day 5 - Biliary tract & pancreas + UPPER GI

Question 1

Congenital abnormalities of the oesophagus

Answer 1

These include the absent or short oesophagus, tracheo-oesophageal fistulae, oesophageal atresia, diverticula and congenital stenosis.

Question 2

define Hiatus hernia

Answer 2

A hiatus hernia is defined as partial or total herniation of the stomach or gastro-oesophageal junction through the diaphragmatic hiatus into the thoracic cavity. It is common, particularly after 50 years of age. It may be asymptomatic or produce reflux oesophagitis.

Question 3

aetiology of hiatus hernia

Answer 3

Increased abdominal pressure, low residue diets, and laxity of the diaphragmatic
hiatus or peri-oesophageal attachments contribute to development of a hiatus hernia.

Question 4

pathology of hiatus hernia

Answer 4

There are two main types of hiatus hernia, which may coexist. The sliding hiatus
hernia is the more common. It occurs when the gastro-oesophageal junction +/- stomach are pulled up through the diaphragmatic hiatus. The para-oesophageal hiatus hernia represents only 5% of all gastric herniations and involves part of the stomach (usually the greater curve) sliding through the hiatus between the oesophagus and diaphragm, while the gastro- oesophageal junction remains secure. This type occurs four times more often in females than males. In extreme cases, the entire stomach herniates into the thoracic cavity producing an upside down stomach. Complications are similar to those of reflux oesophagitis.

Question 5

symptoms of Oesophagitis

Answer 5

Oesophageal inflammation occurs in 5% of the adult western population. There is usually retro-sternal burning (heartburn), which is often worse on leaning forward or drinking hot liquids. In severe cases there may be dysphagia, bleeding, haematemesis and melaena.

Question 6

Aetiology and Pathogenesis Oesophagitis

Answer 6

Oesophagitis is caused by damage to the oesophageal mucosa. It mainly results
from gastro-oesophageal reflux disease, but can rarely be due to infection (candida, herpes virus, CMV, bacteria), chemicals (NSAIDs, bleach), radiation therapy or Crohn’s disease.

Question 7

what is Gastro-oesophageal reflux disease (GORD)

Answer 7

A small amount of gastro-oesophageal reflux is a normal physiological phenomenon. It occurs when gastro-duodenal contents enter the lower oesophagus. A small proportion of people develop abnormal reflux, causing oesophagitis. Only some of these become symptomatic. Factors predisposing to GORD produce either increased abdominal pressure (pregnancy, obesity, trauma, vomiting), incompetence of the lower oesophageal sphincter (smoking, alcohol, hiatus hernia, systemic sclerosis) or reduced mucosal protection (NSAIDs). Investigation is by endoscopy and biopsy.

Question 8

histology of GORD

Answer 8

There is poor correlation between the severity of symptoms and histological findings.
On endoscopy the oesophagus may appear erythematous or normal. The three diagnostic histological features seen in biopsies are hyperplasia of the stratified squamous epithelium, congestion of the lamina propria and chronic inflammatory cells within the mucosa. The presence of neutrophils suggests ulceration. The most important complications are mucosal erosions, ulceration, lower oesophageal stricture, bleeding and Barrett’s oesophagus.

Question 9

Erosive and ulcerative oesophagitis

Answer 9

Erosive or ulcerative oesophagitis is usually clearly identifiable at endoscopy. The features are similar to those of erosions and ulcers found in the stomach.

Question 10

Benign stricture of the oesophagus

Answer 10

Recurrent or persistent ulceration leads to oesophageal fibrosis. Fibrosis can be focal or circumferential and may lead to stenosis and dysphagia. Symptoms may resolve with treatment of the underlying cause or may require surgical intervention.

