Upper GI and hepatobiliary

Question 1

Risk factors for GORD?

Answer 1

age
male gender
obesity
alcohol and smoking
intake of caffeinated drinks or fatty / spicy foods

Question 2

Presentation of GORD?
Red flag sxs?

Answer 2

burning retrosternal chest pain
Aggravating: worse after meals, lying down, bending over, or straining
Relieving: antacids

Associated sxs:
excessive belching
odynophagia
chronic / nocturnal cough

Red flags:
malaise
dysphagia
weight loss
early satiety and loss of appetite

Question 3

What is the Los Angeles classification?

Answer 3

The L.A classification can be used to grade reflux oesophagitis based on severity from the endoscopic findings of mucosal breaks in the distal oesophagus:

Grade A – breaks ≤5mm
Grade B – breaks >5mm
Grade C – breaks extending between the tops of ≥2 mucosal folds, but<75% of circumference
Grade D – circumferential breaks (≥75%)

Question 4

What should be done for patients with GORD in whom medical treatment fails and surgery is being considered?

Answer 4

24h pH monitoring alongside oesophageal manometry studies to exclude oesophageal dysmobility

Question 5

3 main indications for surgery in GORD?

Answer 5

Failure to respond to medical therapy
Patient preference to avoid life-long medication
Patients with complications of GORD (in particular respiratory complications, such as recurrent pneumonia)

Question 6

The main surgical intervention that can be offered for patients with GORD is a fundoplication. Outline this procedure.
What are the main complications?

What are the other options for surgical intervention?

Answer 6

The gastro-oesophageal junction and hiatus are dissected and the fundus wrapped around the GOJ, recreating a physiological lower oesophageal sphincter

Complications:
dysphagia, bloating, and inability to vomit, however these often settle after 6 weeks in most patients

Other options:
Stretta: uses radio-frequency energy to cause thickening of the LOS
Linx: a string of magnetic beads is inserted around the LOS laparoscopically to tighten it

Question 7

Complications of GORD?

Answer 7

aspiration pneumonia
Barrett’s oesophagus
oesophageal strictures and oesophageal cancer

Question 8

What are the 2 major types of oesophageal cancer?
Risk factors for each?

Answer 8

SCC:
typically affects upper 2/3
developing world
RF: smoking, excess alcohol, chronic achalasia, vit A deficiency

Adenocarcinoma:
lower 1/3
progresses from Barrett’s oesophagus
developed world
RF: GORD, obesity and high fat intake

Question 9

Any patient with a suspected oesophageal malignancy should be offered urgent upper GI endoscopy within 2 weeks. What other investigations can be offered?

Answer 9

CT CAP and PET scan are used together to investigate for distant metastases

Endoscopic USS to measure penetration into the oesophageal wall (T stage) and assess and biopsy suspicious mediastinal lymph nodes

Staging laparoscopy (for junctional tumours with an intra-abdominal component) to look for intra-peritoneal metastases

FNA of any palpable cervical lymph nodes

Question 10

What is the curative management for the 2 types of oesophageal cancer?

Answer 10

SCC - difficult to operate so definitive chemo-radiotherapy is the tx of choice

Adenocarcinomas – neoadjuvant chemotherapy or chemo-radiotherapy followed by oesophageal resection

Question 11

What is the problem with surgery for oesophageal cancer?

Answer 11

majority of patients present with advanced disease- 70% of patients are treated palliatively

Surgery is a major undertaking as both the abdominal and chest cavities need to be opened and it takes 6-9 months for patients to recover to their pre-operative QoL

Question 12

What are the different approaches to oesophagectomy?

Answer 12

Right thoracotomy with laparotomy (Ivor-Lewis procedure)

Right thoracotomy with abdominal and neck incision (McKeown procedure)

Left thoracotomy with or without neck incision

Left thoraco-abdominal incision (one large incision starting above the umbilicus and extending round the back to below the left shoulder blade)

Question 13

What are the main complications of oesophagectomy?

Answer 13

anastomotic leak (8%), re-operation, pneumonia (30%), and death (4%)

Post-operative nutrition is a major problem as patients lose the reservoir function of the stomach
- can routinely insert a feeding tube into the small bowel (a “feeding jejunostomy”) to aid nutrition

Question 14

What palliative management is available for oesophageal cancer?

Answer 14

Dysphagia:
Oesophageal stent
Radiotherapy/chemotherapy to reduce tumour size
Radiologically-Inserted Gastrostomy (RIG) tube

Cachexia:
Nutritional support with thickened fluids and supplements

Question 15

What is the prognosis for oesophageal cancer?

