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Gastro-Esophageal Reflux Disease (GERD) Endoscopy: locate GE Pathology: for histological

junction, to assist biopsies diagnosis
Definition: is medical condition in which the gastric content (acid are obtained (2cm from
& stomach contents) back up into esophagus and causing NERD GEJ)
(Non-Erosive Reflux Disease) or RE (Reflux esophagitis))

Columnar-appearing distal Intestinal metaplasia
Symptoms – NERD

Gastric content – esophagus (Non-erosive Reflux Disease)
Clinical manifestation
Esophagitis – RE
 Some patient: asymptomatic
(Reflux Esophagitis)
 Heartburn (Classic  Chest pain
 Dysphagia
 Regurgitation (Sour taste)
1) Anti-reflux barrier: LES-Lower Esophageal Sphincter, Hiatus  Odynophagia (severe
Hernia  Belching pain on swallowing)

2) Esophageal clearance: Primary & Secondary peristaltis  Water brash (sudden appearance in the mouth slightly sour or
salty fluid)
3) Esophageal mucosal resistance / Esophageal sensitivity

4) Stimulation of the regurgitant gastric content  GERD: heartburn (classical symptoms), dysphagia,
regurgitation (especially postprandially & at night), water
5) Other: Neonate, pregnant, obesity, scleroedema, DM, brash, & belching
Mellitus, Seroperitoneum
 Peptic stricture: hearthburn + dysphagia

 Alternative diagnose: severe inflammation without
stricture, peristaltic dysfunction, and an esophageal cancer
arising in Barrett’s esophagitis

 Patients with GERD may present with extraesophageal
symptoms, including chest pain and respiratory, ear, nose
and throat problems.

 Chronic cough, recurrent aspiration pneumonia, and
pulmonary fibrosis may be related to GERD

 Hoarseness, sore throat, halitosis, vocal cord granuloma,
and even laryngeal cancer may be caused by intermittent
aspiration of gastric contents
 Hyperemia ,edema, erosion ,ulcer


Distal esophagus


 GI bleeding: hematemesis, melena

 Barrett esophagus (BE)-columnar lined esophagus  Esophagostenosis: dysphagia
 BE: pre-canceriosis
 Diagnosis: endoscopy and pathology
Investigation test  H2RA (H2 receptor antagonists)

 X-ray: barium meal (hiatal hernia)  Cimitidine  Famotidine

 Endoscopy: esophagitis, complication, differential diagnosis.  Ranitidine  Nizatidine

 24-hour pH test: PH<4  Prokinetic agents

 Esophageal manometry: LES’s pressure  Metoclopramide  Cisapride

 PPI (Proton-pump inhibitor) test: omeprazole (OME) 20mg  Domperidone  Mosapride
2/d x 7ds
 Protective agent of gastric mucosa
 Hydrotalcite  Smecta
Symptoms + endoscopy (esophagitis) + 24-h pH test + PPI test
 Ulcerlmin  De-Nol
 Atypical cases: analysis
3) Operation under endoscopy
by endoscopy, 24-h pH
test and PPI test.
 BE (cut off, electrocoagulation, argon plasma
coagulation (APC) )
 Classification:
 Stricture (Esophageal stent, Balloon dilation )
4) Surgical Operation
 RE
 Fundoplication / Laparoscopic fundoplication
 BE

Differential diagnosis

 Coronary heart disease, angina

 Carcinoma of esophagus

 Achalasia (Bird beak)

 Asthma


1) Change life style

 Elevated the head at bed time to allow stomach acid stays
down reducing burning

 Quit smoking & dringking Gastritis

 Pay attention to diet Definition

 Gastritis: is defined as inflammation of the gastric mucosa
(generally accompanied with epithelial damage and
2) Drugs regeneration), regardless of its etiology

