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Block 15 > Inflammation Of The Bowel > Flashcards

Inflammation Of The Bowel Flashcards

1
Q

What are the functions of the small intestine?

A

Enzymatic digestion, absorption of nutrients
Duodenum – iron
Jejunum – sugars, amino acids, fatty acids
Ileum – vitamin B12, bile salts

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2
Q

What is the histology/important cells of the small intestine?

A 
Columnar epithelium 
Endocrine cells
Paneth cells
Intraepithelial lymphocytes 
Brunner's gland 
Lymphoid tissue (GALT)
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3
Q

Describe the columnar epithelium of the small intestine

A

goblet cells, enterocytes (absorptive cells), brush border (increasing surface area for absorption of nutrients)

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4
Q

Describe the endocrine cels in the small intestine?

A

amongst columnar epithelial cells, within crypts, elaborate gut hormones and aid motility

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5
Q

Describe the paneth cells of the small intestine?

A

base or crypts, contain eosinophilic lysozyme-rich granules, possible role in regulating cell proliferation and differentiation

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6
Q

What are the intraepithelial lymphocytes?

A

less than 20 per 100 enterocytes, villous tips < base

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7
Q

What are the brunner’s gland of the small intestine?

A

duodenal submucosal glands producing alkaline mucous secretions, also rich is epidermal growth factor, encouraging mucosal regeneration after injury

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8
Q

Describe the lymphoid tissue (GALT) in the small intestine?

A

dense aggregates in terminal ileum (Peyer’s patches), important in immunity, predominantly T suppressor cells maintaining tolerance to food antigens

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9
Q

What are the functions of the large intestine?

A

Storage and elimination of food residues
Maintaining fluid and electrolyte balance
Bacterial degradation of complex carbohydrates and other nutrients

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10
Q

Describe the histology of the large intestine?

A 
Mucosa
Basement membrane 
Lamina propria 
Muscularis mucosae 
Submucosa 
Muscularis propria 
Subserosa 
Serosa
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11
Q

Describe the mucosa of the large intestine?

A

Smooth surface
Crypts – tubular, regular spacing o Epithelium
• Goblet cells – apical mucin
• Absorptive colonocytes – principle cell, responsible for ion and water
transportation, eosinophilic cytoplasm with minimal mucin, striate border on
apical surfaces, mucosal immunity
• Endocrine cells – confined to crypts, inverse polarity, peptide hormones e.g.
serotonin and neurotensin (right), enteroglucagon/glicentin (distal colon and
rectum)
• Paneth cells – eosinophilic apical granules, innate immunity, physiological
features of right colon, pathological manifestation of metaplasia

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12
Q

Describe the lamina propria of the large intestines?

A

Fibroblast
Myofibroblasts
Inflammatory cells

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13
Q

Describe the muscularis mucosae of the large intestine

A

thin layer of muscle transversed by various vessels, lymphatics and nerves

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14
Q

Describe the submucosa of the large intestine?

A

collagen, smooth muscle, adipose tissue, blood vessels, lymphatics and cells of enteric nervous system (Meissner’s and Henle’s), regulates gut motility via interstitial cells of Cajal and ganglia

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15
Q

Describe the muscularis propria of the large intestine?

A

Third plexus (Auerbachs)

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16
Q

Describe the subserosa of the large intestine

A

outside muscle coat, comprise fat with blood vessels and lymph nodes

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17
Q

Describe the Serosa of the large intestine

A

Shiny layer or peritoneum

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18
Q

What is coeliacs disease

A

immunologically mediated inflammatory disorder due to intolerance in genetically susceptible individuals of ‘gluten’q

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19
Q

Describe the epidemiology of coeliacs disease?

A

Commonly presents in childhood, but minority diagnosed in adults and elderly
Affects 1 in 2000 individuals in UK, but 1 in 300 in Ireland
Increasingly recognised in East, possibly due to introduction of wheat into diet, and
increasing trend of autoimmune diseases
Female > Male (2:1)

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20
Q

Describe the pathophysiology of coeliacs disease?

A

Strong association with HLA-DQ2 in 90% (remainder HLA-DQ8)
Combination of genetic susceptibility and sensitivity to gliadin may be triggered by other
factors e.g. viral infection
Gliadin thought to be toxic component where it effects an immune response resulting in
increased intraepithelial T-cell lymphocytes

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21
Q

Describe the presentation f coeliac disease

A 
Malabsorption
Classical
o Weight loss
o Chronic diarrhoea
o Failure to thrive (children)
Non-classical
o Irritable bowel syndrome type symptoms o Abdominal pain
o Altered bowel habit
o Anaemia (iron deficiency)
22
Q

Describe the serology of coeliac disease?

A 
Tissue transglutaminase (tTG) antibody – first line test due to high sensitivity and negative predictive value, if this is elevated the patient will then an endoscopy to confirm diagnosis and assess response to gluten in the diet
Endomysial antibody (EMA) – labour intensive
Deaminated gliadin peptide (DGP) antibody – recently introduced but less inferior to tTG assays and not recommended
23
Q

Describe the histology in coeliacs disease?

