HPB Flashcards

1
Q

Gallstone pathophysiology

A

Bile is formed from cholesterol, phospholipids and bile pigments
Form as a result of supersaturation of bile:
1) Cholesterol stones – excess cholesterol production
2) Pigment stones – excess bile pigment production (commonly seen in those with known haemolytic anaemia)
3) Mixed stones – cholesterol and bile pigments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Gallstone risk factors

A

Fat
Female
Forty
Fertile
Family history
Pregnancy, oral contraceptives, haemolytic anaemia & malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Biliary colic

A

Gallbladder neck is impacted by a gallstone
No inflammatory response, but contraction of the gallbladder against the occluded neck will result in pain
Pain – sudden, dull & colicky, focused in the RUQ but may radiate to the epigastrium/back, may be precipitated by fatty foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Acute cholecystitis

A

Constant pain in RUQ or epigastrium, associated with signs of inflammation
Tender in the RUQ & may demonstrate a positive Murphy’s sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Gallstone and acute cholecystitis investigations

A

Lab test
* FBC & CRP
* LFTs
* Amylase
Imaging – trans-abdominal ultrasound is first line
* MRCP is gold standard if US scans are inconclusive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Biliary colic management

A

Should be prescribed analgesia
Patient should be advised about lifestyle factors
Elective laparoscopic cholecystectomy is warranted & should be offered within 6 weeks of first presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute cholecystitis management

A

Should be started on appropriate IV abx (co-amoxiclav +/- metronidazole)
Laparoscopic cholecystectomy is indicated within 1 week of presentation, ideally within 72 hours of presentation
For those not fit for surgery & not responding to antibiotics, a percutaneous cholecystostomy can be performed to drain the infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mirizzi syndrome

A

Stone located in Hartmanns pouch/cystic duct itself can cause compression of the adjacent hepatic duct
Results in obstructive jaundice
Diagnosis is confirmed by MRCP & management is usually with laparoscopic cholecystectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Gallbladder empyema

A

Gallbladder becomes filled with pus
Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis
Condition is diagnosed by either US scan/CT scan
Treatment – via laparoscopic cholecystectomy/percutaneous cholecystostomy (if unsuitable for surgery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Chronic cholecystitis

A

Typically have a history of recurrent/untreated cholecystitis -> led to persistent inflammation of the gallbladder wall
Patients present with ongoing RUQ/epigastric pain with associated N&V
Diagnosed typically by CT imaging
Management – uncomplicated cases is via elective cholecystectomy
Main complications – gallbladder carcinoma & biliary-enteric fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Bouveret’s syndrome and gallstone ileus

A

Inflammation of the gallbladder can cause a fistula to form (cholecystoduodenal fistula) allowing gallstones to pass directly into the small bowel
Bouveret’s syndrome – stone impacts in the proximal duodenum, causing a gastric outlet obstruction
Gallstone ileus – a stone impacts at the terminal ileum, causing small bowel obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pre-hepatic jaundice

A

Excessive red cell breakdown -> overwhelms the liver’s ability to conjugate bilirubin
Causes an unconjugated hyperbilirubinemia (remains in the blood steam to cause jaundice)
E.g. haemolytic anaemia, Gilbert’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hepatocellular jaundice

A

Dysfunction of the hepatic cells
Loses the ability to conjugate bilirubin & also causes where it may become cirrhotic -> compresses the intra-hepatic portions of the biliary tree to cause a degree of obstruction
Both unconjugated and conjugated bilirubin
e.g. alcoholic liver disease, viral hepatitis, hereditary haemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Post-hepatic jaundice

A

Obstruction of biliary drainage
Conjugated hyperbilirubinemia
e.g. gallstones, cholangiocarcinoma, strictures, pancreatic cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cholangiocarcinoma risk factors

A

Primary sclerosing cholangitis
Congenital – Caroli’s disease, choledochal cyst
Intraductal gallstone formation
Infective – liver flukes, hepatitis
Toxins – chemicals in rubber & aircraft industry
Liver cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cholangiocarcinoma clinical features

A

Intrahepatic – generally asymptomatic until a late stage in the disease
Extrahepatic – typically present early
Jaundice, pruritus, steatorrhea, non-specific abdominal pain, dark urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Courvoisier’s law