Question 11

what happens in Barrett’s oesophagus (or columnar-lined oesophagus)

Answer 11

Barrett’s oesophagus is a complication of chronic oesophagitis. It is characterized by replacement of distal oesophageal stratified squamous epithelium by columnar epithelium of gastric or intestinal type (a process termed gastric, intestinal, columnar or glandular metaplasia). It occurs in 10% of patients with symptomatic GORD and up to 40% of peptic oesophageal strictures.
Morphology

Question 12

endoscopy and microscopy of Barrett’s oesophagus

Answer 12

At endoscopy, abnormal red mucosa lies as islands or as a circumferential band
between the normal white stratified squamous epithelium of the oesophagus and the normal gastric mucosa. Microscopically, Barrett’s oesophagus appears as a sudden transition from squamous epithelium to columnar gastric or intestinal-type epithelium, proximal to the gastro-oesophageal junction.

Question 13

complications of Barrett’s oesophagus

Answer 13

The significance of Barrett’s oesophagus lies in its association with a 30-40-fold
increase in the risk of developing adenocarcinoma of the oesophagus, and so patients with this undergo frequent endoscopic follow-up with repeated biopsy. The aim is to detect and treat dysplastic changes before they can progress to invasive cancer and to treat invasive disease as early as possible.

Question 14

Oesophageal neoplasms

Answer 14

Malignant oesophageal neoplasms represent 5% of cancers. Squamous carcinoma (SCC) and adenocarcinoma are the most common types. Worldwide, SCC makes up 90% of oesophageal carcinomas. There are geographical pockets of high incidence, particularly in China and Japan. In the western world, adenocarcinoma is nearly as common as SCC. They both present with dysphagia, weight loss and anaemia.

Question 15

epi of Squamous cell carcinoma of the oesophagus

Answer 15

Squamous cell carcinoma usually presents in the 5th decade and is more common in males. It is most importantly associated with diet (ingestion of nitrates from smoked and pickled food, smoking, alcohol, nutritional deficiency) and host factors (long-standing oesophagitis, achalasia, Plummer-Vinson syndrome).

Question 16

pathogenesis of Squamous cell carcinoma of the oesophagus

Answer 16

Many genetic abnormalities have been identified within SCC but their role in
tumorigenesis has not been well characterized. Lesions are thought to progress from epithelial dysplasia (abnormal epithelium), to carcinoma in-situ (intraepithelial neoplasia) to invasive carcinoma.

Question 17

morphology of Squamous cell carcinoma of the oesophagus

Answer 17

80% of squamous carcinoma affect the lower 2/3 of the oesophagus. Endoscopically, they appear as protruding (60%), flat (15%) or excavating (25%) lesions. Microscopically, oesophageal tumors can be divided into early and advanced lesions. Early lesions do not invade through the submucosa, whereas advanced lesions do. As with most tumors, SCC can be well differentiated (look like squamous cells with keratinization and intercellular bridges) or poorly differentiated. Local and distant spread occurs early to lymph nodes, mediastinum, liver and bone. Staging is by the TNM classification.

Question 18

pathogen of Adenocarcinoma of the oesophagus

Answer 18

Adenocarcinoma is becoming as common as SCC in western society, with a slight preponderance for men. It presents most commonly in the 5th decade. It is associated with smoking, alcohol and most importantly Barrett’s oesophagus.
Pathogenesis
The vast majority of adenocarcinomas arise in areas of Barrett’s oesophagus.
Mutations in the p53 gene and chromosome 17p allele loss are thought to be important in the tumorigenesis. They are often found in association with dysplastic epithelium but the progression from in-situ lesion to carcinoma is less well characterized than with SCC.

Question 19

morphology of Adenocarcinoma of the oesophagus

Answer 19

Most adenocarcinomas arise in the distal oesophagus appearing as flat, ulcerating,
infiltrative lesions. They may also be divided into early and advanced lesions. Microscopically, these show intestinal-type or, less commonly, gastric-type differentiation, often with mucus production.

Question 20

clinical course of Adenocarcinoma of the oesophagus

Answer 20

Most oesophageal carcinomas are advanced at the time of diagnosis, often
extending to surrounding structures. Only a minority are early lesions as diagnosis is usually delayed until the cancer is large enough to produce dysphagia or local complications. Survival at 5 years for early lesions is about 75% but overall only 5-10% survive 5 years.

