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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
Q

ASCITES

What are some causes of ascites with a SAAG >11g/L?

A
  • 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
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26
Q

ASCITES

What are some causes of ascites with a SAAG <11g/L?

A
  • Hypoalbuminaemia = nephrotic syndrome, severe malnutrition (Kwashiorkor)
  • Malignancy/infections = peritoneal cancer, TB
  • Other = pancreatitis, bowel obstruction
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27
Q 
ASCITES
What is a key complication of ascites?
What is a common cause of it?
How does it present?
How is it diagnosed?
A
  • Spontaneous bacterial peritonitis
  • E. Coli
  • Ascites, abdominal pain + fever
  • Paracentesis = neutrophil count >250 cells/uL
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28
Q

ASCITES

What is the management of spontaneous bacterial peritonitis?

A
  • IV cefotaxime

- Prophylaxis with PO ciprofloxacin or norfloxacin if previous SBP or cirrhosis + ascites protein ≤15g/L until resolved

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29
Q

ASCITES

What is the conservative and medical management of ascites?

A
  • Reduce dietary salt + fluid restrict if Na <125mmol/L

- Aldosterone antagonists e.g., spironolactone ± adjuvant loop diuretic

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30
Q

ASCITES
What is the management of tense ascites?
What is a potential complication and how this is managed?

A
  • 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
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31
Q

ASCITES

What surgical intervention may be considered in ascites?

A
  • Transjugular intrahepatic portosystemic shunt (TIPS)
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32
Q

PORTAL HYPERTENSION

How are the causes of portal hypertension classified?

A
  • Pre-hepatic = portal vein thrombosis
  • Hepatic = cirrhosis #1 UK, schistosomiasis #1 worldwide
  • Post-hepatic = Budd-Chiari syndrome
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33
Q

PORTAL HYPERTENSION

What is Budd-Chiari syndrome?

A
  • Hepatic vein obstruction usually secondary to haem disorder like thrombophilia, polycythaemia
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34
Q

PORTAL HYPERTENSION
How does Budd-Chiari syndrome present?
How is it investigated?
How is it managed?

A
  • Abdo pain (acute severe), ascites + tender hepatomegaly
  • USS with doppler flow studies
  • Anticoagulants
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35
Q

PORTAL HYPERTENSION

What are the clinical features of portal hypertension?

A

SAVE –

  • Splenomegaly (decreased WCC + platelets)
  • Ascites
  • Varices
  • Encephalopathy
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36
Q

PORTAL HYPERTENSION
What are varices?
Where do varices occur?

A
  • Dilated veins at junction between portal/systemic circulation due to diversion of blood from increased pressure
  • Distal oesophagus (UGI bleed), proximal stomach (Caput Medusae)
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37
Q

NAFLD

What is the pathophysiology of non-alcoholic fatty liver disease (NAFLD)?

A
  • Thought to represent hepatic manifestation of metabolic syndrome + hence insulin resistance (T2DM) thought to be key mechanism
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38
Q

NAFLD

What is the spectrum of disease seen in NAFLD?

A
  • Steatosis = fat in liver
  • Steatohepatitis = fat with inflammation
  • Progressive disease > fibrosis + liver cirrhosis
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39
Q

NAFLD

What are some associated factors with NAFLD?

A
  • CVD risk factors = obesity, T2DM, high cholesterol + smoking
  • Sudden weight loss/starvation
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40
Q

NAFLD
How does NAFLD present?
What initial investigations would you conduct?

A
  • Asymptomatic, maybe hepatomegaly
  • LFT = ALT typically > AST
  • Non-invasive liver screen = hep B/C serology, autoAb, caeruloplasmin, A1AT, iron studies, USS liver (increased echogenicity)
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41
Q

NAFLD

After initial investigations, what other tests would you consider?

A
  • Enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis on incidental NAFLD Dx
  • Transient elastography
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42
Q

NAFLD

What is the management of NAFLD?

