CASE 13

IRRITABLE & INFLAMMATORY

BOWEL DISEASES.

contents:
1. Inflammatory bowel disease:
a. Crohn’s disease.
b. Ulcerative colitis.
2. Irritable bowel syndrome
3. Diarrhea.
4. Constipation.
5. Dyspepsia.
a. Functional dyspepsia.
6. Somatic symptom disorder (somatization disorder).
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Inflammatory bowel diseases
- It is an immune-mediated chronic disease that cause inflammation of the intestine.
- It has 2 types:
o Ulcerative colitis (UC): Diffuse inflammatory disease limited to mucosa of colon
& rectum.
o Crohn disease (CD).
o Indeterminate colitis: 10% of cases are indistinguishable between UC and CD.

Crohn's disease (CD)

Defintion: Chronic, relapsing, transmural, usually segmental, granulomatous inflammatory
disorder involving any portion of the GI tract, most common in the terminal ileum.

Epidemiology:
• Incidence is 3-6/100,000.
• Prevalence is 25-100/100,000.
• High in Jewish, low in African black.
• Female > male.
• Bimodal distribution (1st: 25-40 years/ 2nd: 50-65 years of old).

Pathophysiology and risk factors:

1) Genetic susceptibility.
2) Environmental factors.
3) The intestinal microbiota.
4) Host immune response.

1) Genetic susceptibility:
a. Family history is the largest independent risk factor for IBD.
b. The major genetic factors for CD include:
i. The IBD1 gene which encode NOD2 protein on ch 16: It is an intracellular
sensor of bacterial peptidoglycan.
ii. The Th17 pathway (IL- 23–type 17 helper T cells).

2) Environmental factors:
a. Smoking:
i. Increase the risk of CD.
ii. Protective against UC.
b. NSAIDs: In both.
c. Hygiene: Poor and large families have lower risk of developing CD.
d. Nutritional factors: Breast feeding is protection against IBD.
e. Psychological factors: Chronic stress and depression increase relapses.
f. Appendicectomy:
i. Increase the risk of CD.
ii. Protective against UC.
g. Oral contraceptive pills: Increase the risk of CD.
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3) Intestinal microbiota:
a. Intestinal dysbiosis: Alteration in the bacterial flora in patients with CD:
i. Higher concentrations of Bacteroides and E. coli
4) Immune response:
a. The luminal antigen enters the cell due to many factors through the APCs >>
These cells activate CD4 T cells >> This cell will stimulate the macrophages to
secrete cytokines >> Most important ones are TNF-a, IL1 and IL >> These
cytokines will cause chronic inflammation.
i. TNF-a it’s the most important one.

Distribution:
1- Ileocecal area: 40-50-%. 2- Small intestine: 30-40%.
3- Isolated colon: 20%. 4- Upper GI: <5%.

Pathology:
• Can involve one small area of the gut (terminal ileum) or multiple areas.
• Normal bowel in between lesions (skip lesions).
• Macroscopic changes:
- Thickened bowel and narrowed.
- Deep ulcers and fissures in the mucosa produce a cobblestone appearance.
• Microscopic changes:
- Non-caseating granulomas (non-caseating epithelioid cell aggregates with
Langhian’s’ giant cells).
- Increase in chronic inflammatory cells and lymphoid hyperplasia.

Clinical features:
CD typically has a chronic intermittent course with episodic acute flares and periods of
remission.
1) Intestinal manifestation:
a. Triad of Crohn's disease includes:
i. Recurrent colicky abdominal pain associated with distention, increased by
food.
ii. Non-bloody watery diarrhea
iii. Weight loss, fever, and other constitutional symptoms.
2) Features of CD complications:
a. Anorectal lesions: Chronic, recurrent, or nonhealing anal fissures, ulcers, complex
anal fistulas, perirectal abscesses.
i. Perianal fistulas (50%) and abscesses are often the first signs of CD.
b. Malnutrition: Protein-losing enteropathy, steatorrhea, vitamin deficiencies (A, D,
E, K, B12), failure to thrive.
c. Strictures may cause obstructive symptoms.
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3) Extra-intestinal manifestations: Box 32.29.

