IBD Flashcards

1
Q

Inflammatory Bowel Disease (IBD)

general

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Crohn’s Disease

general

A

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”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Crohns

RF

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Crohns

patho

A

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 cytokinesintestinal 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Crohn’s

Location & Pattern of Inflammation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Crohns

General manifestations

A

Low-grade fever
Fatigue
Loss of appetite
Weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Crohns

GI manifestations

A
  • 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Crohn s

Extraintestinal manifestations

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
A

aphthous ulcers, erythema nodusum, pyoderma gangrenosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

chrohns

lab Dx

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

crohns

Stool studies

A

May be used to exclude other causes of inflammatory diarrhea
Clostridioides difficiletoxin studies in cases of recent antibiotic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Crohns

Imaging

A

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”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Crohns

Endoscopy/Colonoscopy

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Crohns

Drug classes for Tx (4)

A
  1. Abx
  2. corticosteroids
  3. immunomodulators
  4. biologics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

crohns

Antibiotics

A

Metronidazole or ciprofloxacin
Used for complications such as abscesses and fistulas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

crohns

Corticosteroids

A

Budesonide (mild) or prednisone (moderate-severe disease)

Used for acute disease flare-ups
Duration is limited due to complications of long-term use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

crohns

Immunomodulators

A

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

18
Q

crohns

Biologics

A

Infliximab, adalimumab, golimumab (anti-tumor necrosis factor agents) or vedolizumab (adhesion molecular inhibitors)
For induction and maintainingremission

probably specialist noy us

19
Q

crohns

general Tx

A

Smoking cessation
Vitamin B12and D for severe disease or prior to ileal resection
Avoidance of NSAIDs (exacerbate disease)
Antidiarrheal agents

20
Q

crohns

Surgical intervention:

A

Intestinal resection, reserved for medical treatment failure
May also be necessary in case of complications such as fistulas,perforation, or obstruction

21
Q

crohns

Colorectal screening

A

Colonoscopyto screen forcolorectal cancer
8–10 years after initial diagnosis
Every 1–2 years thereafter

22
Q

Crohns

complications

A

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

23
Q

UC

general

A

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

24
Q

UC

Risk Factors

A

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

25
Q

UC

Pathophysiology

A

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

26
Q

UC

Location & Pattern of Inflammation

A

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

27
Q

UC

General manifestations

A

Signs ofanemia
Weight loss
Low-gradefever

28
Q

UC

GI manifestations

A

Bloodydiarrheathat lasts from weeks to months (with or without mucus)
Fecal urgency and/or incontinence
Tenesmus
Colicky lower abdominalpainthat istemporarily relieved bydefecation

29
Q

UC

Extraintestinal manifestations

A

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

30
Q

UC

Lab and stool studies

A

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

31
Q

UC

imaging

lead pipe, loss of haustration
A

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

32
Q

UC

Colonoscopy

A

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

33
Q
don't memorize
A
34
Q

UC

Drug classes for Tx (5)

A
  1. corticosteroids
  2. Aminocalicylates
  3. immunuomodulators
  4. biologics
  5. antidiarrhea agents
35
Q

UC

Corticosteroids

A

For acute disease flare-ups
Duration is limited due to complications of long-term use

36
Q

UC

Aminosalicylates

A

Mesalamine

37
Q

UC

General and surgical Tx

A

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

38
Q

UC

preventative care

A

Preventative care:
Colonoscopy to screen forcolorectal cancer(higher risk inpatients with UC)
8–10 years after initial diagnosis
Every 1–2 years thereafter

39
Q

UC

Complications

A

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

40
Q
A