = alcoholic liver disease, NAFLD, hepatitis B + C

- Rarer = A1AT, autoimmune hepatitis, PBC, haemochromatosis, Wilson’s, CF

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8
Q

LIVER CIRRHOSIS

What are the features of compensated liver cirrhosis?

A
  • Fatigue, anorexia

- Nausea, abdo pain

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9
Q

LIVER CIRRHOSIS

What are the features of decompensated liver cirrhosis?

A
  • Jaundice + hepatosplenomegaly
  • Spider naevi, palmar erythema
  • Gynaecomastia, ascites, caput medusae
  • Asterixis
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10
Q

LIVER CIRRHOSIS

What are some complications of liver cirrhosis?

A
  • Portal HTN + varices
  • Ascites + SBP
  • Hepatorenal syndrome
  • Malnutrition
  • Liver failure
  • HCC
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11
Q

LIVER CIRRHOSIS

What initial investigations would you consider in cirrhosis?

A
  • FBC = raised WCC ?infection, low platelets (chronic liver disease), anaemia
  • U&E for baseline renal function
  • INR + clotting (coagulopathy)
  • LFTs
  • Hepatitis + CMV serology, auto-antibodies, A1AT, iron studies, caeruloplasmin
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12
Q

LIVER CIRRHOSIS

What imaging might you consider to screen for cirrhosis?

A
  • Transient elastography if hep C, men >50units/w, women >35units/w or Dx alcohol-related liver disease (biopsy if not suitable)
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13
Q

LIVER CIRRHOSIS
What scoring system is used to assess the severity of cirrhosis?
What are the components to it?

A
  • Child-Pugh classification

- Albumin, bilirubin, PT/INR, presence of encephalopathy + presence of ascites

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14
Q

LIVER CIRRHOSIS

What is the management of liver cirrhosis?

A
  • USS liver + serum AFP every 6m to monitor for HCC
  • Endoscopy if new cirrhosis Dx to look for varices
  • Ultimate treatment = liver transplant
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15
Q

ACUTE LIVER FAILURE

What is acute liver failure and how is it sub-divided?

A
  • Rapid onset of liver dysfunction

- Hyperacute ≤7d, acute 8–21d, subacute >21d–26w

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16
Q

ACUTE LIVER FAILURE

What are some causes of acute liver failure?

A
  • Paracetamol overdose, alcohol
  • Hepatitis A/B/E, CMV
  • Acute fatty liver of pregnancy, NAFLD, autoimmune hepatitis, Wilson’s
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17
Q

ACUTE LIVER FAILURE

What is the clinical presentation of acute liver failure?

A
  • Triad = encephalopathy, jaundice + coagulopathy (raised INR/PT)
  • Hypoalbuminaemia > ascites
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18
Q

ACUTE LIVER FAILURE

What investigations would you do in acute liver failure?

A
  • FBC, U&E, CRP, LFT (albumin), clotting

- Investigate cause (e.g., paracetamol levels, peritoneal tap, abdominal USS)

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19
Q

ACUTE LIVER FAILURE

What are some complications of acute liver failure?

A
  • Most common = infection
  • Bleeding = may need vitamin K and FFP
  • Hepatic encephalopathy
  • Hepatorenal syndrome
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20
Q

ACUTE LIVER FAILURE

What is the pathophysiology of hepatic encephalopathy and how does it present?

A
  • Ammonia accumulates in the circulation, crosses BBB > cerebral oedema
  • 4 stages = altered mood/behaviour > drowsiness, confusion > asterixis > coma
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21
Q

ACUTE LIVER FAILURE

What is the management of hepatic encephalopathy?

A
  • First = lactulose (encourages nitrogenous waste loss through bowels)
  • Second = rifaximin
  • IV mannitol to reduce cerebral oedema
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22
Q

ACUTE LIVER FAILURE

What is the management of hepatorenal syndrome?

A
  • May need haemofiltration

- If need fluid resus, use human albumin solution

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23
Q

ACUTE LIVER FAILURE

What is the management of acute liver failure and the criteria?