Question 21

what is gastritis

Answer 21

Gastritis is an inflammatory condition of the stomach, caused by damage to the gastric mucosa. There are two distinct forms, acute and chronic gastritis. They are pathologically distinct and have different clinical connotations.

Question 22

characteristics of Acute gastritis

Answer 22

Acute gastritis is characterized by a transient acute inflammatory response to gastric mucosal damage. It is usually superficial and self-limiting, producing only epigastric burning, nausea and sometimes vomiting. In severe cases there is mucosal erosion, ulceration, haemorrhage or acute necrotizing gastritis, with a history of severe pain, haematemesis (vomiting blood), melaena (tarry faeces stained black by blood that is partially digested by gastric secretions) or shock.

Question 23

Aetiology and Pathogenesis of acute gastritis

Answer 23

Acute gastritis is mainly caused by chemicals (alcohol, smoking, NSAIDs,
chemotherapy, bile reflux), stress (being in hospital, trauma, burns) and infections (Herpes simplex virus, CMV). Inflammation is promoted either by compromising mucosal defences against gastric secretions by decreasing gastric blood flow and disrupting the protective gastric mucus layer, or by direct epithelial damage.

Question 24

morphology of acute gastritis

Answer 24

In most cases, the mucosa looks normal or slightly erythematous. The microscopic
features of acute gastritis are oedema, vascular congestion and acute inflammatory cells (neutrophil polymorphs) in the mucosa. There may also be erosions, ulceration and haemorrhage. The presence of both erosions and haemorrhage is termed acute erosive gastritis.

Question 25

what is chronic gastritis

Answer 25

Chronic gastritis is characterized by chronic inflammation of the gastric mucosa, mucosal atrophy and epithelial metaplasia, usually without erosions. In the absence of complications, chronic gastritis usually produces few symptoms, but there may be episodic pain, nausea or vomiting. Complications include anaemia, peptic ulcer disease and gastric carcinoma.

Question 26

Aetiology and Pathogenesis chronic gastritis

Answer 26

There are distinct aetiological subgroups: Autoimmune gastritis, Bacterial gastritis (H
pylori), Chemical gastritis and miscellaneous (Crohn’s disease, radiation therapy).

Question 27

Autoimmune gastritis

Answer 27

Autoimmune gastritis accounts for less than 10% of chronic gastritis. It is characterized by autoantibodies to gastric parietal cells (90%) or intrinsic factor (60%). There is immune- mediated destruction of gastric glands, chronic inflammation and mucosal atrophy. In 10% of patients, lack of intrinsic factor and reduced gastric acid production reduces absorption of dietary vitamin B12 resulting in pernicious anaemia. Autoimmune gastritis is associated with other autoimmune disorders such as Hashimoto’s thyroiditis and Addison’s disease.

Question 28

Bacterial gastritis (Helicobacter pylori gastritis)

Answer 28

Helicobacter pylori accounts for up to 90% of chronic antral gastritis. It is associated with an increased risk of peptic ulcer disease and possibly gastric cancer. H pylori is a Gram- negative rod that has adapted to living in the stomach. It does not invade the mucosa, but adheres to the surface epithelium and survives the harsh environment by using the enzyme urease to degrade urea into ammonia, which buffers local gastric acid. The mechanism by which H pylori stimulates and maintains a chronic mucosal inflammatory response is not fully understood.

Question 29

Morphology of chronic gastritis

Answer 29

Autoimmune gastritis mostly affects the gastric body/fundus. H pylori gastritis mainly
affects the antrum, but may also affect the body/fundus. Initially, the mucosa appears hyperaemic, coarse and boggy, but in long-standing atrophic disease, the mucosa is flattened and thin.

The four main microscopic features are relatively constant. There are inflammatory aggregates composed of lymphocytes and plasma cells within the lamina propria, intestinal metaplasia, glandular atrophy and neutrophils within the glandular epithelium. If H pylori organisms are present, they are found in the superficial mucus layer. They do not colonize areas of intestinal metaplasia and so are absent from Barrett’s oesophagus and duodenal or pyloric metaplasia.

Long standing gastritis leads to epithelial atypia and dysplasia which may account for the increased risk of cancer. These changes are particularly associated with atrophic gastritis and pernicious anaemia.

