Intestine

Question 1

Lacteals

Answer 1

One of the lymphatic vessels which convey chyle from the small intestine through the mesenteric glands to the thoracic duct; a chyliferous vessel.

chyle: a milky fluid containing fat droplets which drains from the lacteals of the small intestine into the lymphatic system during digestion.

Question 2

Intestines; Congenital Anomalies

Answer 2

1. Intestinal atresia and stenosis
2. Meckel’s diverticulum
3. Intestinal malrotation

Question 3

Intestinal Atresia

Answer 3

It is the congenital absence of lumen, most commonly affecting the ileum or duodenum. The proximal segment has a blind end which is separated from distal segment freely, or the two segments are joined by a fibrous cord.

Question 4

Intestinal Stenosis

Answer 4

It is congenital narrowing of the lumen affecting a segment of the small intestine. Intestinal segment above the level of obstruction is dilated and that below it is collapsed.

Question 5

Meckel’s Diverticulum

Answer 5

Is known as the ‘‘left-sided’’ appendix.

It is almost always lined by small intestinal type of epithelium; rarely it may contain islands of gastric mucosa and ectopic pancreatic tissue.

It is more common in males.

It represents the remnant of the omphalomesenteric (vitelline) duct presenting as an outpouching of the ileum. A useful mnemonic is four 2s:

• Present in 2% of normal people.
• 2 feet from the ileocolic junction (80–90 cm).
• 2% may become symptomatic and cause symptoms similar to appendicitis or volvulus.
• Site of 2% of ectopic ulcers.

The common complications of Meckel’s diverticulum are perforation, haemorrhage and diverticulitis.

Question 6

Volvulus

Answer 6

Abnormal twisting of a portion of the gastrointestinal tract, usually the intestine, which can impair blood flow. Volvulus can lead to gangrene and death of the involved segment of the gastrointestinal tract, intestinal obstruction, perforation.

Volvulus is the twisting of loop of intestine upon itself through 180° or more. This leads to obstruction of the intestine as well as cutting off of the blood supply to the affected loop. The usual causes are bands and adhesions (congenital or acquired) and long mesenteric attachment.

Occurs most often in the sigmoid colon.

Question 7

Intestinal Malrotation

Answer 7

Malrotation is a developmental abnormality of the midgut (i.e. the portion of intestine between the duodenojejunal flexure and the middle of transverse colon). Due to failure of normal rotation of midgut, the following consequences can occur:

1. Exomphalos i.e. intestinal eventration at the umbilicus.
2. Misplacement of the caecum, appendix and ascending colon.
3. Mobile caecum.

Question 8

Hirschsprung disease

Answer 8

Also known as congenital megacolon or megacolon with congenital agangliosis.

• Incidence is 1 in 5000 infants.
• Male infants are more often affected (male-to-female ratio is 4:1).
• Multifactorial inheritance is suggested by higher incidence in some families.
• Dilatation of the colon is proximal to an aganglionic segment of the rectum.
• The defect in innervation results from faulty migration of precursors of intestinal ganglionic cells. These cells develop from the neural crest and migrate into fetal intestine. Normally, these cells populate the entire colon, but if they do not reach the terminal part of the rectum, this segment remains aganglionic.
• The diagnosis is made clinically (chronic constipation in a young child) but must be confirmed by biopsy, which typically shows an absence of ganglion cells.
• The part of the intestine that does not contain ganglion cells must be resected.

Question 9

Classify the causes of intestinal obstruction.

Answer 9

1. Mechanical Obstruction
2. Neurogenic Obstruction
3. Vascular Obstruction

*Out of the various causes listed above, conditions producing external compression on the bowel wall are the most common causes of intestinal obstruction (80%).