A
  • Treat underlying
  • Liver transplantation based on King’s College Hospital criteria > paracetamol = arterial pH <7.3 after 24h, non-paracetamol = PT >100s
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24
Q

ASCITES
What is ascites?
How are the causes grouped?

A
  • Abnormal accumulation of fluid in the abdomen

- Serum-ascites albumin gradient (SAAG) from ascitic tap either >11g/L (indicates portal HTN) or <11g/L

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25
ASCITES | What are some causes of ascites with a SAAG >11g/L?
- Liver disease #1 = cirrhosis, alcoholic liver disease, acute liver failure, liver mets - Cardiac = RHF, constrictive pericarditis - Other = Budd-Chiari syndrome (hepatic vein thrombosis), portal vein thrombosis
26
ASCITES | What are some causes of ascites with a SAAG <11g/L?
- Hypoalbuminaemia = nephrotic syndrome, severe malnutrition (Kwashiorkor) - Malignancy/infections = peritoneal cancer, TB - Other = pancreatitis, bowel obstruction
27
``` ASCITES What is a key complication of ascites? What is a common cause of it? How does it present? How is it diagnosed? ```
- Spontaneous bacterial peritonitis - E. Coli - Ascites, abdominal pain + fever - Paracentesis = neutrophil count >250 cells/uL
28
ASCITES | What is the management of spontaneous bacterial peritonitis?
- IV cefotaxime | - Prophylaxis with PO ciprofloxacin or norfloxacin if previous SBP or cirrhosis + ascites protein ≤15g/L until resolved
29
ASCITES | What is the conservative and medical management of ascites?
- Reduce dietary salt + fluid restrict if Na <125mmol/L | - Aldosterone antagonists e.g., spironolactone ± adjuvant loop diuretic
30
ASCITES What is the management of tense ascites? What is a potential complication and how this is managed?
- Therapeutic abdominal paracentesis - Large-volume >5L can lead to paracentesis-induced circulatory dysfunction > ascites recurrence, hepatorenal syndrome, dilutional low Na+ and mortality - Cover with IV human albumin solution
31
ASCITES | What surgical intervention may be considered in ascites?
- Transjugular intrahepatic portosystemic shunt (TIPS)
32
PORTAL HYPERTENSION | How are the causes of portal hypertension classified?
- Pre-hepatic = portal vein thrombosis - Hepatic = cirrhosis #1 UK, schistosomiasis #1 worldwide - Post-hepatic = Budd-Chiari syndrome
33
PORTAL HYPERTENSION | What is Budd-Chiari syndrome?
- Hepatic vein obstruction usually secondary to haem disorder like thrombophilia, polycythaemia
34
PORTAL HYPERTENSION How does Budd-Chiari syndrome present? How is it investigated? How is it managed?
- Abdo pain (acute severe), ascites + tender hepatomegaly - USS with doppler flow studies - Anticoagulants
35
PORTAL HYPERTENSION | What are the clinical features of portal hypertension?
SAVE – - Splenomegaly (decreased WCC + platelets) - Ascites - Varices - Encephalopathy
36
PORTAL HYPERTENSION What are varices? Where do varices occur?
- Dilated veins at junction between portal/systemic circulation due to diversion of blood from increased pressure - Distal oesophagus (UGI bleed), proximal stomach (Caput Medusae)
37
NAFLD | What is the pathophysiology of non-alcoholic fatty liver disease (NAFLD)?
- Thought to represent hepatic manifestation of metabolic syndrome + hence insulin resistance (T2DM) thought to be key mechanism
38
NAFLD | What is the spectrum of disease seen in NAFLD?
- Steatosis = fat in liver - Steatohepatitis = fat with inflammation - Progressive disease > fibrosis + liver cirrhosis
39
NAFLD | What are some associated factors with NAFLD?
- CVD risk factors = obesity, T2DM, high cholesterol + smoking - Sudden weight loss/starvation
40
NAFLD How does NAFLD present? What initial investigations would you conduct?
- Asymptomatic, maybe hepatomegaly - LFT = ALT typically > AST - Non-invasive liver screen = hep B/C serology, autoAb, caeruloplasmin, A1AT, iron studies, USS liver (increased echogenicity)
41
