HPB Flashcards

1
Q

What are the screening questionnaires for alcohol consumption?

A

CAGE

AUDIT

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2
Q

What are the signs of alcoholic liver disease?

A
Jaundice + scleral jaundice
Palmar erythema
Hepatomegaly
Spider naevi
Caput medusa
Flapping tremor (asterixis)
Ascites
Gynaecomastia
Unexplained bruising
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3
Q

How is alcoholic liver disease diagnosed?

A

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

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4
Q

What is the management of alcoholic liver disease?

A
  1. Stop drinking / detox programme
  2. Calorie and nutrition support- incl thiamine
  3. Consider suitability for transplant
  4. Symptomatic treatment
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5
Q

What are the stages of alcohol withdrawal?

A
  1. 6-12 hrs: tremors, sweating, headache, cravings and anxiety
  2. 12-24 hrs: hallucinations and tactile disturbance - characteristically insects crawling
  3. 24-48hrs: seizures
  4. 48-36 hrs: delirium tremens
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6
Q

What is delirium tremens?

A

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

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7
Q

What classification system is used in alcohol withdrawal?

A

CIWA-AR tool

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8
Q

How should you manage acute alcohol withdrawal?

A

Benzodiazepine e.g. chlordiazepoxide (librium) titrated regimen
Thiamine: IV pabrinex followed by oral thiamine
Manage any seizures/other symptoms

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9
Q

What are the 3 features of Wernicke’s encephalopathy?

A

Confusion
Ataxia
Occulomotor disturbance

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10
Q

What are the three features of Korsakoff’s syndrome?

A
  1. Amnesia- anterograde and retrograde
  2. Confabulation
  3. Behavioural change: lack of insight, apathy
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11
Q

What are the causes of liver cirrhosis?

A

Common:

  1. Alcoholic liver disease
  2. Non-alcoholic steatohepatitis
  3. Chronic viral hepatitis
  4. Drug causes

Less common

  1. a1-antitripsin deficiency
  2. Wilson’s disease
  3. Haemochromatosis
  4. Primary biliary cirrhosis
  5. Autoimmune hepatitis
  6. Cystic fibrosis
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12
Q

Which drugs most commonly cause liver cirrhosis?

A
  1. Methotrexate
  2. Amiodarone
  3. Sodium valproate
  4. Chemotherapy agents

TPN is also associated with liver injury and fibrosis.

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13
Q

What are the signs of liver cirrhosis?

A
Palmar erythema
Asterixis 
Jaundice
Spider naevi, caput medusa
Ascites and oedema
Bruising and bleeding
Pale stool and dark urine
Splenomegaly
Gynaecomastia
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14
Q

What investigations should be done in liver cirrhosis?

A
  1. LFTs: raised AST/ALT, raised ALP, low albumin, high bilirubin, ?gamma gt
  2. Coagulation: prolong PT
  3. AFP: marker for HCC
  4. U&E: can cause deranged urea and creatinine, hyponatraemia due to dilution
  5. Hepatitis viral screen and autoantibody testing
  6. USS abdomen and Fibroscan
  7. CT scan and biopsy
  8. Endoscopy looking for varies

Enhanced liver fibrosis blood test= new test, not available in all centres

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15
Q

What are the scoring systems for liver cirrhosis?

A

Child-Pugh score - indicated severity

MELD score- done 6 monthly in those with compensated cirrhosis to estimate mortality and need for transplant

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16
Q

How should patients with liver cirrhosis be managed?

A

Avoid alcohol!

  1. Vitamin and nutrition replacement - high protein, low sodium, vitamin supplements
  2. Coagulopathy management
  3. Diuretics for ascites
  4. BP control for hepatorenal syndrome
  5. Consideration for transplant
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17
Q

What are the complications of cirrhosis?

A
Ascites + SBP
Portal hypertension
Varices + variceal bleeding
Hepatorenal syndrome
Encephalopathy
Bleeding/bruising
Malnutrition
HCC
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18
Q

What is the blood marker for HCC?

A

AFP

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19
Q

How are stable varices managed?

A
  1. Stop drinking if alcohol-related / abstain either way
  2. Propranolol to reduce BP
  3. Elective banding procedure
  4. TIPS procedure
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20
Q

How are unstable varices managed?