Question 10

Mechanical Obstruction

Answer 10

• Internal Obstruction (intramural and intraluminal):
  
  • Inflammatory strictures (e.g. Crohn’s disease) Congenital stenosis, atresia, imperforate anus
  • Tumours
  • Meconium in mucoviscidosis
  • Roundworms
  • Gallstones, faecoliths, foreign bodies
  • Ulceration induced by potassium chloride tablets prescribed to counter hypokalaemia.
• External compression:
  
  • Peritoneal adhesions and bands
  • Strangulated hernias
  • Intussusception
  • Volvulus
  • Intra-abdominal tumour

Question 11

Neurogenic Obstruction

Answer 11

It occurs due to paralytic ileus i.e. paralysis of muscularis of the intestine as a result of shock after abdominal operation or by acute peritonitis.

Question 12

Vascular obstruction

Answer 12

• Thrombosis
• Embolism
• Accidental ligation

Question 13

Peritoneal adhesions and bands

Answer 13

Adhesions and bands in the peritoneum composed of fibrous tissue result following healing in peritonitis. Rarely, such fibrous adhesions and bands may be without any preceding peritoneal inflammation and are of congenital origin.

Question 14

Hernias

Answer 14

Hernia is protrusion of portion of a viscus through an abnormal opening in the wall of its natural cavity.

External hernia is the protrusion of the bowel through a defect or weakness in the peritoneum.

Internal hernia is the term applied for herniation that does not present on the external surface.

Two major factors involved in the formation of a hernia are as under: i) Local weakness, ii) Increased intra-abdominal pressure.

Inguinal hernias are more common, followed in decreasing frequency, by femoral and umbilical hernias. Inguinal hernias may be of 2 types: Direct and indirect.

When the blood flow in the hernial sac is obstructed, it results in strangulated hernia. Obstruction to the venous drainage and arterial supply may result in infarction or gangrene of the affected loop of intestine

Question 15

Intussusception

Answer 15

Intussusception is the telescoping of a segment of intestine into the segment below due to peristalsis.

The telescoped segment is called the intussusceptum and lower receiving segment is called the intussuscipiens. The condition occurs more commonly in infants and young children, more often in the ileocaecal region when the portion of ileum invaginates into the ascending colon without affecting the position of the ileocaecal valve.

The main complications of intussusception are intestinal obstruction, infarction, gangrene, perforation and peritonitis.

Question 16

How does intussusception develop?

Answer 16

• In small children with very active peristalsis: In these children, one small intestinal loop invaginates into another, like the finger of an inverted glove. The loop is said to be ‘‘telescoped into another loop’’ (because the loops resemble the old navigators’ telescopes), and intussusceptum is strangulated by the out-sided intussuscipient. The inner loop may become necrotic unless the invagination is everted surgically (or spontaneously, as may sometimes occur).
• In the presence of tumors: Small pedunculated tumors carried by peristalsis may pull forward the loop to which such a tumor is attached.

Question 17

Ischaemic Bowel Disease (Ischaemic Enterocolitis); Transmural Infarction

Answer 17

Ischaemic necrosis of the full-thickness of the bowel wall is more common in the small intestine than the large intestine.

G/A: Irrespective of the underlying etiology, infarction of the bowel is haemorrhagic (red) type. The affected areas become dark purple and markedly congested and the peritoneal surface is coated with fibrinous exudate. The wall is thickened, oedematous and haemorrhagic. The lumen is dilated and contains blood and mucus. In arterial occlusion, there is sharp line of demarcation between the infarcted bowel and the normal intestine, whereas in venous occlusion the infarcted area merges imperceptibly into the normal bowel.

M/E: There is coagulative necrosis and ulceration of the mucosa and there are extensive submucosal haemorrhages. The muscularis is less severely affected by ischaemia. Subsequently, inflammatory cell infiltration and secondary infection occur, leading to gangrene of the bowel

Question 18

Ischaemic Bowel Disease;

Mural & Mucosal Infarction (Haemorrhagic gastroenteropathy, membranous colitis)

Answer 18

Mural and mucosal infarctions are limited to superficial layers of the bowel wall, sparing the deeper layer of the muscularis and the serosa. The condition is also referred to as haemorrhagic gastroenteropathy, and in the case of colon as membranous colitis.

