This is most likely ulcerative colitis. Note that aphthous oral ulcers can be seen in both ulcerative colitis and Crohn’s disease. However, commonly, literature would classify aphthous oral ulcers to be a feature seen only in Crohn’s disease. It is also noted that this patient has blood when he passes stools of which the history points towards ulcerative colitis.

CROHN’S DISEASE VS ULCERATIVE COLITIS :

It is important to know the differences between ulcerative colitis and Crohn’s disease as it is very commonly asked.

These are some key differences that will help you with your exam:

Crohn’s disease:

* Usually non bloody

* Abdominal mass palpable in right iliac fossa

* Increased goblet cells on histology

* Granulomas seen on histology

* Weight loss is more prominent 

* Transmural, skip lesions, cobblestone appearance on endoscopy.

Ulcerative colitis:

* Bloody diarrhoea is more common

* Abdominal pain in the left lower quadrant

* Decreased goblet cells on histology

* Granulomas are infrequent in histology

* Primary sclerosing cholangitis is more common

* Loss of haustration, drain pipe colon is seen on barium enema.

This scenario shows a classical picture of Clostridium difficile. Broad-spectrum antibiotics always have the potential to kill off normal gut flora leaving C. Difficile the chance to grow. Metronidazole is usually used as first-line to manage Clostridium difficile. As this is not an option here, use the second line which is vancomycin.

Vancomycin is usually reserved for more severe colitis with severe bloody diarrhoea, severe abdominal pain, and temperatures above 38.5 C. Woman always want a “strong” antibiotic to treat their urinary tract infections but they are not aware that antibiotics such as cephalosporins and amoxicillin are commonly implicated in C. difficile infections.

This is a very good reason why we should always start with narrow-spectrum antibiotics such as trimethoprim and nitrofurantoin for simple urinary tract infections. In the exam, look out for antibiotic usage like cephalosporins, clindamycin, co-amoxiclav, and amoxicillin as a cause for Clostridium difficile.

CLOSTRIDIUM DIFFICILE :

Clostridium difficile is a Gram-positive rod often encountered in hospital practice. It is transmitted via the fecal-oral route by spores that are resistant to antibiotics. It produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis.

Clostridium difficile develops when the normal gut flora is suppressed by broad-spectrum antibiotics.

The most common antibiotics implicated in Clostridium difficile infections are :

• Clindamycin

• Cephalosporins (in particular second and third-generation cephalosporins)

• Quinolones

• Co-amoxiclav

• Aminopenicllins (amoxicillin and ampicillin)

Features :

• Diarrhoea - may be mild diarrhoea or serious bloody diarrhoea

• Abdominal pain – can sometimes be severe enough to mimic an acute abdomen

• Raised white blood cell count

• Fever

Diagnosis : Clostridium difficile toxin (CDT) detected in the stool

Management :

• Stop the causative antibiotic (if possible)

• First-line therapy is oral metronidazole

• If severe or not responding to metronidazole then oral vancomycin may be used. Another method of treating Clostridium difficile is faecal microbial transplantation but we shall not discuss this in case you are about to eat lunch.

Note: Treatment is not usually needed if the patient is asymptomatic.

The World Health Organisation classification of diarrhoea is as follows:

• Diarrhoea > 3 loose or watery stools per day

• Acute diarrhoea < 14 days

• Chronic diarrhoea > 14 days.

According to the above classification, it is too early to decide in this patient if he is suffering from ulcerative colitis or not because he has had diarhoea for only the last seven days. At this stage, it is best to exclude the infectious causes first by doing a stool microscopy, culture, and sensitivity test. In such cases, the investigations largely depend on the clinical setting.

For example, in primary care, the main aim is to make the diagnosis, and in secondary care, to confirm the diagnosis as well as to assess the severity and extent of the disease. In primary care, the test must include a stool culture and sensitivity to exclude the infectious causes of diarrhoea such as salmonella, shigella, escherichia coli, clostridium difficile, campylobacter, and giardiasis. Once the infectious causes are excluded, further diagnostic tests like colonoscopy with biopsy can be done in secondary care.

Faecal test is not the correct option. A faecal fat test is primarily ordered when a person has signs and symptoms of malabsorption such as steatorrhea, persistent diarrhoea, abdominal pain, bloating, weight loss, and failure to thrive (in children) The faecal antigen test is a stool test that is used to detect helicobacter pylori. It is an irrelevant test to perform on this particular patient.

Benign oesophageal strictures – are usually the result of scarring from acid reflux in severe and persistent GORD. It may also follow the ingestion of corrosives. While the area heals, a scar forms, causing the tissue to pull and tighten, leading to difficulty in swallowing. Certain drugs like alendronate and NSAIDs have the potential to cause strictures due to their side effects which worsen GORD.

This is seen in this stem where the patient is taking alendronate. This is the reason that it is so important to advise patients not to lie down for at least 30 minutes after taking alendronate as this will help alendronate reach the stomach faster and prevent irritation of the oesophagus.

Oesophageal carcinoma - The absence of any significant weight loss makes oesophageal carcinoma a less likely diagnosis.

However, it is important to note that any cause of dysphagia can essentially cause weight loss. This includes both benign oesophageal stricture and achalasia.

Barrett’s oesophagus - Would also have a long history of gastro-oesophageal reflux which is seen in this stem however, the symptoms of dysphagia are usually occasional rather than persistent.

Pharyngeal pouch - Usually presents with a history of halitosis and regurgitation of undigested food, a sensation of a lump on the throat, and neck bulge.

Achalasia - While the most common feature is dysphagia, regurgitation is a very common feature of achalasia and occurs in around 80-90% of sufferers. Please note that if this stem did not include the history of taking Alendronate, the answer is still likely to be benign oesophageal stricture given that there is less evidence for any other option.

Acute cholecystitis presents with severe continuous right upper quadrant pain which can be seen to radiate to the right flank and back. A fever like in this stem is also associated with it.

Nausea and vomiting are often seen with cholecystitis. Jaundice can be a feature of obstruction of the biliary tract and can be seen in cholecystitis however, it is often mild or not seen unless there is the presence of gallstones in the common bile duct (choledocholithiasis). In this stem, jaundice is absent.

The examination here shows a positive Murphy’s sign. Remember, the Murphy sign is not just pain, but it is the arrest of inspiration when pressing the right costal margin at the midclavicular line. It is a sign of acute cholecystitis.

It is sensitive, but not specific to cholecystitis. There is an elevation of ALP in this stem which ALP rises much higher than ALT which points towards a form of biliary obstruction with cholestasis. The likely scenario here is that there are gallstones that are obstructing the cystic duct causing acute cholecystitis.

Remember, more than 90% of the time, acute cholecystitis occurs from blockage of the cystic duct by a gallstone.

When this occurs, the patient would experience biliary colic. Chronic cholecystitis is incorrect here as chronic cholecystitis occurs when there are repeated episodes of infection causing thickening and fibrosis of the gallbladder. Acute pancreatitis is incorrect as the amylase is within normal limits in this stem.

Acute cholecystitis follows stone or sludge impaction in the neck of the gallbladder, which may cause continuous epigastric or RUQ pain (referred to the right shoulder), vomiting, fever, local peritonism, or a gallbladder mass.

The main difference from biliary colic is the inflammatory component (local peritonism, fever, and elevated WCC). If the stone moves to the common bile duct (CBD), obstructive jaundice and cholangitis may occur Murphy’s sign is positive when you lay 2 fingers over the RUQ and ask the patient to breathe in which causes pain & arrest of inspiration as an inflamed gallbladder impinges on your fingers.

It is only positive if the same test in the LUQ does not cause pain.

Tests: WCC would be elevated.

Ultrasound shows a thick-walled, shrunken gallbladder

Management: Nil by mouth, pain relief, IV fluids, and antibiotics.

Once symptoms settle, do a laparoscopic cholecystectomy.

Laparoscopic cholecystectomy is the treatment of choice for all patients fit for general anaesthesia. Open surgery is required if there is gall bladder perforation.

There is an association between type 1 diabetes and coeliac disease. The gold standard to diagnose coeliac disease is a jejunal/duodenal biopsy. In the past, small-bowel biopsies for the diagnosis of coeliac disease were taken from the jejunum, but nowadays most gastroenterologists take endoscopic biopsies from the distal duodenum. Coeliac disease is caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption.

Signs and symptoms :

• Chronic or intermittent diarrhoea

• Stinking stools / steatorrhoea

• Persistent or unexplained gastrointestinal symptoms including bloating, nausea and vomiting

• Fatigue

• Recurrent abdominal pain, cramping or distension

• Sudden or unexpected weight loss

• Unexplained iron, vitamin B12 or folate deficiency.

Note that the one of them a common presentation of coeliac disease is iron deficiency anaemia. Also, folate deficiency is more common than vitamin B12 deficiency in coeliac disease.

Complications -

• Osteoporosis

• T-cell lymphoma of small intestine (rare) Investigation.

Diagnosis is made by a combination of immunology and jejunal biopsy. Any test for coeliac disease is accurate only if a gluten-containing diet is eaten during the diagnostic process. The person should not start a gluten-free diet until the diagnosis is confirmed. If patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at least 6 weeks before testing.

Specific auto-antibodies -

• Tissue transglutaminase (TTG) antibodies (IgA) are first-choice.

• Endomysial antibody (IgA)

Jejunal/duodenal biopsy - A biopsy is still needed to diagnose coeliac disease even if antibody tests confirm the diagnosis of coeliac disease. It shows :

• Villous atrophy

• Crypt hyperplasia

• Increase in intraepithelial lymphocytes

Management -

• Gluten-free diet.

The corkscrew pattern gives it away. This can only be an oesophageal spasm.

Diffuse Esophageal Spasm (DES) :

Clinical Presentation - These patients present with intermittent chest pain and dysphagia. The pain can simulate that of a myocardial infarction, but it bears no relationship with exertion.

The pain can be precipitated by drinking cold liquids.

Diagnosis - Barium studies may show a "corkscrew" pattern at the time of the spasm. The most accurate test is manometric studies, which will show high-intensity, disorganized contractions. Because the contractions are disorganized, they do not lead to the forward flow of food and peristalsis.

Treatment - Calcium-channel blockers, such as nifedipine, and nitrates.

The diagnosis of Crohn’s disease is quite clear here. Fistulas help differentiate between ulcerative colitis and Crohn’s. Since fistulas are present, it can only be Crohn’s disease.

