Gastroenterology - Diseases of the small intestine Flashcards Preview

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Flashcards in Gastroenterology - Diseases of the small intestine Deck (89):
1

What is the main function of the small intestine?

The main role of the small intestine is digestion and absorption of nutrients. Vitamin B12 and bile salts have specific receptors

2

What are the presenting symptoms of small bowel disease?

Presenting symptoms of small bowel disease include diarrhoea, steatorrhoea, abdominal pain or discomfort and anorexia causing weight loss. Small bowel disease may also be found after investigation for specific deficiencies such as vitamin B12. The two most common causes of small bowel disease in the western world are coeliac disease and Crohn's disease. Investigation of suspected small bowel disease is initially with coeliac screen, small bowel barium follow or MRI and endoscopic small bowel biopsy.

3

What disorders of the small intestine are associated with malabsorption?

Coeliac disease
Crohn's disease
Dermatitis herpetiformis
Tropical sprue
Bacterial overgrowth
Intestinal resection
Whipple's disease
Radiation enteritis
Parasite infection - e.g. Giardia intestinalis

4

What is Coeliac disease?

This is an autoimmune condition characterised by an abnormal jejunal mucosa that improves when gluten (contained in wheat, rye and barley) is withdrawn from the diet, and relapses when gluten is reintroduced. About 1 in 100 individuals in European derived populations have coeliac disease, most of whom are undiagnosed.

5

What is the pathogenesis of coeliac disease?

There is a strong association between coeliac disease and HLA DQ2 and DQ8. The peptide alpha gliadin is the toxic portion of gluten. Gliadin is resistant to proteases in the small intestinal lumen and passes through a damaged (as a result of infection or possibly gliadin itself) epithelial barrier of the small intestine where it is deaminated by tissue transglutaminase so increasing its immunogenicity.

Gliadin then interacts with antigen presenting cells in the lamina propria via HLA DQ2 and HLA DQ8 and activates gluten sensitive T cells. The inflammatory cascade that follows and release of mediators contributes to the villous atrophy and crypt hyperplasia that are the typical histological features of coeliac disease. There is an increase in intraepithelial lymphocytes but the pathogenic role of these lymphocytes, compared with lamina propria lymphocytes is not known.

6

What are the clinical features of coeliac disease?

Presentation is at any age but there are two peaks in incidence; in infancy (after weaning on to gluten containing foods) and in adults in the fifth decade. There may be non specific symptoms of tiredness and malaise, or symptoms of small intestinal disease. Physical signs are usually few and non specific, and related to anaemia and nutritional deficiency. There is an increased incidence of atopy and autoimmune diseases.

7

Which individuals should be offered screening for coeliac disease?

Autoimmune diseases
- type 1 DM
- thyroid disease
- autoimmune liver disease
- Addison's disease
IBS (symptoms may be similar to coeliac disease)
Unexplained osteoporosis
Those with a first degree relative
Downs syndrome (20 fold increase)
Turners syndrome
Infertility and recurrent miscarriage

8

What investigations should be performed in patients with suspected coeliac disease?

1) Serum autoantibodies
2) Distal duodenal biopsy
3) FBC
4) Small bowel radiology or capsule endoscopy
5) Bone densitometry

9

What serum antibodies are present in coeliac disease?

IgA tissue transglutaminase antibodies have a very high sensitivity and specificity for coeliac disease. False negatives occur in IgA deficiency when IgG based tests should be used. IgA endomysial antibodies are less sensitive.

Serological testing is offered to patients with signs and symptoms or in conditions where there is an increased risk. Patients with positive serology, or if serology is negative but disease is strongly suspected, are referred for endoscopic biopsy.

10

What is required for a definitive diagnosis of coeliac disease?

Distal duodenal biopsy. Histological changes are of variable severity and show an increase in the number of intraepithelial lymphocytes, crypt hyperplasia with chronic inflammatory cells in the lamina propria and villous atrophy. The latter is seen in other conditions (e.g. tropical sprue, Whipple's disease), but coeliac is the commonest cause of subtotal villous atrophy.

11

What important findings are seen on the blood count in coeliac disease?