A

Blunting and atrophy of mucosa
Crypt hyperplasia (more crypts)
Increased intraepithelial T-lymphocytes (more than 20 per 100 enterocytes, and increased
numbers around villous tips - loss of decrescendo pattern) = damaged epithelial cells may
produce tumour necrosis factors-alpha, which attracts more intraepithelial lymphocytes
Increased lamina propria chronic inflammatory cells

24
Q

What are the complications due to coeliacs disease?

A

Malabsorption due to
o Mucosal damage, reduced surface area
o Immature enterocytes incapable of normal absorption
o Disaccharide deficiency
o Reduction in hormone production
Lymphoma – enteropathy-associated T-cell lymphoma (EATL)
o 4-fold risk of developing non-Hodgkin lymphoma compared to general population

25
Q

What drugs can affect the GI tract

A

NSAIDs – non-selective COX inhibitors e.g. indomethacin > specific COX-2 inhibitors
65% on long term use develop ulcers, erosions, usually distal ileum and duodenum, right
colon
Complications: perforations, focal active colitis, chronic NSAID enteropathy - ‘diaphragm
disease’, usually affect ileum, suppositories - localised proctitis, ulceration, strictures

26
Q

What is COX1

A

constitutive (continuously stimulated by body), produces prostaglandin for basic house-keeping purposes, stimulate normal body functions such as stomach mucous
production, regulation of gastric acid and kidney water excretion

27
Q

What is COX2

A

induced (not normally present in cells), produces prostaglandins for inflammatory response, used for signalling pain and inflammation

28
Q

Describe pseudomembranus colitis?

A

Complex ecosystem of microbes act as a natural barrier against colonisation by enteropathogens
• broad spectrum antibiotics develop diarrhoea(antibiotic-associated colitis)
• Iatrogenic disease caused by Clostridium difficle and its associated toxins resulting in fulminant colitis, profuse diarrhoea, dehydration and in some debilitated patients, death
o C. difficle – spore-forming Gr+ anaerobe
o 2 toxins – A and B detected in faeces
o Primarily colonic, but may be accompanying ileitis, in immunosuppressed individuals o 25% all antibiotic-associated diarrhoea
o Histologically, ‘volcano’-like eruption of mucus, epithelial cells, neutrophils and fibrin on surface = pseudomembrane

29
Q

What is the most common surgical emergency?
What is this condition caused by?
What are the complications?

A

Appendicitis
Inflammation due to obstruction by faecoliths, food residues, lymphoid hyperplasia (children, viral infections), diverticulosis and neoplasia (carcinoid). Other aetiology: specific infections (Yersinia, tuberculosis), inflammatory bowel disease
Complications
o Abscess formation
o Extensive necrosis (gangrenous)
o Perforation
o Spread of suppurative inflammation (liver) o Septicaemia

30
Q

What is diverticular disease?
What causes it?
What are the symptoms?
What are the complications?

A

Common condition causing considerable morbidity in Western countries
Due to high intraluminal pressure causing
o Hypertrophy of muscular layers
o Herniation of mucosa through area of weakness (where vessels enter into mucosa) -
protrusion of diverticula which can be obstructed by faecoliths etc.
Can occur anywhere in intestinal tract, sigmoid commonest site
Abdominal pain, altered bowel habit, bleeding
Complications
o Diverticulitis – inflammation of diverticula
o Pericolic abscess
o Perforation
o Fistula – communication between 2 organs

31
Q

What is diverticulitis colitis/diverticulosis associated colitis?

A

Mucosal inflammation limited to segment affected by diverticulosis
Mucosa proximal and distal (rectum) normal
Histologically, inflammation confined to mucosa with crypt architectural changes, but can be
transmural with lymphoid aggregates and fistula formation – mimicking inflammatory bowel disease

32
Q

What is infective enterocolitis?

A

Acute GI infection is major cause of morbidity throughout the world with viruses playing a leading role, and small intestine is usually main site
Tuberculosis and Yersiniosis – affects terminal ileum/caecum, chronic granulomatous inflammation and endoscopically and histologically mimics Chron’s disease

33
Q

What is chronic inflammatory bowel disease (CIBD)?

A

chronic relapsing condition encompassing Crohn’s disease and ulcerative colitis

34
Q

What is Crohn’s disease?

A

Proposed genetic defect that prevents a controlled and effective immune response to causative agent
Support for genetic role from twin study: 44-70% monozygous twins had Crohn’s compared to 4% in dizygous twins
HLA-DR1 and DQw5
Frequency of involvement
o Small intestines – 33% o Ileocolic – 45%
o Large intestines – 20%

35
Q

Describe the epidemiology of Crohn’s disease?

A

Higher incidence in northern Europe and US
Incidence varies from 4-65 per 100,000 population
Bimodal incidence (2 peaks): 20-30yrs and 60-70yrs, can occur in children
Becoming more prevalent than ulcerative colitis
Incidence rising in Asia

36
Q

Describe the aetiology of Crohn’s disease?

