# data[].attributes.attachment_link.description
Case study 65 yo female Widowed 2 Adult sons 3 cats Limited income - Social Security Benefits - minimal savings No transportation relies on others Independent and private about cares NJ case study N.J. 65 yo Caucasian female widowed 2 sons "limited contact" prefers 6 cats over

# data[].attributes.attachment_link.readable_text
Continuing Education Activity

Lactose intolerance is a clinical syndrome that manifests with characteristic signs and symptoms upon consuming food substances containing lactose, a disaccharide. Normally upon lactose consumption, it is hydrolyzed into glucose and galactose by the lactase enzyme, which is found in the small intestinal brush border. Deficiency of lactase due to primary or secondary causes results in clinical symptoms. This activity describes the pathophysiology of lactose intolerance and highlights the role of the interprofessional team in its management.

Objectives:

Review the pathophysiology of lactose intolerance.

Describe the presentation of a patient with lactose intolerance.

Summarize the management options for lactose intolerance.

Outline the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by lactose intolerance.

Access free multiple choice questions on this topic.
Introduction

Lactose intolerance is a clinical syndrome that manifests with characteristic signs and symptoms upon consuming food substances containing lactose, a disaccharide. Normally upon lactose consumption, it is hydrolyzed into glucose and galactose by the lactase enzyme, which is found in the small intestinal brush border.[1] Deficiency of lactase due to primary or secondary causes results in clinical symptoms. Disease severity varies among individuals. Lactose is present in dairy, milk products, and mammalian milk.[2] It is also sometimes referred to as lactose malabsorption.

Lactase deficiency is the commonest type of disaccharidase deficiency. Enzyme levels are at the peak shortly after birth and decline after that, despite continued lactose intake. Among the animal world, nonhuman mammals generally lose their ability to digest lactose into its components as they reach adulthood. Certain populations of the human species, such as those of South American, Asian, and African descent, tend to develop lactase deficiency. On the contrary, people of northern Europe origin or northwestern India usually retain the ability to digest lactose into adulthood.[3]

Lactose intolerance presents with abdominal bloating and pain, loose stools, nausea, flatulence, and borborygmi.[4][5] Many people start avoiding milk as soon as a diagnosis is made, or even the suggestion of lactose intolerance is put forward. This leads to consuming specially prepared products with digestive aids, adding to the health care burden.

Etiology

Lactase enzyme deficiency can occur in individuals with lower levels of this enzyme, resulting in failure to hydrolyze lactose into absorbable glucose and galactose components. There are four leading causes of lactase deficiency.

Primary Lactase Deficiency

It is the most common cause of lactase deficiency, also known as lactase non-persistence. There is a gradual decline in lactase enzyme activity with increasing age. Enzyme activity begins to decline in infancy, and symptoms manifest in adolescence or early adulthood. More recently, it has been observed that lactase non-persistence is of the ancestral form (normal Mendelian inheritance), and lactase persistence is secondary to mutation.[6][7][8]

Secondary Lactase Deficiency

Due to several infectious, inflammatory, or other diseases, injury to intestinal mucosa can cause secondary lactase deficiency.[9] Common causes include:

Congenital Lactase Deficiency

There is a decrease or absence of lactase enzyme activity since birth due to autosomal recessive inheritance.[10][11] It manifests in the newborn after ingestion of milk. It is a rare cause of the deficiency, and its genetics are not very well known.[12]

Developmental Lactase Deficiency

It is seen in premature infants born at 28 to 37 weeks of gestation.[13] The infant's intestine is underdeveloped, resulting in an inability to hydrolyze lactose. This condition improves with increasing age due to the maturation of the intestine, which results in adequate lactase activity.