As the patient has watery diarrhoea instead of bloody diarrhoea, think of giardiasis. Many cases of giardiasis are associated with recent foreign travel. Giardiasis can present as a traveler's diarrhoea with symptoms lasting more than ten days. Symptoms of giardiasis include bloating, flatulence, abdominal pain, loose stool, and explosive diarrhoea. The symptoms may begin after returning from travel and may be associated with weight loss.

Giardiasis can cause both acute and chronic diarrhoea. In this stem, it is likely chronic diarrhoea as there is a history of weight loss.

The clinical features of giardiasis are slightly different compared to campylobacter enteritis.

In campylobacteriosis, clinical features usually include a prodromal illness of headache and myalgia with fevers as high as 40°C.

This is followed by abdominal pains and profuse diarrhoea. The stool is often bloody. The reason many choose campylobacter as the answer is because campylobacter is the most common bacterial cause of infectious intestinal disease. But this is incorrect for this stem.

Important keynotes :

• Campylobacter, Shigella, Salmonella usually cause bloody diarrhoea.

• Giardiasis causes non-bloody diarrhoea

• Giardiasis can cause chronic diarrhoea associated with weight loss

• Campylobacter has a prodrome of headache, myalgia, and fever.

Findings on examination for B12 deficiency may include lemon tinge to the skin and glossitis. These findings together with a history of gastric resection whereby malabsorption of B12 could occur, point towards the diagnosis of B12 deficiency.

B12 DEFICIENCY Vitamin B12 is found in meat, fish, and dairy products, but not in plants.

Body stores are sufficient for 4 years. B12 then binds to intrinsic factors in the stomach, and this complex is absorbed in the terminal ileum.

Clinical presentation

• Symptoms are those of chronic anemia, i.e. fatigue, dyspnoea on effort

• Neurological symptoms may also be present ? Classically peripheral paresthesia and disturbances of position and vibration sense

• If uncorrected, the patient may develop subacute combined degeneration of the spinal cord leading to permanent ataxia Causes of B12 deficiency:

• Pernicious anaemia ?Commonest cause. It is due to autoimmune gastric atrophy resulting in a loss of intrinsic factor production required for the absorption of B12.

It is usually associated with other autoimmune problems e.g.hypothyroidism

• Dietary (e.g. vegans)

• Following total gastrectomy

• Ileal disease ? Resection of ileum, Crohn’s disease

• Malabsorption disorders ? Coeliac disease, tropical sprue. One distinction that may help you choose between B12 and folate deficiency is the diet. Good food sources of folate include broccoli, brussels sprouts, asparagus, and peas(basically vegetables). Thus if the given scenario is a vegetarian, it is unlikely that he is suffering from folate deficiency. In that case, pick B12 deficiency. Haematological abnormalities of B12 deficiency

• Macrocytic anaemia and the MCV is usually >110fL

• Hypersegmented neutrophils

• Serum B12 is low Management: Hydroxocobalamin IM.

Achalasia is the idiopathic loss of the normal neural structure of the lower oesophageal sphincter. The lower oesophageal sphincter is usually contracted to prevent the acidic gastric contents from refluxing backward into the oesophagus. For swallowing to occur, there is normally a relaxation process of the lower oesophageal sphincter to allow food to pass into the stomach. Inhibitory neurons are stimulated, blocking the impulses that cause constriction. In achalasia, these inhibitory neurons have been lost, as well as the ability to relax the lower oesophageal sphincter.

Presentation:

• Progressive dysphagia to both solids and liquids simultaneously and can have regurgitation several hours after eating

• There can also be weight loss

• Achalasia has no relationship with alcohol or tobacco use

• Note: This is different from oesophageal cancer, which usually not only presents with dysphagia to solid foods that progresses to difficulty swallowing liquids, but also is more common in older patients with a long history of alcohol and tobacco use.

Investigations:

• Barium swallow shows dilation of the esophagus, which narrows into a "bird beak" at the distal end

• The most accurate test overall is esophageal manometry.

Manometry shows increased lower oesophageal resting pressure

Management:

• Dilatation of the lower oesophageal sphincter

This man is suffering from coeliac disease. Malabsorption typically presents with diarrhoea and weight loss. The malabsorption from coeliac disease can result in either iron deficiency, folate, or B12 deficiency anemias. In this case, since the MCV is high, it is likely folate or B12 deficiency (more often folate deficiency). The term dimorphic red blood cells is used when one observes two types of distinct morphology in the circulating red cell population.

It is seen in B12 and folate deficiencies, sideroblastic anemias, post-transfusions, myelodysplasia, and iron deficiencies. Coeliac disease is confirmed by finding villous atrophy on small bowel biopsy (usually duodenum) by endoscopy.

The GP would likely have sent off specific auto-antibodies, such as tissue transglutaminase (TTG) antibodies (IgA) to investigate for coeliac disease when ordering the initial blood test. This information was omitted as the answer would then be too obvious.

An acute abdomen. The X-ray which shows free air under the diaphragm is classical for a perforation. Lying motionless and having a rigid, tender abdomen with signs of guarding is typical for a perforated peptic ulcer. Perforated peptic ulcer Perforation of a gastric or duodenal ulcer is usually a severely painful sudden event. It may occur in those without known peptic ulcer disease, as well as those with previously diagnosed problems.

However, close questioning may reveal recent symptoms attributed to ‘indigestion’. Sudden localized epigastric pain spreads to the remainder of the abdomen the pain is worse on coughing or moving and may radiate to the shoulder tip Examination Although distressed, the patient often prefers to lie still, rather than roll about.

Absent bowel sounds, shock, generalized peritonitis, and fever develop as time passes. Investigations An erect chest X-ray will demonstrate free gas under the diaphragm In those cases where the diagnosis is suspected, but not proven by X-ray, a contrast CT scan may help.

Treatment;

 • Provide IV analgesia

• Give an antiemetic (eg IV metoclopramide 10mg).

• Resuscitate with IV 0.9 % saline.

• Refer to the surgeon and give IV antibiotics.

High MCV and low Hb – Macrocytic anaemia These findings together with a history of ileal resection whereby malabsorption of B12 could occur, point towards the diagnosis of B12 deficiency.

COMPARISON OF CAUSES BETWEEN VITAMIN B12 AND FOLATE DEFICIENCY 

Vitamin B12 deficiency

- Malabsorption

-Pernicious anaemia

- Medical conditions of small intestine (coeliac disease, tropical sprue, Crohn’s disease)

- Gastric resection (for reasons of obesity or cancer)

- Inadequate dietary intake

- Low intake of cobalamin-rich foods.

Folate deficiency :

- Malabsorption

- Poor bioavailability

- Medical conditions

- Inflammation of small intestine (coeliac disease, tropical sprue, Crohn's disease)

- Inadequate dietary intake

- Low intake of folate-rich foods (usually vegetables).

In exam, one distinction that may help you choose between B12 and folate deficiency is the diet.

Good food sources of folate include broccoli, brussels sprouts, asparagus, and peas (basically vegetables). Thus if the given scenario is a vegetarian, it is unlikely that he is suffering from folate deficiency. In that case, pick B12 deficiency.

This patient is less than 55 years old and does not have any red flags. As his initial antibodies for Helicobacter pylori are negative and his symptoms have not resolved, it would be appropriate to refer this patient for an endoscopy. On the other hand, if his serum antibodies for Helicobacter pylori were initially positive, then a urea breath test would be appropriate.

GENERAL MANAGEMENT FOR DYSPEPSIA, HELICOBACTER PYLORI TESTING :

Whilst we have put in this diagram to use H. pylori antibody testing if no response to lifestyle modifications and antacids, NICE recommends any locally validated test for H. pylori which includes the carbon-13 urea breath test, stool antigen test, or serum antibody testing.

In practice, if the patient is taking proton pump inhibitors, remember to stop it for 2 weeks before performing a urea breath test or stool antigen test.The only test that you need to remember for re-testing for H. pylori is the carbon-13 urea breath test as NICE recommends this as there is still insufficient evidence to recommend stool antigen test as a test for eradication.

Serological tests have no value in confirming successful eradication because the antibodies persist after successful eradication.

Mediastinitis may occur after oesophageal perforation or rupture, due to a variety of reasons with endoscopy being one of them. Oesophageal perforation or rupture should not be taken lightly as it is a life-threatening condition. Often air along the subcutaneous planes or into the mediastinum would cause chest pain, dyspnoea, and fever. This patient should be considered critically ill and require management in the intensive care unit. It may be difficult to catch the diagnosis early in the course of mediastinitis as the signs and symptoms may be subtle.

However, as the condition progresses, patients would experience increasing chest pain, respiratory distress, and odynophagia. The most prominent symptom of mediastinitis is chest pain and this is localized depending on the portion of mediastinum involved. In anterior mediastinitis, pain is located at the substernal region while in posterior mediastinitis, the pain is localized to the epigastric region with radiation to the interscapular region.

A chest X-ray may show a widened mediastinum or air in the mediastinum. Water-soluble contrast can be added if needed. If there is diagnostic uncertainty, a direct visualization using endoscopy is used to confirm the diagnosis. The principles of managing mediastinitis due to oesophageal perforation include repairing the defect and treatment with antibiotics.

The likely diagnosis is acute pancreatitis. The most useful investigation is a serum lipase, looking for an elevation of more than 3 times the upper limit of normal. While abdominal X-rays are not useful in the diagnosis of pancreatitis, they are routinely ordered to exclude other potential causes of abdominal pain such as perforation or bowel obstruction. Ultrasound is useful to detect the presence of gallstones but it is not a good diagnostic test for acute pancreatitis.

The pancreas is poorly visualized in 25-50% of cases. Urea and electrolytes and liver function tests do not directly aid the diagnosis of pancreatitis however, they help assess the severity of the disease (e.g. showing the degree of leucocytosis or hypovolaemia) or give clues of the aetiology of pancreatitis (e.g. gallstone pancreatitis). Acute pancreatitis Aetiology The vast majority of cases are caused by gallstones and alcohol.

A popular mnemonic to remember is " GET SMASHED "

• Gallstones

• Ethanol

• Trauma

• Steroids

• Mumps (other viruses include Coxsackie B)

• Autoimmune (e.g. polyarteritis nodosa), Ascaris infection

• Scorpion venom

• Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia

• ERCP

• Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide,furosemide, pentamidine, steroids, sodium valproate)

Clinical features :

• Gradual or sudden severe epigastric or central abdominal pain (radiates to back, sitting forward may relieve it)

• Vomiting is prominent

• Tachycardia

• Fever,

• Jaundice

• Shock

• Rigid abdomen with local or general tenderness

• Periumbilical bruising (Cullen’s sign)

Investigation :

• Raised serum amylase (>1000U/mL or around 3-fold upper limit of normal).However, lipase levels are more sensitive and more specific.

