Upper GI and Hepatobiliary surgery Flashcards
The epiploic foramen of Winslow is an important anatomical landmark as it is the only communication between the greater and the lesser sac. Of the five structures listed below, which one is not a border of the epiploic foramen of Winslow?
A. Inferior vena cava
B. First part of the duodenum
C. Hepatoduodenal ligament
D. Gallbladder
E. Caudate lobe of the liver
D. Gallbladder
the gallblader is seperate from the the epiploic foramen of Winslow. It is important to be aware of the structures contained within the Hepatoduodenal ligament; the portal triad. The triad is made up of the Hepatic artery, portal vein, and the common ble duct.
Of the following, which is not a risk factor for gastric cancer?
A. Pernicious anaemia
B. Helicobacter pylori
C. Partial gastrectomy
D. Blood group O
E. Dried fish
D. Blood group O
Incidence of gastric cancer in the UK has declined to 16:100,000. It is more common in Japan, Dried meats and fish are associated with an increased risk due to high quantities of nitrosamines.
All of the factors here are risks for gastric cancer, except blood group O, it is Blood group A that carries a higher risk (for reasons unclear).
Which of the following investigations are not used in staging of oesophageal
malignancy?
A. Mediastinoscopy
B. High-resolution computed tomography scanning
C. Endoscopy
D. Endoluminal ultrasound
E. Laparoscopy
C. Endoscopy
Due to the insidious nature of oesophageal cancer it is often diagnosed late and 75% of cases will have metastasied by the time of diagnsis, as such it carries a 5% 5-year survival.
The appropriate staging investigation will depend on the location of the primary tumour, however endoscopy is a diagnostic and grading (biopsy) investigation. Endoscopy is limited to visualising the surface of the tumour and taking samples, it cannot identify the depth of the tumour, the nodal involvement or the prescence of mets.
The blood supply to the oesophagus is derived from which three vessels?
A. Inferior thyroid artery, descending aorta, left gastric artery
B. Internal carotid, descending aorta, oesophageal artery
C. Lateral thoracic artery, phrenic artery, right gastric artery
D. Pharyngeal artery, long thoracic artery, phrenic artery
E. Ascending aorta, common hepatic artery, left gastric artery
A. Inferior thyroid artery, descending aorta, left gastric artery
At first sight this question looks daunting but applying some basic anatomy it can be narrowed down.
We can exclude option (B) straight away as the internal carotid doesn’t branch until it is within the cranial vault.
The lateral thoracic artery runs in the mid axillary line supplying the lateral chest wall, and the long thoracic artery is fictitious so that takes out (C) and (D).
with option (E) the common hepatic and the ascending aorta are not related to the oesophagus in any way.
(A) is the correct answer, the first third is supplied by the inferior thyroid artery abd drained by the inferior thyroid veins and deep cervical lymph nodes. The second third is supplied by the descending aorta and drained by azygos vein and the posterior mediastinal lymph nodes. The lower third is supplied by the oesophageal branches of the left gastric artery and drained by the left gastric vein into the portal sysem (hence varicies), and its the lymph nodes of the coeliac plexus that drains it.
A 58-year-old patient presents with a 6-week history of increasing difficulty
swallowing. He first noticed problems when eating meat which became stuck
‘behind his heart’, but this gradually began to include other foods. The patient is currently worried because he is now struggling with thick fluids and has noticed some involuntary weight loss. What is the most appropriate investigation?
A. Staging computed tomography
B. Barium meal
C. Upper gastrointestinal endoscopy
D. Barium swallow
E. Electrocardiography
C. Upper gastrointestinal endoscopy
With this patient’s age, the rapidly worsening dysphagia, and weight loss is calls it to mind the potential for malignancy. The gold standard for diagnosis is an endoscopy (C), as it enables visualisation and biopsy.
Barium meal (B) is a technique more suited to gastric pathology.
Barium Swallow (D) is more utilised for neuromuscular causes of dysphagia, such as achalasia. With mechanical causes of dysphagi it has largely been replaced by endoscopy.
Not sure why ECG (E) is an option here, even if it was a cardiac cause a 6 week history excludes ACS.