A

In the presence of jaundice and an enlarged/palpable gallbladder, malignancy of the biliary tree/pancreas should be strongly suspected as the cause is unlikely to be gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cholangiocarcinoma investigations

A

Bloods – elevated bilirubin, ALP & yGT
Tumour markers – CEA and CA19-9 may also be elevated
MRCP – gold standard imaging modality
CT, ERCP/PTC (obtain tissue brushings for cytological diagnosis)
Triple phase CT imaging/contrast-enhanced MRI of the liver – staging of the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cholangiocarcinoma management

A

Definitive cure – complete surgical resection (only 10-15% patients are suitable)
Both chemotherapy and radiotherapy may be used in some cases as adjuvant treatments after surgery
Palliative
1) Stenting – relieve obstructive symptoms
2) Surgery – bypass procedures if obstruction cannot be relieved by stenting
3) Medical – palliative radiotherapy/chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Cholangitis

A

Infection of the biliary tract
Caused by a combination of biliary outflow obstruction & biliary infection
During an obstruction, stasis of fluid allows bacterial colonisation of the biliary tree to become pathological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cholangitis causes

A

(any condition that causes occlusion of the biliary tree)
Gallstones
ERCP
Cholangiocarcinoma
Most common infective causes – E coli, Klebsiella species & enterococcus

22
Q

Cholangitis clinical presentation

A

Charcot’s triad – jaundice, fever, RUQ pain
Reynold’s pentad – jaundice, fever, RUQ pain, hypotension & confusion

23
Q

Cholangitis investigations

A

Routine bloods – esp, FBC & LFTs
Blood cultures – should always be taken in suspected cases
Imaging – biliary tract USS, ERCP is gold standard as it is both diagnostic & therapeutic

24
Q

Cholangitis management

A

Immediate – IV access, fluid resus, routine bloods, blood cultures, broad spectrum IV abx (co-amoxiclav & metronidazole)
Definitive – endoscopic biliary decompression, ERCP should clear any obstruction (PTC is second line for patients too unwell)

25
Q

Complications of ERCP

A

Repeated cholangitis
Pancreatitis
Bleeding
Perforation

26
Q

Hepatocellular cancer aetiology

A

Arises as a result of a chronic inflammatory process affecting the liver (80-90% seen with background of established liver cirrhosis)
Mainly due to viral hepatitis, other causes: chronic alcohol excess, hereditary haemochromatosis, PBC

27
Q

Hepatocellular cancer risk factors

A

Liver cirrhosis
Aflatoxin exposure
Hepatocellular adenoma
Smoking
Advancing age
Positive family history

28
Q

Hepatocellular cancer clinical features

A

Many cases picked up on surveillance imaging
Fatigue, weight loss
Examination – irregular enlarged liver, features of decompensated liver disease (ascites, jaundice or confusion)

29
Q

Hepatocellular cancer investigations

A

Routine bloods, AFP
Imaging – USS in screening, MRI/CT are both useful to further assess lesions
Biopsy can be obtained for histological diagnosis by either ultrasound-guided/CT-guided percutaneous biopsy

30
Q

Hepatocellular cancer management

A

Decided by discussion by a MDT
Curative options – liver transplantation/liver resection, ablative techniques
Metastatic disease – systemic therapies are indicated

31
Q

Acute pancreatitis

A

Inflammation of the pancreas
Distinguished from chronic pancreatitis by its limited damage to the secretory function of the gland

32
Q

Acute pancreatitis aetiology

A

Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune disease – SLE/Sjogren’s syndrome
Scorpion venom
Hypercalcaemia
ERCP
Drugs – azathioprine, NSAIDs/diuretics

33
Q

Acute pancreatitis pathophysiology

A

Each cause will trigger a premature and exaggerated activation of digestive enzymes in the pancreas
Pancreatic inflammatory response -> increase in vascular permeability & subsequent fluid shifts
Enzymes are released into systemic circulation -> autodigestion of fats & blood vessels
Fat necrosis can cause release of free fatty acids -> react with calcium, resulting in hypocalcaemia
Eventually -> partial/complete necrosis of the pancreas

34
Q

Acute pancreatitis clinical features

A

Severe epigastric pain, which can radiate through to the back, with nausea & vomiting
Examination – often epigastric tenderness, Cullen’s sign (bruising around the umbilicus) & Grey Turner’s sign (bruising in the flanks) – representing retroperitoneal haemorrhage
Tetany (from hypocalcaemia)