• CT scan with contrast enhancement may be diagnostic where clinical and biochemical results are equivocal on admission.

This patient is suffering from an acute flare of ulcerative colitis. The stem gives multiple clues that allude to the severity such as bloody diarrhea (which is the hallmark of the disease), several bowel motions a day, tachycardia, and pyrexia. Intravenous corticosteroids are used for the treatment of acute and severe ulcerative colitis. This patient displays signs and symptoms of a severe exacerbation and should be referred to the medical team.

Topical aminosalicylates and oral corticosteroids have their place in the management of mild to moderate exacerbation of the disease but not in severe flare-ups like this.

It is also worth mentioning that if the question had asked for an appropriate investigation, an abdominal X-ray would be very appropriate in this setting to look for features suggestive of toxic megacolon.

ULCERATIVE COLITIS MANAGEMENT - Inducing remission

• First line – topical aminosalicylates e.g. Rectal mesalazine o Rectal aminosalicylates are better than rectal steroids and also better than oral aminosalicylates alone

• If not responding, then add 5-ASA (e.g. oral mesalazine)

• If still not responding, then add oral prednisolone If severe colitis, treat in the hospital with IV steroids as first-line In the exam, how do you know if this is severe colitis?

It is severe if the following are present:

• More than 6 bowel movements

• Visible blood in large amounts

• Pyrexia more than 37.8 C

• Tachycardic

• Anaemic

• ESR more than 30

Maintaining remission -

• Oral aminosalicylates e.g. mesalazine

• If remission is not well maintained, consider oral azathioprine or mercaptopurine.

The diagnosis here is achalasia. In achalasia, dysphagia is often with both fluids and solids and in fact, solids are affected more than soft food or liquids. It can sometimes present as chest pain or with recurrent chest infections. Chest infections or aspiration pneumonia results from untreated achalasia that leads to nocturnal inhalation of material lodged in the oesophagus and aspiration pneumonia.

Pernicious anaemia is caused by autoimmune atrophic gastritis, leading to achlorhydria and a lack of gastric intrinsic factor secretion. Injections are required. Note: if the cause of B12 deficiency is not due to pernicious anaemia (e.g. dietary), then oral B12 can be given after the initial acute course.

This is a difficult question to answer as there is not much background information in terms of patient history or signs and symptoms in terms of patient presentation. Based on the histology, we would be tempted to choose Crohn’s disease as a diagnosis as Crohn's disease is known to have histopathology of:

· Abdominal mass palpable in right iliac fossa

· Increased goblet cells on histology

· Granulomas seen on histology

· Transmural, skip lesions, cobblestone appearance on endoscopy

· Kantor's string sign, rose thorn ulcers and fistulae are seen on a small bowel enema.

Based on the histopathology ALONE the correct answer is D.

In reality, the patient presents with the classical signs and symptoms of Crohn’s disease i.e:

· diarrhoea (which may be bloody and become chronic - if present for more than six weeks)

· abdominal pain and/or weight loss

· periods of acute exacerbation, interspersed with remissions or less active disease.

· Systemic symptoms of malaise, anorexia, or fever

· Abdominal tenderness or distension, palpable masses.

· Anal and perianal lesions (pendulous skin tags, abscesses, fistulae) are characteristic.

· Mouth ulcers.

Some additional points to remember to diagnose UC or CD:

1. Fecal calprotectin

2. Abdominal X Ray - to exclude colonic dilatation

3. Stool exam

4. Barium fluoroscopy

5. Sigmoidoscopy/colonoscopy + biopsy

Ulcerative Colitis Management - Inducing remission

Topical * Rectal Mesalazine is better than rectal steroids  1st line

* 5-ASA (e.g. oral mesalazine) 2nd line.

* Oral Prednisolone - If severe colitis, is treated in the hospital with IV steroids as the first line. Maintaining remission oral aminosalicylates e.g. mesalazine

Management of Crohn’s disease Inducing remission :

1st line * Oral Prednisolone 2nd line *5-ASA drugs (e.g. mesalazine) azathioprine or mercaptopurine may be used as an add-on medication to induce remission but is not used as monotherapy metronidazole is often used for isolated perianal disease. Maintaining remission 1st line * azathioprine or mercaptopurine.

Recurrent abdominal pain with episodic headaches in a child with no abnormal findings examination and investigation points towards a diagnosis of Abdominal Migraine.

Abdominal migraines are a type of functional pain. It is usually characterized by having:

• Paroxysmal episodes of intense, acute periumbilical pain lasting for one or more hours

• Pain is dull or "just sore" quality

• Intervening periods of usual health, lasting weeks to months

• The pain interferes with normal activities

• The pain is associated with two or more of the following: anorexia, nausea, vomiting

• Not attributed to another disorder Reassurance is all that is needed.

Chronic pancreatitis often presents with abdominal pain. Classically, the pain is located at the epigastrium and radiates to the back.

The pain is worse after eating leading to a dislike of eating with consequent weight loss. The second most predominant feature is malabsorption which is represented here by steatorrhoea. Malabsorption again contributes to weight loss.

Alcohol is one of the significant risk factors for chronic pancreatitis but it is not a good hint to pick chronic pancreatitis as the answer based on an alcohol history as alcohol also contributes to acute pancreatitis, gastro-oesophageal reflux, oesophagitis, and indirectly to pancreatic cancer.

One might consider “Carcinoma of the head of the pancreas” as the answer given the similar symptoms of weight loss, epigastric pain, and history of alcohol. In reality, it is difficult to differentiate the two hence the importance of imaging modalities such as ultrasounds and CT scans.

In chronic pancreatitis, plain abdominal films of the pancreas can show diffuse calcifications which indicate significant damage to the pancreas. X-rays of the abdomen are not one of the main imaging modalities of the pancreas, and it is usually done for other reasons such as to exclude bowel perforation in A&E. Again to stress that ultrasound and CT scans would be better imaging modalities for pancreatic diseases. 

Transmural granulomatous inflammation involving the ileocaecal junction is one of the features seen in Crohn’s disease.

The combination of deranged LFTs combined with secondary amenorrhoea in a young female strongly suggests autoimmune hepatitis. In autoimmune hepatitis, serum aminotransferases: aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are usually elevated at initial presentation.

Serum alkaline phosphatase is normal or only mildly raised. A more than two-fold elevation suggests an alternative or additional diagnosis. Occasionally, the stem would include a form of another autoimmune disease such as Addison’s disease, vitiligo, or an autoimmune thyroid disorder as this may be present with autoimmune hepatitis.

Autoimmune hepatitis (AIH) is a chronic disease of unknown cause, characterized by continuing hepatocellular inflammation and necrosis, which tends to progress to cirrhosis.

• Predominantly affects young or middle-aged women

• Up to 40% present with acute hepatitis and signs of autoimmune disease, eg fever, malaise, urticarial rash, polyarthritis, pleurisy, pulmonary infiltration, or glomerulonephritis. The reminder present with gradual jaundice or are asymptomatic and diagnosed incidentally with signs of chronic liver disease.

Amenorrhoea is common and the disease tends to attenuate during pregnancy.

Investigations:

The diagnosis rests on a combination of compatible biochemical, immunological and histological features together with the exclusion of other liver diseases. Associated diseases : Concurrent autoimmune disorders occur in approximately 40% of patients, particularly autoimmune thyroid disorders.

The likely diagnosis is acute pancreatitis. Serum amylase and lipase are appropriate investigations, looking for an elevation of more than 3 times the upper limit of normal.

While abdominal X-rays are not useful in the diagnosis of pancreatitis, they are routinely ordered to exclude other potential causes of abdominal pain such as perforation or bowel obstruction. Ultrasound is useful to detect the presence of gallstones but it is not a good diagnostic test for acute pancreatitis. The pancreas is poorly visualized in 25-50% of cases.

Urea and electrolytes and liver function tests do not directly aid the diagnosis of pancreatitis however, they help assess the severity of the disease (e.g. showing the degree of leucocytosis or hypovolaemia) or give clues of the aetiology of pancreatitis (e.g. gallstone pancreatitis).

Hepatoma (more often called hepatocellular carcinoma) is a primary malignancy of the liver. The given scenario has features of hemochromatosis which is among the causes of restrictive cardiomyopathy. It is a very well-known fact that. patients with hemochromatosis have an increased risk of developing hepatocellular carcinoma. The liver is a primary storage area for iron and will naturally accumulate excess iron. Over time the liver is likely to be damaged by iron overload causing cirrhosis.

Cirrhosis and hemochromatosis together will increase the risk of hepatocellular carcinoma.

HAEMOCHROMATOSIS :

Hereditary haemochromatosis (HHC) is an autosomal recessive genetic disease in which increased intestinal absorption of iron causes accumulation in tissues, especially the liver, which may lead to organ damage. Other organs that may be affected by iron deposits include the pancreas, joints, heart, skin, and gonads.

Presentation :

• Early diagnosis is difficult because HHC is often asymptomatic until the latest of disease.

• Symptoms usually start between ages 40-60

• Initial symptoms are usually vague and nonspecific - eg, fatigue, weakness heart problems

• HHC may be diagnosed incidentally - eg, following abnormal serum ferritin or lifts

• Symptoms of advanced disease include:

o Diabetes

o Bronzing of the skin

o Hepatomegaly

o Cirrhosis

o Arthropathy

o Cardiac disease - arrhythmias or cardiomyopathy

o Neurological or psychiatric symptoms

- impaired memory, mood swings, irritability, depression

Remember the triad of diabetes, hepatomegaly, and bronze pigmentation. This is seen in 30% of patients with hemochromatosis and is a common presentation given in the questions.

The diagnosis of Crohn’s disease is quite clear here. Skip lesions are a give away that this is Crohn’s disease. This is also supported by the weight loss and the perianal skin tags.

The diagnosis here is a perforated peptic ulcer induced by NSAIDs. The sudden onset, rigid abdomen, silent and no bowel sounds are all hints that point toward perforated peptic ulcer.

