Week 3

Question 1

What is the primary environmental trigger that induces the inflammatory response and mucosal injury in coeliac disease?

Answer 1

Gluten (fragments of gliadin)

Question 2

What is the clinical term that encompasses defects occurring during the digestion and absorption of food nutrients by the gastrointestinal tract?

Answer 2

Malabsorption syndrome.

Question 3

What is the term used to describe the impaired transport of nutrients from the intestine into the blood?

Answer 3

Malabsorption

Question 4

What is the concordance rate of coeliac disease in monozygotic (identical) twins?

Answer 4

70 - 75%

Question 5

Which hormone is primarily responsible for stimulating the secretion of pancreatic enzymes?

Answer 5

Cholecystokinin (cck)

Question 6

Which chromosome region has been associated with a susceptibility locus for insulin-dependent diabetes mellitus (iddm) in coeliac disease?

Answer 6

Chromosome region 15q26

Question 7

What percentage of individuals with coelia disease are positive for the HLA- DQ2 haplotype?

Answer 7

90%

Question 8

What serological test is considered the gold standard for screening and diagnosis of celiac disease?

Answer 8

Anti-tissue transglutaminase ( anti- tTG ) antibody

Question 9

What is the primary cause of malabsorption due to defective intraluminal digestion?

Answer 9

Pancreatic exocrine insufficiency

Question 10

What is the primary cause of maldigestion?

Answer 10

Deficiency of digestive enzymes

Question 11

What is inflammatory bowel disease; its epidemiology and the two classifications?

Answer 11

It is not synonymous with inflammatory bowel syndrome; it is more common in females and presents in teen and early twenties.it is more prominent in caissons of Ashkenazi Jews. There is increased incidence in Africas South America; this may be due to hygiene practices such as storage of food to reduce contamination.it is subdivided into ulcerative colitis and Crohn’s disease.

Question 12

What is the relation between UC and Crohn’s disease?

Answer 12

May be the result of defects in host interactions with intestinal flora, intestinal epithelial dysfunction and aberrant mucosal immune response. Nod 2 gene may play a role in Crohn’s disease in Caucasians of European descent. Inappropriate and persistent t-cell activation plays a role in both diseases. Intestinal ford contributes to the pathogenesis but exact role is unknown.

Question 13

What are the most important features of ulcerative colitis?

Answer 13

Present with episodes of chronic mucous & bloody diarrhoea; it often affects the rectum but may extend proximally to affect the entire colon (pancolitis). It may also affect the ileum in backwash ileitis; does not involve the anal canal and continuous without skiplesions. Only affects the mucosa & submucosa therefore is superficial.

Question 14

What are the gross findings in UC?

Answer 14

Red & granular appearance; extensive broad based ulcers with abrupt transition. Orientated along the long axis & formation of pseudopolyps and mucosal bridges. The wall is not thickened therefore strictures do not occur

Question 15

Carefully list the complications of UC

Answer 15

Toxic megacolon due to dilatation; blood loss & electrolyte disturbances are all acute while malignancy is chronic

Question 16

What are the features of Crohn’s disease which are important to remember?

Answer 16

May involve any part of the git tract but mainly involves the terminal ileum; ileocaecal value and caecum. Skip lesions are characteristic and involves the entire thickness of the mucosa with resulting strictures.

Question 17

What are the characteristic gross findings of Crohn’s disease?

Answer 17

Apthous ulcers that turn elongated along the axis of the bowel. Patchy involvement; leading to cobblestone appearance of bowel. Fistula tracts or perforations may form. The intestinal wall thickens with rubbery consistency and the mesenteric fat creeps along the sides of the bowel (fat wrapping).

Question 18

What is the hallmark of Crohn’s disease?

Answer 18

Non-caseating granulomas

Question 19

What is the hallmark intestinal lesson seen in celiac disease, a condition that leads to malabsorption due to primary mucosal cell abnormalities?

Answer 19

Villas atrophy

Question 20

What is a risk factor for the development of Barret’s aesophagus?

Answer 20

Chronic gastroesophageal reflux disease (GERD)

Question 21

What iatrogenic cause can lead to malabsorption?

