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Crohns Disease
Alex Chan FHCC NYCOM Family Medicine

Today, we are going to talk about

IBD: Crohns Disease Definition/Epidemiology Risk Factors Pathogenesis Pathology Clinical Manifestations Differential Diagnosis Diagnosis Treatment Preventive Measure

Definition/Epidemiology: Crohns Disease

Inflammatory Bowel Disease: is a chronic condition resulting from inappropriate mucosal immune activation.

Epidemiology: Men and women are equally distributed bimodal distribution that occurs between ages 15-40 and between 50 and 80 eastern European (Ashkenazi) Jewish descent most common in North America, northern Europe, and Australia worldwide is on the rise Africa, South America, and Asia

+ Risk Factors I

Ethnicity and race Both UC and CD are more common in individuals with Jewish ancestry than those without Jewish ancestry.

Age Bimodal distribution: b/t ages 15 and 40 years with a second peak between age 50 and 80 years.
Gender: M = W Family history Approximately 10 to 25 percent of affected patients have a first degree relative with CD.

W/ evidence of concordance in disease type, location, and severity of the clinical course.

Genetic susceptibility genes The IBD gene (IBD1) encodes a product NOD2 also referred to as CARD 15 increased risk of CD. Smoking Cigarette smoking decreases the risk of developing UC and increases the risk for CD.

Diet "Western" style diet (processed, fried, and sugary foods) is associated with an increased risk of developing CD

Risk Factors II +

Oral contraceptives conflicting data pertaining to oral contraceptives and IBD. Given the uncertainty, it is reasonable to continue oral contraception in patients with IBD who are doing well, but stop if otherwise. Perinatal events Studies have demonstrated a 4x risk of IBD in those who had "health events" such as a diarrheal illness during the perinatal period. Nonsteroidal antiinflammatory drugs (NSAIDs) Reports suggest that NSAIDs increase the risk for the development of IBD and may exacerbate underlying IBD. Data pertaining to COX-2 selective inhibitors is limited.

Most patients can tolerate at least short-term treatment without exacerbation of disease.

Psychosocial factors Stress does not appear to be related to the onset of IBD but may have a role in the exacerbation of symptoms.

+ Pathogenesis?

Idiopathic disorder So what are we thinking? Yesit all leads to something

genetic eventually.

NOD2, ATG16L, and IRGM

combination of defects in host interactions with intestinal microbiota, intestinal epithelial dysfunction, and aberrant mucosal immune responses

Pathology

Clinical Manifestations I
Distribution Small bowel (distal ileum) Ileocolitis (both ileum and colon) ~80% ~50% Percentage

Colon (exclusively)
Anal involvement Perianal Disease Predominant in mouth or gastroduodenal area Esophagus and Proximal small bowel

~20%
50% of Colon exclusive patients ~33% <5% Few percent

+ Clinical Manifestations II Systemic: fever, weight loss

Abdominal pain Crampy abdominal pain is a common, regardless of disease distribution. Non Bloody Diarrhea fluctuates over a long period of time. However, the stool may be guiac positive but gross blood is uncharacteristic of Crohns Disease Transmural inflammation can cause: Fistulas: (33 and 50 percent after 10 and 20 years, and up to 45% in patients before diagnosis)

Enteroenteric fistulas may be asymptomatic or present as a palpable mass Enterovesical fistulas lead to recurrent urinary tract infections, often with multiple organisms, and to pneumaturia Fistulas to the retroperitoneum may lead to psoas abscesses or ureteral obstruction with hydronephrosis Enterovaginal fistulas may present with passage of gas or feces through the vagina Enterocutaneous fistulas can cause bowel contents to drain to the surface of the skin.

Phlegma: a walled off inflammatory mass without bacterial infection that may be palpable on physical examination Abscesses Perianal disease

Clinical Manifestations III

Malabsorption

absorbed by specific receptors in the distal ileum > = 50 to 60 cm of terminal ileum is diseased or resected.

Unabsorbed bile salts enter the colon resulting in a secretory or "bile salt" diarrhea.
INC in synthesis of bile salts will compensate UNTIL

more than 100 cm involvement of the terminal ileum

depletion of the bile salt pool and fat malabsorption, which causes:

Watery diarrhea:

effects of bile acids on colonic water and electrolyte absorption. bile acid malabsorption since the concentration of bile acids required for micelles for fat absorption is impaired. bacterial overgrowth from small bowel strictures, enterocolonic fistulas (b/t small bowel and colon), and extensive jejunal disease.