The likely cause is oesophageal cancer where a malignant stricture or mass has resulted in difficulty in swallowing. An endoscopic biopsy is the definitive investigation. Oesophageal cancer Adenocarcinoma has now overtaken squamous cell carcinoma as the most common type of oesophageal cancer

Risk factors :

• Smoking - risk factor for both adenocarcinoma and squamous cell carcinoma, but associated with a much higher risk for squamous cell carcinoma than adenocarcinoma.

• Alcohol

• GORD

• Barrett's oesophagus - which is a precursor of adenocarcinoma

• Achalasia - Chronic inflammation and stasis from any cause increase the risk of oesophageal squamous cell carcinoma Very often in the stem, there would be a patient with a history of gastro-oesophageal reflux disease (GORD) or Barrett's oesophagus. Sometimes, they would give a history of increasing dysphagia and weight loss.

Diagnosis :

• Upper GI endoscopy with brushings and biopsy of any lesion seen is the first line test

• CT or MRI scan of the chest and upper abdomen is performed for staging purposes.

The scenario shows a classical picture of Clostridium difficile for which oral metronidazole is a treatment.

The two risk factors here are:

• Clindamycin – increased risk of Clostridium difficile infections

• Recently been in hospital – likely where she may have picked up C. diff In the exam, look out for antibiotic usage like cephalosporins, clindamycin, co-amoxiclav, and amoxicillin as a cause for Clostridium difficile.

The lump in the left supraclavicular region is known as a Virchow’s node. It is indicative of carcinoma of the stomach. The weight loss and decreased appetite support the diagnosis of gastric cancer.

Spidernaevi and ascites are suggestive of liver disease. It is likely that with the history of alcohol, and his signs and symptoms, he has a diagnosis of chronic liver disease which has resulted in portal hypertension and bleeding from oesophageal varices.

Oesophageal varices :

• Dilated sub-mucosal veins in the lower third of the oesophagus. This can lead to variceal haemorrhage which occurs from the dilated veins (varices) at the junction between the portal and systemic venous systems. The bleeding is often severe and life-threatening. The majority of the patients would have a history of chronic liver disease.

Presentation:

• Haematemesis (most commonly), melaena

• Signs of chronic liver disease

Investigation:

• Endoscopy at early stage Acute management of variceal bleeding

• Always start with ABC

• Correct clotting: FFP, vitamin K

• Vasoactive agents like terlipressin Terlipressin should be offered to patients suspected variceal bleeding at presentation

• Antibiotic prophylaxis  reduces mortality in patients with acute upper GI bleeding in association with chronic liver disease

• Endoscopic variceal band ligation If band ligation is not available, emergency sclerotherapy as first-line

• Sengstaken-Blakemore tube if uncontrolled haemorrhage

• Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if still unable to control bleeding

Prophylaxis of variceal haemorrhage :

• Propranolol is often given at discharge to reduce portal pressure to decrease the risk of repeat bleeding.

Gilbert's syndrome is usually an autosomal recessive disorder and is a common cause of unconjugated hyperbilirubinemia due to decreased UGT-1 activity which is the enzyme that conjugates bilirubin with glucuronic acid. It may go unnoticed for many years and usually presents in adolescence with intermittent jaundice occurring during illness, physical exertion, stress, or fasting. In this stem, the jaundice was precipitated by infection.

Investigations usually show a mildly raised serum bilirubin but the other LFTs remain within normal ranges as seen in this stem.

FBC would show normal reticulocyte count -this helps distinguish Gilbert’s syndrome from other types of haemolysis.

Urine dipsticks would be seen as normal as it is the unconjugated bilirubin that is high (not the conjugated bilirubin as would be seen in Dubin-Johnson syndrome). Remember, viral infections are common triggers for a rise in bilirubin in patients with Gilbert's syndrome.

Acute fatty liver of pregnancy (AFLP) and HELLP (Haemolysis, Elevated Liver enzymes, Low Platelets) syndrome both have low platelets and deranged liver function as part of the clinical picture. However, low serum glucose and/or raised serum ammonia are more suggestive of AFLP. Vomiting is also more commonly seen in AFLP than HELLP syndrome.

Acute fatty liver of pregnancy Acute fatty liver pregnancy (AFLP) is a rare form of jaundice in pregnancy. It occurs late in pregnancy and may be life-threatening.

The aetiology of AFLP is unknown. It is part of the spectrum of disorders related to pre-eclampsia. Differentiation from HELLP(Haemolysis, Elevated Liver enzymes, Low Platelets) syndrome can be difficult as signs and symptoms can overlap.

Risk factors ;

• Pre-eclampsia - There is associated pre-eclampsia in 30–60% of AFLP

• First pregnancies

• Multiple pregnancy

Presentation :

• Presents acutely with: o Nausea o Vomiting o Abdominal pain o Fevers o Headache o Pruritus o Jaundice

• Begins typically after 30 weeks of gestation

• It also may appear immediately after delivery. Severe hypoglycaemia and clotting disorder may develop causing coma and death

Investigations :

• Liver transaminases are elevated (ALT is typically elevated more than 500 U/L)

• Raised serum bilirubin

• Hypoglycaemia

• Abnormal clotting with coagulopathy (prolongation of prothrombin and partial thromboplastin times)

• Biopsy would be diagnostic

Management :

 • Treat hypoglycemia

• Correct clotting disorders

• N-acetylcysteine (NAC) 

• Consider early delivery

A DIFFERENTIATING AFLP FROM HELLP :

Acute fatty liver of pregnancy vs Haemolysis, Elevated Liver Enzymes, Low Platelets syndrome.

HELLP AFLP Epigastric pain ++ + Vomiting ++ Hypertension ++ + Proteinuria ++ + ALT/AST + + Hypoglycaemia ++ Hyperuricaemia + ++ DIC + ++ Thrombocytopenia ++ + WBC + ++ Ammonia ++ Acidosis ++ Haemolysis ++

If patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at least 6 weeks before testing. Serology tests and jejunal biopsies may come back negative if the patient is currently on a gluten-free diet.

The patient is suffering from Crohn’s disease. In this scenario, we have multiple clues which point towards Crohn’s disease such as diarrhoea with the location of abdominal pain. The common site of the pain in Crohn’s disease is the lower right side of the abdomen due to the involvement of the small intestine (ileum). Other common features are weight loss and mouth ulcers. Another subtle hint is the smoking history.

Smoking increases the risk of developing Crohn’s by about three to four times. While ulcerative colitis also can present as chronic diarrhoea, it more often involves the other part of the colon (left-sided colitis) In coeliac disease, the diarrhoea is mainly due to malabsorption, which leads to abnormally high levels of fat in stools termed steatorrhoea, which is not the case in this patient.

Colon cancer is the last thing that you should be thinking of in a patient in this age group. Medications are not the right option as there is no significant past medical history in this patient.

The clinical features and treatment after colonoscopy suggest a diagnosis of ulcerative colitis for which the initial treatment of mild to moderate symptoms is mesalazine.

The best answer here is coeliac disease. Whilst coeliac disease indeed causes malabsorption which accounts for intermittent diarrhoea and abdominal bloating, the more specific answer is still Coeliac disease since there is a history of wheat in the diet. Eggs do not exacerbate coeliac disease as it is not gluten however her meals which contain wheat is likely the cause of her malabsorption symptoms. 

The diagnosis here is haemochromatosis. The liver is a primary storage area for iron and will naturally accumulate excess iron. Over time, the liver is likely to be damaged by iron overload causing cirrhosis. Cirrhosis and hemochromatosis together will increase the risk of hepatocellular carcinoma. 

Reassurance is the correct option here. It is reserved for patients who are asymptomatic and have stones in their gallbladder. Stones that are found incidentally, as a result of imaging investigations unrelated to gallstone disease in asymptomatic patients do not require any intervention. But be aware that if the gallstones were found in the common bile duct instead of the gallbladder, then a laparoscopic cholecystectomy may be needed regardless if they are symptom-free or have symptoms. 

This is a case of perforated peptic ulcer with the features of shock, abdominal rigidity, and raised temperature. Perforation of a peptic ulcer causes an acute abdomen with epigastric pain that may progress to generalized rigidity. The stress of an operation may cause the body to produce higher amounts of acid, which can irritate preexisting ulcers leading to easy perforation. A diagnosis is made by taking an erect abdominal/chest X-ray (seeking air under the diaphragm).

When someone presents with dysphagia, glossitis, and iron deficiency anaemia, Plummer-Vinson syndrome is your answer. Plummer Vinson syndrome • A condition where iron deficiency is associated with a post-cricoid oesophageal web The syndrome most often affects middle-aged women.

Presentation:

• Painless, intermittent dysphagia due to oesophageal webs

• Symptoms of iron-deficiency anaemia

Management:

• Iron supplements

• Dilation of the webs

As she is symptomatic, reassurance is out of the question. The two remaining options are laparoscopic cholecystectomy and emergency laparotomy. Laparoscopic cholecystectomy is the preferred option here as there are no signs of gallbladder perforation. Laparotomy has a higher risk as it is much more invasive.

In haemochromatosis, characteristically, the iron is found predominantly in a periportal distribution (acinar zone 1) within the hepatic lobule, with virtually all iron deposited in parenchymal hepatocytes and none in Kupffer cells. By contrast, iron overload in haemosiderosis causes to accumulation of iron granules predominantly in kupffer cells and more in the central area rather than peripheral hepatocytes. Since the question gives a pathology report of a large amount of iron pigment in hepatocytes rather than Kupffer cells, the diagnosis is haemochromatosis.

These findings together with a history of a gastric resection whereby malabsorption of B12 could occur, point towards the diagnosis of B12 deficiency. Mean cell volume is also increased which supports that diagnosis. Hypersegmented neutrophils are seen on blood smears in megaloblastic anaemias.

Perianal haematoma strictly speaking, it is a clotted venous saccule. It appears as a 2-4mm ‘dark blueberry’ (purple color) under the skin at the anal margin. It is seen as swollen and acutely tender perianal lumps.

Management: It may be evacuated under local anaesthesia or left to resolve spontaneously.

• Incision and drainage of the clot relieve pain but the thrombosis often recurs and there may be persistent bleeding.

• Conservative treatment includes analgesia, ice packs, and stool softeners. A topical calcium antagonist may help to relieve pain. If managed conservatively, symptoms usually settle within 10-14 days.

In autoimmune hepatitis, serum aminotransferases: aspartate aminotransferase (AST)and alanine aminotransferase (ALT) are usually elevated at initial presentation. Serum alkaline phosphatase is normal or only mildly raised. A more than two-fold elevation suggests an alternative or additional diagnosis.

