Oesophageal carcinoma is cancer arising in the lining of the oesophagus, usually appearing as squamous cell carcinoma or adenocarcinoma. Progressive difficulty swallowing, especially solids followed by liquids, requires urgent medical assessment because early diagnosis can expand cancer treatment options.

Diagnosis commonly combines upper gastrointestinal endoscopy with biopsy, CT, PET-CT, and sometimes endoscopic ultrasound. Treatment may include surgery, chemotherapy, chemoradiation therapy, radiation therapy, immunotherapy, or symptom-focused care, depending on stage, tumour type, and overall fitness.

Key takeaways

  • Squamous cell carcinoma arises in the upper two thirds; adenocarcinoma in the lower third.
  • Barrett's oesophagus is the precursor to adenocarcinoma, through metaplasia and dysplasia.
  • Progressive dysphagia, to solids then to liquids, is the cardinal symptom.
  • NICE NG12 refers anyone with dysphagia on a suspected cancer pathway, at any age.
  • The oesophagus is about 25 cm long, which matters when you describe the level of a lesion.

What Is Oesophageal Carcinoma?

Oesophageal carcinoma is a malignant tumour that develops from cells lining the oesophagus and can interfere with swallowing, nutrition, breathing, or nearby organs.

Oesophageal carcinoma is a cancer arising from the lining of the oesophagus, the muscular tube connecting the pharynx to the stomach. In American usage, this is called oesophageal cancer. It can obstruct swallowing, invade nearby structures, and spread through lymphatic and blood vessels.

Oesophageal carcinoma is the American spelling for a malignant tumour of the oesophagus. The terms oesophageal cancer and oesophageal cancer describe the same broad condition, although tumours differ by histology, location, and molecular features.

Oesophageal squamous cell carcinoma develops from squamous lining cells, whereas oesophageal adenocarcinoma develops from glandular cells. Oesophageal scc is an abbreviation commonly used for oesophageal squamous cell carcinoma.

Anatomy and tumour location

The oesophagus is approximately 25 cm long. It begins at the level of C6, passes through the thorax, crosses the diaphragm at T10, and joins the stomach around T11. Important anatomical relations include the trachea, left main bronchus, aortic arch, and recurrent laryngeal nerves.

For MRCS Part B, remember the typical distribution:

  • Squamous cell carcinoma (SCC): usually affects the upper two-thirds.
  • Adenocarcinoma: usually affects the lower third, often near the gastro-oesophageal junction.

SCC develops from squamous epithelium. Risk factors include smoking, alcohol, achalasia, caustic injury, and diets containing carcinogens. Adenocarcinoma develops from glandular epithelium. It is strongly associated with Barrett’s oesophagus, which results from chronic gastro-oesophageal reflux.

In current terminology, oesophageal adenocarcinoma usually describes a lower-tube malignancy associated with Barrett oesophagus, obesity, and GERD. Oesophageal squamous cell carcinoma more often affects the upper or middle tube and is associated with tobacco, alcohol, nutritional deficiency, or caustic injury.

Barrett’s oesophagus involves replacement of normal squamous epithelium by columnar epithelium. This metaplasia can progress through dysplasia to invasive adenocarcinoma. Therefore, surveillance and biopsy findings are central to clinical assessment. These are distinct diseases that share the same anatomical site.

Barrett oesophagus is a change in the lower oesophageal lining caused by long-term exposure to stomach contents. It is not cancer, but it can increase the likelihood of oesophageal adenocarcinoma when dysplasia develops.

Clinical and pathology points

Progressive dysphagia is the cardinal symptom. Patients typically struggle with solids first, followed by liquids as the tumour enlarges and narrows the lumen. Weight loss, odynophagia, reflux, cough, haematemesis, or recurrent chest infections may also occur.

Initial investigation is usually upper gastrointestinal endoscopy, or OGD. It allows direct visualisation and biopsy for histological diagnosis. CT of the chest, abdomen, and pelvis assesses local invasion, lymph nodes, and distant metastases. Further staging may guide chemotherapy, radiotherapy, endoscopic treatment, or surgery.

Local spread can cause recurrent laryngeal nerve palsy, Horner’s syndrome, tracheo-oesophageal fistula, or superior vena cava obstruction. Treatment depends on histology, stage, fitness, and resectability. Curative surgery commonly involves oesophagectomy with perioperative systemic treatment.