Answer 15

Poor - five-year survival is 5-10%

Question 16

Outline the principles of definitive management for an oesophageal tear following immediate resucitation

Answer 16

1. Control of the oesophageal leak
2. Eradication of mediastinal and pleural contamination
3. Decompress the oesophagus (typically via a trans-gastric drain or endoscopically-placed NG tube)
4. Nutritional support

Question 17

Who is suitable for non-operative management of oesophageal tear and what are the options ?

Answer 17

patients with iatrogenic perforations- often more stable
minimal contamination
contained perforation
no symptoms or signs of mediastinitis
no solid food in pleura or mediastinum
too frail for surgery

Non operative management options:
Initial resuscitation and transfer to ICU/HDU
Appropriate abx and anti-fungal cover
Nil by mouth for 1-2 weeks, with endoscopic insertion of an NG tube on drainage
Large-bore chest drain insertion
Total Parenteral Nutrition (TPN) or feeding jejunostomy insertion

Question 18

Initial investigation for suspected oesophageal rupture?

Answer 18

CT CAP with IV and oral contrast

Question 19

Describe the anatomy of the oesophagus

Answer 19

Upper third – composed of skeletal muscle
Middle third – transition zone of both skeletal and smooth muscle
Lower third -composed of smooth muscle

Question 20

What controls the peristaltic waves of the oesophagus?

Answer 20

The primary wave is under control of the swallowing centre and the secondary wave is activated in response to distention.

Question 21

What other sxs might someone with achalasia present with (other than progressive dysphagia/regurgitation)?

Answer 21

respiratory complications (either a nocturnal cough or aspiration)
chest pain
dyspepsia
weight loss

Question 22

How can achalasia be classified?

Answer 22

Type I = classical achalasia, no evidence of pressurisation
Type II = achalasia with compression or compartmentalisation in the distal oesophagus >30mmHg
Type III = two or more spastic contractions

Question 23

Outline the medical and surgical management of achalasia and the associated risks of each

Answer 23

Medical:
CCBS e.g. Nifedipine to inhibit LOS muscle contraction
Botox injections into LOS via endoscopy

Surgical:
Laparoscopic Heller Myotomy
– the division of the specific fibres of the LOS
- lower side-effect profile compared to endoscopic treatment

Per Oral Endoscopic Myotomy (POEM)
– a cardiomyotomy at the LOS is performed from the inside of the oesophageal lumen, through a submucosal tunnel
- good clinical response although rates of post-operative GORD are high

Endoscopic Balloon Dilatation – insertion of a balloon into the LOS, which is dilated to stretch the muscle fibres
- carries the risks of perforation and the need for further intervention, reserved for well patients with type II pattern

End-stage refractory achalasia may eventually require an oesophagectomy.

Question 24

What is diffuse oesophageal spasm?

Answer 24

a disease characterised by multi-focal high amplitude contractions of the oesophagus

caused by the dysfunction of oesophageal inhibitory nerves

can progress to achalasia

Question 25

Clinical features of DOS?

Answer 25

severe dysphagia to both solids and liquids central chest pain, exacerbated by food pain can respond to nitrates, making it difficult to distinguish from angina pectoris examination usually normal

Question 26

What will be shown on endoscopy and manometry for DOS? Finding on barium swallow?

Answer 26

Endoscopy: normal Manometry: repetitive, simultaneous, and ineffective contractions of the oesophagus Barium swallow - “corkscrew” appearance

Question 27

Give 3 causes of oesophageal dysmobility other than achalasia and DOS. How are they treated?

Answer 27

systemic sclerosis (most common) polymyositis dermatomyositis Tx: tx underlying cause e.g. immunosuppression nutritional modification PPIs

Question 28

What is a hiatus hernia? How common are they?

Answer 28

the protrusion of an organ from the abdominal cavity into the thorax through the oesophageal hiatus (typically the stomach) Present in 1/3 of people >50 yrs

Question 29

What are the two subtypes of hiatus herniae?

Answer 29

Sliding hiatus hernia (80%)– the GOJ and frequently the cardia of the stomach move or ‘slide’ upwards through the diaphragmatic hiatus into the thorax. Rolling or Para-Oesophageal hernia (20%) – an upward movement of the gastric fundus occurs to lie alongside a normally positioned GOJ, which creates a ‘bubble’ of stomach in the thorax. This is a true hernia with a peritoneal sac.

Question 30

What are the risk factors for hiatus herniae?

