IBD- UC + Crohn's Clinical

Question 1

Clinical Presentation of Crohn’s

can be confused with intestinal tuberculosis

Answer 1

abdominal cramps/pain
fever
diarrhoea
weight loss
PR bleeding (per rectum bleeding)

Question 2

another name for Crohn’s disease

Answer 2

regional ileitis

Question 3

what is Crohn’s disease + what are the commonest sites of the GI it affects

Answer 3

Chronic inflammatory and ulcerating condition of GI tract

Can affect any site in GI luminal tract from mouth  anus

Commonest sites include terminal ileum and colon

Question 4

epidemiology of Crohn’s

Answer 4

Young patients
Disease most often diagnosed between ages 20-30yrs (50%)
90% of affected individuals are 10-40yrs
Higher incidence in urban areas vs rural areas
Men and women are equally likely to be affected by Crohn’s (Crohn’s & Colitis Foundation)

Question 5

PR bleeding causes

Answer 5

1. if bright red blood = lower GI source i.e. fresh
   - hemorrhoids
   - anal fissures
   - rectal cancer
2. if dark/maroon blood = mid-GI source
   - diverticular disease
   - colitis
3. if mixed with stool = more proximal colonic source
   - inflammatory bowel disease, IBL
   - colorectal cancer

1. Hemorrhoids – Painless bright red blood on toilet paper or in the bowl.
   
   2. Anal Fissures – Painful bleeding, often after straining.
   3. Diverticular Disease – Sudden, painless, large-volume bleeding.
   4. Colorectal Cancer – Blood mixed with stool, weight loss, or altered bowel habits.
   5. Inflammatory Bowel Disease (IBD) – Bloody diarrhea, abdominal pain, weight loss.
   6. Infectious Colitis – Bloody diarrhea with fever and cramping.
      Angiodysplasia – Small vascular malformations in the colon, leading to intermittent bleeding.

Question 6

define
diverticulosis
diverticulitis
diverticular bleeding

Answer 6

• Diverticulosis. This is when you have one or more tiny pouches called diverticula in your colon.
  
  • Diverticulitis. This is when the pouches in your colon get inflamed with or without infection.
    Diverticular bleeding. This happens when a small blood vessel in a pouch breaks open and bleeds.

Question 7

Crohn’s disease is a chronic condition. it can have periods of exacerbation followef by remission

true or false

Answer 7

true

Question 9

endoscopic appearance of Crohn’s

Answer 9

Canker sores — or aphthous ulcers — are small, shallow ulcers that occur in the lining of your mouth. A canker sore starts as a white or yellowish mouth sore with a red border.

Question 10

endoscopic distribution of Crohn’s

Answer 10

Question 11

see oneNote

Pathological features of Crohn’s disease

Answer 11

Summary of Pathological Features:
Segmental (patchy) disease
Chronic active inflammation
Transmural inflammation
Ulceration including deep “knife like” fissuring
Granulomas, non-caseating

transmural = passing or administered through an anatomical wall.

Question 12

paneth cells function

Answer 12

secrete antimicrobial peptides and proteins, which are “key mediators of host-microbe interactions, including homeostatic balance with colonizing microbiota and innate immune protection from enteric pathogens.”

Question 13

crypt epithelial cells function

Answer 13

secretory in function—water and electrolytes are secreted into the intestinal lumen to solubilize the chyme and neutralize gastric acid.

Question 14

pyloric glands function

Answer 14

cover the **gastric antrum and pylorus **and contain G-cells that secrete gastrin into the circulation.

The** rugae** are folds in the stomach lining. Surface epithelial cells, specialized mucus cells of the neck, and mucus cells in the glands also secrete mucin, a high molecular weight glycoprotein.