Epidemiology

Lactose intolerance is a common disease; however, it is rare in children younger than 5. It is most often seen in adolescents and young adults. On average, 65% of the world's population is lactose intolerant.[14] The prevalence of lactose intolerance is variable among different ethnicities. It is most common in African Americans, Hispanics/Latinos, and Asians and least prevalent in people of European descent.[15] Ethnic groups with a higher prevalence of lactose intolerance also are more likely to have lactose non-persistence.[16][17]

The primary form is the commonest (found in up to 70% of the world's population, but not all of them are symptomatic).[18][19][20] On the contrary, the congenital type is extremely rare (with around 40 cases reported worldwide to date).[6]

In the US, the primary disease is much more common in certain ethnicities, such as African-Americans, American Indians, Hispanics or Latinos, and Asian-Americans, than in White Americans.[21][22][23][24][21] North Americans, Australians, and White Northern Europeans have the lowest rates, ranging between 2% and 15%.[21][22] On the contrary, the prevalence of lactose intolerance is 50% to 80% in South Americans, around 100% in American Indians and some East Asians, and around 60% to 80% in Ashkenazi Jews and Africans.[21][23][24]

The age-related decline in lactase activity is generally complete during childhood; however, the decline has also been seen to occur later, in adolescence, particularly in Whites.[25] The eventual level and the duration of loss of lactase expression vary considerably per ethnicity. Chinese and Japanese people lose between 80% and 90% of activity within three to four years after weaning. Jews and Asians lose 60% to 70% over many years after weaning, and for White Northern Europeans and North Americans, it could take between 18 and 20 years for lactase expression to reach its lowest levels.[18] A low prevalence of lactase non-persistence is noted in patients of mixed ethnicity, whereas an increased prevalence is observed in the native ethnic group.

The onset of the disease is generally subtle and progressive in primary illness, and many patients first experience symptoms of intolerance in late adolescence and adulthood.[2][3] As opposed to White Northern Europeans, Australians, and North Americans, earlier presentation is noted in Native Americans, Asian-Americans, African-Americans, and Hispanics/Latinos.[21] The secondary disease is commoner in children, particularly in developing countries where infections are a common cause.[9]

The sexes are affected equally.

Pathophysiology

The lactase enzyme is located in the brush border of the small intestinal mucosa. Deficiency of lactase results in the presence of unabsorbed lactose within the bowel. This results in an influx of fluid into the bowel lumen resulting in osmotic diarrhea. Colonic bacteria ferment the unabsorbed lactose-producing gas (hydrogen, carbon dioxide, and methane), which hydrolyzes lactose into monosaccharides.[26] This results in an additional influx of fluid within the lumen. The overall effect of these mechanisms results in various abdominal signs and symptoms.

An association has been reported between certain single nucleotide polymorphisms with lactose tolerance in a northeastern Brazilian population. In Indo-Europe, lactose intolerance is linked with rs4982235 SNP (or -13910C>T).[27]

Histopathology

In lactose intolerance, microscopic findings of the small intestine vary depending on the cause of lactase deficiency. In primary lactase deficiency, the mucosa appears normal. Lactase activity can be measured to assess the severity of the disease. The mucosa may be abnormal in secondary lactase deficiency, depending upon the underlying cause. It helps determine the secondary causes of the disease, such as celiac disease. Biopsy results may be normal if the mucosal abnormality is focal or patchy.[28]

History and Physical

Signs and symptoms of lactose intolerance manifest 30 minutes to 1 to 2 hours after ingesting milk (dairy) products. The severity of symptoms depends upon the amount of lactose consumed, the residual lactase function, and the small bowel transit time.[29] Common signs and symptoms may include the following:

Less commonly, it can present with headache, muscle pain, joint pain, mouth ulcers, urinary symptoms, and loss of concentration.[32][33]

Evaluation

Lactose intolerance is evaluated by getting a careful history, performing a physical exam, and medical tests.

History

It is essential to take a past medical, family, and dietary history to determine the cause of lactose intolerance and exclude secondary causes.

Physical Exam

Assess for the presence of abdominal bloating, tenderness, and pain.