NAFLD | After initial investigations, what other tests would you consider?
- Enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis on incidental NAFLD Dx - Transient elastography
42
NAFLD | What is the management of NAFLD?
- Mainstay of treatment is lifestyle changes, especially weight loss
43
VIRAL HEPATITIS Give an overview of hepatitis A How is it spread?
- RNA virus with 2–4w incubation period | - Faecal-oral, often from shellfish
44
VIRAL HEPATITIS How may hepatitis A present? Are there complications associated with hepatitis A?
- Flu-like prodrome, RUQ pain, tender hepatomegaly, cholestatic LFTs - Does NOT cause chronic disease or increase HCC risk
45
VIRAL HEPATITIS | What is the management of hepatitis A?
- Supportive | - Vaccination prophylaxis = MSM, IVDU, chronic liver disease, travellers
46
VIRAL HEPATITIS Give an overview of hepatitis B How is it spread? How may it present?
- Double-stranded DNA virus - Blood borne (IVDU, sex, vertical transmission) - Jaundice, fever, malaise
47
VIRAL HEPATITIS | What are the 4 main components to hepatitis B serology?
- Surface antigen = HBsAg - Surface antibodies = anti-HBs - Core antibodies = anti-HBc - E antigen = HBeAg
48
VIRAL HEPATITIS In terms of hepatitis B serology, what do the following show... i) HBsAg? ii) anti-HBs?
i) Ongoing infection + causes anti-HBs production, if present for >6m = chronic disease ii) Immunity (exposure OR vaccine) is –ve in chronic disease
49
VIRAL HEPATITIS In terms of hepatitis B serology, what do the following show... i) anti-HBc? ii) HBeAg?
i) Previous INFECTION, C = caught, not seen in vaccinated (IgM = acute/recent, IgG = persists after acute) ii) Breakdown of core antigen from infective liver cell + so marker of infectivity
50
VIRAL HEPATITIS In terms of hepatitis B serology, what would the following show... i) previous immunisation? ii) previous hep B >6m + not carrier? iii) chronic hep B infection?
i) Anti-HbS +ve, others –ve ii) Anti-HBc +ve, HBsAg –ve iii) Anti-HBc +ve, HBsAg +ve
51
VIRAL HEPATITIS | What are some complications with hepatitis B?
- Chronic hepatitis (ground-glass hepatocytes on light microscopy) - HCC - Polyarteritis nodosa
52
VIRAL HEPATITIS | What is the management of hepatitis B?
- Pegylated interferon first line - Anti-viral tenofovir second line - Vaccination with inactive HBsAg (occupational, childhood vaccines, IVDU)
53
VIRAL HEPATITIS Give an overview of hepatitis C How is it spread?
- RNA virus | - Blood borne (IVDU, vertical, sexual)
54
VIRAL HEPATITIS What are some complications of hepatitis C? What is the management of hepatitis C?
- 75% > chronic (HCV RNA in blood >6m) = cirrhosis, HCC, arthritis - Depends on viral genotype, usually combination of protease inhibitors like sofosbuvir ± ribavirin
55
VIRAL HEPATITIS Give an overview of hepatitis D How is it spread?
- Incomplete RNA virus which requires HBsAg to complete replication + transmission cycle - Blood + bodily fluids
56
VIRAL HEPATITIS What are some complications of hepatitis D? What is the management?
- Superinfection (HBsAg +ve > Hep D) associated with high risk of fulminant hepatitis, chronic hepatitis + cirrhosis - Complete prophylaxis if hep B vaccinated, interferon treatment
57
VIRAL HEPATITIS Give an overview of hepatitis E How is it spread? What are some features?
- RNA virus - Faecal-oral route - Like hep A but significant mortality in pregnancy, does NOT cause chronic disease or increased HCC risk
58
GALLSTONES What are gallstones made of? What are some risk factors?
- Majority mixed composition, some pure cholesterol | - Fat, Female, Forty, FHx, also Crohn's + haemolytic anaemia
59
GALLSTONES | What is the classic clinical presentation of gallstones?
- Biliary colic due to gallstone obstructing cystic duct leading to gallbladder contraction - Colicky RUQ pain - Worse postprandially, especially after fatty foods (CCK) - May radiate to R scapula, N+V
60
GALLSTONES | What important symptoms should be negative in simple biliary colic?