 PPI (Proton Pump Inhibitors)  Gastropathy: is reserved for mucosal alterations (epithelial
damage and regeneration without inflammation) resulting
 Omeprazole (Losec)  Rabeprazole from chemical injuries or vascular disturbances

 Lansoprazole  Esomeprazole Classification
 Pantoprazole  Acute  Chronic gastritis
Acute Gastritis Prostaglandin decrease


 Acute Gastritis is defined as acute gastric mucosa
inflammation resulting from various damage factors  Clinical manifestation:

 Gastric mucosal congestion, edema, hemorrhage and  Nausea, vomit, epigastric pain or discomfort, melena,
erosion (superficial ulcers) can be verified by endoscopy hematemesis, early saturation, fullness sensation

 Lamina propria mucosae infiltrated by Inflammatory  Active bowel sound
cells (mainly neutrophils) is a histopathologic feature
 Stool occult blood positive
 Positive findings by endoscopy within 24-48 hours
 Acute helicobacter pylori gastritis

 Acute gastritis infected with other pathogens

 Acute erosive-hemorrhagic gastritis

Acute helicobacter pylori gastritis

 Diffuse gastritis associated with epigastric pain, nausea,
and vomiting, last for few days or a week. Chronic Gastritis
 Diagnosed by a positive urea breath test or by the Characteristic
combination of positive histology and negative serology for
anti–H. pylori IgG (proof for acute infection)  Defined as chronic inflammation of gastric mucosa
Acute gastritis infected with other pathogens  Mucosal infiltration of lymphocytes and plasmocytes is a
histopathologic feature
 Mucosa damage result from pathogenic organisms infection
and/or their toxin Classification (Sydney system)

 The infection rarely happens except those patients who suffer
from severe immunodeficiency.

Acute erosive-hemorrhagic gastritis

 Characterized by multiple mucosal erosion, hemorrhage
and transient superficial ulceration

 Common damage factor include: Helicobacter pylori – Induce Gastritis

Chemical Stress Characteristic

 NSAID- indomethacin,  Severe trauma  G- bacteria microaerophilic organism, cause chronic, serious
aspirin infection
 Operation
 Some chemotherapeutics-  It produces urease, which appears to be important in
fluorouracil  Burning colonization of the gastric mucosa

 Potassium chloride  MOF  Have long latent period with small proportion of infected
individuals experiencing clinical illness
 Iron supplements
Transmission & Causes
Pathogenesis: Pathogenesis:
 Transmission is opportunistic (person-person)
 Direct epithelial damage  Mucosal ischemia and
hypoxia play a key role in  Bad household hygiene, contact of contaminated food or
 Weakend epithelial pathogenesis water, gastric juice of infected individuals (nasogastric tubes
regeneration or endoscopes)

 Cyclooxygenase respression

 Male predominance of clinical disease, with M:F ratio

 Most typically is acquired in childhood

 Mostly asymptomatic, 15% develop Peptic ulcer disease &
0.05% develop gastric cancer or lymphoma

H. pylori pathophysiology
 Motility
 Duodenal ulcer: due to gastric metaplasia of the duodenal
 Adherence to gastric epithelial layer bulb and gastric acid hypersecretion

 Virulence factors:  Gastric ulcer & gastric carcinoma: due to gastric atrophy
(and relative hypochlorhydria)
 Urease (protect from gastric juice)
 Gastric lymphoma (rare): excessive lymphoproliferative
 Vac A cytotoxin (associated with development of peptic response
ulcer, also gastric cancer & lymphoma)


 Early stage: characterized by colonization of the host stomach

 Late stage: characterized by clinical disease

Clinical findings
 Anorexia  Vomiting

 Epigastri  Hematem
c pain esis Treatment

 Nausea  “Coffee 1) Life style modification
grounds” emesis
 Quit Smoking and alcohol
 There is poor correlation between symptoms
and the number or severity of endoscopic abnormalities  Avoid spicy food when disease is active