Medical Tests

1. Hydrogen breath test: This test measures the hydrogen content of breath after lactose ingestion. The test is positive for lactose malabsorption if the post-lactose breath hydrogen value rises >20 ppm compared with the baseline.[34]

2. Stool acidity test: Unabsorbed lactose is fermented by colonic bacteria into lactic acid, which lowers the stool pH.

3. Dietary elimination: One way to assess the underlying illness is to eliminate lactose-containing food products, which would result in the resolution of symptoms. Resumption of symptoms with the reintroduction of these products will indicate lactose intolerance.[35]

4. Milk tolerance test: Administer 500 mL of milk and obtain the blood glucose level. A rise in blood sugar of less than 9 mg/dL shows lactose malabsorption.[36]

5. Lactose tolerance test: This test determines lactose absorption after ingestion of a lactose-containing liquid. Measure serial blood glucose levels after giving an oral lactose load. After obtaining a fasting serum glucose level, 50 g of lactose is administered.[34] Serum glucose level is then measured at 0, 60, and 120 minutes. Failure of blood glucose levels to rise by 20 g may indicate lactose intolerance. This test has a specificity of 96% and a sensitivity of 75%. False-negative results may occur in patients with diabetes or small bowel bacterial overgrowth. The results are also affected by abnormal gastrointestinal emptying.[37]

6. Small bowel biopsy: This test is rarely performed as it is invasive. It is only indicated to rule out secondary causes of lactose intolerance.

7. Genotyping: It is an emerging test with higher sensitivity and specificity. It has been used in Germany and the Nordic states, but it is yet not widely available or practiced elsewhere.[38]

Treatment / Management

Management of lactose intolerance consists of dietary modification, lactase supplementation, and treating an underlying condition in people with secondary lactase deficiency.

Dietary Modification

Lactase-containing milk products and calcium supplements are recommended. Limiting the dietary intake of lactose by avoiding the intake of lactose-containing products improves the symptoms of the disease. The following products contain lactose and, therefore, must be avoided:

Yogurt contains varying amounts of lactose and may cause symptoms in some patients. Greek yogurt has the least. Yogurt culture microorganisms can produce β-galactosidase as part of their lactose utilization pathway. This may promote lactose digestion in vivo.[39] Plant-based milk alternatives are becoming more available; however, technological issues, palatability, and nutritional balance remain concerns.[40][41] Probiotics have been observed to improve symptoms, such as the DDS-1 strain of Lactobacillus acidophilus.[42][43] Calcium and vitamin D supplements should also be recommended. In patients with secondary lactase deficiency, treatment should be directed at the underlying cause.[44]

Lactase Supplements

Lactase enzyme supplements contain lactase which breaks down lactose in milk and milk-containing products. They are available as lactase enzyme tablets or drops.

Differential Diagnosis

Other conditions to be considered in the list of differential diagnoses of lactose intolerance include:

Pertinent Studies and Ongoing Trials

Emerging treatments include the following:

Fungal Beta-galactosidases

Two fungal beta-galactosidases from Aspergillus carbonarius ATCC6276 are beta-gal 1 and beta-gal 2. They can be given alone or in combination and may be used as an enzyme supplement for lactose intolerance.[45] Unlike current commercialized supplemental lactases, these purified enzymes demonstrate significant stability on exposure to simulated gastric conditions.

Nutrigenomics

Nutrigenomics may be used in the future management of hypolactasia through prompt identification of specific mutations or haplotype patterns that modulate dietary responses in affected individuals.[46]

Prognosis

Lactose intolerance has an excellent prognosis. Most patients have a considerable improvement in signs and symptoms with dietary modification alone. Lactose intolerant may lead to osteopenia.[47][48][49] Vitamin D deficiency is linked to the LCT-13910C>T gene variant of lactose intolerance among Whites.[49]

Complications

Following are some common complications:

Consultations

Once a diagnosis of lactose intolerance is made, consultation should be made with a gastroenterologist and dietician.