- No fever, murphy's sign and usually no jaundice | - If transient obstructive jaundice may have pale stools + dark urine
61
GALLSTONES | What investigations would you do in gallstones?
- LFTs = obstructive jaundice (raised ALP + bilirubin) | - Abdominal USS = acoustic shadow, dilated ducts >6mm, wall oedema
62
GALLSTONES | What is a key complication of gallstones?
- Gallstone ileus = gallstone erodes through gallbladder wall leading to gallbladder-small bowel (cholecystoenteric) fistula
63
GALLSTONES What is a consequence of gallstone ileus? How can it appear on XR?
- Large gallstone > fistula > trapped in narrow areas of small bowel > SBO (commonly terminal ileum around ileo-caecal valve) - Air in biliary tree (pneumobilia) + dilated small bowel
64
GALLSTONES | How do you manage gallstones?
- Expectant if asymptomatic | - Elective laparoscopic cholecystectomy if symptomatic
65
ACUTE CHOLECYSTITIS | What is acute cholecystitis?
- Gallbladder inflammation often secondary to gallstones (calculous) but can be acalculous (e.g., hospital/severely ill > gallbladder stasis, hypoperfusion, infection)
66
ACUTE CHOLECYSTITIS | What is the clinical presentation of acute cholecystitis?
- RUQ pain which may radiate to R scapula - Fever + systemically unwell - Murphy's sign = inspiratory arrest on palpation of RUQ (absent in LUQ)
67
ACUTE CHOLECYSTITIS | What investigations would you do in acute cholecystitis and what might they show?
- FBC (raised WCC), raised CRP, LFTs often normal - USS abdomen = first line choice - Magnetic resonance cholangiopancreatography (MRCP) if ?CBD stone
68
ACUTE CHOLECYSTITIS What are some complications of acute cholecystitis? How do you manage this?
- Sepsis, gangrenous gallbladder, perforation | - Gallbladder empyema = IV Abx + either cholecystectomy or cholecystostomy with drain insertion
69
ACUTE CHOLECYSTITIS | What is the management of acute cholecystitis?
- NBM - IV fluids - IV Abx - Early laparoscopic cholecystectomy <1w of Dx
70
ASCENDING CHOLANGITIS | What is the pathophysiology of ascending cholangitis?
- Bacterial infection of the biliary tree due to obstruction in the common bile duct causing biliary stasis allowing intestinal bacteria to migrate up via Ampulla of vater
71
ASCENDING CHOLANGITIS | What are the causes of infection and obstruction in ascending cholangitis?
- Infection = E. coli commonly, Klebsiella | - Obstruction = mostly gallstones, can be benign biliary strictures or malignancy
72
ASCENDING CHOLANGITIS | What is the clinical presentation of ascending cholangitis?
- Charcot's triad = RUQ, fever (+ rigors) + jaundice | - Reynold's pentad = above PLUS hypotension + confusion
73
ASCENDING CHOLANGITIS | What investigations would you do in ascending cholangitis?
- FBC (raised WCC), raised CRP - LFTs = cholestatic picture = raised ALP + bilirubin - USS abdomen first line - MRCP is most accurate for visualisation
74
ASCENDING CHOLANGITIS | What is the management of ascending cholangitis?
- IV Abx + endoscopic retrograde cholangiopancreatography (ERCP) after 24–48h to relieve any obstruction + biliary drainage
75
ACUTE PANCREATITIS What is the pathophysiology of acute pancreatitis? What are some causes?
``` - Autodigestion of pancreatic tissue by pancreatic enzymes > necrosis GET SMASHED – - Gallstones - Ethanol - Trauma - Steroids - Mumps - Autoimmune - Scorpion sting - Hyperlipidaemia, Hypercalcaemia, Hypothermia - ERCP - Drugs (azathioprine, mesalazine) ```
76
ACUTE PANCREATITIS | What is the clinical presentation of acute pancreatitis?
- Severe epigastric pain, radiates through to back, relieved by sitting forward - Vomiting common, low-grade fever - Signs = periumbilical (Cullen's) + flank bruising (Grey-Turner's), shock
77
ACUTE PANCREATITIS What initial investigations would you do in acute pancreatitis? How would you diagnose it?
- FBC (raised WCC), U&E, LFT, Ca2+, CRP, ABG, amylase | - Dx = characteristic pain + serum amylase/lipase >3x upper limit of normal
