IBD, IBS and Small intestine Flashcards
1
Q
Conditions in IBD
A
Crohn’s disease
Ulcerative colitis
2
Q
What are the causes of IBD
A
Idiopathic, but genetics + environment + immunity have been claimed to have an effect on development of IBD
3
Q
What genes are claimed to have an impact on IBD
A
NOD2 , HLA-DR2, HLA-DQw5
4
Q
Risk factors for Crohn’s
A
Young age Male Family history of IBD NSAID Smoking
5
Q
How may the immune system have an effect on development of Crohn
A
Predominantly TH1 response (TH1 > TH2)
excess TNF-alpha (proinflammatory cytokine)
6
Q
Difference between Crohn’s disease and ulcerative colitis
A
- Crohn’s affect anywhere in GI tract whereas UC only affects rectum and colon
- Crohn’s causes transmural inflammation whereas UC only causes submucosal inflammation
- Crohn’s causes skip lesions whereas UC is continuous inflammation
- Crohn’s is associated with mouth ulcers whereas UC is not
- Smoking increases risk of Crohn’s whereas smoking protects against UC
- Crohn’s forms non-caseating granuloma whereas UC does not have any granuloma
7
Q
Most common site of Crohn’s disease
A
small intestine
8
Q
Which age group is at most risk for Crohn’s
A
Younger people, 10-40 years old
And elderly 60-80 years old
9
Q
What are the pathophysiological changes seen in Crohn’s
A
- cobblestone pattern
- patchy, discontinuous inflammation
- non-caseating granuloma
- rosethorn ulcers
10
Q
What causes cobblestone pattern in crohn’s
A
Ulcers connecting together
11
Q
What causes rose thorn ulcer appearance in IBD
A
Transmural inflammation of Crohn’s disease
12
Q
What does transmural inflammation mean
A
Inflammation across all layers of mucosa
13
Q
What are the histological findings for Crohn’s
A
Non-caseating granuloma Inflammatory cells bursting into crypts Lymphoid hyperplasia Increase in inflammatory cells in lamina propria loss of crypts Increase in goblet cells
14
Q
What do macrophages look like under microscope
A
Pale pink cytoplasm
15
Q
Symptoms of Crohn’s disease
A
Diarrhea +/- blood Vomiting Weight loss Abdominal pain Pale due to anaemia tender abdomen
16
Q
Which site of inflammation causes pain in peri umbilical region
A
small intestine
17
Q
Which site of inflammation causes lower abdominal pain
A
Colon
18
Q
Diagnosis for Crohn’s
A
Blood tests Stool culture Faecal calprotectin colonoscopy / upper gi endoscopy small bowel MRI
19
Q
What would blood tests show if the patient has IBD
A
Increase in CRP
Decrease in albumin
Decrease in Hb
20
Q
Why do we need to measure faecal calprotectin
A
To differentiate between IBD and IBS
21
Q
What will the faecal calprotectin level be in IBD
A
Elevated
22
Q
2 main objectives in managing Crohn’s
A
To induce remission
To maintain remission
Because this is a lifelong disease, there will be exacerbations and remissions, goal is to induce and maintain remission
23
Q
First line drug to induce remission in Crohn’s
A
Glucocorticoids - prednisolone or IV hydrocortisone
24
Q
Why isn’t steroids used in young children
A
Because it causes stunted growth
25
Second line drug to induce remission in Crohn's
Azathioprine / methotrexate / mercaptopurine
26
First line drug used to maintain remission in Crohn's
Azathioprine / mercaptopurine
27
When is methotrexate used in maintaining remission
In Crohn's disease when azathioprine / mercaptopurine are not tolerated or ineffective
28
Surgery is curative in Crohn's disease or UC
UC
29
When is surgery used in Crohn's
for fistula repair / perianal repair / stricturoplasty
30
What should surgeons be cautious about when dealign with Crohn's
Limiting the amount resected to avoid e.g. short bowel syndrome causing malabsorption
31
What are the complications of Crohns
```
Stricture of bowel
Perforation
Fistula
Malabsorption / gall stones
Anal diseases
Increases risk for colonic cancer
amyloidosis
Continous diarrhea
```
32
Why may perforation and fistula occur in Crohn's
Due to transmural inflammation
33
How may Crohn's disease increase risk of gall stone formation
1) Reduces ability to reabsorb bile acids = Decreases enterohepatic recycling
2) Depletion of bile acids
3) decrease in cholesterol absorption
4) cholesterol collect in gall bladder and because gall bladder concentrates bile, excess cholesterol may become crystalized and form gall stones
34
What is a fistula