A 27-year-old patient presents with a 3-month history of increasing difficulty in
swallowing. He first noticed the problem when drinking fluids, but is now
commonly experiencing it when eating food as well. He has presented as
regurgitation of food is becoming a problem and he has noticed unintentional
weight loss. A chest radiograph shows a widened mediastinum. What is the most likely diagnosis?
A. Thoracic aortic aneurysm
B. Oesophageal malignancy
C. Plummer–Vinson syndrome
D. Achalasia
E. Oesophageal spasm
D. Achalasia
Achalasia is a neuromuscular disorder caused by te degeneration of Auerbach’s plexus which causes a failure of the lower oesophageal plexus to relax.
It typically presents as difficulty swallowing fluids initially followed by food. Chest pain and weight loss are common. The progression from liquids to solids is the opposite to the history of a mechanical cause such as malignancy (B). The patient’s age is also a factor that makes malignancy less likely. The widend mediastinum is a dillated oesophagus loaded with food.
an aortic anueurysm (A) would be unlikely to cause dysphagia, if it did then it would be an obstructive presentation.
Plummer-Vinsn syndrome (C) is charecterised by severe iron deficiency and hyperkeratinisation of the upper third of the oesophagus, which causes web formation and obstructive dysphagia.
Oesophageal spasm (E) is a differential diagnosis for cardiac chest pain, it can also be relieved by GTN. Dysphagia does occur but weght loss is almost never a feature.
The severity of acute pancreatitis can be assessed using the Glasgow criteria.
Which of the following is not used in the calculation?
A. Serum amylase
B. White cell count
C. Serum calcium
D. Alanine aminotransferase
E. Serum urea
A. Serum amylase
The Glasgow criteria is the most commonly applied prognostic criteria for acute pancreatitis, as such it is the one you should probably remember.
One point is awarded for each criteria and a score of 3 points within 48hrs of onset indicates severe disease. The criteria can be remembered by the mnenomic PANCREAS:
- P – pO2 <8kPa
- A – age >55 years
- N – neutrophil count >15 x 109/L
- C – calcium <2mmol/L
- R – raised urea >16mmol/L
- E – enzymes; LDH >600 IU/L, AST >300 IU/L
- A – albumin <32 g/L
- S – sugar (glucose) >10 mmol/L
CREST syndrome is an autoimmune condition which is associated with atrophy
and fibrosis of the oesophageal musculature resulting in dysphagia and reflux-type symptoms. Which of the following is not a feature of CREST syndrome?
A. Raynaud’s phenomenon
B. Erythematous malar rash
C. Sclerodactyly
D. Soft tissue calcification
E. Telangiectasia
B. Erythematous malar rash
Scleroderma is a spectrum of disorders that affect the connective tissues. There is localised scleroderma (skin involvement), Raynaud’s, and systemic sclerosis (made up of diffuse cutaneous systemic sclerosis, and limited cutaneous systemic sclerosis [also known as CREST syndrome]).
Both forms os systemic sclerosis affect the lungs and kidneys, leading to fibrosis and failure. In DCSS skin involvement is severe and widespread but organ involvement is maximal at 3 years and then typically improves. In CREST skin involvement is confined to the face and extremities but organ involvement tends to be severe and progresive. CREST is an acronym for the cardinal features: Calcinosis, Raynaud’s, esophageal (american spelling) disorders, sclerodactyly and telangiectasia.
Diagnosis is clinical and suported by anti-nuclear antibodies. anti-SCL-70 is positive in 40%, anti-centromere antibody occurs in 80-90% of CREST. However all of this testing is non-specific.
The gastro-oesophageal sphincter is not a true sphincter in that it does not rely on a ring of contractile muscle to maintain patency. It therefore relies on several other mechanisms to prevent reflux. Which of the following does not contribute to gastro-oesophageal sphincter function?
A. Left crus of diaphragm
B. Smooth muscle of the lower oesophageal sphincter
C. Angle of His
D. Right crux of diaphragm
E. Intra-abdominal pressure
A. Left crus of diaphragm
The gastro-oesophageal sphincter is made up of three components. The lower oesophageal sphincter (B) is a 4cm long section of hypertropic muscle, it maintains a tonic contraction resulting in a pressure equal to 25cm H2O above resting intragastric pressure.