A

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

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21
Q

How does ascites form?

A

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

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22
Q

How should ascites be managed?

A
  1. Low sodium diet
  2. Spironolactone
  3. 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.
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23
Q

What are the most common organisms causing SBP?

A

Ecoli
Klebsiella
Gram positive cocci

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24
Q

What are the symptoms of SBP?

A
May be asymptomatic
Ascites
Abdominal pain
Fever
Sepsis
Ileus
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25
Q

How is SBP diagnosed?

A

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

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26
Q

How is SBP managed?

A

IV antibiotics - usually cefotaxime

Ascitic drain - albumin replacement for each L of fluid drained

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27
Q

What is hepatorenal syndrome?

A

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.

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28
Q

What is the cause of hepatic encephalopathy?

A

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.

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29
Q

What are the symptoms of hepatic encephalopathy?

A

Flapping tremor
Reduced GCS
Confusion, change in behaviour/personality

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30
Q

How do you manage hepatic encephalopathy?

A

Laxatives to increase excretion of intestinal ammonia
Enemas
Oral rifampicin to kill bacteria and reduce ammonia production
Nutritional support

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31
Q

What can precipitate hepatic encephalopathy?

A
  1. Constipation
  2. Renal impairment
  3. Infection
  4. GI bleed
  5. Excess protein
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32
Q

How is non-alcoholic fatty liver disease diagnosed?

A

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

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33
Q

What is the management for non-alcoholic fatty liver disease?

A

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

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34
Q

What is the inheritance pattern for a1-antitrypsin deficiency?

A

Autosomal recessive

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35
Q

How is hepatitis A diagnosed?

A

Symptom profile= N&V, anorexia, jaundice, cholestasis, hepatomegaly, fever
HAV IgM

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36
Q

What percentage of HBV and HCV become chronic infections?

A

HBV: 10%
HCV: 75%

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37
Q

What do each of the serology factors mean in HBV?

HBsAg, HBeAg, Anti-HBc, Anti-HBs, HBV DNA

A
HBsAG= presence of infection
HBeAg= indication of viral replication and infectivity
Anti-HBc= Current or past infection
Anti-HBs= resolution of infection
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38
Q

What would you expect to see on serology in acute HBV infection?

A
  1. HBsAg +ve
  2. HBeAg +ve
  3. Anti-HbC IgM
  4. HBV DNA +ve

Raised ALT

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39
Q

What would you expect to see on serology in chronic HBV infection?

A
  1. HBsAg +ve
  2. HBeAg +ve or -ve
  3. Anti-HbC IgG
  4. HBV DNA +ve

Elevated ALT

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40
Q

What would you expect to see on serology in somebody who has recovered from HBV infection?

A

Anti-HBs
Anti-HBc IgG

Normal ALT
No Antigens or DNA

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41
Q

What would you expect to see on serology for somebody who has been vaccinated against HBV?

A

Anti-HBs
Normal ALT
No antigens or DNA

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42
Q

How is HBV managed?

A
  1. Testing for other BBVs, informing public health
  2. Reduce risk factors: stop smoking, alcohol abstinence
  3. Monitoring for complications: Fibroscan, USS
  4. Antivirals to slow progression (no cure)
  5. Transplant
43
Q

How is HCV diagnosed?

A

Anti-HCV Ab = screening test

HCV RNA= diagnostic confirmation, viral load

44
Q

How is HCV managed?

A

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

45
Q

What is the main complication of chronic hepatitis?

A

Hepatocellular carcinoma

46
Q

When should you worry about HEV?

A

In pregnant women or immunocompromised -> can cause chronic hepatitis and liver failure in these populations

47
Q

What are the two types of autoimmune hepatitis?

A

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

48
Q

How is autoimmune hepatitis diagnosed and managed?

A
  1. Liver biopsy + antibody testing

2. Managed using high-dose prednisolone (tapering), azathioprine and transplant in end-stage disease

49
Q

What are the symptoms of haemochromatosis?

A

Fatigue, Joint pain, Hair loss
Bronze/grey pigmentation
Mood/memory disturbance
Amenorrhoea, erectile dysfunction

50
Q

What is the inheritance pattern of haemochromatosis?

