CAPA Conference 2015 1 Student Challenge Bowl Inflammatory Bowel Disease Greg Mennie, MSEd, PA-C Associate Professor Marshall B. Ketchum University School of Physician Assistant Studies Polling Instructions • To Use the CAPA Events App: Open the CAPA App, go to “Agenda” and find this session. Click on the session and go to the tab for “Polls.” Answer each polling question when instructed. • For Text Polling from Your Phone: You will be provided the Question ID on upcoming poll slides. Text the Question ID to 79905 and you will be given the opportunity to provide your answer.
Transcript
CAPA Conference 2015
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Student Challenge Bowl
Inflammatory Bowel Disease
Greg Mennie, MSEd, PA-CAssociate Professor
Marshall B. Ketchum UniversitySchool of Physician Assistant Studies
Polling Instructions
• To Use the CAPA Events App: Open the CAPAApp, go to “Agenda” and find this session. Clickon the session and go to the tab for“Polls.” Answer each polling question wheninstructed.
• For Text Polling from Your Phone: You will beprovided the Question ID on upcoming poll slides.Text the Question ID to 79905 and you will begiven the opportunity to provide your answer.
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Objectives
• Compare and contrast the different presenting symptomsof the Inflammatory Bowel Diseases.
• Note the different gastrointestinal structures involved inCrohn’s disease vs Ulcerative Colitis.
• Understand the diagnostic criteria for the InflammatoryBowel Diseases.
• Know the current treatment recommendations for Crohn’sDisease and Ulcerative Colitis.
• List the medical (prescription and non-prescription) andsurgical treatment modalities available for InflammatoryBowel Disease.
• Understand the current diagnostic and monitoringcomponents for patients with Inflammatory Bowel Disease.
SA-CME Question 1
A 21 yo female presents to your office after moving to the area torestart her college career. She states she has always had “stomachproblems”, but feels since moving here she has noticed a lot morecramping and occasional bouts of brown non-bloody diarrhea. Shedenies any travel or other associated symptoms, her weight is stableand her family history is non-contributory. She had a normal CT scan ofher abdomen in the Emergency room approximately 6 monthsago. On this brief history the patient’s most likely diagnosis is:
• 42 year old woman who died after several months of bloodydiarrhea and fever
• 1909– Hawkins described the natural history of UC– Hurst describe the sigmoidoscopic appearance
Epidemiology
• Approximately 1.6 million Americans currentlyhave IBD
• 163 genes associated with IBD (whites)
• Mother may pass along bacteria
– mother mouse can pass along gut-residingbacterium called Sutterella
Inflammatory Bowel Disease
• Ulcerative Colitis– 100,000k new cases annually– Men>women
• > men diagnosis ages 50-60yo
– Median age of diagnosis 34.9 years– family member with IBD– Jewish descent– >Denmark, Iceland, U.S.– Physical/Sexual abuse during childhood (2x’s higher rate)1
• Crohn’s Disease– 33k new cases annually– Men=women– Median age of diagnosis 29.5 years– family member (primary) with IBD– Tobacco use– > Canada
Fuller-Thomson E1, West KJ, Sulman J, Baird SL. Childhood Maltreatment Is Associated with Ulcerative Colitis but Not Crohn'sDisease: Findings from a Population-based Study. Inflamm Bowel Dis. 2015 Jul 30. [Epub ahead of print]
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IBD Distribution• Age
– Peak diagnosis 15 – 35 yo• Rare < 8yo
– Median Age• ulcerative colitis 35 years• Crohn’s disease 30 years
• Gender– men = women– Men
• > North American ulcerative colitis• Older age of diagnosis for ulcerative colitis (50-60 yo)
• Race/Ethnicity– Unclear data
• Increased rates when immigrate to U.S.– Only as a child
Bernstein CN, Shanahan F. Disorders of a modern lifestyle: reconciling the epidemiology of inflammatorybowel diseases. Gut. 2008;57(9):1185–1191.