A mild anaemia is present in 50% of cases. There is almost always folate deficiency, commonly iron deficiency and rarely vitamin B12 deficiency. Target cells, spherocytes and Howell-Jolly bodies are due to hyposplenism.

12

How often is small bowel radiography or capsule endoscopy performed in coeliac disease?

These are usually only performed when a complication is suspected such as lymphoma.

13

What other scan should be performed at diagnosis of coeliac disease?

Bone densitometry - increased risk of osteoporosis.

14

How is coeliac disease managed?

Treatment is with lifelong gluten free diet and correction of any vitamin deficiencies. Pneumococcal vaccine is given as coeliac disease is associated with hyposplenism. Symptoms and serologic testing (undetectable antibodies indicate a response) are used to monitor recovery and compliance with the diet. Re biopsy is reserved for patients who do not respond or in whom there is diagnostic uncertainty.

15

What complications are associated with coeliac disease?

There is an increased incidence of malignancy, particularly intestinal T cell lymphoma, small bowel and oesophageal cancer. The incidence may be reduced by a gluten free diet.

16

What is dermatitis herpetiformis?

This is an itchy, symmetrical eruption of vesicles and crusts over the extensor surfaces of the body with deposition of granular immunoglobulin (IgA) at the dermoepidermal junction of the skin, including areas not involved with the rash. Patients also have a gluten sensitive enteropathy, which is usually asymptomatic. The skin condition responds to dapsone, but both the gut and the skin will improve on a gluten free diet.

17

What is tropical sprue? How is it treated?

This is a progressive small intestinal disorder presenting with diarrhoea and steatorrhoea and megaloblastic anaemia. It occurs in residents or visitors to endemic areas in the tropics (Asia, the Carribean, Puerto Rico, parts of South America). The aetiology is unknown but likely to be infective.

Diagnosis is based on demonstrating evidence of malabsorption (particularly of fat and vitamin B12) together with a small bowel mucosal biopsy showing features similar, but not identical, to those in untreated coeliac disease. Infective causes of diarrhoea, particularly Giardia intestinalis, should be excluded. Treatment is with folic acid and tetracycline for 3-6 months and correction of nutritional deficiencies.

18

What is bacterial overgrowth?

Sometimes called "blind loop syndrome", bacterial overgrowth occurs when there is stasis of intestinal contents as a result of abnormal motility - e.g. systemic sclerosis or hypogammaglobulinaemia or a structural abnormality - e.g. previous small bowel surgery or a diverticulum. The upper small intestine is almost sterile.

19

What are the clinical features of bacterial overgrowth?

The bacteria deconjugate bile salts causing diarrhoea and/or steatorrhoea and metabolise vitamin B12 which may result in deficiency.

20

How is bacterial overgrowth diagnosed?

A therapeutic trial of antibiotics is given when clinical suspicion is high. Otherwise, diagnosis is usually by a hydrogen breath test in which hydrogen is measured in exhaled air after oral lactulose. With bacterial overgrowth an early peak is seen in the breath hydrogen followed by a later colonic peak (normally present due to metabolism of lactulose by colonic bacteria).

Serum B12 concentrations are low; folate levels are normal or elevated. Immunoglobulin levels may exclude hypogammaglobulinaemia.

21

How is bacterial overgrowth managed?

The underlying cause should be corrected if possible. Otherwise, rotating courses of antibiotics - e.g. tetracycline and metronidazole are given.

22

How does intestinal resection cause malabsorption?

The effects of small intestinal resection depend on the extent and the area involved. Resection of the terminal ileum leads to malabsorption of:
- vitamin B12 leading to megaloblastic anaemia
- bile salts which overflow into the colon. This causes secretion of water and electrolytes and diarrhoea, and increased oxalate absorption which may result in renal oxalate stones

Ileal resection is usually performed as a treatment for Crohn's disease. Parenteral administration of vitamin B12 and colestyramine or aluminium hydroxide for the diarrhoea are usually needed.

23

What is the short bowel syndrome?

More extensive resection leaving less than 1m of small bowel is followed by the short bowel syndrome. The majority of cases occur after resection for Crohn's disease, mesenteric ischaemia, trauma, volvulus or surgical complications.

