Gastrointestinal System/Adomen/Abdomen Wall Flashcards

Question

A 42-year-old man is admitted with a hematemesis. On examination he has a blood pressure of 95/60 mmHg and a pulse rate of 104 bpm. He has yellowish sclerae, scratch marks and bruises on his arms. Several spider nevi are noted on his chest and abdomen. His abdomen is distended and soft with evidence of shifting dullness. Dilated veins are easily visible in the subcutaneous tissue and the liver is palpable two finger-breadths below the costal margin. Which one of the following could be the most likely underlying cause of his problem? A. Alcoholic liver disease. B. Biliary cirrhosis. C. Schistosomiasis. D. Budd-Chiari syndrome. E. Hepatitis C cirrhosis.

Answer 1

**A. Alcoholic liver disease.** Upper gastrointestinal bleeding may have different causes, but I this man having the clinical features of liver disease and cirrhosis, bleeding from esophageal varices would be the most likely cause of bleeding. Cirrhosis results in portal vein hypertension. When the portal vein is obstructed, shunting between the portal vein and systemic veins start to develop. This shunts lead to dilated veins around the umbilicus (caput medusa), in the lower gastrointestinal tract (hemorrhoids), or in the upper gastrointestinal tract (esophageal varices). In **Australia alcoholic liver disease** is the **most common cause of chronic liver disease and cirrhosis**, followed by hepatitis C infection. Biliary cirrhosis, schistosomiasis, and Budd-Chiari syndrome can all potentially lead to liver cirrhosis, but are much less common than alcoholic liver disease.

Answer 2

**B. The serum albumin concentration.** The clinical picture is suggestive of ascites in the background of chronic liver disease. The **Child-Pugh system** is used to assess the prognosis of patients with liver disease and cirrhosis by calculating 1-year survival rate. This system takes into account the following 5 parameters for determination of the prognosis: 1. The presence of ascites 2. Bilirubin level 3. Albumin level 4. Prothrombin time 5. Encephalopathy The Child-Pugh score is then calculated according to the following table: (see photo) Based on the Child-Puch score, the patients are categorized as follows: * Class A (scores 5-6): well-compensated disease – one- and two-year survival are 100% and 85% respectively. * Class B (scores 7-9): functional compromise – one- and two-year survival are 80% and 60% respectively. * Class C (scores 10-15): decompensated disease - one- and two-year survival are 45% and 35% respectively. Of the given options, the only one contributing to prognosis is serum albumin concentration.

Answer 3

**C. Gatro-esophageal junction stricture.** Dysphagia to solid food is more likely to be caused by mechanical obstruction due to strictures, tumors, rings or webs. With the history of protracted gastro-esophageal reflux disease (GERD), the most likely cause of this presentation would be stricture. Inflammation and scarring of the esophagus result in stenosis of the esophagus most often at the site of junction to the stomach. **Resolution of GERD symptoms supports the diagnosis: when the stricture develops, the amount of acid reflux is decreased.** Option A: Esophageal cancer is another important differential diagnosis that has to be excluded, but not the most likely diagnosis given the absence of other symptoms such as significant weight loss, anemia, etc. Option B: Achalasia causes dysphagia to *both solids and liquids*. Dysphagia to solids, but not to liquids is against out achalasia as a probability diagnosis. Option D: Para-esophageal hernias may present with GERD and GERD, over time, may result in this clinical picture. The stricture, however, is caused by the GERD, not directly by the hernia. Option E: Ulcerative esophagitis is very rarely complicated by strictures, especially in patients with HIV; hence, an unlikely diagnosis in this HIV negative patient. | Esophageal Stricture

Answer 4

**B. Hemangioma.** The patient has the provisional diagnosis of the biliary colic, most likely due to biliary stones. The ultrasound scan – as the best initial diagnostic tool –has been used to confirm the diagnosis. Furthermore, any associated inflammation would be evaluated. Inflammation of the gallbladder manifests as the thickening of the wall of the gallbladder and the presence of pericholecystic fluid. Stones might be seen in the common bile duct as well; however, the sensitivity of ultrasound for detection of ductal stones is low (30%-50%). As a routine procedure, when scanning for biliary problems, the sonographer will scan the liver as well. In this case the sonographer has encountered an incidental finding, irrelevant to the presenting symptoms, for which a triphasic CT scan of the liver has been performed. **Early prominent dense enhancement of the lesion during the arterial phase is characteristic of liver hemangioma (the most common benign liver tumor). Hemangiomas are seen in approximately 20% of the general population. They may be solitary or multiple. The lesions typically show intense enhancement during the arterial phase of triphasic CT scan and retain a blush of contrast during the portal venous phase.** Option A and C: Most malignant liver tumours (primary or metastatic) are hypovascular and will not have the early enhancement during the arterial phase; rather, they become more pronounced during the portal venous phase. Option D: Cystic lesions in the liver may be simple, multiple (polycystic liver disease), neoplastic or infective (hydatid cysts). Simple cysts are extremely common and usually asymptomatic. On imaging, these cysts have a low-density homogenous appearance. With polycystic disease, the number and size of the cysts often lead to symptoms. Option E: Hydatid cysts have a characteristic septate appearance and heterogenous appearance if they contain daughter cysts. Liver abscesses are usually symptomatic and more likely to have a heterogenous appearance.

Answer 5

**C. Lacunar ligament, femoral vein, femoral artery, femoral nerve.** Femoral triangle consists of three borders: * Upper border: inguinal ligament * Medial border: lateral border of adductor longus * Lateral border: medial border of sartorius The contents of the femoral triangle from medial to lateral are: 1. Lacunar ligament and deep femoral lymph nodes 2. Femoral vein 3. Femoral artery 4. Femoral nerve `Remember LEVAN: Lymph node chain / lacunar ligament, Empty space, Vein, Artery and Nerve for the order of contents from medial to lateral.` The lacunar ligament is a ligament in the inguinal region that connects the inguinal ligament to the pectineal ligament near the point where they both insert on the pubic tubercle. This ligament comprises the medial border of the femoral canal.

Answer 6

**E. Renal failure.** Acute pancreatitis can be classified into acute interstitial (most common) and acute hemorrhagic (least common). In the first type, the gland architecture is preserved but is edematous. Inflammatory cells and interstitial edema are prominent within the parenchyma. **In hemorrhagic type, there is marked necrosis, hemorrhage, and fat necrosis. There is marked pancreatic necrosis along with vascular inflammation and thrombosis.** Hemorrhagic pancreatitis can rapidly result in **severe hemorrhage, hypovolemia, shock and acute renal failure.** Other options are also potential complications of acute pancreatitis but often do not occur as early as acute renal failure.

Answer 7

**D. Drainage through ERCP.** A **pancreatic pseudocyst** is a collection of pancreatic juice encased by reactive granulation tissue (not epithelial tissue) in or around the pancreas. Pseudocysts can be single or multiple, small or large, and can be located either within or outside the pancreas. Most pseudocysts communicate with the pancreatic ductal system and contain high concentrations of digestive enzymes such as amylase and lipase. The walls of pseudocysts are formed by adjacent structures such as the stomach, transverse mesocolon, gastrocolic omentum, and pancreas. The lining of pancreatic pseudocysts consists of fibrous and granulation tissue; the lack of an epithelial lining distinguishes pseudocysts from true pancreatic cysts. The mechanism by which a pseudocyst is formed is necrosis and liquefaction of the pancreatic necrosis of pancreatic or peripancreatic tissue. Pseudocyst can be seen in the following situations: * After an episode of acute pancreatitis (in 10% of patients) - necrosis of peripancreatic tissue progresses to liquefaction and pseudocyst formation. Alternatively, a pseudocyst may result from parenchymal necrosis leading to the complete ductal disruption, and gross leakage of pancreatic juice. * In patients with chronic pancreatitis – pseudocysts may develop after acute attacks of pancreatitis or after the pancreatic duct is obstructed. The latter causes increased intraductal pressure and leakage of pancreatic juice. * After blunt or penetrating abdominal trauma (including iatrogenic injuries) - The injury can directly disrupt the duct and causes leakage. Clinical manifestations and complications of pancreatic pseudocysts include: * Expansion of the pseudocyst can produce abdominal pain, duodenal or biliary obstruction, vascular occlusion, or fistula formation into adjacent viscera, the pleural space, or pericardium. * Spontaneous infection. * Digestion of an adjacent vessel can result in a pseudoaneurysm, which can produce a sudden, painful expansion of the cyst or gastrointestinal bleeding due to bleeding into the pancreatic duct. * Pancreatic pleural effusion -can result from disruption of the pancreatic duct with fistulization into the chest. * Pancreatic peritonitis - can be caused by disruption of the pancreatic duct with fistulisation to the abdomen. `NOTE - up to 40% of pseudocysts resolve without intervention; however, they can produce a wide range of clinical problems depending on the location and extent of the fluid collection and the presence of infection.` Pancreatitis pseudocysts are diagnoses with CT or ultrasound scan. Where the diagnosis is in doubt, the content can be aspirated (under endoscopic ultrasonography or CT scan) and examined. The old rule mentioning that intervention is needed if the cysts are larger than 6 cm or persist beyond 6 weeks is no longer in use, and surgical intervention should be considered if any of the following is present: * Compression of large vessels (clinical symptoms or seen on CT scan) * Gastric or duodenal outlet obstruction * Stenosis of the common bile duct due to compression * Infected pancreatic pseudocysts * Hemorrhage into pancreatic pseudocyst * Pancreatico-pleural fistula * Pancreatic pseudocysts and symptoms: --- Early satiety --- Nausea and vomiting --- Pain --- Upper gastrointestinal bleeding * Asymptomatic pancreatic pseudocyst AND either of the following: --- Pseudocysts > 5cm, unchanged in size and morphology for more than 6 weeks --- Diameter > 4cm and extrapancreatic complications in patients with chronic alcoholic pancreatitis --- Suspected malignancy Surgical drainage is the criterion standard against which all other interventions are measured in terms of success rate, mortality and recurrence rate. In recent years, however, **endoscopic drainage has been introduced and can be applied provided that the cyst is near the stomach or duodenal wall**: There are two main types of endoscopic drainage: * Transmural drainage: in this method, using endoscopy, a small incision is made in the stomach (endoscopic cystgastrostomy [ECG]) or in duodenum (endoscopic cystduodenostomy [ECD]) to let the pseudocyst drain into the stomach or duodenum. ECD is preferred over ECG. NOTE - pseudocysts should have a mature capsule (wall thickness>3mm and < 1cm), bulge the lumen and have minimum size of 5-6 cm to become eligible for endoscopic drainage. * Transpapillary drainage: this method is safer and more effective than transmural drainage, but requires that the cyst communicates with the pancreatic duct because this method includes entering the pancreatic duct by ERCP, and from there, into the pseudocyst. Stents may be left in place to facilitate drainage. Generally, endoscopic drainage methods are preferred over open surgical treatment if eligibility is met and there is no contraindication because these methods are less invasive and associated with fewer complications. Laparotomy with cyst excision and internal and external drainage is still the gold standard management option; however it is ONLY considered first-line therapy for surgical intervention in the following conditions: * Complicated pseudocysts i.e. infected or necrotic * Pseudocysts associated with pancreatic duct stricture and a dilated pancreatic duct * Suspected cystic neoplasia * Presence of pseudoaneurysm, unless it has been embolised before the procedure * Coexistence pseudocysts and bile duct stenosis * Complications such as compression of the stomach or the duodenum, perforation or pseudoaneursyms `NOTE - pseudoaneurysm is an absolute contraindication to endoscopic drainage unless it is embolized prior to the procedure.` Generally, patients with symptomatic pseudocysts should undergo interventional measures for pseudocyst drainage. The procedure of choice is endoscopic drainage. This cyst is 10 cm in size (>5cm) and amenable to endoscopic drainage either by endoscopic transmural or transpapillary drainage. Transpapillary drainage has the lowest complication rate of all the mentioned procedures and is the method of choice if the pseudocyst communicates with the pancreatic duct. Fortunately, 80% of pseudocysts communicate with the pancreatic duct. Option A: Endoscopic cystgastrostomy (ECG) or duodenostomy (ECD) are methods of choice if the pseudocyst is not communicating with the pancreatic duct. Option B: Laparotomy and surgical removal of the cyst is considered if endoscopic methods fail or there is a contraindication. Option C: Percutaneous catheter drainage has low success rate and high recurrent rates. It is never considered for treatment of a pancreatic pseudocyst. However, in infected pseudocysts it is the procedure of choice for sampling and examining the material as the most appropriate initial step. Option E: Conservative management is not an appropriate option for symptomatic pseudocysts. | Pancreatic Pseudocysts

Answer 8

**C. Observation.** A pancreatic pseudocyst is a collection of pancreatic juice encased by reactive granulation tissue (and not epithelial tissue) in or around the pancreas. Pseudocysts can be single or multiple, small or large, and can be located either within or outside of the pancreas. Most pseudocysts communicate with the pancreatic ductal system and contain high concentrations of digestive enzymes such as amylase and lipase. The walls of pseudocysts are formed by adjacent structures such as the stomach, transverse mesocolon, gastrocolic omentum, and pancreas. The lining of a pancreatic pseudocysts consists of fibrous and granulation tissue. Lack of an epithelial lining distinguishes pseudocysts from true pancreatic cysts. The mechanism by which a pseudocyst is formed is necrosis and liquefaction of the pancreatic necrosis of pancreatic or peripancreatic tissue. Pseudocyst can be seen in the following situations: * After an episode of acute pancreatitis (in 10% of patients) - necrosis of peripancreatic tissue progresses to liquefaction and pseudocyst formation. Alternatively, a pseudocyst may result from parenchymal necrosis leading to the complete ductal disruption, and gross leakage of pancreatic juice. * In patients with chronic pancreatitis - pseudocysts may develop after acute attacks of pancreatitis or after the pancreatic duct is obstructed. The latter causes increased Intraductal pressure and leakage of pancreatic juice. * After abdominal blunt or penetrating trauma (including iatrogenic injuries such as pancreatic surgery - injury can directly disrupt the duct and causes leakage. Clinical manifestations and complications of pancreatic pseudocysts include: * Expansion of the pseudocyst can produce abdominal pain, duodenal or biliary obstruction, vascular occlusion, or fistula formation into adjacent viscera, the pleural space, or pericardium. * Spontaneous infection. * Digestion of an adjacent vessel can result in a pseudoaneurysm, which can produce a sudden, painful expansion of the cyst or gastrointestinal bleeding due to bleeding into the pancreatic duct. * Pancreatic pleural effusion -can result from disruption of the pancreatic duct with fistulization to the chest. * Pancreatic pleural effusion: can be caused by disruption of the pancreatic duct with fistulization to the abdomen. `NOTE - up to 40% of pseudocysts resolve without intervention; however, they can produce a wide range of clinical problems depending on the location and extent of the fluid collection and the presence of infection.` Pancreatitis pseudocysts are diagnoses with CT or ultrasound scan. If the diagnosis is in doubt, contents can be aspirated and examined. The dictum mentioning that intervention is needed if the cysts are larger than 6 cm or persist beyond 6 weeks is no longer in use, and surgical intervention should be considered in (even one criterion is sufficient): * Compression of large vessels (clinical symptoms or seen on CT scan) * Gastric or duodenal outlet obstruction * Stenosis of the common bile duct due to compression * Infected pancreatic pseudocysts * Hemorrhage into pancreatic pseudocyst * Pancreatico-pleural fistula * Pancreatic pseudocysts and symptoms: --- Early satiety --- Nausea and vomiting --- Pain --- Upper gastrointestinal bleeding * Asymptomatic pancreatic pseudocyst AND either of the following: --- **Pseudocysts > 5cm**, unchanged in size and morphology for more than 6 weeks --- Diameter > 4cm and extrapancreatic complications in patients with chronic alcoholic pancreatitis --- Suspected malignancy Surgical drainage (laparotomy and internal and external drainage) is the criterion standard against which all other interventions are measured in terms of success rate, mortality and recurrence rate. In recent years however **endoscopic drainage** has been introduced and can be applied provided that the cyst is near the stomach or duodenal wall: There are two main types of endoscopic drainage: * Transmural drainage: in this method, using endoscopy, a small incision is made in the stomach (endoscopic cystgastrostomy [ECG]) or in duodenum (endoscopic cystduodenostomy [ECD]) to let the pseudocyst drain into the stomach or duodenum. ECD is preferred over ECG. * Transpapillary drainage: this method is safer and more effective than transmural drainage, but requires that the cyst communicates with pancreatic duct. Using ERCP and through the pancreatic duct, the cyst is reached and poked so that its content can drain into the pancreatic duct. Stents may be used to facilitate drainage. `NOTE - pseudocysts should have a mature capsule (wall thickness>3mm and <1cm), bulge the lumen and have minimum size of 5-6 cm to become eligible for endoscopic drainage.` Generally, endoscopic drainage methods are preferred over open surgical treatment if eligibility is met and there is no contraindication, because these methods are less invasive and associated with fewer complications. Laparotomy with cyst excision and internal and external drainage is still the gold standard management option; however it is considered first-line therapy for surgical intervention if: * Complicated pseudocysts i.e. infected and necrotic pseudocysts * Pseudocysts associated with pancreatic duct stricture and a dilated pancreatic duct * Suspected cystic neoplasia * Presence of pseudoaneurysm unless it has been embolized before the procedure * Coexistence pseudocysts and bile duct stenosis * Complications such as compression of the stomach or the duodenum, perforation or pseudoaneursyms `NOTE - pseudoaneurysm is an absolute contraindication to endoscopic drainage unless it is embolized prior to the procedure.` Generally, patients with symptomatic pseudocysts should undergo interventional measures for pseudocyst drainage. The procedure of choice is endoscopic drainage, but as mentioned before, for a pseudocyst to be amenable to this procedure, it `has to be at least 5-6 in size as well as bulging into the lumen`. **This cyst with 4 cm in size is unlikely to be drained by endoscopic measures; therefore, open decompression (surgical drainage) should be considered; however, since the pain is mild, a watchful observation would be best management here in an attempt to avoid the high rates complications associated with surgical drainage. If the symptoms were more pronounce, intolerable or indicative of more serious complications, surgical drainage (open surface drainage) would have been the option of choice.** Percutaneous catheter drainage has low success rate and high recurrent rates. It is never considered for treatment of a pancreatic pseudocyst. However, in infected pseudocysts it is the procedure of choice for sampling and examining the material as the most appropriate initial step.