SA-CME Question 3
The following differentiate UC from Crohn’s except:
1. UC only involves the colon and rectum
2. UC effects the upper most layers of the intestinalwall
3. The lesions of UC are noted as skipped lesions
4. Smoking is considered protective
Take the poll in the CAPA App or text 37195 to 79905
Inflammatory Bowel Disease
• Ulcerative Colitis– Colon and rectum
• Continuous• begins in the rectum and sigmoid• innermost layer of the lining of the intestine
– (mucosa/Submucosa)
• Crohn’s Disease– Any part of the GI tract
• Patches• Transmural
– > the ileum
• Indeterminate Colitis– 10–15%– difficulty distinguishing between ulcerative colitis and Crohn’s
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Inflammatory Bowel Disease
Ulcerative ColitisCrohn’s Disease
Histopathology
• Ulcerative colitis
– confluent inflammatory cellular infiltration closest to the epithelial surface
• Crohn’s disease
– patchy, deep and focal inflammatory cell infiltrates and macrophages
– noncaseating granulomas containing giant cells
UlcerativeColitis
Cro
hn
’s
SA-CME Question 4
A 29 yo Caucasian male states he has had intermittent LLQ pain with bloodydiarrhea over the last 2 months. He states the bouts of pain and diarrhea arebecoming more frequent and he now has the urge to defecate all the time. Herecalls that he had blood in his stool a few years ago and it resolved on itsown so he thought it was related to a hemorrhoid. His weight has decreasedby 7 pounds over the last 2-3 months, and he does note that he occasionallygets some mild pain and swelling in his hands and wrist, which he alsobelieves is much more persistent with his current symptoms. He is otherwisehealthy, takes no medication, and has a non-contributory family history. Withthe current information the patient’s most likely diagnosis is:
• hepatic– primary sclerosing cholangitis, hepatitis, and cirrhosis
Levine, J. S., & Burakoff, R. (2011). Extraintestinal Manifestations of Inflammatory Bowel Disease. Gastroenterology & Hepatology, 7(4),235–241.
Immune Disturbance
Environmental factors
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Genes• 5% to 20% first-degree relative
– > Crohns than Ulcerative Colitis
• Genes affect three types of traits:– Balance of the immune system– Mucosal barrier (first line of defense in the intestine)– Controlling the growth of bacteria
Which of the following is associated withDysbiosis:
1. Marked increase in bacterial diversity
2. Decrease in beneficial bacteria
3. Normal epithelial barrier
4. Decrease in pathogenic bacteria
Take the poll in the CAPA App or text 37197 to 79905
microbiome• Microorganisms that reside in or on the
human body
– bacteria, viruses, fungi, and other microbes
• identifying the constellation of bacteria that reside inthe intestines and understanding how theycommunicate and interact within the intestines andwith the immune system
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Cause or effect
• Symbiosis
– Intestinal balance of bacteria
• Dysbiosis
– overgrowth of harmful organisms
• Bacteria
• Fungal
• Protozoa
• Viral
Dysbiosis• Off Balance
– commensal bacteria vs harmful bacteria in the gut• variations in how the host interacts with its microbiota
– alterations in epithelial barrier function– level of innate and adaptive immunity to the microbiota
• UC– Unclear what initiates or maintains the inflammatory process in UC.– Opposing views regarding dysbiosis
• ? Campylobacter and Salmonella initiates
• Crohn’s– Stronger association– Host’s relationship to its own microbial environment
• specific transmissible agent• markedly reduced bacterial diversity
– decrease in beneficial bacteria» Bifidobacteria, Lactobacilli, Bacteroides and Firmicutes
– increase in pathogenic bacteria» Escherichia coli, Mycobacterium avium paratuberculosis
U. Gophna, K. Sommerfeld, S. Gophna, W. F. Doolittle, and S. J. O. Veldhuyzen Van Zanten, “Differences between tissue-associatedintestinal microfloras of patients with Crohn's disease and ulcerative colitis,” Journal of Clinical Microbiology, vol. 44, no. 11, pp. 4136–4141, 2006.Bernstein CN, Shanahan F. Disorders of a modern lifestyle: reconciling the epidemiology of inflammatory bowel diseases. Gut.2008;57(9):1185–1191.Kaakoush NO, Day AS, Huinao KD, et al. Microbial dysbiosis in pediatric patients with Crohn’s disease. J Clin Microbiol.2012;50(10):3258–3266.
