301 IBD Flashcards
What are the abdominopelvic regions?
- Right hypochondriac region
- Epigastric region
- Left hypochondriac region
- Right lumbar region
- Umbilical region
- Left lumbar region
- Right iliac region
- Hypogastric region
- Left iliac region
How does the sigmoidoscope work?
Passed through anus into colon
How does colonoscope work?
Passed through anus into colon
Sigmoidoscopy: procedure and outcomes
- Routine in patients with lower abdominal symptoms or in diarrhoea cases
- Normal mucosa is shiny with superficial vessels & no contact bleeding, biopsy if needed
Can identify: colitis, polyps (+ removal), haemorrhoids, neoplasms
Flexible sigmoidoscopy: procedure and outcomes
- Reach up splenic flexure, requires bowel preparation, routine in patients w/ increased stool frequency/looseness/rectal bleeding
- Normal mucosa is shiny with superficial vessels & no contact bleeding, biopsy if needed
Can identify: colitis, polyps (+ removal), haemorrhoids, neoplasms
Gastroscopy or OGD: procedure and outcomes
- Upper GI disorders, visual endoscopes relay colour images to HD monitor, therapeutic OGD treats upper GI bleeding & obstruction, requires fasting
- Can identify: reflex oesophagitis, gastritis, ulcers & cancer
Colonoscopy: procedure and outcomes
- Good visualisation of whole colon & terminal ileum, biopsies obtained, polyps removed, benign strictures dilated, malignant strictures stented, oral iron stopped 1 week prior, bowel cleanse required
- Can identify: cancer, polyps, diverticular disease, IBD
Proctoscopy: procedure and outcomes
- For all patients with history of bright red rectal bleeding to look for anorectal pathology, rigid sigmoidoscope is too narrow & long to enable adequate exam of anal canal
- Haemorrhoids are seen as purplish veins, fissures may be seen
What is IBD?
Immune-mediated chronic intestinal condition
UC or CD
CUTE (colitis of uncertain type of etiology)
Possible causes of IBD
Genetics
Environment
Smoking
OCP
Appendectomy
Abx
NSAIDs
Diet
Infection
Gut microflora
Host immunity
Genome wide studies of IBD
- NOD 2/CARD15 on chromosome 16
- Autophagy genes (ATG16L1, IRGM)
- IL23 and Th17 cytokines
- HLA genes on chromosome 6 modifies disease
- DRB0103 allele: aggressive UC, colonic CD
- DRB0103 and MICA010: perianal disease
- DRM0701: Ileal CD
Crohn’s disease immune response
- In Crohn’s disease, Th1 cells release cytokines (INF-gamma and TNF-alpha), which stimulate macrophages
- Macrophages release harmful substances such as free radicals, proteases & platelet-activating factor
- Leads to unregulated inflammation & tissue destruction
- This process contributes to the ongoing inflammation characteristic of CD
Colonic mucosa comparison: CD and UC
- CD: “cobble-stoning”, fat-wrapping with thicken colon wall & fissures
- UC: ulceration, surviving mucosa (pseudo-polyps), loss of haustra & crypt distortion
Extraintestinal symptoms of CD and UC
Eyes: episcleritis more in CD & uveitis & iritis more in UC
Mucocutaneous lesions
Skin effects
Weight loss
Anaemia
UC less associated w/ gallstones, fistulas or renal stones
Goals of IBD treatment
- Reduce colorectal cancer risk
- Treat & reduce intestinal inflammation
- Promote mucosal healing
- Maintain remission
- Improve QoL
- Treat complications
- Replenish nutritional deficits
- Address psychosocial issues
- Minimise toxicity
- Control & relieve symptoms
Not curative
IBD pharmacological management
Anti-inflammatory drugs
Immunosuppressants
Biologics
Others (antibiotics, analgesics, vitamins)
Crohn’s disease
Any part of GIT (mouth ulcers/anal skin tags)
‘Skip lesions’
Macrophage, neutrophils, T-lymphocytes involvement
Transmural inflammation
What does Crohn’s cause?
Malabsorption (folate deficiency, decreased vitamin B12 (megaloblastic anaemia), decreased iron (iron deficiency anaemia))
What increases Crohn’s risk?