Clinical features include:
- large volume jejunostomy fluid loss
- if colon is preserved, diarrhoea and steatorrhoea
- dehydration and signs of hypovolaemia
- weight loss, loss of muscle bulk and malnutrition

24

How is short bowel syndrome treated?

Parenteral nutrition is the mainstay of treatment for patients in whom absorptive function has failed.

The ability of patients to cope without supplemental IV fluids or nutritions depends on:
- AMOUNT of resected bowel - most patients with <100cm of jejunum and no colon will require supplements
- LOCATION of resected bowel (jejunal resection is better tolerated than ileal)
- COLON intact which absorbs water and electrolytes
- HEALTH of residual tissue - i.e. there are fewer problems after resection following trauma than in patients with Crohns

25

What is Whipple's disease?

This is a rare disease caused by the bacterium Tropheryma whipplei. Steatorrhoea, abdominal pain, lymphadenopathy, arthritis, cardiac (pericarditis, myocarditis, endocarditis) and neurological involvement occur. Small bowel biopsy shows periodic acid schiff (PAS) positive macrophages which on electron microscopy are seen to contain the causative bacteria. Treatment is with co-trimoxazole for 1 year after two weeks of IV ceftriaxone.

26

What is radiation enteritis? What are the clinical features?

Intestinal damage occurs in 10–15% of patients undergoing radiotherapy for abdominal or pelvic malignancy. The risk varies with total dose, dosing schedule and the use of concomitant chemotherapy.

Acutely, there is nausea, vomiting, cramping abdominal pain and diarrhoea. When the rectum and colon are involved, mucus, bleed- ing and tenesmus occur. The chronic phase develops after 5–10 yrs in some patients and may feature bleeding from telangiectasis, fis- tulae, adhesions, strictures or malabsorption.

27

How is radiation enteritis managed?

Acute phase: codeine, loperamide, corticosteroid enemas for proc- titis and antibiotics for bacterial overgrowth.

Nutritional supplements for malabsorption; colestyramine for bile salt malabsorption may be necessary.

Endoscopic laser or argon plasma coagulation therapy: may reduce bleeding from proctitis.

Surgery should be avoided, because the injured intestine is difficult to resect and anastomose, but it may be necessary for obstruction, perforation or fistula.

28

What is norovirus?

Norovirus (Norwalk agent) is the most common cause of infectious gastroenteritis in the UK and causes outbreaks in closed communities, such as hospital wards. Food handlers may also transmit norovirus. It is highly infectious via the faecal oral root and causes prominent vomiting and dirrahoea after an incubation period of 24-48 hours. Diagnosis is by electron microscopy or PCR of stool samples. Case isolation and rehydration is the main management.

29

What is the most common virus to cause diarrhoea in young children?

Rotavirus is the major cause of diarrhoeal illness in young children. Infection is endemic in developing countries. There are winter epidemics in developed countries, particularly hospitals. The virus infects enterocytes causing decreased surface absorption and loss of enzymes on the brush border.

The incubation period is 48 hours, and patients present with watery diarrhoea, vomiting, fever, and abdominal pain. The disease is self limiting but dehydration needs appropriate management. Effective vaccines have been developed.

30

What serotypes of adenovirus are associated with diarrhoeal illness?

40 and 41

31

What is gastroenteritis?

Gastroenteritis is acute diarrhoea with or without vomiting that is due to gastrointestinal infection with bacteria, viruses or protozoa. Gastroeneteritis can happen at home or whilst travelling abroad.

Not all cases of gastroenteritis are food poisoning as the pathogens are not always food or water borne - e.g. C.difficile as a complication of antibiotic therapy. Individuals at risk of infection include infants and young children, the elderly, travellers, the immunocompromised, and those with reduced gastric secretions (e.g. individuals using PPIs or with pernicious anaemia). Viral gastroenteritis is a common cause of diarrhoea and vomiting in young children.

32

What are the three mechanisms that bacteria can cause diarrhoea?

Bacteria cause diarrhoea by either:
- mucosal adherence (watery diarrhoea - e.g. Enteropathogenic E.coli, Enteroaggregative E.coli)
- mucosal invasion (bloody diarrhoea - e.g. Shigella, Campylobacter, Enteroinvasive E.coli)
- toxin production

Toxins can either be enterotoxic which causes fluid secretion without mucosal damage, or cytotoxic causing damage to the mucosa.