Answer 30

Age is the biggest- age-related loss of diaphragmatic tone, increasing intrabdominal pressures (e.g. repetitive coughing), and increased size of diaphragmatic hiatus Pregnancy Obesity Ascites

Question 31

Presenting features of hiatus herniae?

Answer 31

Normally asymptomatic Potentially: vomiting and weight loss (a rare but serious presentation due to gastric outflow being blocked) swallowing difficulties (oesophageal stricture formation or rarely incarceration of the hernia) bleeding / anaemia ( oesophageal ulceration) hiccups or palpitations (irritation to either the diaphragm or the pericardial sac) Examination usually normal but may be bowel sounds in chest if large

Question 32

What is the gold standard investigation for hiatus herniae?

Answer 32

Oesophagogastroduodenoscopy (OGD) - shows upwards displacement on GOJ (Z line)

Question 33

The first line pharmacological management for a symptomatic hiatus hernia is a PPI and lifestyle modification - WL, alteration of diet (low fat, earlier meals, smaller portions), and sleeping with the head of the bed raised. When is surgical intervention indicated?

Answer 33

Remaining symptomatic despite maximal medical therapy Increased risk of strangulation/volvulus (rolling type or mixed type hernia, or containing other abdominal viscera) Nutritional failure (due to gastric outlet obstruction)

Question 34

What are the 2 types of surgery for hiatus herniae?

Answer 34

Cruroplasty – The hernia is reduced from the thorax into the abdomen, large defects usually require mesh to strengthen the repair Fundoplication – The gastric fundus is wrapped around the lower oesophagus and stitched in place Aims to strengthen the LOS and keep the GOJ in place below the diaphragm

Question 35

Complications of hiatus herniae surgery?

Answer 35

Recurrence of the hernia Abdominal bloating (inability to belch due to the improved anti-reflux mechanism of the procedure) Dysphagia may occur if the fundoplication is too tight or if the crural repair is too narrow – relatively common early after surgery due to oedema Fundal necrosis, if the blood supply via the left gastric artery and short gastric vessels has been disrupted - surgical emergency, typically requiring major gastric resection

Question 36

Complications of untreated hiatus herniae?

Answer 36

Incarceration and strangulation Gastric volvulus- stomach twists on itself by 180 degrees

Question 37

How can gastric volvulus present?

Answer 37

Borchardt’s triad: Severe epigastric pain Retching without vomiting Inability to pass an NG tube

Question 38

Where are peptic ulcers most commonly located?

Answer 38

lesser curvature of the proximal stomach or the first part of the duodenum.

Question 39

Risk factors for peptic ulcers?

Answer 39

MAJOR: H. pylori infection and prolonged NSAID use Other risk factors include: corticosteroid use (when used with NSAIDs) previous gastric bypass surgery physiological stress (such as severe burns (Curling’s ulcer) or head trauma (Cushing’s ulcer) Zollinger-Ellison syndrome (rare)

Question 40

NICE guidelines suggest that a referral for urgent upper Oesophago-Gastro-Duodenoscopy (OGD) should be done for patients presenting with either:

Answer 40

New-onset dysphagia Aged >55 years with weight loss and either upper abdominal pain, reflux, or dyspepsia New onset dyspepsia not responding to PPI treatment

Question 41

What triad is found in Zollinger-Ellison syndrome?

Answer 41

1. severe peptic ulcer disease 2. gastric acid hypersecretion 3. gastrinoma

Question 42

Why does NICE recommend all gastric ulcers be biopsied?

Answer 42

Malignant potential

Question 43

The majority (>90%) of gastric cancers arise from where?

Answer 43

Gastric mucosa- adenocarcinomas

Question 44

Major risk factors for gastric cancer?

Answer 44

older male H. pylori infection smoking and alcohol consumption salt in diet positive family history pernicious anaemia.

Question 45

Presenting symptoms of gastric cancer? Examination findings?

Answer 45

Sxs: dyspepsia (particularly if new onset or not responsive to simple PPI treatment) dysphagia early satiety vomiting or melena Examination findings: (late stage) Epigastric mass Troisier sign - palpable Virchow's node Signs of metastatic disease: hepatomegaly, ascites, jaundice, or acanthosis nigricans

Question 46

Investigations for suspected gastric cancer?

Answer 46

OGD and biopsy Biopsies should be sent for: Histology – for classification and grading of any neoplasia present CLO test – for the presence of H. Pylori HER2/neu protein expression – this will allow for targeted monoclonal therapies if present CT CAP and staging laparoscopy

Question 47

What operations can be performed for gastric cancers in different locations?