Hypoalbuminaemia and prolongation of prothrombin time are markers of severe hepatic synthetic dysfunction. These lab tests do not rule out other liver diseases but given the combination of the presence of another autoimmune disease like hypothyroidism, the most likely diagnosis here is autoimmune hepatitis.

The gastrin levels need to be checked to rule out a gastrinoma. A gastrinoma is a neuroendocrine tumor usually found in the pancreas or duodenum. These tumours secrete gastrin which stimulates parietal cells of the stomach to secrete hydrochloric acid into the stomach cavity leading to intractable peptic ulcerations. Gastrinomas are suspected when peptic ulcers occur at unusual sites, such as the second part of the duodenum or the jejunum, or ulcers recur after adequate surgery.

One-third of patients have watery diarrhea due to high gastric output. Diagnosis is made by measurement of fasting gastrin levels or secretin stimulation test.

ZOLLINGER-ELLISON SYNDROME :

Zollinger-Ellison syndrome is characterized by gastric acid over-secretion due to excessive levels of gastrin secreted from tumours found in the duodenum or pancreas. It presents as severe peptic ulcer disease, gastro-oesophageal reflux, and diarrhoea. When to suspect Zollinger-Ellison syndrome Suspect in those with:

• Multiple peptic ulcers resistant to drugs

• If associated with diarrhoea or steatorrhoea

• Associated with a family history of peptic ulcers.

One must remember the cancer risk associated with coeliac disease. Intestinal lymphoma is one of them.

This is a very high-yield question and you need to remember that villous adenoma is one of the causes of hypokalaemia.

Dysphagia from inoperable oesophageal cancer is a complex issue with little consensus on the ideal management approach. For advanced cases of oesophageal cancer that are causing dysphagia, insertion of a stent into the oesophagus may be recommended.

The stent expands once in place and holds the oesophagus open to manage symptoms of dysphagia. Although radiotherapy also provides symptom relief (long-term relief), the waiting times for initiation of radiotherapy are long, and there are long lag times between initiation of treatment and relief of symptoms. Endoluminal stents provide more rapid and effective early relief for symptomatic patients.

Percutaneous endoscopic gastrostomy (PEG) is an endoscopic medical procedure in which a tube is passed into a patient’s stomach through the abdominal wall to provide a means of feeding when oral intake is not adequate. This is usually in stroke patients who are at risk of aspiration pneumonia or decompressing the stomach in cases of gastric volvulus.

OESOPHAGEAL STENT : An oesophageal stent is a tube placed in the oesophagus to keep a blocked area open so that the patient can swallow soft food and liquids. Oesophageal stents may be self-expandable metallic stents, or made of plastic, or silicone. They are used primarily in palliative cancer treatment.

Since this patient is on treatment for prostate cancer and bone metastasis, logic dictates that he would also be taking a large amount of opioid medication.

One of the side effects of opioid-based medication, such as morphine, is constipation. Since he is only complaining of constipation and not hard stool, stool softeners are incorrect. He has no evidence of having impacted stool and therefore, phosphate enema is incorrect. A low-residue diet is a low fibre diet.

This is the blatantly incorrect answer in the choices. So we are left with two choices: senna and lactulose.

1. High fibre diet

2. Stimulatant laxative (senna)

3. Osmotic laxative (lactulose/macrogol)

4. Add on a prokinetic agent such as metoclopramide, domperidone, or erythromycin

5. Consider the use of a dantron-containing laxative

6. Seek specialist advice if the patient is still experiencing constipation.

The lump in the left supraclavicular region is known as a Virchow’s node. It is indicative of carcinoma of the stomach. The weight loss and decreased appetite support the diagnosis of gastric cancer.

It is only necessary to check for the eradication of Helicobacter pylori in patients whose symptoms return. In this case, the patient tested positive for Helicobacter pylori and started on triple therapy. His history shows that his compliance was good and that he successfully finished his treatment.

However, he still complains of indigestion. So the issue in this question is to choose the single best test that will confirm the eradication of Helicobacter pylori.

We know that the answer is a urea breath test as that is the only test that NICE recommends post-eradication, but is the answer a C13 urea breath test or a C14 urea breath test.

The urea breath test is the only current valid method for detecting eradication of Helicobacter pylori infection. Urea can be labeled with two different carbon isotopes: C14 and C13. 

The main difference between them is that the former is radioactive, whereas the latter is stable. The C13 urea breath test is the recommended test to perform. This is because it is a non-radioactive isotope that can be used safely for repeated testing, which is frequently required in clinical practice. Endoscopy is only required if H. pylori is completely eradicated, as shown by urea breath testing, to further investigate the cause of dyspepsia. 

Note that in achalasia the symptoms can also be intermittent. It usually presents with gradually progressive, intermittent dysphagia. The dysphagia associated with oesophageal carcinoma is more rapid than achalasia. In achalasia, they may have a history of recurrent respiratory tract infections like in this stem. 

The likely diagnosis is acute pancreatitis given the elevated amylase. The initial treatment for acute pancreatitis is supportive and includes early fluid resuscitation, analgesia, and nutritional support. Parenteral nutrition is only used when the enteral route is not tolerated, or if it is not meeting specific caloric requirements. Surgical debridement may be required where there is proven infection and necrosis.

Note that laparoscopic surgical debridement has largely been replaced by newer minimally invasive techniques such as transgastric endoscopy and video-assisted translunar retroperitoneal necrosectomy followed by closed lavage of infected pancreatic necrosis so urgent laparoscopy is not the answer here. Also, remember that there needs to be some evidence of necrosis before surgical debridement is considered.

Intravenous antibiotics (e.g. IV imipenem) can be started in moderate to severe cases even without evidence of infected necrosis. This should preferably follow percutaneous aspiration of peritoneal fluid for culture however in this case, fluid resuscitation, analgesia and nutritional support are more important than just antibiotics. 60% of acute pancreatitis in adults are due to gallstones and thus cholecystectomy can be considered but should only be considered after the initial symptoms of acute pancreatitis have resolved.

The pain started when he drank a cold drink. The most likely answer here is an oesophageal spasm.

The diagnosis of Crohn’s disease is quite clear here. Lethargy and weight loss are nonspecific signs that can occur in Crohn’s disease. The giveaway here is the cobblestone mucosa that is seen on endoscopy which is pathognomic for Crohn’s disease.

Haematogenous spread to the liver from the lung is the most common route of metastases. TTF-1 is a protein seen by immunostaining which is used as a clinical marker of lung adenocarcinoma.

Enteropathy-associated T-cell lymphoma (EATL) is a celiac disease (CD) complication. This tumor derives from the neoplastic transformation of aberrant intraepithelial T lymphocytes emerging in coeliac patients unresponsive to a gluten-free diet.

The biopsy may show lymphomatous infiltrates accompanied by a prominent mixed-inflammatory infiltrate composed of histiocytes, small lymphocytes, plasma cells, and eosinophils, which may obscure the neoplastic cells. Just keep in mind that lymphoma should be at the top of the list of answers when you see a patient with coeliac disease in the exam.

The deep tan color of the skin with the combination of diabetes is termed “bronze diabetes”: and it is seen in haemochromatosis. Iron overload can also cause symptoms of arthropathy and gynaecomastia.

Please see Q-17

A colonoscopy would be able to diagnose the majority of the causes of changes in bowel habits and weight loss. The likely diagnosis here is colorectal cancer although inflammatory bowel disease could also present with similar features (e.g. weight loss, abdominal pain, and anaemia). Whatever the cause, a colonoscopy and biopsy is the gold standard to give us a diagnosis. Colonoscopy is still the preferred diagnostic investigation.

Alternatives to colonoscopy include barium enema and CT colonography. If a patient is without major comorbidities, a colonoscopy should be offered to diagnose colorectal cancer.

If a lesion suspicious of cancer is detected, a biopsy sample should be sent for histology. Flexible sigmoidoscopy, then barium enema can be used as an alternative to colonoscopy for patients with major comorbidity. Barium enema may also be used if a colonoscopy fails to visualize the caecum or if the patient is unable to tolerate the colonoscopy procedure.

Computed tomographic (CT) colonography can also be used as an alternative if the local radiology service can demonstrate competency in this technique. If a lesion suspicious of cancer is detected on CT colonography, a colonoscopy with biopsy to confirm the diagnosis should be performed. The tumour marker Carcinoembryonic Antigen (CEA) is of no use for diagnosis or staging but can be used to monitor disease relapse if raised at diagnosis and falls to normal after resection.

The most common organism that causes traveler’s diarrhoea is E. coli. It will usually cause mild self-limiting diarrhoea for less than 72 hours.

Around 80% of chronic pancreatitis results from alcohol excess in developed countries. Given his recurrent presentation over several months, we can say this is chronic. Patients with chronic pancreatitis usually have constant and relapsing episodes of upper abdominal pain lasting for days or weeks. He would likely go on to have a CT scan of his abdomen as the CT of the pancreas is often the imaging modality of choice. Cystic fibrosis is incorrect.

This is a genetic disorder that affects people from birth and is associated with respiratory complications. Furthermore, sadly most sufferers will not live beyond the age of 30 years.

CHRONIC PANCREATITIS :

• Alcohol - seen in the majority of cases

• Smoking

• Autoimmune

Clinical features :

• Classically presents with epigastric pain radiating into the back

o Pain is relieved when sitting forward

o Pain is the most common presentation of chronic pancreatitis

o Pain is episodic with short periods of severe pain

o Eating may exacerbate the pain

• Steatorrhoea

o Steatorrhoea occurs due to the malabsorption of fats from the lack of pancreatic lipase secretion which could subsequently cause weight loss

o Occasionally, the question writers may use words like “offensive stools which are difficult to flush” which in other words represent the term steatorrhoea.

o This is a later presentation due to obstruction of the common bile duct when the head of the pancreas becomes fibrosed. Remember, patients with chronic pancreatitis seek medical attention mainly because of symptoms of abdominal pain or maldigestion and weight loss.