Answer 9

**C. Pancreatic pseudocyst.** The round lesion with hypodense homogenous content and the thin smooth wall in the vicinity of and obliterating the pancreas is highly suggestive of a pancreatic cyst or pseudocyst. With the history of previous acute pancreatitis, a pseudocyst would be the most likely diagnosis. A pancreatic pseudocyst is a collection of pancreatic juice encased by reactive granulation tissue (and not epithelial tissue) in or around the pancreas. Pseudocysts can be single or multiple, small or large, and can be located either within or outside of the pancreas. Most pseudocysts communicate with the pancreatic ductal system and contain high concentrations of digestive enzymes such as amylase and lipase. The walls of pseudocysts are formed by adjacent structures such as the stomach, transverse mesocolon, gastrocolic omentum, and the pancreas. The lining of pancreatic pseudocysts consists of fibrous and granulation tissue. Lack of an epithelial lining distinguishes pseudocysts from true pancreatic cysts. The mechanism by which a pseudocyst is formed is necrosis and liquefaction of the pancreatic necrosis of pancreatic or peripancreatic tissue. Pseudocyst can be seen in the following situations: * After an episode of acute pancreatitis (in 10% of patients) - necrosis of peripancreatic tissue progresses to liquefaction and pseudocyst formation. Alternatively, a pseudocyst may result from parenchymal necrosis leading to the complete ductal disruption, and gross leakage of pancreatic juice. * In patients with chronic pancreatitis - pseudocysts may develop after acute attacks of pancreatitis or after the pancreatic duct is obstructed. The latter causes increased Intraductal pressure and leakage of pancreatic juice. * After abdominal blunt or penetrating trauma (including iatrogenic injuries such as pancreatic surgery - injury can directly disrupt the duct and causes leakage. Clinical manifestations and complications of pancreatic pseudocysts include: * Expansion of the pseudocyst can produce abdominal pain, duodenal or biliary obstruction, vascular occlusion, or fistula formation into adjacent viscera, the pleural space, or pericardium * Spontaneous infection * Digestion of an adjacent vessel can result in a pseudoaneurysm, which can produce a sudden, painful expansion of the cyst or gastrointestinal bleeding due to bleeding into the pancreatic duct * Pancreatic pleural effusion -can result from disruption of the pancreatic duct with fistulisation to the chest * Pancreatic peritonitis - can be caused by disruption of the pancreatic duct with fistulisation to the abdomen

Answer 10

**C. Endoscopy after 24 months.** The photograph shows Barrett’s esophagus. Barrett’s esophagus refers to metaplasia of the squamous epithelium of the distal esophagus to columnar epithelium of the intestinal type. The metaplasia is believed to be due to GERD in a susceptible individual. Barrett’s esophagus is often associate with severe reflux disease, esophagitis, or strictures, but is also seen in asymptomatic or minimally symptomatic patients. Barrett’s esophagus is a premalignant condition with a 40- to 125-fold increase in the incidence of adenocarcinoma of the lower esophagus; however, the absolute risk is relatively small and approximately 0.5% per year. Every patient with the alarming symptoms of weight loss, anemia, heme-positive stool, and dysphagia, or GERD for more than 5 years should undergo endoscopy and biopsy. Further management depends on the histological findings and is summarized in the following: `ENDOSCOPIC FINDINGS - MANAGEMENT` * **Barrett’s esophagus (metaplasia) - Repeat endoscopy every 2-3 years for lesions ≥ 3cm and every 3-5 years for lesions < 3 cm.** * Low-grade dysplasia - Repeat endoscopy in 6 months. * High grade dysplasia - Distal esophagetomy. This patient has metaplastic changes involving an area of more than 3cm; therefore, the next step in management would be repeating the endoscopy in 2-3 years. Option A: Pneumatic dilation is not a management option for GERD or Barrett's esophagus. Option B: Although proton pump inhibitors (PPIs) may be associated with the appearance of squamous islands and possibly some degree of regression, there is no evidence that PPIs reduce the incidence of esophageal cancer in patient’s with Barrett’s esophagus. Option D: Endoscopy after 3-6 months (current recommendations: every 6 months) was the choice of management if low-grade dysplasia (not metaplasia) would be found on histological studies. Option E: This patient needs close surveillance and follow-up and action should be taken for early detection of esophageal malignancies.

Answer 11

**C. Transabdominal ultrasound.** The clinical picture and history of excessive alcohol use makes **chronic pancreatitis** the most likely diagnosis. Chronic pancreatitis presents with epigastric pain as the most dominant feature. The natural history of pain in chronic pancreatitis is highly variable. Most patients experience intermittent attacks of pain at unpredictable intervals, while a minority of patients have chronic pain. In most patients, pain severity either decreases or resolves over 5-25 years. In alcohol-induced disease, alcohol cessation may reduce the severity of pain. The pain is constant, often radiates to back and may be associated with nauseas and vomiting. It is often felt in the epigastric area but may be felt on the left side or even right side. The pain may or may not be related to eating. If related, there may be weight loss due to fear of eating. At times of pain patients bend forward to the so-called “pancreatic position” or lie in the knee-chest position on their right or left side to decrease the pain intensity. Patients with severe pancreatic exocrine dysfunction cannot properly digest complex foods and absorb partially digested breakdown products. Nonetheless, clinical significant protein and fat deficiencies does not develop until more than 90% of the pancreatic function is lost. However, fear of eating due to pain brought up by eating, can result in early weight loss. With severe chronic pancreatitis, insulin deficiency and diabetes mellitus may also develop. Abdominal CT scan, MRI, ultrasound, plain X-ray films and ERCP can be used for diagnosis, but **CT scan is the best initial test used for imaging studies when chronic pancreatitis is suspected**. CT scans are 75-90% sensitive and 85% specific. **Ultrasound is the second-line initial imaging study** with a sensitivity of 60-70% and specificity of 80-90% and the best among option in the absence of CT scan. Calcifications within the pancreatic duct are present on plain films in approximately 30% of cases, making palne films a less desirable option. The characteristic finding on imaging is pancreatic duct calcifications, ductal dilation, enlargement of the pancreas and fluid collection. Calcium deposition is most commonly seen in alcoholic pancreatitis, but is also present hereditary and tropical forms of the disorder. It is rare in idiopathic pancreatitis. Magnetic resonance cholangiopancreatography (MRCP) is becoming the diagnostic test of choice since it can show calcification, without any radiation risks, but is expensive and not readily available. For this reason, it is not an ideal option for initial assessment. Endoscopic retrograde cholangiopancreatography (ERCP) is reserved for situations where non-invasive modalities are not available, are equivocal and for intervention.

Answer 12

**B. Acute pancreatitis.** The clinical picture and the history of heavy alcohol use suggest acute pancreatitis as the most likely diagnosis. The cardinal symptom of acute pancreatitis is abdominal pain. The pain is characteristically described as dull, boring and constant. The pain is often sudden-onset and gradually becomes worse. Most often, the pain is felt in the upper abdomen usually in the epigastric region, but sometimes is perceived more on the right or left side, depending on which part of the pancreas is involved. In about 50% of the patients, the pain directly radiates through the abdomen to the back. The duration of pain is variable but typically lasts more than 1 day. Restless and agitation may be noted. At times of pain patients bend forward to the so-called “pancreatic position” or lie in the knee-chest position. Anorexia, nausea and vomiting, and diarrhea are other likely symptoms. Acute pancreatitis secondary to alcohol, frequently occurs 1 to 3 days after a binge drinking.It can also occur after cessation of drinking. The patient should be asked about recent operative or other invasive procedures such as ERCP, family history of hypertriglyceridemia, previous biliary colic and binge alcohol drinking as the major causes of acute pancreatitis. Option A: Acute cholecystitis causes pain in right upper quadrant, fever and leukocytosis. Murphy’s sign is usually positive: the patient is asked to inspire deeply while the right subcostal area is palpated. The Murphy sign is cessation of inspiration due to pain. Patients with acute cholecystitis may experience increased discomfort and hold in mid-inspiration. Abdominal examination may show voluntary and involuntary guarding. Option B: Acute gastritis usually can present with pain in epigastrium associated with nauseas and vomiting and epigastric tenderness but fever would not be a feature. Option D: Gastroesophageal reflux disease (GERD) presents with heartburn, chronic cough, a metalic taste in the mouth. The given clinical picture is completely different from that of GERD. Option E: Patients with alcohol intoxication presents with slurred speech, nystagmus, disinhibited behavior, incoordination, unsteady gate, memory impairment, stupor, or coma depending on the severity of intoxication.

Answer 13

**A. Gastric outlet obstruction.** The picture shows a contrast CT scan of the abdomen. On the right side of the picture (left side of the patient) a distended contrast-filled stomach is seen. Duodenum is on the left side of the picture. It also contains contrast media. The right kidney is another structure seen on the CT scan. In front of the vertebral body and slightly to the left, the aorta (containing contrast material) is noticed. Other structures seen on this cut of the CT scan are lower part of the right hepatic lobe, left hepatic lobe, spleen and parts of the pancreas. The **distended and fluid filled stomach** is suggestive of **gastric outlet obstruction (GOO)**. The **distended duodenum** indicates that the **obstruction** has occurred at the duodenum level. Clinical entities that can result in GOO generally are categorized into two groups – benign and malignant. In the past, peptic ulcer disease (PUD) was the most common cause of GOO, but currently, 50-80% of GOOs are due to malignancies such as pylorus adenocarcinoma, lymphoma and gastrointestinal stromal tumour (GIST). Benign causes of GOO include pancreatic pseudocysts, gastric varices, infections such as tuberculosis, and rarely gall stones. At this level no pancreatic or hepatic lesion is seen. Cancer of the stomach would have given an obstruction in upper parts if it involves the pylorus. Besides, this might be the underlying cause of the CT scan findings not the interpretation.

Answer 14

**B. Pneumatic dilation.** **Achalasia** is a primary esophageal motility disorder characterized by the **absence of esophageal peristalsis and impaired relaxation of the lower esophageal sphincter (LES)** in response to swallowing. These abnormalities cause a `functional obstruction` at the gastroesophageal junction. The goal of treatment is to reduce the resistance of the LES and overcome the obstruction. Currently, standard of care for achalasia is based on guidelines from the American College of Gastroenterology and is as follows: * **Initial therapy** should be either **graded pneumatic dilation (PD)** or **laparoscopic surgical myotomy** in patients who are fit for such surgeries. * Botulinum toxin injection into the LES is considered for patients who are not appropriate candidates for surgery. * Pharmacologic therapy can be used for patients not undergoing PD or myotomy and who have failed botulinum toxin therapy (nitrates and calcium channel blockers most common) For this patient, either pneumatic dilation or endoscopic myotomy (not an option) is the most appropriate initial management option. Option A: Pyloromyotomy is the procedure used for treatment of hypertrophic pyloric stenosis or obstruction. Option C: In patients with mild symptoms or in those who are not appropriate candidates for pneumatic balloon dilation or surgery, injection of botulinum toxin is considered the next most appropriate treatment. Botulinum toxin injection has been associated with symptoms improvement, but may need to be repeated at intervals of 3-12 months. Option D and E: Pharmacological therapy can be used for those patients not undergoing pneumatic dilation or myotomy, and who have failed botulinum toxin therapy. These medications, however, may not be desirably effective. First-line medical treatment is with glyceryl trinitrate (oral or sublingual spray). If the episodes are associated with spasms or are frequent or disabling, a trial of diltiazem, nifedipine, or isosorbide dinitrate can be considered. | Achalasia

Answer 15

**C. Cecal volvulus.** The X-ray shows an extensively air-filled dilated proximal colon arising from the right side and extending to the left. With these X-ray findings, along with the history and physical findings, cecal volvulus is the most likely diagnosis. Volvulus occurs when a segment of viscus twists around its axis and results result in obstruction as well as blood supply compromise. The most common types of volvulus are sigmoid volvulus (more common) and cecal volvulus (less common). Cecal volvulus tends to occur in younger patients (30-60 years) compared to sigmoid volvulus that often is seen in elderly patients, who are bedridden or nursing home residents. Option A: There are no suggestive clues to acute appendicitis as a precipitating event for an appendix abscess to form. Option B: Although the clinical findings and history of warfarin use can make rectus sheath hematoma a likely diagnosis, the abdominal X-ray is consisetent with csecal volvulus. Option D: With leaking abdominal aortic aneurysm, a tender pulsatile mass would be expected in the midline, not in the right iliac fossa. Option E: With fecal impaction, fecal material was expected to be seen in colon (left side). Focal tenderness is not a dominant feature in fecal impaction.

Answer 16

**C. CT angiography.** The case scenario is an example of obscure gastrointestinal tract (GIT) bleeding. Obscure GIT bleeding is defined as bleeding from the GIT that persists or recurs without an obvious etiology found on upper endoscopy and colonoscopy and radiologic evaluation of the small bowel (such as by small bowel follow-through or enteroclysis). Obscure GIT bleeding accounts for approximately 5% of patients with GIT bleeding. In 75% of these patients, the source of bleeding is in small bowel. The remainder of cases are due to missed lesions in either upper or lower GI tract. Obscure bleeding is subdivided into overt or occult, depending upon the presence or absence of clinically-evident bleeding: Obscure occult (inactive) bleeding – This is manifested as iron deficiency anemia or recurrent positive Fecal Occult Blood Test (FOBT) results. Obscure overt (active) bleeding – This is manifested as recurrent episodes of clinically evident bleeding (e.g., melena or hematochezia), or persistent blood loss. Patients with ongoing blood loss so significant to necessitate transfusion are considered to have life-threatening active bleeding. Further management of obscure GI bleeding depends on whether the bleeding is clinically active (overt) or inactive (occult): **Active obscure GI bleeding:** In patients presenting with active bleeding, radiological investigations are the mainstay of diagnostic approach, given their high sensitivity and non-invasiveness. **CT Angiography (CTA) can detect bleeding rates of 0.5 ml/min and above.** A negative CTA signifies that catheter angiography is not indicated since the latter is less sensitive than the CTA and has been shown to detect the source of bleeding only if the rate of blood loss is greater than 0.5 ml/min. With a negative CTA and continuous bleeding, technetium 99m – labeled RBC nuclear scan is used as the second-line investigation at some institutions while others may use this as the first-line investigation. Among available modalities, RBC nuclear scan is most sensitive for active GI bleeding and can detect bleeding rates as low as 0.1 mL/min. `NOTE - Life-threatening hemorrhage should indicate catheter angiography as first-line management. A hemorrhage so significant is very likely to light up on catheter angiography. With catheter angiography, the site of bleeding can be found and controlled at the same time.` **Inactive obscure GI bleeding:** Capsule endoscopy is the option of choice. However, a negative test demands CT angiography or other radiologic modalities (radionuclide scan, etc.) for further assessment. ----- This patient has low hemoglobin despite several transfusions; however, he does not have urgent life-threatening hemodynamic instability such as low blood pressure, tachycardia, shortness of breath, chest pain, or hypoperfusion-related altered mental state. **For him a CTA would be the most appropriate next step in management to find the source of bleeding.** Option A: Capsule endoscopy is the first option for patients with occult obscure GI bleeding i.e. iron deficiency anemia or recurrent positive Fecal occult blood test (FOBT) results. Option B: Interventional angiography was the option of choice if the patient had immediate life-threatening hemodynamic instability at the moment. Although this patient has low hemoglobin, more transfusion can temporarily stabilize him to fulfill the criteria for CTA. Option D: Repeating the endoscopic studies is unlikely to add any information regarding the site of bleeding, as this measure has already failed to do so. Option E: Radionuclide imaging is used when there is obscured GI bleeding of unknown origin despite CT angiography or capsule endoscopy. The test takes a long time to perform. This patient with brisk and significant blood loss is not a good candidate for this test.