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Pro Biotics• Live micro-organisms, such as bacteria and yeasts , that offer a health benefit when taken
– Align (B. infantis)– Culturelle (L. rhamnosus GG)– DanActive (L. casei)– Florastor (S. boulardii)– Mutaflor (E. coli Nissle 1917)– VSL#3 - Lactobacillus acidophilus, L. bulgaricusm, and multiple others
• Mechanisms– Suppression of growth or epithelial binding/invasion by pathogenic bacteria– Improvement of intestinal barrier function– Modulation of the immune system.– Modulation of pain perception. micro-opioid and cannabinoid receptors in intestinal epithelial
• The Jury is still out– Animal models show promise– Human models limited
Doherty GA, Bennett GC, Cheifetz AS, Moss AC. Meta-analysis: targeting the intestinal microbiota in prophylaxis for post-operative Crohn's disease. AlimentPharmacol Ther. 2010;31(8):802.
Butterworth AD, Thomas AG, Akobeng AK. Probiotics for induction of remission in Crohn's disease. Cochrane Database Syst Rev. 2008.
Ghouri YA, Richards DM, Rahimi EF, Krill JT, Jelinek KA, DuPont AW. Systematicreview of randomized controlled trials of probiotics, prebiotics, and synbioticsin inflammatory bowel disease. Clinical and Experimental Gastroenterology. 2014; (7) :473—487.
UC
Crohn’s
SA-CME Question 6
The following are all considered potentialenvironmental risk factors for the developmentof Crohn’s except:
1. Un-Sanitary living conditions
2. Appendectomy
3. Early Antibiotic exposure
4. Smoking
Take the poll in the CAPA App or text 37198 to 79905
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Environmental influence
• Development of IBD
– Difficult to truly note cause and effect
– Some areas identified
• Multiple hypotheses'
Ng, S.C. et al. Geographical variability and environmental risk factors in inflammatory bowel disease. Gut 2013;62, 630-649
Environmental Factors• Smoking
– Current – 2x’s more likely to develop Crohn’s– Decreased risk of ulcerative colitis
• Antibiotics– May increase the risk for Crohns and Ulcerative Colitis
• NSAIDS– May increase risk Crohn’s and Ulcerative Colitis– Inc. Flares
• Appendectomy– Decreased risk for ulcerative colitis– Increased risk of developing Crohn’s disease
• Diet– No increase in developing Crohn’s or Ulcerative Colitis– Some association of distribution and prevalence– May aggravate symptoms
• Breast Feeding– Decreased risk Crohn’s and UC +/-
Loftus EV, Jr. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastroenterology.2004;126(6):1504-1517.Bernstein CN. Assessing environmental risk factors affecting the inflammatory bowel diseases: a joint workshop of the Crohn’s & Colitis Foundations ofCanada and the USA. Inflamm Bowel Dis. 2008;14(8):1139-1146.Klement E, Cohen RV, Boxman J, Joseph A, Reif S. Breastfeeding and risk of inflammatory bowel disease: a systematic reviewwith meta-analysis. Am J ClinNutr 2004;80:1342–52.
• The Netherlands (Population-based case–control study)– cola drinks and chocolate are potential risk factors for IBD
• Increased IBD rates– Europe and USA 1940 to 1960– Asia early 1990’s
• Introduction and expansion of fast food• Processed/packaged food• Increased use of antibiotics• Increased aluminum foils
Ng, S.C. et al. Geographical variability and environmental risk factors in inflammatory bowel disease. Gut 2013;62, 630-649
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Hygiene
• ‘hygiene hypothesis‘– raised in a sanitary environment
• more likely to develop IBD– lack of childhood exposure to enteric pathogens
– loss of saprophytic microorganisms
• Canada– highest rates of IBD in the world
– First Nations Manitobans• low rates of IBD
– crowded and poor conditions and
» infected with pinworms, hepatitis A and H pylori.