Deterrence and Patient Education

Lactose-intolerant patients and their families should be advised that ingestion of lactose-containing products generally only leads to reversible symptoms without causing permanent damage to the gastrointestinal tract (unlike celiac disease). Also, there are no long-term complications if an adequate intake of proteins, calories, calcium, and vitamin D is ensured.[21]

Primary and congenital lactase deficiency can not be prevented. However, secondary lactase deficiency could be prevented if underlying secondary causes are diagnosed early and promptly instituted appropriate treatment to preserve intestinal mucosal integrity. In addition, avoiding lactose-containing foods helps limit long-term disease severity.

Pearls and Other Issues

To avoid their use, people with lactose intolerance can check the ingredients on food labels for lactose on food products.

Some people with lactose intolerance can tolerate some milk and milk-containing products and may not need to avoid them completely.

Lactose intolerance is commonly confused with milk allergy. Lactose intolerance is a gastrointestinal disorder, while milk allergy is an autoimmune reaction against specific milk proteins. Milk allergy is life-threatening and presents early in infancy, while Lactose intolerance usually presents in adolescence or early adulthood.

Milk is rich in calcium and vitamin D. Prolong avoidance of milk in people with lactose intolerance can result in calcium and vitamin D deficiency.

Enhancing Healthcare Team Outcomes

The diagnosis and management of lactose intolerance are with an interprofessional team that includes a nurse practitioner, primary care provider, pediatrician, gastroenterologist, and an allergist. Lactose intolerance is commonly confused with milk allergy. Lactose intolerance is a gastrointestinal disorder, while milk allergy is an autoimmune reaction against certain milk proteins. Milk allergy is life-threatening and presents early in infancy, while Lactose intolerance usually presents in adolescence or early adulthood. It is important to educate the patient that they should always check the ingredients on food labels for lactose on food products to avoid their use when they have lactose intolerance. However, some people with lactose intolerance can tolerate some milk and milk-containing products and may not need to avoid them completely. Prolonged avoidance of milk in people with lactose intolerance can result in calcium and vitamin D deficiency.[50] [level 5]

References

Disclosure: Talia Malik declares no relevant financial relationships with ineligible companies.

Disclosure: Kiran Panuganti declares no relevant financial relationships with ineligible companies.

# data[].attributes.attachment_link.description
Lactose intolerance is a clinical syndrome that manifests with characteristic signs and symptoms upon consuming food substances containing lactose, a disaccharide. Normally upon lactose consumption, it is hydrolyzed into glucose and galactose by the lactase enzyme, which is found in the small intestinal brush border.[1] Deficiency of lactase due to primary or secondary causes results in clinical symptoms. Disease severity varies among individuals.

# data[].attributes.attachment_link.readable_text
Continuing Education Activity

Crohn disease (CD) and ulcerative colitis (UC) are two conditions commonly referred to as inflammatory bowel disease (IBD). They are immunologically mediated inflammatory diseases of the gastrointestinal tract. In Crohn disease, the inflammation extends through the entire thickness of the bowel wall from the mucosa to the serosa. The disease runs a relapsing and remitting course. With multiple relapses, Crohn disease can progress from initially mild to moderate inflammatory conditions to severe penetrating (fistulization) or stricturing disease. This activity reviews the etiology, presentation, evaluation, and management of Crohn disease and highlights the role of the interprofessional team in evaluating, diagnosing, and managing the condition.

Objectives:

Review the pathophysiology of Crohn disease.

Describe the extraintestinal manifestations of Crohn disease.

Summarize the management of Crohn disease.

Explain the importance of interprofessional team strategies for improving care coordination and communication to aid in prompt diagnosis of Crohn disease and improving outcomes in patients diagnosed with the condition.

Access free multiple choice questions on this topic.
Introduction

Crohn disease (CD) and ulcerative colitis (UC) are two conditions commonly referred to as inflammatory bowel disease (IBD). They are immunologically mediated inflammatory diseases of the gastrointestinal tract. In CD, the inflammation extends through the entire thickness of the bowel wall from the mucosa to the serosa. The disease runs a relapsing and remitting course. With multiple relapses, the CD can progress from initially mild to moderate inflammatory conditions to severe penetrating (fistulization) or stricturing disease.[1][2][3][4][5]

Crohn disease can affect any part of the gastrointestinal tract. About one-third of patients have small bowel involvement, especially the terminal ileum, another 20% have only colon involvement and about 50% have involvement of both the colon and small bowel. There is no cure and most patients experience bouts of remissions and relapse at unpredictable times. This disease leads to a very poor quality of life.