Answer 17

**D. Vomiting after one hour of meals.** Gastric outlet obstruction (GOO), is the consequence of any disease producing a mechanical obstruction to gastric emptying. Clinical entities that can cause GOO are generally categorized into benign and malignant. Peptic ulcer disease (PUD) is among the benign causes of GOO; however, the incidence of ulcer-induced GOO has dramatically declined owing to adequate and efficient treatment of PUD. The mechanism of obstruction by PUD can be either edema around the ulcer, or scar formation after the ulcer heals. The most common symptoms of GOO, regardless of the underlying etiology, are bloating, anorexia, nausea and vomiting. Vomiting usually is described as nonbilious, and characteristically containing undigested food particles. Patients with gastric outlet obstruction from a duodenal ulcer or incomplete obstruction typically present with symptoms of gastric retention, including early satiety, bloating or epigastric fullness, indigestion, anorexia, nausea, vomiting, epigastric pain, and weight loss. They are frequently malnourished and dehydrated and have a metabolic insufficiency. Weight loss is frequent when the condition is chronic and is most significant in patients with malignant disease. Abdominal pain is not frequent and usually relates to the underlying cause, e.g., PUD, pancreatic cancer. The time of vomiting can suggest the site of obstruction. In pyloric obstruction (more proximal) the time of vomitus is usually within the first hour of eating, whereas in pyloric stenosis, or duodenal stenosis or obstruction (more distal) the vomiting occurs after one hour because normally it takes 45 minutes to 1 hour for the food to reach the duodenum. Option A: If the patient has 3 or 4 meals a day he may vomit 3 to 4 times within one hour after each meal, but vomiting 3 to 4 times a day by itself is not a common presentation of gastric outlet obstruction. Option C: Right upper quadrant abdominal pain is seen in hepatobiliary diseases and is not a characteristic feature of gastric outlet obstruction. Option B: Abdominal distension is a feature of bowel obstruction, particularly obstruction of the large bowel. Option E: Early morning vomiting is associated with raised intra-cranial pressure and pregnancy, and is not a feature of gastric outlet obstruction.

Answer 18

**B. ERCP.** The clinical and laboratory picture suggests **acute pancreatitis secondary to gallstones and common bile duct obstruction** that has led to LFT abnormalities as well. Gallstone pancreatitis necessitates specific therapeutic consideration in addition to conventional treatment of acute pancreatitis. Multiple studies suggest that **early endoscopic retrograde cholangiopancreatography (ERCP), within 24-48 hours**, with papillotomy, or **surgical intervention** to remove bile duct stones is beneficial in patients with acute biliary pancreatitis and the presence of the following: * Concomitant acute cholangitis * Persisted common bile duct obstruction evident by worsening signs or symptoms of obstruction (clinical deterioration), or deteriorating liver function tests Endoscopic papillotomy is typically accompanied by placement of a plastic biliary stent to decrease the risk of post-ERCP pancreatitis. With increased liver function tests (LFTs), especially the elevated conjugated bilirubin, this patient should be considered to have concomitant cholangitis until proven otherwise. Considering the likelihood of acute cholangitis caused by CBD obstruction, this patient should undergo **early ERCP** as the most appropriate next step in management, **after rehydration, analgesia, and antibiotics**. LFTs are used to monitor the response to treatment. An **ultrasound** scan (not an option) is the **very first imaging investigation** for patients with signs and symptoms of pancreatitis or pancreatic cancer if manifestations of biliary obstruction are also present. Otherwise, **Abdominal CT scan** is used; However, in the absence of clinical features of biliary obstruction, CT scan is the preferred diagnostic modality. CT scan is the most important imaging test for the diagnosis of acute pancreatitis, its severity and potential complication Patients with clinical and biochemical features of acute pancreatitis. CT scan is indicated if: * there is no improvement with conservative therapy * complications are suspected * other diagnoses than pancreatitis is suspected | Acute Pancreatitis

Answer 19

**D. Intravenous fluids, analgesics and antiemetics.** This patient has clinical diagnosis of acute pancreatitis, most likely secondary to gallstones; however, a non-dilated common bile duct (CBD) and normal bilirubin excludes CBD obstruction. Management of the acute pancreatitis should be started with intravenous fluids, analgesia and antiemetics. The patient should be nil by mouth (NPO) and NG tube inserted for GI decompression. Further attention then should be paid to biliary stones as the underlying cause. Early ERCP (within 24-48 hours) is recommended for patients with acute biliary pancreatitis and either of the following: * Concomitant acute cholangitis * Persisted common bile duct obstruction evident by worsening sign or symptoms of obstruction, or deteriorating liver function tests Elevated liver enzymes and/or CBD stone on ultrasound are pointers towards a biliary cause for acute pancreatitis; however, normal level of bilirubin and the non-dilated of CBD on ultrasound exclude cholangitis with high certainty. For this patient early ERCP is not indicated, but ideally the patient should undergo semi-elective cholecystectomy during this hospital stay. CT scan is the most important imaging test for diagnosis of acute pancreatitis and its intraabdominal complications and also for assessment of severity. Patients with clinical and biochemical features if acute pancreatitis, who do not improve with initial conservative therapy or who are suspected of having complications or other diagnoses should undergo CT scan of the abdomen. This patient may need CT scan later (usually not earlier than 72 hours) in the course of the disease but not now as the most appropriate next step. Monitoring LFTs are required for assessment of response to treatment, but not a priority in initial management.

Answer 20

**C. Esophagoscopy.** The clinical picture including the history of heavy smoking and GERD, as well as the characteristics of the dysphagia is suggestive of mechanical dysphagia most likely caused by esophageal cancer. Weight loss can be seen in any kind of dysphagia; however, a significant weight loss of 15 kg in only 3 months suggests a more malignant etiology. Anemia is another clue to malignancy. When esophageal cancer is suspected, the best initial test is endoscopy (esophagoscopy) and biopsy for definite diagnosis. Option B: Barium swallow is very sensitive for detection of strictures and intraluminal masses but does not allow staging and biopsy. It is now rarely used when cancer is suspected. Option A, D and E: Bronchoscopy , chest X-ray , and CT scan of the chest are all used as tools for further evaluation and staging of the tumor, once esophagoscopy established a diagnosis of esophageal cancer. Bronchoscopy may be used for malignancies of upper (and middle) esophagus because it is common for tumors of these parts to invade the tracheobronchial tree. `NOTE - The extent of tumor spread to the mediastinum and para-aortic lymph nodes should be assessed by CT scanning of the chest and abdomen and endoscopic ultrasound. Endoscopic ultrasonography is the most sensitive test for assessment of the tumor depth. Other studies to consider for staging are bone scan and liver function tests.`

Answer 21

**B. Barrett’s esophagus.** While smoking and alcohol are the two most common risk factors for squamous cell carcinoma of the esophagus, Barrett's esophagus is the most significant risk factor for development of esophageal adenocarcinoma. Option A: Achalasia has been associated with esophageal cancer but is not as significant as other factors such as smoking and alcohol in squamous cell carcinoma and Barret's esophagus in adenocarcinoma of the esophagus. Option C: Although implicated in some studies, low-fiber diet is not as significant as other risk factors for esophageal cancer. Option D: Smoking and chronic alcohol ingestion are the most common and important risk factors for development of esophageal squamous cell carcinoma. Option E: Gastro-esophageal reflux disease is not a risk factor for esophageal adenocarcinoma unless it results in Barrett’s esophagus (indirect effect). `NOTE - Obesity is considered another important risk factor, mostly because it predisposes to reflux disease. However, the outcome of these conditions – GERD and the consequent Barrett’s esophagus, remains the main and most significant risk factor through producing metaplastic changes that can progress to dysplasia and eventually cancer.`

Answer 22

**E. Acute cholangitis.** The clinical picture is highly suggestive of acute cholangitis as the most likely diagnosis. This patient has signs and symptoms consistent with diagnosis of acute cholangitis. Fever is present in approximately 90% of patients. Abdominal pain and jaundice occurs in 70% and 60% of patients, respectively. The patient can become quickly septic and hypotensive with altered level of consciousness. Option A: Septic shock can result from acute cholangitis, and is a clinical syndrome not a diagnosis. Option B: Choledocholithiasis is the presence of gallstones within the common bile duct. A patient with uncomplicated common bile duct stones typically develops abdominal pain with mild liver function abnormalities. Fever is not a usual fever in uncomplicated patients. The two major complications associated with choledocholithiasis are acute cholangitis and acute pancreatitis. Option C: In acute pancreatitis, the abdominal pain is typically accompanied by nausea and vomiting, which may persist for many hours. The patient is often restless. Jaundice is not a feature unless there is concomitant common bile duct (CBD) obstruction and cholangitis. Option D: Acute cholecystitis is inflammation of the gallbladder, characterized by right upper quadrant pain and tenderness, fever, and leukocytosis. Gallstones are the most common etiology. Jaundice is not a feature of acute cholecystitis.

Answer 23

**B. Abdominal ultrasonography.** The clinical presentation is highly suggestive of pancreatic head carcinoma. This is evident by painless obstructive jaundice and a distended gallbladder (the right upper quadrant mass that moves with respiration). Pancreatic cancer can present with the following (percentages are from one recent study of 186 patients with pancreatic cancer): * Malaise and fatigue – 86% * Weight loss – 85% * Anorexia – 83% * Abdominal pain – 79% * Epigastric pain – 71% * Dark urine – 59% * Jaundice – 56% * Nausea – 51% * Back pain – 49% * Diarrhea- 44% * Vomiting – 33% * Steatorrhoea – 25% * Thrombophlebitis – 3% The most frequent signs are: * Jaundice – 55% * Hepatomegaly- 39% * Right upper quadrant mass – 15% * Cachexia – 13% * Courvoisier’s sign (nontender but palpable distended gallbladder at the right costal margin) – 13% * Epigastric mass – 9% * Ascites – 5% Of all pancreatic malignant tumors, most are found in the pancreatic head as the most common site. Pancreatic body and tale are second and third most common sites, respectively. Initial imaging study for assessment of suspected pancreatic cancer depends on the presenting symptoms. For patients with jaundice, the initial imaging study is typically a transabdominal ultrasound. It has high sensitivity for detecting biliary tract dilation and determining the level of the obstruction. It also has high sensitivity (>95%) for detection of a mass in the pancreas. The sensitivity is lower for tumours < 3 cm. Option A: Abdominal CT , however, is the preferred initial imaging modality in patients with epigastric pain and weight loss, but without jaundice. A contrsast-enhanced CT scan of the abdomen is alwasy considered for such patients. Option C: Chest X-ray is not indicated for diagnostic imaging of pancreatic cancer. Option D and E: ERCP and MRCP may be indicated in further assessment, in cases with obstructive jaundice. | Cholestatic Jaundice

Answer 24

**D. Ultrasonography of the pelvis and the abdomen.** The clinical picture is suggestive of pelvic appendicitis. The most common symptom of appendicitis is abdominal pain. Typically, symptoms begin as periumbilical or epigastric pain migrating to right lower quadrant of the abdomen. This pain migration is the most characteristic feature in the patient’s history. However, in up to 30% of the time, the appendix may be hidden from the anterior peritoneum by being in pelvic, retroileal or retrocolic (retroperitoneal retrocecal) position. The hidden position of the appendix may significantly alter the clinical manifestation of the appendicitis. A patient with a pelvic appendix may show no abdominal signs, but rectal examination may cause tenderness in cul-de-sac. Additionally, an obturator sign (pain on passive internal rotation of the flexed right thigh) may be present in a patient with pelvic appendix. With typical presentation of appendicitis, imaging studies are not necessary and the patient will be taken to the operating room for appendicectomy, but when diagnosis of appendicitis is not certain (such as in this case) imaging studies are required for confirmation. CT scan, specially the technique of appendiceal CT, is the most accurate imaging study (more accurate than ultrasonography). Appendiceal CT gives the highest diagnostic yield. If appendiceal CT is not available, standard abdominal/pelvic CT with contrast remains highly useful and may be more accurate than ultrasonography. However, because of concerns about patient exposure to radiation during CT scans, ultrasonography has been suggested as a safer primary diagnostic modality for appendicitis, with CT scanning used secondarily when ultrasounds are negative or inconclusive. A healthy appendix usually cannot be viewed with ultrasonography. When appendicitis occurs, the ultrasonogram typically demonstrates a noncompressible tubular structure of 7-9 mm in diameter. CT scan is the next step if ultrasound is non-diagnostic. `NOTE - Pelvic appendicitis may present with:` * An absence of abdominal wall rigidity and tenderness * Tenderness in the rectovesical pouch and Pouch of Douglas on rectal examination * Spasm of psoas muscle on right-hand-side * Diarrhea due to rectal irritation by the inflamed appendix * Frequency of micturition due bladder irritation by the inflamed appendix * Hypogastric pain on flexing and internally rotating the hip - due to contact of inflamed appendix with obturator internus muscle

Answer 25

**D. Distal splenocaval shunt.** The history of alcoholic liver disease and the bright red bleeding indicates variceal bleeding with high certainty. Varicose esophageal veins are the most common cause of variceal bleeding. Although at occasions gastric varices can be the source. Currently, endoscopic therapy is the definitive treatment for active variceal bleeding. It can be performed at the same time of the diagnostic endoscopy. Two forms of endoscopic treatment are commonly used: Sclerotherapy - Sclerotherapy includes injection of a sclerosant solution into the varices through an injection needle that is placed through the endoscope. Variceal band ligation – The procedure is similar to hemorrhoidal banding and involves placing small elastic bands around varices in the distal 5 cm of the esophagus. Surgical intervention is another option. Surgical procedures fall into either of these two categories: 1- Shunt surgeries – a shunt is created between portal and systemic venous system 2- Non-shunt surgeries - the two procedures used are (a)esophageal transection and (b) devascularization of gastro-esophageal junction Shunt surgeries can be categorized as: Nonselective - those that decompress the entire portal tree and divert all flow away from the portal system, such as portacaval shunts Selective - those that compartmentalize the portal tree into a decompressed variceal system while maintaining sinusoidal perfusion via a hypertensive superior mesenteric-portal compartment, such as a distal splenorenal shunt, or a distal splenocaval shunt Partial - those that incompletely decompress the entire portal tree and thereby, maintain some hepatic perfusion Selective shunting maintains near normal portal flow while decompresses the varicose veins. Since the portal flow is normal the risk of hepatic encephalopathy is minimal compared to TIPS, non-selective, or partial shunting. Of the options, the only one that can be applied as the next best step in management to both stop the bleeding and decrease the risk of hepatic encephalopathy is splenocaval shunting. Of all patients with selective shunting, only 10-15% develop encephalopathy; however, since retroperitoneal lymphatics are diverted, ascites is a common complication. `NOTE - The routine procedure after endoscopic measures fail is TIPS despite the higher risk of hepatic encephalopathy; however, the question does ask about the procedure to choose with the lowest risk of hepatic encephalopathy.` Attempting a third endoscopy (option B) or medical treatment with octreotide (option A) are not likely to stop the bleeding and are incorrect options. Renocaval shunting (option E) does not lead to decompression of portal system.

Answer 26

**A. Postoperative adhesions.** Post-operative adhesions are the **most common cause of small bowel obstruction (SBO)**. The risk of developing an obstruction after surgery from postoperative adhesions is estimated to be 9% within the first year after abdominal surgery, 19% by 4 years, and 35% by 10 years. The incidence of adhesive SBO seems to be **higher in open surgeries than in laparoscopic surgeries**. The cause for such difference is not clear, but is likely to be related to the degree of manipulation and trauma to the intraabdominal tissues. *Malignant tumors* are the second most common cause of SBO, accounting for about 20% of cases. SBO has been described in as many as 42% of women with ovarian carcinoma and 28% of patients with colorectal carcinomas. *Hernias* are the third leading cause of SBO and account for approximately 10% of all cases. *Ventral and inguinal hernias* are most commonly associated with obstruction; however, internal hernias, femoral, obturator and parastomal hernias also can contribute to SBO. Other less common causes of small bowel obstruction include: * Strictures e.g. caused by *Crohn’s disease* * Small bowel tumors * Trauma * Intussusception * Bezoars * Gallstone ileus (pseudo-obstruction) * Superior mesenteric artery syndrome * *Hypokalemia* (pseudo-obstruction) | Small-Bowel Obstruction

Answer 27

**D. Escherichia coli.** **Acute cholangitis** is a clinical syndrome characterized by **fever, abdominal pain and jaundice, developing as a result of stasis and infection in the biliary tract**. It can rapidly progress to sepsis. Biliary system obstruction is the most common predisposing factor. Culture of bile, ductal stones, and blocked biliary stents are positive in over 90% of cases, yielding a mixed growth of gram negative and gram positive bacteria. The most common bacteria isolated have colonic origin. `Escherichia coli is the major bacterium isolated (25 to 50%)`, followed by **Klebsiella** (15-20% percent) and **Enterobacter** species (5-10%). **Enterococcus** species (e.g. enterococcus fecalis) are the most common gram positive bacteria (10-20%). Anaerobes, such as bacteroides and Clostridia, are usually present as isolated pathogens , but they are rarely the sole infecting organisms and it is not clear if they play a role in acute cholangitis.