 PE is nonspecific finding  Reduce Coffee, tea ,cola consumption

2) Drugs therapy

 Antacid and cytoprotective drugs:

 Antacid compounds are based on aluminium and
magnesium hydroxide

 Sucralfate: 1~2 pills tid

 Bismuth compounds
Diagnosis (H. pylori test)
 Antisecreroty drugs:
 Noninvasive modalities: serology with enzyme-linked
immunosorbent assay for IgG or IgA antibodies, 13C-urea  PPIs-proton pump  Prostaglandin analogues:
or 14C-urea breath tests, stool antigen testing inhibitors: Omeprazole, misoprostol
pantoprazole, lansoprazole
 Invasive (endoscopic): histologic examination, urease  Muscarinic (M1) receptor
testing of antral biopsy specimens, or culture  H2-receptor antagonists: inhibitors: atropine
Famotidine, cimetidine
 Prokinetic agents:  Imbalance between aggressive factors and
mucosal defenses
 Metoclopramide  Cisapride
 Domperidone  Mosapride
 Common in men
 Anti Hp therapy
 DU is more common than GU
 Triple-therapy
 DU 10x more common than GU in young patient, while
PPIs + metronidazole/tinidazole + clarithromycin relatively equal in older group

PPIs+ amoxicillin + clarithromycin Pahtogenesis

PPIs+ amoxicillin + metronidazole
 Fail to repair and healing (GU)
(Other antibiotics: tetrocycile, gentamycin, Furazolidone)
 Defense mechanisms are compromised by Hp-induced
 Quadruple-therapy inflammation & NSAID-induced reduction of prostaglandin
synthesis. (PU)
Triple-therapy +bismuth (colloidal bismuth subcitrate)
 7-14 days
1) H. Pylori and Peptic Ulcer

 Main cause of chronic gastritis & PU

 >90% of DU & >75% of GU are associated with Hp

 Destroy the balance between the aggressive factors and
defensive/repairing factors

Hp → inflamation & immune response → damage the
mechanism of mucosal defense and repair.

Hp → gastrin↑, acid↑.

2) NSAIDs and Peptic Ulcer
Peptic ulcer  Mechanism:

Definition: ulceration which may occur at any site in the  Damage directly gastric mucosal barrier.
gastrointestinal tract that is exposed to acid-pepsin secretion.
Defects in the gastrointestinal mucosa are extending through the  Inhibit the production of endogenous prostaglandin
muscularis mucosae into the submucosa or muscularis (PG)

Typical ulcers  Risk factor:

 GU (Gastric Ulcer)  Age: elderly individuals, >60

 DU (Duodenal Ulcer)  Previous history of ulcers or complications

Major cause  Duration of therapy: the first week and the first month of
 Hp (helicobacter pylori)
 Dose and duration of action and use of multiple NSAIDs
 NSAIDs (nonsteroidal anti-inflammatory
 Dyspepsia
 Cotherapy with corticosteroids
 Others: Hp infection, smoking, etc.
3) Acid-pepsin and peptic ulcer  DU:

 PU formation → depend on acid-peptic activity in gartric o hunger (2-3hours after meals): when acid is secreted in
juice the absence of food buffer

 Peptic activity is linked to gastric pH o At night(11pm-2am)/nocturnal pain : when the
circadian stimulation of acid secretion is maximal
 Adequate acid secretion is necessary for DU, GU may occur
in low acid concentrations o Relieved when intaking alkali, food, antisecretory
 Cause of excess of gastric acid secretion in DU: Amount of
parietal cells↑, Susceptibility of parietal cells to stimulators↑,  GU:
Normal feedback inhibitory, Tension of vagal nerve↑
o Less likely to be relieved by food or antiacids
4) Other factors and PU
o More likely to display food provocation (within 1 hour
 Disturbance of gastric emptying and bile reflux. after meals)