The next component is the is the extrinsic sphincter formed of skeletal muscle fibres of the right crus of the diaphragm that form a sling around the eosophagus. as well as support during rest these fibres contract with inspiration and abdominal straining to prevent reflux.
The final component is the ‘physiological sphinter’, as the oesophagus projects 2-3cm into the abdomen any rise of abdominal pressure compresses the lower part of the oesophagus. this effect is synergistic with the angle of His, this provides a flap valve which also helps to prevent reflux. It can be seen that this knowledge is important in evaluating the effect of a hiatus hernia on reflux.
A 58-year-old builder is referred to outpatients with a long history of retrosternal chest pain associated with food. His GP has started a trial of daily proton-pump inhibitor without symptomatic relief. Oesophagogastroduodenoscopy was performed which showed grade 2 oesophagitis with a hiatus hernia. The stomach and duodenum were normal. What is the most appropriate management?
A. Triple eradication therapy
B. Add H2 antagonist
C. Nissen’s fundoplication
D. Increase proton-pump inhibitor dose with yearly endoscopic surveillance
and biopsy
E. Supportive gusset
B. Add H2 antagonist
Hiatus hernias are common, affecting 30% of the population aged over 50, and 50% of those with hiatus hernias complain of symptomatic GORD. A minority of hiatus hernis (8%) are sliding hernias, these do not routinly require surgical repair. Rolling Hiatus hernias, however, may strangulate and so require surgical repair.
The Los Angeles classification grades oesophagitis as four grades;
Grade 1- small mucosal breaks, not continous over 2 mucosal folds
Grade 2- Mucosal break >5mm long, not continous over 2 mucosal folds
Grade3- Mucosal breaks extending across more than 2 mucosal folds
Grade 4 - Circumfrential mucosal breakdown involving >75% of the mucosal circumference.
Complications of oesophagitis include; Barrett’s oesophagus, malignancy, bleeding (usually chronic small bleeds), and stricture.
Surgery is the last line treatment and should be reserved for life-altering severe symptoms and refractory oesophagitis. The first treatmetn options are optimal life-style management and best medical therapy.
The next step with this patient is to add another medical treatment such as a H2 antagonist as the effect is synergistic with the PPI.
Triple eradication therepy (A) is a treatment option for H.pylori and so relevant to gastric/duodenal ulcers.
Which one of the following is not a recognized long-term complication of
partial/total gastrectomy?
A. Gastric malignancy
B. Obstruction
C. Folate deficiency
D. Iron deficiency
E. Vitamin B1 deficiency
E. Vitamin B1 deficiency
Gastrectomy is less commonly performed now as modern medical and endoscopic procedures are generally effective.
The most common indication for gastrectomy now is for gastric malignancy, although bypass surgery is a growing trend.
Therefore it is important to be aware of the side effects of surgery, there is a lifelong increased risk of malignancy after partial gastrectomy (A).
There is always an increased risk of obstruction with any abdominal surgery (B)
There are several malabsorption syndromes associated with gastrectomy; B12, Iron, and folate deficiency (C)(D).
Thiamine (Vitamin B1) difeciency is not associated ith gastrectomy (E)
Other side effects include; abdominal discomfort and early saity due to reduced gastric volume. There is a specific complication, ‘Dumping syndrome’, this is where a large volume of chyme is rapidly dumped in the duodenum. These sugars are rapidly absorbed leading to an exaggerated insulin spike, leading to; hot flushes, palpitations, and syncope, much like a hypoglaecimic episode.
A 45-year-old man presents to the emergency department with a history of coffeeground vomiting. He also reports that for 2 days his stool has appeared darker than usual. Which of the following gives the most sensitive guide as to the severity of his gastrointestinal haemorrhage?
A. Haemoglobin
B. Systolic blood pressure
C. Pulse rate
D. Volume of vomitus/melaena
E. Lying and standing blood pressure
E. Lying and standing blood pressure
There is a strong sugesstion of gastrointestinal bleeding in this scenario. this patient needs a endoscopy .
Parameters such as heart rate and BP (B)(C) will be preserved in a fit patient until severe haemodynamic compromise.
The most sensitive measure is to assess the dynamic cardiac reserve with a lying/standing blood pressure.