Answer 47

Proximal gastric cancers – total gastrectomy Distal gastric cancers (antrum or pylorus) – subtotal gastrectomy early T1a tumours (tumours confined to the muscularis mucosa) - Endoscopic Mucosal Resection (EMR) (All surgery should be performed alongside peri-operative chemotherapy - 3 cycles of neoadjuvant and 3 cycles of adjuvant)

Question 48

What is the most commonly used method in reconstructing the alimentary anatomy?

Answer 48

Roux-en-Y reconstruction as it gives the best functional result

Question 49

Complications of gastrectomy?

Answer 49

death anastomotic leak re-operation dumping syndrome vitamin B12 deficiency (patients need 3-monthly vitamin B12 injections)

Question 50

What is dumping syndrome?

Answer 50

Sudden and large passage of hypertonic gastric contents into the small intestine, resulting in an intraluminal fluid shift and subsequent intestinal distention

Question 51

10-year survival rate for stomach cancer?

Answer 51

15%

Question 52

List 3 pre hepatic causes of jaundice

Answer 52

Haemolytic anaemia Gilbert’s syndrome Criggler-Najjar syndrome (absence of enzyme that conjugates bilirubin)

Question 53

List some hepatic causes of jaundice

Answer 53

Alcoholic liver disease Hepatitis - viral / autoimmune Hereditary haemochromatosis Primary biliary cirrhosis or primary sclerosing cholangitis Hepatocellular carcinoma Iatrogenic e.g. medication

Question 54

List some post hepatic causes of jaundice (intraluminal, mural and extra-mural)

Answer 54

Intra-luminal causes: gallstones Mural causes: cholangiocarcinoma, strictures, or drug-induced cholestasis Extra-mural causes: pancreatic cancer or abdominal masses (e.g. lymphomas)

Question 55

What viral serology and non-infective markers can be investigated for acute liver injury?

Answer 55

Viral Serology: Hepatitis A, B, C, and E CMV and EBV Non-infective markers: Paracetamol level Caeruloplasmin Antinuclear antibody and IgG subtypes

Question 56

What viral serology and non-infective markers can be investigated for chronic liver injury?

Answer 56

Viral serology: Hepatitis B and C Non-infective markers: Caeruloplasmin Ferritin and transferrin saturation Tissue Transglutaminase antibody Alpha-1 antitrypsin Autoantibodies

Question 57

Imaging for jaundice?

Answer 57

USS of abdomen first line Then MRCP to visualise biliary tree

Question 58

Causes of splenic rupture?

Answer 58

Abdo trauma - commonly seatbelt injuries or falls onto the left side in the elderly Iatrogenic Secondary to underlying splenomegaly- EBV, malignancy

Question 59

Clinical features of splenic rupture?

Answer 59

Signs of hypovolaemic shock LUQ tenderness Peritonism (more generalised as blood loss increases) Kehr's sign- free blood irritates diaphragm and causes referred left shoulder tip pain

Question 60

Investigations for splenic rupture?

Answer 60

Patients who are haemodynamically unstable with peritonism following trauma have abdominal bleeding until proven otherwise = immediate laparotomy haemodynamically stable with suspected abdominal injury = urgent CT CAP with IV contrast

Question 61

How should you manage haemodynamically stable patients with grade 1–3 splenic injuries without active extravasation?

Answer 61

Conservative tx : Admitted to HDU for observation (strict bed rest) Serial abdo exams for deterioration Resuscitated using the principle of permissive hypotension Repeat CT scan at 1-week post-injury There should be a low threshold for re-imaging and / or laparotomy with any evidence of increasing tenderness or peritonitis Prophylactic vaccinations at discharge

Question 62

Complications of conservative management for splenic rupture?

Answer 62

Ongoing bleeding Splenic necrosis Splenic abscess or cyst formation Thrombocytosis

Question 63

What are the 3 main types of gallstones?

Answer 63

Cholesterol stones – linked with poor diet and obesity Pigment stones – composed purely of bile pigments, from excess bile pigments production- seen in those with haemolytic anaemia Mixed stones – comprised of both cholesterol and bile pigments

Question 64

Risk factors for gallstones?

Answer 64

“5 F’s”: Fat, Female, Fertile, Forty, Family history diabetes mellitus Crohn's disease rapid weight loss e.g. weight reduction surgery drugs: fibrates, combined oral contraceptive pill

Question 65

What is a positive Murphy's sign?

Answer 65

Whilst applying pressure in the RUQ, ask the patient to inspire. Murphy’s sign is positive when there is a halt in inspiration due to pain, indicating an inflamed gallbladder - acute cholecystitis

Question 66

Investigations for suspected cholecystitis?