 Genetic factors.  Located at epigastric portion

 Circumstance factors: Smoking, foods, infections (HSV-1,  Character of pain: dull pain, hungrily pain, gnawing
CMV), season and geographic difference.
 Degree: mild, moderate, severe
 Stress ulcer
 Frequency: paroxysmal, persistent
5) Comorbid ulcer
 Relieve/enhance factor
 COPD- 30% case has PU
2) Other dyspepsia symptoms & complication’s symptoms
 Cirrhosis
Acid reflux, belching, heartburn, epigastric fullness and
 Renal failure discomfort, bloating, early satiety, nausea and vomiting,
hematemesis, melena, weight loss, anorexia, etc
 Organ transplant


 Mild, localized epigastric tenderness, often unremarkable
 Signs of ulcer complications
 Site:  GU: Lesser curvature
 DU: anterior wall of duodenal bulb
1) Bleeding/hemorrhage (Most common)
 Number: mostly solitary
 Most common cause of UGI bleeding
 Size: GU: <2cm
 The most common cause of ulcer-related death
DU: <1.5cm
2) Perforation (2nd most common)
 Depth: Extending through muscularis mucosa into submucosa
or muscularis Typical clinical manifestation

Symptoms  Acute onset of severe, intolerable abdominal pain

1) Abdominal pain, characteristic: o Unremitting & exacerbated by any movement

 Chronic: recurrent, weeks, months, years o Precisely identification of exact time the pain began

 Periodically: cluster of pain lasting a few  Peritoneal irritation sign
days/weeks/months, followed by pain free periods of week
or months o Tenderness; Rebound tenderness; Muscle guarding

 Rhytmically
 Bowel sound ↓ 4) X-ray barium-contrast meal: direct sign (niche); indirect sign
(mucosal fold, oval scar surrounded with edema)
 Free air underneath the diaphragm (abdominal X-ray)
5) Endoscopy: gold standard for determining benign or malignant
3) Obstruction

 Acute ulcers ⇒ obstruction due to edema ± motor dysfunction
(functional obstruction) Diagnosis

 Chronic ulcer ⇒ obstruction occur secondary to scarring of an  Clinical feature (history, symptoms, signs)
ulcer in pyloric channel or duodenum (organic obstruction)
 X-ray barium-Contrast meal
 Presentation:

Gastric retention → frequent vomiting  Endoscopy and mucosal biopsy

→ Succussion splash Differential diagnosis

4) Canceration  Functional dyspepsia  Gastric cancer

 Chronic Cholecystitis &  Gastrinoma
 GU: 1%-2% of GU pts, Alert signals (Chronic GU history,
Above 45y, Recurrent ulcers, Continuing occult blood test
(OB) positive)
 DU: No canceration tendency 1) General

Special type of PU  Diet

 Silence ulcer: asymptomatic ulcer, more commom in  Emotion
 Regular life
 The aged ulcer: atypical, GU≥DU

 Complex ulcer :combined gastric and duodenal ulcers

 Pyloric channel ulcer: acid↑, vomit,obstruction 2) Drug therapy

 Postbulbar ulcer: 5% of DU, night pain, back pain,  Eradication of H. pylori
 PPIs–based triple therapy / Bismuth-based triple therapy:
 Giant ulcers: DU>2cm,GU>3cm Double standard amount of PPI (bismuth subsalicylate) +
two antibiotics (7-14d)
 Refractory ulcer: chronic, repeatedly
 Quadruple-therapy

 Stress ulcer: Cushing’s, Curling’s o When Triple-therapy failed

 Kissing ulcer: the anterior wall and back wall of o Triple-therapy + PPI / Bismuth subsalicylate
duodenal bulb.
 Confirmation of Hp cure: stoping medication for
Assistant test: sufficient time, followed by HP test (histologycal, culture,
1) Diagnostic test for Hp
 Antisecretory drugs
 Non-invasive: Serology (Anti-Hp IgG antibodies), Carbon
13 or 14 breath test (UBT), Stool antigen test  H2 receptor antagonists (H2RAs)