A
  • Mainstay of treatment is lifestyle changes, especially weight loss
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43
Q

VIRAL HEPATITIS
Give an overview of hepatitis A
How is it spread?

A
  • RNA virus with 2–4w incubation period

- Faecal-oral, often from shellfish

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44
Q

VIRAL HEPATITIS
How may hepatitis A present?
Are there complications associated with hepatitis A?

A
  • Flu-like prodrome, RUQ pain, tender hepatomegaly, cholestatic LFTs
  • Does NOT cause chronic disease or increase HCC risk
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45
Q

VIRAL HEPATITIS

What is the management of hepatitis A?

A
  • Supportive

- Vaccination prophylaxis = MSM, IVDU, chronic liver disease, travellers

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46
Q

VIRAL HEPATITIS
Give an overview of hepatitis B
How is it spread?
How may it present?

A
  • Double-stranded DNA virus
  • Blood borne (IVDU, sex, vertical transmission)
  • Jaundice, fever, malaise
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47
Q

VIRAL HEPATITIS

What are the 4 main components to hepatitis B serology?

A
  • Surface antigen = HBsAg
  • Surface antibodies = anti-HBs
  • Core antibodies = anti-HBc
  • E antigen = HBeAg
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48
Q

VIRAL HEPATITIS
In terms of hepatitis B serology, what do the following show…

i) HBsAg?
ii) anti-HBs?

A

i) Ongoing infection + causes anti-HBs production, if present for >6m = chronic disease
ii) Immunity (exposure OR vaccine) is –ve in chronic disease

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49
Q

VIRAL HEPATITIS
In terms of hepatitis B serology, what do the following show…

i) anti-HBc?
ii) HBeAg?

A

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

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50
Q

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?

A

i) Anti-HbS +ve, others –ve
ii) Anti-HBc +ve, HBsAg –ve
iii) Anti-HBc +ve, HBsAg +ve

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51
Q

VIRAL HEPATITIS

What are some complications with hepatitis B?

A
  • Chronic hepatitis (ground-glass hepatocytes on light microscopy)
  • HCC
  • Polyarteritis nodosa
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52
Q

VIRAL HEPATITIS

What is the management of hepatitis B?

A
  • Pegylated interferon first line
  • Anti-viral tenofovir second line
  • Vaccination with inactive HBsAg (occupational, childhood vaccines, IVDU)
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53
Q

VIRAL HEPATITIS
Give an overview of hepatitis C
How is it spread?

A
  • RNA virus

- Blood borne (IVDU, vertical, sexual)

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54
Q

VIRAL HEPATITIS
What are some complications of hepatitis C?
What is the management of hepatitis C?

A
  • 75% > chronic (HCV RNA in blood >6m) = cirrhosis, HCC, arthritis
  • Depends on viral genotype, usually combination of protease inhibitors like sofosbuvir ± ribavirin
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55
Q

VIRAL HEPATITIS
Give an overview of hepatitis D
How is it spread?

A
  • Incomplete RNA virus which requires HBsAg to complete replication + transmission cycle
  • Blood + bodily fluids
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56
Q

VIRAL HEPATITIS
What are some complications of hepatitis D?
What is the management?

A
  • Superinfection (HBsAg +ve > Hep D) associated with high risk of fulminant hepatitis, chronic hepatitis + cirrhosis
  • Complete prophylaxis if hep B vaccinated, interferon treatment
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57
Q

VIRAL HEPATITIS
Give an overview of hepatitis E
How is it spread?
What are some features?

A
  • RNA virus
  • Faecal-oral route
  • Like hep A but significant mortality in pregnancy, does NOT cause chronic disease or increased HCC risk
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58
Q

GALLSTONES
What are gallstones made of?
What are some risk factors?

A
  • Majority mixed composition, some pure cholesterol

- Fat, Female, Forty, FHx, also Crohn’s + haemolytic anaemia

59
Q

GALLSTONES

What is the classic clinical presentation of gallstones?

A
  • 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
Q

GALLSTONES

What important symptoms should be negative in simple biliary colic?