G/A: The lesions affect variable length of the bowel. The affected segment of the bowel is red or purple but without haemorrhage and exudation on the serosal surface. The mucosa is oedematous at places, sloughed and ulcerated at other places.

M/E: There is patchy ischaemic necrosis of mucosa, vascular congestion, haemorrhages and inflammatory cell infiltrate. The changes may extend into superficial muscularis but deeper layer of muscularis and serosa are spared. Secondary bacterial infection may supervene resulting in pseudomembranous enterocolitis.

Question 19

Ischaemic Colitis

Answer 19

G/A: Most frequently affected site is the splenic flexure; other site is rectum. Ischaemic colitis passes through 3 stages: infarct, transient ischaemia and ischaemic stricture. However, the surgical submitted specimens generally are of the ischaemic stricture. External surface of the affected area is fusiform or saccular. On cut section, there are patchy, segmental and longitudinal mucosal ulcers.

M/E: The ulcerated areas of the mucosa show granulation tissue. The submucosa is characteristically thickened due to inflammation and fibrosis. The muscularis may also show inflammatory changes and patchy replacement by fibrosis.

Question 20

Necrotising enterocolitis

Answer 20

Necrotising enterocolitis is an acute inflammation of the terminal ileum and ascending colon, occurring primarily in premature and low-birth-weight infants within the first week of life and less commonly in full-term infants.

Found in: Infants fed on commercial formulae than breast-fed, implying the role of immunoprotective factors.

G/A: The affected segment of the bowel is dilated, necrotic, haemorrhagic and friable. Bowel wall may contain bubbles of air (pneumatosis intestinalis).

M/E: The changes are variable depending upon the stage. Initial changes are confined to mucosa and show oedema, haemorrhage and coagulative necrosis. A pseudomembrane composed of necrotic epithelium, fibrin and inflammatory cells may develop. As the ischaemic process extends to the subjacent layers, muscle layer is also involved and may lead to perforation and peritonitis.

Question 21

Inflammatory bowel disease (IBD)

Answer 21

The term ‘inflammatory bowel disease (IBD)’ is commonly used to include 2 idiopathic bowel diseases having many similarities but the conditions usually have distinctive morphological appearance. (Crohn’s disease or Regional enteritis & Ulcerative colitis)

Question 22

What are the differences between UC and CD?

Answer 22

Question 23

Can one distinguish UC from CD by intestinal biopsy?

Answer 23

The diagnosis of UC and CD is made by exclusion and by correlating all the clinical, endoscopic, radiologic, and pathologic findings.

Negative bacteriologic and confirmatory biopsy findings are of paramount importance for such an exclusion diagnosis.

Histologic findings are useful to confirm active inflammation. However, biopsy findings do not allow a clear distinction between UC and CD.

Finding of granulomas (50% of cases) is typical of CD.

Involvement of the ileum also favors CD over UC.

Question 24

Infective Enterocoltis

Answer 24

These are a group of acute and chronic inflammatory lesions of small intestine and/or colon caused by microorganisms (bacteria, viruses, fungi, protozoa and helminths). All these are characterised by diarrhoeal syndromes.

Pathogenetically speaking, these microorganisms can cause enterocolitis by 2 mechanisms—

• by enteroinvasive bacteria producing ulcerative lesions
• by enterotoxin-producing bacteria resulting in non-ulcerative lesions.

Question 25

Primary Intestinal Tuberculosis

Answer 25

In the pre-pasteurisation era, it used to occur by ingestion of unpasteurised cow’s milk infected with Mycobacterium bovis. But now-a-days due to control of tuberculosis in cattle and pasteurisation of milk, virtually all cases of intestinal tuberculosis are caused by M. tuberculosis.

G/A: The affected lymph nodes are enlarged, matted and caseous (tabes mesenterica). Eventually, there is healing by fibrosis and calcification.

M/E: In the initial stage, there is primary complex or Ghon’s focus in the intestinal mucosa as occurs elsewhere in primary tuberculous infection. Subsequently, the mesenteric lymph nodes are affected which show typical tuberculous granulomatous inflammatory reaction with caseation necrosis.