Answer 28

**A. Invasion to tracheobronchial tree.** **Surgery is the cornerstone of treatment for esophageal cancer**; however, in the following situations surgery is contraindicated: * Distant metastases – the presence of peritoneal, lung, bone, adrenal, brain, or liver metastasis, or extraperitoneal lymph node spread (e.g., paraaortic or mesenteric lymphadenopathy). Approach to patients with celiac lymph node involvement remains controversial. * Invasion to adjacent structures – invasion of the tumor to the aorta, **trachea**, heart, great vessels, or the presence of tracheoesophageal fistula (tumor stage: T4b) `NOTE - With invasion to the pleura, pericardium, or diaphragm the cancer is classified as T4a, and considered potentially resectable.` In addition, the presence of severe, associate comorbid conditions such as cardiovascular or respiratory diseases decreases a patient’s chance of survival and success of esophageal resection. Every patient should undergo **cardiac and respiratory function assessment prior to the surgery**. A forced expiratory volume in 1 second (FEV1) less than 1.2 L and a left ventricular ejection fraction of less than 40% are relative contraindications to the surgery. Of the options, only invasion of the tumor to the tracheobronchial tree is a contraindication to surgical resection.

Answer 29

**A. He should be monitered every 2-3 years by endoscopy and biopsy.** With metaplasia present in this patient, surveillance with endoscopy and biopsy should be performed every 2-3 years. Other options are incorrect. Barrett’s esophagus is a condition in which metaplastic columnar epithelium replaces the stratified squamous epithelium of the distal esophagus. The metaplastic epithelium is acquired as a **consequence of chronic gastro-esophageal reflux disease (GERD)**. Hiatus hernia predisposes to GERD and indirectly to development Barrett’s esophagus. Barrett’s esophagus is a premalignant condition with a 40- to 125-fold increase in the incidence of adenocarcinoma of the lower esophagus; however, the absolute risk relatively small and approximately 0.5% per year. Every patient with the alarming symptoms of weight loss, anemia, heme-positive stool, and dysphagia, or GERD for more than 5 years should undergo endoscopy and biopsy. Further management depends on the histological findings and is summarized in the following table:

Answer 30

**C. Dilation of bile ducts.** Jaundice can be caused by a variety of etiologies that broadly are categorized into extrahepatic or intrahepatic. A careful history and physical examination is essential. Laboratory tests follow for further evaluation.. The most important laboratory values to consider are bilirubin (total and unconjugated), hepatic transaminases, gamma glutamyl transpeptidase (GGT), alkaline phosphatase and coagulation profile. If the history, physical exam, and initial laboratory studies suggest obstruction of the biliary tree as the underlying pathophysiology of jaundice, an imaging study is indicated to differentiate extrahepatic and intrahepatic causes of cholestatic jaundice. The imaging tests that can be used are abdominal ultrasonography, endoscopic ultrasonography, abdominal CT scan, ERCP, and MRI. **Abdominal ultrasonography** is the **initial imaging** modality of choice, becasue it is inexpensive and readily available. In evaluation of jaundice, the **most important finding to look for is obstruction of the biliary tree, evident by biliary duct dilation**. Sensitivity of abdominal sonography ranges between 55% and 91% according to different studies. The sensitivity increases with increased serum bilirubin and duration of the jaundice. Ultrasound can also show stones; however, common bile duct (CBD) stones may not be visualized enough due to the duodenal gas obscuring the distal CBD. Gallstones, hepatic masses and pancreas may also be visualized on ultrasonography. Gallbladder thickening suggests cholecystitis. Cholecystitis per se does not result in jaundice, unless cholangitis or distal biliary tree obstruction occurs.

Answer 31

**D. Pseudo-obstruction.** Of the options, the most consistent one with the **history of fall (trauma)** and the given clinical presentation is `acute colonic pseudo-obstruction`, also known as `Ogilvie syndrome`. Acute colonic pseudo-obstruction is a disorder characterized by **gross dilatation of the cecum and the right hemicolon in the absence of an anatomic lesion obstructing intestinal flow**. `Acute colonic pseudo-obstruction is associated with an underlying disease in 95% of patients, including:` * Non-operative trauma * Infection * Myocardial infarction/ heart failure * Obstetric or gynecologic disease * Abdominal/pelvic surgery * Neurological problems e.g. Parkinson disease, spinal cord injury, multiple sclerosis, Alzheimer disease, etc * Orthopedic surgery * Miscellaneous medical conditions e.g. metabolic, cancer, respiratory failure, renal failure * Miscellaneous surgical conditions e.g. urologic, thoracic, neurosurgery Studies suggest that **non-operative trauma** is among the most common causes of acute colonic pseudo-obstruction. Acute colonic pseudo-obstruction is more common in men and in patients over the age of 60 years. Nausea, vomiting, abdominal pain, constipation, and, paradoxically, diarrhea are the primary manifestations. Abdominal distention is always present and can cause difficulty breathing. On physical examination, the abdomen is tympanic; however, bowel sounds are present in almost 90% of patients. Peritoneal signs are absent in the early stages of the disease; if they develop, they suggest impending perforation. Option A and B: Volvulus (cecal or sigmoid) is associated with *acute onset of pain and obstruction*, but a volvulus of three-day duration would have resulted in a *very ill and toxic patient* due to *ischemia* of the affected part of the colon and signs of *peritoneal irritation*. Option C: Pneumatosis coli is the presence of gas in the large intestinal wall. It is a *condition* not a diagnosis. Option E: Patients with toxic megacolon typically appear *very ill with fever, tachycardia and abdominal tenderness*. There is often a history of *bloody diarrhea* or other signs and symptoms of chronic inflammatory bowel disease. | Acute colonic pseudo-obstruction (Ogilvie's syndrome)

Answer 32

**E. Advice dietary changes.** With gasterectomy in history, dumping syndrome is the most likely underlying cause to this presentation. **Dumping syndrome is the effect of altered gastric reservoir function, abnormal gastric motor function, and/or pyloric emptying mechanism.** In terms of temporal relation to eating, dumping syndrome can have early or late manifestations: **Early dumping** Symptoms of early dumping syndrome occur 30-60 minutes after a meal, and are hypothesized to result from accelerated gastric emptying of hyperosmolar contents into the small bowel. The hyperosmolarity of the bowel content leads to fluid shift from the intravascular compartment into the bowel lumen, resulting in rapid small bowel distention and increase in the frequency of bowel contractions. With rapid shift of fluid into the intestinal lumen, circulating volume contraction follows, triggering a vasomotor response that presents with tachycardia, lightheadedness, etc **Late dumping** Late dumping occurs 1-3 hours after a meal, probably through development of hyperinsulinemic (reactive) hypoglycemia. Rapid delivery of a meal to the small intestine results in an initial high concentration of carbohydrates in the proximal small bowel and rapid absorption of glucose, hypoglycemia, and a hyperinsulinemic response. The high insulin levels stay for longer period and are responsible for the subsequent hypoglycemia. The following diagram summarizes the mechanism through which the dumping syndrome develops: (see photo) The clinical presentation of dumping syndrome can be categorized as abdominal versus vasomotor symptoms, and based on the time of onset as early versus late. Early dumping systemic symptoms: * Desire to lie down * Palpitations * Fatigue * Faintness * Syncope * Diaphoresis * Headache * Flushing Early dumping abdominal symptoms: * Epigastric fullness * Diarrhea * Nausea * Abdominal cramps * Borborygmi These symptoms can be collectively referred to as **dyspepsia**. Late dumping symptoms: * Perspiration * Shakiness * Difficulty to concentrate * Decreased consciousness * Hunger `For patients with dumping syndrome, dietary modification is the first-line management option. The following pieces of advice are appropriate:` * Daily energy intake is divided into 6 meals. * Fluid intake during and with meals be restricted and liquids be avoided for at least half an hour after a meal. * Avoiding simple sugars. * Milk and milk products are generally not tolerated and should be avoided. * Because carbohydrate intake is restricted, protein and fat intake should be increased to fulfill energy needs. Additional points to consider: Supplementation with dietary fiber has proven effective in the treatment of hypoglycemic episodes. Many medical therapies have been tested, including pectin, guar gum, and glucomannan. These dietary fibers form gels with carbohydrates, resulting in delayed glucose absorption and prolongation of bowel transit time. Dietary change to a low-carbohydrate, high protein diet, as well as the use of alpha-glucosidase inhibitors, may be useful to control the symptoms of dumping. This is preferential to subtotal or total pancreatectomy in those persons with severe symptoms. Most patients have relatively mild symptoms and respond well to dietary changes. In some patients with postprandial hypotension, lying supine for 30 minutes after meals may delay gastric emptying and also increase venous return, thereby minimizing the chances of syncope. | RACGP - AFP - The bariatric surgery patient

Answer 33

**B. Squamous cell carcinoma.** The epidemiology of esophageal carcinoma has markedly changed over the past several decades. **Worldwide**, squamous cell carcinoma is the most common type of esophageal malignancies. **Smoking and alcohol** are the most significant risk factors for this type of esophageal cancer. However, in `developed countries` such as United States of America, UK, and Australia, the incidence of `adenocarcinoma` of the distal esophagus and gastro-esophageal junction has progressively increased and accounts for over 70% of all cases of esophageal cancer. Gastroesophageal reflux disease (GERD) can result in `Barrett’s esophagus` which is the most significant risk factor for adenocarcinoma of the esophagus.

Answer 34

**D. Ruptured a hepatic adenoma.** The **age of the patient, the acute onset of the presentation and the history of OCP** use make a ruptured hepatic adenoma the most likely diagnosis. **Hepatocellular adenomas (HCAs)**, also known as hepatic adenomas or liver cell adenomas, are rare, **benign tumors of epithelial origin** and occur in less than 0.004% of the population at risk. HCAs occur mostly in **women of childbearing age** and are strongly associated with the use of oral contraceptive pills **(OCPs) and other estrogens**. This is reflected by a dramatic increase in the incidence of this disease since OCPs were introduced in the 1960s. The clinical presentation varies widely. Main features in history and physical examination may include the following: * Pain in the right upper quadrant or epigastric region in 25-50% of patients with HCAs * Lesions may be noticed by patients as a palpable mass. Lesions may also be discovered incidentally during an abdominal imaging study for an unrelated reason * History of birth control or anabolic steroid use should be checked in patients with suspected hepatocellular adenomas. * Patients may present with severe, acute abdominal pain with bleeding into the abdomen, which results in signs of shock such as hypotension, tachycardia, and diaphoresis * Hemoperitoneum occurs more frequently if the patient is taking a high-dose OCP, is actively menstruating or pregnant, or is within 6 weeks postpartum. Location of the lesion also is important, with those near the surface of the liver more prone to causing hemoperitoneum. Option A: A strangulated hernia is very unlikely to present with this clinical picture and an onset so acute. Option B: Mesenteric artery occlusion is usually seen in *elder patients* with *risk factors for thrombosis or embolus formation*. There is often a concomitant medical condition predisposing the patient to embolus formation such as atrial fibrillation. The condition presents with postprandial diarrhea, abdominal pain and abdominal exam findings that are usually disproportionate to the symptoms. Rectal bleeding may be found on digital rectal exam. Option C: Abdominal aortic aneurysm (AAA) is a disease seen in *older male patients*. Rupture of an AAA may present similarly; however, the age and gender of this patient make this diagnosis very unlikely. Option E: Acute appendicitis presents with vague *periumbilical pain that gradually localizes in the right lower quadrant*. Symptoms of peritonitis and shock develop later following rupture of the inflamed appendix. Acute appendicitis is a very unlikely explanation for this presentation.

Answer 35

**A. Surgical exploration.** The clinical picture is suggestive of a **femoral hernia** as the most likely diagnosis. Irreducibility and the fact the swelling is not altered by cough or straining suggests that the hernia has been **incarcerated**. Tenderness to palpation, if present, indicates **strangulation**. Femoral hernias account for 2-4% of groin hernias, are more common in women, and are more likely to present with strangulation requiring emergency surgery. An incarcerated hernia needs watchful monitoring for signs of strangulation while semi- elective surgery is arranged. Where clinical picture suggests **strangulation, emergency surgical intervention should be performed without delay.** For most hernias (as in this case), the location will be obvious on physical examination. **Femoral hernias most commonly present inferior to the inguinal ligament and medial to the femoral artery. They present with a swelling below and lateral to the pubic tubercle, in contrast to inguinal hernias that present as a swelling medial to the pubic tubercle.** Most of the time, the diagnosis is evident by physical exam; however, in situations when the physical exam is uncertain, such as in obese patients, additional imaging studies are recommended. This is particularly important owing to the fact that femoral hernias are approached differently from inguinal hernias. **While watchful waiting may be an option for asymptomatic or minimally symptomatic inguinal hernia, this is not recommended for femoral hernias due to the high risk of complications.** Option A: Ultrasonography is used when the diagnosis is uncertain clinically. CT scan is used if ultrasound results are equivocal and non-diagnostic. MRI has the highest accuracy but is not readily available and cost-effective. Option C: Femoral hernias have a high rate of incarceration and strangulation and it is unlikely that an incarcerated femoral hernia resolves with bowel rest. Option D and E: The diagnosis is certain in this case scenario. Fine needle or excisioanl biopsies are not necessary when hernia is suspected.

Answer 36

**A. Rectal examination.** In approach to every patient with **rectal bleeding**, a complete history should be taken and physical examination performed. **Inspection of the anus and a digital rectal exam must be carried out for every patient presenting with rectal bleeding as the most important initial step.** If available, **anoscopy or proctoscopy** is an appropriate means of inspecting the anorectal area, especially during active bleeding. Although often benign in nature, rectal or occult bleeding should always be attributed to more serious causes until proven otherwise by endoscopic testing. Flexible sigmoidoscopy in low-risk younger patients or colonoscopy in most other patients establishes the diagnosis of hemorrhoids, and excludes other causes of bleeding such as colitis, tumors, polyps, or vascular malformations. Option B: Occult blood testing in the presence if overt bleeding is not indicated. Option C and D: Imaging modalities such as CT scan or MRI are not routinely used for evaluation of rectal bleeding. Option E: Colonoscopy is considered if the source of bleeding is suspected to be more proximal. With colonoscopy the entire colon can be often visualized.

Answer 37

**C. Internal hemorrhoid.** **Fresh blood covering the stool** in the **background history of prolonged constipation** is most likely caused by internal hemorrhoid. Typical pattern of rectal bleeding in internal hemorrhoids is usually associated with a bowel movement. Bright-red blood typically coats the stool at the end of defecation. Blood may also drip into the toilet bowl or stain toilet paper. Hemorrhoidal bleeding is **almost always painless**, and **painful defecation prompts investigation for other causes such as anorectal fissures**. Although the pattern of rectal bleeding in this man is more likely to have been caused by hemorrhoids, overt or occult rectal bleeding should not be merely attributed to hemorrhoids until other less common b**ut more serious causes of rectal bleeding have been excluded by endoscopic testing**. **Flexible sigmoidoscopy or anoscopy in low-risk younger patients** or **colonoscopy in most other patients** establishes the diagnosis of hemorrhoids, and excludes other causes of bleeding such as colitis, tumors, polyps, or vascular malformations. Option A: Presence of rectal bleeding in this patient should also raise suspicion against colorectal cancer. However, this diagnosis is less likely because firstly, there are no other suggestive findings such as weight loss, altering bowel habits, etc. and secondly, hemorrhoids are more common than cancers statistically. Option B and E: External hemorrhoid and anal fissure are associated with *significant anal pain* and are very unlikely to be the diagnosis in this patient who has no pain on defecation. Option D: Anorectal fistulae are associated with *soiling* rather than rectal bleeding. It is unlikely that painless fresh rectal bleeding is the only presentation of anorectal fistulae. Addendum: Faecal soiling occurs when sticky faeces stays behind in the anorectal canal and gives a local reaction at the anodermal skin which results in itching, dermatitis and loss of small amounts of brown fluid.

Answer 38

**A. Digital rectal exam (DRE).** **Rectal bleeding** is often caused by benign conditions such as hemorrhoids or anal fissures. However, it is possible that this assumption masks serious and more proximal pathologies such as colorectal cancer. To avoid missing patients with sinister conditions, either as the cause of bleeding or a concomitant problem, all such patients should be assessed even if based on the history the etiology is clear. Approach to patients with rectal bleeding starts with a thorough history followed by physical exam. The physical examination should be directed at identifying possible or definite sources of bleeding and at finding worrisome distal lesions that may be detectable on examination. A detailed physical examination must include** external inspection of the anus and a digital rectal exam as initial investigations**. Having the patient bear down during the examination may induce prolapse of a hemorrhoid or bleeding of a superficial lesion. Moreover, when available, office-based anoscopy or proctoscopy (option B) should be performed in patients who present with acute rectal bleeding. These are simple measures not requiring bowel preparation. Sigmoidoscopy (option C and D) or colonoscopy (option E) is indicated in patients in whom initial assessment suggests *more proximal lesions* as the cause.