Antibiotics• 9 observational studies
– + association abx and IBD development
• Abx create Imbalance in normal gut microbiota– Sustained effect on gastrointestinal immune tolerance and sensitivity to pathogens
• + Association antibiotic use in the first year of life and the development of IBD– Newborns –
• Sterile intestinal tract• get mother flora
– First year of life• stabilization for gut flora
• Danish prospective cohort study in children– Higher risk (Crohn’s)
• > first 3 months• >7 courses of antibiotics
Shaw SY, Blanchard JF, Bernstein CN. Association between the use of antibiotics in the first year of life and pediatricinflammatory bowel disease. Am J Gastroenterol. 2010;105:2687–92.
Virta L, Auvinen A, Helenius H, et al. Association of repeated exposure to antibiotics with the development of pediatricCrohn’s disease—a nationwide, register-based Finnish case–control study. Am J Epidemiol 2012;175:775–84.
Patterns of Antibiotic Exposure and Clinical Disease Activity inInflammatory Bowel Disease: A 4-year Prospective Study
718 patients -59.9% had Crohn's disease, whereas 38.6% had ulcerative colitis
• Outcomes:• Short IBD Questionnaire scores• C-reactive protein levels• health care utilization• medication use
• 66.3% were exposed to antibiotics• Antibiotic-exposed patients were more likely to have Crohn's disease
– < mean Short IBD Questionnaire (poor)– > C-reactive protein– > health care utilization
• “The majority of patients with IBD receive antibiotic treatment, and these individuals demonstrate a moresevere clinical course”.
Hashash JG, Chintamaneni P, Ramos Rivers CM, Koutroubakis IE, Regueiro MD, Baidoo L, Swoger JM, Barrie A, Schwartz M, Dunn MA,Binion DG. Patterns of Antibiotic Exposure and Clinical Disease Activity in Inflammatory Bowel Disease: A 4-year Prospective Study.Inflamm Bowel Dis. 2015 Aug 20. [Epub ahead of print] http://www.ncbi.nlm.nih.gov/pubmed/26296061
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SA-CME Question 7
Which of the following diagnostic findings would youexpect to find in patients with Ulcerative Colitis?
1. Endoscopic findings showing continuousinflammation of the intestinal mucosa isolated torectum and colon
2. Elevated C-reactive protein3. Bio marker profile of ASCA - / pANCA +4. All of the above
Take the poll in the CAPA App or text 37199 to 79905
– High ASCA titers have a higher chance ofcomplicated disease course (fistula,stricture..)
Sensitivity Specificity
Imaging
• MRI
– Crohn’s
• higher sensitivity and specificity than ileocolonoscopy
• diagnosing and monitoring severity
• useful for evaluating pelvic and perianal disease
Imaging
• Eval small bowel– Capsule endoscopy– CT enterography or magnetic resonance (MR)
enterography is replacing small bowel follow-through(SBFT) studies
• better distinguish between inflammation and fibrosis
• Endoscopy -Gold Standard– Sigmoidoscopy
• Biopsy• Visualization
– Colonoscopy• Biopsy• Visualization
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Treatment endpoints
• Mucosal visualization
– Index scoring
– Direct observation to assess remission andresponse
• Histopathology
• Lab response
– CBC, ESR, CRP…
• The Patient
Crohn's Disease EndoscopicIndex of Severity
• CDEIS
– gold standard
• assessment of endoscopic activity of Crohn's disease
– Objective
• observer variations
– May not correlate with pt
• <6 endoscopic remission
• Treat patients not scores
active inflammation in the last 20 cmclassified as endoscopic remission
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Endoscopic Index Strengths Weaknesses
Mayo score
4-point scale with the parameters stool frequency,rectal bleeding, endoscopy and physician's globalassessment, easy to use even in daily routine.Endoscopic subscore provided (0–3)
Definition of mucosal healing not validated