Question 26

Secondary Intestinal Tuberculosis

Answer 26

Self-swallowing of sputum in patients with active pulmonary tuberculosis may cause secondary intestinal tuberculosis, most commonly in the terminal ileum and rarely in the colon.

The intestinal lesions are prominent than the lesions in regional lymph nodes as in secondary pulmonary tuberculosis. The lesions begin in the Peyer’s patches or the lymphoid follicles with formation of small ulcers that spread through the lymphatics to form large ulcers which are transverse to the long axis of the bowel, (c.f. typhoid ulcers of small intestine, described below). In advanced cases, transverse fibrous strictures and intestinal obstruction are seen.

Question 27

Hyperplastic Caecal Tuberculosis

Answer 27

This is a variant of occurring secondary to pulmonary tuberculosis.

G/A:The caecum and/or ascending colon are thick-walled with mucosal ulceration.

M/E: The presence of caseating tubercles distinguishes the condition from Crohn’s disease in which granulomas are non-caseating.

Question 28

What is enteric fever?

Answer 28

Enteric fever is a form of diarrhea that is of protracted duration and is associated with signs of systemic disease, such as high fever, rash, and respiratory or neurologic symptoms. Salmonella typhimurium and Salmonella paratyphi are the most common causes.

Question 29

Enteric Fever; Pathogenesis

Answer 29

1. The typhoid bacilli are ingested through contaminated food or water.
2. During the initial asymptomatic incubation period of about 2 weeks, the bacilli invade the lymphoid follicles and Peyer’s patches of the small intestine and proliferate.
3. Following this, the bacilli invade the blood-stream causing bacteraemia, and the characteristic clinical features of the disease like continuous rise in temperature and ‘rose spots’ on the skin are observed.
4. Eventually, the bacilli are localised in the intestinal lymphoid tissue (producing typhoid intestinal lesions), and in the mesenteric lymph nodes (leading to haemorrhagic lymphadenitis).

G/A: Terminal ileum is affected most often, but lesions may be seen in the jejunum and colon. Peyer’s patches show oval typhoid ulcers with their long axis along the length of the bowel, (c.f. tuberculous ulcers of small intestine, described above). The base of the ulcers is black due to sloughed mucosa. The regional lymph nodes are invariably enlarged

*Though enteric fever is an example of acute inflammation, neutrophils are invariably absent from the cellular infiltrate and this is reflected in the leucopenia with neutropenia and relative lymphocytosis in the peripheral blood.

Question 30

Bacterial Food Poisoning

Answer 30

This is a form of acute bacterial illness that occurs following ingestion of food or water contaminated with bacteria other than those that cause specific acute intestinal infections like typhoid, paratyphoid, cholera or dysentery bacilli.

The commonest causes of bacterial food poisoning resulting in enteritis or enterocolitis are as under:

1. Staphylococcal food poisoning,
2. Clostridial food poisoning,
3. Botulism
4. Salmonella food poisoning (Salmonellosis).

Question 31

Dysentry

Answer 31

The term ‘dysentery’ is used to mean diarrhoea with abdominal cramps, tenesmus and passage of mucus in the stools, from any cause.

Question 32

Bacillary Dysentry

Answer 32

Bacillary dysentery is the term used for infection by shigella species: S. dysenteriae, S. flexneri, S. boydii and S. sonnei. Infection occurs by foeco-oral route and is seen with poor personal hygiene, in densely populated areas, and with contaminated food and water. The common housefly plays a role in spread of infection.

G/A: The lesions are mainly found in the colon and occasionally in the ileum. Superficial transverse ulcerations of mucosa of the bowel wall occur in the region of lymphoid follicles but perforation is seldom seen.

M/E: The mucosa overlying the lymphoid follicles is necrosed. The surrounding mucosa shows congestion, oedema and infiltration by neutrophils and lymphocytes. The mucosa may be covered by greyish-yellow ‘pseudomembrane’ composed of fibrinosuppurative exudate.

