Inflammation of the GI tract Flashcards

(47 cards)

1
Q

What are the causes of mucosal injury?

A

-GI tract secretions
=Acid and pepsin in stomach
=Biliary and pancreatic secretions
-Ischaemia
-Drugs
=NSAIDs, antibiotics, steroids
=Chemotherapy (5-fluorouracil)
-Immunological
=Coeliac disease
-Infections
=Helicobacter, Salmonella, Shigella, E. Coli, C. difficle, CMV
-Radiation (rectal inflammation following radiotherapy for prostate cancer)
-Trauma (complications of endoscopic procedures)
-Idiopathic (ulcerative colitis and Crohn’s disease)

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2
Q

Describe the manifestations of mucosal injury

A
  • Inflammation
  • Apoptosis (drugs, graft versus host disease in bone marrow transplantation, HIV) or necrosis (ischaemia, infections)
  • Erosion and ulceration
  • Hypoplasia and atrophy
  • Hyperplasia
  • Metaplasia
  • Dysplasia and or neoplasia
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3
Q

What is the classification system for Gastritis?

A
  • Sydney System= endoscopic features, histology and aetiology to classify gastritis
  • Acute gastritis
  • Chronic gastritis
  • Special forms of chronic gastritis
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4
Q

Describe acute gastritis

A

-Acute gastritis
=Acute erosive/ haemorrhagic gastritis (ingestion of irritant chemicals/ acute H.pylori infection- usually no or minor symptoms so not seen in biopsy)

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5
Q

Describe chronic gastritis

A

-Chronic gastritis
=Non-atrophic gastritis (chronic H.pylori infection)
=Atrophic gastritis (autoimmune gastritis- antibodies against parietal cells detected in blood, loss of intrinsic factor secretion for B12 absorption= megaloblastic anaemia, chronic H.pylori infection)
=Loss of acid-secreting parietal cells and pepsin-secreting cells in mucosa
=Metaplasia and neuroendocrine cell hyperplasia- corkscrew glands (elongated)

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6
Q

Describe special forms of chronic gastritis

A

-Special forms of chronic gastritis (based on aetiology)
=Chemical gastritis (bile reflux, NSAIDs)
=Radiation
=Lymphocytic (coeliac association)
=Non-infectious granulomatous (Crohn’s, sarcoidosis)
=Eosinophilic (food sensitives- Type 1, reaction to parasitic infection)
=Other infectious gastritis (non-H.pylori) - bacteria, viruses (CMV), fungi, parasites

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7
Q

Describe the histology of chronic H.pylori infection

A
  • Chronic inflammation within lamina propria= lymphocytes and plasma cells
  • Ongoing acute inflammation in petitis= neutrophil infiltrating epithelium of gastric pits
  • Biopsies taken for patients taking PPIs
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8
Q

What is the hallmark of intestinal metaplasia?

A

-Presence of goblet cells (large pale staining cells containing mucin vacuoles)

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9
Q

Describe coeliac disease

A
  • Gluten-sensitive enteropathy
  • Hypersensitivity to glutamine rich proteins in wheat, barley and rye (gliadins, hordeins and secalins)
  • UK prevalence 1 in 300
  • Strong link to certain HLA class 2 genes that code for MHC class 2 in antigen presenting cells (HLA-DQ2 and HLA-DQ8)
  • Leads to malabsorption
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10
Q

How is coeliac disease diagnosed?

A
  • Combination of histology (duodenum), serology (auto-antibodies in blood) and response to gluten-free diet
  • Often picked up in asymptomatic individuals on routine haematology (iron deficiency anaemia, consequence of malabsorption)
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11
Q

What other conditions are associated with coeliac?

A
  • Endocrine (type 1 diabetes, thyroid disorders)
  • Liver (primary biliary sclerosis and autoimmune hepatitis)
  • Skin (dermatitis herpetiformis)- often presented first
  • Neurological
  • Cardiac
  • Others
  • 30 x increased risk of small bowel adenocarcinoma, 20 x increased risk of enteropathy associated T-cell lymphoma
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12
Q

Describe the histology of coeliac disease

A
  • Variable villous atrophy (complete or partial loss)
  • Chronic inflammation in lamina propria
  • Increased CD8+ cytotoxic T-lymphocytes in epithelium
  • Epithelial damage
  • Crypt hyperplasia (attempt regeneration and repair)
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13
Q

Which bacterial infections can be diagnosed with a biopsy (visible/ pattern of injury)?

A
  • H.pylori
  • Shigella
  • Salmonella
  • Campylobacter jejuni
  • E.coli (0157)
  • Clostridium difficile (=pseudomembranous colitis)
  • Vibrio cholera
  • Mycobacterium tuberculosis
  • Atypical mycobacteria (MAI)
  • Yersinia enterocolitica (neutrophil rich granulomas)
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14
Q

What inclusion bodies (large quantities of viral protein) can be diagnosed with biopsies?