a. Joint complications are most common.
b. The peripheral arthropathies are classified as:
i. Type 1 (pauciarticular):
1. attacks are acute and shorter.
2. occur with IBD relapses
ii. Type 2 (polyarticular):
1. Arthropathy lasts longer (months to years)
2. Independent of IBD activity
3. Usually associated with uveitis.
Diagnosis:
1) Blood test:
a) CBC: Anemia duo to either iron, B12, folate deficiency.
b) Hypoalbuminemia.
c) High Inflammatory markers: ESR, CRP.
d) Serological markers: ASCA+, ANCA-.

2) Stool test:
- Fecal calprotectin and lactoferrin are raised in active intestinal disease.
- Fecal calprotectin is useful for:
o Disease monitoring in IBD.
o Distinguishing IBD from IBS.
- C. difficile toxin assay should always be performed if diarrhea is present.

3) Radiographic findings:
a) Upper Gl with small bowel follow-through or enteroclysis:
- Narrowed terminal ileum (Kantor string sign), fistulas, nodules.
b) Barium enema:
- Thickened wall, longitudinal ulcers, transverse fissures, cobblestone formation, & rectal
sparing.
- Terminal ileum may contain strictures (string sign).
c) Abdominal CT:
- Intraabdominal abscesses, thickened bowel wall, and/or fistulas.

4- Colonoscopy:
- The gold standard.
- Rectum is normal (rectal sparing) in 40%-50% of patients
- Characteristic lesions:
o Aphthous ulcers (early feature).
o Mucosal ulcerations.
o Anal fissures.
o Cobblestoning.
o Segmental (skip) lesions.
o Fibrosis, strictures, and fistulas in either small or large intestine.
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Complications:
1- Intestinal obstruction 40%.
2- Abscess formation 30%.
3- Fistulas (specific to Crohn's disease):
• Entero-enteric fistulae: Cause diarrhea and malabsorption due to blind loop syndrome.
• Entero-vesical fistula: Causes recurrent urinary infections and pneumaturia.
• Entero-vaginal fistula: Causes a feculent vaginal discharge.
• Fistulation from the bowel: Cause perianal abscesses, fissures and fistulae.
4- Anorectal lesions: Abscess, fistula, and/or fissure.
5- Free perforation and hemorrhage: Rare because of gradual fibrosis and formation of strictures.
6- Carcinoma: It is less common than UC
7- Toxic megacolon:
• Nonobstructive colonic dilatation larger than 6 cm and signs of systemic toxicity.
• In 5% of patients with colonic involvement.

Management:
Seven categories:
1) Induction of remission.
2) Maintenance therapy.
3) Fistula.
4) Perianal disease.
5) Acute flare of CD.
6) Supportive therapy.
7) Surgical therapy.

Commonly used medications:

1) Corticosteroids.
2) Anti-TINF-a antibodies (adalimumab, infliximab, certolizumab).
3) Immunomodulators (azathioprine, 6-mercaptopurine, methotrexate)
4) 5-aminosalicylic acid derivative (sulfasalazine): May be considered to induce remission
of mild to moderate colonic or ileocolonic CD.
5) Antibiotics: Metronidazole may be beneficial in the prevention of postoperative
recurrence of CD.

1) Induction of remission:
a. Glucocorticoids is the 1st choice:
i. Start with budesonide, if fail >> Prednisolone.
ii. Calcium & Vit.D should be co-prescribed.
b. If fail to respond to glucocorticoids, or severe ileal or panenteric disease >> anti-
TNF agent.
2) Maintenance therapy:
a. Immunosuppression with thiopurines (azathioprine, 6-mercaptopurine) is the 1st
choice
b. If fail >> Anti-TNF
c. The combination of immunosuppressant & anti-TNF is the most effective
strategy, but costs are high and increased risk for side effects.
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3) Fistula: Anti-TNF, if fail >> Surgery.