Investigations :

• Serum lipase and lipase

o May be slightly elevated however in contrast to acute pancreatitis, the serum amylase and lipase levels are not strikingly elevated

• Transabdominal ultrasound scans

o Often as part of the initial assessment

• Contrast-induced spiral CT scan

o Remains the gold standard for imaging technique for pancreatic disease

o Shows evidence of pancreatic calcification

Management - Think of the individual clinical features and how to manage them

• Pain – analgesia

• Steatorrhoea or malabsorption – Pancreatic enzymes supplements and fat-soluble vitamins

• Diabetes – oral hypoglycaemics and insulin

Ulcerative colitis is often episodic and presents with chronic diarrhoea that can be bloody. Systemic symptoms include fever and malaise. In moderate to severe attacks, blood tests would show raised white blood cells and CRP with anaemia (iron deficiency anaemia).

The features that she presents within the hospital are consistent with a toxic megacolon. This is characterized by a very dilated colon accompanied by abdominal distension, abdominal pain, and in some cases shock. Toxic megacolon is one of the well-known complications of ulcerative colitis.

A normal rectal examination and flexible sigmoidoscopy exclude the other options. Only proctalgia fugax is left.

Proctalgia fugax - Severe recurrent rectal pain in the absence of any organic disease. Attacks may occur at night, after bowel actions, or following ejaculation. Anxiety is said to be an associated feature.

The diagnosis here is primary biliary cirrhosis. The classic presentation is itching in a middle-aged woman as we see here. Often asymptomatic and diagnosed after finding alkaline phosphatase on routine LFT. Lethargy, sleepiness, and pruritus may precede jaundice. There is an association with Sjögren syndrome.

Antimitochondrial antibodies (AMA) are the hallmark of this disease.

To help remember: Think of the M rule for Primary biliary cirrhosis.

• IgM

• anti-Mitochondrial antibodies

• Middle-aged females

PRIMARY BILIARY CIRRHOSIS VS PRIMARY SCLEROSING CHOLANGITIS :

Primary Biliary Cirrhosis :

• Autoimmune, idiopathic

• Association - Sjogren

• Pruritus, raised ALP

• Antimitochondrial antibody (AMA) positive

• Management involves ursodeoxycholic acid, cholestyramine

Primary Sclerosing Cholangitis :

• Autoimmune, idiopathic

• Association - IBD (especially UC)

• Pruritus, raised ALP

• ERCP is the most specific test

• Management involves ursodeoxycholic acid, cholestyramine

The diagnosis of Crohn’s disease is quite clear here. A transmural, cobblestone appearance mucosa is a giveaway that this is Crohn’s disease.

The blistering rash over her elbows is called dermatitis herpetiformis. Dermatitis herpetiformis, is a skin condition linked to coeliac disease.

Typical symptoms of dermatitis herpetiformis are red, raised patches, often with blisters and severe itching. The low haemoglobin is another clue towards coeliac as one of the most common presentation of coeliac disease is iron deficiency anaemia. Folate and B12 deficiency can also occur.

The shortening of villi (villous atrophy) and lymphocytosis on jejunal biopsy is provides us with the diagnosis of coeliac disease. One may be thinking of tropical sprue as a diagnosis as it also has villous atrophy on jejunal biopsy and has a similar presentation.

But tropical sprue does not present with dermatitis herpetiformis and it is also much rarer as compared to coeliac disease.

Please see Q No-11

Crypt abscesses (Crypts of Lieberkühn) are typical of ulcerative colitis, though not diagnostic. They are mucosal crevices that are seen in the normal gastrointestinal tract. In ulcerative colitis, these get clogged up with neutrophilic exudates, forming “crypt abscesses.” These are not “real” abscesses and do not require surgical drainage. It is important to know the differences between ulcerative colitis and Crohn’s disease as it is very commonly asked.

Barrett’s oesophagus results from prolonged exposure of normal oesophageal squamous epithelium to the refluxate of GORD. This causes mucosal inflammation and erosion, leading to the replacement of the mucosa with metaplastic columnar epithelium. The most significant associated morbidity is oesophageal adenocarcinoma.

The diagnosis here is Achalasia. It can sometimes present as chest pain. The productive cough in this question points towards aspiration pneumonia secondary to retained food and fluid in the oesophagus. Regurgitation of undigested food and difficulty swallowing both food and liquids are classic for achalasia.

A chest X-ray would also show a large oesophagus in Achalasia.

While some might argue that the answer here could potentially be the pharyngeal pouch due to the regurgitation of undigested food and aspiration pneumonia. Question would provide other hints if a pharyngeal pouch was the answer such as halitosis which may occasionally be seen in a pharyngeal pouch. Furthermore, the megaesophagus points towards achalasia as being the answer to this question. 

In previous recommendations, patients aged 55 years or older with unexplained and persistent recent-onset dyspepsia should be referred urgently for endoscopy. In recent years, the recommendations have changed to consider routine endoscopic investigations in patients over the age of 55 where symptoms persist despite Helicobacter pylori testing and acid suppression. Since this question is asking for an investigation that would lead to a diagnosis, endoscopy is the best answer to investigate a peptic ulcer. 

If constipation is not treated and is left to manifest for a long period, it can result in the development of faecal impaction whose symptoms may be seen as dehydration, tachycardia, tachypnoea, agitation, and confusion if severe. A person with faecal impaction may require emergency treatment or hospitalization.

For rapid action, phosphate enema is preferred. Phosphate enemas contain sodium acid phosphate and sodium phosphate. The osmotic activity of the former increases the water content of the stool so that rectal distension follows and it is thought that this induces defecation by stimulating rectal motility. It has a very quick onset of action which makes enemas useful for when a rapid evacuation of a stony dull faecal impaction is required.

The anaemia and low ferritin and folate levels are characteristic of coeliac disease. This is in combination with the endomysial antibodies. A jejunal biopsy should be done to confirm this diagnosis.

Inadequate vitamin B12 absorption can be due to chronic pancreatitis. Neuropsychiatric features of B12 deficiency include dementia which is why he is having memory loss and difficulties with thinking. Peripheral paraesthesia and disturbances of position and vibration sense are classically seen in B12 deficiency. Treat with hydroxocobalamin.

The diagnosis of Crohn’s disease is quite clear here. Lethargy and weight loss are nonspecific signs that can occur in Crohn’s disease. The giveaway here is the deep ulcers, and skip lesions that are seen on endoscopy which is pathognomic for Crohn’s disease. Note that although Crohn’s disease usually has non-bloody diarrhoea, it occasionally may present with bloody diarrhoea.

High MCV and low Hb – Macrocytic anaemia.

These findings together with a history of ileal resection whereby malabsorption of B12 could occur, point towards the diagnosis of B12 deficiency.

This patient has hypoalbuminaemia. When plasma proteins, especially albumin, no longer sustain sufficient colloid osmotic pressure to counterbalance hydrostatic pressure, oedema, and ascites develops. Intravenous albumin may be used to increase a colloid osmotic pressure to draw fluid back into the intravascular compartment to reduce oedema and ascites.

It restores intravascular plasma volume with less exacerbation of salt and water overload than isotonic solutions. Albumin infusion produces only a transient effect but it is useful in cases like this where surgery may not be an option and treatment of intravascular fluid deficit and oedema is required. It is also useful to obtain diuresis in hypoalbuminaemia patients. Haloperidol has no role in causing hypoalbuminaemia.

Peptic strictures have an association with gastro-oesophageal reflux disease and can cause dysphagia. The fact that there is no weight loss and haemoglobin is normal points towards a benign cause. Esophageal cancer in this age group is also uncommon.

Inflammatory bowel disease remains the best choice among the rest. All the symptoms stated in the question including tenesmus can occur in inflammatory bowel disease. The answer is unlikely to be diverticulosis as diverticulosis is defined as the presence of asymptomatic diverticula. This patient has symptoms. Blood in stools is not seen in irritable bowel disease. Remember, passing blood is not a symptom of IBS. The symptoms are not at all consistent with adenomyosis or endometriosis.

The history of sudden onset epigastric pain, chills, and nausea in the postpartum period with a likely history of an uneventful pregnancy make cholecystitis the most likely diagnosis. Symptomatic gallstone disease is the second most common abdominal emergency in pregnant women. Pregnancy alters bile composition and gallbladder emptying slows in the second trimester, increasing the risk of gallstones. The raised ALT is of something to note. The causes of raised liver enzymes in the postpartum period is endless.

They include:

• Pregnancy-related liver diseases such as:

o Obstetric cholestasis

o Pre-eclampsia, eclampsia,

o HELLP syndrome

o Acute fatty liver of pregnancy

o Viral hepatitis

o Autoimmune liver disease

o Wilson’s disease

o Budd-Chiari syndrome

o Acute cholecystitis

o Drug-induced hepatotoxicity

As there is no protein in the urine and blood pressure has been normal throughout pregnancy, pre-eclampsia is unlikely. As haemoglobin levels and platelet levels are within a normal range for someone who has just delivered a baby, HELLP syndrome is unlikely. Obstetric cholecystitis may have aminotransferase levels as high as 20 times the normal limits, but the raised bile acids would cause significant pruritus which would be the main presenting feature rather than epigastric pain. Biliary colic occurs when a stone temporarily occludes the cystic duct. There is a colicky pain in the right upper quadrant radiating to the right shoulder.

The episode is usually self-limiting. Ultrasound establishes the diagnosis of gallstones. The diagnostic accuracy of ultrasound for detecting gallstones is 95%. The main difference between biliary colic and acute cholecystitis is the inflammatory component. In acute cholecystitis, there is local peritonism, fever, and elevated WCC.

This man has a peptic ulcer disease which is causing his upper GI bleeding. Part of the management involves resuscitation with intravenous fluids, intravenous analgesia, antiemetics, and intravenous PPI if known peptic ulcer disease. Intravenous antibiotics are only considered prophylactically if we are considering upper GI bleeding from varices or a perforated peptic ulcer. There is no reason to administer fresh frozen plasma or intravenous steroids in this stem. 

Loss of haustration is pathognomonic for Ulcerative Colitis. Cobblestone appearance is seen on an endoscopy for Crohn’s disease. Kantor's string sign rose thorn ulcers, and fistulae are seen on a small bowel enema in Crohn’s disease.

The correct answer is option C. Ascending cholangitis.

This is a classical presentation with Charcot’s triad of fever, RUQ pain, and jaundice. Abdominal sepsis is one of the three most common types of sepsis, particularly as this lady recently had a procedure at the time of presentation and is most suspicious of an infective pathology.

Acute pancreatitis is incorrect as this typically / classically presents with profuse vomiting and central (umbilical) abdominal pain that radiates under the ribs.

This distribution of pain relates to the embryonic origins of the pancreas which is the midgut. Acute cholecystitis is incorrect as although it is a good differential given the presentation, it is not the single best answer given the history of jaundice. Jaundice is not typically present in cholecystitis.