Truelove and Witts score Possibility to stratify patients by their disease severityNo detailed endoscopic analysis, based onthe presence of blood in stool rather thanthe presence of ulcers
Baron score 4-point scale, easy to use in daily practiceLacks assessment of ulcerations, novalidation of definition of mucosal healing
Modified Baron score 5-point scale, easy to use in daily practiceNo validation of definition of mucosalhealing
12-point index with four components (granulation,vulnerability, vascular pattern, mucosal damage)
Potential underestimation of activity, aseven scores in the presence of ulcers mayresult in the assessment 'inactive disease'
UCEIS
Only validated endoscopic index for UC, accounting for94% of variance between endoscopists for the overallassessment of severity. Simple scale based on threedescriptors, each with 3–4 levels
Responsiveness and clinical relevanceneed further testing, not used in clinicaltrials so far
Endoscopic SCORES
Walsh A, et al. Gastrointest. Endoscopy Clin. N. Am. 2014; 24 (3), 367-78: 367–378
SA-CME Question 8
All of the following are important factors fortreating patients with IBD except:
1. Mitigate disease complications
2. Improve patients Lifestyle
3. Preserve patient’s GI function
4. Decrease Colon cancer risk rate
Take the poll in the CAPA App or text 37200 to 79905
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Treatment endpoints
• The Patient
– Mitigate complications
– Preserve function
– Lifestyle
Treatment
• Tailored approach to treatment– 5 med areas
– Surgery
– Other
• Prior treatment and response
• Severity
• Anatomic location
• Co-Morbidities
• Side effect Profile
SA-CME Question 9
Mild UC disease is treated with whichmedication class:
1. Immunmodulators
2. Antibiotics
3. Aminosalicylates
4. Biologic therapies
Take the poll in the CAPA App or text 37201 to 79905
– Mesalamine (asacol), sulfasalazine, balsalazide,, and olsalazine
• - Antinflammatory– Decrease inflammation at intestinal wall– Rectal or Oral
– Corticosteroids• Short term• Flares
– prednisone, prednisolone, and budesonide
– Antibiotics• ciprofloxacin and metronidazole minimal benefit• Infections or abscess treatment
– Immunomodulators• azathioprine, 6-mercaptopurine (6-MP), and methotrexate• maintain remission in people
– Biologic therapies• moderate to severe active disease• poor response to other therapies• Anti-TNF (tumour necrosis factor)
– a molecule responsible for increasing levels of inflammation– adalimumab, certolizumab pegol, golimumab and infliximab
• Alpha 4 Integrin antibody– Monotherapy– Block leukocyte migration from the blood vessels to sites of inflammation by inhibiting the action of cell adhesion– Natalizumab and vedolizumab
Surgical Treatment
• Ulcerative Colitis– 30% after 30 years
– require surgery• removal of the colon and rectum.
– ileal pouch anal anastomosis (IPAA)
» patient to pass stool through the anus
• Crohn’s disease– 70% surgical intervention
• 30% after 3 yr recurrence
– 60% after 10 yrs
Mortality endpoint?
• Usual goal of therapy is mitigation of sxs andavoidance of colectomy
– Elective colectomy seemed to be associated withimproved survival relative to medical therapy inUC.
• improved survival with surgery in patients aged 50years or older with advanced UC
• Unable to calculate in years– 5year mortality 30%lower in surgical group
Bewtra M, Newcomb CW, Wu Q, Chen L, Xie F, Roy JA, et al. Mortality Associated With Medical Therapy Versus ElectiveColectomy in Ulcerative Colitis: A Cohort Study. Ann Intern Med. [Epub ahead of print 14 July 2015] doi:10.7326/M14-0960
Kansal S, Wagner J, Kirkwood CD, Catto-Smith AG. Enteral nutrition in crohn’s disease: an underused therapy. Gastroenterol Res Pract.2013;2013:482108
Other• Stem Cell
– repair systems for specific inflammatory responses.