4) Perianal disease:
a. Ciprofloxacin/metronidazole + anti-TNF.
b. If fail >> Surgery.
5) Acute flare of CD:
a. Hemodynamic support as needed: IV fluids, electrolyte repletion.
b. Abdominal plain XR to exclude obstruction or megacolon.
c. Determine choice of induction therapy:
i. IV hydrocortisone 100 mg tid and close monitoring
ii. If insufficient response by day 3 >> Initiate infliximab or cyclosporine.
d. Prophylaxis against common infectious diseases.
e. Initiate thromboprophylaxis as needed (LMWH).
f. Identify and treat malnutrition micronutrient and deficiency.

6) Supportive therapy:
a. Antidiarrheal therapy: loperamide OR cholestyramine.
b. Smoking cessation, NSAID avoidance.
c. Stress, depression, and anxiety management.
d. Identify and treat micronutrient deficiency:
i. Iron deficiency, vitamin D, and vitamin B deficiency are common.
e. Identify and treat malabsorption syndrome.

7) Surgical treatment:
a. Eventually required in 70%-75% of cases over lifetime of disease.
b. Reserved for treatment of complications only, because surgery is not curative.
c. Indications for surgery:
i. Small bowel obstruction often caused by strictures.
ii. Fistula.
iii. Abscess.
iv. Hemorrhage.
v. Perianal disease unresponsive to medical therapy.
vi. Toxic megacolon.
vii. Dysplasia seen on biopsy.
d. Surgery can lead to remission but is not curative.
e. Short bowel syndrome “condition when bowel fail to absorb nutrient, water &
electrolytes which lead to intestinal failure” occur after multiple procedures.
f. Recurrence rates 10 years after initial operation is approximately 50%.

Indeterminate colitis
• Typically present with symptoms similar to ulcerative colitis.
• Endoscopic and pathologic findings include features common to both UC and CD.
Ulcerative colitis 6
Defintion: Chronic inflammatory disease characterized by recurrent episodes of
inflammation limited to the mucosal layer of the rectum and colon. Starts at the rectum then
extends proximally.
Epidemiology:
Incidence: 10 per 100,000 persons.
Prevalence: 80-150 per 100,000 persons.
Onset: 2/3 by age 30 (with second peak after 50).
M>F.
Higher in White & Ashkenazi Jewish descent, low in African.
Small hereditary contribution.
Smoking & Appendectomy are protective.

Pathophysiology: Abnormal interactions between host immune cells&commensal

bacteria:
1- Dysregulation of intestinal epithelium: Increased permeability for luminal bacteria →
Activation of macrophages & dendritic cells → Antigen presentation to macrophages and
naive CD4+ cells leads to:
a. Secretion of proinflammatory cytokines (IL-6, IL-12, TNF-α) and chemokines
→ Recruitment of other immune cells (e.g., neutrophils) to the site.
2- Dysregulation of the immune system: Upregulation of lymphatic cell in bowel walls →
Inflammation with local tissue damage (ulcerations, erosions, necrosis).
a. Autoantibodies (pANCA) against cells of the intestinal epithelium.
3- Pattern of involvement:
a. Ascending inflammation begins in the rectum and spreads continuously
proximally throughout the colon.
b. Inflammation is limited to the mucosa and submucosa.

Pathology:
Macroscopic:
• Mucosa reddened, inflamed, and bleeds easily (friability).
• In severe cases: There may be extensive ulceration, with adjacent mucosa appearing as post-
inlammatory (pseudopolyps).
Microscopic:
• Mucosa shows a chronic inflammatory cell iniltrate in the lamina propria.
• Crypt abscesses (cryptitis) and goblet cell depletion.
• Colonic involvement is continuous in ulcerative colitis, unlike the patchy nature of CD.
*N.B: It is occasionally not possible to distinguish between UC and CD, particularly if biopsies
are obtained in the acute phase, and such patients are considered to have indeterminate colitis.