A
  • Rotaviruses
  • Enteric adenoviruses
  • Herpes viruses (HSV)
  • Cytomegalovirus (CMV)- big cell virus, immunosuppressant
  • HIV
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15
Q

What fungal infections can be diagnosed?

A
  • oesophageal
  • Candida
  • Histoplasmosis
  • Murcormycosis
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16
Q

What protozoal infections can be diagnosed?

A
  • Giardia lamblia (UK, duodenum)
  • Entamoeba histolytica (large organism, engulfed red blood cells, pinker staining)
  • Cyrptosporidia (opportunistic, immunocompromised)
  • Microsporidia
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17
Q

What helminths can be diagnosed?

A

Worms

  • Enterobius (pinworm/threadworm, routine appendiscectomy)
  • Ascaris
  • Tapeworms
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18
Q

Describe pseudomembranous colitis

A
  • Yellowish material= fibrin and pus erupting from dilated crypts (volcano lesions)
  • Clostridium difficile
  • Antibiotic associated
  • Mimicked by ischaemic colitis (localised and patchy)
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19
Q

What is inflammatory bowel disease?

A
  • Could in theory refer to any inflammatory disorder of the small and large intestine
  • Clinically= ulcerative colitis and Crohn’s disease
20
Q

Describe the aetiology of IBD

A

-Idiopathic
-Inherited susceptibility
=Family member with IBD= greatest risk factor
=Monozygotic twin studies shower greater concordance for Crohn’s than UC
=NOD2 in Crohn’s, bacterial recognition
-Immunological abnormalities
-Environmental factors
=food antigens
=smoking (decreases risk of UC, aggravates Crohn’s)
-Infection
=Mycobacteria, Yersinia, viruses
=No definitive link identified
-Loss of tolerance to normal commensal bacteria
=Increased IgG levels to commensals
=Improvement in disease flares with antibiotics

21
Q

Describe endoscopic biopsies in IBD

A
  • Excludes other aetiologies (infection)
  • Make initial diagnosis
  • Distinguish between Crohn’s and UC
  • Assess response to treatment
  • Look for complications/ other pathology (superimposed infection)
  • Surveillance for dysplasia
  • Multiple sites as distribution of inflammation within colon and terminal ileum used in distinction
22
Q

What are the pathological features in the epithelium in IBD?

A
  • Epithelial damage/ erosion/ ulceration
  • Mucin depletion
  • Neutrophil infiltration (cryptitis and crypt abscesses)
  • Metaplasia
23
Q

What are the pathological features in the lamina propria in IBD?

A
  • Inflammatory cell infiltrate
  • Cell types (plasma cells, neutrophils)
  • Density of inflammatory infiltrate
  • Distribution of infiltrate (patchy vs. diffuse)
  • Presence of granulomas
24
Q

What are the changes to the general architecture of the mucosa in IBD?

A
  • Surface topography (villous change in colon)