Etiology

Although the exact etiology of inflammatory bowel disease (IBD) is not known, there is substantial evidence to suggest that the disease is resulting from an inappropriate immune response in the bowel to situations from environmental factors such as drugs, toxins, infections, or intestinal microbes in a genetically susceptible host. More than a hundred genes associated with IBD have been identified. In Crohn disease particularly, there appears to be a genetic association with phenotypes. Specifically, NOD2/CARD15 mutations were found to be associated with a phenotype of Crohn disease which was associated in those diagnosed at a younger age, with ileal involvement, increased severity of ileal disease requiring surgical intervention/reoperation. In the future, this genotyping could potentially provide prognostic information on the severity of the disease. Furthermore, it could predict which patient should be considered for surgical management vs. medical management based on a more detailed understanding of genetic analysis.[6]

Epidemiology

Crohn disease (CD) is most commonly seen in the western developed world in North America, northern Europe, and New Zealand. Its incidence has a bimodal distribution with the onset occurring most frequently between ages 15 to 30 years and 40 to 60 years old. It is more prominent in urban than rural areas. There is a high incidence in Northern Europeans and Jewish descent (incidence 3.2/1000) contrasting to a significant infrequent prevalence in Asians, Africans, and South Americans.[7] However, recent studies have shown a significant increase in incidence in rapidly industrializing areas of Asia, Africa, and Australasia.[8]

Pathophysiology

The pathophysiology is multifactorial and involves genetic predisposition, infectious, immunological, environmental, and dietary. The characteristic transmural inflammation can include the entire GI tract from mouth to the perianal area; although most frequently involve terminal ileum and right colon. The initial lesion starts out as an infiltrate around an intestinal crypt. This goes on to develop ulceration first in the superficial mucosa and involves deeper layers. As the inflammation progresses, non-caseating granulomas form involving all layers of the intestinal wall. It can develop into the classic cobblestone mucosal appearances and skip lesions along the length of the intestine sparing areas with normal mucosa. As the flare of Crohn settles, scarring replaces the inflamed areas of the intestines.[9]

Granuloma formation is very common in Crohn disease but their absence does not exclude the diagnosis. The ongoing inflammation and scarring lead to bowel obstruction and stricture formation. Crohn disease is also associated with enterovesical, enteroenteral, enterocutaneous, and enterovaginal fistulas.

Toxicokinetics

The immune-mediated response in Crohn disease involves both innate and acquired mechanisms by macrophages, neutrophils, and T-cells in the intestine which promote pro-inflammatory mediators like tumor necrosis factor-alpha. Colonic Crohn lesions were found to have high levels of cytokines like interferon-gamma, IL-2, IL-12, and IL-18. Crohn disease is primarily regulated by hepler T 1 and 17 mediated processes.[10]

History and Physical

Patients with flare-ups of Crohn disease typically presents with abdominal pain (right lower quadrant), flatulence/bloating, diarrhea (can include mucus and blood), fever, weight loss, anemia. In severe cases, perianal abscess, perianal Crohn disease, and cutaneous fistulas can be seen.

When the small bowel is involved, it may present with diarrhea, malabsorption, weight loss, abdominal pain, and anorexia. Enterovesical fistulae may present with pneumaturia, recurrent urinary tract infections, and feculent vaginal discharge.

Crohn disease is associated with extraintestinal manifestations including episcleritis, uveitis, stomatitis, aphthous ulcers, liver steatosis, gallstones, cholangitis, primary sclerosing cholangitis, nephrolithiasis, hydronephrosis, urinary tract infections, arthritis (spine - sacral, knee, ankles, hips, wrist, elbows), ankylosing spondylitis, erythema nodosum, and pyoderma gangrenosum.[11]

Thromboembolic disease is now recognized to be a common complication of Crohn disease. It may present with deep vein thrombosis, stroke, or pulmonary embolism.