78
ACUTE PANCREATITIS What is significant about the degree of elevation of amylase? When is lipase more useful?
- Nothing – it's not related to severity of disease | - Longer half-life so may be useful for late presentations >24h
79
ACUTE PANCREATITIS | What imaging would you consider in acute pancreatitis?
- Early USS abdo to assess aetiology - ERCP/MRCP - CT abdomen if complications suspected
80
ACUTE PANCREATITIS How is the severity of acute pancreatitis measured? How do you manage this?
- Modified Glasgow criteria = PaO2 <8, >55y, WCC >15, Ca2+ <2, urea >16 etc. - ≥3 = ITU/HDU transfer for intensive monitoring
81
ACUTE PANCREATITIS | What are some complications of acute pancreatitis?
- ARDS - Peripancreatic fluid collections = most resolve but can develop pseudocysts/abscess - Pancreatic pseudocyst - Pancreatic necrosis, abscess + haemorrhage
82
ACUTE PANCREATITIS What is a pancreatic pseudocyst? How is it managed?
- Peripancreatic fluid collection with a fibrous wall (after 4w) - Observe for 12w as 50% resolve, if not cystogastrostomy or aspiration
83
ACUTE PANCREATITIS | What is the management of acute pancreatitis?
- ABCDE = aggressive IV fluids, anti-emetics, analgesia - Not routinely NBM unless vomiting but enteral nutrition if mod sev–severe (e.g., transient or persistent organ failure) - Do NOT offer prophylactic Abx - Treat underlying cause
84
CHRONIC PANCREATITIS | What is the pathophysiology of chronic pancreatitis?
- Chronic inflammation in the pancreas leading to fibrosis + reduced functioning + can affect both exocrine + endocrine functions of the pancreas
85
CHRONIC PANCREATITIS | What are the causes of chronic pancreatitis?
- Chronic alcohol excess = #1 - Genetic = CF, haemochromatosis - Ductal obstruction = tumours, stones
86
CHRONIC PANCREATITIS | What is the clinical presentation of chronic pancreatitis?
- Chronic epigastric pain, worse 15–30m following meal, sitting forward relieves - Exocrine dysfunction = malabsorption + steatorrhoea - Endocrine dysfunction = DM (often years after onset)
87
CHRONIC PANCREATITIS | What investigations would you do in chronic pancreatitis?
- AXR = may show pancreatic calcification but CT abdomen is more sensitive for this - Faecal elastase to assess exocrine function
88
CHRONIC PANCREATITIS | What are some complications of chronic pancreatitis?
- Formation of strictures, pseudocysts, abscesses + pancreatic cancer risk
89
CHRONIC PANCREATITIS | What is the management of chronic pancreatitis?
- Stop alcohol, analgesia, insulin if DM - ERCP with stenting if strictures + obstruction - Pancreatic enzyme supplementation (Creon)
90
PARACETAMOL OVERDOSE | What is the pathophysiology of paracetamol overdose?
- Metabolism of paracetamol results in build-up of toxic NAPQI - NAPQI is inactivated by glutathione but in overdose, stores are rapidly depleted meaning NAPQI is left un-metabolised causing liver + kidney damage
91
PARACETAMOL OVERDOSE What is the clinical presentation of paracetamol overdose? What are some risk factors for increased hepatotoxicity in paracetamol overdose?
- Varies from asymptomatic, N+V, abdo pain, jaundice + severe metabolic acidosis - P450 inducers (PC BRAS), malnourished, HIV, chronic (NOT acute) alcohol excess
92
PARACETAMOL OVERDOSE | What investigations would you do in paracetamol overdose?
- FBC, U&E, LFTs, clotting, VBG | - Paracetamol levels 4h after
93
PARACETAMOL OVERDOSE When would you consider using activated charcoal? What is the mechanism of action?
- Ingestion <1h | - Reduce drug absorption
94
PARACETAMOL OVERDOSE | What other treatment would you consider in paracetamol overdose and when would you use it?
- N-acetylcysteine (NAC) - Staggered overdose (tablets not all taken within 1h) or ingestion >15h - Nomogram shows above treatment line
95
PARACETAMOL OVERDOSE | What is associated with NAC and how do you manage this?