Answer 39

**C. Diet counselling.** The presentation and the **history of gastric bypass surgery** make dumping syndrome the most likely diagnosis. **Dumping syndrome is the effect of altered gastric reservoir function, abnormal gastric motor function, and/or pyloric emptying mechanism.** In terms of temporal relation to eating, dumping syndrome can have early or late manifestations: **Early dumping** Symptoms of early dumping syndrome occur 30-60 minutes after a meal, and are hypothesized to result from accelerated gastric emptying of hyperosmolar contents into the small bowel. The hyperosmolarity of the bowel content leads to fluid shift from the intravascular compartment into the bowel lumen, resulting in rapid small bowel distention and increase in the frequency of bowel contractions. With rapid shift of fluid into the intestinal lumen, circulating volume contraction follows, triggering a vasomotor response that presents with tachycardia, lightheadedness, etc **Late dumping** Late dumping occurs 1-3 hours after a meal, probably through development of hyperinsulinemic (reactive) hypoglycemia. Rapid delivery of a meal to the small intestine results in an initial high concentration of carbohydrates in the proximal small bowel and rapid absorption of glucose, hypoglycemia, and a hyperinsulinemic response. The high insulin levels stay for longer period and are responsible for the subsequent hypoglycemia. The following diagram summarizes the mechanism through which the dumping syndrome develops: (see photo) The clinical presentation of dumping syndrome can be categorized as abdominal versus vasomotor symptoms, and based on the time of onset as early versus late. Early dumping systemic symptoms: * Desire to lie down * Palpitations * Fatigue * Faintness * Syncope * Diaphoresis * Headache * Flushing Early dumping abdominal symptoms: * Epigastric fullness * Diarrhea * Nausea * Abdominal cramps * Borborygmi These symptoms can be collectively referred to as dyspepsia. Late dumping symptoms: * Perspiration * Shakiness * Difficulty to concentrate * Decreased consciousness * Hunger `For patients with dumping syndrome, dietary modification is the first-line management option. The following pieces of advice are appropriate:` * Daily energy intake is divided into 6 meals. * Fluid intake during and with meals be restricted and liquids be avoided for at least half an hour after a meal. * Avoiding simple sugars. * Milk and milk products are generally not tolerated and should be avoided. * Because carbohydrate intake is restricted, protein and fat intake should be increased to fulfill energy needs. Additional points to consider: Supplementation with dietary fiber has proven effective in the treatment of hypoglycemic episodes. Many medical therapies have been tested, including pectin, guar gum, and glucomannan. These dietary fibers form gels with carbohydrates, resulting in delayed glucose absorption and prolongation of bowel transit time. Dietary change to a low-carbohydrate, high protein diet, as well as the use of alpha-glucosidase inhibitors, may be useful to control the symptoms of dumping. This is preferential to subtotal or total pancreatectomy in those persons with severe symptoms. **Most patients have relatively mild symptoms and respond well to dietary changes. In some patients with postprandial hypotension, lying supine for 30 minutes after meals may delay gastric emptying and also increase venous return, thereby minimizing the chances of syncope.**

Answer 40

**C. Erect and supine x-ray films of the abdomen.** The lump can be a segment of a small bowel loop entrapped in the inguinal region, namely **inguinal hernia**. Absent cough impulse is a pointer towards **incarceration of the hernia**. There are two points in the question. The first and most important one is the presence of constipation and abdominal distention consistent with **bowel obstruction**. The second point is the presence of an **inguinal lump** with no cough impulse, no pain, and no tenderness. The history and physical findings make `small bowel obstruction (SBO)` the most likely diagnosis and the first condition to exclude. The initial imaging of choice in assessment of suspected bowel obstruction is **plain X-rays films**. At least two views are required: **upright view and supine view**. Plain abdominal films can confirm the diagnosis in most patients without the need for further diagnostic testing, but they can be equivocal in 20-30% of patients, or normal or misleading in 10-20%. `Abdominal X-rays are always the first imaging step in diagnosis.` Currently the best and `most accurate diagnostic test` for SBO is abdominal `CT scan` (option D) with both intravenous and oral contrast. CT scan can simultaneously provide information about the presence, level, severity and cause of obstruction. In addition, other abdominal pathologies can be detected. In some cases, closed-loop or strangulating obstruction may be revealed. CT scanning has been replaced with barium follow-through, which previously was the gold-standard diagnostic test for SBO. Follow-through series are now reserved for cases in which CT is not diagnostic. The question, however, asks about the initial investigation not the most accurate one. Abdominal ultrasound scan (option B) is sometimes used for assessment of bowel obstruction, and is the only modality with the ability to assess the bowel pristaltism. However, plain X-rays remain the standard initial investigation. This lump is very likely to be an incarcerated inguinal hernia which justifies both the lump and the obstruction. However, other differential diagnoses such as an inguinal lymph node should be considered as well once SBO, as the most likely cause, is excluded. In that case, ultrasound of the lump (option A) and biopsy (option E) if the lump turns out to be a lymph node, are indicated.

Answer 41

**A. Resistance to clarithromycin.** Triple therapy with clarithromycin, amoxicillin and a proton pump inhibitor (PPI) for 7-14 days is the regimen of choice for treatment of H.pylori infection with over 90% response. Clarithromycin is the most effective antibiotic against H.pylori. The most common cause of treatment failure with this regimen is the **increasing rates of resistance of H.pylori to clarithromycin**. This resistance cannot be overcome by dose increase or lengthening the duration of therapy. `NOTE - In those with penicillin hypersensitivity, in whom amoxicillin cannot be used, metronidazole can replace amoxicillin. So the regimen would be a combination of metronidazole, clarithromycin and a PPI. In such cases, resistance to either metronidazole or clarithromycin, or even both, can be the cause of treatment failure.`

Answer 42

**C. Gastroesophageal disease (GERD).** Option A: Correct- There is strong evidence that H. pylori contributes to the development of gastric cancer. Option B: Correct- H. pylori infection can also lead to the development of mucosa-associated-lymphoid-tissue (MALT) lymphoma, a type of cancer of the stomach. Treatment and eradication of H. pylori infection can result in regression of this malignancy in up to 75% of cases. Option C: Incorrect- To date, there has been NO study suggesting a strong link between H.pylori and GERD. Eradication of H.pylori has NOT shown effective in treatment of GERD. Option D: Correct- Chronic H.pylori-induced inflammation can eventually lead to loss of normal gastric mucosal architecture, with destruction of gastric glands and replacement by fibrosis and intestinal-type epithelium. This process of atrophic gastritis and intestinal metaplasia occurs in approximately 50% of the H.pylori-colonized population. Option E: Correct- Helicobacter pylori (H.pylori) has been strongly linked to the development of gastric and duodenal ulcers. Eradication of H. pylori can prevent ulcers forming. Indeed patients presenting with ulcers should be tested for H. pylori and treated because eradication of H. pylori in patients with pre-existing ulcers cures ulcer disease and can prevent most recurrences.

Answer 43

**C. Adenocarcinoma.** The epidemiology of esophageal carcinoma has markedly changed over the past several decades. Previously, squamous cell carcinoma was the most common type of esophageal malignancies worldwide (90-95% of cases); however, over the past 4 decades and in **developed countries such as United States of America, UK, and Australia**, the incidence of **adenocarcinoma** of the distal esophagus and gastro-esophageal junction has progressively increased. Currently, adenocarcinomas account for more than 70% of all cases of esophageal cancers in Australia. **Barrett’s esophagus caused by gastroesophageal reflux disease (GERD)** is the most significant **risk factor** for development of esophageal carcinoma of adenocarcinoma type. `NOTE - Squamous cell carcinoma remains the leading type of esophageal carcinoma worldwide with smoking and chronic alcohol as the most significant risk factors.`

Answer 44

**D. He should reduce weight.** Advice regarding **lifestyle modification** has been historically a part of management plan, **in conjunction to antacid therapy**, for **gastroesophageal reflux disease (GERD)**. Mild cases will respond to simple measures (e.g., bed head elevation), while most will need proton pump inhibitors (PPIs) as the cornerstone of the treatment. `Lifestyle modifications that are often advised include:` * Weight reduction * Bed head elevation during sleep * Avoiding spicy foods * Last meal not later than 2-3 hours before bed time * Avoiding or reducing alcohol and caffeine intake * Quitting smoking Of these, however, only **elevation of the head of the bed and weight reduction** seems to have an effect more than placebo. While widely encouraged, other measures appear to be associated with improved overall health with no specific effect on GERD, at least not in all patients. | Gastro-oesophageal reflux disease

Answer 45

**C. Colon capsule endoscopy(CCE).** **In the elderly, gastrointestinal bleeding** should be attributed to **colorectal malignancies until proven otherwise**. In such patients, **the whole length of the colon should be thoroughly investigated with colonoscopy** as the most appropriate diagnostic modality. An incomplete colonoscopy examination may occur in up to 5-10% of cases due to patient discomfort, a colon with many twists, postoperative adhesions, or hernia. In such cases, either a **CT colonography (CTC)** or `colonic capsule endoscopy (CCE)` may be performed. The latter, based on recent studies, is associated with `higher diagnostic value`. Option A: Forcing the colonoscope is likely to cause damages such as mucosal tear or even perforation. Option B: Tagged red cells are used in cases of acute lower gastrointestinal bleeding when colonoscopy cannot spot the bleeding site. it is not useful for tumor detection. Option D: Compared to first-generation capsules, CTC was superior to CCE, but `with the advent of newer capsules, diagnostic value of CCE has surpassed that of CTC`. Option E: Double contrast barium enema was traditionally used in cases of incomplete colonoscopy, but retrospective studies demonstrated that this method could miss more malignant lesions than CTC and CCE; hence, these procedures have superseded double contrast barium enema.

Answer 46

**D. Painful swallowing.** **Achalasia** is a primary esophageal motility disorder characterized by the **absence of esophageal peristalsis and impaired relaxation of the lower esophageal sphincter (LES) in response to swallowing**. The LES is hypertensive in about 50% of patients. These abnormalities cause a `functional obstruction` at the gastroesophageal junction. Option A and B: **Dysphagia for solids (91%) and liquids (85%) are the primary clinical feature of achalasia**. Although dysphagia for liquids can occur in patients with other esophageal motility disorders (e.g., progressive systemic sclerosis), this symptom is most characteristic of achalasia and strongly suggests the diagnosis. **Regurgitation of food** (option C) is another important feature of achalasia. It can be **worse at night (nocturnal regurgitation)** (option E) when the patient is recumbent. Patients can find undigested food particles on their pillow in the morning. Regurgitation is a problem in 40-60% of patients with achalasia. **Weight loss in the range of 5-10 kg is common** (40-60%). Profound weight loss can also occur. **Difficulty belching** is another important symptom that is seen in 85% of patients. **Chest pain and heart burn** can also be present. Painful swallowing (odynophagia) is not a feature of achalasia and, if present, another diagnosis must be thought of.

Answer 47

**C. She can go to school now.** The `incubation period of hepatitis A is 15 to 50 days`, but more commonly 28 to 30 days. The usual **clinical presentation is acute fever, malaise, anorexia, nausea and abdominal discomfort (prodromal symptoms), followed by dark urine and jaundice a few days later**. Symptoms usually last several weeks. The likelihood that symptoms will follow infection increases with age: jaundice occurs in only a small proportion of infants and young children, but a majority of adults. Infants and children infected with HAV may have mild or no symptoms. The viral load in the stool (and infectivity) is highest just before the onset of jaundice. Patients are considered **infectious from a few days before onset of prodromal symptoms to a few days after onset of jaundice**, and `non-infectious one week after onset of jaundice (if it occurs) or two weeks (14 days) after onset of prodromal symptoms, whichever comes first`. Kim has had jaundice 8 days ago and she does not seem to be infectious anymore because more than 7 days has past since jaundice. She can go back to school now. **Serum IgM anti-HAV is the gold standard for diagnosis**. The antibody becomes positive at the onset of symptoms, peaks during the acute or early convalescent phase, and remains positive for approximately 4 to 6 months. Liver function tests may also remain deranged beyond the infections period. Liver function tests or HAV antibodies are not appropriate indicators for infectivity. `NOTE - exclusion of contacts is not necessary.`

Answer 48

**E. Post-cholecystectomy syndrome.** The **dyspepsia manifested by bloating and belching after cholecystectomy** is suggestive of post-cholecystectomy syndrome (PCS) as the most likely diagnosis. PCS affects between 10-15% of patients with cholecystectomy and is characterized by a heterogenous group of symptoms including: * Upper abdominal pain * Nausea and vomiting * Diarrhea * Jaundice * Bloating * Excessive gas * Dyspepsia. These symptoms can be the continuation of symptoms thought to be caused by gallbladder pathology, the development of new symptoms normally attributed to the gallbladder, or symptoms caused by removal of the gallbladder. In 90% of the time an etiology can be found. The most common etiologies are: * Choledocholithiasis – stones remained or formed in the common bile duct or cystic duct remnant * Biliary dyskinesia * Continuously increased bile flow to the GI tract * Dilation of cystic duct remnant `NOTE - choledocholithiasis is the most common cause of PCS. It can involve the common bile duct of the cystic duct remnant. Choledocholithiasis is classified as retained, if found within 2 years of cholecystectomy or recurrent, if the stone is found 2 years after the surgery. Recurrent stones formed as result of the biliary stasis are often caused by strictures, papillary stenosis, and biliary dyskinesia.` `NOTE - ultrasonography is the initial imaging study of choice for patients with suspected PCS.` PCS is a **provisional diagnosis** and the presentation should be renamed after a specific cause as an explanation for the symptoms is clinched. Option A: The presentation is quite different from acute pancreatitis due to chronicity of symptoms and lack of the typical presentation. Chronic pancreatitis can cause dyspepsia but other features suggestive of the diagnosis are absent. Chronic pancreatitis presents with abdominal pain that can radiate to the back, chronic diarrhea due fat malabsorption and other signs and symptoms caused by pancreatic insufficiency. Option B: Cystic duct stump syndrome or cystic duct remnant syndrome refers to gastrointestinal symptoms of bloating, dyspepsia, nausea, etc caused by dilation of the remnant cystic duct. It is among the etiologies for PCS. The patient is likely to have PCS either due to this condition or other causes. Unless further studies establish the exact etiology, it cannot be said that cystic duct stump syndrome is the most likely cause to this presentation. Option C: Retained stones can also be an etiology for PCS and the presentation; however an intra-operative cholangiogram has been clear, making this condition less likely, yet not impossible. Option D: A clear cholangiogram makes this option correct but again this is not an etiology.

Answer 49

**C. Esophageal varices.** Dysphagia means difficulty in swallowing and can be classified as **three types**: **Oropharyngeal dysphagia** – difficulty in passing liquids more than solids due to neurologic or muscular problems such as: * Parkinsonism * Myasthenia gravis – the upper one-third of the esophagus has striated muscle. If myasthenia gravis affects this part, dysphagia ensues. * Prolonged intubation * Zenker’s diverticulum **Esophageal dysphagia** – difficulty in passing solids more than liquids due to local obstruction in the following conditions: * Strictures * Schatzki ring * Webs * Carcinoma. **Motility-related dysphagia** – difficulty in passing both solids and liquids at the same time, seen in conditions such as: * Achalasia * Scleroderma At occasions, there is odynophagia that is painful swallowing. In fact, in **odynophagia the difficulty in swallowing is caused by the pain, not by structural abnormalities**. Monilial (candida) esophagitis and pill esophagitis are two examples of conditions leading to odynophagia. Of the given options, the only condition which is not associated with dysphagia (or odynophagia) is esophageal varices.

Answer 50

**B. Gallstones.** Most RUQ pains in adults are usually due to biliary or hepatic diseases. Biliary causes of the RUQ pain include: * Gallstones * Acute cholecystitis * Acute cholangitis * Dysfunction of the Sphincter of Oddi Hepatic etiologies include: * Hepatitis * Perihepatitis * Liver abscess * Budd-Chiari syndrome * Portal vein thrombosis **Gallstones are very common among different populations**. They could be **asymptomatic and incidentally found** during evaluation for another reason, or cause problems such as biliary colic, cholecystitis, choledocholithiasis, and cholangitis. Of the options, gallstones are the most common ultrasonographic findings in patients with RUQ pain. Thickened gallbladder wall and extravasation is the diagnostic finding seen in patients with RUQ with cholecystitis. Gallstones, either as the cause, or as an incidental finding may be noted. Pericholecystic edema can be noticed as well. Bile duct dilation can be seen in patients with RUQ caused by bile duct obstruction.

