Upper GI and Hepatobiliary surgery Flashcards

1
Q

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

A

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.

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2
Q

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

A

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).

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3
Q

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

A

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.

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4
Q

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

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.

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5
Q

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

A

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.

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6
Q

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

A

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.

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7
Q

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

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
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8
Q

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

A

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.

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9
Q

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

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.

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10
Q

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

A

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.

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11
Q

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

A

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.

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12
Q

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

A

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.

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13
Q

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

A

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.

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14
Q

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

A

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)

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15
Q

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

A

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.

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16
Q

A patient is admitted from the emergency department following a large-volume
haematemesis. Oesophagogastroduodenoscopy is performed, which identifies a
posteriorly positioned duodenal ulcer that is actively bleeding. The vessel
responsible is:
A. Gastroduodenal artery
B. Abdominal aorta
C. Right gastric artery
D. Left gastric artery
E. Right gastroepiploic artery

A

A. Gastroduodenal artery

All of the blood supply to the stomach arises from the coeliac plexus at T12, the lesser curve is supplied by the right and left gastric vessels. The greater curve is supplied by the right and left gastroepiploic vessels. The right gastroepiploic artery is a branch of the gastroduodenal artery, which passes under teh first part of the duodenum close to the posterior wall. Therefore any erosion of a posterior duodenal ulcer is likely to breech the gastroduodenal artery.

17
Q

A patient is admitted to hospital following referral by his GP for melaena. An
oesophagogastroduodenoscopy identifies an actively bleeding gastric ulcer.
Haemostasis is achieved. You are called to see the patient 48 hours later by nursing staff concerned that the patient has again passed black stool. On examination the patient is comfortable, blood pressure is 120/80 mmHg lying and 115/85 mmHg standing, pulse rate is 70 beats/min and respiratory rate is 16 breaths/min. Rectal examination reveals black stool on glove. The next best course of action should be:

A. Urgent endoscopy
B. Repeat the full blood count
C. Intravenous fluids and colloid
D. Intravenous terlipressin
E. Nothing, this is normal following upper gastrointestinal bleeding

A

B. Repeat the full blood count

This patient is not shocked as seen by the observations and the lack of significant postural hypotensive drop. Therefore an ongoing haemorrhage is unlikey, we can exclude (A), (C), and (D).
There can be a continuation of malaena up to three days after bleeding has stopped, even longer if there is constipation. As such option (E) is a reasonable concept and the patient can be reassured that the continued maelena is not necessarily a sign of continued bleeding. The safest and most through step, however, is to repeat the FBC (B) to exclude an occult haemorrhage. #The scenarion would be of more concern if there had been a period of normal stool before the reoccurence of maelena and the finding of a fall in haematoctit; this would necessitate a repeat endoscopy.

18
Q

Which of the following syndromes is associated with multiple duodenal ulcers not
amenable to conventional medical therapy?

A. Hereditary non-polyposis colon cancer (HNPCC)
B. Plummer–Vinson syndrome
C. Gardner’s syndrome
D. Zollinger–Ellison syndrome
E. CREST syndrome

A

D. Zollinger–Ellison syndrome

Zollinger-Ellison syndrome (D) is caused by a non-insulin secreting tumour of the pancreas. It releases high levels of gastrin-like hormone, leading to hyper-acidity of the stomach and therefore, extensive duodenal ulceration.

HNPCC (A) also known as Lynch syndrome is an autosomal dominant condition that leads to a high risk of colon cancer, as well as; endometrial, ovary, stomach, small intestine, hepatobiliary tract, upper urinary tract, brain, and skin. It is due to an inherited mutation of the DNA mismatch repair mechanism.

Plummer-Vinson (B) is a condition of unclear aeitology that leads to iron deficiency anaemia and oesophageal webs, causing dysphagia. It is also associated with glossitis and cheilosis. It is generally seen in post-menopausal women, and carries an increased risk of oesophageal and pharyngeal carcinomas.

Gardner’s syndrome (C) is familial colorectal polyposis, it is autosomal dominant and presents with thousands of polyps in the colon and has an extremely high risk of colon cancer.

CREST (E) is a form of limited cutaneous scleroderma charecterised by the cardinal signs of; Calcinosis, Reynauds, oEsophageal dysmotility, Sclerodactly, Telangectasia.