Question 30

what are Erosions and ulcers

Answer 30

Erosions and ulcers are pathological defects in epithelial surfaces that result from acute or chronic mucosal damage. They can occur anywhere in the gastrointestinal tract but are most common in the stomach and duodenum.

Erosions are superficial mucosal defects which do not breach the muscularis mucosae. They are commonly associated with acute gastritis but may occur in chronic gastritis. Macroscopically they appear as small, flat, hyperaemic patches. Histologically, there is epithelial disruption associated with an acute inflammatory response in the lamina propria. Healing is usually swift once the stimulus is removed.

Ulcers are more severe mucosal defects, which extend through the muscularis mucosae into the submucosa or deeper. Acute ulceration is associated with NSAIDs, severe physiological stress [shock, sepsis, burns (Curling’s ulcer)] or chemical poisoning. 5- 10% of ITU admissions develop acute ulceration. Acute ulcers tend to be multiple, small (<1cm) and surrounded by mucosa which is initially normal but progressively becomes inflamed and haemorrhagic. There is no scarring and healing may be seen in days to weeks. The microscopic features of acute ulcers are mucosal excavation with superficial fibrinoid necrosis, acute inflammation within the mucosa and active granulation tissue. Chronic ulceration occurs on a background of sustained mucosal injury. Most chronic ulcers are peptic ulcers.

Question 31

what is peptic ulcer disease

Answer 31

The lifetime risk of developing a peptic ulcer is 10% for men and 5% for women. Duodenal ulcers are 3 times more common in men and gastric ulcers are slightly more common in women. Peptic ulcers often have a relapsing and remitting course. Symptoms vary widely and do not correlate well with endoscopic or pathological findings. There is epigastric pain, nausea and often vomiting. Pain is often worse at night and 1-3 hours after food (duodenal ulcers), or immediately after food (gastric ulcers), and relieved with antacids. In severe cases there may be a history of haematemesis or melaena. There may also be weight loss and anaemia. In acute perforation there may be signs of peritonism and shock.

Question 32

Aetiology and Pathogenesis of peptic ulcer disease

Answer 32

The role of H. Pylori in PUD cannot be over-emphasized. Colonization is present in
100% of duodenal PUD and 75% of gastric PUD. Other causes include NSAIDs, smoking, alcohol, hypercalcaemia and Zollinger-Ellison syndrome. Peptic ulceration is thought to result from an imbalance between mucosal defences and the harmful effects of pepsin and acid. Hyperacidity is not a prerequisite but the action of pepsin is potentiated by acid. The effects of multiple aetiological factors are additive.

Question 33

morphology of peptic ulcer disease

Answer 33

98% of PU’s are in the duodenum (75%) or the stomach (25%), most of which are on the lesser curve. 10-20% of patients with a gastric ulcer also have a duodenal ulcer. They are also found in the gastro-oesophageal junction, gastrojejunostomy sites, the jejunum (Zollinger-Ellison Syndrome) and a Meckel’s diverticulum.

Macroscopically peptic ulcers have a diagnostic appearance. They are solitary and less than 4 cm in diameter. They are round, punched-out mucosal defects with vertical walls. Heaping up of the edge is more characteristic of carcinoma. The base may reveal muscularis mucosae, vessels or omentum in the case of perforation. Scarring may produce a puckered mucosa, which radiates from the central ulcer. There is usually background chronic gastritis. Chronic gastritis is not usually present with acute erosive gastritis or stress ulcers.

The microscopic appearance of ulcers varies from active necrosis to chronic ulceration to that of healing. Active ulceration has four elements: superficial fibrinoid necrosis with mucosal excavation, mixed inflammatory cell infiltrate within the lamina propria, active granulation tissue and underlying fibrosis.

Question 34

complications of peptic ulcer disease

Answer 34

PUD tends to cause recurrent morbidity rather than mortality. The most important
complication are bleeding 15-20% (25% of ulcer deaths), perforation 5% (66% of ulcer deaths), obstruction 2%, anaemia, intractable pain and malignancy (increased risk of malignancy probably results from underlying gastritis or malignant lesion previously thought to be a benign ulcer).