- Anaphylactoid reactions | - Not true anaphylaxis so stop transfusion temporarily + restart at slower rate
96
PARACETAMOL OVERDOSE | What might be require in severe paracetamol overdose and the indication for this?
- Liver transplantation | - Arterial pH <7.3 24h after ingestion
97
PANCREATIC CANCER What cancer type is commonly seen in pancreatic cancers? What is the difficulty with pancreatic cancers?
- Majority adenocarcinoma occurring at head of pancreas | - Diagnosed late as non-specific presentation + early spread to liver + lungs
98
PANCREATIC CANCER | What are some associations with pancreatic cancer?
- Increasing age, smoking, DM - Chronic pancreatitis - HNPCC, MEN
99
PANCREATIC CANCER | What is the clinical presentation of pancreatic cancer?
- Classically painless obstructive jaundice = pale stools, dark urine + pruritus - Loss of exocrine (steatorrhoea) + endocrine (DM) function - Weight loss
100
PANCREATIC CANCER | What 2 eponymous phrases are linked with pancreatic cancer?
- Courvoisier's law = painless obstructive jaundice + palpable gallbladder is unlikely to be due to gallstones - Trousseau's sign = migratory thrombophlebitis (paraneoplastic)
101
PANCREATIC CANCER | What investigations would you do in pancreatic cancer?
- LFTs (cholestatic), CA 19-9 (marker for monitoring) - USS abdomen - HR CT abdo/pelvis = investigation of choice > double-duct sign (simultaneous dilatation of CBD + pancreatic ducts)
102
PANCREATIC CANCER | What is the management of pancreatic cancer?
- <20% suitable for surgery > Whipple's resection (pancreaticoduodenectomy) if resectable lesion in head of pancreas + adjuvant chemo - ERCP with CBD stenting for palliation
103
LIVER CANCER | What are the two main types of primary liver cancer?
- Hepatocellular carcinoma (HCC #1) | - Cholangiocarcinoma (bile duct adenocarcinoma)
104
LIVER CANCER What are some causes of HCC? What are some risk factors?
- Cirrhosis, chronic hep B (#1 worldwide), chronic hep C (#1 Europe) - A1AT, haemochromatosis, Wilson's, alcohol, NAFLD, PBC
105
LIVER CANCER | What are some risk factors for cholangiocarcinoma?
- PSC (+ so ulcerative colitis) | - Liver flukes (parasitic infection)
106
LIVER CANCER | What is the clinical presentation of HCC?
- Pre-existing cirrhosis with mass discovered on screening USS
107
LIVER CANCER | What is the clinical presentation of cholangiocarcinoma?
- Painless obstructive jaundice (pale stools, dark urine, pruritus) - Palpable gallbladder (Courvoisier's law) - EXAM NOTE: pancreatic cancer is more common with these Sx
108
LIVER CANCER What investigations would you do in HCC? Any investigations you would avoid?
- AFP almost always raised, USS abdomen - CT/MRI imaging modalities of choice - Avoid biopsy as seeds tumour cells
109
LIVER CANCER | What investigations would you do in cholangiocarcinoma?
- LFTs = obstructive jaundice - CA 19-9, CEA and CA 125 often raised - CT/MRI + MRCP are imaging methods of choice
110
LIVER CANCER What is the management of... i) HCC? ii) cholangiocarcinoma?
i) Surgical resection mainstay, ?transplant | ii) Surgical resection, palliative ERCP stenting
111
HAEMOCHROMATOSIS | What is the pathophysiology of haemochromatosis?
- Autosomal recessive disorder of iron absorption + metabolism > iron accumulation + deposition due to mutations in HFE gene on chromosome 6
112
HAEMOCHROMATOSIS | What is the clinical presentation of haemochromatosis?
- Early = fatigue, ED + arthralgia (hands) - Bronze skin, T2DM, liver cirrhosis - Cardiac failure 2º to dilated cardiomyopathy
113
HAEMOCHROMATOSIS What investigation is useful for screening in the general population? What investigation is used on family members? What other investigations would you do and what would they show?
- Transferrin saturation - HFE mutation genetic testing - Iron studies = HIGH transferrin saturation + ferritin, LOW TIBC - Joint XR = chondrocalcinosis
114
HAEMOCHROMATOSIS | What are the reversible and irreversible complications of haemochromatosis?