When the fissure penetrates through the adjacent organ and forms an abnormal connection
35
What is vesicocolic fistula
Fistula between colon and bladder
36
Examples of anal diseases caused by Crohns'
fissures
| abscesses
37
What is amyloidosis
Abnormal build up of amyloid in organs, disrupting function
38
How does smoking affect UC
Protects against UC
39
Pathophysiological changes in UC
```
Crypt abscesses
Branching and irregular crypts
Inflammatory infiltration into lamina propria
Continuous inflammation
Loss of goblet cells
```
40
What may low grade activity of UC eventually lead to
Persistent inflammation -> fibrosis -> loss of crypts -> no longer functional
41
Which type of T cell is associated in development of UC
Th2
42
Symptoms of UC
Diarrhea + blood
Need to go to toilet for a lot of times
tenesmus
abdominal pain at left iliac fossa
43
When do UC symptoms usually occur
At night
44
What is tenesmus
feeling to pass stool even though you already did
45
What is Truelove and WItts used for
assess severity for UC
46
What is considered as mild in Truelove and Witts
pass stools for < 4 times
| small amount of blood
47
What is considered as intermediate in Truelove and Witts
pass stools for 4-6 times
| mild - severe amount of blood
48
What is considered as severe in Truelove and Witts
pass stools for more than 6 times
bloody
pyrexic / tachycardic / increase in ESR
49
What is ESR
erythrocyte sedimentation rate ; measures the distance red blood cells travel in one hour in a sample of blood as they settle to the bottom of a test tube
50
What does elevated ESR mean
Inflammation
51
First line management of mild UC
topical or oral aminosalicylate
52
Second and third line management of mild UC
if 5ASA ineffective = + oral prednisolone
| If 5ASA + steroid ineffective = + oral tacrolimus
53
First line management of severe UC
IV corticosteroids
54
Second line management of severe UC
+ IV ciclosporin
| or surgery
55
Complications of UC
Toxic megacolon
Increases risk for colorectal carcinoma
Hypokalaemia
Extra GI manifestations
56
What is toxic megacolon
When the colon swells up and fills up with fluid due to inflammation. It can eventually burst and release all contents into peritoneal cavity -> peritonitis, sepsis, death
57
What is the urgent treatment for toxic megacolon
Immediate colectomy
58
Which IBD condition increases risk for colorectal cancer more
UC
59
What does the extent of increase in risk of colorectal cancer depend on
The more colon is affected , the greater the risk
| Having UC for over 10 years
60
Extra GI manifestations of IBD
Eyes - uveitis
Liver - primary sclerosing cholangitis (UC)
joints - arthritis, ank spondylitis, clubbing
skin - painful purple nodules on skin (erythema nodosum), aphthous ulcer
anaemia , thromboembolism
61
Which extra GI manifestation is the most common due to UC
Arthritis
62
What is IBS
functional bowel disease characterised by abdominal pain and altered bowel habits
63
What does functional bowel disease mean
There are no structural / biochemical dysfunction. Most likely due to dysregulation in communication between the gut and brain
64
Causes of IBS
Abnormal motility
Visceral hypersensitivity
Altered gut flora
Altered mucosal and immune function
65
What does visceral hypersensitivity mean
Nocireceptors (pain receptors) are more stimulated than usual
66
What is visceral hypersensitvity mediated by
Mast cells releasing histamine and enteroendocrine cells release serotonin
67
What condition may cause secondary IBS and why
Gastroenteritis due to increase in activation of immune cells
68
Types of IBS
IBS-C
IBS-D
IBS-M
69
Which type of IBS is the most common
IBS-C
70
Risk factors for IBS
```
Female
Family history of IBS
young age
mental health problems - depression / traumatic life events/ anxiety / personality disorder
Previous gastroenteritis
```
71
Symptoms of IBS
Abdominal pain for at least 1 day per week over last 3 months
Abdominal pain related to defaecation
Abdominal pain worse when eating
Changed bowel habits - constipation / diarrhea
Bloating
Belching
nausea
72
What chart is used to describe the type of faeces
Bristol stool chart
73
What is type 7 on Bristol stoll chart
Severe diarrhea; no solid pieces
74
What is type 1 on bristol stool chart
Severe constipation; separate, hard lumps
75
Diagnosis of IBS
```
Symptom fitting criteria:
