IBD Flashcards
Inflammatory Bowel Disease (IBD)
general
Term that describes disorders involving long-standing (chronic) inflammation of the digestive tract caused by an abnormal immune response in the bowel
Occurs in genetically susceptible individuals
Types include:
Crohn’s disease
Ulcerative colitis
Differentiation:
Location and depth of involvement in the bowel wall
Spectrum of disease:
Mild symptoms – debilitating condition with life-threatening complications
Crohn’s Disease
general
Chronic, recurrent condition that causes patchy transmural inflammation that can involve any part of the gastrointestinal tract (mouth to anus)
Epidemiology:
Incidence:bimodal distribution
15–25 years(slightly younger average than in ulcerativecolitis)
Smaller peak occurs between 50 and 70 years of age
Most common among whites and eastern European (Ashkenazi) Jews
“skip lesions”
Crohns
RF
Smoking- (not a RF for UC)
Genetics:
HLA-B27
NOD2gene mutation → affects the body’s ability to recognize and attack luminal pathogens (bacterial)
Family historyofIBD
Twin concordance rate is 55%
15% ofpatientswith CD have an affected first-degree relative
Decreased physical activity
Decreased fiber intake
Increased dietary fat intake
Crohns
patho
Multifactorial
Combination of dysregulation of the intestinalepithelium and theimmune system
Mutations of the NOD2gene→ defects in the epithelial barrier of the gastrointestinal (GI) tract → more pathogens penetrate the GI tract →recruitmentand activation ofcytotoxiccells that release pro-inflammatory cytokines →intestinal inflammation
Lack of thedown-regulationof immune responsiveness →chronic inflammation → granulomas
Intestinal tissue damage includingedema, ulcerations, erosions, andnecrosis
Inflammationis transmural and may lead tointestinal perforation and fistulas
Chronic and repetitive episodes →scarring,fibrosis, and obstruction of the intestinal wall
Crohn’s
Location & Pattern of Inflammation
May include any portion of the GI tract
The most common sites:
Terminal ileum
Proximal colon
Associated withskip lesions (discontinuous patchy inflammation)
Therectum is often spared
Inflammation extends through the entire thickness of the bowel wall
Crohns
General manifestations
Low-grade fever
Fatigue
Loss of appetite
Weight loss
Crohns
GI manifestations
- Chronic, intermittent,diarrhea (usually non-bloody)
-
Crampyabdominal pain(diffuse or localized to theright lower quadrant)
Flatulence andbloating - Signs ofmalabsorption with vitamin B12and D deficiencies andiron deficiencyanemia
gallstones more common in Crohns (not UC)
Crohn s
Extraintestinal manifestations
- Aphthous ulcers
- Gallstones → decreased bile acid reabsorption
- Pyoderma gangrenosum: rapidly progressive painful, red papules → pustules → deep ulcers with centralnecrosis
- Erythema nodosum: painful, red nodules that usually appear on theshins
- Eyeinflammation(uveitis,iritis, episcleritis)
- Peripheralarthritis,ankylosing spondylitis, orosteoporosis
aphthous ulcers, erythema nodusum, pyoderma gangrenosum
chrohns
lab Dx
Complete blood count → anemia,leukocytosis, and thrombocytosis
Basic metabolic panel → electrolyte imbalance
↑ESR and CRP
Malabsorption evaluation
Fecal calprotectin (concentrations demonstrate good correlation with intestinal inflammation)
crohns
Stool studies
May be used to exclude other causes of inflammatory diarrhea
Clostridioides difficiletoxin studies in cases of recent antibiotic use
Crohns
Imaging
Imaging Studies
CT scan of abdomen and pelvis, abdominal MRI, or abdominal x-ray with barium swallow
Assess the extent and severity of disease as well as any complications (perforation, fistulas, abscess, stenosis)
Signs of intestinal inflammation: wall thickening with mucosal enhancement, distortion, and hyperintensity
Narrowing of the intestinal lumen giving a “string sign”
Crohns
Endoscopy/Colonoscopy
with biopsy
Gold standard for diagnosis
Transmural inflammation
Skip lesions in any portion of the GI tract, usually sparing therectum
Ulcers, fissures, and fistulas (cobblestone appearance)
Crohns
Drug classes for Tx (4)
- Abx
- corticosteroids
- immunomodulators
- biologics
crohns
Antibiotics
Metronidazole or ciprofloxacin
Used for complications such as abscesses and fistulas
crohns
Corticosteroids
Budesonide (mild) or prednisone (moderate-severe disease)
Used for acute disease flare-ups
Duration is limited due to complications of long-term use
crohns
Immunomodulators
Methotrexate, azathioprine or sulfasalazine
Used after corticosteroid induction therapy to allow tapering and withdrawal ofcorticosteroids
Also used in combination with anti-TNF agents to induce remissionand reduce the likelihood of treatment failure
probaby specialist not us
crohns
Biologics
Infliximab, adalimumab, golimumab (anti-tumor necrosis factor agents) or vedolizumab (adhesion molecular inhibitors)
For induction and maintainingremission
probably specialist noy us
crohns
general Tx
Smoking cessation
Vitamin B12and D for severe disease or prior to ileal resection
Avoidance of NSAIDs (exacerbate disease)
