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Y3 Surgery > Upper GI and hepatobiliary > Flashcards

Upper GI and hepatobiliary Flashcards

1
Q

Risk factors for GORD?

A

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

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2
Q

Presentation of GORD?
Red flag sxs?

A

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

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3
Q

What is the Los Angeles classification?

A

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%)

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4
Q

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

A

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

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5
Q

3 main indications for surgery in GORD?

A

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)

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6
Q

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?

A

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

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7
Q

Complications of GORD?

A

aspiration pneumonia
Barrett’s oesophagus
oesophageal strictures and oesophageal cancer

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8
Q

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

A

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

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9
Q

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

A

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

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10
Q

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

A

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

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

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11
Q

What is the problem with surgery for oesophageal cancer?

A

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

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12
Q

What are the different approaches to oesophagectomy?

A

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)

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13
Q

What are the main complications of oesophagectomy?

A

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

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14
Q

What palliative management is available for oesophageal cancer?

A

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

Cachexia:
Nutritional support with thickened fluids and supplements

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15
Q

What is the prognosis for oesophageal cancer?

A

Poor - five-year survival is 5-10%

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16
Q

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

A
  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
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17
Q

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

A

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

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18
Q

Initial investigation for suspected oesophageal rupture?

A

CT CAP with IV and oral contrast

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19
Q

Describe the anatomy of the oesophagus

A

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

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20
Q

What controls the peristaltic waves of the oesophagus?

A

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

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21
Q

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

A

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

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22
Q

How can achalasia be classified?

A

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

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23
Q

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

A

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.

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24
Q

What is diffuse oesophageal spasm?

A

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

caused by the dysfunction of oesophageal inhibitory nerves

can progress to achalasia

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25
Q

Clinical features of DOS?

A

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

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26
Q

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

A

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

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27
Q

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

A

systemic sclerosis (most common)
polymyositis
dermatomyositis

Tx:
tx underlying cause e.g. immunosuppression
nutritional modification
PPIs

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28
Q

What is a hiatus hernia? How common are they?

A

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

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29
Q

What are the two subtypes of hiatus herniae?

A

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.

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30
Q

What are the risk factors for hiatus herniae?

A

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

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31
Q

Presenting features of hiatus herniae?

A

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

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32
Q

What is the gold standard investigation for hiatus herniae?

A

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

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33
Q

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?

A

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)

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34
Q

What are the 2 types of surgery for hiatus herniae?

A

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

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35
Q

Complications of hiatus herniae surgery?

A

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

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36
Q

Complications of untreated hiatus herniae?

A

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

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37
Q

How can gastric volvulus present?

A

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

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38
Q

Where are peptic ulcers most commonly located?

A

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

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39
Q

Risk factors for peptic ulcers?

A

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)

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40
Q

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

A

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

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41
Q

What triad is found in Zollinger-Ellison syndrome?

A
  1. severe peptic ulcer disease
  2. gastric acid hypersecretion
  3. gastrinoma
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42
Q

Why does NICE recommend all gastric ulcers be biopsied?

A

Malignant potential

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43
Q

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

A

Gastric mucosa- adenocarcinomas

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44
Q

Major risk factors for gastric cancer?

A

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

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45
Q

Presenting symptoms of gastric cancer?
Examination findings?

A

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

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46
Q

Investigations for suspected gastric cancer?

A

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

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47
Q

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

A

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)

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48
Q

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

A

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

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49
Q

Complications of gastrectomy?

A

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

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50
Q

What is dumping syndrome?

A

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

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51
Q

10-year survival rate for stomach cancer?

A

15%

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52
Q

List 3 pre hepatic causes of jaundice

A

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

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53
Q

List some hepatic causes of jaundice

A

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

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54
Q

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

A

Intra-luminal causes: gallstones

Mural causes: cholangiocarcinoma, strictures, or drug-induced cholestasis

Extra-mural causes: pancreatic cancer or abdominal masses (e.g. lymphomas)

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55
Q

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

A

Viral Serology:
Hepatitis A, B, C, and E
CMV and EBV

Non-infective markers:
Paracetamol level
Caeruloplasmin
Antinuclear antibody and IgG subtypes

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56
Q

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

A

Viral serology:
Hepatitis B and C

Non-infective markers:
Caeruloplasmin
Ferritin and transferrin saturation
Tissue Transglutaminase antibody
Alpha-1 antitrypsin
Autoantibodies

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57
Q

Imaging for jaundice?

A

USS of abdomen first line
Then MRCP to visualise biliary tree

58
Q

Causes of splenic rupture?

A

Abdo trauma - commonly seatbelt injuries or falls onto the left side in the elderly

Iatrogenic

Secondary to underlying splenomegaly- EBV, malignancy

59
Q

Clinical features of splenic rupture?

A

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

60
Q

Investigations for splenic rupture?

A

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

61
Q

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

A

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

62
Q

Complications of conservative management for splenic rupture?

A

Ongoing bleeding
Splenic necrosis
Splenic abscess or cyst formation
Thrombocytosis

63
Q

What are the 3 main types of gallstones?

A

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

64
Q

Risk factors for gallstones?

A

“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

65
Q

What is a positive Murphy’s sign?

A

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

66
Q

Investigations for suspected cholecystitis?

A

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

67
Q

What might be seen on USS in gallstone disease?

A

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)

68
Q

Management of acute cholecystitis?

A

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)

69
Q

What is Mirizzi syndrome?

A

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

70
Q

Complications of cholecystitis?

A

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

71
Q

Causes of cholangitis?

A

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

72
Q

Most common infective organisms in cholangitis?

A

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

73
Q

Two common eponymous syndromes associated with cholangitis are:

A

Charcots Triad: Jaundice, Fever, and RUQ Pain

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

74
Q

What is the gold standard investigation for cholangitis?