Question 33

Amoebic Dysentry

Answer 33

This is due to infection by Entamoeba histolytica. It is more prevalent in the tropical countries and primarily affects the large intestine. Infection occurs from ingestion of cyst form of the parasite.

The trophozoites of Entamoeba are seen in the inflammatory exudate and are concentrated at the advancing margin of the lesion.

Intestinal amoebae characteristically have ingested red cells in their cytoplasm. Oedema and vascular congestion are present in the area surrounding the ulcers.

Question 34

Pseudomembranous Enterocolitis (Antibiotic-Associated Diarrhoea)

Answer 34

Numerous studies have established the overgrowth of Clostridium difficile with production of its toxin in the etiology of antibiotic-associated diarrhoea culminating in pseudomembranous colitis.

Oral antibiotics such as clindamycin, ampicillin and the cephalosporins are more often (20%) associated with antibiotic-associated diarrhoea, while development of pseudomembranous colitis may occur in 1-10% cases.

G/A: The lesions may be confined, to the large intestine or small intestine, or both may be involved. The mucosa of the bowel is covered by patchy, raised yellow-white plaques.

M/E: The ‘pseudomembrane’ is composed of network of fibrin and mucus, in which are entangled inflammatory cells and mucosal epithelial cells. There is focal necrosis of surface epithelial cells.

Question 35

Malabsorption Syndrome

Answer 35

The malabsorption syndrome (MAS) is characterised by impaired intestinal absorption of nutrients especially of fat; some other substances are proteins, carbohydrates, vitamins and minerals. MAS is subdivided into 2 broad groups:

• Primary MAS, which is due to primary deficiency of the absorptive mucosal surface and of the associated enzymes.
• Secondary MAS, in which mucosal changes result secondary to other factors such as diseases, surgery, trauma and drugs.

Question 36

What are the laboratory and clinical findings in malabsorption syndrome?

Answer 36

Question 37

Malabsorption Syndrome; Celiac Disease (Celiac Sprue or Gluten Sensitive Enteropathy or Non-troical sprue)

Answer 37

It is a disease characterized by increased sensitivity to a protein called gluten or its alcohol soluble fraction α-gliadin Q present in the grains like wheat, oat, barley and rye resulting in a T-cell mediated chronic inflammatory reaction in the small intestine and impaired absorption. It is associated with HLA-DQ2 or HLA-DQ8.

Clinical features include diarrhea, flatulence, weight loss and fatigue and a characteristic skin lesion called ‘dermatitis herpetiformis’.

Biopsy of the intestine shows the diffuse enteritis (lymphocytes and plasma cells in lamina propria) with marked atrophy of the villi and elongated and hyperplastic crypts (overall mucosal thickness is unalteredQ). The disease also demonstrates the presence of antigliadin, antiendomysialQ (most useful) or antitransglutaminase antibodiesQ (useful for screening test)

Treatment is intake of the gluten-free diet and substitution by rice, millet, tapioca, potato and maize in the diet.

Question 38

Malabsorption Syndrome; Tropical Sprue (Post Infectious Sprue) is now called as Environmental Enteropathy

Answer 38

It is a disease similar in features to celiac sprue but present in the tropical region. Though the exact cause is unknown, but bacterial overgrowth particularly E. coli and Hemophilus have been implicated. Biopsy of the intestine shows the diffuse enteritis with atrophy of the villi. Treatment is done with the help of antibiotics.

• There is characteristically involvement of the proximal intestine in celiac sprue resulting in iron deficiency anemia whereas in tropical sprue, there is generalized involvement of the small intestine (resulting in megaloblastic anemia because B12 and folic acid are absorbed from the terminal ileum).
• Another important difference between the two is that tropical sprue is not associated with cancer development whereas celiac sprue is associated with cancers like non Hodgkin’s lymphoma, small intestine adenocarcinoma and esophageal squamous cell cancer.