– Promising• Ongoing
• Fecal transplant– Saline reduced stool donation NG tube placement
• 18 studies – meta analyses– Safe
– ? Better for Crohns
– Still unclear
Colman R, Rubin D. Fecal microbiota transplantation as therapy for inflammatory bowel disease: A systematic review andmeta-analysis. Journal of Crohn's and Colitis Volume 8, Issue 12, 1 December 2014, Pages 1569–1581
Complications
• Bleeding
• Perforation
• Anatomical disruption
• Acute Dilation
• Pseudopolyps
• Colon Cancer
• Extraintestinal manifestations
• Lifestyle disruption
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Crohn’s Complications
• > Obstruction• Strictures• Fistulas• Abscesses
• Infection– –Clostridium difficile
• >Abx use
– –Cytomegalovirus• >steroid use
• Depression
• Complications of surgical resection– Bile acid diarrhea– Steatorrhea– Small bowel bacterial overgrowth– Short bowel syndrome
SA-CME Question 10
IBD Patients have higher risk for all of thefollowing complications except:
1. Primary Sclerosing Cholangitis (PSC)
2. Barret’s esophagitis
3. Lymphoma
4. Colo-Rectal Cancer (CRC)
Take the poll in the CAPA App or text 37202 to 79905
Other risks
• Inc risk for CRC– > eight to ten years after initial diagnosis– 18% of people with IBD may develop colorectal cancer at 30 years– Frequent colonoscopies
• every one to two years after eight years of disease– Perforation
• Lymphoma– 3-4 x’s increased rate of lymphoma in IBD patients
• > Use of immunomodulators or biologic therapies– <1% of IBD patients
• DVT– 3x’s risk increase
• Primary Sclerosing Cholangitis (PSC)– > ulcerative colitis than Crohn’s disease– > men than women– 75% of all patients that have PSC had IBD
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Crohn's Disease Ulcerative Colitis
Location Any area of the GI tract> cecum
Colon and Rectum
Distribution Patches Continuous
Pain Right lower abdomen Left lower abdomen
Colonoscopy Thickened rocky appearing bowelwallDeep ulcersAll layers of bowel wall
Thinner inflammation of bowelwall+/- superficial ulcers
Rectal Bleeding Bleeding from the rectum duringbowel movements is not common
Bleeding from the rectum duringbowel movements
Summary
SA-CME Question 1
A 21 yo female presents to your office after moving to the area to restart hercollege career. She states she has always had “stomach problems”, but feelssince moving here she has noticed a lot more cramping and occasional boutsof brown non-bloody diarrhea. She denies any travel or other associatedsymptoms, her weight is stable and her family history is non-contributory. Shehad a normal CT scan of her abdomen in the Emergency room approximately6 months ago. On this brief history the patient’s most likely diagnosis is:
A. Ulcerative Colitis (IBD)
B. Irritable Bowel Syndrome (IBS)
C. Dyspepsia
D. Crohn’s Disease (IBD
B. Irritable Bowel Syndrome (IBS)
IBS is a functional gastrointestinal disorder, - a syndrome not adisease. Patient symptoms usually entail cramping andalternating bouts of diarrhea and constipation. There is no GIbleeding associated with IBS, and most sxs are self-limitingand resolve without any intervention. Unlike IBD, There is noobjective sign of disease or abnormalities when the colon isexamined. While IBS can cause significant life quality of lifeconcerns for patients, it is a much less serious disease processthan IBD, and does not cause physical destruction of apatient’s intestinal tract. Treatment for IBS rarely requiressignificant interventions such as surgery or hospitalization, nordoes it require significant pharmaceutical intervention.