A

Autosomal recessive

51
Q

How is haemochromatosis diagnosed?

A
Serum ferritin ^
Serum transferrin saturation ^
Genetic testing
Liver biopsy with PERL'S STAIN- show's parenchymal iron concentration
CT abdomen
52
Q

What is the treatment for haemochromatosis?

A
  1. Weekly venesection and serum iron monitoring
  2. Genetic counselling
  3. Monitor for complication e.g. liver cirrhosis and avoid alcohol
53
Q

What are the complications of haemochromatosis?

A
Liver cirrhosis
T1DM
Endocrine disturbance e.g. DI
HCC
Cardiomyopathy
Hypothyroidism
54
Q

What is the inheritance pattern for Wilson’s disease?

A

Autosomal recessive

55
Q

What are the features of Wilson’s disease?

A

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

56
Q

How is Wilson’s disease diagnosed?

A

Liver biopsy for copper content= gold standard
Serum caeruloplasmin = low (protein carrying copper)
Serum copper
Genetic testing

57
Q

How is Wilson’s disease managed?

A

Copper chelation: penicillamine

58
Q

What is primary biliary cirrhosis?

A

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

59
Q

What are the symptoms of primary biliary cirrhosis?

A
RUQ pain
Jaundice
Fatigue
Steatorrhoea + dark urine, itching
Xanthelasma, xanthomata
Signs of cirrhosis
60
Q

How is primary biliary cirrhosis diagnosed?

A

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

61
Q

What is the antibody most associated with primary biliary cirrhosis?

A

Anti-mitochondrial antibody

62
Q

How is primary biliary cirrhosis managed?

A
  1. Ursedoxycholic acid to decrease intestinal cholesterol absorption
  2. Cholestyramine to prevent bile acid absorption
  3. Transplant in end-stage disease
  4. Steroids used in some
63
Q

What are the indications for liver transplant?

A
  1. Acute liver failure - most commonly paracetamol OD
  2. Chronic liver failure and cirrhosis
  3. Hepatocellular carcinoma

Contraindications:
Alcohol, significant comorbidity, malnutrition, active infection, end-stage HIV

64
Q

What condition is most commonly associated with primary sclerosing cholangitis?

A

Ulcerative colitis

65
Q

What is primary sclerosing cholangitis?

A

Stricturing and fibrosis of the intra/extrahepatic ducts -> obstruction of bile flow
Chronic obstruction -> hepatitis, fibrosis, cirrhosis

66
Q

What is the triad of symptoms for primary sclerosing cholangitis?

A

RUQ pain
Jaundice
Pruritus

67
Q

How is primary sclerosing cholangitis diagnosed?

A
  1. LFTs: Cholestatic pictire
  2. Autoantibodies: p-ANCA and ANA
  3. MRCP - gold standard test
68
Q

How is primary sclerosing cholangitis managed?

A

ERCP to dilate and stent ducts
Cholestyramine to reduce bile acid absorption
Vitamin supplementation
Monitor complications - key = cholangiocarcinoma
Transplant can be curative

69
Q

What are the risk factors for HCC?

A

Alcoholic Liver Disease
Chronic hepatitis
Non-alcoholic fatty liver disease
Liver cirrhosis of different aetiology

70
Q

What are the symptoms of HCC?

A

Often asymptomatic / normal symptoms of liver disease
RUQ pain, jaundice, ascites, nausea, pruritus
Weight loss, malaise

71
Q

How is HCC diagnosed?

A

AFP = serum marker
LFTs
USS liver
CT scan and liver biopsy

72
Q

How is HCC treated?

A

Resection if extremely localised
Liver transplant if confined to liver
Chemo/radiotherapy
Kinase inhibitor can prolong survival

73
Q

What is the main risk factor for cholangiocarcinoma?

A

Primary sclerosing cholangitis

74
Q

What are the symptoms of cholangiocarcinoma?

A

Often asymptomatic until quite advanced
Painless jaundice- like pancreatic cancer
Weight loss, fatigue, night sweats

75
Q

How is cholangiocarcinoma diagnosed?

A
CA19-9 = blood marker
LFTs
USS
CT scan
ERCP to take brushings/biopsy
76
Q

How is cholangiocarcinoma managed?