Why does dysphagia progress from solids to liquids? A solid-food bolus is affected first by mechanical narrowing. Liquids become difficult when the lumen is severely narrowed or oesophageal motility is impaired.

Oesophageal carcinoma classically presents with progressive dysphagia, with SCC in the upper two-thirds and adenocarcinoma in the lower third. > Key clinical insight: Solids-first dysphagia suggests a structural narrowing, while simultaneous difficulty with solids and liquids may indicate a motility disorder.

How does oesophageal carcinoma present?

Oesophageal carcinoma often presents with gradually worsening swallowing difficulty. Early symptoms can be subtle, especially in patients with longstanding reflux or indigestion. The tumour may arise in the upper, middle, or lower oesophagus, producing local and systemic features.

Dysphagia usually develops when the oesophageal lumen narrows below approximately 13 mm, suggesting locally advanced disease.

Typical symptoms and red flags

  • Progressive dysphagia for solids followed by liquids is the cardinal symptom of oesophageal carcinoma and requires urgent investigation.
  • Odynophagia, or painful swallowing, may indicate mucosal ulceration, inflammation, or direct tumour involvement of the oesophageal wall.
  • Unintentional weight loss reflects reduced oral intake, cancer-related metabolism, and advanced disease, particularly when rapid or severe.
  • Retrosternal pain, heartburn, regurgitation, and persistent indigestion can mimic reflux but may signal underlying oesophageal cancer.
  • Persistent symptoms despite appropriate reflux treatment, especially dysphagia, should prompt urgent referral rather than repeated empirical treatment.

Dysphagia for solids before liquids suggests a mechanical obstruction, such as a tumour. As the lumen becomes narrower, even fluids cannot pass easily. This differs from motility disorders, where solids and liquids often cause difficulty from the outset. Ask when symptoms began, whether they are worsening, and whether food sticks in the throat or behind the sternum.

Symptoms of other symptoms include excessive salivation, regurgitation, nausea, and hiccups. Persistent cough may result from reflux, aspiration, or a fistula between the oesophagus and airway. Hoarseness suggests recurrent laryngeal nerve involvement. Haematemesis or melaena may indicate tumour bleeding and requires urgent assessment.

MRCS-style assessment of dysphagia

Start by assessing the patient’s airway, breathing, circulation, and ability to manage secretions. Stridor, respiratory distress, inability to swallow saliva, or active haematemesis are immediate concerns.

Use a structured history:

  • Define the onset, progression, and consistency of affected foods.
  • Separate oropharyngeal symptoms from oesophageal symptoms.
  • Ask about odynophagia, reflux, regurgitation, chest pain, and vomiting.
  • Check for weight loss, fatigue, bleeding, cough, aspiration, and voice change.
  • Establish smoking, alcohol, reflux, Barrett’s oesophagus, achalasia, and previous caustic ingestion.
  • Ask about previous cancer, family history, and functional impact on eating.

Examine the patient’s nutritional state, hydration, cervical lymph nodes, mouth, chest, and abdomen. Look for a left supraclavicular node, hepatomegaly, or signs of metastatic disease. Assess the voice and listen for cough or aspiration. Hoarseness, Horner syndrome, superior vena cava obstruction, bone pain, jaundice, or neurological symptoms suggest local invasion or metastases.

What causes oesophageal carcinoma?

Oesophageal carcinoma develops when abnormal cells grow within the oesophagus. Risk depends on the tumour type, inherited susceptibility, and long-term damage to the lining. Some causes can be reduced, while others cannot. The two main histological types are squamous cell carcinoma and adenocarcinoma.

The direct answer is that smoking and alcohol mainly increase squamous cell carcinoma risk. Obesity, gastro-oesophageal reflux disease (GORD), and Barrett’s oesophagus mainly increase adenocarcinoma risk. Other recognised risks include dietary deficiencies, caustic injury, achalasia, previous radiotherapy, and inherited syndromes.

Aetiology means the cause or set of causes underlying a condition. The aetiology of oesophageal cancers is multifactorial, involving tobacco, alcohol, reflux, obesity, chronic inflammation, inherited susceptibility, and environmental exposures.

Modifiable risk factors

Tobacco exposure is a major risk factor for oesophageal cancer. This includes cigarettes, cigars, pipes, and, to a lesser extent, chewing tobacco. Alcohol has a strong association with squamous cell carcinoma. Combined smoking and alcohol exposure increases risk more than either factor alone.