All three of these mechanisms produce either watery or bloody diarrhoea (called dysentery).

33

Does acute diarrhoea require investigation?

Most infectious causes of diarrhoea are self limiting. Routine stool examination for culture and microscopy for ova and parasites and stool testing for C.difficile toxin is not usually necessary other than in the following groups of patients:
- immunosuppressed patients with IBD (to distinguish a flare from infection)
- certain employees such as food handlers
- bloody diarrhoea
- persistant diarrhoea (>7 days, possible Giardia, Cryptosporidium)
- severe symptoms (fever, volume depletion) or recent antibiotic treatment or hospitalisation

34

How are patients with acute diarrhoea managed?

Management of patients with acute diarrhoea includes adequate hydration and antimotility agents such as loperamide (other than those with bloody diarrhoea or fever). Antibiotic therapy is not given in most cases since the illness is usually self limiting. Antibiotics are avoided in patients with suspected or proven enterohaemorrhagic E.coli infection as they may increase the risk of haemolytic uraemic syndrome. Empiric antibiotic therapy - e.g. ciprofloxacin and metronidazole - is given to patients with severe symptoms or bloody diarrhoea, pending the results of stool testing.

35

What agents typically cause acute food poisoning?

Staphylococcus aureus
Bacillus cereus
Clostridium perfringens

36

What is the typical history of staphylococcal food poisoning?

Severe nausea and vomiting develop after 1-6 hours. Diarrhoea may not be marked. There is a short incubation period and cases usually resolve within 24 hours. Diagnosis is clinical. Mainstay of treatment is anti-emetics and rehydration. Public health authorities should be notified if the source is a street vendor.

37

What two types of illness are seen with bacillus infection?

Bacillus cereus causes:
- vomiting within 6 hours, stereotypically due to rice and ingestion of preformed enterotoxins produced during storage
- diarrhoeal illness occurring after 6 hours due to ingestion of viable organisms, leading to a longer incubation period

The disease is self limiting and management in both cases is with supportive therapy.

38

How does clostridium perfringens cause illness?

Spores of C.perfringens are widespread in the guts of large animals and in soil. In anerobic conditions, C.perfringens spores in incompletely cooked contaminated germinate and viable organisms multiple. Subsequent reheating of food causes heat shock sporulation of the organisms, during which they release an enterotoxin. Symptoms (diarrhoea and cramps) occur 6-12 hours following ingestion.

"Point source" outbreaks, in which a small number of cases all become symptomatic following ingestion, classically occur after school or canteen lunches where meat stews are served.

39

What is the typical history associated with Campylobacter infection?

A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody. Campylobacter jejuni is a zoonoses carried in the gut of cattle and poultry. The most common source of infection is chicken. Most adult infections last 5-7 days and are self limiting. Between 10-20% have prolonged symptoms and need treatment with antibiotics such as erythromycin, as ciprofloxacin resistance is common.

GBS is one of the recognised complications.

40

What are the two distinct clinical infections produced by Salmonella spp?

1) Serotypes S.typhi and S.paratyphi A, B and C have a purely human reservoir and produce the septicaemic illness "enteric fever"

2) Other Salmonella serotypes are subdivided into five distinct subgroups that produce gastroenteritis, of which S.enteritidis and S.typhimurium are the most important

Transmission is by contaminated water or food, particularly poultry and egg products. The incubation period is 12-72 hours and the predominant feature is diarrhoea, sometimes containing blood. Reactive arthritis occurs in 2%. Antibiotics are not indicated unless there is bacteraemia, which is a CLEAR indication for antibiotic therapy, as Salmonella are notorious for persistent infection and for colonising endothelial surfaces.

41

What are the 5 clinico-pathological patterns of disease seen in E.coli infection?

E.coli is a major member of the enterobacteriaceae. The 5 subtypes all cause diarrhoea and are:
1) Enterotoxigenic E.coli (ETEC)
2) Enteroinvasive E.coli (EIEC)
3) Enteropathogenic E.coli (EPEC)
4) Enteroaggregative E.coli (EAEC)
5) Enterohaemorrhagic E.coli (EHEC)

42

What clinical condition does Enterotoxigenic E.coli cause (ETEC)?