A

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

75
Q

Definitive management of cholangitis?

A

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

76
Q

Complications of ERCP?

A

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

77
Q

What factors increase the mortality rate of cholangitis?

A

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

78
Q

What is the most common histological subtype of cholangiocarcinoma seen?

A

Adenocarcinomas (95%)

79
Q

What are Klatskin Tumours?

A

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

80
Q

What are the main risk factors for cholangiocarcinoma?

A

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

81
Q

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?

A

jaundice and pruritus
steatorrhea
dark urine
non specific abdo pain
WL

82
Q

What is Courvoisier’s Law?

A

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

83
Q

How is cholangiocarcinoma investigated and managed?

A

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

84
Q

How is cholangiocarcinoma managed?

A

definitive tx is complete surgical resection

majority of patients have inoperable disease at the time of presentation - palliative care and symptomatic relief with stents

85
Q

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

A

Stenting – relieve obstructive symptoms

Surgery – Surgical bypass procedures if the obstruction cannot be relieved by stenting

Medical – Palliative radiotherapy or chemotherapy

86
Q

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

A

in the right lobe

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

87
Q

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

A

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

88
Q

How can polycystic liver disease be managed?

A

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

89
Q

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?

A

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

90
Q

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

A

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

91
Q

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

A

Liver lobe resection

92
Q

Commonest causes of liver abscesses?
Common offending organisms?

A

cholecystitis, cholangitis, diverticulitis, appendicitis, septicaemia

E. Coli, K. pneumoniae, and S. constellatus

93
Q

Pyogenic abscess should be considered in which patients?

A

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

94
Q

How do patients with liver abscesses present?

A

fever, rigors, and abdominal pain
bloating
nausea
anorexia and weight loss
fatigue
jaundice

On examination: RUQ tenderness +/- hepatomegaly

95
Q

What will be found on investigation for liver abscesses?

A

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

96
Q

How can liver abscesses be managed?

A

image-guided aspiration of the abscess and abx

97
Q

What is the most common extra-intestinal manifestation of amebiasis infection, caused by the organism Entamoeba histolytica?

What will be seen in blood results?

A

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

98
Q

Tx for an amoebic liver abscess?

A

metronidazole or tinidazole

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

99
Q

Causes of HCC?

A

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

100
Q

Risk factors for HCC?

A

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

101
Q

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

A

alpha fetoprotein (AFP) level

102
Q

Appearance of HCC on USS? CT?

A

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

103
Q

How is HCC staged?

A

The Barcelona Clinic Liver Cancer staging system (BCLC)

0 (very early), A (early), B (intermediate), C (advanced) and D (terminal)

104
Q

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

A

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

105
Q

What is the Milan criteria to qualify for liver transplant?

A

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

106
Q

Approximately half of metastasis to the liver arise from where?

A

colorectal primary tumours, due to spread via the portal circulation

also pancreas, breast, and lung

107
Q

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

A

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

108
Q

Systemic complications of acute pancreatitis?

A

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

109
Q

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

A

gallstones and alcohol

110
Q

Local complications of acute pancreatitis?

A

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

111
Q

What Serum amylase level is diagnostic of acute pancreatitis?

A

3 times the upper limit of normal

112
Q

How is acute pancreatitis managed?

A

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

113
Q

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

A

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

114
Q

How should chronic pancreatitis be managed medically?

A

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)

115
Q

How should chronic pancreatitis be managed surgically?

A

large ductal stones = Frey’s procedure may be performed

pancreatic head disease but without ductal stones = lateral pancreaticojejunostomy

116
Q

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

A

Ductal adenocarcinoma - arise from the exocrine portion

Risk factors:
smoking, chronic pancreatitis, and dietary factors (high red meat intake, low fruit and vegetables intake)

117
Q

How does pancreatic cancer present?

A

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

118
Q

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

A

CA19-9

119
Q

What investigations can be done for pancreatic cancer?

A

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

120
Q

How are pancreatic tumours classified?

A

resectable, borderline resectable, or locally advanced

at diagnosis, <20% of patients have a resectable tumour

121
Q

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

A

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

122
Q

Prognosis of pancreatic cancer?

A

Very poor - 5-year survival rate around 10%

123
Q

Pancreatic cysts are fluid-filled lesions found within the pancreas, usually asymptomatic.

How are pancreatic cysts classified?

A

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

124
Q

How should pancreatic cysts be managed?

A

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)

125
Q

Presenting features of acute pancreatitis?

A

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

126
Q

Key investigation to perform early in acute pancreatitis?

A

USS

127
Q

Presenting features of chronic pancreatitis?

A

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

128
Q

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

A

acute cholecystitis or cholangitis rather than biliary colic

if abnormal LFTs - suggests ascending cholangitis

129
Q

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

A

Serum lipase - longer half-life than amylase

130
Q

Outline the Glasgow scale of Pancreatitis Severity (PANCREAS):

A

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

131
Q

indicator of pancreatitis severity?

A

presence of hypocalcaemia

132
Q

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

A

no fever and liver function tests/inflammatory markers are normal

133
Q

First line tx in low grade gastric MALT lymphoma?

A

H.pylori eradication

Omeprazole, amoxicillin and clarithromycin

134
Q

Causes of acute pancreatitis?

A

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)

135
Q

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

A

Subacute combined degeneration of the cord due to B12 deficiency

136
Q

Blockage of which hepatobiliary duct is least associated with jaundice?

A

Cystic duct

137
Q

investigation of choice for suspected Boerhaave’s syndrome?

A

CT contrast swallow

138
Q

What are pigmented gallstones associated with?

A

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

139
Q

Absolute contraindications to laprascopic surgery?

A

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

140
Q

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

A

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

Y3 Surgery (8 decks)

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