- Reversible = cardiomyopathy, skin pigmentation | - Irreversible = liver cirrhosis + HCC, DM, arthropathy
115
HAEMOCHROMATOSIS What is the first line management of haemochromatosis and what are the treatment targets? What is the second line?
- Venesection (transferrin saturation <50% + serum ferritin conc <50ug/L - Desferrioxamine
116
WILSON'S DISEASE | What is the pathophysiology of Wilson's disease?
- Autosomal recessive disorder characterised by excessive copper deposition in tissues due to a defect in the ATP7B gene on chromosome 13
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WILSON'S DISEASE | What are some clinical features of Wilson's disease?
- Liver = hepatitis, cirrhosis - Neuro = dystonia, Parkinsonism (basal ganglia), psychosis, dementia - Kayser-Fleischer rings - Blue nails, renal tubular acidosis + haemolysis
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WILSON'S DISEASE What are Kayser-Fleischer rings? How do you assess them?
- Green-brown rings in periphery of iris | - Slit-lamp examination
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WILSON'S DISEASE What is the first line investigation of Wilson's disease? What other investigations would you do? What are the diagnostic investigations?
- Caeruloplasmin (low) - Reduced total SERUM copper, increased 24h URINARY copper excretion - Liver biopsy + genetic analysis for ATP7B gene
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WILSON'S DISEASE | What is the management of Wilson's disease?
- Penicillamine = first line copper chelation agent (also trientine) - Avoid high copper food = liver, nuts, chocolate
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A1AT DEFICIENCY | What is the pathophysiology of alpha 1 antitrypsin (A1AT) deficiency?
- Autosomal recessive disorder of deficiency of protease inhibitor alpha 1 antitrypsin which usually inhibits neutrophil elastase + protects tissues on chromosome 14
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A1AT DEFICIENCY | What is the clinical presentation of A1AT deficiency?
- Lungs = emphysema, most marked in lower lobes (young onset COPD) - Liver = cirrhosis + HCC, cholestasis in paeds
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A1AT DEFICIENCY | What investigations would you do in A1AT deficiency?
- Serum A1AT concentrations = diagnostic | - Spirometry = obstructive
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A1AT DEFICIENCY | What is the management of A1AT deficiency?
- Supportive = bronchodilators, physio, no smoking (exacerbates) - IV A1AT is expensive + not widely used - Surgery = consider lung volume reduction surgery or full transplantation
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PRIMARY BILIARY CHOLANGITIS | What is the pathophysiology of primary biliary cholangitis (PBC)?
- Autoimmune condition that results in interlobular bile duct damage from chronic inflammation leading to progressive cholestasis > cirrhosis
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PRIMARY BILIARY CHOLANGITIS | What are some conditions that PBC is associated with?
- Sjögren's = #1 - RA - Systemic sclerosis - Thyroid disease
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PRIMARY BILIARY CHOLANGITIS What is the clinical presentation of PBC? What are some specific features?
- Pruritus, cholestatic jaundice (pale stools, dark urine), xanthelasma - Rule of Ms = IgM, anti-Mitochondrial Ab (M2 subtype), Middle aged females
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PRIMARY BILIARY CHOLANGITIS | What investigations would you do in PBC?
- LFTs = raised ALP, GGT | - USS abdomen or MRCP for Dx
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PRIMARY BILIARY CHOLANGITIS | What are some potential complications of PBC?
- Cirrhosis > portal HTN > ascites, variceal haemorrhage - Osteomalacia + osteoporosis - HCC
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PRIMARY BILIARY CHOLANGITIS | What is the management of PBC?