Distribution (Types):
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Clinical features:
- Hematochezia (bloody diarrhea).
a. May have nonbloody diarrhea at first.
b. Proctitis is characterized by frequent passage of blood & mucus, urgency and
tenesmus.
2- Abdominal pain.
3- Bowel movements are frequent but small.
4- Fever, anorexia, and weight loss (severe cases).
5- Tenesmus (Pain during defecation).
6- Extraintestinal symptoms (e.g., jaundice, uveitis, arthritis, skin lesions).
*N.B: The first attack is usually the most severe and is followed by relapses and remissions.
• Emotional stress, infection, gastroenteritis, antibiotics or NSAID may all provoke a relapse.

Differential diagnosis: See the table.

*Backwash ileitis: Inflammation of terminal ileum in the context of UC (few cm proximal
to the ileocecal valve). Affects 10–20% of all patients with UC. Clinically, its presence
makes it harder to differentiate between UC & CD.

Diagnosis:
1) Blood tests:
a. CBC:
i. High WBC and platelet counts in moderate to severe attacks.
ii. Iron deiciency anaemia is present.
b. ESR and CRP: Often raised (high CRP is a sign of poor prognosis).
c. Liver biochemistry:
i. Hypoalbuminaemia in severe disease (a sign of poor prognosis).
ii. High ALP, GGT in patients with concurrent PSC.
d. pANCA: May be positive. Contrary to CD, where pANCA is usually negative.

2) Stool tests and C. difficile toxin:

a. These should always be performed to exclude infective causes of colitis.
b. Faecal calprotectin/lactoferrin will be elevated.

3) Imaging:
a. A plain abdominal X- ray is essential in patients with acute severe attacks to
exclude colonic dilation.
i. However, extent of disease cannot be assessed dusing this investigation.
b. Other imaging modalities are rarely used in the assessment of patients with UC.

4) Colonoscopy:
a. Endoscopy with mucosal biopsy is the ‘gold standard’ for diagnosis of UC.
b. Also allows assessment of disease activity and extent.
c. In long-term colitis, chromoendoscopy is used to diagnose dysplasia.
d. Full colonoscopy should not be performed in severe attacks of disease for fear of
perforation.
i. Instead, a limited unprepared flexible sigmoidoscopy should be used to
confirm diagnosis.
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5) Important points:
a. The most important issue is to distinguish first attack of colitis from infection.
i. In general, diarrhea lasting >10 days is unlikely to be a result of infection.
b. Faecal calprotectin has high sensitivity for GI inflammation and may be
elevated, even when CRP is normal.
i. It is particularly useful for distinguishing IBD from IBS, and for
subsequent monitoring of the disease.

Assessment of severity: See the table.

Complication:
1) Toxic megacolon:
a. Is the leading cause of death in UC and affects <5% of patients.
b. Associated with risk of perforation.
c. The plain abdominal X- ray shows a dilated, thin-walled colon with a
diameter of >6 cm; it is gas-filled and contains mucosal islands.
d. Urgent surgery is required in all patients who not resolved within 48 hours.
e. High mortality (15–25%).
2) GI bleeding (both acute and chronic).
3) Perforation (peritonitis).
4) Fulminant colitis: > 10 stools/day, lower GI bleeding, abdominal pain, and distention.
5) ↑ Risk of cancer: Risk increases with duration and extent of disease, in distal proctitis
there is no increased risk of CRC.
6) Colonic stricture.
7) Amyloidosis.

Management:
1- Aminosalicylate (5-ASA):
a. Mainstay of treatment.
b. Sulfasalazine is 1st choice in patients with coexistent arthropathy.
2- Oral glucocorticoids.
3- TNF inhibitors (infliximab, adalimumab).
4- Immunosuppressive agents thiopurine (6-mercaptopurine, azathioprine).
5- Surgical:
a. Often curative (unlike Crohn disease) and involves total colectomy.
b. Indications for surgery (Box):
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Approach:
1)Active proctitis:
- 1 g mesalazine suppository (topical), but some require additional oral (5-ASA) therapy.
- If fail>> Topical glucocorticoids (budesonide).
- If fail >> Systemic glucocorticoids and immuno-suppressants.
- A stool softener may be required to treat proximal constipation.