- Crypt architecture abnormalities, crypt atrophy

25
What is Ulcerative Colitis?
- Chronic relapsing and remitting condition typically presenting with recurrent episodes of rectal bleeding - Mild and infrequent vs severe - Highest incidence 15-25 years, smaller peak at 60-70 years, no gender difference - Inflammation confined to mucosa unless severe - Typically involves rectum +/- left colon (variable length) - Involvement of whole colon (pancolitis) continuous distribution but generally limited to colon and rectum
26
What does ulcerative colitis look like in the rectum?
- Congested - Erythematous - Ulceration - Granular appearance - Flat (loss of normal mucosal folds in large bowel) - Sharp demarcation of diseased segments and normal mucosa
27
What are the hallmarks of active ulcerative colitis?
-Infiltration of colonic crypts by neutrophils -Formation of crypt abscesses -Inflammatory polyps -Some pseudo polyps= islands of residual mucosa appear polyp as surrounded by areas of extensive ulceration =Broad and flat bottomed, extend into submucosa, undermine adjacent mucosa, rupture of crypt abscesses
28
Describe the distribution of UC
- Limited to rectum only (proctitis) - Rectum and variable length of colon in continuity - Rectum and variable length of colon in continuity and discontinuous involvement of caecum and appendix (caecal patch lesion) - Entire colon and rectum (pan-proctocolitis)
29
What are the hallmarks of chronic ulcerative colitis?
-Irregular, shortened and branched crypts and increased inflammatory cells in mucosa
30
What is Crohn's Disease?
- "Regional enteritis" - Chronic, multifocal, relapsing condition that can affect any part of the GI tract (mouth to perianal skin) - Peak incidence 20-30 years with smaller peak 60-70 years, no gender difference - Variety of presentations depending on part of GI tract involved- abdominal pain, diarrhoea, weight loss, strictures and obstruction, fistulae - Transmural (all layers) inflammation often patchy and discontinuous (skip lesions)
31
Describe the distribution of Crohn's disease
- Small intestine (30-35%) - Colon (25-30%) - Small intestine and colon (30-40%) - Anus/ perianal region (50%) - Stomach and duodenum (5%, more common in children) - Oesophagus (2%, more common in children)
32
How are granulomas a diagnostic feature of Crohn's disease?
``` -Granulomas =aggregates of activating macrophages =70% cases =Fewer in right colon than left =Commoner in children =Tend to be larger in adults =Fewer after 2 years of illness =Particularly helpful in diagnosis when present deeper within wall/ within draining lymph nodes =Mucosal granulomas least specific as can occur in UC but usually associated with damaged crypts in lamina propria ```
33
Describe ulceration in Crohn's disease
- Aphthous ulcers - Not broad based and flat like UC - Small superficial ulcers overlying patches of mucosa-associated lymphoid tissue - In rectum, ulceration extends into anal canal, involves perianal skin - Ulceration typically along border of colon to which the mesocolon is attached - More severe= crisscrossing linear ulceration= cobblestone mucosa - Fissuring ulceration= deep and knife-like, can extend through to muscularis propria, can give rise to fistula
34
What other diagnostic features are associated with Crohn's?
- As involves full thickness= fibrosis - Narrowed lumen, stricture formation - Lymphoid aggregates
35
What are the GI tract complications of IBD?
*All from Crohn's -Subacute intestinal obstruction =Fistulae =Malabsorption (small bowel involvement) *with UC as well =Toxic dilation (distended large bowel loops as damage to nerve supply) =Perforation =Haemorrhage =Amyloidosis =Neoplasia
36
Describe neoplasia in IBD
- Risk increased in both UC and CD (highest in UC) - Risk increases with time since diagnosis (mean duration 17-21 years) - Risk increases with severity and extent of disease - Most commonly colorectal adenocarcinomas but also increased risk of small bowel carcinomas and other malignancies (bile duct carcinomas, leukaemias) - Affects about 5% of patients with CD and 11% of UC
37
What are the musculoskeletal conditions associated with IBD?
Arthritis and ankylosing spondylitis - UC + - CD +++
38
What are the Hepatobiliary conditions associated with IBD?
``` -Primary sclerosing cholangitis =UC +++ =CD + -Bile duct carcinoma =UC +++ =CD + ```
39
What are the skin conditions associated with IBD?
``` -Erythema nodosum =UC +++ =CD +++ -Pyoderma gangrenosum =UC +++ =CD + ```
40
What are the other conditions associated with IBD?
``` -Oral ulceration =UC + =CD +++ -Eye lesions =UC +++ =CD +++ -Amyloid (rare) =UC + =CD +++ ```
41
Contrast the typical microscopic features of UC and CD
- UC= Cryptitis, crypt abscesses, mucin depletion, crypt architectural distortion and crypt loss in chronic UC, paneth cell metaplasia - CD= patchy inflammation, lymphoid aggregates, cryptitis and mucin cell depletion less prominent, pyloric metaplasia in small intestine, cobblestone pattern from linear ulcers running in different direction
42
What mimics IBD?
- Infective colitis mimics CD= bacterial and parasitic, sextually trasnmitted chlamydia and syphilis cause inflammation in rectum that resembles UC - Ischaemic colitis= most common in region of splenic flexure and descending colon - Diverticular disease= most common in sigmoid colon, can result in fistulas to bladder - Drug induced colitis (NSAIDs, ileocolic inflammation where CD usually presents) - Radiation colitis- proctitis - Neoplasia= CD= mass lesions, fistulae and strictures
43
What is diverticular disease?
- Characterised by outpouching of bowel mucosa through weak points in the wall - Consequence of high intra-lumenal pressure in chronic constipation - Outpouchings can rupture= abscesses= fistulae
44
What are the causes of colonic strictures?
- CD - Ischaemic colitis - Diverticular disease - Diaphragm disease (NSAIDs)= thin membrane like strictures due to repeated episodes of ulceration and healing - Neoplasia
45
What is microscopic colitis?
-Older patients -Usually presents as chronic watery diarrhoea over several months -Normal appearance of colonic and rectal mucosa at endoscopy -Increase in chronic inflammatory cells in lamina propria -Two patterns =Collagenous colitis (thick band of thick collagen within superficial lamina propria, mucosal fragility- detached from collagen band) =Lymphocytic colitis (numerous intraepithelial lymphocytes, CD3 immunohistochemistry)
46
What is the cause of microscopic colitis?
- Cause often not identified - Lymphocytic colitis can be associated with coeliac disease - Drugs implicated in both forms, lansoprazole (PPI for acid suppression, collagenous) and NSAIDs
47
What is the treatment for microscopic colitis?
Steroids (budesonide)