Question 35

epidem of gastric neoplasms

Answer 35

90% of gastric malignancies are adenocarcinomas. The rest include lymphomas (4%), carcinoids (3%) and sarcomas (2%). In western society, the incidence is 8/100,000 for men and 4/100,000 for women and they represent 2.5% of cancer deaths. The incidence is 5 times greater in Japan and China. There is a typically insidious onset of non-specific changes such as weight loss, pain, anorexia, vomiting, altered bowel habit, anaemia and occasionally haemorrhage.

Question 36

Aetiology and Pathogenesis of gastric neoplasms

Answer 36

The most important aetiological factors are environmental. Dietary nitrites, derived
from smoked, salted and pickled foods, and lack of fruit and vegetables, are associated with increased risk. Smoking increases the risk by 1.5-3 times. Host factors are the second major contributor. H. pylori infection is associated with gastric carcinoma but causality has not been proved. Chronic gastritis/autoimmune atrophic gastritis increases risk by 2-4 times.

Question 37

Morphology of gastric neoplasms

Answer 37

Gastric carcinoma affects the pylorus/antrum 50%, cardia 25%, body 25%, and
favours the lesser curve of the stomach. Macroscopically, carcinoma may be exophytic (nodular), flat (difficult to identify clinically or radiographically) or excavating (mimic PUD but tend to have a heaped up edge and necrotic centre). Carcinomas that infiltrate the wall of the stomach, creating a rigid tube, are known as linitis plastica.
Microscopically, in-situ lesions are confined to the epithelium, early lesions are confined to the submucosa and advanced lesions extend into the muscular wall. There are two main histological subtypes (Lauren classification). Intestinal-type tumors resemble colonic adenocarcinoma; they grow with a cohesive front and often form glandular epithelium with mucin vacuoles. Diffuse-type tumors resemble cells of gastric mucosa, infiltrate as clusters and single cells, and do not form glands. Signet ring cells are commonly seen.

Question 38

Clinical Course of gastric neoplasms

Answer 38

Prognosis is heavily influenced by the depth of invasion. The 5 year survival for early
lesions (10-15% of new diagnoses) is 90% and for advanced lesions is 15%. Average survival at 5 years after diagnosis is 20%. Carcinomas characteristically invade the duodenum, pancreas and retroperitoneum. Sometimes there is spread to the supraclavicular lymph nodes (Virchow’s node).

Question 39

what is Cholelithiasis

Answer 39

Gallstones!

Cholelithiasis is caused by the accretion of bile constituents and mucus into solid stones within the biliary tract. Gallstones are found in up to 20 % of western adults, and are twice as common in women as in men. Incidence increases with age, with >50% prevalence over 80 years of age.
Only 10-20% of cases are symptomatic and symptoms depend on the location of the stone. There is usually RUQ pain, which may be severe and is often spasmodic due to rhythmic contraction of the gallbladder against an impacted stone (biliary colic). Stones in the common bile duct may result in cholestasis, jaundice (conjugated hyperbilirubinaemia) and pancreatitis. Attacks may be characteristically provoked 30mins after eating bacon sandwiches.

Question 40

Pathogenesis of Cholelithiasis

Answer 40

There are two main types of stones, cholesterol (80%) and pigment (20%). They are
formed as a consequence of bile supersaturation, gallbladder hypomobility, and mucus hypersecretion. Cholesterol stones contain 50-100% cholesterol monohydrate and small amounts of calcium salts +/- bilirubin. They are associated with obesity, rapid weight loss, high oestrogen states (OCP, pregnancy), family history, congenital errors of metabolism and clofibrate treatment. Pigment stones contain a mixture of insoluble calcium salts of unconjugated bilirubin and inorganic molecules. They are more common in haemolysis, severe ileal dysfunction and bacterial contamination of the biliary tract.

Question 41

Morphology of Cholelithiasis

Answer 41

Cholesterol stones are usually multiple with a smooth, yellow surface. Some have a
lamellar cut surface, and 15% contain sufficient calcium carbonate to be radio-opaque. Pigment stones are usually numerous with a black, facetted surface and 50-75% are radio- opaque.