http://www.aafp.org/afp/2012/0901/p419.html
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SA-CME Question 2
It is believed that Inflammatory Bowel Disease results from a complexinteraction between genetics and environmental risk factors that :
A. create changes in vitamin D absorption leading to mucosaldestruction
B. trigger an exaggerated immune response in the intestinal mucosa
C. cause the loss of intrinsic factor
D. block the body’s immune system and other normal protectiveresponses along the brush border of the intestines
B. trigger an exaggerated immuneresponse in the intestinal mucosa.
The prevailing hypothesis regarding the pathophysiologyof inflammatory bowel disease (IBD) is related to theinteraction of 3 major factors: genetics, environment andimmune response. Approximately 160 potential geneshave been identified in the pathogenesis of IBD. Faults ingenes that have the ability to recognize bacteria (nod 2)have been shown to be the most significantly involved.These gene mutations, along with some level ofenvironmental trigger, allow the body’s immune systemto develop a sustained response within the GI tract,altering its’ structure and immunity creating thesymptoms and pathology findings seen in IBD patients.
3. The following differentiate UC from Crohn’sexcept:
A. UC only involves the colon and rectum
B. UC effects the upper most layers of the intestinalwall
C. The lesions of UC are noted as skipped lesions
D. Smoking is considered protective
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C. The lesions of UC are noted asskipped lesions
UC and Crohn’s have a number of differentiatingfindings. The endoscopic finding of UC is noted ascontinuous. Skipped lesion or patches within theIntestinal tract usually signify Crohn’s lesions.Microscopically, UC only affects the uppermostlayers of the intestinal mucosa, whereas Crohn’s is atransmural process of the bowel wall. Crohn’slesions may be found in any part of the GI tractwhereas UC is isolated to the large bowel andrectum. Smoking has been shown to lower one’srisk for UC.
SA-CME Question 4
A 29 yo Caucasian male states he has had intermittent LLQ pain with bloody diarrheaover the last 2 months. He states the bouts of pain and diarrhea are becoming morefrequent and he now has the urge to defecate all the time. He recalls that he hadblood in his stool a few years ago and it resolved on its own so he thought it wasrelated to a hemorrhoid. His weight has decreased by 7 pounds over the last 2-3months, and he does note that he occasionally gets some mild pain and swelling in hishands and wrist, which he also believes is much more persistent with his currentsymptoms. He is otherwise healthy, takes no medication, and has a non-contributoryfamily history. With the current information the patient’s most likely diagnosis is:
A. Crohn’s disease
B. Irritable Bowel Syndrome
C. Colon Cancer
D. Ulcerative Colitis
D. Ulcerative Colitis
Caucasians are more likely to develop IBD. LeftLower abdominal pain and bloody diarrhea is ahallmark symptom of IBD, and is more prevalent inpatients with Ulcerative Colitis (UC) than Crohn’s(minimal blood in stool and RLQ pain). Individualswith UC can have mild sxs and long remissions.Patients with IBD can develop malabsorption issuesthat lead to weight loss has UC and Crohn’s bothcan manifest extra-intestinal manifestations of thedisease, such as arthralgias.
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SA-CME Question 5
Which of the following is associated with Dysbiosis:
A. marked increase in bacterial diversity
B. decrease in beneficial bacteria
C. normal epithelial barrier
D. decrease in pathogenic bacteria
B. decrease in beneficial bacteriaThe human GI tract is essentially an eco-system, relying ondiversity with a balance of bacteria (pathogenic andbeneficial), and an intact barrier system to maintain normalfunction. If this complex system is “off-balance” or becomesdysbiotic it may create an environment that is non-functionaland susceptible to exaggerated immune responses. Dysbiosisrefers to a state of imbalance, specifically in the microbiomeof the GI tract, an increase in harmful bacteria and decrease inbeneficial bacteria or lack of appropriate diversity betweencommensal bacteria and harmful bacteria. The initiation ofIBD, may in fact derive from this imbalance and decrease inthe bacterial diversity.