- Roman IV criteria
- Manning criteria
Faecal calprotectin
Blood tests
```
76
Describe Roman IV criteria
Abdominal pain for at least 1 day per week over the last 3 months
Pain must be at least one of them:
- related to defaecation
- associated with change in appearance of stool
- associated with change in frequency of stool
77
Describe Manning criteria
```
Recurrent abdominal pain for at least 4 months + pain relieved by defaecation / associated with change in stool form or bowel frequency
Associated with at least 2:
- altered stool passage
- bloating
- symptoms worsen due to eating
- passage of mucus
```
78
How to differentiate between IBD and IBS
Faecal calprotectin not elevated in IBS
IBS diarrhea normally not bloody
FBC / ESR / CRP not raised in IBS
79
Lifestyle management for IBS
avoid mushroom / onions / garlic / bean
avoid lactose if lactose intolerant
avoid skins / seeds
limit fruit and fruit juice intake for IBS-D
80
What drugs are used to relief pain for IBS
Antispasmodics
| Tricyclic antidepressants
81
Example of antispasmodics
Buscopan
Mebeverine
Colpermin
82
Examples of anti-depressants
amitriptyline
| nortriptyline
83
First line drug treatment for IBS-C
Bulk forming laxatives - ispagula husk
84
Second and third line treatment for IBS-C
Osmotic Laxative - MgOH , polyethene glycol, movicol
5-HT4 agonists
Guanylate cyclase
Selective C2 chloride channel activators
85
Example of 5-HT4 agonist
Prucalopride
| tegaser
86
Example of guanylate cyclase
linaclotide
87
Drug treatment for IBS-D
Loperamide
Bile acid sequestrants
5-HT3 receptor antagnoists
Rifaximin
88
Example of bile acid sequestrants
cholesystamine
| colesevelam
89
Most common site of colorectal cancer
Left side of colon
90
What type of cancer is colorectal cancer
Adenocarcinoma
91
What is a polyp
A protrusion above an epithelial surface
| Does not indicate benign/malignant
92
Most common type of polyp
Adenoma
93
Why should polyps be sent for histopathological studies
Because it can be neoplastic (there is dysplasia) which can mean it is an adenoma
94
Describe adenoma-carcinoma sequence
The development of adenocarcinoma from adenoma
1) Small adenoma; Mutation in APC gene, leading to hyperproliferative epithelium
2) Large adenoma; Mutation in KRAS (proto-oncogene -> oncogene)
3) Mutation in p53 (tumour suppressor gene)
4) Adenocarcinoma
95
What is oncogene
Mutated version of proto-oncogene, causing the proto-oncogene to be permanently turned on, stimulating cell division when they are not supposed to be dividing
96
What are tumour suppressor genes
Normal genes that slow down cell division and repair DNA mistakes
97
What happens when there is a mutation at tumour suppressor gene
Tumour suppressor gene not functional so the cell undergoes uncontrolled cell division
98
What is adenoma
Benign lesion, does not metastasize
| But can develop into malignant adenocarcinoma
99
Which are the most common sites of metastasis for colorectal cancer
Liver, lung, peritoneum
100
Symptoms of colorectal cancer
```
Weight loss
Malaise
Change in bowel habits
tenesmus
Malena - bright red
Pallor (skin is lighter)
Jaundice
Lymphadenopathy
```
101
What symptom is specific for right side colorectal cancer
iron deficiency anaemia
102
Investigations for colorectal cancer
Colonoscopy / sigmoidoscopy
CT colongraphy
CEA
PET
103
What is CEA
Carcinoembryonic antigen - a serum marker for colorectal cancer
104
Staging of colorectal cancer - T
T1 - invades submucosa but not muscularis propria
T2 - invades muscularis propria
T3 - invades through muscularis propria into pericolorectal tissues
T4 - invades through visceral peritoneum
105
Staging of colorectal cancer - N
N1 - metastasis in 1 - 3 regional lymph nodes
| N2 - metastasis in 4 or more lymph nodes
106
Why should all adenoma be removed
Because they are premalignant; can develop into adenocarcinoma
107
Symptoms specific to left side colorectal cancer
Worsening constipation due to obstruction
108
What hereditary syndromes increases the risk of colorectal cancer
HNPCC
| FAP
109
What is HNPCC
Hereditary Non Polyposis Coli (Lynch syndrome)
110
Mutations in which genes occur in Lynch syndrome
MLH1, MSH2, MSH6 and PMS2
111
What type of genes are mutated in HNPCC
DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2)
112
HNPCC is autosomal recessive or dominant?