Heavy smoking increases exposure to carcinogens that damage DNA in squamous lining cells. Smoking is especially relevant to oesophageal scc, although it can contribute to several forms of oesophageal cancer.

Obesity increases the risk of adenocarcinoma, particularly in Western populations. It can promote reflux by increasing abdominal pressure. Chronic GORD exposes the lower oesophagus to acid and bile. Persistent inflammation may lead to Barrett’s oesophagus.

GERD, also written as gerd, means gastroesophageal reflux disease. Gerd can cause repeated acid exposure, while acid reflux describes the movement of stomach contents into the oesophagus. Long-term gerd is particularly relevant to oesophageal adenocarcinoma.

Barrett’s oesophagus is metaplasia of squamous epithelium into specialised columnar epithelium. Continued injury can cause dysplasia, which may progress to adenocarcinoma. Therefore, Barrett’s is a premalignant condition rather than a cancer itself. Endoscopic surveillance may detect dysplasia before invasive disease develops.

Barrett oesophagus is a recognised precursor to oesophageal adenocarcinoma. The terms Barrett oesophagus, Barrett’s oesophagus, and intestinal metaplasia may appear in clinical records, but biopsy interpretation determines whether dysplasia or invasive cancer is present.

Symptoms of dietary risks include low fruit and vegetable intake and diets containing nitrosamines or preserved foods. These factors are classically linked with squamous cell carcinoma. Caustic ingestion can cause severe oesophageal injury, strictures, and later malignancy. The increased risk may remain for many years.

Non-modifiable and less common risks

Achalasia causes prolonged stasis and irritation within the oesophagus. It increases the risk of squamous cell carcinoma. Previous radiotherapy to the chest or neck can also increase later cancer risk.

Inherited conditions tested in MRCS questions include tylosis (Howell–Evans syndrome). This autosomal dominant disorder causes thickened skin on the palms and soles and increases squamous cell carcinoma risk. Plummer–Vinson syndrome, with iron-deficiency anaemia and swallowing difficulty, is another recognised association.

Age, male sex, and a relevant family history are non-modifiable risks. MRCS pathology questions commonly test the anatomical pattern: squamous cell carcinoma usually affects the upper two-thirds, while adenocarcinoma usually affects the lower third near the gastro-oesophageal junction.

Which risk factor most strongly suggests adenocarcinoma? Long-standing GORD with Barrett’s oesophagus, especially alongside obesity. Which risks suggest squamous cell carcinoma?

Smoking, excess alcohol, achalasia, caustic injury, and tylosis. Smoking and alcohol favour squamous cell carcinoma, while obesity, GORD, and Barrett’s oesophagus favour lower oesophageal adenocarcinoma.

Research from the National Cancer Institute shows that risk patterns vary by geography and histology. In epidemiology, incidence describes new cases in a population, whereas prevalence describes existing cases. The incidence of oesophageal squamous cell carcinoma remains substantial in several regions, while oesophageal adenocarcinoma has increased in some Western populations.

How Is Oesophageal Carcinoma Diagnosed and Staged?

Diagnosis establishes whether malignant cells are present, while staging determines the tumour’s extent and guides treatment. Suspected oesophageal carcinoma requires urgent upper gastrointestinal endoscopy with biopsy. CT, PET-CT, endoscopic ultrasound, and selected bronchoscopy then assess tumour spread, lymph nodes, metastases, and resectability.

Progressive dysphagia, weight loss, or upper gastrointestinal bleeding should prompt urgent investigation. The first diagnostic test is usually an upper gastrointestinal endoscopy, also called an OGD. This allows direct inspection of the oesophagus, gastro-oesophageal junction, and stomach.

Confirming the diagnosis

During endoscopy, the clinician takes several biopsies from any abnormal area. The pathologist examines these samples for malignant cells and confirms the tumour type. Most oesophageal cancer cases are either squamous cell carcinoma or adenocarcinoma. Squamous tumours often affect the upper or middle oesophagus, while adenocarcinoma commonly affects the lower third.

Histological confirmation means that cancer cells have been identified in tissue under a microscope. Imaging may suggest oesophageal cancer, but it cannot replace a biopsy in most patients.