Question 39

Malabsorption Syndrome; Whipple’s Disease

Answer 39

• It is a systemic infectious disease caused by an actinomycete, Tropheryma whippelii affecting the triad of small intestine, CNS and jointsQ. The bacteria characteristically proliferate inside the macrophages without getting destroyed.
• The hallmark feature of the disease is small intestinal mucosa having macrophages in the lamina propria and these macrophages show the presence of PAS positive, diastase resistant granulesQ and rod shaped bacteria on electron microscopy. There is mucosal edema, dilation of the lymphatics and involvement of mesenteric lymph nodes. The macrophages having the bacteria can also be found in the joints, brain, cardiac valves etc with absence of inflammation being a typical feature.
• Clinical features include arthropathy (initial presentation), diarrhea, weight loss, hyperpigmentation and dementia. The diarrhea is due to impaired lymphatic transport.
• Diagnosis is confirmed by identification of T. whipplei by polymerase chain reaction (PCR). Treatment is done with cotrimoxazole (drug of choice) for one year.

Question 40

Carcinoid Tumor

Answer 40

Carcinoid tumor arises from the endocrine cells called as argentaffin tissue (also called as Kulchitzsky cells of crypts of Lieberkuhn) with the GIT and the lungs as the main sites of origin of this cancer. The clinical features are due to release of peptide and non-peptide hormones from these cells.

The gastrointestinal carcinoid tumors can be of the following types:

1. Foregut carcinoid tumors: Arise from the esophagus, stomach and the duodenum proximal to the ligament of Treitz, these are usually benign.
2. Midgut carcinoid tumors: Arise from the jejunum and ileum; these are aggressive and metastasize frequently.
3. Hindgut carcinoid tumors: Arise from the appendix, colon and rectum; usually benign.

Question 41

Clinical features of carcinoid syndrome are:

Answer 41

S - Systemic fibrosis (Affects cardiac valves, endocardium, retroperitoneal and pelvic fibrosis)

H - Hepatomegaly (Because of metastasis)

I - Intestinal hypermotility (Vomiting, diarrhea, cramps, nausea)

V - Vasomotor symptoms like flushing and cyanosis of the skin

A - Asthma like features (Cough, wheezing, dyspnea)

*Hepatic metastasis is usually present in this tumor. The most sensitive screening test for small intestine carcinoids is the plasma level of chromogranin A. The levels of 5-HT and its metabolite 5-hydroxyindoleacetic acidQ (5-HIAA) is elevated in the urine

Question 42

What are intestinal polyps?

Answer 42

Polyps are benign tumors or tumor-like protrusions of the intestinal mucosa. Polyps are classified as neoplastic and nonneoplastic

Question 43

What are juvenile (retention) polyps?

Answer 43

These polyps are hamartomas typically found in the rectum of children aged younger than 10 years. They are pedunculated, round, and have a smooth surface. Histologically, they are composed of mucus-filled cystic glands and edematous, usually inflamed stroma.

Question 44

What is Peutz–Jeghers syndrome?

Answer 44

An autosomal dominant syndrome characterized by:

1. Multiple hamartomatous intestinal polyps (Polyps may be found in any part of the intestine but are most numerous in the small intestine.)
2. Pigmented macules on the lips and the perioral skin
3. Increased risk of cancer in the lungs, breast, uterus, and pancreas
4. Intestinal polyps composed of irregularly arranged glands surrounded by strands of smooth muscles (These polyps are not precancerous and only exceptionally progress to adenocarcinoma.)

Question 45

What is familial adenomatous polyposis (FAP) coli?

Answer 45

• It is an autosomal dominant hereditary tumor syndrome.
• It is linked to deletion of the tumor suppressor gene called adenomatous polyposis coli (APC) on chromosome region 5q21.
• The colon contains numerous (>100) tubular adenomas.
• Tumors are not present at birth but appear in childhood and become clinically evident in the second decade of life.
• Adenocarcinoma develops in all patients. By age 40 years, cancer is found in 100% of patients.
• Prophylactic colectomy must be performed in midlife.

Question 46

Discuss the other hereditary colonic cancer syndromes.

