IBD Flashcards

1
Q

Contrast the presenting symptoms of UC and CD.

A

UC: continuous inflammation, colon only, superficial inflammation

CD: patchy inflammation, most to anus involvement, full thickness inflammation, fistulas

both: risk of colon cancer, extraluminal manifestations, strictures

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2
Q

When does dx. of IBD often occur?

A

presentation esp. during adolescence and young adult years (suggesting hormonal factors at play); controversial second peak between 5th and 6th decades of life

sigh male predominance of UC, slight female predominance of CD

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3
Q

Explain the pathology of IBD (working hypothesis).

A

IBD results from dysregulated response of the mucosal immune system towards intraluminal antigens of bacterial origin in genetically predisposed individuals, thought to be triggered by some environmental cue

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4
Q

In what layers of the intestine are GALT found?

A

within the mucosa or spanning the mucosa and submucosa (macroscopically visible as Peyer’s patches)

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5
Q

What role does immune tolerance play in IBD?

A

IBD is thought to include over-responsiveness of mucosal T-cells to normal bowel flora- lack of immune tolerance- possibly due to a defect in the suppression by T effector cells leading to expansion and ineffective apoptosis

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6
Q

What is the predominant immune response in CD and UC?

A

CD: T-cell driven, TH1 cytokine response (IL-12, INF-y and TNF-a)

UC: enhanced humoral response and T-cell response, TH2 cytokine driven (IL-5, IL-13)

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7
Q

Highlight some genetic factors that are thought to have a role in IBD.

A

NOD2/CARD15: mediates innate immune response to microbial pathogens, mutation leads to abnormal production of inflammatory cytokines (confers higher risk for fibrostenosis)

IL-23 receptor variants: dives innate and T-cell mediated intestinal inflammation; can be protective or confer risk

ATG16L1: defect in genes involved in autophagy (important in restricting microbe growth) found in patients with CD

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8
Q

How does smoking effect IBD?

A

UC: current smokers have some degree of protection

CD: smoking increases risk of disease and more frequent flares

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9
Q

How do NSAIDs, OCs, diet and infection interact with IBD?

A

NSAIDs can worsen flairs
OCs have a controversial role in IBD
diet has no proven connection to development of IBD
multiple bacteria have been studied in connection with IBD but none have shown definitive connection

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10
Q

Explain the “hygiene hypothesis and how it relates to IBD.

A

IBD is thought to be more common in the developed world due to low level/delayed exposure to common childhood infectious agents due to improved hygiene negatively effecting immune development

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11
Q

Describe the prevalence of Crohn’s disease by location.

A

45% ileocolitis
30% Ileitis/jejunoiletis
20% colitis
5% Gastroduodenitis

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12
Q

What are the presenting signs and symptoms of CD?

A

abdominal pain, diarrhea (usually non-bloody except with colon involvement), weight loss, fatigue, iron deficiency anemia, extra intestinal manifestations

ileocolitis: RLQ pain, diarrhea, may mimic appendicitis
ileitis/jejunitis/jejunoilietis: diarrhea, bloating, bowel obstruction
colitis: hematochezia, diarrhea, tensemus

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13
Q

Describe the perianal disease of CD.

A

occurs in 20% of patients with CD

common accompanied by elephant ear skin tags, fissures, fistula +/- abscess

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14
Q

What are possible complications of Crohns?

A

vitamin/mineral deficiency (iron, B12, Vit D)
stricture (active inflammation may be treatable medically)
fistula formation
perforation (require broad spectrum abx and surgery)
abscess formation
colon cancer (colon must be included in disease)

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15
Q

What other diseases could present similar to CD and UC?

A

infectious colitis, mesenteric ischemia, radiation enteritis, microscopic colitis, graft-host dz, systemic vasculitis, ischemic colitis, diverticular disease associated colitis

NSAID use, gold, solitary rectal ulcer syndrome, anal fissure, hemorrhoids

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16
Q

What labs might you get on initial assessment of CD suspected patient?

A

CBC, CRP, ESR, fecal calprotectin (fecal leukocytes)

possible imaging by CT, MR, colonoscopy with biopsy to confirm dx, capsule entersscopy with biopsy and capsule endoscopy (second line)

17
Q

What findings of colonoscopy are common in Crohn’s disease?

A

linear,s stellate ulcers

cobblestoning

18
Q

What serologic studies may be helpful in differentiating Crohns and UC?

A

ASCA is expressed in 60% of patients with CD (not specific enough for dx)

19
Q

List the signs and symptoms of UC.

A

fecal urgency, tenses, hematochezia, abdominal pain, fever, iron deficiency anemia and extra intestinal manifestations

20
Q

Name complications of UC.

A

iron deficiency anemia, uncontrolled GI bleeding, toxic megacolon/perforation (requires emergency colectomy), PSC, colon cancer

21
Q

T/F UC patients with disease of only proctitis are at 50% increased risk of CRC.

A

false- those with proctitis have risk of the general population for colorectal cancer

note for all other manifestations risk increases 8-10 years after dx at which time surveillance should be initiated (those with no dysplasia and extensive colitis require repeat q 1-2yrs)

22
Q

When would you expect to see the extra intestinal manifestations of IBD?

A

may precede development of bowel disease and while some may closely related to bowel disease course, others are independent

sym. usually respond to standard IBD therapy and can effect all organ systems

23
Q

List common extra intestinal manifestations of IBD.

A

erythema nodosom, pyoderma gangrenosum

enterpathic arthritis, spondyltitis, sacroilitis

iriitis, uveitis, episcerititis