Answer 66

Bloods: FBC and CRP – inflammatory response LFTs – biliary colic and acute cholecystitis are likely to show raised ALP (ductal occlusion), but ALT and bilirubin should remain within normal limits (unless a Mirizzi syndrome) Amylase (or lipase) -evidence of pancreatitis A urinalysis ( including a pregnancy test if relevant) - exclude renal or tubo-ovarian pathology Imaging: trans-abdominal USS first line to look for gallstones

Question 67

What might be seen on USS in gallstone disease?

Answer 67

The presence of gallstones or sludge (the start of gallstone formation) Gallbladder wall thickness (if thick walled, then inflammation is likely) Bile duct dilatation (indicates a possible stone in the distal bile ducts)

Question 68

Management of acute cholecystitis?

Answer 68

IV abx (such as co-amoxiclav +/- metronidazole) analgesia and antiemetics laparoscopic cholecystectomy indicated within 1 week of presentation (ideally should be done within 72hrs) percutaneous cholecystostomy can be performed to drain the infection (in patients who aren't suitable for surgery)

Question 69

What is Mirizzi syndrome?

Answer 69

A stone located in Hartmanns pouch or in the cystic duct itself causes compression on the adjacent common hepatic duct = obstructive jaundice Confirmed with MRCP

Question 70

Complications of cholecystitis?

Answer 70

Mirizzi syndrome Gallbladder empyema (dx with USS or CT) Chronic cholecystitis (ongoing RUQ pain and N+V, diagnosed by CT) Bouveret’s Syndrome – stone impacts in the proximal duodenum, causing a gastric outlet obstruction Gallstone Ileus– a stone impacts at the terminal ileum causing a small bowel obstruction

Question 71

Causes of cholangitis?

Answer 71

Any condition which causes occlusion of the biliary tree (stasis of fluid and increased intraluminal pressure allows for bacterial colonisation) Gallstones (most common) , ERCP (iatrogenic), and cholangiocarcinoma

Question 72

Most common infective organisms in cholangitis?

Answer 72

Escherichia Coli (27%), Klebsiella species (16%), and Enterococcus (15%)

Question 73

Two common eponymous syndromes associated with cholangitis are:

Answer 73

Charcots Triad: Jaundice, Fever, and RUQ Pain Reynold’s Pentad: Jaundice, Fever, and RUQ Pain, Hypotension, and Confusion

Question 74

What is the gold standard investigation for cholangitis?

Answer 74

ERCP- diagnostic and therapeutic USS will show bile duct dilation (>6mm)

Question 75

Definitive management of cholangitis?

Answer 75

endoscopic biliary decompression, removing the cause of the blocked biliary tree In patients who are too sick to tolerate ERCP, percutaneous transhepatic cholangiography (PTC) is the second line intervention

Question 76

Complications of ERCP?

Answer 76

repeated cholangitis pancreatitis (in 3-5% of patients) bleeding (more common when a sphincterotomy is performed) perforation

Question 77

What factors increase the mortality rate of cholangitis?

Answer 77

delayed diagnosis, liver failure, cirrhosis, CKD, hypotension, female gender, and >50yrs

Question 78

What is the most common histological subtype of cholangiocarcinoma seen?

Answer 78

Adenocarcinomas (95%)

Question 79

What are Klatskin Tumours?

Answer 79

Also known as hilar cholangiocarcinoma bile duct cancers at the bifurcation of the right and left hepatic ducts invade local structures, such as the portal vein and hepatic arteries, and metastasise to local lymph nodes

Question 80

What are the main risk factors for cholangiocarcinoma?

Answer 80

Primary sclerosing cholangitis (lifetime risk of 10-20%) Congenital (Caroli’s disease, choledochal cyst) Intraductal gallstone formation Infective (Liver flukes, hepatitis virus) Toxins (Chemicals in rubber and aircraft industry) Liver cirrhosis

Question 81

Intrahepatic cholangiocarcinoma is generally asymptomatic until a late stage in the disease, whereas extrahepatic cholangiocarcinoma will typically present early. How do they present when symptomatic?

Answer 81

jaundice and pruritus steatorrhea dark urine non specific abdo pain WL

Question 82

What is Courvoisier’s Law?

Answer 82

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

Question 83

How is cholangiocarcinoma investigated and managed?

Answer 83

Bloods- obstructive jaundice (elevated bilirubin, ALP, and ɣGT) tumour markers CEA and CA19-9 Mainstay is radiology - MRCP gold standard Staging via a combination of contrast-enhanced triple phase CT and contrast-enhanced MRI of the liver

Question 84

How is cholangiocarcinoma managed?