A

Surgical resection if small and localised
Chemo/radiotherapy - resistant disease, poor prognosis
ERCP stenting of the bile ducts

77
Q

What are the key risk factors for gallstones?

A

Female
Fat
Fair
Forty

78
Q

What are the symptoms of gallstones?

A

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

79
Q

How are gallstones diagnosed?

A

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

80
Q

How are gallstones managed?

A
  1. If asymptomatic, no management required
  2. ERCP removal of stones
  3. Cholecystectomy
81
Q

What is post-cholecystectomy syndrome?

A

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

82
Q

What are the symptoms of acute cholecystitis?

A

RUQ pain -> may be referred to R shoulder
Fever, tachycardia, tachypnoea
Nausea and vomiting

83
Q

What are the signs of acute cholecystitis on examination?

A

^ RR, HR, temp
RUQ tenderness and guarding
Murphy’s sign +ve - pain on inspiration
Peritonism in severe disease

84
Q

How would you investigate acute cholecystitis?

A

A-E assessment
Bloods: FBC, U&E, LFT, CRP, lipase,
USS abdo: thickened wall, stones / sludge in the gallbladder, fluid around the gallbladder
MRCP

85
Q

How to manage acute cholecystitis?

A
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)
86
Q

What are the main causes of ascending cholangitis?

A

Gallstones

ERCP

87
Q

What are the most common causative organisms in ascending cholangitis?

A

E-coli
Klebsiella
Enterococci

88
Q

What are the symptoms of ascending cholangitis?

A

Charcot’s triad:

Fever, RUQ pain, Jaundice

89
Q

How is ascending cholangitis diagnosed?

A

Symptom profile
Bloods: Raised WCC and CRP, obstructive liver picture
Blood cultures
USS -> CT -> MRCP
ERCP actually most sensitive but also most invasive

90
Q

How is ascending cholangitis managed?

A
A-E
Make NBM and get IV access
NG tube if vomiting
IV fluids, analgesia, antibiotics
ERCP to remove any stones / stent ducts
91
Q

What are the causes of pancreatitis?

A
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hypercalcaemia, hyperlipidaemia
ERCP
Drugs
92
Q

What are the common drugs causing pancreatitis?

A
Thiazide diuretics
Furosemide
Amiodarone
Propofol
Azathioprine
93
Q

What are the symptoms of pancreatitis?

A

Epigastric pain radiating to the back, better when leant forwards
Nausea and vomiting
Fever, ^HR, RR
Epigastric tenderness and guarding

94
Q

What is the severity scoring for pancreatitis?

A
GLASGOW score- PANCREAS
PaO2
Age
Nutrophils
Calcium levels
R uRea
Enzymes: LDH, liver enzymes, lipase
Albumin
Sugar

0-1= mild
2=moderate
3+= severe

95
Q

How is pancreatitis diagnosed?

A
  1. Raised WBC, CRP, serum lipase/amylase
    ABG, LFT, calcium, U&E, blood cultures
  2. USS
  3. CT abdomen
96
Q

How is pancreatitis managed?

A

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

97
Q

What are the complications of acute pancreatitis?

A
Pseudocyst formation
Abscess formation
Perforation
Sepsis
Chronic pancreatitis
Pancreatic necrosis
98
Q

What are the complications of acute pancreatitis?

A
Pseudocyst formation
Abscess formation
Perforation
Sepsis
Chronic pancreatitis
Pancreatic necrosis
99
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol excess

100
Q

What are the symptoms of chronic pancreatitis?

A
Chronic epigastric pain
Steatorrhoea
Diabetes features
Malnutrition
Recurrent episodes of acute pancreatitis
101
Q

How is chronic pancreatitis managed?

A
Stop alcohol and smoking
Pancreatic enzyme supplements + nutrition support
Analgesia
ERCP and stunting of ducts
Surgical removal of necrotic pancreas
102
Q

What are the symptoms of pancreatic cancer?

A

Painless jaundice
Dark urine, pale stool, itch
Nausea and vomiting
Weight loss, night sweats, fatigue

103
Q

How is pancreatic cancer diagnosed?

A

CA 19-9
USS/MRCP
ERCP and biopsy
CT scan staging

104
Q

How is pancreatic cancer managed?

A

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