These cause most cases of travellers diarrhoea in developing countries, although other causes are possible. The organism produces an enterotoxin causing fluid secretion without mucosal damage. This leads to marked secretory diarrhoea and vomiting after 1-2 days incubation. Ciprofloxacin has been used to limit the duration of symptoms but benefit is unproven.

43

What are the symptoms of Enteroinvasive E.coli (EIEC)?

Enteroinvasive E.coli penetrates and damages the intestinal mucosa. It produces an illness very similar to Shigella dysentery. No enterotoxin is produced. Acute watery and bloody diarrhoea are common. Symptoms are rarely severe and usually self limiting.

44

What is Enteropathogenic E.coli (EPEC)?

These are very important in infant diarrhoea. They attach to gut mucosa which causes destruction of microvilli and disruption of normal absorptive capacity. The symptoms vary from mild non bloody diarrhoea to quite severe illness.

45

What are the symptoms of Enteroaggregative E.coli (EAEC)?

These strains adhere to the mucosa and produce a locally active enterotoxin. A "stacked brick" aggregation is seen in the small bowel. They have been associated with prolonged diarrhoea in children in South America, South-east Asia and India.

46

What are the clinical features of Enterohaemorrhagic E.coli (EHEC) infection?

Initial watery diarrhoea becomes frankly and uniformly blood-stained in 70% of cases and is associated with severe and often constant abdominal pain. There is little systemic upset, vomiting or fever. Enterotoxins, if produced, have both a local effect on the bowel and a distant effect on particular body tissues such as glomerular apparatus, heart and brain. The potentially life-threatening haemolytic uraemic syndrome (HUS) occurs in 10–15% of sufferers from this infection, arising 5–7 days after the onset of symptoms. It is most likely at the extremes of age, is heralded by a high peripheral leucocyte count and may be induced, particularly in children, by antibiotic therapy. HUS is treated by dialysis if necessary and may be averted by active intervention with processes such as plasma exchange.

47

What toxin is produced by EHEC?

A number of distinct ‘O’ sero- types of E. coli produce two distinct enterotoxins (verocytotoxin), which are identical to toxins produced by Shigella (‘shiga toxins 1 and 2’). E. coli O157:H7 is perhaps the best known of these verocy- totoxigenic E. coli (VTEC), but others, including types O126 and O11, are also implicated.

48

What does C.difficile infection cause?

C.difficile is responsible for some cases of antibiotic related diarrhoea and nearly all cases of pseudomembranous colitis. It may also induce a relapse in patients with IBD.

49

What is the pathology of C.difficile infection?

C.difficile can be cultured from the stool of 3% of healthy adults and about one third of hospital in patients. Most colonised patients remain asymptomatic. Clinical disease develops when the normal colonic flora is altered, usually by antibiotics, and creates an environment where C.difficile can thrive. Infection with toxigenic strains of C.difficile causes colonic inflammation and diarrhoea by secretion of toxins A and B, which induces expression of cytokines such as IL-8 in intestinal epithelial cells, causes loss of barrier function and causes cell death by apoptosis. There is focal epithelial ulceration and an inflammatory exudate that appears as a pseudomembrane on endoscopic examination. The clinical picture varies from mild diarrhoea, to life-threatening severe disease with profuse diarrhoea, abdominal pain and toxic megacolon.

50

How is C.difficile infection diagnosed?

Demonstration of toxins A/B in stool samples or the characteristic appearance of pseudomembranes at endoscopy. A raised WCC is characteristic.

51

How is acute C.difficile infection managed?

Management is to prevent cross infection (isolate hospitalised patients in a side room, barrier nursing) stop offending antibiotics where possible and treat with oral metronidazole (500mg TDS) for 10-14 days. Vacomycin is given for severe disease. Recurrent disease (relapse of diarrhoea after initial resolution of infection) occurs in 15-30% of cases and is usually treated with pulsed tapering doses of vancomycin.

52

How should refractory cases of C.difficile infection be treated?