Question 42

Complications of Cholelithiasis

Answer 42

Cholecystitis is the most common complication, and the most common indication for
emergency cholecystectomy. Other complications include empyema, perforation, fistulae, cholangitis, cholestasis, pancreatitis, and increased risk of carcinoma of the gallbladder.

Question 43

what is Cholecystitis

Answer 43

Inflammation of the gallbladder can be acute, chronic or acute on chronic. It is almost always associated with gallstones (calculous cholecystitis) but not always (acalculous cholecystitis).

Question 44

what is Acute cholecystitis

Answer 44

Acute cholecystitis is an acute inflammatory condition of the gall bladder, precipitated in 90% of cases by gallstone obstruction of the neck of the gallbladder or the cystic duct. Acute acalculous cholecystitis occurs in the severely ill patient, post major (non-biliary) surgery, trauma, burns, organ failure, sepsis and postpartum.

Question 45

Pathogenesis of acute cholecystitis

Answer 45

The balance between mucosal defences and the effects of bile salts is lost. The
mucosa is exposed to the detergent action of bile salts and an inflammatory response ensues. Initially there is no infection, but this may subsequently supervene. In calculous cholecystitis, stone impaction causes bile stasis, which raises intraluminal pressure and produces gallbladder distension. Distension of the gallbladder reduced blood flow to the mucosa and compromises mucosal defenses. Acalculous cholecystitis results mainly from ischaemic mucosal damage.

Question 46

Morphology of acute cholecystitis

Answer 46

The gallbladder is enlarged, tense and mottled. The wall is thickened, oedematous and hyperaemic, or green/black in gangrenous cholecystitis. There are usually gallstones and sometimes pus or mucosal perforation. Microscopically there is non-specific acute inflammation, oedema, vascular congestion and neutrophils possibly with abscess formation and necrosis.

Question 47

Clinical Course of acute cholecystitis

Answer 47

Symptoms may be mild and transient or present as a surgical emergency. There is
RUQ pain, fever, nausea and vomiting. Jaundice is uncommon but raised bilirubin suggests common bile duct obstruction. There may be high WCC and cholestatic liver enzymes. Untreated, spontaneous resolution occurs in 1-10 days, but recurrence is common. 25% of patients progressively worsen, requiring surgery. Acalculous cholecystitis tends to be more insidious and obscured by the primary illness. Failure to diagnose it may give a fatal outcome. Onset may be indolent in outpatients with chronic gallbladder ischaemia.

Question 48

what happens in Chronic cholecystitis

Answer 48

Chronic cholecystitis is often asymptomatic, but may result from recurrent, symptomatic bouts of acute cholecystitis. 90% of cases are associated with gallstones. Diagnosis is important in order to prevent complications.
The serosa is often dulled by fibrosis and the wall is thickened, opaque and stiff. The mucosa is generally preserved with variable subepithelial chronic inflammation and fibrosis. There may be diverticula, with epithelium protruding through the muscular layer of the gallbladder wall (Rokitansky-Aschoff sinuses).

Question 49

Complications of Chronic cholecystitis

Answer 49

Complications
It is important to treat early and avoid complications which include cholangitis, sepsis,
perforation with abscess formation, peritonitis, cholecystenteric fistula with the risk of gallstone ileus, bacterial infection and bile drainage to adjacent organs. Cholecystitis may also precipitate decompensation in patients with pre-existing renal, hepatic, cardiac or pulmonary disease.

Question 50

what is pancreatitis

Answer 50

Pancreatitis is an inflammatory condition of the pancreas caused by enzymatic auto- digestion of pancreatic tissue. It is classified into acute, chronic and obstructive forms. Obstructive pancreatitis is caused by obstruction of the pancreatic duct. The features are those of acute and chronic pancreatitis.