The pathology report may describe the tumour type, differentiation, and other features. These findings help the multidisciplinary team plan treatment. A biopsy can also exclude other causes of narrowing, such as benign strictures, inflammatory disease, or external compression.

Oesophageal adenocarcinoma is confirmed when malignant gland-forming cells are identified in an appropriate tissue sample. Oesophageal adenocarcinoma may coexist with Barrett oesophagus, but a biopsy must distinguish intestinal metaplasia, dysplasia, and invasive tumour.

Endoscopy is mainly a diagnostic investigation. It confirms the lesion and obtains tissue. It may also show the length and position of the tumour, but it cannot reliably assess the full depth of invasion or distant spread.

Staging the tumour

Staging determines how far the oesophageal cancer has spread. Doctors use the TNM system:

  • T (tumour): how deeply the tumour invades the oesophageal wall and nearby structures.
  • N (nodes): whether regional lymph nodes contain cancer.
  • M (metastases): whether the cancer has spread to distant organs.

A contrast-enhanced CT scan of the chest, abdomen, and pelvis provides a broad assessment. It can identify enlarged lymph nodes, liver lesions, lung deposits, pleural disease, and invasion of surrounding structures. CT is central to metastatic assessment and initial evaluation of resectability.

A PET-CT combines anatomical imaging with information about increased metabolic activity. It can detect otherwise occult metastatic disease and may alter the proposed treatment. However, inflammation and infection can also appear active on PET imaging.

Endoscopic ultrasound passes an ultrasound probe through the endoscope. It provides detailed local staging, particularly the depth of tumour invasion and nearby lymph nodes. Suspicious nodes may undergo fine-needle aspiration during the procedure. EUS is especially useful when deciding whether an apparently local tumour could be removed with surgery.

Bronchoscopy may be used for upper or middle oesophageal tumours. It assesses possible invasion of the trachea or bronchi and helps determine whether curative surgery is technically possible. This is a targeted investigation, not a routine test for every patient.

Assessing resectability

Resectability means whether the tumour can be removed completely with an acceptable operation. The MDT combines endoscopy, histology, CT, PET-CT, EUS, and sometimes bronchoscopy to make this decision. Major vessel invasion, airway invasion, or distant metastases may make curative surgery unsuitable.

The final stage guides treatment, such as endoscopic therapy, chemotherapy, radiotherapy, surgery, or palliative treatment.

In summary, endoscopy with biopsy confirms oesophageal carcinoma, while CT, PET-CT, EUS, and selected bronchoscopy establish TNM stage and resectability. A stage cancer classification is not based only on tumour size. It incorporates invasion, lymph nodes, metastases, grade, and sometimes tumour location. Accurate staging also prevents inappropriate surgery when cancer spread has already occurred.

How is oesophageal carcinoma treated?

Cancer treatment for oesophageal carcinoma is selected according to stage, histology, location, molecular findings, and fitness.

What determines treatment?

Treatment depends on tumour stage, location, histology, patient fitness, and treatment intent. Staging usually includes endoscopy with biopsy, CT of the chest, abdomen and pelvis, and often PET-CT and endoscopic ultrasound.

Curative treatment aims to eradicate all visible cancer. It is usually considered for stages I–III disease without distant metastases. Stage IV disease is generally treated with palliative intent, although selected patients may receive more intensive treatment after multidisciplinary review.

Histology also matters:

  • Squamous cell carcinoma is more common in the upper and middle oesophagus.
  • Adenocarcinoma usually affects the lower third and gastro-oesophageal junction.
  • Barrett’s oesophagus can progress from metaplasia to dysplasia and then adenocarcinoma.

Fitness affects whether a patient can tolerate major surgery, chemotherapy, or radiotherapy. Frailty, cardiopulmonary disease, nutritional status, renal function, and patient preference must be assessed. Only around one-third of patients are suitable for potentially curative surgery at presentation, because of advanced disease or poor physiological reserve.

Treatment should be planned by a specialist multidisciplinary team. Options include endoscopic treatment, surgery, chemotherapy, radiotherapy, or combinations of these treatments.

How is potentially curable disease treated?

Very early lesions, such as selected T1a cancers limited to the mucosa, may receive endoscopic mucosal resection or endoscopic submucosal dissection. This avoids oesophagectomy but requires careful staging and surveillance. Further treatment may be needed if there is poor differentiation, lymphovascular invasion, or incomplete excision.