Treatment options for refractory disease, particularly if severe, are escalating doses of oral vancomycin, or vancomycin and metronidazole IV together. Rifampicin and IVIg (400mg/kg) or occasionally colectomy, but post operative mortality is high.

53

How is C.difficile infection prevented?

Prevention is by preventing cross infection and reducing overprescribing and inappropriate antibiotic use. Clindamycin is historically associated with causing Clostridium difficile but the aetiology has evolved significantly over the past 10 years. Second and third generation cephalosporins are now the leading cause of Clostridium difficile.

54

What is travellers diarrhoea?

This is one of the most common illnesses in people who travel internationally and affects 20-50% of patients depending on the destination. The risk is highest in people travelling to areas with poor food and water hygiene.

55

What are the clinical features of travellers diarrhoea?

There is diarrhoea (with or without blood), abdominal cramps, fever, nausea and vomiting which usually resolves without treatment over several days. A prolonged illness lasting weeks or more is likely to be caused by protozoan parasites.

56

How is travellers diarrhoea prevented?

To reduce the risk of infection, travellers are advised to drink bottled water, peel fruit before eating it and avoid salads because the ingredients my have been washed in contaminated water. Antibiotic prophylaxis with ciprofloxacin is not indicated for most travellers but is given when a trip is vital or when an underlying medical illness would be compromised by diarrhoea - e.g. ileostomy, immunosuppression, and chronic kidney disease.

57

How is travellers diarrhoea treated?

Treatment of travellers diarrhoea is symptomatic with rehydration and antidirrahoeal agents - e.g. loperamide. Empirical antibiotics are given to patients with moderate to severe symptoms (fever, tenesmus, bloody diarrhoea) after obtaining a stool sample.

Fluoroquinolones (e.g. oral ciprofloxacin 500mg BD for 1-3 days) are used in most cases. Rifaximin (a poorly absorbed derivative of rifamycin) is used where E.coli predominates and azithromycin is increasingly used due to emergence of fluorquinolone resist Campylobacter.

58

What is the most common cause of travellers diarrhoea?

Bacteria account for 70-90% of cases and E.coli (enterotoxigenic) is the most common organism.

59

What is Yersinia enterocolitica?

This organism found commonly in pork, causes mild to moderate gastroenteritis and can produce significant mesenteric adenitis after an incubation period of 3-7 days. It predominantly causes disease in children but adults may also be affected. The illness resolves slowly, with 10-30% of cases complicated by persistent arthritis or Reiter's syndrome.

60

What is Amoebiasis?

Amoebiasis is caused by the protozoal organism Entamoeba histolytica. Infection occurs world wide, although much higher incidence rates are found in the tropics and sub tropics. Transmission of infection is by ingestion of cysts in contaminated food and water or spread directly by person to person contact.

61

What are the clinical features of amoebiasis?

1) Intestinal amoebiasis (amoebic dysentery) E. histolytica invades the colonic epithelium leading to tissue necrosis and ulceration. Ulceration may deepen and progress under the mucosa to form typical flask like ulcers. The presentation varies from mild blood diarrhoea to fulminating colitis, with the risk of toxic dilatation, perforation and peritonitis. An amoeboma (inflammatory fibrotic mass) may develop, commonly in the caecum or rectosigmoid junction which may bleed, cause obstruction or intussusception, or be mistaken for carcinoma.

2) Amoebic liver abscess - an amoebic liver abscess (often single and in right lobe of the liver) develops when organisms invade through the bowel serosa, enter the portal vein and pass into the liver. There is tender hepatomegaly, a high swinging fever and profound malaise. There may not be a history of colitis

62

What is the differential diagnosis of amoebiasis?

Amoebic colitis must be differentiated from other causes of bloody diarrhoea: IBD, bacillary dysentery, E.coli, Campylobacter sp, Salmonellae and rarely pseudomembranous colitis. Amoebic liver abscesses must be differentiated from pyogenic abscess and/or hydatid cyst.

63

How is amoebiasis managed?

Colitis - oral metronidazole for 5 days followed by luminal amoebicide such as diloxanide furoate to the clear the bowel of parasites

Liver abscess - metronidazole for 5 days. A large tense abscess may require percutaneous drainage under ultrasound guidance

64

What is Shigellosis?