Question 15

microscopic appearance of Crohn’s

Answer 15

Patchy disease throughout GI tract on biopsy
”Chronic active inflammation”
Mucosal crypt architectural distortion
Inflammation in lamina propria  lymphocytes / plasma cells
Pyloric gland metaplasia
Paneth cell metaplasia
Cryptitis (active inflammation in crypts)
Crypt abscesses
Ulceration

Question 16

describe the features of anal disease

Answer 16

Sinuses: tunnel-like passage (fistula) between anal canal and skin
Fissures
Skin tags
Abscesses

Question 18

what are sinuses

Answer 18

tunnel-like passage (fistula) between anal canal and skin

Question 19

complications of Crohn’s disease

Answer 19

:
Malabsorption
- Hypoproteinaemia
- Vitamin deficiency
- Anaemia

Gallstones: interrupts enterohepatic circulation

Short bowel syndrome: repeated resections of small bowel  reduces absorptive capacity in small bowel

Fistulas: abnormal channels forming between two organs:
Vesico-colic
Entero-colic
Gastro-colic
Recto-vaginal
Tubo-ovarian abscess

“Blind loop” syndrome: food passage is slowed or bypassed, resulting in bacterial overgrowth and malabsorption

Failure to respond to medical therapy
Ongoing symptoms
Requiring surgical resection
Bowel obstruction
Perforation
Amyloidosis
Malignancy
Extra-intestinal Crohn’s
Toxic megacolon

Question 20

what is amyloidosis

Answer 20

group of rare conditions where a protein called amyloid builds up in your body. It can affect organs such as your heart, kidneys, liver, nerves or digestive system. It cannot be cured, but there are treatments that may help with symptoms.

cause by: Chronic infectious or inflammatory diseases:

symptoms:
- purpura around the eyes
- enlarged tongue

Question 21

what is blind loop syndrome

Answer 21

: food passage is slowed or bypassed, resulting in bacterial overgrowth and malabsorption

Question 22

describe the immmune response in Crohn’s disease

Answer 22

Immune Response
Persistent activation of T cells and macrophages
Excess pro-inflammatory cytokine production
Exaggerated response to changes in gut microflora

Question 23

what is ulcerative colitis + age group commonality

Answer 23

Chronic inflammatory disorder
Mucosal and submucosal (i.e. superficial) inflammation
Colon and rectum

Bimodal age distribution: 15-30yrs and 50-70yrs

Question 24

what type of infections increases the risk of UC post-infection

Answer 24

1. Salmonella
2. Shigella
3. Campylobacter

Question 25

sites of UC

Answer 25

Sites: Colon Rectum (almost always involved) Continuous and confluent disease, extends from rectum proximally for varying lengths

Question 26

Clinical presentaiton of UC

Answer 26

Presentation: Diarrhoea Mucous/blood PR ## Footnote Increased bowel frequency (HOW OFTEN?) Night rising for bowels Urgency Tenesmus Incontinence Lower abdo pain (esp. LIF) (proctitis can cause constipation)

Question 27

describe the clinical course of UC

Answer 27

Periods of disease exacerbation followed by remission Continuous low grade disease activity Single episode of disease Acute fulminant colitis  toxic megacolon

Question 28

microscopic features of ulcerative colitis

Answer 28

Microscopic Features Superficial: involves mucosa + superficial submucosa Chronic active colitis Crypt architectural distortion Lamina propria basal lymphoplasmacytic infiltrate Cryptitis Crypt abscess Ulceration +++ (with fibrinopurulent exudate) Massive influx of inflammatory cells including lymphocytes/plasma cells in lamina propria Shortening and branching of crypts (architectural distortion)

Question 29

describe the macroscopic features of chronic inactive UC

Answer 29

CRYPT DISTORTION low grade chronicn inflammation atrophied mucosa

Question 30

where is the site of inflammation in UC

Answer 30

NB. Inflammation is superficial – confined to mucosa + submucosa i.e. no transmural inflammation seen Except in toxic megacolon

Question 31

pathological features of UC

Answer 31

Summary of Pathological Features: Continuous, diffuse disease Almost always involves rectum Superficial inflammation and ulceration Chronic active colitis No granulomas