A
  • No fever, murphy’s sign and usually no jaundice

- If transient obstructive jaundice may have pale stools + dark urine

61
Q

GALLSTONES

What investigations would you do in gallstones?

A
  • LFTs = obstructive jaundice (raised ALP + bilirubin)

- Abdominal USS = acoustic shadow, dilated ducts >6mm, wall oedema

62
Q

GALLSTONES

What is a key complication of gallstones?

A
  • Gallstone ileus = gallstone erodes through gallbladder wall leading to gallbladder-small bowel (cholecystoenteric) fistula
63
Q

GALLSTONES
What is a consequence of gallstone ileus?
How can it appear on XR?

A
  • 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
Q

GALLSTONES

How do you manage gallstones?

A
  • Expectant if asymptomatic

- Elective laparoscopic cholecystectomy if symptomatic

65
Q

ACUTE CHOLECYSTITIS

What is acute cholecystitis?

A
  • Gallbladder inflammation often secondary to gallstones (calculous) but can be acalculous (e.g., hospital/severely ill > gallbladder stasis, hypoperfusion, infection)
66
Q

ACUTE CHOLECYSTITIS

What is the clinical presentation of acute cholecystitis?

A
  • RUQ pain which may radiate to R scapula
  • Fever + systemically unwell
  • Murphy’s sign = inspiratory arrest on palpation of RUQ (absent in LUQ)
67
Q

ACUTE CHOLECYSTITIS

What investigations would you do in acute cholecystitis and what might they show?

A
  • FBC (raised WCC), raised CRP, LFTs often normal
  • USS abdomen = first line choice
  • Magnetic resonance cholangiopancreatography (MRCP) if ?CBD stone
68
Q

ACUTE CHOLECYSTITIS
What are some complications of acute cholecystitis?
How do you manage this?

A
  • Sepsis, gangrenous gallbladder, perforation

- Gallbladder empyema = IV Abx + either cholecystectomy or cholecystostomy with drain insertion

69
Q

ACUTE CHOLECYSTITIS

What is the management of acute cholecystitis?

A
  • NBM
  • IV fluids
  • IV Abx
  • Early laparoscopic cholecystectomy <1w of Dx
70
Q

ASCENDING CHOLANGITIS

What is the pathophysiology of ascending cholangitis?

A
  • 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
Q

ASCENDING CHOLANGITIS

What are the causes of infection and obstruction in ascending cholangitis?

A
  • Infection = E. coli commonly, Klebsiella

- Obstruction = mostly gallstones, can be benign biliary strictures or malignancy

72
Q

ASCENDING CHOLANGITIS

What is the clinical presentation of ascending cholangitis?

A
  • Charcot’s triad = RUQ, fever (+ rigors) + jaundice

- Reynold’s pentad = above PLUS hypotension + confusion

73
Q

ASCENDING CHOLANGITIS

What investigations would you do in ascending cholangitis?

A
  • FBC (raised WCC), raised CRP
  • LFTs = cholestatic picture = raised ALP + bilirubin
  • USS abdomen first line
  • MRCP is most accurate for visualisation
74
Q

ASCENDING CHOLANGITIS

What is the management of ascending cholangitis?

A
  • IV Abx + endoscopic retrograde cholangiopancreatography (ERCP) after 24–48h to relieve any obstruction + biliary drainage
75
Q

ACUTE PANCREATITIS
What is the pathophysiology of acute pancreatitis?
What are some causes?

A 
- 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
Q

ACUTE PANCREATITIS

What is the clinical presentation of acute pancreatitis?

A
  • 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
Q

ACUTE PANCREATITIS
What initial investigations would you do in acute pancreatitis?
How would you diagnose it?

A
  • FBC (raised WCC), U&E, LFT, Ca2+, CRP, ABG, amylase

- Dx = characteristic pain + serum amylase/lipase >3x upper limit of normal

78
Q

ACUTE PANCREATITIS
What is significant about the degree of elevation of amylase?
When is lipase more useful?