19
Q

A patient presents with a short history of perfuse, projectile vomiting without bile staining. He has a history of peptic ulceration and chronic dyspepsia and has noticed increased bloating over the preceding 9 months. On examination there is distension in the epigastric region and a succession splash. The abdominal radiograph shows a grossly distended stomach and collapsed bowel. The most likely cause is:
A. Carcinoma of the pylorus
B. Carcinoma of the head of pancreas
C. Fibrotic stricture
D. Compression by malignant nodes
E. Chronic pancreatitis

A

C. Fibrotic stricture

The most common causes of gastric outlet obstruction in an adult is a fibrotic stricture (C) secondary to duodenal ulceration and cancer of the pylorus (A). As such the other causes presented here are more unusual, particularly without a suggestive history.

Distinguishing betwen the two possibilities here is somewhat tricky. Both present with painless projectile vomiting which is not bile stained, but contains stale food and smells faeculant. Significant weight loss is a feature of both conditons.

The long history of peptic ulcer disease points to a likey diagnosis of fibrotic stricture (C), this is supported by the gross distention which is a process that occurs over a period of years as there is gastric hypertrophy. A carcinoma (A) and (B) presents much more acutely.

The only way to reliably identify the cause is through endoscopy.

20
Q

Which of the following is not a lifestyle change which might reduce the occurrence of reflux-type symptoms?

A. Smoking cessation
B. Abdominal exercise
C. Avoid tight clothing
D. Eat smaller portions more often
E. Raise the head of the bed at night

A

B. Abdominal exercise

Gastro-oesophageal reflux is a common symptom affecting the majority of the population, the serious sequale of oesophagitis, anaemia, strictures, and Barrett’s oesophagus are far less common. For example Barrett’s oesophagus affects 2% of the population, and of those, 2% will develop malignancy.

The majority of reflux can be managed conservatively/lifestyle modification such as smoking cessation (A), weight loss, avoidance of tight clothing (C), avoiding large meals (D), and raising the head at night (E).

Abdominal exercises may excacerbate the problem (B).

Failure to respond to a PPI and conservative management may require an endoscopy to exclude a hiatus hernia or other cause.

New onset dyspepsia in patients over 55 or the prescence of ‘red flas’ should lead to urgent endoscopic investigation.

the red flags can be remembered with teh mnenomic ALARMS:

  • Anemia
  • Loss of weight
  • Anorexia
  • Recent onset of rapidly progressing symptoms
  • Melaena
  • Swallowing difficulty
21
Q

Which one of the following statements regarding gallstone disease is incorrect?

A. Gallstones occur in 15 per cent of all people over 65 in Western
countries
B. 85 per cent of gallstones are asymptomatic
C. 10 per cent are identifiable using plain film radiography
D. Gallstones are more common in males
E. Gallstone disease is the most common cause of acute pancreatitis

A

D. Gallstones are more common in males

Gallstones are present in around 15% of the population over 60 (A), but only produce symptoms in 15% of those patients (B).

Stones come in three varieties: cholesterol (15%), pigment (5%) and mixed stones (80%).

Pigment sones are seen in haemolytic anaemias and are irregular, small, black, multiple and fragile.

Cholesterol stones are often large single stones (solitare) but can form multiple small stones (mulberry stones). Pure cholesterol stones contain crystals.

Mixed stones are often multiple and have a laminated cross section, and 15% are radio-opaque due to calcification (C)

Gallstone pancreatitis accounts for 45% of all acute pancreatits in western countries (E) the next most common cause being alcohol in 25% of cases.

Gallstone disease is slightly more common in females, making statement (D) incorrect.

22
Q
  • Which of the following is not a risk factor for gallstone formation?

A. Smoking
B. Pregnancy
C. Crohn’s disease
D. Diet high in fats
E. Contraceptive pill

A

A. Smoking

Factors that predispose gallstone formation include sepsis within the biliary tree, anatomical variants that lead to stasis, and changes to the bile composition that predispose to stone formation. The lithogenic composition of bile is represented by Amirand’s triangel, essentialy as the ratio of cholesterol increases relative to bile salts or phospholipids then stone formation is more likely.

There are several risk factors for gallstone formation;

  • Race - higher rats in black and asian populations
  • High fat diet, history of hypercholesterolaemia
  • Obesity
  • High oestrogen states (OCP, Pregnancy, PCOS,)
  • Haemolytic states

The loss of the terminal ileum (site of bile salt reabsorption) also increases the risk of stone formation, as is seen in chron’s disease.

There is no known association with smoking and stone formation.