Answer 84

definitive tx is complete surgical resection majority of patients have inoperable disease at the time of presentation - palliative care and symptomatic relief with stents

Question 85

The palliative treatment options in cholangiocarcinoma (most patients) include:

Answer 85

Stenting – relieve obstructive symptoms Surgery – Surgical bypass procedures if the obstruction cannot be relieved by stenting Medical – Palliative radiotherapy or chemotherapy

Question 86

Simple liver cysts are simple fluid-filled epithelial-lined sacs within the liver. Where do they most commonly occur? What causes them?

Answer 86

in the right lobe congenitally malformed bile duct cells (failing to connect to the extrahepatic ducts) which leads to a local dilatation

Question 87

What characterises polycystic liver disease? What are the 2 main causes?

Answer 87

the presence of ≥20 cysts within the liver parenchyma, each of which are ≥1cm in size Autosomal dominant polycystic kidney disease (ADPKD) - mutations in the PKD1 (chromosome 16) and PKD2 (chromosome 4) genes - commonest extra-renal manifestation Autosomal dominant polycystic liver disease (ADPLD) - mutations in the PRKCSH (chromosome 19) or SEC63 (chromosome 6) genes - no renal involvement

Question 88

How can polycystic liver disease be managed?

Answer 88

left alone and monitored potential short-term benefit for somatostatin analogues in symptomatic relief- reduce cyst volume Can do surgery if v symptomatic or worried about malignancy - US guided aspiration or laparoscopic de-roofing

Question 89

True cystic neoplasms of the liver are rare and account for <5% of liver cysts. What is the most common subtype? How should it be investigated?

Answer 89

cystadenomas - premalignant lesions CT imaging with contrast for further delineation +/- evidence of metastasis Aspiration or biopsy should be AVOIDED if a cystic neoplasm is suspected as can result in peritoneal seeding of the malignancy

Question 90

There are several features that can be seen on imaging for liver cysts that can suggest a sinister pathology. What are they?

Answer 90

Suspicious for malignancy (1) septations (2) wall enhancement (3) nodularity Suspicious for abscess (1) debris within the lesion (2) Loculation (may also suggest malignancy) Suspicious for hydatid cyst (1) Calcification (2) “Daughter cysts” around the main lesion

Question 91

What is the treatment of choice for both cystadenomas and cystadenocarcinomas?

Answer 91

Liver lobe resection

Question 92

Commonest causes of liver abscesses? Common offending organisms?

Answer 92

cholecystitis, cholangitis, diverticulitis, appendicitis, septicaemia E. Coli, K. pneumoniae, and S. constellatus

Question 93

Pyogenic abscess should be considered in which patients?

Answer 93

patients presenting with pyrexia of unknown origin associated with associated abdominal pain or bloating

Question 94

How do patients with liver abscesses present?

Answer 94

fever, rigors, and abdominal pain bloating nausea anorexia and weight loss fatigue jaundice On examination: RUQ tenderness +/- hepatomegaly

Question 95

What will be found on investigation for liver abscesses?

Answer 95

FBC - raised WCC and ALP in most cases and deranged ALT and bilirubin in some USS - poorly-defined lesions with hypo- and hyper-echoic areas Peripheral blood and fluid cultures sent for microscopy

Question 96

How can liver abscesses be managed?

Answer 96

image-guided aspiration of the abscess and abx

Question 97

What is the most common extra-intestinal manifestation of amebiasis infection, caused by the organism Entamoeba histolytica? What will be seen in blood results?

Answer 97

amoebic liver abscess presents with vague symptoms of abdominal pain, nausea, fever or rigors, weight loss, and bloating Cases should be suspected in patients with a history of recent travel (<6 months) to an endemic region leucocytosis with deranged LFTs

Question 98

Tx for an amoebic liver abscess?

Answer 98

metronidazole or tinidazole large cysts or those which do not respond well to antibiotic therapy - surgical drainage / luminal agents such as paromomycin

Question 99

Causes of HCC?

Answer 99

Most commonly viral Hep chronic alcohol excess hereditary haemochromatosis primary biliary cirrhosis (PBC) aflatoxin exposure (a toxic fungal metabolite)

Question 100

Risk factors for HCC?

Answer 100

Liver cirrhosis Hepatocellular adenoma Aflatoxin exposure Smoking Advanced age (>70yrs) Positive family history

Question 101

What test is useful as measure of disease response or surveillance in HCC?