Answer 51

**D. Chronic pancreatitis.** Epigastric pain can have a myriad of etiologies. Cardiac ischemia, peptic ulcer disease, hepatobiliary diseases, pancreatitis, and lower lobe pneumonia can all cause epigastric pain. Of the options, however, chronic pancreatitis is the most likely diagnosis. Chronic pancreatitis presents with **epigastric pain that typically radiates to back**. The pain **may or may not be triggered by eating** and **lasts for several hours**. **Serum amylase and lipase are often normal, or just slightly elevated**. Characteristic finding on imaging is calcification of the pancreas. Ultrasound shows **calcifications** in only 60 to 70% of patients. 30 to 40% of patients may have **normal ultrasound** scan results. Option A: Duodenal ulcer presents with epigastric pain. It can radiate to back. Laboratory findings and ultrasound scan are inconclusive; however, it is worse with hunger and relieved by eating. Option B: Esophagitis presents with dysphagia (difficulty swallowing) and/or odynophagia (pain on swallowing). Laboratory tests and ultrasound exam findings are unremarkable; however, it is uncommon for the pain to radiate to back. Retrosternal chest pain and heart burn are other features associated with esophagitis. Option C: A normal ECG makes acute coronary syndrome (ACS) less likely. On the other hand, chronicity of the pain and the episodic nature excludes ACS with high certainty. Option E: Cholecystitis can presents with pain often *aggravated by eating, especially eating fatty foods*. The pain can be felt in the right upper quadrant or epigastrium. *The pain can radiate to the tip of right shoulder*. Furthermore, *fever* is a common feature. *Alkaline phosphates and gamma glutamyl transpeptidase (GGT) are often elevated*. Lipase and amylase are normal or only slightly elevated. It is unlikely that sonography misses the diagnosis. | Chronic Pancreatitis

Answer 52

**D. Surveillance colonoscopy in 3 years.** Although adenomatous polyps (adenomas) of the colon and rectum are **benign growths** arising from the colonic and rectal mucosa, there is a **risk of progression to carcinoma in-situ and eventually to invasive colorectal cancer**, therefore, **surveillance is required**. The nature and interval of such surveillance depends on the size, number, and histopathological examination of the polyps (adenomas). As per current National Guidelines by the National Health and Medical Research Council (NHMRC), any colorectal polyps observed during colonoscopy should be resected and sent for histopathological exam, and surveillance program is considered. Current Australian guidelines recommend the following surveillance program for colorectal polyps: **Group A (low risk) – any patient with the following falls into this group:** * one to 2 adenomas; AND * all < 10mm; AND * no villous features; AND * no high-grade dysplasia For group A surveillance includes colonoscopy at 5-year intervals, or fecal occult blood test (FOBT) every 1-2 years. **Group B (high risk) – any patient with any of the following falls into this group:** * three to 4 adenomas; OR * any adenoma ≥10mm; OR * villous features; OR * high-grade dysplasia For group B surveillance includes `colonoscopy at 3-year intervals`. **Group C (multiple) – this group includes patients with ≥5 adenomas.** For group C, surveillance includes colonoscopy at 1-year intervals if the number of adenomas is 5-9 and sooner if ≥10. **Group D (possible incomplete or piecemeal excision of large or sessile adenomas)** Surveillance in this group consists of colonoscopy at 3- to 6-months intervals until no residual adenoma is detected after that time surveillance continues at 1-year intervals. ----- For Robert, either the number of adenomas (3) or the high-grade dysplasia histopathology of the adenoma resected from the transverse colon puts him in **group B (high-risk)**; therefore, **colonoscopic surveillance at 3-year intervals** is the most appropriate investigation for him. Option A: CT colonography is a new safe and well tolerated tool for diagnosis of colonic polyps and masses and, when performed by experienced hands, is as accurate as traditional colonoscopy. However, cost and training issues are needed to be addressed before it is widely accepted beyond the current indications of incomplete colonoscopy or patients who are unfit to undergo optic colonoscopy. Option B and C: CT scan of the abdomen and pelvis is not an effective tool for surveillance of colorectal adenomas. It is used, however, in cases of colorectal cancer to assess the extent of the disease and staging. Rectal ultrasound is not an assessment tool for surveillance of colorectal adenomas. It is neither sensitive nor specific. Option E: Serum tumor markers such as AFP and CEA are used if the diagnosis is invasive carcinoma. Such markers are used for assessment of the tumor burden as well as monitoring for any post-treatment recurrence.

Answer 53

**A. CT scan of the abdomen.** This patient is very likely to have bowel obstruction, and with the 2-month history of constipation and radiological finding of a sudden cut-off of the sigmoid and dilated proximal colon, **sigmoid volvulus** is the most likely diagnosis. Once colonic volvulus is suspected based on the history and physical findings and **the patient is stable**, confirmatory imaging should follow for confirmation of the diagnosis and prompt action should follow to reduce the risk of complications (if not already developed). **The initial imaging to consider is a plain abdominal x-ray.** Abdominal x-rays reveal a distended loop of colon that may resemble a **coffee bean or a dilated U-shaped colon with a cut-off point at the site of obstruction**. Plain abdominal x-rays may also show distention of the small bowel with air-fluid levels and decompressed colon distal to the point of volvulus. Further diagnostic modalities to consider for more accurate diagnosis and determination of the exact anatomical site of obstruction are contrast-enhanced CT scan and water-soluble contrast enema. Currently, `contrast-enhanced abdominal CT scan is the preferred confirmatory diagnostic tool for both cecal and sigmoid volvulus` because it is noninvasive, almost readily available, accurate for both cecal and sigmoid volvulus, and has the advantage of identification of incidental pathology that may be missed with plain radiographs or contrast studies. `In addition, abdominal CT may facilitate the diagnosis of colonic ischemia` (A is correct). Option B: Barium, as a contrast matter, is contraindicated if bowel perforation is suspected. Although this patient does not have signs of bowel perforation or even ischemia, barium should be avoided. Should enema be considered as a diagnostic tool, a *water-soluble contrast* is the option. `NOTE - Avoid barium if viscus perforation is suspected or if the goal is to assess the post-operative leak.` Option C: Rigid or flexible sigmoidoscopy is the most appropriate initial treatment option for patients in whom bowel perforation or ischemia has been excluded with high certainty. After endoscopic detorsion, a rectal tube is left in place for 1 to 3 days to maintain reduction. Colonoscopy is only used in unusual cases in which the obstruction point is beyond the reach of shorter scopes. Definitive treatment is with surgery. Option D: Ultrasound scan is not an appropriate diagnostic tool for suspected colonic volvulus. It has no benefit over plain radiograph for this purpose. Option E: Barium meal and follow through is an investigation to consider for suspected small bowel obstruction.

Answer 54

**A. Sigmoid volvulus.** The history of prolonged constipation, as well as the exam findings of a tympanic distended abdomen, colicky abdominal pain and an empty rectum is more consistent with sigmoid volvulus as the most likely diagnosis. A colonic volvulus occurs when a part of the colon twists around its mesentery and causes colonic obstruction. Such obstruction can be acute, subacute or chronic. Although volvulus can occur in any portion of the large bowel, the sigmoid colon is the most frequently affected part, followed by volvulus of the right colon and terminal ileum, namely cecal or cecocolic volvulus. In very rare cases, volvulus may develop in the transverse colon or the splenic flexure. Patients with colonic volvulus are commonly elderly, debilitated, and bedridden. A history of dementia or neuropsychiatric impairment is often present. The symptoms are acute in more than 60-70% of patients, while the rest present with subacute or chronic symptoms. A history of chronic constipation is common. The patient may describe previous episodes of abdominal pain, distention, and obstipation, which suggest repeated subclinical episodes of volvulus. Regardless of its anatomic site, colonic volvulus presents the same way with cramping abdominal pain, distention, constipation and/or obstipation. Abdominal distention often increases progressively. The distention is characteristically tympanic over the gas-filled, thin-walled colon loop. Tenderness or rebound tenderness indicates that peritonitis has occurred or is imminent. With progressive obstruction, nausea and vomiting occur. The development of constant abdominal pain is an ominous sign indicating the development of a closed-loop obstruction with significant intraluminal pressure. This leads to the development of ischemic gangrene and bowel wall perforation. Depending on the extent of bowel ischemia or fecal peritonitis, signs of systemic toxicity may be present. Because of the massive abdominal distention, the patient may have respiratory and cardiovascular compromise. Plain abdominal films are the initial imaging choice. Massive dilation of the sigmoid colon loop arising from the pelvis and extending to the diaphragm is a typical finding of sigmoid volvulus. The walls of the loop are evident as three bright lines converging in the pelvis to create a beak-like appearance. Option B: A sigmoid tumor can also be the underlying cause of this clinical picture. Left-sided colon cancer can present with bloody stool, changes in bowel habits and abdominal pain specially if the tumor has caused partial or complete obstruction. However, a sigmoid tumor large enough to cause complete obstruction of the colon to result in obstipation is expected to have more pronounced exam findings. Option C: Obstruction caused by the entrapment of a loop of the small bowel in an adhesion band formed from previous surgery can cause small bowel obstruction. In fact, adhesions from previous abdominal surgeries are the most common cause of small bowel obstruction. In this patient, however, the clinical picture more favors large bowel rather than small bowel obstruction because in small bowel obstruction nausea and vomiting are prominent features occuring earlier in the course of the process. This patient has not vomited until after 24 hours of symptoms onset. The clinical presentation of small bowel obstruction includes the following: * Nausea/vomiting (60-80%): The vomitus can often be bilious in nature * Constipation/absence of flatus (80-90%): Typically, a later finding of SBO * Abdominal distention (60%) * Fever and tachycardia: Late findings and may be associated with strangulation Option D: An obstructed hernia is expected to cause **constant** abdominal pain and tenderness. In early stages and before the strangulation occurs, there is no tenderness. This patient has a mass suggestive of hernia. However, the mass is **reducible** indicating that the hernia is not yet incarcerated or strangulated. A reducible hernia does not cause obstruction. Even in case of incarceration, it is the small bowel that becomes entrapped; therefore, symptoms would be expected to be in favor of small bowel obstruction. This patient has the clinical presentation of a large bowel obstruction. Option E: As the name implies, this kind of obstruction is caused by impaction of fecal matter often in the rectum. An empty rectum excludes this diagnosis.

Answer 55

**B. Diarrhea, bloody stool and abdominal pain.** Bloody stool (rectal bleeding), bowel habit changes mostly in form of diarrhea or altered stool caliber, and abdominal pain are the most common presenting symptoms in order of incidence in rectal cancer. **Rectal cancers** present with a variety of sign and symptoms including the following: * **Rectal bleeding** – bleeding is the most common presenting symptom of rectal cancer, occurring in 60% of patients. It should be noted, however, that profuse bleeding and anemia are rare. Occult bleeding detected through a fecal occult blood test (FOBT) is present in 26% of all cases. * **Changes in bowel habits** – this is the second most common presenting symptom, occurring in 43% of patients. Bowel habit changes is often in form of **diarrhea rather than constipation**. Some patients report a decrease in stool caliber. Large tumors can cause obstruction and obstructive symptoms. Tumors located low in the rectum can cause a feeling of incomplete evacuation and tenesmus. * Back pain is usually a late sign caused by a tumor invading or compressing nerve trunks. * Urinary symptoms may also occur if the tumor is invading or compressing the bladder or prostate. * Malaise is a nonspecific symptom and present in 9% of rectal cancer cases. * Bowel obstruction due to a high-grade rectal lesion is rare, occurring in 9% of all cases. * Pelvic pain is a late symptom, usually indicating nerve trunk involvement, and is present in 5% of all cases. * Other manifestations include emergencies such as peritonitis from perforation (3%) or jaundice, which may occur with liver metastases (< 1%). Option A: Melena is the black stool caused by oxidation of blood in the GI. Melena is a feature in upper gastrointestinal rather than lower gastrointestinal bleeding, and not a presenting symptom in rectal cancers. Although a change in bowel habit is the second most presenting symptom of rectal cancers, this change is more often in form of diarrhea rather than constipation. Lower abdominal pain due to partial or complete obstruction can be a feature. Option C: As mentioned earlier, diarrhea is more common than constipation in rectal cancers. Option D: External hemorrhoids (a thrombosed anal vein) is not a common presenting complaint in patients with rectal cancer. Option E: Fatigue is feature more commonly seen in *right-sided colon cancers*. As the blood mixes with the stool, bloody stool is a less frequently encountered presentation. On the other hand, bleeding from right-sided lesions result in diarrhea (blood is cathartic) and anemia. The latter is the main cause of fatigue in patients with right-sided malignant lesions. Fatigue or malaise is seen in only 9% of patients with rectal cancer.

Answer 56

**A. Sexual intercourse.** **Hepatitis B virus is a blood-borne virus**, meaning that the virus should enter the blood stream in order to cause infection. Modes of transmission include: * sharing contaminated objects that pierce the skin or mucous membranes, such as needles, tattoo equipment, body-piercing equipment, acupuncture equipment, razor blades and toothbrushes * sexual contact (heterosexual or homosexual, more common with homosexual contact) * perinatal transmission from an infected mother to her infant (vertical transmission) * needlestick injuries * contact between infective fluid and mucous membranes, such as a splash of blood into eyes or mouth * invasive medical or dental procedures if there has been inadequate infection control * transfusion of infected blood or blood products * human bites and other direct contact with the blood or open spores of an infected person Of these routes, some are more common than the others in different parts of the world, depending on the regional prevalence of the chronic hepatitis B infection: * Low-prevalence areas: Such areas include the United States, Canada, Western Europe, **Australia**, and New Zealand. The prevalence of hepatitis B in such areas is ≤2% (0.1- 2%). Less than 12% HBV infected individuals live in these areas. **The most common route of transmission in these countries are sexual transmission and percutaneous transmission.** * Intermediate-prevalence areas: Sexual and percutaneous transmission and transmission during delivery are the major transmission routes in areas of intermediate prevalence (rate of 3-5%). These regions include Eastern and some areas of Northern Europe, Japan, some Mediterranean countries, Latin and South America, and Central Asia. * High-prevalence areas: Such areas include China, Southeast Asia, sub-Saharan Africa, Pacific Islands, Parts of Middle East and Amazon Basin. The prevalence in ≥8% (often 10-20%). Perinatal infection including vertical transmission from the mother to the infant is the predominant mode of transmission. Australia has a chronic hepatitis B prevalence of less than 0.5% and is among low-prevalence regions of the world. The most common mode of transmission of hepatitis B infection in Australia is h**eterosexual and homosexual sexual intercourse with the latter being associated with higher risk of transmission**. This is followed by percutaneous transmission such as in injecting drug use and non-sterile procedures such as piercing, tattooing, etc. Option B: In Australia, screening of blood and organ donors using serological, and subsequently nucleic acid amplification testing, has virtually eliminated the risk of transmission of hepatitis B through blood transfusion and organ transplants. Option C: Injecting drug use predominates other modes of transmission in newly infected individuals with hepatitis C in Australia. It is also an important mode of transmission in hepatitis B after sexual intercourse. Option D: Perinatal transmission including vertical transmission from the mother to the infant is the predominant route of transmission of hepatitis B infection in areas with high prevalence of HBV infection. In such areas the prevalence is ≥8% (generally 10-20%). These areas include China, Southeast Asia, Indonesia, sub-Saharan Africa, Pacific Islands, parts of the Middle East, and the Amazon Basin. Due to perinatal care and administration of hepatitis B vaccine within the 12 hours of birth, this route of transmission is not common in Australia. Option E: Breast feeding does not appear to be a significant route of transmission, neither are fecal-oral and vector-borne modes. `NOTE - Saliva may contain levels of virus that are likely to be infective only if inoculated directly into tissue (ocular or mucous membranes). The risk of transmission by inadvertent inoculation by other means, such as by toothbrush, razor etc., or through close personal contact in households in which one or more infected persons reside, is low but not negligible.`

Answer 57

**B. A trial of proton pump inhibitors.** **Primary eosinophilic esophagitis (EoE)** is an increasingly recognized medical condition characterized clinically by symptoms related to esophageal dysfunction, and histologically by eosinophilic inflammation in the esophagus. EoE is hypothesized to be an atopic inflammatory disease caused by an abnormal immune response to antigenic stimulation, mostly foods. Normally, eosinophils are normal component of mucosal infiltrates in all-length of the gastrointestinal tract except the esophagus. `Eosinophils in the esophageal mucosa are always pathologic.` Generally, the clinical symptoms of EoE are nonspecific, and the patients are in good physical condition resulting in a delayed diagnosis (years) in some cases. The presenting symptoms vary depending on the age of the onset: Children - children tend to present with nausea and vomiting, weight loss, anemia, and failure to thrive. In neonates and infants, refusal of food is the most common presenting symptom. Adults - the characteristic symptoms in adults include dysphagia for solid foods, retrosternal pain and food impaction. Some patients also present with gastroesophageal reflux disease (GERD) symptoms unresponsive to medical anti-reflux therapy. A subset of patients have been recognized to have a typical clinical presentation of EoE in the absence of GERD who show a clinicopathologic response to PPIs. This condition is currently referred to as PPI-responsive EoE. There is no Australian guidelines for diagnosis and management of EoE and current recommendation is based on the guidelines by the American College of Gastroenterology (ACG). According to the ACG, diagnostic criteria for EoE include all of the following: * Symptoms related to esophageal dysfunction. * ≥15 eosinophils/hpf on esophageal biopsy * **Persistence of eosinophilia after a proton pump inhibitor (PPI) trial ** * Secondary cause of esophageal eosinophilia excluded This patient has symptoms related to esophageal dysfunction (dysphagia and odynophagia) and established eosinophilia on histological studies. `In order for EoE to be the definite diagnosis, it is necessary that eosinophilia persists after an 8-week trial of a PPI.` **The rationale behind this trial is that GERD may mimic EoE, coexist with it, or contribute to it.** Conversely, EoE may contribute to GERD; therefore, the diagnosis of EoE is generally made after the symptoms persist after an 8-week course of proton pump inhibitors (PPIs) as the best initial step in management. PPIs may benefit patients with EoE either by reducing acid production in patients with co-existent GERD, or by other unknown anti-inflammatory mechanisms. The main three components of treatment in established EoE are (1) dietary advice and alteration, (2) pharmacotherapy, and (3) surgical intervention. For pharmacological intervention topical **swallowed steroids (e.g., fluticasone, budesonide) are considered the main treatment options, once the diagnosis of EoE is established either after failed PPI therapy or normal pH studies.** For patients unresponsive to the above measure, oral (systemic) predniso(lo)ne maybe indicated. Option A: The condition is not infectious and antifungal or antimicrobial agents have no role in treatment. Option C: Topical swallowed steroids (e.g., budesonide) are considered as the next step, once the diagnosis of EoE is established either after failed PPI therapy or normal pH studies. Option D: Systemic corticosteroids are a treatment option for patients unresponsive to PPIs or swallowed corticosteroids. Option E: Eradication of H.pylori have not shown efficacy in treatment of EoE. `TOPIC REVIEW` Causes of esophageal eosinophilia: * Eosinophilic esophagitis * GERD * PPI-responsive eosinophilic esophagitis * Achalasia * Crohn’s disease * Parasitic infections * Drug hypersensitivity * Connective tissue disease (e.g., scleroderma, dermatomyositis) * Celiac disease * Hypereosinophilic syndrome

Answer 58

**A. Hepatoma.** Approximately 90% of malignant liver tumors are metastases from other primary malignancies elsewhere. **Hepatoma, also known as hepatocellular carcinoma (HCC) is a primary liver tumor accounting for 10% of malignant liver lesions.** In metastatic liver disease, metastases are usually multiple rather than single; therefore, a **solitary malignant liver tumor is more likely to have caused by HCC** rather than metastasis.