Cancer of the head of the pancreas is incorrect as there is nothing in the question to suggest a malignant pathology such as weight loss.

Furthermore, the classic presentation of cancer of the head of the pancreas is ‘painless jaundice’.

Option E. Upper GI perforation is incorrect as this usually presents with generalized abdominal tenderness with guarding and the patient will typically be much more unwell. This is a good differential to keep in mind as the patient did just have a recent endoscopy.

However, if a perforation had occurred, the patient would have become unwell immediately at the time of the event, not twenty-four hours later!

The diagnosis here is primary biliary cirrhosis. The classic presentation is itching in a middle-aged woman as we see here. Often asymptomatic and diagnosed after finding alkaline phosphatase on routine LFT. Lethargy, sleepiness, and pruritus may precede jaundice. There is an association with Sjögren syndrome. Antimitochondrial antibodies (AMA) are the hallmark of this disease.

This is an example of overflow diarrhoea. Medications such as opioid pain relievers reduce intestinal movement and may cause faecal matter to become too large, hard, and dry making it difficult to expel. Subsequently, faeces become so hard that they cannot be expelled and faecal fluid will flow around the block.

Phosphate enemas contain acid phosphate and sodium phosphate. The osmotic activity of the former increases the water contact of the stool so that rectal distension follows and it is thought that this induces defecation by stimulating rectal motility.

It has a very quick onset of action which makes enemas useful when a rapid evacuation of a stony dull faecal impaction is required. Phosphate enema is the clear answer here as the question addresses the immediate management. It is important to remember the relation between elderly, bedridden individuals and faecal impaction.

Fecal impaction is a fairly common complication of long-term constipation in the elderly and bedridden, occurring in about 30% of all nursing home residents. Hence in the exam, it is likely they would have the words, “Nursing home” in the stem.

Faecal impaction If the patient has faecal impaction, try:

• Bisacodyl suppositories

• Arachis oil retention enema to soften

• Phosphate enema

• An alternative is polyethylene glycol, Movicol taken for three days

• Manual removal (with midazolam, morphine, or caudal anaesthesia)

• Once successful it is imperative to start regular oral measures to prevent recurrence of the problem.

The likely cause is acute pancreatitis. Pancreatitis is one of the most frequent post-ERCP complications. The incidence of this is around 20%. Ascending cholangitis may have a similar presentation but given that she is apyrexial, the likely cause is acute pancreatitis. Note that even in acute pancreatitis, mild pyrexia is common.

The diagnosis of ulcerative colitis is quite clear here. Decreased goblet cells on histology points towards ulcerative colitis.

Achalasia Cardia is a primary motility disorder of the esophagus characterized by peristalsis and defective lower esophageal sphincter relaxation.

The pathogenesis of achalasia cardia is poorly understood. However recent evidences indicate that it is an autoimmune process triggered by some virus (e.g. herpes virus) in a genetically predisposed individual resulting in degeneration of myenteric neurons.

Dysphagia for both solid and liquid or prominently liquid suggests achalasia whereas dysphagia to solid suggests stricture. Also, gross dilatation of oesophagus with smooth narrowing at the lower end is seen in achalasia.

In achalasia, dysphagia is usually described as progressive. The standard of care in patients with achalasia has been pneumatic balloon dilatation and laparoscopic Heller's myotomy. Per oral endoscopic myotomy (POEM) is a novel minimally invasive treatment option for all types of achalasia cardia.

Villous adenoma can cause both hyponatremia and hypokalemia but out of these, better to choose D.

Progressive dysphagia (to mostly solid) is suggestive of peptic stricture which is supported here by the use of prokinetic drugs and H2 blockers which are used for reflux oesophagitis.

Acute gastroenteritis (may be due to bacteria, virus or parasite) may cause transient malabsorption, probably as a result of temporary, superficial damage to the villi and microvilli.

The features like :

i) severe right hypochondrial pain

ii) colicky nature of the pain (comes in waves)

iii) nausea

iv) absence of fever

iv) absence of jaundice favours diagnosis of biliary colic and the most appropriate next investigation is the US abdomen.

Points in favour of achalasia:

Aspiration pneumonia due to retained food and fluid in oesophagus. In achalasia usually, there is no acid reflux.

Dysphagia for both food and drink. Air-fluid level behind the heart.

This is not a hiatus hernia because

i) In a hiatus hernia usually you will get associated GORD

ii) Also in a hiatus hernia there may be nausea or vomiting.

This is not a pharyngeal pouch as there is no halitosis.

Not responding to treatment D/D is:

i) Zollinger Elison syndrome

ii) Ca stomach.

Indications of gastroscopy in a 35 yo man (for men of age <50) :

i) Acute symptoms with H/O previous episode (PUD)

ii) Alarm features : weight loss, anaemia, vomiting, hematemesis and melaena, dysphagia, palpable abdominal mass), fear of cancer, evidence of organic disease.

D/D is rectosigmoidal tumour. As there are no constitutional features of cancer like anorexia, weight loss, or fever rectosigmoid tumour is unlikely.

Crohn’s disease can occur at any age but is most frequently diagnosed in people ages 15 - 35. About 10% of patients are children under age 18.

So Crohn’s disease can occur in this age also and the feature like fistula is a common association of CD.

In UC there is goblet cell depletion and less mucous production in contrast with CD where there may be goblet cell hyperplasia and mucous secretion is not reduced. Please note aphthous ulcers can develop in both CD and UC.

History of diarrhea, abdominal discomfort, and patient being febrile indicate gut inflammation and cobblestone appearance on barium enema is diagnostic of CD.

Diagnosis is achalasia.

Characteristic manometric findings are: Lower esophageal sphincter (LES) fails to relax upon wet swallow (<75% relaxation) Pressure of LES <26 mm Hg is normal,>100 is considered achalasia, > 200 is nutcracker achalasia.

Both A and D are the correct answer as Barrett’s oesophagus is a change known as metaplasia.

Chest pain, unpredictable intermittent dysphagia and food suddenly sticks in the middle of the chest which can be cleared with a drink of water indicates uncoordinated irregular esophageal peristalsis which is characteristic of esophageal spasm! Also “cork-screw esophagus” seen in barium swallow is diagnostic of esophageal spasm.

Whipple’s disease.

Periodic acid-Schiff +ve granules containing macrophages in jejunal biopsy is diagnostic of Whipple's disease. Whipple disease is a systemic disease most likely caused by a gram-positive bacterium, Tropheryma whippelii.

Although the first descriptions of the disorder described a malabsorption syndrome with small intestine involvement, the disease also affects the joints, central nervous system, and cardiovascular system.

Candida and CMV infection both can be the answer but Candida is more common than CMV.

Pain in RIF, diarrhea, granular transmural ulcers near the ileocecal junction points towards the diagnosis of Crohn’s disease (predominantly ileocecal type).

We know for Crohn’s disease treatment options are -

i) Corticosteroids

ii) Immunosuppressants like azathioprine, mercaptopurine, and methotrexate, and

iii) Biological agents like adalimumab, infliximab, vedolizumab and ustekinumab.

However, if the patient is a child (steroid causes growth hamper) or can not tolerate corticosteroid alternate option used is 5-aminosalicylate as Salfasalazine. As the given patient is a child answer for him is A. Salfasalazine.

In diverticulosis there is usually constipation and diarrhea is less common. But in IBD there is usually diarrhea. Occasional blood in stool excludes irritable bowel disease. Adenomyosis can cause menstrual cramps, lower abdominal pressure, and bloating before menstrual periods and can result in heavy periods. UTI does not present like this.

The answer is IBD (Inflammatory bowel disease).

Dysphagia for both solids and liquids suggests neuromuscular dysphagia while dysphagia only for solids suggests mechanical obstruction. Here features are consistent with achalasia for which lower oesophageal sphincter dilation (balloon dilatation) is a treatment modality.

Lichen planus may have a lace-like appearance and not a thick white mark. The aphthous ulcer has a yellowish floor and is surrounded by an erythematous halo.

Smoking may cause tongue coating but not like thick white marks on the inside of the mouth. Leukoplakia with raised edges / Bright white patches and sharply defined and cannot be rubbed out like a candida patch; here also inflamed tongue points towards infection. So candidiasis is the most probable option.

In feacal impaction oral laxative is not the choice but phosphate enema is the best option here.

In benign stricture, esophageal carcinoma, and systemic sclerosis there is persistent dysphagia not intermittent. In oesophageal spasm, there may be intermittent dysphagia but there will be no regurgitation of stale food material and no nocturnal regurgitation in recumbency. The clinical picture described is a well-known feature of the pharyngeal pouch.

Fistula is commonly seen in Crohn’s disease.

Celiac disease.

Diarrhea, abdominal bloating, blistering skin rash over the elbow (Dermatitis herpetiformis), low serum albumin, calcium, and folate conc. Supported by shortening of villi and lymphocytosis on jejunal biopsy is a classic presentation of celiac disease.

The likely diagnosis is pancreatitis. A normal lipase level can range from 0-160 U/L depending on the lab. When the pancreas is damaged, these digestive enzymes can be found in the blood at higher levels than normal. Amylase or lipase results more than three times normal levels are likely to mean pancreatitis.

Mainly colonic anaerobic bacterias produce most of the gas and treated with metronidazole.

Diagnosis is Crohn’s disease.

Crohn's disease is a type of inflammatory bowel disease (IBD) that may affect any segment of the gastrointestinal tract from the mouth to the anus. Symptoms often include abdominal pain, diarrhea (which may be bloody if inflammation is severe), fever, and weight loss.

Clubbing, perianal skin tags, and aphthous ulcers can also be seen. Transmural granulomatous inflammation on colonoscopy is diagnostic of Crohn’s disease.

Diarrhoea causes metabolic acidosis and in response there occurs respiratory compensation [hyperventilation] leading to respiratory alkalosis and low PaCO2 (due to CO2 washout).

The likely diagnosis is IBD. So Colonoscopy should be done.

Oropharyngeal and/or esophageal candidiasis

Elderly patients with RA are usually on NSAIDs which may lead to perforated peptic ulcer which presents as severe epigastric pain, vomiting, and shoulder tip pain. Diagnosis is made by seeing a free gas shadow under the diaphragm on erect CXR.

Endomyseal/alpha-gliadin antibody. [Atrophy of the buttock due to fat malabsorption and distended abdomen (sometimes with everted umbilicus) with frequent offensive smelly stools are seen in coeliac disease. Hence endomyseal/alpha gliadin antibody should be done.