35
Q

Acute pancreatitis investigations

A

Serum amylase/serum lipase – diagnostic if 3x the upper limit of normal
LFTs – assess for any cholestatic element to the clinical picture

36
Q

Acute pancreatitis risk scoring

A

Modified Glasgow criteria – assess the severity of acute pancreatitis within the first 48 hours of admission (> 3 = severe pancreatitis)
PO2 < 8kPa
Age > 55 yrs
Neutrophils > 15 x 10*9L
Calcium < 2mmol/L
Urea > 16mmol/L
LDH > 600U/L or AST > 200U/L
Albumin < 32g/L
Sugar > 10mmol/L

37
Q

Acute pancreatitis imaging

A

Abdominal USS
(not routinely performed but AXR can show sentinel loop sign = dilated proximal bowel loops adjacent to pancreas)
Contrast-enhanced CT scan (after 48hrs of initial presentation) – pancreatic oedema, swelling, pancreatic necrosis

38
Q

Acute pancreatitis management

A

No curative management, treat any underlying cause
IV fluid resus & oxygen therapy as required
NG tube if patient is vomiting
Catheterisation & fluid balance chart
Opioid analgesia
Broad-spectrum abx should be considered for prophylaxis in cases of confirmed pancreatic necrosis

39
Q

Acute pancreatitis systemic complications

A

Disseminated intravascular coagulation
Acute respiratory distress syndrome
Hypocalcaemia
Hyperglycaemia

40
Q

Acute pancreatitis local complications

A

Pancreatic necrosis – should be suspected in patients with evidence of persistent systemic inflammation > 7-10 days, confirmed by CT imaging, treatment is pancreatic necrosectomy, prone to infection (can be confirmed by a fine needle aspiration of the necrosis)
Pancreatic pseudocyst – collection of fluid (pancreatic enzymes, blood & necrotic tissue) anywhere within or adjacent to the pancreas (usually seen in lesser sac), may be found incidentally on imaging/present with symptoms of mass effect, surgical debridement/endoscopic drainage if they don’t spontaneous resolve

41
Q

Chronic pancreatitis

A

Chronic fibro-inflammatory disease of the pancreas, resulting in progressive & irreversible damage to parenchyma
Male to female 4:1, average onset of 40 years

42
Q

Chronic pancreatitis aetiology

A

Chronic alcohol abuse
Idiopathic
Less common – metabolic, infection, hereditary, autoimmune, anatomical or congenital anomalies

43
Q

Chronic pancreatitis clinical features

A

Chronic pain – epigastrium and back, often associated with N&V
Endocrine insufficiency – impaired glucose regulation/eventual diabetes mellitus
Exocrine insufficiency – weight loss, diarrhoea, steatorrhoea
Examination – tender in epigastrium, often evidence of significant cachexia

44
Q

Chronic pancreatitis investigations

A

Urine dip and routine bloods (amylase/lipase levels are often not raised in established disease), blood glucose, faecal elastase level
Imaging – CT imaging, USS, MRI

45
Q

Chronic pancreatitis management

A

Can only be managed definitively by treating any reversible underlying cause, analgesia
Non-surgical – endoscopic management (targetable underlying cause), ERCP, extracorporeal shock wave lithotripsy
Surgical management – Frey’s procedure (large ductal stones), lateral pancreaticojejunostomy, pancreaticoduodenectomy (Whipples procedure) if there is any suspicion of pancreatic head malignancy

46
Q

Pancreatic cancer

A

Most common type – ductal carcinoma
Most arise from the head, then the rest from body & tail/diffuse involvement of the pancreas
80% cases occur between 60-80 yrs old

47
Q

Pancreatic cancer risk factors

A

Smoking
Chronic pancreatitis
Dietary factors – high red meat, low fruit & veg
Family history

48
Q

Pancreatic cancer clinical features

A

Obstructive jaundice – typically painless
Weight loss
Non-specific abdominal pain
Late onset diabetes mellitus
Examination – cachectic, malnourished & jaundiced

49
Q

Pancreatic cancer investigations

A

Routine bloods, CA19-9
Imaging – abdominal USS, CT is gold standard for preliminary diagnosis, endoscopic ultrasound is now largely used in staging & biopsy

50
Q

Pancreatic cancer management

A

Curative option – radical resection
Non-resectable disease – chemotherapy, symptomatic management