2)Active left-sided or extensive ulcerative colitis:

- Combination of once-daily oral & topical 5-ASA (‘top and tail approach’) is effective.
o The topical preparation withdrawn after 1 month.
o The oral is continued long-term to prevent relapse & minimise risk of dysplasia.
- If fail >> Oral prednisolone.
o Simultaneous calcium and vitamin D should be given.
- If fail >> Use Immunosuppressive therapy with a thiopurine.

3)Acute severe colitis:

- Definition: Bloody stool >6/day plus one or more of the following:
o Fever: >37.5 C.
o Tachycardia: >90 bpm.
o ESR: >30 mm/h.
o Anemia: Hb < 100g/L.
o Albumin: < 30g/L.
- Treatment: See box:
o If not respond to hydrocortisone >> Initiate infliximab or cyclosporine.
o If medical treatment or there is colonic dilatation >6cm (toxic megacolon) >>
Urgent colectomy.
- Topical and oral aminosalicylates have no role to play in the acute severe attack!

4)Maintenance of remission:
- Life-long therapy for pts with left-sided/extensive disease but not necessary in proctitis.
- Once-daily oral 5-aminosalicylates are the preferred first-line agents.
- If fail >> Use thiopurines (azathioprine or 6-mercaptopurine).
- If fail >> Use anti-TNF antibodies or anti-a4ß7 integrin antibodies (vedolizumab).
- Glucocorticoids should never be used for maintenance therapy!
Irritable bowel syndrome 10

Definition: Idiopathic disorder in which there is increased frequency of the normal peristaltic
and segmentation contractions of the bowel.

Epidemiology:
- The most common functional GI disorder.
- More common in young women (3-1).
- More common among Caucasians.
- Highest prevalence in individuals aged 20-39.
- Prevalence is 20% of the population are affected at some time but only 10% consult their
doctors because of symptoms.
- Coexisting conditions: Non-ulcer dyspepsia, chronic fatigue syndrome,
dysmenorrhoea and fibromyalgia, and psychiatric conditions.

Pathophysiology:
- IBS is a functional gastrointestinal disorder without a specific organic cause.
- The pathophysiological processes of IBS are multifaceted and not yet fully understood.
- The most common findings associated with IBS are:
o Altered gastrointestinal motility.
o Altered permeability of the gastrointestinal mucosa
o Visceral hypersensitivity/hyperalgesia.
o Psychosocial aspects.

Triggers: See box 32.20.

Subtypes and variants:

1- IBS-D (Diarrhea is the predominant symptom)
2- IBS-C (Constipation is the predominant symptom)
3- IBS‑M (Mixed diarrhea and constipation)
4- IBS‑A (Alternating diarrhea and constipation)

Clinical features:
1) Intestinal symptoms:
a) Chronic abdominal pain:
- Frequency, intensity, and localization generally vary widely from pt to pt:
- More in LLQ.
- Post-prandial worsening of pain for 1-3 hours.
- Worse before and/or during menstruation.
- Typically alleviated by defecation (but it may increase or remain unchanged.)
b) Altered bowel habits: 20% have constipation only, while large percentage have diarrhea alone
or diarrhea alternating with constipation.
c) Other gastrointestinal symptoms
• Nausea, reflux, early satiety
• Passing of mucus, abdominal bloating
• Physical examination: normal

2- Extraintestinal symptoms: See box 32.29.

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Diagnosis:
- IBS is a clinical diagnosis.
- Based on the patient's history (Rome IV criteria) and exclusion of other diseases..
1) Patient history (Rome IV criteria):
- Recurrent abdominal pain (at least 1 day per week during the previous 3 months)
that is associated with 2 or more of the following:
o Pain related to defecation.
o Change in stool frequency.
o Change in stool form or appearance.
- Ruling out organic disease (a disease of exclusion).