Answer 46

• Gardner syndrome: A variant of FAP, it also shows autosomal dominant inheritance of numerous colonic tubular adenomas. In addition, patients have multiple osteomas, fibromatosis, and epidermal inclusion cysts.
• Turcot syndrome: In this rare syndrome, adenomatous polyposis coli is associated with brain tumors (gliomas)
• Hereditary nonpolyposis colorectal cancer (HNPCC): Also known as Lynch’s syndrome, it shows autosomal dominant inheritance of a mutator gene encoding a DNA mismatch repair enzyme. It is characterized by an increased incidence of colonic adenocarcinoma, endometrial, and ovarian cancer. Adenomas of the colon may be present, but most adenocarcinomas develop unrelated to these benign tumors. Colonic adenocarcinomas are often multiple.

Question 47

Which genes are involved in the evolution of cancer from adenomatous polyps?

Answer 47

The so-called adenoma-carcinoma sequence involves several well-defined cancer genes:

• The APC tumor suppressor gene and MSH2 mutator gene involved in DNA mismatch repair set the background for the development of tubular adenomas.
• The k-ras oncogene plays a role in the formation of tubular adenomas.
• The p53 gene is involved in the growth of adenomas and the onset of early malignancy.
• Invasive cancer develops because of the complex interaction of several genes.

Question 48

In which part of the large intestine do most carcinomas develop?

Answer 48

• Rectosigmoid, 40%
• Descending colon, 15%
• Cecum and ascending colon, 35%
• Transverse colon, 10%

Question 49

What are the differences between carcinomas of the right and left colon?

Answer 49

• Histologically, most colorectal carcinomas are adenocarcinomas.
• Carcinomas of the right colon protrude into the lumen and are described as exophytic, polypoid, or craterlike ulcerations with raised margins.
• Carcinomas of the sigmoid are circumferential, napkin-ring-like lesions causing narrowing of the lumen. In barium enema studies, these tumors are described as apple-core-like lesions.

Question 50

Double contrast barium enema

Answer 50

Double contrast barium enema is the radiological investigation of choice which characteristically shows “apple core” appearance of the cancer.

Question 51

The occult blood loss in the stool can be detected with the help of ____.

Answer 51

Guaiac Test

Question 52

Polymorphism of the______ receptor is protective in both the types of inflammatory bowel disease

Answer 52

IL-23 receptor

Question 53

Important features of Crohn’s disease

Answer 53

S – Skip lesions

I – Ileum (MC affected site)

S – Saccharomyces cerevisae antibody present

T – Transmural involvement

E – Extra fibrosis and fistula formation (as compared to ulcerative colitis)

R – Radiological sign- String sign of Kantor, Rectum is usually spared.

Question 54

What is carcinoembryonic antigen (CEA)?

Answer 54

CEA is a glycoprotein secreted by fetal intestinal cells into the meconium. It is also secreted by adenocarcinoma cells and may be found in the blood of patients with colorectal cancer. The CEA test lacks specificity and cannot be used for screening of persons at risk of developing colon cancer. It is useful for monitoring tumor burden and recurrence of cancer following surgical resection of the primary colon cancer.

Question 55

List conditions predisposing to primary GI lymphoma.

Answer 55

• Gastric H. pylori infection
• Celiac disease
• Acquired immune deficiency syndrome
• Mediterranean a-heavy chain disease

Question 56

Where are most carcinoids located?

Answer 56

• Appendix, 40%
• Small intestine, 25%
• Colon, 30%
• Stomach, 5%

Question 57

What are intestinal carcinoid tumors?

Answer 57

• They are low-grade malignant tumors.
• They are composed of neuroendocrine cells.
• Cells with round, uniform nuclei form solid nests or rosettes around blood vessels (and secrete hormones into blood vessels).
• Electron microscopy shows cytoplasmic granules.
• Neuroendocrine hormones are demonstrable by immunohistochemistry.
• Most cases present as small intramucosal or submucosal nodules (95% are 2 cm) metastasize to the liver and other sites.
• May produce carcinoid syndrome (diarrhea, facial flushing, bronchospasm, and right heart failure).
• Urinary 5-hydroxyindolacetic acid may be elevated.