Autosomal recessive
113
Which inherited condition that increases risk of colorectal cancer has 100% penetrance
FAP
114
What is FAP
Familial adenomatous polyposis
115
Difference between FAP and HPNCC
FAP causes formation of more than 100 polyps
FAP is autosomal dominant whereas HPNCC is autosomal recessive
FAP causes a defect in tumour supression whereas HPNCC causes a defect in DNA mismatch repair
FAP causes malignancy throughout the whole colon whereas HPNCC causes malignancy in right side of colon only
116
Which gene is mutated in FAP
APC gene - a tumour suppressor gene
117
Crohn's is associated with changes in what genes
HLA DR1 and HLA DQw5
118
UC is associated with changes in what genes
NOD2 and HLA DR2
119
What is Coeliac disease
An autoimmune disease that is triggered by the ingestion of gluten
120
Cause of Coeliac disease
Intolerance to prolamins e.g. gliadin
121
What HLA proteins are associated to Coeliac disease
HLA DQ8
| HLA DQ2
122
What do type 2 HLA genes code for
MHC II on antigen presenting cells
123
What immune cells are involved in Coeliac Disease
T cells and IEL
124
Are HLA DQ8 and HLA DQ2 type 1 or type 2 HLA
Type 2
125
What infection is associated to the development of Coeliac
Recurrent rotavirus infections during childhood
126
Describe the process leading to epithelial damage in Coeliac Disease
1) Ingested gliadin
2) gliadin may move into the lamina propria
3) gliadin deaminated and presented on HLA DQ2/8 to T cells
4) T cells cause inflammation and subsequent activation of B cells -> epithelial damage
And
1) gliadin irritate the epithelial cells
2) Epithelial cells release IL-15, activating IEL -> epithelial damage
127
What is the most diagnostic test of coeliac
Biopsy
128
What are the histological features of the biopsy for Coeliac disease
- villous atrophy (wasting away)
- crypts hyperplasia
- increase in IEL, inflammatory cells
- flat mucosa
129
Symptoms of Coeliac Disease
```
Bloating
Steatorrhea
Fatigue
Unexplained anaemia
Failure to thrive in children
Muscle wasting
```
130
What are the extra GI manifestations of Coeliac
Osteoporosis
| Dermatitis herpetiformis
131
Which disease is most commonly confused with Coeliac
IBS
132
What would the serology for patients with coeliac show
presence of
- anti tTGA
- anti EMA
133
What immunoglobin may be deficient in patients with coeliac disease
IgA
134
What is the immunoglobin against gliadin
IgG
135
What extra GI manifestation is Crohn's related to
Mouth ulcers (not UC because UC only affects rectum and colon, whereas Crohn's can affect anywhere in GI tract)
136
What extra GI manifestations is UC related to
Arthritis
erythema nodosum
Uveitis
137
What biliary condition is UC related to
PSC
138
What test should be done if suspect Coeliac disease
Total IgA and Anti tTGA
139
What is a marker of colorectal cancer
CEA
140
Which age group is most commonly affected by appendicitis
Young 10-20 years old
141
Which artery supplies the appendix
Appendiceal artery
142
Which artery did the appendiceal artery branch off from
ileocolic artery
143
What are the most common positions of appendix
Retrocaecal
| Pelvic
144
Most common cause of appendicits
Faecolith
145
What is faecolith
Mass of hardened faecal matter
146
Causes of appendicits
Faecolith
Lymphoid hyperplasia
Fibrous stricture
147
How does appendicitis occur
1. Faecolith / lymphoid hyperplasia blocks the appendix
2. this causes overgrowth of bacteria
3. this increases the intraluminal pressure, causing distention of the appendix
4. causes venous and lymphatic congestion and arterial supply become compromised
5. can develop into complications
148
What are the complications of appendicitis
Perforation -> peritonitis
| Gangrene
149
When does visceral pain occur in appendicitis
When the appendix is distended due to increase in intraluminal pressure
150
When does somatic pain occur in appendicitis
When the appendix has perforated
151
Symptoms of acute appendicitis
Mild pyrexia / Mild tachycardia
Pain from periumbilical region moving to RIF
Anorexia
Constipation
152
Clinical signs of acute appendicitis
Rosving's sign
Psoas sign
Guarding
153
What is Rosving's sign
Pressing on the left causes pain on the right
154
What is Psoas sign
Right hip flexed to lift the appendix away from psoas
155
Diagnosis of appendicitis
Bloods - raised CRP, FBC, WCC
Test for pregnancy
Imaging
156
Should imaging be done for every acute appendicitis
No, only done if in doubt
| Do not delay treatment
157
Why should females with acute appendicitis be tested for pregnancy
Because pregnant women with appendicitis can cause high mortality for both the mother and child
158
Management of appendicitis
Analgesia + Antibiotics
| Appendectomy
159
Which abdominal artery is the most common site of blockage
SMA because it is narrower
160
Causes of mesenteric ischaemia
```
Atrial fibrillation (most common)
Virchow's triad
```
161
Patients with mesenteric ischaemia usually have acidosis or alkalosis
Acidosis
162
Management of mesenteric ischaemia
Surgical resection
| SMA embolectomy