- First line = ursodeoxycholic acid to slow disease progression + improve Sx - Pruritus = cholestyramine - Vitamin supplementation fat soluble ADEK - Liver transplant in bilirubin >100
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PRIMARY SCLEROSING CHOLANGITIS What is the pathophysiology of primary sclerosing cholangitis (PSC)? What conditions are associated with PSC?
- Inflammation + fibrosis of intra and extra-hepatic bile ducts > biliary strictures - Majority of patients with PSC have UC, also HIV
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PRIMARY SCLEROSING CHOLANGITIS | What is the clinical presentation of PSC?
- RUQ pain - Hepatomegaly - Fatigue - Cholestasis (jaundice, pruritus, pale stools)
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PRIMARY SCLEROSING CHOLANGITIS What are some investigations in PSC? What is the diagnostic investigation?
- LFTs = cholestasis (raised bilirubin + ALP) - p-ANCA + ANA Ab may be positive - ERCP/MRCP is diagnostic = multiple beaded biliary strictures
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PRIMARY SCLEROSING CHOLANGITIS | What are two key complications of PSC?
- Cholangiocarcinoma | - Colorectal cancer
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PRIMARY SCLEROSING CHOLANGITIS | What is the management of PSC?
- Avoid alcohol - Pruritus = cholestyramine - Fat soluble ADEK vitamins - Dilate strictures via ERCP - ?Liver transplantation
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AUTOIMMUNE HEPATITIS | What are the three types of autoimmune hepatitis?
- I = anti-smooth muscle Ab ± anti-nuclear Ab, adults + paeds - II = anti-liver/kidney microsomal type 1 (LKM1) Ab, paeds - III = soluble liver-kidney antigen, middle-aged adults
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AUTOIMMUNE HEPATITIS | What is the clinical presentation of autoimmune hepatitis and who is commonly affected?
- Young females, PMHx of other autoimmune disorders | - Jaundice, hepatosplenomegaly + abdominal pain
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AUTOIMMUNE HEPATITIS | What investigations might you do in autoimmune hepatitis?
- LFTs = hepatic > raised ALT + bilirubin, normal/mildly raised ALP - ANA/SMA/LKM1 Ab + raised IgG levels - Liver biopsy = diagnostic
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AUTOIMMUNE HEPATITIS | What is the management of autoimmune hepatitis?
- Immunosuppressants (e.g., prednisolone, azathioprine) | - Liver transplantation
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LIVER ABSCESS What are the most common causes of liver abscesses in paeds and adults? What is a cause seen in foreign travel?
- Staph. aureus (paeds), E. coli (adults) | - Entamoeba histolytica = amoebiasis (faecal-oral route)
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LIVER ABSCESS What is the clinical presentation of a liver abscess? What else may be present in amoebiasis?
- Fever, RUQ pain | - Profuse bloody diarrhoea after long incubation
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LIVER ABSCESS What investigations would you do in liver abscess? What would you expect in amoebiasis?
- USS to detect + sample abscess, CT abdo | - Amoebiasis = single R lobe mass
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LIVER ABSCESS What is the management of liver abscess? What is the management of amoebiasis?
- Drainage (percutaneous) + Abx (amox, cipro + metro OR cipro + clinda) - Drainage (contents = anchovy sauce), metronidazole
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POST-OP PYREXIA | What are the causes of post-op pyrexia?
5Ws – - Wind = pneumonia, atelectasis (1–2d) - Water = UTI (>3d) - Wound = infection, anastomotic leak (>5d) - Wonder drugs = anaesthesia - Walking = DVT (>1w) Note: can be physiological systemic inflammatory reaction if within 1d

FINALS (20 decks)

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