Shigellosis is an acute self limiting intestinal infection which occurs worldwide but is more common in tropical countries and areas of poor hygiene. Transmission is by the faecal oral route.

The four Shigella species invade and damage the intestinal mucosa. Some strains of S.dysenteriae secrete a cytotoxin which results in diarrhoea. Differential diagnosis is from other causes of bloody diarrhoea. Sigmoidoscopic appearance may be the same as IBD. Ciprofloxacin 500mg BD is the treatment of choice.

65

What causes cholera? How is it transmitted?

Cholera is caused by the gram negative bacillus, Vibrio cholerae. Infection is common in tropical and subtropical countries and in areas of poor hygiene. Infection is by the faecal oral route and spread is predominantly by ingestion of water contaminated with the faeces of infected individuals. There is no identified animal reservoir.

66

What is the pathology of cholera infection?

Following attachment to and colonization of the small intestinal epithelium, V.cholerae produces its major virulence factor, cholera toxin. The toxin binds to the enterocyte surface receptor which in turn activates cAMP. The increase in cAMP activates intermediaries which then act on the apical membrane causing chloride ion secretion (with water) and inhibition of sodium and chloride absorption. This produces massive secretion of isotonic fluid into the intestinal lumen.

Cholera toxin also increases serotonin release from enterochromaffin cells in the gut, which contributes to the secretory activity and diarrhoea. Profuse watery diarrhoea ("rice water diarrhoea") may result in dehydration, hypotension and death.

67

How is cholera managed?

Management aims at effective rehydration which is mainly oral. Intravenous fluids are given in severe cases. The mechanism of action of oral rehydration solutions (ORS) depends on the fact that there is glucose dependent sodium absorption mechanism not related to cAMP and thus unaffected by the toxin. The WHO ORS contain sodium (75 mmol/L) and glucose (75 mmol/L) along with potassium, chloride and citrate. Single dose azithromycin 1g helps to eradicate infection, decrease stool output and shorten the duration of illness.

68

What causes Giardiasis?

Giardia intestinalis is a flagellated protozoan that is found world wide but is more common in developing countries. It causes travellers diarrhoea and may cause prolonged symptoms.

69

What are the clinical features of giardiasis?

The clinical features are the result of damage to the small intestine mucosa, with subtotal villous atrophy in severe cases. There is diarrhoea, nausea, abdominal pain and distension with malabsorption and steatorrhoea in some cases. Repeated infections can result in growth retardation in children.

70

How is giardiasis investigated?

Treatment is often given based on clinical suspicion. If necessary, the diagnosis is made by finding cysts on stool examination (but negative stools does not exclude the diagnosis) or parasites on duodenal aspirates or biopsies.

71

How is giardiasis treated?

Metronidazole 2g as a single dose daily for 3 days will cure most infections; some patients need two or three courses. Alternative drugs include tinidazole, mepacrine and albendazole.

72

Under what circumstances can a patient develop intestinal tuberculosis?

This results from reactivation of primary tuberculosis caused by Mycobacterium tuberculosis. In developed countries it is most commonly seen in ethnic minority groups or patients who are immunocompromised due to HIV infection or drugs. The ileocaecal valve is most commonly affected.

73

What are the clinical features of intestinal tuberculosis?

There is abdominal pain, diarrhoea, anorexia, weight loss and fever. A mass may be palpable. Presentation can be similar to Crohn's.

74

How is intestinal TB diagnosed?

Imaging - CXR shows evidence of pulmonary tuberculosis in 50% of cases. The small bowel follow through may show features similar to Crohn's disease. US or CT shows mesenteric thickening and lymphadenopathy.

Histology - and culture of the tissue is desirable but not always possible and treatment is started if there is a high degree of suspicion.

75

How is intestinal TB treated?

Management is the same as pulmonary involvement but given for 1 year.

76

What is protein losing enteropathy?

Increased protein loss across an abnormal intestinal mucosa occasionally leads to hypoalbuminaemia and oedema. Causes include Crohn's disease, Menetrier's disease (thickening and enlargement of gastric folds) coeliac disease and lymphatic disorders (e.g. lymphangiectasia).

77

What is Meckel's diverticulum?