Question 51

aetiology of Acute pancreatitis

Answer 51

Acute pancreatitis occurs in 10-20 per 100,000 in western society. Most episodes are mild and self-limiting, but 1/5 cases are severe and may progress to shock, organ failure and death. Patients initially present with rapid onset of upper abdominal pain, nausea, vomiting, tachycardia, a high WCC and raised plasma pancreatic enzyme levels (three-fold at least) within 24 hours. Mild episodes resolve with supportive treatment and minimal organ dysfunction. Severe episodes are associated with considerable pancreatic necrosis (a CT with contrast is the investigation of choice), clinical organ failure and death.

Aetiology
Biliary disease and chronic alcoholism together cause 70% of cases. 20% of cases
are of undetermined cause and the rest are caused by ERCP, trauma, hyperlipidaemia, hypercalcaemia, drugs, infections, and ischaemia.

Question 52

pathogenesis of acute pancreatitis

Answer 52

Acute pancreatitis results from auto-digestion of the pancreas. Damaged acinar cells release pro-enzymes into the interstitium where they are then activated. The mechanisms behind acinar cell injury and enzyme activation are unclear but may include direct acinar cell damage (trauma, infection, alcohol), oxidative stress or acinar cell ischaemia (similar mechanism to cholecystitis with retention of pancreatic secretion, inflammation, oedema and vascular compromise). There is then a combination of acute inflammation with microvascular leakage and oedema, fat necrosis, proteolysis, vascular destruction and haemorrhage.

Question 53

pancreas changes in acute pancreatitis

Answer 53

Mild (interstitial) pancreatitis is limited to interstitial oedema and focal fat necrosis.
The pancreas is swollen and there are superficial white plaques of fat necrosis (fatty acids combined with calcium). Severe (necrotizing) pancreatitis affects acini, ducts and islets and may result in widespread necrosis and haemorrhage. Macroscopically, there are black areas of haemorrhage in yellow-white, chalky fat necrosis. The peritoneum usually contains brown, serous fluid, globules of fat and chalky deposits.

Initial microscopic changes are limited to interstitial oedema and peri-pancreatic fat necrosis. With more severe pancreatitis, necrosis extends further into the substance of the pancreas. There is destruction of acini and blood vessels with haemorrhage and a septal acute inflammatory cell reaction. If there is resolution, it may be complete or associated with focal fibrosis.

Question 54

Clinical Course and Complications of acute pancreatitis

Answer 54

In most cases there is no residual pancreatic dysfunction. Pancreatic abscess,
pancreatic pseudocysts and duodenal obstruction may result from local damage. Systemic complications include multi-organ failure, DIC, ARDS and death. Mortality from severe acute pancreatitis is 30%. Early deaths are from organ failure and late deaths are from infection. 5% die from shock within the first week of presentation.

Question 55

Aetiology and Pathogenesis of chronic pancreatitis

Answer 55

Chronic pancreatitis is defined as sustained inflammation of the pancreas associated with irreversible morphological changes and loss of function. It presents with abdominal pain, maldigestion and diabetes mellitus or occasionally jaundice. It occurs in about 10 per 100,000 of western populations and presents in the 5th decade of life.

Most cases are associated with chronic alcoholism, hypercalcaemia,
hyperlipidaemia, cystic fibrosis, biliary disease and genetic factors as in rare autosomal dominant hereditary pancreatitis, which predisposes to pancreatic carcinoma. 40% of cases have an unknown cause. It is thought that duct plugging by abnormal secretions or repeated bouts of inflammation with fibrosis promote gland distortion making further pancreatitis more likely (necrosis-fibrosis cycle), especially if the stimulus remains, such as alcohol.

Question 56

morphological changes to the pancreas in chronic pancreatitis

Answer 56

Initially, the pancreas is enlarged with septal fibrosis and intra-pancreatic fat
necrosis. More advanced disease produces a shrunken, firm pancreas with extensive fibrosis, calcification and variable dilatation of pancreatic ducts. Pseudocysts are common. The three cardinal microscopic features of chronic pancreatitis are fibrosis, loss of exocrine glands and chronic inflammation (lymphocytes, plasma cells and monocytes).