A
  • Nothing – it’s not related to severity of disease

- Longer half-life so may be useful for late presentations >24h

79
Q

ACUTE PANCREATITIS

What imaging would you consider in acute pancreatitis?

A
  • Early USS abdo to assess aetiology
  • ERCP/MRCP
  • CT abdomen if complications suspected
80
Q

ACUTE PANCREATITIS
How is the severity of acute pancreatitis measured?
How do you manage this?

A
  • Modified Glasgow criteria = PaO2 <8, >55y, WCC >15, Ca2+ <2, urea >16 etc.
  • ≥3 = ITU/HDU transfer for intensive monitoring
81
Q

ACUTE PANCREATITIS

What are some complications of acute pancreatitis?

A
  • ARDS
  • Peripancreatic fluid collections = most resolve but can develop pseudocysts/abscess
  • Pancreatic pseudocyst
  • Pancreatic necrosis, abscess + haemorrhage
82
Q

ACUTE PANCREATITIS
What is a pancreatic pseudocyst?
How is it managed?

A
  • Peripancreatic fluid collection with a fibrous wall (after 4w)
  • Observe for 12w as 50% resolve, if not cystogastrostomy or aspiration
83
Q

ACUTE PANCREATITIS

What is the management of acute pancreatitis?

A
  • 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
Q

CHRONIC PANCREATITIS

What is the pathophysiology of chronic pancreatitis?

A
  • Chronic inflammation in the pancreas leading to fibrosis + reduced functioning + can affect both exocrine + endocrine functions of the pancreas
85
Q

CHRONIC PANCREATITIS

What are the causes of chronic pancreatitis?

A
  • Chronic alcohol excess = #1
  • Genetic = CF, haemochromatosis
  • Ductal obstruction = tumours, stones
86
Q

CHRONIC PANCREATITIS

What is the clinical presentation of chronic pancreatitis?

A
  • Chronic epigastric pain, worse 15–30m following meal, sitting forward relieves
  • Exocrine dysfunction = malabsorption + steatorrhoea
  • Endocrine dysfunction = DM (often years after onset)
87
Q

CHRONIC PANCREATITIS

What investigations would you do in chronic pancreatitis?

A
  • AXR = may show pancreatic calcification but CT abdomen is more sensitive for this
  • Faecal elastase to assess exocrine function
88
Q

CHRONIC PANCREATITIS

What are some complications of chronic pancreatitis?

A
  • Formation of strictures, pseudocysts, abscesses + pancreatic cancer risk
89
Q

CHRONIC PANCREATITIS

What is the management of chronic pancreatitis?

A
  • Stop alcohol, analgesia, insulin if DM
  • ERCP with stenting if strictures + obstruction
  • Pancreatic enzyme supplementation (Creon)
90
Q

PARACETAMOL OVERDOSE

What is the pathophysiology of paracetamol overdose?

A
  • 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
Q

PARACETAMOL OVERDOSE
What is the clinical presentation of paracetamol overdose?
What are some risk factors for increased hepatotoxicity in paracetamol overdose?

A
  • Varies from asymptomatic, N+V, abdo pain, jaundice + severe metabolic acidosis
  • P450 inducers (PC BRAS), malnourished, HIV, chronic (NOT acute) alcohol excess
92
Q

PARACETAMOL OVERDOSE

What investigations would you do in paracetamol overdose?

A
  • FBC, U&E, LFTs, clotting, VBG

- Paracetamol levels 4h after

93
Q

PARACETAMOL OVERDOSE
When would you consider using activated charcoal?
What is the mechanism of action?

A
  • Ingestion <1h

- Reduce drug absorption

94
Q

PARACETAMOL OVERDOSE

What other treatment would you consider in paracetamol overdose and when would you use it?

A
  • N-acetylcysteine (NAC)
  • Staggered overdose (tablets not all taken within 1h) or ingestion >15h
  • Nomogram shows above treatment line
95
Q

PARACETAMOL OVERDOSE

What is associated with NAC and how do you manage this?