Differential diagnoses:

Treatment:
A) Non-medication Therapy (must be individualized):
1- Emotional support and reassurance/Hypnotherapy (most important 50% of treatment).
2- Diet and fiber therapy: Avoidance of foods that cause symptoms.

B) Medical therapy of IBS is symptom‑directed:

1- Diarrhea
- Antidiarrheals “loperamide” (if Diarrhea is predominant symptom).
- Serotonin antagonist.
- Rifaximin (if there is no constipation).
2- Constipation
- Soluble fibers/bulk‑forming laxatives (psyllium).
- Osmotic laxatives (polyethylene glycol).
- Serotonin agonist.
3- Cramping/pain
- Antispasmodics (dicyclomine, hyoscyamine)
- Tricyclic antidepressants (e.g., amitriptyline, nortriptyline).
Diarrhea 12

Defintion: More than three loose stools in 24 hours.

Pathophysiology:
1) Inflammatory diarrhea:
a. Damage to the intestinal mucosa >> Impair absorption.
b. Mucos, blood, and leukocytes present in the stool.
c.Associated disorders: IBD, CRC, Infections (Shigella, salmonella, hemorrhagic E.coli,
amebiasis).

2) Fatty diarrhea: Malabsorption & malabsorption.

a. Associated disorders: Exocrine pancreatic insufficiency, ileal resection, amyloidosis,
infections (SIBO, Whipple disease).

3) Watery diarrhea:
a. Secretory diarrhea: Active secretion of water into lumen via inhibition or activation of
enzymes (e.g., ↑ cAMP activity).
i. Associated disorders:
- Neuroendocrine disorders, e.g.: Carcinoid syndrome, gastrinoma.
- Endocrine disorders, e.g.: Hyperthyroidism, Addison disease, DM.
- Foodborne infections:
1- Cholera (“rice water” diarrhea).
2- Enterotoxigenic E. coli (traveler’s diarrhea).
3- C. difficle (antibiotic & PPI use).
4- Viruses.
b. Osmotic diarrhea:
i.Poor absorption or excessive ingestion of hydrophilic substances (e.g., salts, sugars,
laxatives) causes water to be drawn into the intestinal lumen.
ii.Associated disorders: Osmotic laxative (magnesium citrate), carbohydrate
malabsorption.

c. Functional diarrhea:
i. Rapid intestinal passage due to increased bowel activity.
ii. Associated disorders: Diarrhea-predominant IBS (IBS-D).

Acute diarrhea
Defintion: Diarrhea lasting less than 14 days.

Causes: Usually infectious, mostly viral but sometimes bacterial (more severe cases).
Common infectious causes include:
• Viral infection, e.g. norovirus or rotavirus.
• E. coli food poisoning (causes a secretory diarrhoea).
• Food poisoning from Salmonella, Campylobacter or Staphylo-coccus bacteria.
• Clostridium dificile infection (usually due to recent course ofantibiotics).
• Contaminated food or water.
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Investigations:
1) Stool microscopy culture sensitivities (MCS) should be sent in all patients.
2) Samples for C. difficile toxin should be sent in at risk patients (elderly, nursing home
residents, recent antibiotic use).
3) Stool for ova, cysts and parasites should be sent in the following cases:
a. Persistent diarrhoea (>14 days <30 days).
b. Men who have sex with men.
c. Immunocompromised.
d. Recent travel.
e. If suspecting giardiasis/amoebiasis/cryptosporidium.

Management: Volume repletion, usually oral rehydration, If severe >> IV fluid.

Antibiotics are not usually empirically given, indications for antibiotic treatment include:
• Severe/prolonged symptoms (>5days).
• Systemic signs of infection.
• Extremes of age.
• Immunocompromise.
• Presence of complications.
• Bloody or mucoid stools.

Chronic diarrhea
Definition: Diarrhea lasting more than 30 days.

Causes: Box 32.27.