Antidiarrheal agents
crohns
Surgical intervention:
Intestinal resection, reserved for medical treatment failure
May also be necessary in case of complications such as fistulas,perforation, or obstruction
crohns
Colorectal screening
Colonoscopyto screen forcolorectal cancer
8–10 years after initial diagnosis
Every 1–2 years thereafter
Crohns
complications
Small or largebowel obstruction
GI bleeding
Intestinal perforation
Fistula formation
Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body
Loops of bowel (eneteroenteric)
Intestine andbladder (enterovesical)
Intestine andvagina(enterovaginal)
Intestine andskin (enterocutaneous)
Intra-abdominal or retroperitoneal abscess formation
Perianal disease- Crohns not UC
Skin tags
Anal fissures
Perianal abscesses
Increased risk ofcolorectal cancer
UC
general
Inflammatory condition that involves the mucosal surface of the colon
Epidemiology
Incidence: bimodal distribution
15–35 years
Smaller peak occurs between 50 and 70 years of age
Most common among whites and eastern European (Ashkenazi) Jews
Disease risk islower in smokers
UC
Risk Factors
Genetics:HLA-B27
Family historyofIBD
Twin concordance rate is 10%–15%
First-degree relatives have a 4 times higher risk of developing UC
Increased dietary fat intake
Nonsteroidal anti-inflammatory drug (NSAID) use
Psychological stress and intestinal infectionsmaytrigger disease onset
UC
Pathophysiology
Multifactorial
Combination of dysregulation of the intestinalepithelium and theimmune system
Defects in theepithelial barrier of the gastrointestinal (GI) tract allow for more pathogens to penetrate → recruitmentand activation ofcytotoxiccells
pANCA(perinuclear antineutrophil cytoplasmic antibodies) are thought to recognize nonpathogenic bacteria (E.coli) and epithelial cells as pathogens
Excessivereleaseof pro-inflammatorycytokines which target epithelial cells → intestinalinflammation
Causes intestinalepithelium damage including ulcerations,erosions, andnecrosis
UC
Location & Pattern of Inflammation
Invariablyinvolves therectum and may extend proximally through thecolonin a continuous fashion
Small intestine is unaffected
Skip lesions are not seen
Inflammation is limited to the mucosa
UC
General manifestations
Signs ofanemia
Weight loss
Low-gradefever
UC
GI manifestations
Bloodydiarrheathat lasts from weeks to months (with or without mucus)
Fecal urgency and/or incontinence
Tenesmus
Colicky lower abdominalpainthat istemporarily relieved bydefecation
UC
Extraintestinal manifestations
Aphthous ulcers
Primary sclerosing cholangitis
Pyoderma gangrenosum: rapidly progressive painful, red papules → pustules → deep ulcers with centralnecrosis
Erythema nodosum: painful, red nodules that usually appear on theshins
Eyeinflammation(uveitis, episcleritis)
Peripheralarthritis,ankylosing spondylitis, orosteoporosis
UC
Lab and stool studies
Complete blood count → anemia,leukocytosis, and thrombocytosis
Basic metabolic panel → electrolyte imbalance
↑ESR and CRP
Fecal calprotectin (concentrations demonstrate good correlation with intestinal inflammation)
Stool studies
May be used to exclude other causes of inflammatory diarrhea
Clostridioides difficiletoxin studies in cases of recent antibiotic use
UC
imaging
CT scan of abdomen and pelvis, abdominal MRI, or barium enema with abdominal x-ray
Thickened bowel wall,colondilation
Barium enema: micro-ulcerations, loss ofhaustra with “lead pipe” appearance
Colonoscopy - Gold standard
UC
Colonoscopy
with biopsy
Gold standard for diagnosis
Helps to determine the extent of disease
Contraindicated during an acute exacerbation due to risk of intestinalperforation- use steroids to calm before visualization
Diffuse and continuous mucosal inflammation always involving therectum
Friable mucosa
Pseudopolyps: raised areas caused by recurrent ulceration, healing, andscarringof the mucosa
UC
Drug classes for Tx (5)
- corticosteroids
- Aminocalicylates
- immunuomodulators
- biologics
- antidiarrhea agents
UC
Corticosteroids
For acute disease flare-ups
Duration is limited due to complications of long-term use
UC
Aminosalicylates
Mesalamine
UC
General and surgical Tx
General measures:
Avoid use of NSAIDs
Avoid use of opioids and anticholinergics → increased risk of complications
Surgical intervention:
Colectomy
Considered curative
Reserved for severe diseases, ineffective medical therapy, refractory toxicmegacolon, or biopsy-provenmalignancy
Required in case of complications
UC
preventative care
Preventative care:
Colonoscopy to screen forcolorectal cancer(higher risk inpatients with UC)
8–10 years after initial diagnosis
Every 1–2 years thereafter
UC
Complications
GI bleeding
Large bowel obstruction
Fulminant colitis
Caused by colonic mucosalinflammation
Presents with > 10 bloody stools per day, abdominal painand distension, and systemic symptoms ofshock
Increases risk of developing toxicmegacolon
Toxicmegacolon
Involvesinflammationextending beyond the mucosal layers to the muscular layers of thecolon
Intestinal perforation (rare)
Increased risk ofcolorectal cancer