Question 32

complications of UC

Answer 32

Complications: Continuous diarrhoea Flares can be flared/exacerbated by concomitant infection by bacterial infection/CMV Toxic megacolon  fulminant colitis (entire colon involved); colon becomes extremely swollen  high risk of perforation unless resected  emergency colectomy Complications: Colorectal carcinoma Chronic inflammation  dysplasia  carcinoma Higher risk if: Pancolitis Disease >10yrs Associated primary sclerosing cholangitis Surveillance required Haemorrhage Electrolyte disturbance  hypokalaemia Anal fissures (rare) Extra-GI manifestations: Eyes: uveitis Liver: primary sclerosing cholangitis Joints: ankylosing spondylitis, arthritis Skin: pyoderma gangrenosum, erythema nodosum

Question 33

what is toxic megacolon + diagnosis

Answer 33

Increased diameter of colon -- massive distention of colon Xray

Question 34

smoking is not associated with UC. true or false

Answer 34

true

Question 35

similar features of crohn's and UC

Answer 35

Similar Features of Both: Chronic Relapsing-remitting course Poorly understood aetiology Ulcers Inflammation Diarrhoea PR bleeding Both increase risk of malignancy

Question 36

What does IBDU stand for

Answer 36

Inflammatory Bowel Disease unclassified

Question 37

Sm9ing aggravates crohns disease but protects against UC. True or false?

Answer 37

True

Question 38

What can trigger flares of uc

Answer 38

Nsaids, diet rich in…..

Question 39

most common bowel symptoms

Answer 39

Question 40

name 2 idioapthic chornic inflammatory diseases:

Answer 40

Ulcerative Colitis Crohn's disease

Question 41

desribe the differences in the clinical presentation of Crohn's + UC

Answer 41

diarrhoea, abdominal pain & peri-anal disease (Crohn’s) diarrhoea + bleeding (ulcerative colitis)

Question 42

3 main features of IBD Pathogenesis

Answer 42

## Footnote Positive family history best established risk factor for disease development 1. Genetic Factors : mutated form of NOD2/ CARD15 (IBD-1) --> - Encodes a protein involved in bacterial recognition

Question 43

Gut flora indispensible to the development of animal models of colitis true or false

Answer 43

true

Question 44

antibiotics effective in the treatment of peri-anal Crohn’s Disease true or false

Answer 44

true

Question 45

NOD2 contributes to normal mucosal defences true or false

Answer 45

true

Question 46

Give 2 ways in which maladaptive responses may arise in adaptive mucosal immunity

Answer 46

1. Overactive effector T-cells → Inflammation/ Disease 2. Absence of regulatory T-cells → Uncontrolled Inflammation/ Aggressive Disease

Question 47

what type of T cells arei mplicated in Crohn's disease

Answer 47

Th1 mediated disease

Question 48

what type of T cells arei mplicated in UC

Answer 48

Mixed Th1/ Th2 mediated disease/ Natural Killer T Cells

Question 49

what is a distinguishing feature of Crohn's disease compared to UC in terms of gut antimicrobial activity

Answer 49

colonic tissue from patients with Crohn’s disease has reduced ability to kill bacteria compared to control tissue (and somewhat compared to UC tissue). Crohn’s (compared to UC) is impaired antimicrobial activity, contributing to the pathogenesis and chronic inflammation seen in the disease.

Question 50

smoking aggracates Crohn's disease. True or False

Answer 50

true

Question 51

Recall role of prostaglandins in the GI tract (produced through the COX pathway)

Answer 51

help maintain the integrity of the gastrointestinal lining by promoting mucus and bicarbonate secretion, maintaining blood flow supporting the repair of the mucosal barrier ## Footnote Without adequate prostaglandins, the gut lining becomes more vulnerable to damage. With a compromised mucosal barrier, the gut becomes "leakier," allowing bacteria and toxins to cross the intestinal wall. This can trigger or exacerbate inflammatory responses, particularly in individuals with Crohn's disease who already have an underlying dysregulated immune response. NSAIDs can cause direct irritation or ulceration of the gastrointestinal lining, further increasing the risk of flare-ups in Crohn's disease.