1. U. Gophna, K. Sommerfeld, S. Gophna, W. F. Doolittle, and S. J. O. Veldhuyzen Van Zanten, “Differences betweentissue-associated intestinal microfloras of patients with Crohn's disease and ulcerative colitis,” Journal of ClinicalMicrobiology, vol. 44, no. 11, pp. 4136–4141, 2006.2. Bernstein CN, Shanahan F. Disorders of a modern lifestyle: reconciling the epidemiology of inflammatory boweldiseases. Gut. 2008;57(9):1185–1191.3. Kaakoush NO, Day AS, Huinao KD, et al. Microbial dysbiosis in pediatric patients with Crohn’s disease. J Clin Microbiol.2012;50(10):3258–3266
SA-CME Question 6
The following are all considered potentialenvironmental risk factors for the development ofCrohn’s except:
A. Un-Sanitary living conditions
B. Appendectomy
C. Early Antibiotic exposure
D. Smoking
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D. Un-Sanitary living conditions
Smoking and appendectomy have both been shown todecrease ones risk for developing UC but increase the risk ofthe development of Crohn’s disease. The exact mechanismand reasons are still unknown. Early antibiotic exposure hasbeen shown to increase ones risk for both UC and Crohn’s,some questionable theories include attenuation of the normalgut flora. The Hygiene hypothesis for IBD notes those living insanitary conditions may lack sufficient exposure to entericpathogens necessary for proper gut immunity and response,predisposing one to the development of IBD. Canada has oneof the highest rates of IBD, but shows a disparate low rate ofIBD disease in its First Nation population. This populationtends to live in crowded and poor sanitary conditions andhave high rates of Hep A, H-Pylori, and pinworm infections.
SA-CME Question 7
Which of the following diagnostic findings would you expect to find inpatients with Ulcerative Colitis?
A. Endoscopic findings showing continuous inflammation of theintestinal mucosa isolated to rectum and colon
B. Elevated C-reactive protein
C. bio marker profile of ASCA - / pANCA +
D. All of the above
D. All of the above
The gold standard for diagnosis of IBD , isEndoscopy with biopsy. Usual findings showinflammation of the intestinal mucosa isolated torectum and colon in UC and anywhere along the GItract in Crohn’s. Since IBD is an inflammatoryprocess, the usual serology markers are elevatedsuch as C-reactive protein. There are more specificbio markers, such as ASCA / pANCA ,that can assistin the diagnosis as well as aid in the differentiationbetween UC and Crohn’s.
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SA-CME Question 8
All of the following are important factors fortreating patients with IBD except:
A. Mitigate disease complications
B. Improve patients Lifestyle
C. Preserve patient’s GI function
D Decrease Colon cancer risk rate
D Decrease Colon cancer risk rate
There is no evidence that treating patients withIBD lowers there inherent risk for CRCdevelopment. Despite treatment choice orcontrol of sxs, patients with IBD maintain anincreased risk for the development of CRC, andthus require more frequent colonoscopyscreening exams.
SA-CME Question 9
Mild UC disease is treated with whichmedication class:
A. Immunmodulators
B. Antibiotics
C. Aminosalicylates
D. biologic therapies
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C. Aminosalicylates
Treatment of UC is dependent on the severity ofsymptoms and co-morbidities. As a general rule initialmedical management for UC is the use of anti-inflammatory medications, such as the class ofAminosalicylates (Ssulfasalazine), and/or corticosteroids(Prednisone). These drugs are used in conjunction withother medications for symptomatic control, such as anti-diarrheals. The immunomodulators and biologictherapies are reserved for more severe recalcitrantsymptoms and cases. Antibiotics are only used forpotential secondary infections, and in some studies havebeen shown to prolong the symptoms when used in flareswithout a clear underlying “infectious” process.
SA-CME Question 10
IBD Patients have higher risk for all of thefollowing complications except:
A. Primary Sclerosing Cholangitis (PSC)
B. Barret’s esophagitis
C. Lymphoma
D. Colo-Rectal Cancer (CRC)
B. Barret’s esophagitis
IBD patients have a 3-4x’s risk increase forlymphoma, higher rates of early CRC, and 3x’sthe risk to develop a DVT. PSC is of particularconcern in patients with IBD, specifically UC, as75% of the cases of PSC patients also had IBD.Barret’s esophagitis is not associated with IBD.