Answer 59

**C. Abdominal CT scan.** Simple liver cysts are often congenital and hypothesized to develop from intrahepatic biliary ducts because they have a lining similar to biliary ducts. Simple cysts generally cause no symptoms but may produce dull right-upper-quadrant pain if large in size. Patients with symptomatic simple liver cysts may also report abdominal bloating and early satiety. Occasionally, a cyst is large enough to produce a palpable abdominal mass. Very rarely, jaundice caused by bile duct obstruction or rupture and acute torsion of a mobile cyst may occur. Patients with cyst torsion may present with an acute abdomen. When simple cysts rupture, patients may develop secondary infection, leading to a presentation similar to a hepatic abscess with abdominal pain, fever, and leukocytosis. `It is very important to differentiate a simple cyst from malignant hepatic lesion. One differential diagnosis to exclude is a liver tumor with central necrosis that is often misdiagnosed as simple hepatic cyst. Genuine intrahepatic neoplastic cysts are rare. If a cystic lesion is found on ultrasound, often contrast-enhanced CT scan must be considered to characterize the lesion.` Images are taken during the pre-contrast, arterial and portal venous phase. Option A: Reassuring a patient with a symptomatic cystic lesion is not appropriate unless further investigations are conducted the other causes of such presentation has been excluded. **Symptomatic hepatic cysts usually require treatment.** Option B: Percutaneous aspiration guided by ultrasonography or computed tomography (CT) is technically simple but has been abandoned because the recurrence rates are nearly 100%. Aspiration combined with sclerosis with alcohol or other agents has been successful in some patients but has high failure and recurrence rates. Successful sclerosis depends on complete decompression of the cyst and apposition of the cyst walls. This is not possible if the cyst wall is thickened or if the cyst is large. Percutaneous catheters should not be placed to drain simple cysts, because the cavity becomes contaminated, leading to the development of hepatic abscess. Unlike the typical pyogenic hepatic abscess, this problem is difficult to resolve with repeated catheter placements because of continued secretion from the cyst epithelium. Option D: Laparoscopic unroofing of the cyst by excising the portion of cyst wall that extends to the surface the liver is the **treatment of choice for symptomatic liver cysts**. This, however, should be considered once further investigations establishes the diagnosis of a simple cysts and excludes other differential diagnoses. `NOTE - No medical therapy has proved effective in reducing the size of simple hepatic cysts.` Option E: MRI has a limited role in evaluation of simple cysts and is often unnecessary.

Answer 60

**C. Serum copper and ceruloplasmin level.** Neuropsychiatric problems in a young patient in the presence of a family history of such presentation is suggestive of **Wilson disease**. Wilson disease is a rare (3 in 100000) inherited disease (autosomal recessive) which is caused by **accumulation of copper in the liver and central nervous system**. The genetic basis is a **mutation of a gene on chromosome 13** that codes for a copper transporting ATPase, ATP7B. Over 200 mutations have been identified so far. Total body copper content is 100-150mg with an average intake of 1-5mg/day. The dietary copper is absorbed in the proximal small bowel. Copper is incorporated into ceruloplasmin in the liver. **In Wilson disease copper absorption and transport in the liver are intact but incorporation into ceruloplasmin in the hepatocytes and biliary excretion is impaired.** This results in accumulation of copper in the liver and later on other organs (e.g. CNS). The most common presentations are with liver disease or neuropsychiatric disturbances. Asymptomatic patients are most often detected by family screening. The clinical hallmark of Wilson’s disease is the **corneal Kayser–Fleischer ring**, which is present in 95% of patients with neurologic symptoms and somewhat over half of those without neurologic symptoms. While most affected children present with hepatic involvement (hepatitis, cirrhosis, or fulminant liver failure) adults often present with neuropsychiatric manifestations as the presenting symptoms. Neuropsychiatric manifestations of Wilson disease include dysarthria, dysphagia, dyskinesias, purposeless stereotyped movements, dementia, Parkinsonism, micrographia, clumsiness. There can be also decreased memory, anger outbursts, labile emotions, decreased libido and personality changes. Other possible clinical feature are: * Coombs negative hemolytic anemia * Polyarthritis * Hypermobile joints * Grey skin * Abortions * Hypoparathyrodism **Diagnostic tests include serum copper (increased) and ceruloplasmin (decreased).** It should be noted, however, that ceruloplasmin is an acute phase reactant and may be increased in response to hepatic inflammation, pregnancy, estrogen use, or infection.) The urinary copper excretion rate in patients with Wilson disease is greater than 100 mcg/d (normal < 40mcq/day). Although the sensitivity and the specificity of this test are suboptimal for use as a screening test; it may be useful to confirm the diagnosis and to evaluate the response to chelation therapy. `NOTE - The criterion standard for diagnosis of Wilson disease is liver biopsy. Copper levels of more than 250mcq per each gram of dry weight of the liver in an asymptomatic patient establishes the diagnosis.` Chelation with D-penicillamine or trientine are mainstay of therapy. Patients should be on diets with decreased sources of dietary copper. CT scan of the head (option A) or preferably MRI of the head (option B) are used for the degree of brain involvement in Wilson disease. Option D: Lumbar puncture has no role in diagnosis of Wilson disease. Option E: Liver function tests are impaired in most patients with Wilson disease. These changes are, however, nonspecific and can be seen in a variety of other liver diseases; hence, not diagnostic.

Answer 61

**D. Mallory-Weiss tear.** Although peptic ulcer disease including duodenal ulcers (option A) and gastric ulcers (option C) is the most common cause of bloody vomiting, the fact that the bleeding has followed **frequent retching, makes Mallory-Weiss tear more likely as the diagnosis.** `NOTE - Without the retching in history, peptic ulcer disease would have been the most likely diagnosis.` Mallory-Weiss tear is a linear laceration at the gastroesophageal junction. This tear is hypothesized to occur either by a rapid increase in intragastric pressure and distention, which increases the forceful fluid ejection through the esophagus, or secondary to a significant change in transgastric pressure, which is a difference in pressure across the gastric wall due to negative intrathoracic pressure and positive intragastric pressure. Such change leads to distortion of the gastric cardia, resulting in a gastric or esophageal tear. Mallory-Weiss tears are the cause of hematemesis in 3-5% of cases in adults. The condition is frequently encountered in **binge alcohol drinkers, mostly due to repeated retching and/or vomiting; however, even one single episode of retching or vomiting can result in the tear.** Hematemesis is the presenting symptom in virtually all patients with Mallory-Weiss tears. The diagnosis is **not dependent on the amount** of hematemesis because it can vary from blood flecks or streaks of blood mixed with gastric contents or mucus to a significantly large amount of bright red bloody emesis. Melena is another presentation reported to occur in as many as 10% patients. Other possible symptoms include: Patients with severe vomiting can develop light-headedness or dizziness, or even syncope. These symptoms usually occur secondary to dehydration from the underlying cause of vomiting and are not secondary to blood loss from the Mallory-Weiss tear. Only in rare cases a Mallory-Weiss tear lead to anemia requiring transfusions. Abdominal pain and dyspepsia - As many as 40% of patients may experience epigastric pain or heartburn. These symptoms are often related to the underlying cause of vomiting and not specifically to the Mallory-Weiss tear. Option B: vomiting of a large amount of fresh blood is an unusual presentation for gastric cancer. Additionally, if the cancer was the cause, features such as weight loss as well as other cancer-associated symptoms would have been expected. Option E: Esophagitis can result in a frail mucosa that bleeds easily; however, symptoms related to such bleeding are expected to be iron deficiency anemia (in the long run) and melena (or occult blood in the stool) rather than copious bloody vomitus. | Mallory-Weiss Syndrome

Answer 62

**B. Metronidazole resistance.** The **most common cause of treatment failure against H.pylori infection** is antibiotic resistance. Antibiotics used in multiple drug regimens against H.pylori are clarithromycin, metronidazole, and amoxicillin. Of these three, resistance to `metronidazole and clarithromycin` are the **most common causes of treatment failure**. While resistance to metronidazole **can be overcome by increasing the dose of metronidazole and duration of therapy**, this method is not effective where clarithromycin resistance is the issue. Option A: H.pylori is still susceptible to amoxicillin and resistance to this antibiotic has not been reported as a cause of treatment failure. Option C: A breath urea test is often performed within 4-6 weeks of the commencement of therapy. This patient has presented 10 days after completion of a 14-day course of antibiotics (so 24 days after the commencement of treatment) and nearly about the time of the test. Option D and E: Patients' non-compliance or an unreliable test result with a standard kit are less likely explanations for this patient’s persisting symptoms.

Answer 63

**C. The examiner’s finger cannot get above the swelling.** In indirect inguinal hernia, the bowel enters the scrotum through the inguinal canal. The hernia is often felt as a **swelling filling the scrotum**. Since the swelling **originates from the abdomen and the inguinal area**, the examiner’s finger cannot get above the swelling and this the most important finding that distinguishes a swelling arising from within the scrotum such as a testicular tumor, an epididymal cyst, hydrocele, sebaceous cyst from a swelling originating from out of scrotum. (Options A and B) An indirect inguinal hernia **fills the entire scrotum** not just the anterior or posterior part of it. (Option D) Although a gas-filled loop of bowel in the scrotal sac, as a result of indirect inguinal hernia, can be transilluminable, transillumination is more likely to due to a hydrocele. Even so, what differentiates between these two is that the examiner’s finger cannot get above the swelling in indirect hernia. (Option E) A painful scrotum can be due to a variety of reasons such as epididymo-orchitis, incarcerated or strangulated indirect hernias, testicular torsion or trauma. Presence of pain in a patient with scrotal swelling is not diagnostic for an indirect inguinal hernia. ## Footnote * Medscape – Abdominal Hernias

Answer 64

**E. Achalasia.** This scenario is a very typical picture of achalasia. Achalasia is a primary esophageal motor disorder of unknown etiology characterized manometrically by insufficient relaxation of the lower esophageal sphincter (LES) and loss of esophageal peristalsis; radiographically by aperistalsis, esophageal dilation, with minimal LES opening, ‘bird-beak’ appearance on barium studies, poor emptying of barium; and endoscopically by dilated esophagus with retained saliva, liquid, and undigested food particles in the absence of mucosal stricturing or tumor. Achalasia occurs equally in both genders with prevalence that ranges up to 1 per 10,000 persons. The majority of cases are idiopathic, but the syndrome can be associated with malignancy (especially involving the gastroesophageal junction) and as a part of the spectrum of Chagas disease. Rarely, achalasia is genetically transmitted. In the early stages of the disease, dysphagia may be very subtle and misinterpreted as dyspepsia. The presence of heartburn due to food stasis can add to the diagnostic confusion. **As achalasia progresses, dysphagia to both solids and liquids develops but it is worse to solids. To ease the progression of the food bolus, patients may modify their eating habits including eating more slowly or arching the back (rolling back of the shoulders) or raising the arms when swallowing.** Substernal chest pain during meals in the setting of dysphagia, weight loss, and even heartburn may be accompanying symptoms that often lead to misdiagnosis of achalasia as gastroesophageal reflux disease (GERD). **Achalasia must be suspected in those with dysphagia to solids and liquids and in those with regurgitation unresponsive to initial trial of proton pump inhibitor (PPI) therapy.** `NOTE - Of the symptoms, regurgitation is often more bothersome and more likely as a presenting symptom.` (Options A) occasionally, achalasia may be a result of esophageal malignancy, especially at the gastroesophageal junction. However, esophageal cancer in a young patient with no known risk factors is far less likely than idiopathic achalasia. Moreover, with malignancy, a more rapid course of dysphagia and a more profound weight loss compared to benign causes of dysphagia are expected. (Option B) In esophageal stricture, dysphagia for solids occurs first, and dysphagia to liquids develop later as the stricture progressively narrows the esophageal lumen. (Option C) Scleroderma (systemic sclerosis) is a complex and heterogeneous disease with clinical forms ranging from limited skin involvement (limited cutaneous systemic sclerosis) to forms with diffuse skin sclerosis and severe and often progressive internal organ involvement (diffuse cutaneous systemic sclerosis). Skin involvement (including Raynaud’s phenomenon) is almost always present at the time of presentation and diagnosis. Esophageal involvement in scleroderma may mimic the symptoms of achalasia; however, in the absence of other features of scleroderma, it is a remote possibility for this patient. (Option D) Esophagitis (inflammation of the esophagus) is associated with pain on swallowing (odynophagia) rather than dysphagia. ## Footnote * UpToDate – Achalasia: Pathogenesis, clinical manifestations, and diagnosis * Gut and Liver – The Pathogenesis and Management of Achalasia: Current Status and Future Directions

Answer 65

**B. Abdominal CT scan** The scenario represents a case of **acute-onset abdominal pain with minimal abdominal exam findings** but the presence of a rapid irregular pulse suggestive of **atrial fibrillation**. This constellation of symptoms in a patient over the age of 50 years, especially if male, suggests **acute mesenteric ischemia** as a likely diagnosis. Acute mesenteric ischemia (AMI) is interruption of intestinal blood flow by embolism, thrombosis, or a low-flow state. It leads to mediator release, inflammation, and ultimately intestinal infarction, bowel perforation and peritonitis. The early hallmark of mesenteric ischemia is severe pain which is surprisingly out of proportion to abdominal physical findings. The abdomen is often soft, with mild or no tenderness at early stages. Later, as necrosis develops, signs of peritonitis appear, with marked abdominal tenderness, guarding, rigidity, and absent bowel sounds. The stool may become heme positive. The usual signs of shock develop eventually and frequently result is high mortality. Cited causes for AMI are arterial embolus, atherosclerosis, non-occlusive ischemia such as in heart failure, shock, etc. In some patients, no cause is identified. AF is infamous cause of arterial embolus and a classic risk factor for AMI. Early diagnosis of mesenteric ischemia is particularly important because mortality increases significantly once intestinal infarction sets in. **Mesenteric ischemia must be considered in any patient > 50 with known risk factors or predisposing conditions who develops sudden, severe abdominal pain (AF in this scenario).** Patients with clear peritoneal signs should proceed directly to the operating room for both diagnosis and treatment. For others, **selective mesenteric angiography or CT scan with angiography** is the **diagnostic procedure of choice**. Other imaging studies and serum markers can show abnormalities but lack sensitivity and specificity early in the course of the disease when diagnosis is most critical. CT scanning has also the added benefit of assessment of other abdominal pathologies. Plain abdominal films (option C) are useful mainly in ruling out other causes of pain (e.g., perforated viscus), although portal venous gas or pneumatosis intestinalis may be seen late in the disease. Doppler ultrasonography can sometimes identify arterial occlusion, but sensitivity is low. MRI is very accurate in proximal vascular occlusion, less so in distal vascular occlusion. Serum markers (e.g., creatine kinase, lactate) rise with necrosis but are nonspecific findings that are seen later. Abdominal ultrasound scan (option A) is the choice if conditions such as gallbladder disease or acute appendicitis suggested based on the presentation. While an electrocardiogram (ECG) (option D) should be in the initial workup of this patient to further assess the rapid irregular rhythm as well as cardiac ischemic pain as a possible cause of abdominal pain, it is not diagnostic for AMI. Colonoscopy (option E) is specifically valuable in assessment of intracolonic pathologies such as in gastrointestinal bleeding but is of little if any diagnostic value in this patient with suspected AMI. ## Footnote References * Medscape – Acute Mesenteric Ischemia * John Murthag General Practice - Abdominal Pain