Answer 101

alpha fetoprotein (AFP) level

Question 102

Appearance of HCC on USS? CT?

Answer 102

USS: hypodense heterogenous lesions CT/MRI: mass with vivid enhancement during the late arterial phase and a subsequent rapid wash out

Question 103

How is HCC staged?

Answer 103

The Barcelona Clinic Liver Cancer staging system (BCLC) 0 (very early), A (early), B (intermediate), C (advanced) and D (terminal)

Question 104

How can we mitigate the risk of post-hepatectomy liver failure?

Answer 104

the remnant liver must be a minimum of 20-40% of total liver volume pre-operative portal vein embolisation to the portal vein supplying the side of the liver to be resected

Question 105

What is the Milan criteria to qualify for liver transplant?

Answer 105

One lesion < 5cm or up to three lesions all <3cm There is no vascular infiltration There are no extra-hepatic manifestations

Question 106

Approximately half of metastasis to the liver arise from where?

Answer 106

colorectal primary tumours, due to spread via the portal circulation also pancreas, breast, and lung

Question 107

Whilst not routinely performed for acute pancreatitis, an AXR can show what?

Answer 107

a ‘sentinal loop sign’ - dilated proximal bowel loop adjacent to the pancreas

Question 108

Systemic complications of acute pancreatitis?

Answer 108

Disseminated Intravascular Coagulation (DIC) Acute Respiratory Distress Syndrome (ARDS) Hypocalcaemia Fat necrosis from released lipases→release of free fatty acids→react with serum calcium to form chalky deposits Hyperglycaemia Secondary to destruction of islets of Langerhans

Question 109

Most cases of acute pancreatitis are due to what 2 things?

Answer 109

gallstones and alcohol

Question 110

Local complications of acute pancreatitis?

Answer 110

Pancreatic Necrosis - should be suspected in patients with evidence of persistent systemic inflammation for more than 7-10 days after the onset of pancreatitis, confirm with CT Pancreatic Pseudocyst (lacks an epithelial lining) -50% will spontaneously resolve, if present for longer than 6 weeks unlikely to resolve spontaneously, tx is surgical debridement or endoscopic drainage

Question 111

What Serum amylase level is diagnostic of acute pancreatitis?

Answer 111

3 times the upper limit of normal

Question 112

How is acute pancreatitis managed?

Answer 112

Treatment is conservative and antibiotics should only be used as prophylaxis in cases of confirmed pancreatic necrosis

Question 113

In suspected cases of chronic pancreatitis, what must you check?

Answer 113

blood glucose (secondary to endocrine dysfunction) LFTs (to ensure no concurrent obstructive jaundice) faecal elastase level will be low in most cases of chronic pancreatitis with exocrine insufficiency, often can aid the diagnosis CT to confirm diagnosis

Question 114

How should chronic pancreatitis be managed medically?

Answer 114

Treating any reversible underlying cause + analgesia - neuropathic analgesia (pregabalin) more effective than opioids long term Patients with malabsorption secondary to exocrine dysfunction may benefit from enzyme replacement (including lipases), e.g. Creon Those with pancreatogenic diabetes may benefit insulin regimes ERCP - stone removal, stent placement Extracorporeal shock wave lithotripsy (ESWL)

Question 115

How should chronic pancreatitis be managed surgically?

Answer 115

large ductal stones = Frey’s procedure may be performed pancreatic head disease but without ductal stones = lateral pancreaticojejunostomy

Question 116

What is the most common type of pancreatic cancer? Risk factors?

Answer 116

Ductal adenocarcinoma - arise from the exocrine portion Risk factors: smoking, chronic pancreatitis, and dietary factors (high red meat intake, low fruit and vegetables intake)

Question 117

How does pancreatic cancer present?

Answer 117

Obstructive jaundice – due to compression of the common bile duct (present in 90% of cases at time of diagnosis), typically painless Weight loss – due to the metabolic effects of the cancer, or secondary to exocrine dysfunction Abdominal pain (non-specific) – due to invasion of the coeliac plexus or secondary to pancreatitis

Question 118

What tumour marker can be used for assessing response to treatment in pancreatic cancer?

Answer 118

CA19-9

Question 119

What investigations can be done for pancreatic cancer?

Answer 119

blood tests- FBC (anaemia or thrombocytopenia) and LFTs (raised bilirubin, ALP, and gamma-GT) abdominal USS-pancreatic mass or a dilated biliary tree CT imaging is the gold standard for preliminary diagnosis- can provide staging

Question 120

How are pancreatic tumours classified?