The perineum must be examined in all patients. The inspection may reveal skin tags, ulcers, fistulas, scarring, and abscess. Frank perforation is rare but can be a presentation of Crohn disease. Finally, colon cancer is another complication of Crohn disease.

Evaluation

Stool tests to rule out infections include culture and sensitivities, ovum and parasites, Clostridium difficile toxins, leukocyte count. Stools for calprotectin can detect the active Crohn disease and also used for monitoring disease.[12][13][14][15]

Blood tests including complete blood count and a metabolic panel can highlight the presence of anemia (B12 or iron deficiency) or liver disease. Special serology such as normal anti-neutrophil cytoplasmic antibodies (ANCA) and raised anti-saccharomyces cerevisiae antibodies (ASCA) can distinguish Crohn disease from ulcerative colitis. C-reactive protein (CRP) or erythrocyte sedimentary rate (ESR) can reflect the severity of the inflammation.

A computed tomography scan/magnetic resonance enterography (MRE) of the abdomen and pelvis can detect abscesses and fistulization. The choice between CT or MRE is largely directed at minimizing radiation exposure in younger populations. Both give a higher definition of the diseased intestine. However, MRI can provide more detail when investigating the fistulizing disease. The use of video capsule endoscopy (VCE) can visualize the small bowel for CD when regular endoscopy or colonoscopy cannot reach to visualize these areas. Capsule endoscopy can only detect mucosal changes, whereas MRI can detect transmural inflammation and also identify other complications.

Plain x-rays are ordered when bowel obstruction is suspected.

Small bowel follow-through is often used to assess the involvement of the terminal ileum and can also detect fistulas. The classic string sign due to stricture formation or spasm is often seen.

For those patients too ill to undergo colonoscopy or CT scan, nuclear imaging may reveal sites of inflammation.

Before initiation of any treatment, vaccination history (tetanus, diphtheria, pertussis, human papillomavirus, influenza, pneumococcal, hepatitis A, hepatitis B, measles, mumps, rubella, varicella-zoster virus) should be known, if no prior history titers of hepatitis A, hepatitis B, measles, mumps, rubella, and the varicella-zoster virus should be checked. Baseline Mantoux test with chest radiograph should also be checked before any treatment. Baseline thiopurine methyltransferase (TPMT) levels should be checked before deciding on treatment options. Low levels of TMPT may result in an increased risk of side effects, whereas very high levels may decrease the effectiveness of prescribed treatment.

Treatment / Management

The medical treatment is broadly grouped into two classes:

Mild to moderate disease can be treated by oral mesalamine, immunomodulators such as thiopurines (mercaptopurines, azathioprine), methotrexate, and steroids.

Moderate to severe disease (including fistulizing disease) will be best treated using a combination of immunomodulators and biologics (infliximab, adalimumab, golimumab, vedolizumab) or biologics alone.[10]

Biologics are immunoglobulins engineered to direct against specific cytokines or receptors involving in the inflammation process. Each biologic agent works against one specific site at a molecular level. Anti-tumor necrosis factor (TNF) alpha is a monoclonal antibody that can block the TNF in circulation from their inflammatory actions. Anti-integrin agents are adhesion molecule inhibitors that bind the subunits of the MAdCAM receptors of the endothelial cells at the inflammatory sites. They halt the trafficking of lymphocytes from the circulation into the wall of the intestine, thereby stopping the inflammatory response targeted at the bowel. Examples of anti-TNF agents are infliximab, adalimumab, golimumab. Examples of adhesion molecule inhibitors are natalizumab, vedolizumab. Vedolizumab is gut-specific and has fewer systemic side effects. Many newer therapeutic agents for inflammatory bowel disease are in the pipeline.

