Lynn Takwada 172(1)

Crohn’s disease
is an idiopathic, chronic inflammatory process that can affect any part of
the gastrointestinal tract from the mouth to the anus
Etiology

Genetic,
microbial, -such as Mycobacterium paratuberculosis, Pseudomonas
species, and Listeria
immunologic, -Interleukins and TNF-α
environmental, -such as tobacco
dietary, -high in fatty foods
vascular, and psychosocial factors

Pathogenesis

After activation by antigen presentation, unrestrained responses of type

1 T helper (Th1) cells predominate in Crohn disease as a consequence
of defective regulation. Th1 cytokines such as interleukin (IL)-12 and
TNF-α stimulate the inflammatory response. Inflammatory cells
recruited by these cytokines release nonspecific inflammatory
substances, including arachidonic acid metabolites, proteases, platelet
activating factor, and free radicals, which result in direct injury to the
intestine.

Clinical manifestations
-abdominal pain and prolonged diarrhea,
-Low-grade fever
-generalized fatigability
Investigation
1.Imaging studies
● Plain abdominal radiography

● Barium contrast studies (eg, small bowel follow-through, barium

enema, enteroclysis)
● CT scanning of the abdomen

● CT enterography or magnetic resonance enterography: Replacing

small bowel follow-through studies

● MRI of the pelvis

● Abdominal and/or endoscopic ultrasonography

2. Procedures
● Endoscopic visualization and biopsy (eg, upper gastrointestinal

endoscopy, esophagogastroduodenoscopy, endoscopic retrograde

cholangiopancreatography)
● Colonoscopy, ileocolonoscopy

Small bowel enteroscopy

3. Laboratory Tests

● CBC count
● Chemistry panel
● Liver function tests
● Inflammatory markers
● Stool studies
● Serologic tests

Treatment

● 5-Aminosalicylic acid derivative agents (eg, mesalamine rectal,

mesalamine, sulfasalazine, balsalazide)
● Corticosteroids (eg, prednisone, methylprednisolone, budesonide,
hydrocortisone, prednisolone)
● Immunosuppressive agents (eg, mercaptopurine, methotrexate,
 ●

tacrolimus)
● Monoclonal antibodies (eg, infliximab, adalimumab, certolizumab

pegol, natalizumab, ustekinumab, vedolizumab)

● Antibiotics (eg, metronidazole, ciprofloxacin)

● Antidiarrheal agents (eg, loperamide, diphenoxylate-atropine)

● Bile acid sequestrants (eg, cholestyramine, colestipol)

● Anticholinergic agents (eg, dicyclomine, hyoscyamine,

propantheline)
Prescriptions
Prednisone
Rp:Tab:Prednisolone 0,005 No5
D.S PO4 tab after meal in the morning and 2 after meal

Celiac Disease
also known as celiac sprue or gluten-sensitive enteropathy, is a chronic
disorder of the digestive tract that results in an inability to tolerate
gliadin, the alcohol-soluble fraction of gluten.

Etiology
Celiac disease results from a combination of immunological responses
to an environmental factor (gliadin) and genetic factors.

Pathogenesis

The interaction of alcohol-soluble gliadin in wheat, barley, and rye with

the mucosa of the small intestine is crucial to the pathogenesis of celiac
disease. Endogenous tissue transglutaminase deamidates glutamine in
gliadin, converting it from a neutral to a negatively charged protein.
Negatively charged gliadin has been shown to induce interleukin 15 in
the enteric epithelial cells, stimulating the proliferation of the natural
killer cells and intraepithelial lymphocytes to express NK-G2D, a marker
for natural killer T lymphocytes.