For operable, locally advanced disease, chemotherapy or chemoradiotherapy is often given before surgery. This is called neoadjuvant treatment. It can reduce tumour volume and treat microscopic metastatic disease. The patient then undergoes oesophagectomy if there is no progression.

Chemoradiation is the combined use of anticancer medicines and radiation. Chemoradiation therapy may be used before surgery or as definitive treatment when surgery is unsuitable.

An oesophagectomy removes the tumour with a margin and regional lymph nodes. The stomach is commonly formed into a conduit and joined to the remaining oesophagus in the neck or chest.

An oesophagectomy is an operation that removes part or all of the oesophagus and reconstructs the food passage. An oesophagectomy may be open, minimally invasive, or robotic, depending on expertise and tumour factors.

Key operative approaches include:

  • Ivor Lewis oesophagectomy: abdominal mobilisation followed by right thoracic resection and an intrathoracic anastomosis.
  • McKeown oesophagectomy: abdominal, thoracic, and cervical stages with a neck anastomosis.
  • Transhiatal oesophagectomy: abdominal and cervical dissection without a thoracotomy.

An oesophagectomy requires careful assessment of cardiopulmonary reserve, nutrition, and tumour resectability. Recovery after oesophagectomy involves staged feeding, respiratory physiotherapy, mobilisation, and surveillance for leaks.

Tumour location influences the operation. Lower oesophageal and gastro-oesophageal junction tumours may require distal oesophagectomy, proximal gastrectomy, or extended gastric resection. Upper tumours may require a higher anastomosis and careful recurrent laryngeal nerve preservation.

Symptoms of important complications include anastomotic leak, pneumonia, respiratory failure, chyle leak, recurrent laryngeal nerve injury, conduit ischaemia, and atrial fibrillation. Long-term problems include reflux, dumping symptoms, delayed gastric emptying, and anastomotic stricture.

What is the role of definitive and palliative treatment?

Definitive chemoradiotherapy combines chemotherapy with radiotherapy, without planned surgery. It is especially useful for some squamous cell cancers, cervical oesophageal tumours, and patients who are medically unfit for oesophagectomy. Treatment decisions depend on tumour response, toxicity, and local specialist protocols.

Chemotherapy uses systemic drugs that circulate through the bloodstream. They can kill cancer cells or stop them dividing. Radiotherapy may control local oesophageal cancer but can cause oesophagitis, fatigue, and strictures.

Antineoplastics are medicines used to slow or destroy malignant cells. Common antineoplastics may be combined in regimens, adjusted for kidney function, blood counts, tumour type, and previous therapy. Antineoplastics can cause side effects such as nausea, fatigue, infection risk, neuropathy, or low blood counts.

Immunotherapy and biomarker-guided treatments may be considered for selected advanced tumours. Clinical trials can provide access to new antineoplastics, targeted medicines, immunotherapy combinations, or improved surgical pathways.

Palliative treatment focuses on swallowing, nutrition, pain, bleeding, and quality of life. Dysphagia management may include:

  • Self-expanding metal stent placement for rapid relief of severe obstruction.
  • Radiotherapy for slower, longer-term symptom control.
  • Endoscopic dilatation in carefully selected cases.
  • Nutritional support through oral supplements, a nasogastric tube, or feeding jejunostomy.
  • Analgesia, antiemetics, reflux treatment, and psychological support.

Stents can migrate, block, bleed, or cause chest pain. A feeding route may be preferred when survival is longer or stenting is unsuitable. Decisions should reflect prognosis and patient goals.

Oesophageal cancer treatment is stage- and fitness-dependent—early mucosal disease may be treated endoscopically, locally advanced disease often needs multimodal therapy, and metastatic disease usually receives symptom-directed care.

This quick-reference table shows how stage, tumour characteristics, patient fitness and treatment intent guide decisions for oesophageal carcinoma, helping readers understand why management is individualised after complete staging and multidisciplinary review.

Clinical trials are research studies that test new approaches against current standards. Clinical trials may evaluate surgery, radiation, antineoplastics, immunotherapy, nutrition, or follow-up. A clinical trial requires informed consent and does not guarantee benefit.

What is the prognosis, and what follow-up is needed?