Surgical treatments are used for complications such as bowel obstructions, abscess, fistulas, or perforated bowel.

Dietician input and nutritional supplementation are highly recommended before and during the treatment of Crohn disease.[16][17][18][19]

Guidelines published by the American College of Gastroenterology for the management of Crohn disease in 2018:

1. Fecal calprotectin may help differentiate between IBD and IBS

2. Chromoendoscopy should be utilized during colonoscopy as it may increase diagnostic yield for colorectal dysplasia

3. Avoid NSAIDs as they may exacerbate disease

4. Get mental health counseling as many patients develop depression

5. Sulfasalazine is effective for mild disease

6. Controlled ileal release budesonide can be used for induction of remission in patients with moderate ileocecal disease

7. Avoid the use of metronidazole as it is ineffective in Crohn disease

8. Mild diarrhea can be managed with antidiarrheals

9. Thiopurines can be used for steroid-sparing

10. Anti TNFs can be used in patients resistant to steroids

11. Drain abscess radiologically if possible

Differential Diagnosis

While assessing a patient with Crohn disease following differentials should be kept in mind:

Prognosis

Crohn disease is a chronic inflammatory disorder with no cure. Despite optimal therapy, most patients have a poor quality of life. The life expectancy is slightly reduced to the development of malignancies, genitourinary disease, liver, and biliary tract complications. The majority of Crohn patients who develop complications need surgery and as the disease progresses, some need multiple procedures. Overall, patients with the proximal disease have higher mortality than those with the distal disease.

Complications

Crohn disease is a systemic disease with many intestinal and extra-intestinal complications. Following are few complications caused by Crohn disease:

Deterrence and Patient Education

Education of patients regarding the nature of the disease is very crucial. Patients should undergo screening for skin cancers, irrespective of biological therapy. Bone density should be assessed regularly so that osteoporosis if occurs, is diagnosed early and treated timely. Vaccination against pneumococcus, Haemophilus influenzae, and flu shot should be done. Screening annual colonoscopy should be advised to early detect colon cancer.

Enhancing Healthcare Team Outcomes

Crohn disease is a serious chronic inflammatory disorder that is difficult to diagnose and manage. Besides the GI tract, the disease affects many other organs leading to high morbidity and even premature death. The current consensus is that this disorder should be managed by an interprofessional team dedicated to the management of inflammatory bowel disease.

The diagnosis and management of Crohn disease require an interprofessional team that includes a nurse practitioner or provider assistant, internists, hematologist, gastroenterologist, general surgeon, dietitian, stoma nurse, and a pharmacist. The disorder affects many organs in the body and hence the appropriate specialist should be consulted early on in the disease course.

A nurse practitioner or provider assistant should follow the patient throughout the course and monitor the course of the disease. Any change in the symptoms should be immediately reported to the team. A dietitian should educate the patient on foods to eat and what to avoid. A stoma nurse should educate the patient on the cleaning of the skin and managing everyday problems with this method of stool evacuation.

The pharmacist should educate the patient on the different medications, their benefits, their adverse effects, and the importance of compliance.

Many different providers see these patients as they may develop extraintestinal problems. The patient should be urged to undergo tests to screen for skin and colon malignancies. Finally, most patients develop depression and severe anxiety and hence a mental health nurse should provide continuous counseling.

The disorder is usually managed with medications but complications require surgery. Most patients have relapses and remissions and need lifelong follow-up. The prognosis for most patients with Crohn disease is guarded and the quality of life is poor.[20] An interprofessional team approach can optimize outcomes within the limitations of the condition. (Level 5)

References

# data[].attributes.attachment_link.description
Crohn disease (CD) and ulcerative colitis (UC) are two conditions commonly referred to as inflammatory bowel disease (IBD). They are immunologically mediated inflammatory diseases of the gastrointestinal tract. In CD, the inflammation extends through the entire thickness of the bowel wall from the mucosa to the serosa.

# data[].attributes.attachment_link.title
What is celiac disease, and how does gluten affect the body? | Scienticious - Episode 10