23
Q

A 29-year-old patient presents with a short history of right upper quadrant pain.
She is jaundiced with dark urine and pale stool. She has a fever of 38.9 °C.
Abdominal examination gives no suggestion of a palpable gallbladder. The
diagnosis is:

A. Ascending cholangitis
B. Acute cholecystitis
C. Biliary colic with duct obstruction
D. Pancreatitis
E. Mirizzi’s syndrome

A

D. Pancreatitis

The pyrexia is too high to be typical of any inflammatory processes and should point to an infective cause such as (A) or (B)

Acute cholecystitis (B) is an infection within the gallbladder, most commonly sen due to an obstruction in the biliary tree. It has a presentation of Right upper quadrant pain and fever, and there may or may not be jaundiced. The lack of Murphy’s sign makes it less likely but is not a reliable test.

This patient has a high fever, jaundiced, and has right upper quadrant pain which is termed Charcots triad, classical of ascending cholangitis. This makes (A) the single best answer, but (B) would also be an acceptable answer.

24
Q

A 62-year-old patient is admitted with jaundice. His stool is pale and urine dark
red. On examination he has a palpable gallbladder. The most likely cause is:

A. Ascending cholangitis
B. Impacted stone in the common bile duct (choledocholithiasis)
C. Tumour of the head of pancreas
D. Impacted stone in the neck of the gallbladder
E. Cholangiocarcinoma

A

C. Tumour of the head of pancreas

Here we have the application of Courvoisier’s law, which stated that a palpable gallbladder in the case of an obstructive jandice iprecludes the diagnosis of a stone. This is due to the prescence of a stone causing chronic irritation of the gallbladder leading to it becoming fibrotic and shrinking. As such this precludes options (A), (B) and (D).

This leaves the two malignancies listed here, of which pancreatic (C) is more common.

25
Q

A 63-year-old patient is admitted with colicky right upper quadrant pain and
jaundice. Abdominal ultrasound shows a thickened gallbladder but no identifiable stones. He is treated for biliary colic with fluids and analgesia but fails to improve. His serum bilirubin continues to rise as does his C-reactive protein level and white cell count. Two days after initial presentation he develops a pyrexia of 39.2 °C and his pain is now constant. The next step in management is:

A. Cholecystectomy
B. Endoscopic retrograde cholangiopancreatography
C. Open stone removal with T-tube drainage
D. Magnetic resonance cholangiopancreatography
E. Lithotripsy

A

B. Endoscopic retrograde cholangiopancreatography

This is a case of an obstructive jaundice secondary to gallstones, leading to an ascending cholangitis, it has failed to respond to conservative management.

The majority of biliary colic cases will respond to fluids and analgesia, and then these patients offered a cholecystectomy 6-12 weeks following recovery.

In cases such as this were the jaundice fails to resolve or there is the complication of scute cholecystitis, ascending cholangitis or pancreatitis the priority becomes the decompression of the billiary tree. ERCP is the treatment modality of choice in such a case.

MRCP is diagnositic but cannot treat (D), lithotripsy (E) is for renal calculi within the renal pelvis.

In a young patient or where ERCP fails a T-tube (C) is a valid treatement option.

Cholecystectomy (A) is definitive management and prevents recurrence, but it is not routinely done in an acute setting as the gallbladder is inflammed, adherant and fliable. It is usually offered as an elective procedure following resoloution of symptoms.

26
Q

Which of the following is not a recognized cause of postoperative jaundice
following laparoscopic cholecystectomy?

A. Ascending cholangitis
B. Ligation of the left hepatic duct
C. Ligation of the common hepatic duct
D. Gallstone retention in the common bile duct
E. Thermal injury due to use of electrocautery during dissection

A

B. Ligation of the left hepatic duct

27
Q

Which of the following is not a risk factor for the development of
cholangiocarcinoma?
A. Primary sclerosing cholangitis
B. Choledochal cysts
C. Hepatitis B/C infection
D. Primary biliary cirrhosis
E. Lynch syndrome II

A

D. Primary biliary cirrhosis

Cholangiocarcinoma is a rare primary tumour of the intrahepatic or extrahepatic bile ducts. It accounts for around 20% of primary liver tumours.

to be aware: 20-30% of those with primary sclerosing cholangitis (A) will develop cholangiocarcinoma, there is no association with primary billiary cirrhosis (D)

The other factors here carry increased risk cholangiocarcinoma, there is also an increased risk in IBD.

People with PSC or Choledochal cysts typically develop malignant changes up to two decades before unaffected populations.

28
Q

Whipple’s procedure is an operation used in the management of pancreatic cancer and, more rarely, in chronic pancreatitis. Which of the following structures is not resected during the classical procedure?

A. Duodenum
B. Head of pancreas
C. Gallbladder
D. Common hepatic duct
E. Pylorus

A

D. Common hepatic duct

Whipple’s procedure is indicated in cancer of the pancreatic head or in the management of chronic pancreatitis. As standard it involved removing the gastric antrum, pylorus (E) and proximal duodenum (A). There is a pylorus sparing version but there is no evidence of any survival improvement.