Question 52

How can NSAIDs worsen Crohn's disease

Answer 52

* Inhibition of Prostaglandins: NSAIDs block the cyclooxygenase (COX) enzymes that are responsible for producing prostaglandins. Prostaglandins help maintain the integrity of the gastrointestinal lining by promoting mucus and bicarbonate secretion, maintaining blood flow, and supporting the repair of the mucosal barrier. Without adequate prostaglandins, the gut lining becomes more vulnerable to damage. * Increased Intestinal Permeability: With a compromised mucosal barrier, the gut becomes "leakier," allowing bacteria and toxins to cross the intestinal wall. This can trigger or exacerbate inflammatory responses, particularly in individuals with Crohn's disease who already have an underlying dysregulated immune response. Direct Mucosal Damage: NSAIDs can cause direct irritation or ulceration of the gastrointestinal lining, further increasing the risk of flare-ups in Crohn's disease.

Question 53

Name 3 environmental factors for Crohn's

Answer 53

Smoking, NSAIDs, DIET

Question 54

Location of UC

Answer 54

Affects rectum extending proximally Inflammation is limited to the colon Relapsing & remitting course

Question 55

UC age group

Answer 55

Peak incidence 20-30s

Question 56

UC assessment/diagnosis

Answer 56

Bloods: C-reactive protein (CRP) Albumin (a negative acute phase reactant) Platelets (thrombocytosis indirect marker) Plain AXR Endoscopy Histology

Question 57

Histology of UC. which part of the lining does it affect?

Answer 57

affects mucosal layer only - crypt distortion + abscess - - abscence of goblet cells

Question 58

UC LT complication

Answer 58

Increased risk of colorectal cancer Determined by: severity of inflammation duration of disease disease extent

Question 59

extra intestinal manifestation of UC

Answer 59

Question 60

Inflammation (i.e. thickening) of the wall can result in a fibrotic stricture (i.e. narrowing) true or false

Answer 60

true

Question 61

# PSC = primary sclerosing cholangitis PSC is most commonly associated with UC true or false + name complications

Answer 61

true - cirrhosis - choalgiocarcinoma

Question 62

location/distribution of Crohn's

Answer 62

Can affect any region of GI tract from mouth to anus Skip lesions Transmural inflammation Colonic Crohn’s increasing in incidence

Question 63

Crohn's disease is a peri-anal disease. true or false

Answer 63

true

Question 64

Corhn's can lead to fistula development. true or fase

Answer 64

true

Question 66

describe Crohn's symptoms based on the site of the disease

Answer 66

Question 67

diagnosis/assessment of Crohn's

Answer 67

Clinical exam Evidence of weight loss, RIF mass, peri-anal signs Bloods CRP, albumin, platelets, B12 (terminal ileum), iron stores, FBC Stage disease extent Colonoscopy

Question 68

differences in the histology of Crohn's and UC

Answer 68

Question 69

outline the small bowel assessment tests

Answer 69

CT abdomen & pelvis Small bowel MRI Pelvis MRI (peri-anal disease) Technetium-labelled white cell scan Barium follow through

Question 70

diet is not implicated in the pathogenesis of Crohns, but can influence symptoms. true or false

Answer 70

true

Question 71

# true or false SMOKING aggravates Crohns: worse disease outcome more rapid recurrence post-surgery

Answer 71

true

Question 72

how are fistulas created in Crohns?

Answer 72

In Crohn’s disease, the inflammation goes through the entire thickness of the intestinal wall (transmural inflammation). This deep inflammation can lead to: Ulceration: Deep ulcers form and extend through the bowel wall. Tunnel Formation: The ulcers can eventually create tunnels connecting the bowel to nearby structures (like other parts of the intestine, skin, bladder, etc.). Fistulas: These tunnels, when they connect two different surfaces, are called fistulas.

Question 74

is toxic megacolon associated with UC? why?

Answer 74

yes UC involves continuous inflammation of the colon only, often diffusely affecting large areas of the colonic mucosa. That widespread inflammation can lead to paralysis of the colonic muscles → dilation → toxic megacolon. Crohn’s usually causes segmental and transmural inflammation that can be anywhere in the GI tract, so you’re more likely to see strictures, fistulas, and abscesses, but not as much toxic megacolon.