Made worse by smoking
Appendectomy increases risk
What are the onset ages of Crohn’s
2 age peaks 15-30yo and 60-80yo
Ulcerative colitis affects
Affects rectum, spreads to colon
Superficial mucosal inflammation
Continuous
Appendectomy appears ‘protective’
Corticosteroids in IBD
Immunosuppressive, anti-inflammatory
Short courses to induce remission
Adverse effects with long term use (bone)
Slow tapering regimen vs rapid reduction
Ineffective in maintenance
Aminosalicylates in UC
Sulfasalazine, olsalazine, balsalazine are pro-drugs (metabolised by bacteria in gut to form 5-ASA
Oral mesalazine rapidly absorbed in proximal SI & extensively metabolised (MR preparations designed to release mesalazine in distal lumen/colon (site of UC inflammation))
Aminosalicylates contraindicated by and cause what S/Es
Patients allergic to aspirin
Blood dyscrasias, GI side effects
Aminosalicylates MOA
Inhibits LT and prostanoid formation
Scavenges free radicals
Decreased neutrophil chemotaxis
Thiopurines in IBD and risks
E.g. azathioprine, mercaptopurine
(Azathioprine is prodrug of mercaptopurine)
Unlicensed in IBD
Risk of pancreatitis
Thiopurines MOA
Inhibits RNA synthesis
Modulate T cells
What should be assessed before giving thiopurines?
TPMT activity (enzyme that breaks down this kind of drug, if they have polymorphism for this enzyme, it will be hepatotoxic)
Methotrexate in IBD
No evidence in UC
Unlicensed in IBD
Steroid sparing effect
Antimetabolite
Methotrexate MOA
Inhibits enzyme dihydrofolate reductase
Inhibits lymphocyte multiplication
Methotrexate ADRs and interactions
Hepatotoxicity, pneumonitis
+ folic acid to alleviate GI ADR
Interactions with NSAIDs
Ciclosporin MOA and evidence in IBD
Blocks T-lymphocytes
Prevents production of IL-2 and pro-inflammatory cytokines
No evidence in CD
Unlicensed in IBD
Biologics in IBD
E.g. infliximab, adalimumab
Monoclonal antibodies
Increases risk of infection
TB screening necessary
Biologics MOA
Neutralises TNFα
Interrupt the inflammatory cascade
Suppository - site of action & disease extent
Rectum
Proctitis
Foam (do not spread as far as enemas (due to low volume) but have better retention & acceptability) - site of action & disease extent
Sigmoid colon
Proctosigmoiditis
Enema - site of action & disease extent
Descending colon to splenic flexure (in some cases to distal part of transverse colon)
Left-sided (distal) colitis
Pentasa (500mg mesalazine)
Pressed tablet containing mix of drug microspheres with 1, 2 or 3 layers of ethylcellulose
Octasa (800mg mesalazine)
Release of mesalazine only at pH above 7 (within terminal ileum & colon)
Asacol (400mg mesazaline)
Released in terminal ileum & large bowel by effect of pH above 7, the Eudragit S coat disintegrates & releases active constituent
IBD management
Colonoscopic surveillance after 10 years
Bone health: osteopenia & fracture risk
Growth & pubertal development
What to avoid in ileostomy and jejunostomy?
Avoid enteric coated, MR preparations (active ingredient may not be at site of absorption long enough or may bypass completely), avoid prokinetics, laxatives
Diverticulae
Increased intraluminal pressure, herniation of colonic mucosa through weak areas
Diverticular disease
Problems caused by diverticular e.g. change in bowel habit, abdominal pain
Diverticulitis
Acute inflammation of diverticulae
Which is more common in the UK - UC or CD?
UC more common
What GI symptoms do patients usually present with?
Diarrhoea, rectal bleeding, abdominal pain, weight loss, fatigue and fever
Crohn’s also anal fistulas, abscesses and rectal prolapse
Are extra-GI symptoms more commonly found in UC or CD?
CD, more common before GI symptoms become more prominent
Examples:
CD: pauci-articular arthritis and erythema nodosum
UC: joint pain, swelling, and stiffness
What side effects are commonly associated with aminosalicylates?
Indigestion, heartburn, feeling sick (nausea)
diarrhoea, being sick (vomiting), stomach (abdominal) pain, dizziness
Name 2 types of orally administered medications that might be associate with problems in ileostomy patients
Enteric-coated & modified-release medicines are unsuitable as there may be insufficient release of the active ingredient