Steatorrhea:

Extraintestinal Manifestations I +

These manifestations, which tend to be more frequent with colonic involvement, include: Arthritis primary large joints, most common extraintestinal manifestation Eye involvement uveitis, iritis, and episcleritis (~5%) Skin disorders erythema nodosum, pyoderma gangrenosum (~10%) Primary sclerosing cholangitis approximately 5 percent of patients with an elevation in the serum alkaline phosphatase or gamma glutamyl transpeptidase (GGT) concentration. Secondary amyloidosis is very rare but may lead to renal failure and other organ system involvement Venous and arterial thromboembolism resulting from hypercoagulability

Extraintestinal Manifestations II
Renal stones: Calcium oxalate: due to increase in fat in the colon which causes the calcium to bind to it thus INC free oxalate available for reabsorption Uric acid: due to DEC in urine volume and DEC citrate from the chronic diarrhea. Vitamin B12 deficiency A clinical picture of pernicious anemia can result from severe ileal disease since vitamin B12 is absorbed in the distal 50 to 60 cm of ileum Pulmonary involvement bronchiectasis, chronic bronchitis, ILD, sarcoidosis Bone loss and osteoporosis may result related to glucocorticoid use and impaired vitamin D and calcium absorption

Half time show

Diagnosis

Diagnosis I
A diagnosis

of Crohn's disease should be considered in any patient who presents with: chronic or nocturnal diarrhea (not common in IBD), crampy intermittent abdominal pain (most common), bowel obstruction, weight loss, fever, night sweats, diarrhea (~85%), malaise, arthralgia (most common extraintestinal)

+ Diagnosis II
Laboratory studies:
Laboratory

tests are useful for diagnosing Crohn's disease, assessing disease activity, identifying complications, and monitoring response to therapy. Complete blood count (CBC) Blood chemistry including electrolytes, renal function tests, liver function tests, and blood glucose Erythrocyte sedimentation rate (ESR) C-reactive protein (CRP) Serum iron and vitamin B12 level and nutrition status Culture stool specimen for ova and parasite

Diagnosis III: scopy

Colonoscopic findings in Crohn's disease There are three major endoscopic findings that are specific for the diagnosis of Crohn's disease and help to distinguish it from UC:

Aphthous ulcers Small discrete aphthous ulcers can be seen in early lesions Cobblestoning Serpiginous and linear ulcers can course for several centimeters along the longitudinal axis of the colon Discontinuous lesions They can be adjacent to normal tissue, resulting in "skip areas

Other endoscopic findings that support the diagnosis of Crohn's disease, but are not specific, include the following:

normal rectum supports the diagnosis of Crohn's disease, since UC always involves the rectum. normal vasculature adjacent to affected tissue is seen in Crohn's disease, while loss of vascularity and friability is more typical of UC. Isolated involvement of the terminal ileum is highly suggestive of Crohn's disease.

Diagnosis IV: scopy

Colonoscopy with ileoscopy and biopsy is valuable in the diagnosis of Crohn's disease at the junction of the ileum and colon8 (Figure 1).
Characteristic endoscopic findings include skip lesions, cobblestoning (Figure 2), ulcerations, and strictures. CT enterography (Figure 3) Esophagogastroduodenoscopy:

patients with upper gastrointestinal symptoms asymptomatic patients with iron deficiency anemia;

patients with active Crohn's disease who have a normal colonoscopy.

Procedure depends on anatomic involvement

Differential Diagnosis

Differential Diagnosis of Crohn's Disease Celiac disease Chronic pancreatitis Colorectal cancer Diverticulitis Infection (e.g., Yersinia, Mycobacterium) Irritable bowel syndrome Ischemic colitis Lymphoma of small bowel Sarcoidosis Ulcerative colitis

Staging and Treatment of Crohns Disease

Severity Scale
Severity Criteria

Mild to moderate disease

-ambulatory
-able to take oral alimentation -no dehydration, high fever, abdominal tenderness, painful mass, obstruction, or weight loss of more than 10%

Moderate to severe disease

Severe fulminant disease Remission

-Either patient has failed tx for mild to moderate

disease OR positive pronounced symptoms including fever, significant weight loss, abdominal pain or tenderness, intermittent nausea and vomiting, or significant anemia -Either patient has persistent symptoms despite outpatient steroid therapy OR has high fever, persistent vomiting, evidence of intestinal obstruction, rebound tenderness, cachexia, or evidence of an abscess.

-asymptomatic OR w/o inflammatory sequelae,

including patients responding to acute medical intervention.

Pharmacologic Treatment

+ Just kidding

Severity of disease: Staging and treatment + options III

Supportive and Preventive Measures

Conclusion

Multifactoral pathogenesis: genetics, lifestyle, ethinicity, etc.

Not ONE specific mutation/change will make the diagnosis

Crampy, intermittent abdominal pain, diarrhea, arthritis are very common in patients with Crohns Disease
Evidence of transmural inflammation, fistulas, skip lesions, exclusive terminal ileum involvement, and non-caseating granulomas are some specific indications of disease. Once the diagnosis is made, be sure to stage the severity as best as possible in order to treat the patient using the right medications.

THANK YOU!

Resources

Up To Date: Clinical manifestations, diagnosis and prognosis of Crohn's disease in adults

Robbins Pathological Basis of Disease by Kumar, et al. AAFP: Diagnosis and Management of Crohn's Disease, by Jarvis, T. Wilkins, and Patel, J. 2011

Disclaimer: ALL the information in this powerpoint was retrieved from the above resources. NONE of the information presented here were from my own finding and ALL credit should be given to the hard work to those who have provided the knowledge.