A
  • Anaphylactoid reactions

- Not true anaphylaxis so stop transfusion temporarily + restart at slower rate

96
Q

PARACETAMOL OVERDOSE

What might be require in severe paracetamol overdose and the indication for this?

A
  • Liver transplantation

- Arterial pH <7.3 24h after ingestion

97
Q

PANCREATIC CANCER
What cancer type is commonly seen in pancreatic cancers?
What is the difficulty with pancreatic cancers?

A
  • Majority adenocarcinoma occurring at head of pancreas

- Diagnosed late as non-specific presentation + early spread to liver + lungs

98
Q

PANCREATIC CANCER

What are some associations with pancreatic cancer?

A
  • Increasing age, smoking, DM
  • Chronic pancreatitis
  • HNPCC, MEN
99
Q

PANCREATIC CANCER

What is the clinical presentation of pancreatic cancer?

A
  • Classically painless obstructive jaundice = pale stools, dark urine + pruritus
  • Loss of exocrine (steatorrhoea) + endocrine (DM) function
  • Weight loss
100
Q

PANCREATIC CANCER

What 2 eponymous phrases are linked with pancreatic cancer?

A
  • Courvoisier’s law = painless obstructive jaundice + palpable gallbladder is unlikely to be due to gallstones
  • Trousseau’s sign = migratory thrombophlebitis (paraneoplastic)
101
Q

PANCREATIC CANCER

What investigations would you do in pancreatic cancer?

A
  • 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
Q

PANCREATIC CANCER

What is the management of pancreatic cancer?

A
  • <20% suitable for surgery > Whipple’s resection (pancreaticoduodenectomy) if resectable lesion in head of pancreas + adjuvant chemo
  • ERCP with CBD stenting for palliation
103
Q

LIVER CANCER

What are the two main types of primary liver cancer?

A
  • Hepatocellular carcinoma (HCC #1)

- Cholangiocarcinoma (bile duct adenocarcinoma)

104
Q

LIVER CANCER
What are some causes of HCC?
What are some risk factors?

A
  • Cirrhosis, chronic hep B (#1 worldwide), chronic hep C (#1 Europe)
  • A1AT, haemochromatosis, Wilson’s, alcohol, NAFLD, PBC
105
Q

LIVER CANCER

What are some risk factors for cholangiocarcinoma?

A
  • PSC (+ so ulcerative colitis)

- Liver flukes (parasitic infection)

106
Q

LIVER CANCER

What is the clinical presentation of HCC?

A
  • Pre-existing cirrhosis with mass discovered on screening USS
107
Q

LIVER CANCER

What is the clinical presentation of cholangiocarcinoma?

A
  • Painless obstructive jaundice (pale stools, dark urine, pruritus)
  • Palpable gallbladder (Courvoisier’s law)
  • EXAM NOTE: pancreatic cancer is more common with these Sx
108
Q

LIVER CANCER
What investigations would you do in HCC?
Any investigations you would avoid?

A
  • AFP almost always raised, USS abdomen
  • CT/MRI imaging modalities of choice
  • Avoid biopsy as seeds tumour cells
109
Q

LIVER CANCER

What investigations would you do in cholangiocarcinoma?

A
  • LFTs = obstructive jaundice
  • CA 19-9, CEA and CA 125 often raised
  • CT/MRI + MRCP are imaging methods of choice
110
Q

LIVER CANCER
What is the management of…

i) HCC?
ii) cholangiocarcinoma?

A

i) Surgical resection mainstay, ?transplant

ii) Surgical resection, palliative ERCP stenting

111
Q

HAEMOCHROMATOSIS

What is the pathophysiology of haemochromatosis?

A
  • Autosomal recessive disorder of iron absorption + metabolism > iron accumulation + deposition due to mutations in HFE gene on chromosome 6
112
Q

HAEMOCHROMATOSIS

What is the clinical presentation of haemochromatosis?