Answer 120

resectable, borderline resectable, or locally advanced at diagnosis, <20% of patients have a resectable tumour

Question 121

What are the surgical options for removing a pancreatic tumour? Complications of pancreatic cancer surgery?

Answer 121

Head of the pancreas = pancreaticoduodenectomy (termed a Whipple’s procedure) with regional lymphadenectomy Body or tail of pancreas = distal pancreatectomy +/- splenectomy with regional lymphadenectomy All procedures: adjuvant chemotherapy, typically either with gemcitabine or 5-fluorouracil (5-FU) Complications: pancreatic fistula, delayed gastric emptying, and pancreatic insufficiency

Question 122

Prognosis of pancreatic cancer?

Answer 122

Very poor - 5-year survival rate around 10%

Question 123

Pancreatic cysts are fluid-filled lesions found within the pancreas, usually asymptomatic. How are pancreatic cysts classified?

Answer 123

mucinous (lined with mucin-producing epithelium) OR non-mucinous (namely simple cysts, pseudocysts, and serous cystadenomas) mucinous cysts are higher risk, serous cysts are lower risk

Question 124

How should pancreatic cysts be managed?

Answer 124

Symptomatic cysts, cysts with high-risk features, and those with known high risk for malignancy should be referred for surgical resection the remainder can undergo regular surveillance (MRI pancreas every 6 months-2 years)

Question 125

Presenting features of acute pancreatitis?

Answer 125

severe epigastric pain that may radiate through to the back vomiting is common examination may reveal epigastric tenderness, ileus and low-grade fever periumbilical discolouration (Cullen's sign) and flank discolouration (Grey-Turner's sign) is described but rare

Question 126

Key investigation to perform early in acute pancreatitis?

Answer 126

USS

Question 127

Presenting features of chronic pancreatitis?

Answer 127

pain is typically worse 15 to 30 minutes following a meal steatorrhoea: between 5 and 25 years after the onset of pain diabetes mellitus: typically occurs > 20 years after symptom begin

Question 128

RUQ pain with raised inflammatory markers in a patient with a history of gallstones→

Answer 128

acute cholecystitis or cholangitis rather than biliary colic if abnormal LFTs - suggests ascending cholangitis

Question 129

What test may be useful for late presentations > 24 hours when investigating suspected acute pancreatitis?

Answer 129

Serum lipase - longer half-life than amylase

Question 130

Outline the Glasgow scale of Pancreatitis Severity (PANCREAS):

Answer 130

PaO2< 7.9kPa Age > 55 years Neutrophils (WBC > 15) Calcium < 2 mmol/L Renal function: Urea > 16 mmol/L Enzymes LDH > 600IU/L Albumin < 32g/L (serum) Sugar (blood glucose) > 10 mmol/L

Question 131

indicator of pancreatitis severity?

Answer 131

presence of hypocalcaemia

Question 132

How does biliary colic present differently to other gallstone related conditions?

Answer 132

no fever and liver function tests/inflammatory markers are normal

Question 133

First line tx in low grade gastric MALT lymphoma?

Answer 133

H.pylori eradication Omeprazole, amoxicillin and clarithromycin

Question 134

Causes of acute pancreatitis?

Answer 134

GET SMASHED Gallstones Ethanol Trauma Steroids Mumps (other viruses include Coxsackie B) Autoimmune (e.g. polyarteritis nodosa), Ascaris infection Scorpion venom Hypertriglyceridaemia, Hypercalcaemia, Hypothermia (think in homeless patient found in the street) ERCP Drugs (azathioprine, mesalazine, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)

Question 135

Loss of vibration sense, ataxia and absent ankle reflexes in a patient post gastrectomy?

Answer 135

Subacute combined degeneration of the cord due to B12 deficiency

Question 136

Blockage of which hepatobiliary duct is least associated with jaundice?

Answer 136

Cystic duct

Question 137

investigation of choice for suspected Boerhaave's syndrome?

Answer 137

CT contrast swallow

Question 138

What are pigmented gallstones associated with?

Answer 138

hemolytic anemia (e.g. sickle cell) and liver cirrhosis

Question 139

Absolute contraindications to laprascopic surgery?

Answer 139

haemodynamic instability/shock raised intracranial pressure - pneumoperitoneum created may worsen this acute intestinal obstruction with dilated bowel loops (e.g. > 4 cm) uncorrected coagulopathy

Question 140

What test can be used to determine the cause of hyperbilirubinaemia?

Answer 140

FBC - tells if due to haemolysis or Gilbert's syndrome