Features are suggestive of IBD (inflammatory bowel disease), so barium enema is the most relevant investigation among the given options. Barium contrast dye allows an evaluation of the intestines. This is more commonly used in severe IBD to rule out serious complications like a perforated colon.

Features and treatment after colonoscopy suggest diagnosis of ulcerative colitis for which the initial treatment option is mesalazine.

Dysphagia to both solid and liquid or mostly to liquid is a common feature of achalasia. In the early stages of achalasia there may occur aspiration due to regurgitation during lying down to sleep which may result in recurrent chest infection and cough.

A short history (one week) of bloody diarrhea, abdominal pain with cramps, fever, and tenderness in the lower abdomen is indicative of gastroenteritis.

H. pylori breath test

Cryptosporidiosis mainly affects children. It can affect adults as well. It causes a self-limited diarrheal illness in otherwise healthy adults. However, it is also recognized as a cause of prolonged and persistent diarrhea which can result in malnutrition. Cryptosporidiosis can manifest as chronic severe diarrhea in persons with acquired immunodeficiency syndrome (AIDS).

In medicine, the milk-alkali syndrome is characterized by high blood calcium caused by taking in too much calcium and absorbable alkali; common sources of calcium and alkali are dietary supplements taken to prevent osteoporosis and antacids. If untreated, milk-alkali syndrome may lead to kidney failure or death.

Pancreatic insufficiency can lead to malabsorption and B12 (cobalamin) deficiency. Dementia and diminished vibratory sensation and proprioception in the lower extremities were the most common objective findings of cobalamin deficiency.

The damage to the myelin due to cobalamin deficiency results in a condition known as subacute combined degeneration of the spinal cord (SCDSC). This condition affects various parts of the spinal cord, including the dorsal columns, the lateral corticospinal tracts, and the spinocerebellar tracts, resulting in a loss of proprioception, ataxia, the development of peripheral neuropathy, and dementia.

Mediastinitis usually results from an infection. It may occur suddenly (acute), or it may develop slowly and get worse over time (chronic). It most often occurs in a person who recently had an upper endoscopy or chest surgery. A person may have a tear in their esophagus that causes mediastinitis.

The key is C. CD. [Bloody diarrhea can occur in both CD & UC. Also, weight loss is common! but fistula formation is a well-recognized complication of CD].

Probable diagnosis is Crhon's disease.

Gastrosopy

Usually in hiatus hernia there is acid reflux.

Patient was all right for 3 years after eradication therapy. Now symptoms again may indicate a recurrence of H. Pylori infection which can be demonstrated by a C13 urea breath test. Serum antibodies persist (IgG) for long and are not reliable for recheck.

Probable diagnosis is diverticulitis and the preferred investigation from the given list is colonoscopy. Colonoscopy: It views the colon's interior to see the inflamed, infected pouches. Ultrasound images lack the detail of CT images and cannot evaluate the intestines as well as CT.

Features are consistent with oesophageal candidiasis which is treated with Oral fluconazole (200-400 mg daily) or IV fluconazole for 14-21 days (here iv fluconazole as the patient is immunocompromized due to chemotherapy).

Patients with recurrent symptoms from esophageal rings and webs require repeat esophageal dilation. Repeat esophageal dilation is safe and can relieve symptoms in the long term.

Esophageal spasm.

Epigastric pain radiating to back, worse on lying flat and comfort on bending forward are classic presentation of acute pancreatitis in which serum amylase is increased.

Long-term use of a nsaid predisposes to peptic ulcers. This may cause considerable bleeding leading to shock.

Recurrent abdominal pains, weight loss, and transmural inflammation and granulomata points towards the diagnosis of Crohn’s disease which is treated with sulphasalazine.

Pitting masses throughout the abdomen with dilated rectum indicates retained faecal matter. Enema and laxatives are the treatment.

As the patient has H. pylori infection the most appropriate management is triple therapy. But as it is not in the given options Proton pump inhibitor is the next answer.

A case of autoimmune hepatitis. Autoimmune hepatitis is an uncommon cause of chronic hepatitis which if untreated can lead to cirrhosis. However, the treatment outlook is very good. Smooth muscle antibody is positive in autoimmune hepatitis. The definitive investigation is a liver biopsy. Treated with steroid [start with high dose prednisolone]. Azathioprine is commonly added with steroids to reduce its dose as steroid has more side effects than azathioprine.

Only bilirubin is increased but not the liver enzymes. Also, positive nicotinic acid provocation test is in favour of Gilbert’s syndrome.

Post operative US will not give good results. We shall not go for ERCP first as it has complications like injury and pancreatitis. Acceptable options are CT, MRI and MRCP among which most appropriate is MRCP! But as the Question is most diagnostic it is ERCP. The diagnosis here is choledocolithiasis with cholangitis.

Post-operative US of the abdomen does not give good results for the hepatobiliary system. ERCP is an invasive procedure and it has considerable complications like cholangitis, injury, pancreatitis, etc. Among the given options MRCP is most appropriate. We shall go for ERCP after confirming the diagnosis confirmed. For this MRCP is preferred.

FFP

If the patient experiences serious problems described below his disease has progressed from compensated cirrhosis to decompensated cirrhosis:

1. Bleeding varices (internal bleeding)

2. Ascites (fluid in the belly)

3. Encephalopathy (confusion)

4. Jaundice (yellowing of eyes and skin)

This is a picture suggestive of obstructive jaundice. LFT can give clues like much-raised bilirubin, AST, and ALT not that high and raised alkaline phosphatase but still USG is diagnostic in case of obstructive jaundice.

Autoimmune hepatitis may present as acute hepatitis, chronic hepatitis, or well-established cirrhosis. Autoimmune hepatitis rarely presents as a fulminant hepatic failure. One-third may present as acute hepatitis marked by fever, hepatic tenderness, and jaundice.

Non-specific features are anorexia, weight loss, and behavioural change (here altered sleep pattern and moods).

There may be coagulopathy (here PT 70s) leading to epistaxis, gum bleeding, etc. The presence of another autoimmune disease like hypothyroidism supports the diagnosis of autoimmune hepatitis.

Fat, female, fair, forty, and fertile are the pnemonic for cholecystitis! Here the presentation of severe upper abdominal pain with fever along with the pnemonic features points towards the diagnosis of cholecystitis.

This is obstructive jaundice where the US may show dilatation of common bile duct or stones.

Though biliary infection is possible but acute pancreatitis is a more common complication of ERCP and the absence of any obstruction (stone or tumour which helps biliary infection to occur) makes cholangitis less likely.

Ascites in patients with cirrhosis is the result of portal hypertension and renal salt and water retention. Similar mechanisms contribute to ascites formation in heart failure. Portal hypertension signifies elevation of the pressure within the portal vein. According to Ohm’s law, pressure is the product of resistance and flow. Increased hepatic resistance occurs by several mechanisms. First, the development of hepatic fibrosis, which defines cirrhosis, disrupts the normal architecture of the hepatic sinusoids and impedes normal blood flow through the liver. Second, activation of hepatic stellate cells, which mediate fibrogenesis, leads to smooth-muscle contraction and fibrosis. Finally, cirrhosis is associated with a decrease in endothelial nitric oxide synthetase (eNOS) production, which results in decreased nitric oxide production and increased intrahepatic vasoconstriction. The development of cirrhosis is also associated with increased systemic circulating levels of nitric oxide (in contrast to the decrease seen intrahepatically), as well as increased levels of vascular endothelial growth factor and tumor necrosis factor, that result in splanchnic arterial vasodilation. Vasodilation of the splanchnic circulation results in pooling of blood and a decrease in the effective circulating volume, which is perceived by the kidneys as hypovolemia. Compensatory vasoconstriction via release of antidiuretic hormone ensues; the consequences are free water retention and activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, which lead in turn to renal sodium and water retention.

Cause of edema in cirrhosis:

The condition of Hepatic Cirrhosis is characterized, in part, by hepatic venous outflow obstruction, which in turn expands the splanchnic blood volume, and hepatic lymph formation. Intrahepatic hypertension acts as a stimulus for renal sodium retention and causes a reduction of effective arterial blood volume. These alterations are frequently complicated by hypoalbuminemia secondary to reduced hepatic synthesis, as well as peripheral arterial vasodilation. These effects reduce the effective arterial blood volume, leading to activation of the sodium- and water-retaining mechanisms. The concentration of circulating aldosterone often is elevated by the failure of the liver to metabolize this hormone. Initially, the excess interstitial fluid is localized preferentially proximal (upstream) to the congested portal venous system, causing ascites. In later stages, particularly when there is severe hypoalbuminemia, peripheral edema may develop. A sizable accumulation of ascitic fluid may increase intraabdominal pressure and impede venous return from the lower extremities and contribute to the accumulation of the edema.

In liver cirrhosis ascites (not generalized oedema which is caused by hypoalbuminemia and other mechanisms though they may have roles) is caused by portal hypertension (portal hypertension is invariable in cirrhosis) along with other factors.

Spider nevi and ascites suggest advanced liver disease. Here an alcoholic middle-aged man having large hematemesis with the above-mentioned features are very suggestive of bleeding from esophageal varices secondary to portal hypertension in liver cirrhosis.

Primary biliary cirrhosis, is an autoimmune disease of the liver. It results from a slow, progressive destruction of the small bile ducts of the liver, causing bile and other toxins to build up in the liver, a condition called cholestasis.

Further slow damage to the liver tissue leads to scarring, fibrosis, and eventually cirrhosis.

Pruritus, skin pigmentation (increased amounts of melanin, widely dispersed throughout both epidermis and dermis), raised ALP, and the presence of AMA is diagnostic of primary biliary cirrhosis.

The diagnosis is cholecystitis. The diagnosis of cholecystitis is suggested by the history (abdominal pain, nausea, vomiting, fever) and physical examinations in addition to laboratory and ultrasonographic testing.

Boas's sign which is pain in the area below the right scapula, can be a symptom of acute cholecystitis. The pnemonic for cholecystitis is 5 “f”. Fat, female, fair, forty, fertile = cholecystitis.

Symptoms of Hepatitis : A range from mild nausea to liver failure (very rare). Spread is normally by the faecal-oral route although there are occasional outbreaks through food sources.

Hand washing and good hygiene around food and drink prevent the spread of infection. Increasing age is a direct determinant of disease severity.