Of note lying/standing blood pressure is a good measure of haemodynamic compromise in patient’s who would be otherwise difficult to assess, such as hypertensives or those on b-blockers.
Heamoglobin (A) may indicate the need for transfusion (when less than 80g/l), but it is too variable and difficult to interpret without a baseline to make it any use for assessing haemorrhage.
Assessing the volume of vomitus/malaena (D) is so inaccurate that it is next to wothless.
A 51-year-old patient is brought into the emergency department following a largevolume haematemesis. The patient is a known cirrhotic and previously survived variceal haemorrhage. The patient is haemodynamically stabilized and an emergency endoscopy is performed which identifies actively bleeding varices, and banding is attempted. Shortly following the procedure the patient again has a large-volume haematemesis and becomes haemodynamically compromised. The next step is:
A. Oesophageal transection
B. Transjugular intrahepatic portal–systemic stent shunting
C. Sengstaken–Blakemore tube
D. Repeat endoscopy
E. Angiographic embolisation
C. Sengstaken–Blakemore tube
Oesophageal varicies are the cause of less than 7% of upper GI bleeds, with 80% of cases within the population of cirrhotic patients.
Peptic ulceration accounts for 40% of variceal bleeding, oesophagitis/gastritis for 20% and Malloy-Weiss tears for 15%.
without intervention 30% of varicies will bleed and of those 80% will re-bleed within 2 years. The most effective management is propranolol and repeat endoscopic monitoring and banding.
In an acute setting the first step is, as expected, to haemodynamically stabilise the patient. This can be achieved with endoscopy with sclerotherapy or banding. There needs to also be an infusion of a PPI or terlipressin and any correction of clotting abnormalities.
If this first line treatment fails then the next step is to utilise a Sengstaken–Blakemore tube (C) (effectively a ballon tamponade device).
Repeat endoscopy (D) is unlikely to resolve the bleeding if it failed the first time, although it has a role in the haemodynamically stable patient.
Oesophageal transection (A) is an outdated procedure that is rarely used.
This patient will likely need a TIPSS (B), but it isn’t the immediate next step in an acute scenario. TIPSS carries risks of futire sepsis (blood bypasses the liver), encephalopathy, and risk of reocclusion.
Angiography (E) is inappropriate as this is not an arterial bleed, it is portal-venous.
A 45-year-old patient presents in shock complaining of sudden-onset generalized upper abdominal pain radiating to the right iliac fossa and the tip of his right shoulder. He reports one episode of vomiting but none since. He has no past medical problems. On examination his abdomen is rigid and bowel sounds are absent. The diagnosis is:
A. Caecal volvulus
B. Pancreatitis
C. Perforated duodenal ulcer
D. Ascending cholangitis
E. Appendicitis
C. Perforated duodenal ulcer
This question requires you to exclude the more unlikely pathologies here. The onset of these symptoms is very sudden which goes against a caecal volvulus (A) (as is the lack of vomiting).
With pancreatitis (B) it would be expected to find pain which radiates to the back, and associated vomiting.
With no fever or jaundice ascending cholangitis (D) is unlikely.
Appendicitis (E) is a varied presentation, but shoulder tip pain is uncommon and the rapid onset of generalised peritonitis doesn’t fit/
All things considered the rapid onset upper abdominal pain, with the severe shock and limited vomiting are typical of a perforated duodenal ulcer (C)
Which of the following is not encountered when making Kocher’s (right subcostal)
incision during an open cholecystectomy?
A. Anterior rectus sheath
B. Superior epigastric vessels
C. Eighth intercostal nerve
D. Falciform ligament
E. External oblique
D. Falciform ligament
Kocher’s incision can be on the left or the right, but is most commonly on the right side for biliary tree surgery. It is made 3-5cm below the costal margin, exposing the anterior rectus sheath (A). After dividing the rectus muscles the exposed branches of the superior epigastric vessels (B) are ligated, the lateral abdominal muscles (E) are also encountered as the incision is extended. Within these lateral muscles lie the 8th and 9th intercostal nerves (C), the 8th nerve is often sacrificed.
The falciform ligamenet (D) is attached to the linea alba, which is not encountered in a Kocher’s incision.