Both versions of the procedure involve resection of the gallbladder (C), cystic duct, head of pancreas (B) and distal duodenum. During the procedure the common hepatic duct is preserved (D) and anastomosed to a blind loop of jejunum, the jejunum is also anastomosed to the remnant pancreas and stomach.

29
Q

Which of the following abnormal findings on peripheral blood film is not typical
of changes associated with hyposplenism?
A. Bite cells
B. Howell–Jolly bodies
C. Target cells
D. Ecchinocytes
E. Pappenheimer bodies

A

A. Bite cells

Hyposplenism causes a variety of changes on a peripheral blood film;

Howell-Jolly bodies (B) are DNA remnants within the red blood cells that are usually removed by a functioning spleen. They appear a dark spots within the cells and are a classic finding of hyposplenism.

Pappenheimer bodies (E) are granules seen within iron overloaded cells, which are normally removed by a functioning spleen. They also apear as dark spots in the red blood cells but are smaller than Howell-Jolly bodies.

Target cells (C) and Ecchinocytes (‘Burr Cells’) (D) are red cells with membrane abnormalities, and normally these would be removed by the spleen.

BIte cells (A) are RBCs where a piece of the membrane has be removed, like a bite has been taken. This is charecteristic of G6PD deficiency. During this disease process the haemaglobin becomes oxidised and dentatured, it then aggregates into Heinz bodies and these are removed from the cells by the spleen. As such bite cells cannot exist without a functioning spleen.

30
Q

Which is the most common early complication following splenectomy?

A. Pancreatitis
B. Gastric dilatation
C. Atelectasis
D. Thrombosis
E. Overwhelming post-splenectomy sepsis

A

C. Atelectasis

Splenectomy is performed either laproscopically or open using a left Kocher’s (subcostal) incision. In an emergency it will likely be performed with a midline laporotomy.

With any operation involving an organ adjacent to the diaphragm the most common post-operative complication is atelectasis (C).

There is a paradoxical increase in platelet count following splenectomy, which puts these patients at increased risk of thrombus (D). This risk is present for around 3 weeks tyically, but persists in around 30% of patients. Early mobilisation and thromboembolic prophylaxis are indicated.

Gastric dilatation (B) is also a common complication with potentially serious consequences. It is due to gastric ileus, the danger is that an expanding stomach may disrupt the ligatures on the vessels above. As such, post-splenectomy patients will have an NG tube in situ.

Pancreatitis (A) may occur after splenectomy as the tail of the pancreas and the spleen share a common blood supply.

Overwhelming sepsis (E) is a potential complication post-splenectomy due to teh loss of the spleen’s immunological function. It is for this reason that these patients will be offered vaccines against encapsulated organisms.

31
Q

Splenectomy patients should be immunized against all the following organisms,
except:
A. Haemophilus influenzae
B. Meningococcus B
C. Meningococcus C
D. Streptococcus pneumoniae
E. None of the above

A

E. None of the above

One of the many functions of the spleen is to process antigens and antigen presentation. The spleen is crucial in combating encapsulated organisms such as streptococcus, meningococcus and haemophilus.

Any patients who are having elecitve surgery will have a round of vaccines prior to the procedure and then a series of boosters afterwards. It is also the case that any patients with a traumatic speen injury will recieve these vaccines in case of deterioration leading to splenectomy.

The origional answer to this question was (B) on the grounds that there wasn’t a MenB vaccine, as there is now many trusts reccomend its use for splenectomy patients. As such the answer here is now (E) as all of these vaccines should be given.

32
Q

Which of the following is not secreted by the endocrine or exocrine pancreas?
A. Chymotrypsinogen
B. Glucagon
C. Somatostatin
D. Lipase
E. Gastrin

A

E. Gastrin

The pancreas functions as both an endocrine and exocrine organ, the exocrine component is a compound alveolar gland. The digestiv enzymes are secreted into the alimentary tract via the pancreatic duct (duct of Wirsung) which has a variable course but usually joins the common bile duct to for the ampulla of Vater.

The pancreas produces around 1500ml of secretions per day, this contains both intact enzymes (lipase and amylase) and pro-enzymes (trypsinogen, chymotrypsinogen).

The endocrine pancreas produces 4 peptide hormones; insulin, glucagon, somatostatin, and pancreatic polypeptide.

However, Gastrin (E) is produced by G cells in the gastric wall and regulates acid secretion, gut motility, and mucosal growth. It is produced by the pancreas during fetal life but not in adulthod.