A
  • Early = fatigue, ED + arthralgia (hands)
  • Bronze skin, T2DM, liver cirrhosis
  • Cardiac failure 2º to dilated cardiomyopathy
113
Q

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?

A
  • Transferrin saturation
  • HFE mutation genetic testing
  • Iron studies = HIGH transferrin saturation + ferritin, LOW TIBC
  • Joint XR = chondrocalcinosis
114
Q

HAEMOCHROMATOSIS

What are the reversible and irreversible complications of haemochromatosis?

A
  • Reversible = cardiomyopathy, skin pigmentation

- Irreversible = liver cirrhosis + HCC, DM, arthropathy

115
Q

HAEMOCHROMATOSIS
What is the first line management of haemochromatosis and what are the treatment targets?
What is the second line?

A
  • Venesection (transferrin saturation <50% + serum ferritin conc <50ug/L
  • Desferrioxamine
116
Q

WILSON’S DISEASE

What is the pathophysiology of Wilson’s disease?

A
  • Autosomal recessive disorder characterised by excessive copper deposition in tissues due to a defect in the ATP7B gene on chromosome 13
117
Q

WILSON’S DISEASE

What are some clinical features of Wilson’s disease?

A
  • Liver = hepatitis, cirrhosis
  • Neuro = dystonia, Parkinsonism (basal ganglia), psychosis, dementia
  • Kayser-Fleischer rings
  • Blue nails, renal tubular acidosis + haemolysis
118
Q

WILSON’S DISEASE
What are Kayser-Fleischer rings?
How do you assess them?

A
  • Green-brown rings in periphery of iris

- Slit-lamp examination

119
Q

WILSON’S DISEASE
What is the first line investigation of Wilson’s disease?
What other investigations would you do?
What are the diagnostic investigations?

A
  • Caeruloplasmin (low)
  • Reduced total SERUM copper, increased 24h URINARY copper excretion
  • Liver biopsy + genetic analysis for ATP7B gene
120
Q

WILSON’S DISEASE

What is the management of Wilson’s disease?

A
  • Penicillamine = first line copper chelation agent (also trientine)
  • Avoid high copper food = liver, nuts, chocolate
121
Q

A1AT DEFICIENCY

What is the pathophysiology of alpha 1 antitrypsin (A1AT) deficiency?

A
  • Autosomal recessive disorder of deficiency of protease inhibitor alpha 1 antitrypsin which usually inhibits neutrophil elastase + protects tissues on chromosome 14
122
Q

A1AT DEFICIENCY

What is the clinical presentation of A1AT deficiency?

A
  • Lungs = emphysema, most marked in lower lobes (young onset COPD)
  • Liver = cirrhosis + HCC, cholestasis in paeds
123
Q

A1AT DEFICIENCY

What investigations would you do in A1AT deficiency?

A
  • Serum A1AT concentrations = diagnostic

- Spirometry = obstructive

124
Q

A1AT DEFICIENCY

What is the management of A1AT deficiency?

A
  • Supportive = bronchodilators, physio, no smoking (exacerbates)
  • IV A1AT is expensive + not widely used
  • Surgery = consider lung volume reduction surgery or full transplantation
125
Q

PRIMARY BILIARY CHOLANGITIS

What is the pathophysiology of primary biliary cholangitis (PBC)?

A
  • Autoimmune condition that results in interlobular bile duct damage from chronic inflammation leading to progressive cholestasis > cirrhosis
126
Q

PRIMARY BILIARY CHOLANGITIS

What are some conditions that PBC is associated with?

A
  • Sjögren’s = #1
  • RA
  • Systemic sclerosis
  • Thyroid disease
127
Q

PRIMARY BILIARY CHOLANGITIS
What is the clinical presentation of PBC?
What are some specific features?

A
  • Pruritus, cholestatic jaundice (pale stools, dark urine), xanthelasma
  • Rule of Ms = IgM, anti-Mitochondrial Ab (M2 subtype), Middle aged females
128
Q

PRIMARY BILIARY CHOLANGITIS

What investigations would you do in PBC?

