Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Gastrointestinal > Inflammation of the GI tract > Flashcards

Inflammation of the GI tract Flashcards

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the hallmark of intestinal metaplasia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What fungal infections can be diagnosed?

A
  • oesophageal
  • Candida
  • Histoplasmosis
  • Murcormycosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What helminths can be diagnosed?

A

Worms

  • Enterobius (pinworm/threadworm, routine appendiscectomy)
  • Ascaris
  • Tapeworms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What is Ulcerative Colitis?

A
  • 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
Q

What does ulcerative colitis look like in the rectum?

A
  • Congested
  • Erythematous
  • Ulceration
  • Granular appearance
  • Flat (loss of normal mucosal folds in large bowel)
  • Sharp demarcation of diseased segments and normal mucosa
27
Q

What are the hallmarks of active ulcerative colitis?

A

-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
Q

Describe the distribution of UC

A
  • 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
Q

What are the hallmarks of chronic ulcerative colitis?

A

-Irregular, shortened and branched crypts and increased inflammatory cells in mucosa

30
Q

What is Crohn’s Disease?

A
  • “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
Q

Describe the distribution of Crohn’s disease

A
  • 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
Q

How are granulomas a diagnostic feature of Crohn’s disease?

A 
-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
Q

Describe ulceration in Crohn’s disease

A
  • 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
Q

What other diagnostic features are associated with Crohn’s?

A
  • As involves full thickness= fibrosis
  • Narrowed lumen, stricture formation
  • Lymphoid aggregates
35
Q

What are the GI tract complications of IBD?

A

*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
Q

Describe neoplasia in IBD

A
  • 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
Q

What are the musculoskeletal conditions associated with IBD?

A

Arthritis and ankylosing spondylitis

  • UC +
  • CD +++
38
Q

What are the Hepatobiliary conditions associated with IBD?

A 
-Primary sclerosing cholangitis
=UC +++
=CD +
-Bile duct carcinoma
=UC +++
=CD +
39
Q

What are the skin conditions associated with IBD?

A 
-Erythema nodosum
=UC +++
=CD +++
-Pyoderma gangrenosum 
=UC +++
=CD +
40
Q

What are the other conditions associated with IBD?

A 
-Oral ulceration
=UC +
=CD +++
-Eye lesions 
=UC +++
=CD +++
-Amyloid (rare)
=UC +
=CD +++
41
Q

Contrast the typical microscopic features of UC and CD

A
  • 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
Q

What mimics IBD?

A
  • 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
Q

What is diverticular disease?

A
  • 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
Q

What are the causes of colonic strictures?

A
  • CD
  • Ischaemic colitis
  • Diverticular disease
  • Diaphragm disease (NSAIDs)= thin membrane like strictures due to repeated episodes of ulceration and healing
  • Neoplasia
45
Q

What is microscopic colitis?

A

-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
Q

What is the cause of microscopic colitis?

A
  • 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
Q

What is the treatment for microscopic colitis?

A

Steroids (budesonide)

Gastrointestinal (48 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions