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Y1 GI > IBD, IBS and Small intestine > Flashcards

IBD, IBS and Small intestine Flashcards

1
Q

Conditions in IBD

A

Crohn’s disease

Ulcerative colitis

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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

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3
Q

What genes are claimed to have an impact on IBD

A

NOD2 , HLA-DR2, HLA-DQw5

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4
Q

Risk factors for Crohn’s

A 
Young age
Male
Family history of IBD 
NSAID
Smoking
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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)

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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
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7
Q

Most common site of Crohn’s disease

A

small intestine

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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

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9
Q

What are the pathophysiological changes seen in Crohn’s

A
  • cobblestone pattern
  • patchy, discontinuous inflammation
  • non-caseating granuloma
  • rosethorn ulcers
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10
Q

What causes cobblestone pattern in crohn’s

A

Ulcers connecting together

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11
Q

What causes rose thorn ulcer appearance in IBD

A

Transmural inflammation of Crohn’s disease

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12
Q

What does transmural inflammation mean

A

Inflammation across all layers of mucosa

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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
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14
Q

What do macrophages look like under microscope

A

Pale pink cytoplasm

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15
Q

Symptoms of Crohn’s disease

A 
Diarrhea +/- blood
Vomiting
Weight loss 
Abdominal pain 
Pale due to anaemia 
tender abdomen
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16
Q

Which site of inflammation causes pain in peri umbilical region

A

small intestine

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17
Q

Which site of inflammation causes lower abdominal pain

A

Colon

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18
Q

Diagnosis for Crohn’s

A 
Blood tests
Stool culture
Faecal calprotectin 
colonoscopy / upper gi endoscopy
small bowel MRI
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19
Q

What would blood tests show if the patient has IBD

A

Increase in CRP
Decrease in albumin
Decrease in Hb

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20
Q

Why do we need to measure faecal calprotectin

A

To differentiate between IBD and IBS

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21
Q

What will the faecal calprotectin level be in IBD

A

Elevated

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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

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23
Q

First line drug to induce remission in Crohn’s

A

Glucocorticoids - prednisolone or IV hydrocortisone

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24
Q

Why isn’t steroids used in young children

A

Because it causes stunted growth

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25
Q

Second line drug to induce remission in Crohn’s

A

Azathioprine / methotrexate / mercaptopurine

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26
Q

First line drug used to maintain remission in Crohn’s

A

Azathioprine / mercaptopurine

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27
Q

When is methotrexate used in maintaining remission

A

In Crohn’s disease when azathioprine / mercaptopurine are not tolerated or ineffective

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28
Q

Surgery is curative in Crohn’s disease or UC

A

UC

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29
Q

When is surgery used in Crohn’s

A

for fistula repair / perianal repair / stricturoplasty

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30
Q

What should surgeons be cautious about when dealign with Crohn’s

A

Limiting the amount resected to avoid e.g. short bowel syndrome causing malabsorption

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31
Q

What are the complications of Crohns

A 
Stricture of bowel
Perforation
Fistula
Malabsorption / gall stones
Anal diseases
Increases risk for colonic cancer
amyloidosis 
Continous diarrhea
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32
Q

Why may perforation and fistula occur in Crohn’s

A

Due to transmural inflammation

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33
Q

How may Crohn’s disease increase risk of gall stone formation

A

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

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34
Q

What is a fistula

A

When the fissure penetrates through the adjacent organ and forms an abnormal connection

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35
Q

What is vesicocolic fistula

A

Fistula between colon and bladder

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36
Q

Examples of anal diseases caused by Crohns’

A

fissures

abscesses

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37
Q

What is amyloidosis

A

Abnormal build up of amyloid in organs, disrupting function

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38
Q

How does smoking affect UC

A

Protects against UC

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39
Q

Pathophysiological changes in UC

A 
Crypt abscesses 
Branching and irregular crypts 
Inflammatory infiltration into lamina propria 
Continuous inflammation 
Loss of goblet cells
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40
Q

What may low grade activity of UC eventually lead to

A

Persistent inflammation -> fibrosis -> loss of crypts -> no longer functional

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41
Q

Which type of T cell is associated in development of UC

A

Th2

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42
Q

Symptoms of UC

A

Diarrhea + blood
Need to go to toilet for a lot of times
tenesmus
abdominal pain at left iliac fossa

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43
Q

When do UC symptoms usually occur

A

At night

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44
Q

What is tenesmus

A

feeling to pass stool even though you already did

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45
Q

What is Truelove and WItts used for

A

assess severity for UC

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46
Q

What is considered as mild in Truelove and Witts

A

pass stools for < 4 times

small amount of blood

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47
Q

What is considered as intermediate in Truelove and Witts

A

pass stools for 4-6 times

mild - severe amount of blood

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48
Q

What is considered as severe in Truelove and Witts

A

pass stools for more than 6 times
bloody
pyrexic / tachycardic / increase in ESR

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49
Q

What is ESR

A

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

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50
Q

What does elevated ESR mean

A

Inflammation

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51
Q

First line management of mild UC

A

topical or oral aminosalicylate

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52
Q

Second and third line management of mild UC

A

if 5ASA ineffective = + oral prednisolone

If 5ASA + steroid ineffective = + oral tacrolimus

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53
Q

First line management of severe UC

A

IV corticosteroids

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54
Q

Second line management of severe UC

A

+ IV ciclosporin

or surgery

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55
Q

Complications of UC

A

Toxic megacolon
Increases risk for colorectal carcinoma
Hypokalaemia
Extra GI manifestations

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56
Q

What is toxic megacolon

A

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

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57
Q

What is the urgent treatment for toxic megacolon

A

Immediate colectomy

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58
Q

Which IBD condition increases risk for colorectal cancer more

A

UC

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59
Q

What does the extent of increase in risk of colorectal cancer depend on

A

The more colon is affected , the greater the risk

Having UC for over 10 years

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60
Q

Extra GI manifestations of IBD

A

Eyes - uveitis
Liver - primary sclerosing cholangitis (UC)
joints - arthritis, ank spondylitis, clubbing
skin - painful purple nodules on skin (erythema nodosum), aphthous ulcer
anaemia , thromboembolism

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61
Q

Which extra GI manifestation is the most common due to UC

A

Arthritis

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62
Q

What is IBS

A

functional bowel disease characterised by abdominal pain and altered bowel habits

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63
Q

What does functional bowel disease mean

A

There are no structural / biochemical dysfunction. Most likely due to dysregulation in communication between the gut and brain

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64
Q

Causes of IBS

A

Abnormal motility
Visceral hypersensitivity
Altered gut flora
Altered mucosal and immune function

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65
Q

What does visceral hypersensitivity mean

A

Nocireceptors (pain receptors) are more stimulated than usual

66
Q

What is visceral hypersensitvity mediated by

A

Mast cells releasing histamine and enteroendocrine cells release serotonin

67
Q

What condition may cause secondary IBS and why

A

Gastroenteritis due to increase in activation of immune cells

68
Q

Types of IBS

A

IBS-C
IBS-D
IBS-M

69
Q

Which type of IBS is the most common

70
Q

Risk factors for IBS

A 
Female
Family history of IBS
young age
mental health problems - depression / traumatic life events/ anxiety / personality disorder
Previous gastroenteritis
71
Q

Symptoms of IBS

A

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
Q

What chart is used to describe the type of faeces

A

Bristol stool chart

73
Q

What is type 7 on Bristol stoll chart

A

Severe diarrhea; no solid pieces

74
Q

What is type 1 on bristol stool chart

A

Severe constipation; separate, hard lumps

75
Q

Diagnosis of IBS

A 
Symptom fitting criteria:
- Roman IV criteria
- Manning criteria 
Faecal calprotectin
Blood tests
76
Q

Describe Roman IV criteria

A

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
Q

Describe Manning criteria

A 
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
Q

How to differentiate between IBD and IBS

A

Faecal calprotectin not elevated in IBS
IBS diarrhea normally not bloody
FBC / ESR / CRP not raised in IBS

79
Q

Lifestyle management for IBS

A

avoid mushroom / onions / garlic / bean
avoid lactose if lactose intolerant
avoid skins / seeds
limit fruit and fruit juice intake for IBS-D

80
Q

What drugs are used to relief pain for IBS

A

Antispasmodics

Tricyclic antidepressants

81
Q

Example of antispasmodics

A

Buscopan
Mebeverine
Colpermin

82
Q

Examples of anti-depressants

A

amitriptyline

nortriptyline

83
Q

First line drug treatment for IBS-C

A

Bulk forming laxatives - ispagula husk

84
Q

Second and third line treatment for IBS-C

A

Osmotic Laxative - MgOH , polyethene glycol, movicol
5-HT4 agonists
Guanylate cyclase
Selective C2 chloride channel activators

85
Q

Example of 5-HT4 agonist

A

Prucalopride

tegaser

86
Q

Example of guanylate cyclase

A

linaclotide

87
Q

Drug treatment for IBS-D

A

Loperamide
Bile acid sequestrants
5-HT3 receptor antagnoists
Rifaximin

88
Q

Example of bile acid sequestrants

A

cholesystamine

colesevelam

89
Q

Most common site of colorectal cancer

A

Left side of colon

90
Q

What type of cancer is colorectal cancer

A

Adenocarcinoma

91
Q

What is a polyp

A

A protrusion above an epithelial surface

Does not indicate benign/malignant

92
Q

Most common type of polyp

93
Q

Why should polyps be sent for histopathological studies

A

Because it can be neoplastic (there is dysplasia) which can mean it is an adenoma

94
Q

Describe adenoma-carcinoma sequence

A

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
Q

What is oncogene

A

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
Q

What are tumour suppressor genes

A

Normal genes that slow down cell division and repair DNA mistakes

97
Q

What happens when there is a mutation at tumour suppressor gene

A

Tumour suppressor gene not functional so the cell undergoes uncontrolled cell division

98
Q

What is adenoma

A

Benign lesion, does not metastasize

But can develop into malignant adenocarcinoma

99
Q

Which are the most common sites of metastasis for colorectal cancer

A

Liver, lung, peritoneum

100
Q

Symptoms of colorectal cancer

A 
Weight loss 
Malaise
Change in bowel habits
tenesmus 
Malena - bright red
Pallor (skin is lighter)
Jaundice
Lymphadenopathy
101
Q

What symptom is specific for right side colorectal cancer

A

iron deficiency anaemia

102
Q

Investigations for colorectal cancer

A

Colonoscopy / sigmoidoscopy
CT colongraphy
CEA
PET

103
Q

What is CEA

A

Carcinoembryonic antigen - a serum marker for colorectal cancer

104
Q

Staging of colorectal cancer - T

A

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
Q

Staging of colorectal cancer - N

A

N1 - metastasis in 1 - 3 regional lymph nodes

N2 - metastasis in 4 or more lymph nodes

106
Q

Why should all adenoma be removed

A

Because they are premalignant; can develop into adenocarcinoma

107
Q

Symptoms specific to left side colorectal cancer

A

Worsening constipation due to obstruction

108
Q

What hereditary syndromes increases the risk of colorectal cancer

109
Q

What is HNPCC

A

Hereditary Non Polyposis Coli (Lynch syndrome)

110
Q

Mutations in which genes occur in Lynch syndrome

A

MLH1, MSH2, MSH6 and PMS2

111
Q

What type of genes are mutated in HNPCC

A

DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2)

112
Q

HNPCC is autosomal recessive or dominant?

A

Autosomal recessive

113
Q

Which inherited condition that increases risk of colorectal cancer has 100% penetrance

114
Q

What is FAP

A

Familial adenomatous polyposis

115
Q

Difference between FAP and HPNCC

A

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
Q

Which gene is mutated in FAP

A

APC gene - a tumour suppressor gene

117
Q

Crohn’s is associated with changes in what genes

A

HLA DR1 and HLA DQw5

118
Q

UC is associated with changes in what genes

A

NOD2 and HLA DR2

119
Q

What is Coeliac disease

A

An autoimmune disease that is triggered by the ingestion of gluten

120
Q

Cause of Coeliac disease

A

Intolerance to prolamins e.g. gliadin

121
Q

What HLA proteins are associated to Coeliac disease

A

HLA DQ8

HLA DQ2

122
Q

What do type 2 HLA genes code for

A

MHC II on antigen presenting cells

123
Q

What immune cells are involved in Coeliac Disease

A

T cells and IEL

124
Q

Are HLA DQ8 and HLA DQ2 type 1 or type 2 HLA

125
Q

What infection is associated to the development of Coeliac

A

Recurrent rotavirus infections during childhood

126
Q

Describe the process leading to epithelial damage in Coeliac Disease

A

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
Q

What is the most diagnostic test of coeliac

128
Q

What are the histological features of the biopsy for Coeliac disease

A
  • villous atrophy (wasting away)
  • crypts hyperplasia
  • increase in IEL, inflammatory cells
  • flat mucosa
129
Q

Symptoms of Coeliac Disease

A 
Bloating 
Steatorrhea 
Fatigue 
Unexplained anaemia 
Failure to thrive in children
Muscle wasting
130
Q

What are the extra GI manifestations of Coeliac

A

Osteoporosis

Dermatitis herpetiformis

131
Q

Which disease is most commonly confused with Coeliac

132
Q

What would the serology for patients with coeliac show

A

presence of

  • anti tTGA
  • anti EMA
133
Q

What immunoglobin may be deficient in patients with coeliac disease

134
Q

What is the immunoglobin against gliadin

135
Q

What extra GI manifestation is Crohn’s related to

A

Mouth ulcers (not UC because UC only affects rectum and colon, whereas Crohn’s can affect anywhere in GI tract)

136
Q

What extra GI manifestations is UC related to

A

Arthritis
erythema nodosum
Uveitis

137
Q

What biliary condition is UC related to

138
Q

What test should be done if suspect Coeliac disease

A

Total IgA and Anti tTGA

139
Q

What is a marker of colorectal cancer

140
Q

Which age group is most commonly affected by appendicitis

A

Young 10-20 years old

141
Q

Which artery supplies the appendix

A

Appendiceal artery

142
Q

Which artery did the appendiceal artery branch off from

A

ileocolic artery

143
Q

What are the most common positions of appendix

A

Retrocaecal

Pelvic

144
Q

Most common cause of appendicits

145
Q

What is faecolith

A

Mass of hardened faecal matter

146
Q

Causes of appendicits

A

Faecolith
Lymphoid hyperplasia
Fibrous stricture

147
Q

How does appendicitis occur

A
  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
Q

What are the complications of appendicitis

A

Perforation -> peritonitis

Gangrene

149
Q

When does visceral pain occur in appendicitis

A

When the appendix is distended due to increase in intraluminal pressure

150
Q

When does somatic pain occur in appendicitis

A

When the appendix has perforated

151
Q

Symptoms of acute appendicitis

A

Mild pyrexia / Mild tachycardia
Pain from periumbilical region moving to RIF
Anorexia
Constipation

152
Q

Clinical signs of acute appendicitis

A

Rosving’s sign
Psoas sign
Guarding

153
Q

What is Rosving’s sign

A

Pressing on the left causes pain on the right

154
Q

What is Psoas sign

A

Right hip flexed to lift the appendix away from psoas

155
Q

Diagnosis of appendicitis

A

Bloods - raised CRP, FBC, WCC
Test for pregnancy
Imaging

156
Q

Should imaging be done for every acute appendicitis

A

No, only done if in doubt

Do not delay treatment

157
Q

Why should females with acute appendicitis be tested for pregnancy

A

Because pregnant women with appendicitis can cause high mortality for both the mother and child

158
Q

Management of appendicitis

A

Analgesia + Antibiotics

Appendectomy

159
Q

Which abdominal artery is the most common site of blockage

A

SMA because it is narrower

160
Q

Causes of mesenteric ischaemia

A 
Atrial fibrillation (most common) 
Virchow's triad
161
Q

Patients with mesenteric ischaemia usually have acidosis or alkalosis

162
Q

Management of mesenteric ischaemia

A

Surgical resection

SMA embolectomy

Y1 GI (6 decks)

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