Answer 66

**A. Physiotherapy** The photograph shows a midline swelling starting from the umbilicus extending to halfway between the umbilicus and the xiphoid process of the sternum. The appearance alongside the history and physical finding makes **abdominal recti diastasis (ARD)** the most likely diagnosis. Abdominal rectus diastasis is a condition where the abdominal muscles are separated by an abnormal distance due to widening of the linea alba, which causes the abdominal content to bulge. The rectus fascia is intact, and the condition should therefore not be confused with a ventral hernia. Rectus diastasis can be congenital but is most commonly acquired during pregnancies and/or larger weight gain causing **laxity of linea alba.** ARD presents with visible bulging on exertion or when the intrabdominal pressure is increased (Valsalva maneuvers, coughing, straining, etc.) DRA often develops around the umbilicus but can also occur anywhere between the xiphoid and the pubic bone. It is a common condition in pregnancy with an incidence as high as 66% in the third trimester. In 30–60% cases it persists post-partum. Not all patients with abdominal rectus diastasis are symptomatic. Symptoms, if present, include pain and discomfort in the abdomen, musculoskeletal problems like pelvic instability and lumbar back pain, and urogynecological symptoms such as urinary incontinence, fecal incontinence, and pelvic organ prolapse. In addition, patients with rectus diastasis also experience lower perception of body image, lower body satisfaction, and lower quality of life compared with the general population. Patients with symptoms should receive treatment. Although the efficacy has not been studied adequately, **treatment starts with physiotherapy** of abdominal wall muscles. If a course of months of physiotherapy fails to improve the condition surgical repair comes next. The procedure can be performed via classic abdominoplasty (option E) or endoscopic surgery and stabilization of the defect (option D). Hernioplasty and mesh insertion (option C) is used for hernias. ARD is not a true hernia. An abdominal (hernia) belt or truss (option B) is used to keep the content of a hernia inside the abdominal wall y application of pressure over the defect. They are used to relieve the symptoms of hernia, bridge the surgery, or provide additional support during recovery from the surgery. They are not used as a treatment modality of DRA. ## Footnote * Frontiers in surgery – Treatment Options for Abdominal Rectus Diastasis

Answer 67

**A. Incision under local anesthesia** The picture shows an erythematous raised area near the anus almost covering it. Such appearance, as well as the symptoms and clinical findings, is consistent with a **perianal abscess** as the most likely diagnosis. Physical examination in patients with perianal abscess demonstrates an **erythematous, well-defined, fluctuant, subcutaneous mass near the anal orifice**. Vital signs are often within the normal ranges. As a rule, abscesses have to be treated with **incision and drainage**. Simple perianal abscesses can be treated in the emergency department under local anesthesia followed by administration of systemic antibiotics. More complex perianal abscesses may need treatment in the operating room. (Options B, C and E) Hemorrhoids have a different clinical picture depending on their grade. **Bright rectal bleeding is the most common symptom in internal hemorrhoids**. Other manifestations include **pruritus, mucous discharge and anal pain and discomfort**. A thrombosed anal vein (formerly called external hemorrhoid) presents with a painful and tender bluish mass protruding out of the anus. This patient does not have hemorrhoid; therefore, any option suggesting treatment of hemorrhoids is incorrect. (Option D) Antibiotics alone are inadequate for treatment of a perianal abscess. Clinical suspicion of a perianal abscess warrants surgical incision and drainage. Delaying surgical intervention results in chronic tissue destruction, fibrosis, and stricture formation that may result in impaired anal continence. ## Footnote * Medscape - Anorectal Abscess

Answer 68

**C. Esophageal cancer** Dysphagia and hoarseness can be features seen in esophageal cancer, thyroid cancer or laryngeal cancer. In esophageal cancer, the tumor growth obstructs the esophagus. Dysphagia often occurs to solid foods first, followed by to liquids, as the lumen progressively becomes narrower. Dysphagia often becomes a symptom once the lumen diameter is less than 13 mm. In esophageal cancer, hoarseness occurs if the tumor invades the recurrent laryngeal nerve. This is an indicator of advanced disease and unresectability. A malignant thyroid tumor can also invade the recurrent laryngeal nerve, and cause hoarseness. Dysphagia can also occur due to impingement of the proximal esophagus. Laryngeal cancer, by invasion to structures within the larynx, causes hoarseness or aphonia. Once large enough in size, a laryngeal tumor can compress the proximal esophagus and cause dysphagia as a symptom. Of these three, and given the **history of achalasia as a risk factor** for esophageal cancer and the **presence of a mass in the thoracic inlet on CT scan**, **esophageal cancer** is the most likely diagnosis compared to thyroid and laryngeal cancers. Because a stricture from the previous surgery (option A) in esophagus can explain the dysphagia but not the hoarseness. (Option B) As a malignant thyroid tumor grows, it can compress the adjacent structures in the neck. It can also invade the laryngeal nerve and cause hoarseness. However, a thyroid cancer is most likely to present with a thyroid nodule. It is unusual for a thyroid tumor to be so large to compresses the esophagus but is missed on physical examination of the neck. (Option D) Although laryngeal cancer can cause hoarseness and, if large enough, dysphagia, a neck mass would be expected on imaging. This patient has a mass in the thoracic inlet. This makes laryngeal cancer almost unlikely. Furthermore, the presence of previous achalasia as a risk factor for esophageal squamous cell carcinoma makes esophageal cancer a more likely diagnosis. Important risk factors for laryngeal cancer are smoking and alcohol consumption. (Option E) An apical lung cancer can present with a mass in the thoracic inlet on imaging. A lung cancer can cause hoarseness but is unlikely to cause dysphagia. ***TOPIC REVIEW*** Common clinical manifestations of lung, laryngeal, esophageal, and thyroid cancers: 1. Lung cancer - Cough - Chest pain - Shortness of breath - Coughing up blood - Wheezing - Hoarseness - Recurring infections such as bronchitis and pneumonia - Weight loss and loss of appetite - Fatigue - Metastatic signs and symptoms may include the following: - Bone pain - Spinal cord impingement - Neurologic problems such as headache, weakness or numbness of limbs, dizziness, and seizures 2. Laryngeal cancer - Dysphonia/ aphonia - Dysphagia - Dyspnea - Aspiration - Blood-tinged sputum - Fatigue and weakness - Cachexia - Pain - Halitosis - Expectoration of tissue - Neck mass - Otalgi (ear pain) 3. Esophageal cancer: - Dysphagia (most common); initially for solids, eventually progressing to liquids - Weight loss (second most common) due to dysphagia and tumor-related anorexia. - Bleeding (leading to iron deficiency anemia) - Epigastric or retrosternal pain - Bone pain with metastatic disease - Hoarseness (due to the involvement of the recurrent laryngeal nerve) - Persistent cough or frequent pneumonia due to tracheobronchial fistulas caused by direct invasion of tumor through the esophageal wall and into the main stem bronchus 4. Thyroid cancer - A painless, palpable, solitary thyroid nodule (the most common presentation) - Hoarseness (suggests involvement of the recurrent laryngeal nerve and vocal fold paralysis) - Dysphagia (a sign of esophageal involvement) - Heat intolerance and palpitations (in autonomously functioning nodules) ## Footnote References * Medscape – Esophageal Cancer * Medscape – Thyroid Cancer * Medscape – Malignant Tumors of the Larynx * Medscape – Non-Small Cell Lung Cancer

Answer 69

**E. Familial polyposis coli.** Of the given options, Familial polyposis coli has the strongest association with colorectal cancer and is very significant risk factor for that. **Familial polyposis coli, also termed familial adenomatous polyposis (FAP)** is caused by **mutations in the APC gene** that a person inherits from his or her parents. About 1% of all colorectal cancers are caused by FAP. In the most common type of FAP, hundreds or thousands of polyps develop in a person’s colon and rectum, often starting at ages 10 to 12 years. Cancer usually develops in 1 or more of these polyps as early as age 20 years. **By age 40, almost all people with FAP will have colon cancer if their colon hasn’t been removed to prevent it.** People with FAP also have an increased risk for cancers of the stomach, small intestines, pancreas, liver, and some other organs. (Option A) Adenomatous polyp: About 70 % of all polyps are adenomatous, making it the most common type of colon polyp. When this type of polyp is found, it is tested for cancer. Only a small percentage actually become cancerous, but nearly all malignant polyps began as adenomatous. (Option B) Melanosis coli: is a condition that can be caused by chronic laxative abuse. Studies have not found an association between melanosis coli and an increased risk of colorectal cancer in humans. Or it may be that the factors that contributed to constipation itself, such as a diet that's too low in fiber, are the reason why this possible higher risk of cancer exists (Option C) Diverticulitis: the risk of colorectal cancer is increased in the short-term period after hospitalization related to diverticular disease. According to a recent systematic review and meta-analysis, the prevalence of colorectal cancer is 1.6% in patients with acute diverticulitis who underwent colonoscopy. (Option D) Ulcerative colitis: The risk of colorectal cancer for patients with ulcerative colitis is increased, and is estimated to be 2% after 10 years, 8% after 20 years and 18% after 30 years of disease ## Footnote * Cancer Council Australia – Familial Bowel Cancer

Answer 70

**C. Dysphagia for both solids and liquids** Achalasia is caused by lack of a relaxation of the lower esophageal sphincter and aperistalsis of the esophageal body. The condition is characterized by degeneration of the nerves innervating the esophagus of unknown cause. Symptoms of achalasia include the following: - Dysphagia – the most common symptom: like other motility disorders of the esophagus there is dysphagia for both liquids and solids at the same time. - Regurgitation – regurgitation of achalasia is worse at night when the patient is in lying position, but that of retropharyngeal pouch (Zenker’s diverticulum) occurs even when the patient is standing. - Chest pain - Heart burn - Weight loss – weight loss can occur with all types of dysphagia Of the symptoms, dysphagia to both liquids and solids is the cardinal and the most common symptom of achalasia. (Option A) Dysphagia for solids as the prominent feature is characteristic of conditions that cause a narrowing within the lumen such as a tumor. (Option B) Dysphagia for liquids as the cardinal symptom seen in oropharyngeal dysphagia such as in Zenker’s diverticulum, Parkinsonism, stroke and myasthenia gravis. (Option D) Regurgitation in recumbency is also a feature of achalasia but it is not as common as dysphagia (~40% vs. 80%). Regurgitation is also seen in other conditions such as retropharyngeal pouch and is not a feature specific to achalasia. (Option E) Weight loss can be a manifestation of all esophageal diseases. It is not an exclusive feature of achalasia.

Answer 71

**D. Intussusception.** The dark spots on the lips and buccal mucosa of this patient is highly suggestive of Peutz Jeghers syndrome. **Peutz Jeghers syndrome (PJS) is an autosomal dominant inherited condition characterized by freckling, gastrointestinal polyposis, and increased risk of certain cancers. ** Features seen in PJS are: 1. **Freckling** - Most people with PJS have flat deeply pigmented spots around and inside their mouth, on their lips, fingers and toes. Less commonly, these spots can be seen on hands and feet, in the mucosa of the nose, conjunctiva or rectum. Freckles are benign and develop early in childhood and may disappear into adulthood. 2. **Polyposis** - Patients with PJS will typically develop dozens to thousands of hamartomas, usually beginning in childhood. These polyps primarily develop in small bowel (jejunum, ileum and duodenum); however, they can also occur anywhere in the in the gastrointestinal (GI) tract. 3. **GI problems** - GI symptoms arise mostly from the complications of hamartomas. Bleeding can occur as a GI hamartoma rubs against intestinal lining. GI bleeding in PJS may preset as blood in stool either occult or overt, anemia, etc. Bloating and abdominal pain may be seen. One important well-known complication in GI polyps of PJS is **intussusception** (infolding of one part of the intestine into another) of the small bowel. Other - Very early puberty can occur and occasionally male patients develop gynecomastia. The disease is different in each patient meaning that not all patients show all of the features of the disease or any particular feature to the same extent as other patients `NOTE - PJS is associated with an increased risk of specific cancers such those of stomach, small intestine, colon, pancreas, breasts, ovaries, cervix or testes. Not everyone with PJS will develop cancer, but those affected are at an increased risk and with a younger age of onset than those in the general population.` This patient has the clinical picture of small bowel obstruction. Given the PJS in history, **small bowel intussusception** would be the most likely diagnosis. Small bowel obstruction presents with central colicky abdominal pain, early development of nausea and vomiting, mild to moderate abdominal distention, and constipation/ obstipation. As the condition deteriorates, bowel ischemia, necrosis, perforation, and peritonitis can develop. (Option A) Although people with PJS are at increased risk of GI cancers at younger ages, cecal cancer is a less likely diagnosis in this scenario. Cecal cancer presents with fatigue due to chronic blood loss rather than signs and symptoms of bowel obstruction. (Option B) Acute appendicitis can also present with periumbilical pain that gradually shifts and fixes in the right lower quadrant. Nausea and probably vomiting may follow the pain. The patient usually has anorexia and regional tenderness and often rebound in the right lower quadrant. However, bowel obstruction, as seen in this patient, is not a feature. (Option C) In sigmoid volvulus, the sigmoid colon twists around the mesenteric axis and causes bowel obstruction. Abdominal distention is a prominent feature as are other signs and symptoms of large bowel obstruction such as an empty rectum on DRE. Sigmoid volvulus is typically seen in elderly patients who are bed-ridden and have chronic constipation. The location of the pain, the age of the patient, and the quick start of the nausea and vomiting are against large bowel obstruction on this patient. Moreover, with Peutz Jeghers syndrome, intussusception of the small bowel and small bowel obstruction are stronger possibilities. (Option E) Bowel perforation presents with signs and symptoms of peritonitis such as abdominal tenderness and rebound tenderness, board-like rigidity, and guarding in an ill and toxic patient. ## Footnote * Cancer Council – Peutz-Jeghers syndrome * Medscape – Peutz Jeghers Syndrome

Answer 72

**D. Rectal schistosomiasis** Rectal cancer (option A) can cause altered bowel motions and bleeding. Anal fissures are not a feature of rectal cancer though. Given the patient is young and has anal fissure, rectal cancer is unlikely to be the predisposing factor to this presentation. Hemorrhoids (option B) present with painless rectal bleeding, and there is no pain on defecation. Although chronic constipation can be a predisposing factor for both hemorrhoids and anal fissure, hemorrhoids do not cause anal fissure. Perianal abscesses (option C) can present with painful or tender swellings around the anus. Although they might cause pain on defecation as the feces passes and compresses an abscess, they do not cause rectal bleeding or anal fissure. Perianal fistulae, however, can develop as a consequent of perianal abscess. High-fiber diet (option E) do not predispose to anal fissure. In fact such diet, by constipation prevention, is a management step in both hemorrhoids and anal fissures Given the fact that the patient is an immigrant from **Somali**, where **schistosomiasis is endemic**, rectal schistosomiasis is most likely to have predisposed to the anal fissure and such presentation. Schistosomiasis is either **intestinal or urogenital**, depending on where the adult flukes are located. In intestinal schistosomiasis, adult worms occupy mesenteric veins, and their eggs pass into the lumen of the intestine and reach the faeces. In the Eastern Mediterranean Region, Somalia and Sudan remain the most endemic countries. Gastrointestinal schistosomiasis due to S. mansoni, S. japonicum and S. mekongi can cause bowel lesions such as ulceration, pseudopolyps, and microabcesses. Gastrointestinal schistosomiasis clinically presents with abdominal pain, altered bowel habits, and blood in stool. Liver enlargement and periportal fibrosis are common in advanced cases, and is generally linked with ascites and portal hypertension. Other well-documented clinical signs include superficial abdominal blood vessel dilatation, spleen enlargement, and bleeding- prone esophageal varices. Patients with severe hepatosplenic schistosomiasis may die from ruptured esophageal varices. Some studies suggest an association of S. mansoni and S. japonica and cancer development in the liver and colon, but no hard evidence exists to support the association. Chronic schistosomiasis commonly affects the sigmoid colon and rectum and usually presents with abdominal pain, diarrhea, bleeding, or ulcerations. Given its location of infection, it can also lead to anal fistulas, fissures, or abscesses. ## Footnote * WHO – Schistosomiasis

Answer 73

**D. Ganciclovir** **Individuals with HIV infection** are at an increased risk for **esophagitis caused by cytomegalovirus (CMV)** as an AIDS-defining illness **when the CD4+ lymphocyte counts decline below 100 cells/µL.** Such as in any other type of esophagitis, CMV esophagitis presents with **odynophagia (pain on swallowing)** as the main symptom. The most constant endoscopic finding in CMV esophagitis is **mucosal ulceration**. The ulcers may be single or multiple, deep, or shallow, and could be several centimeters or more in diameter. The ulcers mostly affect the middle and distal parts of the esophagus. Histopathologic findings include: - **Basophilic inclusion bodies** in the nucleus and cytoplasm (intranuclear and intracytoplasmic inclusion bodies) - **Arrogates of macrophages** The **treatment of choice** for CMV esophagitis is **ganciclovir or valganciclovir**, usually in intravenous form. **Foscarnet** is used as an alternative if resistance occurs. Acyclovir (option E) is not potent enough for the treatment of CMV esophagitis. Combination therapy with IV ganciclovir and IV foscarnet is used when monotherapy fails; however, this regimen is associated with significant toxicity. Longer-term oral ganciclovir is considered for patients who require long-term suppressive treatment, and patients with HIV infection with CD4+ lymphocyte counts of less than 50 cells/µL. PPIs (option A) and H2-receptor antagonists (option B) (e.g., ranitidine) are used for reflux disease, peptic ulcer disease, or gastritis none of which is the case here. Swallowing inhaled corticosteroids (option C) is the treatment of choice, after a trial of PPIs, for eosinophilic esophagitis. The clinical picture does not fit eosinophilic esophagitis. ## Footnote Medscape - Cytomegalovirus Esophagitis NIH - Cytomegalovirus Esophagitis

Gastrointestinal System/Adomen/Abdomen Wall Flashcards

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