A
  • LFTs = raised ALP, GGT

- USS abdomen or MRCP for Dx

129
Q

PRIMARY BILIARY CHOLANGITIS

What are some potential complications of PBC?

A
  • Cirrhosis > portal HTN > ascites, variceal haemorrhage
  • Osteomalacia + osteoporosis
  • HCC
130
Q

PRIMARY BILIARY CHOLANGITIS

What is the management of PBC?

A
  • First line = ursodeoxycholic acid to slow disease progression + improve Sx
  • Pruritus = cholestyramine
  • Vitamin supplementation fat soluble ADEK
  • Liver transplant in bilirubin >100
131
Q

PRIMARY SCLEROSING CHOLANGITIS
What is the pathophysiology of primary sclerosing cholangitis (PSC)?
What conditions are associated with PSC?

A
  • Inflammation + fibrosis of intra and extra-hepatic bile ducts > biliary strictures
  • Majority of patients with PSC have UC, also HIV
132
Q

PRIMARY SCLEROSING CHOLANGITIS

What is the clinical presentation of PSC?

A
  • RUQ pain
  • Hepatomegaly
  • Fatigue
  • Cholestasis (jaundice, pruritus, pale stools)
133
Q

PRIMARY SCLEROSING CHOLANGITIS
What are some investigations in PSC?
What is the diagnostic investigation?

A
  • LFTs = cholestasis (raised bilirubin + ALP)
  • p-ANCA + ANA Ab may be positive
  • ERCP/MRCP is diagnostic = multiple beaded biliary strictures
134
Q

PRIMARY SCLEROSING CHOLANGITIS

What are two key complications of PSC?

A
  • Cholangiocarcinoma

- Colorectal cancer

135
Q

PRIMARY SCLEROSING CHOLANGITIS

What is the management of PSC?

A
  • Avoid alcohol
  • Pruritus = cholestyramine
  • Fat soluble ADEK vitamins
  • Dilate strictures via ERCP
  • ?Liver transplantation
136
Q

AUTOIMMUNE HEPATITIS

What are the three types of autoimmune hepatitis?

A
  • 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
137
Q

AUTOIMMUNE HEPATITIS

What is the clinical presentation of autoimmune hepatitis and who is commonly affected?

A
  • Young females, PMHx of other autoimmune disorders

- Jaundice, hepatosplenomegaly + abdominal pain

138
Q

AUTOIMMUNE HEPATITIS

What investigations might you do in autoimmune hepatitis?

A
  • LFTs = hepatic > raised ALT + bilirubin, normal/mildly raised ALP
  • ANA/SMA/LKM1 Ab + raised IgG levels
  • Liver biopsy = diagnostic
139
Q

AUTOIMMUNE HEPATITIS

What is the management of autoimmune hepatitis?

A
  • Immunosuppressants (e.g., prednisolone, azathioprine)

- Liver transplantation

140
Q

LIVER ABSCESS
What are the most common causes of liver abscesses in paeds and adults?
What is a cause seen in foreign travel?

A
  • Staph. aureus (paeds), E. coli (adults)

- Entamoeba histolytica = amoebiasis (faecal-oral route)

141
Q

LIVER ABSCESS
What is the clinical presentation of a liver abscess?
What else may be present in amoebiasis?

A
  • Fever, RUQ pain

- Profuse bloody diarrhoea after long incubation

142
Q

LIVER ABSCESS
What investigations would you do in liver abscess?
What would you expect in amoebiasis?

A
  • USS to detect + sample abscess, CT abdo

- Amoebiasis = single R lobe mass

143
Q

LIVER ABSCESS
What is the management of liver abscess?
What is the management of amoebiasis?

A
  • Drainage (percutaneous) + Abx (amox, cipro + metro OR cipro + clinda)
  • Drainage (contents = anchovy sauce), metronidazole
144
Q

POST-OP PYREXIA

What are the causes of post-op pyrexia?

A

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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