33
Q

Of the following, which is not a clearly recognized cause of acute pancreatitis?
A. 5-acetyl salicylic acid
B. Furosemide
C. Coxsackie B virus
D. Hyperlipidaemia
E. Magnetic resonance cholangiopancreatography

A

E. Magnetic resonance cholangiopancreatography

The answer here is obvious if you pay attention to the question, MRCP is a completely non-invasive echnique and so has no possible mechanism to cause pancreatitis.

The causes of acute pancreatitis are varied and cover more than is included in the acronym GET SMASHED, se below.

• Gallstones – the most common cause, accounting for 45 per cent of
acute pancreatitis.
• Ethanol – the second most common cause, accounting for 25 per
cent of acute pancreatitis.
• Trauma – contusion or laceration of the gland precipitates a
generalized inflammatory reaction.
• Steroids – a common pharmacological cause (see below for more
detail).
• Mumps – and other viral infections affecting exocrine glands
(Coxsackie B).
• Autoimmune – rarely in isolation; usually occurs in the presence of
PSC, PBC, Sjögren’s.
• Scorpion sting – a species of Trinidadian scorpion (Tityus trinitatis),
the poison of which is a powerful pancreatic secretagogue that
causes pancreatic injury.
• Hyperlipidaemia (types I and IV), Hypothermia, Hypercalcaemia,
Hypotension
• ERCP – accounts for 5 per cent of all pancreatitis.
• Drugs – collectively the third most common cause; causative agents
include thiazide diuretics, furosemide, azathioprine, 5-
aminosalicylate, 6-mercaptopurine, metronidazole, tetracycline,
oestrogens.

34
Q

A 48-year-old patient is admitted into hospital with acute-onset abdominal pain
and perfuse vomiting. Serum amylase is 2500 IU/mL, C-reactive protein is 250
mg/L. The patient is managed conservatively, but 48 hours later you are called to see him as the nursing staff have become concerned. On examination the patient is distressed and combative. His blood pressure is 105/65 mmHg, pulse rate is 130 beats/min and respiratory rate is 38 breaths/min. Arterial blood gases show pH 7.20, pO2 7.9 and pCO2 5.8. The most likely cause of his deterioration is:

A. Septic shock
B. Acute respiratory distress syndrome
C. Pancreatic pseudocyst
D. Acute alcohol withdrawal
E. Disseminated intravascular coagulation

A

B. Acute respiratory distress syndrome

Acute pancreatitis is a serious systemic insult, even with optimal management there is still a 10% mortalitiy. Patients who present seemingly well will deteriorate over the course of a few days, as in this case.

Causes of mortality are various, but can arise from cardiovascular collapse (secondary to hypovolaemia), gastrointestinal bleeding, thrombosis, renal failure, coagulation derangement (Rarely severe).

The patient in this scenario is in respiratory failure, there can be respiratory complication in pancreatitis due to atelectasis and acute lung injury or ARDS. ARDS may be due to a primary lung injury or an inflammatory insult, it has a poor prognosis and often leads to ITU admission.

35
Q

A patient was admitted for acute pancreatitis secondary to alcohol misuse. He was treated conservatively and discharged for outpatient follow-up. He presents to your clinic after 8 weeks complaining of continued abdominal pain in the epigastrium radiating into the back. Serum amylase is 7800 IU/L. On examination he is tender over the epigastrium. Blood pressure, pulse rate and temperature are all unremarkable. The diagnosis is:
A. Pancreatic pseudocyst
B. Cholecystitis
C. Chronic pancreatitis
D. Recurrent acute pancreatitis
E. Pancreatic abscess

A

A. Pancreatic pseudocyst

A pancreatic psudocyst is a common (20% of cases) late complication of pancreatitits, this is a classic presentation.

Patients will tend to present 6-8 weeks following acute pancreatitis, there will commonly be a persistently raised amylase. Without any deranged observations or pyrexia it is unlikely to be reccurrent acute pancreatitis, and precludes a pancreatic abcess.

Chronic pancreatitis and cholecystitis are differentials but should only be considered after the exclusion of a pancreatic psudocyst.

These psudocysts are a collection of pancreatic juices enclosed in a non-epithelial sac of fibrous and granulomatous tissue. They can occur in the pancreas, but are more commonly in the lesser sac. Comnplications include; infection (then termed a pancreatic abcess), vesel erosion, duodenal obstruction, billiary obstruction or rupture.

Smaller cysts often resolve and are managed conservatively, large cysts (6cm pr greater) or complicated cysts may be drained with the aid of CT or ultrasound imaging, endoscopic drainage, or open pancreatectomy.