Prognosis describes expected outcome, while survival reflects how long people live after diagnosis or treatment. Oesophageal carcinoma is a serious cancer whose outcome depends mainly on stage, spread, and the patient’s fitness for treatment.

Prognosis

Prognosis is best when the tumour is localised and complete resection is possible. Outcomes worsen with deeper invasion, involved lymph nodes, and distant metastatic disease. Liver, lung, bone, or peritoneal metastases usually indicate incurable disease, although systemic treatment may control symptoms and prolong survival.

Histology also affects outcome. Squamous cell carcinoma and adenocarcinoma have different risk factors and anatomical patterns. Tumour biology, response to chemotherapy or radiotherapy, resection margins, and lymphovascular invasion also influence recurrence risk.

Performance status is central to treatment planning. A patient who is independent and medically fit may tolerate multimodal treatment or oesophagectomy. Frailty, malnutrition, major cardiopulmonary disease, and poor functional status may limit treatment options.

Only a minority of patients present with disease suitable for curative surgery, and overall five-year survival remains poor. Reported survival varies widely according to stage and histology. Survival figures should therefore support, not replace, an individual discussion with the oncology team.

Survival estimates should be interpreted alongside newer staging systems, molecular testing, and access to immunotherapy or clinical trials. A population statistic cannot predict an individual’s outcome, particularly after a strong response to treatment.

Complications After Treatment

Oesophagectomy has significant morbidity. Surgical trainees should recognise these complications:

  • Anastomotic leak: Look for fever, tachycardia, chest pain, sepsis, respiratory decline, or increasing drain output. Management may include drainage, antibiotics, nutritional support, endoscopic therapy, or reoperation.
  • Recurrent laryngeal nerve injury: This causes hoarseness, weak cough, and aspiration risk. Assess the voice and arrange early laryngoscopy when indicated.
  • Respiratory complications: Atelectasis, pneumonia, aspiration, and respiratory failure are common. Early mobilisation, physiotherapy, analgesia, and careful fluid management help reduce risk.
  • Chyle leak: Milky drain fluid, especially after feeding, suggests thoracic duct injury. Confirm with drain triglycerides and manage with dietary restriction, specialist nutrition, or intervention.
  • Anastomotic stricture: Progressive dysphagia after recovery may result from scarring. Endoscopic balloon dilatation is commonly required.

Symptoms of other problems include delayed gastric emptying, reflux, dumping symptoms, vocal changes, and wound infection. These can reduce quality of life after technically successful surgery.

Recurrence and Follow-Up

Recurrence may be local, nodal, or metastatic. New dysphagia, weight loss, pain, cough, hoarseness, or jaundice requires assessment. Follow-up usually combines clinical review, nutritional assessment, imaging, and endoscopy when symptoms or findings indicate. Surveillance schedules vary between centres and depend on treatment and recurrence risk.

Dietitians should monitor weight, hydration, swallowing, micronutrient intake, and tolerance of small frequent meals. A feeding jejunostomy may support nutrition during recovery. Multidisciplinary follow-up should include upper gastrointestinal surgery, oncology, radiology, pathology, endoscopy, specialist nursing, speech and language therapy, and dietetics.

For MRCS revision, practise related pathology questions, operative complication scenarios, examination stations, and communication tasks on Mrcspartbquestions. The platform offers more than 3,500 interactive questions, explanations, and surgical skills practice across devices.

For oesophageal cancer, stage and fitness guide prognosis, while early recognition of postoperative complications protects recovery and survival.

What are the key differences between the main tumour types?

Oesophageal squamous cell carcinoma, oesophageal scc, and adenocarcinoma are distinct histological diagnoses. Oesophageal squamous cell carcinoma usually arises from squamous lining cells, while oesophageal adenocarcinoma forms glandular structures and often develops near the gastroesophageal junction.

Oesophageal adenocarcinoma is associated with Barrett oesophagus, gerd, obesity, and chronic acid exposure. Oesophageal squamous cell carcinoma is associated with smoking, alcohol, caustic injury, and achalasia. Oesophageal adenocarcinoma may therefore prompt assessment of reflux history, whereas oesophageal scc may prompt a detailed tobacco and alcohol history.

How is this topic marked in MRCS Part B?

MRCS Part B marks a surgical pathology station out of 20, with all 20 marks for clinical knowledge and its application. Two of the seventeen examined stations are surgical pathology, the second titled surgical pathology and/or microbiology.