Question 57

Complications in chronic pancreatitis

Answer 57

About 70% of patients develop local complications such as biliary, duodenal or
colonic obstruction; pseudocysts; haemorrhage; ascites or gastric varices. Secondary diabetes due to islet damage and malabsorption due to acinar damage are also common. There is also an increased risk of pancreatic carcinoma, which probably relates to alcohol and smoking.

Question 58

what is a pseudocyst

Answer 58

A pseudocyst is a localized collection of pancreatic secretions that develops after pancreatic inflammation or trauma. It is to be distinguished from a sterile pancreatic abscess, which is filled with liquefactive necrosis of the pancreas. Both lack the epithelial lining of a true cyst. They both commonly produce abdominal pain and may be mistaken for a malignancy. Complications include haemorrhage and infection with peritonitis.
Morphology
They are usually solitary lesions up to 10cm in diameter, either within or adjacent to
the pancreas. Pancreatic secretions, which have drained from damaged ducts, are walled off by fibrotic tissue forming a fluid-filled pseudocyst. They are often calcified.

Question 59

epidem and presentation of Neoplasms of the exocrine pancreas

Answer 59

A variety of benign and malignant, solid and cystic neoplasms affect the exocrine pancreas. Over 80% are ductal adenocarcinomas, derived from ductal epithelium. It has an incidence of 10 per 100,000 per annum and is the fifth most common cause of cancer death in western societies. Cystic neoplasms represent <5% of pancreatic neoplasms. The benign form (cystadenoma) and malignant form (cystadenocarcinoma) are distinguished by microscopy after excision.

Pancreatic carcinoma presents insidiously with non-specific features such as abdominal pain, weight loss, anorexia and vomiting. More than 50% develop jaundice at some time but less than 20% are jaundiced at presentation. There is migratory thrombophlebitis (Trousseau’s sign), with appearing/disappearing thrombosis present in 10%, or painless distension of the gallbladder (Courvoisier’s sign). Pancreatic carcinoma is often associated with many and varied incidental chemical abnormalities or non-specific symptoms.

Question 60

Aetiology of Neoplasms of the exocrine pancreas

Answer 60

Pancreatic carcinoma is increased several-fold in smokers. Associations with alcohol
and hyperlipidaemia are not consistent and although there is some familial clustering, genetic factors have yet to be well characterized.

Question 61

Morphology of Neoplasms of the exocrine pancreas

Answer 61

Carcinoma of the pancreas affects the head (60%), body (15%) and tail (5%) or is
diffuse (20%). These are gritty, hard pale masses with poorly defined infiltrating edges, which eventually invade into the adjacent structures. Microscopically these neoplasms are usually poorly to moderately differentiated adenocarcinomas with an infiltrating pattern of cell clusters. 10% are adeno-squamous/giant cell/sarcomatoid-type.

Question 62

Clinical Course of Neoplasms of the exocrine pancreas

Answer 62

These present late, often with pain secondary to nerve compression or invasion, at
which point cure is not possible. They have often spread locally into the peritoneum, spine and liver, with distant metastasis to the lungs and bones at diagnosis. Most cases are incurable and the majority of patients are dead within 18 months. Under 15% are resectable at diagnosis with surgery often being undertaken for palliation of symptoms only.

Question 63

anatomical divisions of the stomach

Answer 63

fundus, body and antrum

Question 64

what is a MALT LYMPHOMA

Question 65

what is a GIST

Answer 65

GIST – Gastrointestinal Stromal Tumour

Question 66

what is achalasia

Answer 66

Achalasia (/eɪkəˈleɪʒə/; a- and -chalasia “no relaxation”) is a failure of smooth muscle fibers to relax, which can cause a sphincter to remain closed and fail to open when needed. Without a modifier, “achalasia” usually refers to achalasia of the esophagus, which is also called esophageal achalasia, achalasia cardiae, cardiospasm, and esophageal aperistalsis. Achalasia can happen at various points along the gastrointestinal tract; achalasia of the rectum, for instance, is Hirschsprung’s disease.

Question 67

what is Dyspepsia

Answer 67

Dyspepsia = Dys + pepsia (difficult) (digestion)Pain or discomfort in the upper abdomen