Clinical manifestations

Gastrointestinal symptoms

Gastrointestinal symptoms may include the following:

Diarrhea - 45-85% of patients
Flatulence - 28% of patients

Borborygmus - 35-72% of patients

Weight loss - 45% of patients;

Weakness and fatigue - 78-80% of patients; usually related to general

poor nutrition

Severe abdominal pain - 34-64% of patients

Extraintestinal symptoms
Anemia - 10-15% of patients
Osteopenia and osteoporosis - 1-34% of patients

Neurologic symptoms - 8-14% of patients; include motor weakness,

paresthesias with sensory loss, and ataxia;

Skin disorders - 10-20%

Investigations
1. Laboratory tests
antibody testing, especially immunoglobulin A anti-tissue
transglutaminase antibody (IgA TTG),

Other laboratory tests include the following:

-Electrolytes and chemistries - Electrolyte imbalances; evidence of
malnutrition
-Hematologic tests - Anemia, low serum iron level, prolonged
prothrombin time (PT), international normalized ratio (INR)
-Stool examination - Fat malabsorption
-Oral tolerance tests - Lactose intolerance
-Serology - Immunoglobulin A (IgA) antibodies
2. Imaging studies

Radiographic evaluation
-Abnormal radiographic findings can include dilatation of the small
intestine, a coarsening or obliteration of the normally delicate mucosal
pattern, and fragmentation or flocculation of the barium in the gut
lumen.
3. Endoscopy and biopsy

Treatment
-dietary. Removal of gluten from the diet is essential, although complete
avoidance of gluten-containing grain
-corticosteroids

Ulcerative Colitis
ulcerative colitis characteristically involves the large bowel
Etiology
-genetic factors,
-immune system reactions,
-environmental factors, -For example, sulfate-reducing bacteria,
nonsteroidal anti-inflammatory drug (NSAID) use,
low levels of antioxidants, psychological stress factors, a smoking
history, and consumption of milk products.

Pathogenesis

A complex contribution of environmental and host factors that increase

the susceptibility of developing UC, and disease onset is triggered by
events that perturb the mucosal barrier, alter the healthy balance of the
gut microbiota, and abnormally stimulate gut immune responses. Here,
we discuss the general aetiological factors that increase the risk of
developing UC

Clinical manifestations
● Rectal bleeding

● Frequent stools

● Mucous discharge from the rectum

● Tenesmus (occasionally)

● Lower abdominal pain and severe dehydration from purulent rectal

discharge

Investigations
1. Laboratory studies

● Serologic markers (eg, antineutrophil cytoplasmic antibodies

[ANCA], anti– Saccharomyces cerevisiae antibodies [ASCA])
● Complete blood cell (CBC) count
● Comprehensive metabolic panel

● Inflammation markers (eg, erythrocyte sedimentation rate [ESR], C-

reactive protein [CRP])
● Stool assays
2. Endoscopy and biopsy,
Abnormal erythematous mucosa, with or without ulceration, extending
from the rectum to a part or all of the colon
Uniform inflammation, without intervening areas of normal mucosa
Contact bleeding may also be observed, with mucus identified in the
lumen of the bowel
3. Imaging modalities

● Plain abdominal radiography

● Double-contrast barium enema examination
● Cross-sectional imaging studies (eg, ultrasonography, magnetic
resonance imaging, computed tomography scanning)

Treatment

Medical treatment of mild UC includes the following:

● Mild disease confined to the rectum: Topical mesalazine via

suppository (preferred) or budesonide rectal foam

● Left-side colonic disease: Mesalazine suppository and oral

aminosalicylate (oral mesalazine is preferred to oral sulfasalazine)

● Systemic steroids, when disease does not quickly respond to

aminosalicylates
● Oral budesonide

● After remission, long-term maintenance therapy (eg, once-daily

mesalazine)

Medical treatment of acute, severe UC may include the following:

● Intravenous high-dose corticosteroids

● Alternative induction medications: Cyclosporine, tacrolimus,

infliximab, adalimumab, golimumab

Indications for urgent surgery include the following:

 ● Toxic megacolon refractory to medical management
● Fulminant attack refractory to medical management
● Uncontrolled colonic bleeding

Indications for elective surgery include the following:

● Long-term steroid dependence

● Dysplasia or adenocarcinoma found on screening biopsy

● Disease being present for 7-10 years

Surgical options include the following

● Total colectomy (panproctocolectomy) and ileostomy

● Ileoanal pouch reconstruction or ileorectal anastomosis

● In an emergency, subtotal colectomy with end-ileostomy

Prescriptions
Mesalazine
Rp:Tab Mesalazine 0,5 No 100
D.S 1 Tab PO 3 t/d

Prednisone
Rp:Tab Prednisoloni 0,005 No5
DS PO 4 Tab after meal