Investigations:
1) CBC, Cr & electrolytes, thyroid function.
2) Coeliac screen (TTG) or (EMA).
3) Faecal calprotectin.
4) Stool MCS, C. dificile toxin.
5) If the above not reveal a cause >> Flexible sigmoidoscopy.
a. In the following circumstances, patients should undergo a full colonoscopy:
‣ Iron deficiency anaemia.
‣ Abnormal faecal calprotectin with suspicion of IBD.
‣ Older patients when screening for polyps and CRC.
6) Further investigations include bowel imaging, endoscopy, SeHCAT scan and lactose
hydrogen breath tests. The choice will depend on symptoms.

Management: Treating the underlying cause.

Constipation 14

Definition: Persistent, difficult, infrequent, or seemingly incomplete defecation.

Epidemiology:
• Prevalence is 14% of the population experiences chronic constipation.
• Increasing prevalence with age.
• Female>Male.

Causes:
1- Primary constipation (functional constipation): most common
a. Functional, idiopathic attributed to colon dysmotility.
b. Most commonly due to poor diet and insufficient exercise.
2- Secondary constipation: See box 32.43.

Investigations:
1- CBC, Electrolytes (hypokalemia) TSH, Calcium, Glucose.
2- Abdominal x-ray.
3- Colonoscopy, CT colonography: To exclude mechanical obstruction; (e.g., tumor, stenosis),
especially in the presence of red flags,

Management:
1- Treat underlying causes.
2- Approach in adults:
pomp
• Begin with lifestyle changes: High-fiber diet,
increased fluid intake, and exercise.
• If constipation persists, start bulk forming laxatives.
• If unsuccessful, add a osmotic or stimulant laxative.
3- Pharmacology:

Dyspepsia (indigestion)

Definition: Spectrum of epigastric symptoms (heartburn, acidity, bloating, epigastric

pain/discomfort, nausea, fullness, belching, wind).

Alarm symptoms (indication of endoscopy):

1- Dysphagia, weight loss, persistent vomiting, GI bleeding.
2- Iron deficiency anemia, Family Hx of cancer.
3- Nocturnal Sx, recent onset dyspepsia (>50YO).

Causes: See table 21.14.

• Most common causes are GERD and functional dyspepsia.
 Functional dyspepsia 15
(indigestion)
Types and diagnosis:
1- Postprandial distress syndrome (70%): Postprandial fullness or early satiety severe
enough to impact on regular activities or finishing a regular-size meal.
a. To diagnose: 3 or more days per week in the past 3 months.
2- Epigastric pain syndrome: Bothersome epigastric pain or epigastric burning 1 or more
days per week in the past 3 months
a. To diagnose: 1 or more days per week in the past 3 months.
*The diagnosis must be made after excluding all other organic causes (disease of exclusion).

Treatment:
a) First-line treatment: PPIs for 8 weeks at standard dose.
b) Second-line treatment: Tricyclic antidepressants (e.g., amitriptyline)
c) Third-line treatment:
• Prokinetic therapy (e.g., metoclopramide)
• Psychological therapy (e.g., cognitive behavioral therapy)

Somatic symptom disorder (somatization disorder)

(indigestion)
Definition: Mental illness that causes one or more bodily symptoms, including pain.

Epidemiology:
• Female > Male.
• Prevalence in adults: 5–7%.

Clinical features:
• The symptoms can involve one or more different organs and body systems, such as:
◦ Pain, neurologic problems, GI complaints, or sexual symptoms.
• People with SSD are not faking their symptoms!

Diagnosis: DSM-5 diagnostic criteria must be met:

a) ≥ 1 somatic symptom (e.g., heartburn, fatigue, headache, pain) that causes significant distress.
b) Excessive thoughts, feelings, or behaviors related to the somatic symptoms or health concerns,
manifesting as ≥ 1 of the following:
• Disproportionate and constant thoughts of symptom severity.
• Constant and significant anxiety about symptoms or general health.
• Excessive amounts of time and energy spent attending to symptoms or health concerns.
c) Duration: ≥ 6 months

Management: Psychotherapy.