A

Cigarette smoking increases risk in genetically susceptible individuals
Microvascular infarction – oral contraceptive pill (procoagulant)
Triggers appear to be infective agents – e.g. mycobacteria, measles virus

37
Q

Describe the presentation of Crohn’s disease?

A

Depends on disease location
o Colon: bloody diarrhoea
o Upper GI/small intestine: severe abdominal pain, vomiting, weight loss, small intestinal obstruction due to strictures
o Perianal: ulcers, fissures, perianal abscess, fistula

38
Q

Describe the macroscopic appearance of Crohn’s disease

A

Serosal fat wrapping
‘Cobblestone’ – transverse ulcers intersecting oedematous mucosa
Serpiginous ulcers – longitudinal

39
Q

Describe the microscopic appearance of Crohn’s disease?

A

Flat surface
Crypt architecture often preserved
Ulcer, patchy activity (cryptitis and crypt abscess o Plasma cell-rich infiltrate
Granuloma
Resection shows
• Fissuring ulcers
• Transmural chronic inflammation (affects all layers of wall) with lymphoid
aggregates along muscular coat
• Muscular hypertrophy and neural hyperplasia
• Pyloric metaplasia – response to chronic inflammation/injury
• Granuloma – collection of macrophages

40
Q

What are the indications for surgery with Crohn’s disease?

A

Complications of disease process - e.g. fistula, strictures, intra-abdominal abscess, perforation
Main principle of surgery is to preserve bowel length, avoiding short bowel syndrome and intestinal failure

41
Q

What are the complications of Crohn’s disease?

A

Malabsorption – short loop/bowel syndrome
Fistula formation
Anal lesions (60%) – fissures, fistula
Perforation, haemorrhage, toxic dilation not as frequent as ulcerative colitis
Increased risk of malignancy of small intestine but less frequent than UC

42
Q

What is ulcerative colitis?

A

Always begins in rectum
Can remain limited to rectum (ulcerative proctitis)
Extends proximally to a variable length, or involve the entire large intestine (pancolitis) in a
continuous manner
Changes always most severe distally
Primarily affects mucosa, but in severe disease, deeper layers can be involved - fulminant
colitis (toxic megacolon)

43
Q

Describe the epidemiology of ulcerative colitis?

A

Peak incidence -3rd decade
Can present in very young children or elderly
Anglo-Saxon individuals – North America, North Western Europe, New Zealand, Scandinavia
– approx. 100 per 100,000 population

44
Q

What is the aetiology of ulcerative colitis?

A

Inappropriate immune response to an unknown environmental stimulus in the colon
Unknown cause – infection, diet, environmental factors, primary immunological
defects, abnormalities in mucin, genetic disorders, psychomotor disorder
Appendicectomy may be protective, delay onset, producing a milder form
Smoking appears to be preventive – could be linked to increased glycoprotein synthesis
maintaining protective mucosal barrier
QNSAIDs known to reactivate CIBD, especially UC, and in some patients, implicated in
initiating UC

45
Q

What is the macroscopic appearance of ulcerative colitis?

A

Length may be shortened, reduction in transverse calibre – increase in sarcorectal
distance radiologically
Normal serosa except in toxic megacolon
Granular/valvety friable surface
Ulcers – flasked-shaped, or undermining
Polyps (inflammatory - granulation tissue) vs pseudopolyps (mucosal islands)

46
Q

What is the microscopic appearance of ulcerative colitis?

A

Irregular surface
Diffuse crypt architectural distortion
Diffuse chronic inflammatory cell infiltrate, rich in plasma cells

47
Q

What are the indications for surgery in ulcerative colitis?

A

Resistance to medical therapy or dependence on unacceptable levels of therapy (majority of the patients on immunosuppression to dampen the body’s immune response)
Severe disease
Complications – dysplasia (unregulated cell proliferation), carcinoma

48
Q

What are the extra-intestinal manifestations of inflammatory bowel disease?

A

-Liver pathology – incidence depends on severity and extent of colitis, but significant liver problems in 5-8%
-Coincidental – fatty change (nutritional and absorptive problems), cholelithiasis (CD>UC)
-Primary sclerosing cholangitis – disease of biliary tract, most commonly seen with pancolitis
(ulcerative colitis)
o 1-5% of patients with IBD have PSC
o 50-75% of patients with PSC have IBD
-Skin – pyoderma gangrenosum, erythema nodosum
-Eyes – iritis, uveitis, episcleritis
-Joints – ankylosing spondylitis

49
Q

What is the incidence and age of onset for ulcerative colitis

A

11/100000

15-30 and 60-80

50
Q

What is the incidence and age of onset of Crohn’s disease?

A

7/100000

15-30 and 60-80

51
Q

What is the male female ratio for

  1. Ulcerative colitis
  2. Crohn’s disease
A
  1. 1:1

2. 1.8: 1

52
Q

What affect can smoking, appendectomy and the oral contraceptive have on ulcerative colitis and Crohn’s disease?

A

smoking-Prevent disease in ulcerative colitis and may cause it in crohns
Appendectomy may be protective in ulcerative colitis
Oral contraceptive relative risk of 1.9 in Crohn’s

Block 15 (11 decks)

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