Crohn disease Flashcards

1
Q

definition of crohn’s

A

inflammatory bowel disease,

mostly affects young adults and adolescents between the ages of 15 and 35
second peak at 60 years
m>f
whites and jews

located in the terminal ileum, but can discontinuously (skip lesion) affect the entire gastrointestinal tract

eads to complications such as fistulas, abscesses, and stenosis

linical features include diarrhea, weight loss, and abdominal pain in the right lower quadrant (RLQ), as well as extraintestinal manifestations in the eyes, joints, or skin.

difficult to diagnose because there is no confirmatory test

Acute episodes rx w/ corticosteroids,
severe cases,: immunosuppressants

Crohn disease cannot be cured!!! (in contrast to ulcerative colitis). The goal of treatment is thus to avoid the progression and recurrence of inflammatory episodes.

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2
Q

what causes crohn’s dusease

A

balance between proinflammatory and anti-inflammatory mediators from unknown cause

Nicotine consumption is the only (known) controllable risk factor for Crohn disease.
RF
1)Nicotine abuse
-Nicotine consumption is the only (known) controllable risk factor f

2) Familial predisposition -mutation of the NOD2(all ppl w/ CD have nod2 but not all pl w/ NOD2 mutation have CD)
- HLA-B27 association

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3
Q

pathophys of CD

A

Unknown mechanisms (possibly NOD2) lead to the activation of lymphatic cells (Th1) in the intestinal walls
→ inflammation
→ local tissue damage (edema, ulcers, necrosis) → obstruction
d/2 fibrotic scarring, stricture, and strangulation of the bowel

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4
Q

pathophys of abscess & fistulae

A
intestinal aphthous ulcers form 
→ transmural fissures and inflammation of  intestinal walls 
→ adherence to other organs or skin 
→ penetration of adjacent organs/skin 
→ microperforation
→abscess formation  
or 
→ macroperforation into these structures 
→ fistula formation
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5
Q

where does crohn’s disease

A

usually terminal ileum/ colon or entire GI stystem from mouth to anus in skip leasion manner

SPARES RECTUM

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6
Q

how may NOD2 mutation increase risk of CD

A

1)loss of function mutations in NOD2
→ allow bacteria to enter the intestinal mucosa
→ cause an unregulated inflammation

2)Dysfunctional NOD2
→ cause overactivity of the NF-κB signaling pathway
→ ↑ production of pro-inflammatory cytokines and antimicrobial peptides
→ chronic autoinflammation

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7
Q

sx of CD

A

non-bloody, chronic diarrhea (micro bleeding w/ occult blood causes iron def anemia!!)

Abdominal pain, typically in the RLQ

malabsoprtion sx

  • failure to thrive
  • vitb12 def ( inflamed terminal ileum)

sx d/2 reduced bile acid absorption in intestines

  • -def of fat sol vit
  • -gallstones
  • -kidney stones(d/2/ excess ffa d/e/ loss of bile acids, Ca2 binds to ffa instead of oxalate, oxalate accum in kidney and stone forms)

abscesses & enterocutaneous fistula between ileium and perianal reion (FIRST SIGNS)

bowel obstruction

peirtonitis d/2 perforation

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8
Q

extraintestinal sx of CD

A

Joints: enteropathic arthritis (e.g., sacroiliitis)

Eye: iritis, episcleritis, uveitis

skin diseases;
-Erythema nodosum
(inflammation of subcutaneous fat caused by a delayed hypersensitivity reaction)

-Acrodermatitis enteropathica
(Zinc deficiency may cause bullous skin abrasions, especially on the hands, feet, and genital area. not specific for crohn’s)

Pyoderma gangrenosum
( very painful, rapidly-progressive, red spots that can change into purulent pustules or deep ulcerated lesions with central necrosis)

oral apthae

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9
Q

dg of CD

A

Laboratory tests

1) Blood
- inflamm markers↑ CRP, ↑ –ESR, ↑ thrombocytes, and ↑ leukocytes
- Anemia
- ↑ ASCA (Anti-Saccharomyces cerevisiae mannan antibodies for UC dx)

Feces
Stool analysis to rule out gastroenteritis caused by bacteria
occult blood

IMAGING
-axr
-barium swallow
String sign ( inflammation and fibrosis may narrow the intestinal lumen in other sections)
Creeping fat

US: see abscesses/fistulas

Endoscopy confirms the diagnosis, assesses the extent of the disease, differentiates CD from other diseases

HISTOLOGY: Non-caseating granulomas & Giant cells

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10
Q

which sign on barium swallow is pathognomic for CD

A

creeping fat: Proliferated mesenteric fat between the intestinal loops is pathognomonic for CD.)

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11
Q

Ileocolonoscopy findings

A

typical segmental/ discontinuous involvment of intestines (skip lesions)

Linear/transmural ulcers (snail trails)

aphthous hemorrhagic mucosa

Cobblestone sign: characteristic appearance of Inflamed sections followed by deep ulcerations that resemble uneven cobblestones

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12
Q

rx of CD (no cure)

A

general rx

  • nicotine asbstinence
  • lactose freee diet d/2 2ndairy lactase def
  • vit su for mmalabsoprtion
  • excacerbation:avoid dietary fibre & parenteral nutrition
pharmacotherapy 
w/ step up therapy// top down therapy
-antidiarrhoea med(loperamide)
-systemic corticosteriods (prednisone) 
-immunosuppresents if steroids fail (tnf alpa ab's (infliximab)// methotrexate) 

surgery(aims to resect non func/ damaged intestines but preserve overall func/health

  • ileostomy, ileocolostomy, colectomy,proctocolectomy
  • abscess:percutaneous drainage/ surgical drainage of
  • fistula: fistulectomy
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13
Q

indications of surgery in CD

A

Failed medical therapy

Severe complications abscesses, perforation, toxic megacolon, obstruction, stricture, hemorrhage

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14
Q

why do pt w/ cronh’s need freq check ups e/ endoscopy

A

increased risk of colorectal carcinoma and/or recurrence of the disease

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15
Q

complications of crohn’s

A

colorectalcarcinoma

short bowel sx after surgery

osteoporosis

reduced growth!

fistula’s (3)

  • enterocutaneous fistulas: inestinal content on skin
  • gasstrocolic fistulas: weight loss. abd pain, foul burps
  • rectovaginal fistula: stool via vag
  • aortoenteric fistula: rectal bleed
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16
Q

prognosis

A

no cure

common relapses

common development of complications

normal life expectancy w/ rx