A diverticulum projects from the wall of the ileum approximately 60cm from the ileocaecal valve. About 50% contain gastric mucosa which secretes acid, and peptic ulceration may occur. Presentation is with lower gastrointestinal bleeding, perforation, inflammation (presents similar to appendicits) or with obstruction (due to associated band). Treatment is surgical removal.

78

When does intestinal ischaemia occur?

Ischaemia is usually due to reduced blood inflow as a result of atheroma, embolism (e.g. AF) vasculitis, or profound and prolonged shock. It presents acutely with severe abdominal pain but often little to find on abdominal examination. Surgery is necessary to resect the gangrenous bowel and the mortality rate is high. It may also present chronically with post prandial abdominal pain and weight loss. Diagnosis is made by angiography.

79

How do tumours of the small intestine present?

These are rare and present with abdominal pain, diarrhoea, anorexia, and anaemia. Carcinoid tumours have additional clinical features.

80

What is the most common malignant tumour of the small intestine?

Adenocarcinoma accounts for 50% of malignant tumours of the small intestine; there is an increased incidence in coeliac disease and Crohn's disease. Non Hodgkin lymphoma constitutes 15% of malignant bowel tumours and may be B or T cell in origin. The latter occur with increased frequency in coeliac disease. Treatment is surgical excision with or without chemo and radio therapy.

81

What are the most important types of benign small bowel tumour?

1) Peutz-Jeghers syndrome
- autosomal dominant condition
- mucocutaneous pigmentation (circumoral, hands and feet) and hamartomatous gastrointestinal polyps
- polyps can occur anywhere but most common in small bowel
- may bleed or cause intussusception and may undergo malignant change

2) Adenomas, leiomyomas and lipomas are rare
3) FAP

82

What are carcinoid tumours? What is the definition of carcinoid syndrome?

These originate from enterochromaffin cells (serotonin producing) of the intestine. Carcinoid syndrome is the term applied to the symptoms that arise as a result of serotonin, kinins, histamine and prostaglandins, released into the circulation by the tumour.

83

What are the clinical features of carcinoid tumours?

Patients with gastrointestinal carcinoid tumours have the carcinoid syndrome only if they have liver metastases. Tumour products are then able to drain directly into the hepatic vein (without being metabolised by the liver) and into the systemic circulation, where they cause flushing, wheezing, diarrhoea, abdominal pain and right sided cardiac valvulvar fibrosis causing stenosis and regurgitation.

84

How are carcinoid tumours investigated?

A high level of 5-hydroxyindoleacetic acid (5-HIAA), the breakdown product of serotonin, is found in the urine in the carcinoid syndrome. A liver ultrasound confirms the presence of metastases.

85

How is carcinoid syndrome managed?

Treatment of the carcinoid syndrome is symptomatic and aimed at:
- inhibition of tumour products with somatostatin analogue, octreotide, or with 5-HT antagonists e.g. cyproheptadine

- reducing tumour size through surgical resection, hepatic artery embolization, radiofrequency ablation or chemotherapy

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What is Meckel's diverticulum?

Meckel's diverticulum is a vitelline duct remnant.
It is a true diverticulum (all layers present)
Mnemonic, rule of "2s" - 2 inches long, 2 feet from the ileocaecal valve, 2% of the population, 2% symptomatic

It contains pancreatic rests and heterotropic gastric mucosa. This increases the risk of bleeding.

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What are the clinical features of Meckel's diverticulum?

1) Newborn finding
- faecal material in umbilical area due to persistence of vitelline duct

2) Bleeding (most common finding)
- common cause of iron deficiency in newborns and young children
- symptoms usually arise during the first and second year of life

3) Diverticulitis
- clinically impossible to distinguish Meckel's diverticulitis from appendicitis

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How is Meckel's diverticulum diagnosed?

Tc99 nuclear scan identifies parietal cells in ectopic gastric mucosa. Treatment is surgery.

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What is a small bowel pulsion diverticula?

Duodenum is the most common site
- wide mouthed diverticula suggests systemic sclerosis.

Complications include:
- diverticulitis (danger of perforation)
- bacterial overgrowth (may produce bile salt deficiency and vitamin B12 deficiency)

Decks in Year 4 - SPM Class (129):