Answer 21

Surgical resection of the small intestine

Question 22

What is the defining histological feature of Barrett’s oesophagus?

Answer 22

Replacement of the normal squamous epithelium of the oesophagus with specialized intestinal metaplastic epithelium.

Question 23

What is intussusception and the underlying pathophysiology?

Answer 23

Occurs when the proximal segment of the bowel telescope into a distal segment and pushed deeper due to peristalsis.it commonly occurs in the ileum through the ileacaecal value into the colon. The classical sign is a redcurrant jelly stool caused by venous obstruction as a result there is oedema and mucosal bleeding.

Question 24

What is diverticula disease and diverticulitis?

Answer 24

Diverticula disease is the presence of symptoms resulting from existing diverticula in the intestines; an acquired conditions where there are small out-pouching of intestines. while diverticulitis is inflammation of one/more diverticula.it is more common in females and 50% of patients over 70 years have them.it is said to be associated with a low fibre diet. More common in the sigmoid colon.

Question 25

What is the association between a low fibre diet and formation of diverticula?

Answer 25

In the presence of a low fibre diet; the muscles of the colon must work harder to move faeces along; this causes high pressure in the colon and as a result parts of the colon will form out-pouchings. The teen cold does the cover the entire colon therefore herniation will occur between the bands. There may be muscle changes such as fibrosis

Question 26

What is the pathogenesis of typhoid fever?

Answer 26

Hyperplasia of peyer’s patches of the terminal ileum with infiltration of histiocytes (Mallory cells) the reform become necrotic and form ulcers. The ulcers are ovoid in shape and orientated longitudinally with the long axis of of the great (contrast with tuberculosis)

Question 27

What is the pathology of a polyp?

Answer 27

Tumourous mass that protrudes into the lumen, sessile without a definable stalk; pedunculated polyp. Formed as a result of abnormal mucosal maturation, inflammation or architecture owing to proliferation & dysplasia. A precursor to carcinoma.

Question 28

What is the inheritance pattern of familial adenomatous polyposis (fap)?

Answer 28

Autosomal dominant caused by a mutation at the APC gene; colorectal adenocarcinoma develops if untreated. Treatment via colectomy but still at risk of developing malignancies at other sites like ampulla of Vater or stomach

Question 29

What is the genetic pattern and features of HNPCC?

Answer 29

Also known as Lynch syndrome; it is autosomal dominant in nature, familial clustering of cancers in colorectal etc wherein there are defects in mismatch repair genes(MSH 2 & MLH1). Colorectal cancer tends to occur at younger ages and are located in the right colon.

Question 30

What is the aetiology of typhoid fever?

Answer 30

Humans are the only host of s.typhi; bacteria is shed in bodily fluids of acutely ill patients & in faeces of chronic carriers. There are 3 stages wherein week 1 is bacteraemia; week 2 is rash and week 3 is ulceration of the Peyer’s patches

Question 31

What is the pathophysiology of typhoid fever?

Answer 31

Taken up by lymphoid tissues of the git especially Peyer’s patches and lymphoid follicles of the colon. Spread occurs through mesenteric lymph & haematogenously to liver; gallbladder & spleen. There is hyperplasia of the Peyer’s patches and infiltration of histiocytes (Mallory cells). Peyer patches become necrotic and form ulcer. Ulcers are ovoid in shape and orientated longitudinally with the long axis of the gut.

Question 32

Acute pseudomembranous colitis

Answer 32

Associated with use of broad spectrum antibiotics; patients develop a fulminant colitis with diarrhoea and dehydration → owing to suppression of normal bowel hard & overgrowth of C. Difficult. There is loss of epithelial cells and a volcano-like eruption of mucin, neutrophils and fibrin forming a pseudomembrane

Question 33

Amoebic colitis

Answer 33

Entamoeba histolytica presenting with dysentery with faecal-oral transmission of cysts with release of trophozoutes. Spread laterally in the mucosa and submucosa to form flask-shaped ulcers. Ulcers can communicate to form tunnels of necrotic tissue. Entamoeba organisms seen within floor of the exudate.