 Invasive (endoscopic biopsy required): rapid urease test  Proton pump inhibitors (PPIs)
from biopsy, histology culture
 Anticholinergics
2) Fasting serum gastrin level: gastrinoma  Antacids (neutralize gastric acids)
3) Gastric juice analysis  Calcium carbonate antacids
 Magnesium-containing antacids  For patients with liver cirrhosis → precipitating hepatic
encephalopathy or hepatorenal syndrome
 Aluminum-containing antacids
 For patients with underlying ischemic heart disease →
developing angina because of hypoperfusion

 Enhancement mucosal defense
 Sucralfate
Upper GI Bleeding (75% of Lower GI Bleeding (24%)
 Bismuth all GI bleeding)

 Prostaglandin E1 analogue (Misoprostol)  Mallory-Weiss tear  Cancer or polyps

 Treatment of NSAID ulcers  Varices  Upper GI
bleeding(need to rule it out)
 Anti-ulcer drugs: PPIs (for ulcer healing), Prostaglandins  Gastritis/Gastric
for prevention (not good for healing), (H2RAs, sucralfate cancer  Colitis
and antacids) are inadequate
 Arteriovenous  Angiodysplasia
 Prevention: Prostaglandins (misoprostosol 200mg, qd); malformation
PPIs (low dose); not H2RA (doesn’t prevent)  Diverticulosis
 Ulcer(peptic)
 Refractory & recurrent illness  Hemorrhoids

Maintenance therapy (for prevention), PPIs (standard dose),
H2RA (half-dose) 1. Nonvariceal esophageal bleeding
3) Surgical  Typical present with hematemesis or melena
Indication: complication, refractory ulcers  Mallor-weiss tear: retching, vomiting, or coughing before

 Reflux esophagitis: occurs in a subset of GERD

2. Peptic ulcer disease (most common cause of upper GI
GI bleeding bleeding)

Definition: any bleeding that stars in GI tract, which extends from 3. Acute Gastropathy (Acute mocosa lesions)
mouth to anus.
 Involve gastric body & fundus
 Cause by NSAIDs, alcohol, stress
According to Microscopic bleeding (occult)
amount  Treatment: ↑gastric pH, H2RAs
Overt bleeding
4. Portal hypertensive GI bleeding (highest mortality)
Massive bleeding
 Conseguences: varices formation (in stomach, esophagus,
According to Upper GI bleeding (from mouth-upper part small bowel, & colon), vascular congestion (Portal
location (ligament of small intestine)
hypertensive gastropathy, enteropathy, and colopathy →
of treitz)
Lower GI bleeding (small intestine- anus) mucosal bleeding), development varices into cirrhosis

 Portal hypertensive gastropathy:
GI bleeding induced
 Mechanism: ↑ mucosal blood flow & passive congestion of
 Prolonged microscopic bleeding → leading to loss of iron, the submucosa
causing anemia
 Can lead to chronic blood loss
 Acute, severe, massive bleeding → leading to hypovolemia,
shock, and even death 5. Obscure upper GI bleeding

 Gastric Antral Vascular Estasia (GAVE)
o Experiencing occult bleeding & anemia o Oliguria o Sweating

o High frequency with autoimmune disorders & atrophic  Signs: o Blood pressure↓ o Pulse↑
gastritis, hypergastrinemia, cirrhosis, or portal hypertension
 Vital sign: o Postural o Tachycardia
o Treatment: supportive treatment or surgical treatment hypertension
(orthostatic o Recumbent
hypertension, ↓ hypotension
 Dieulafoy’s Lesion
3) Anemia and blood abnormality
o It is a large artery that penetrates thee gastric wall
 Symptoms: o Pale o Dyspnea
o Presentation: Hematemesis (usually) or hematochezia (1/3)
o Dizziness o Fatigability
6. Lower GI bleeding (Hemorrhoidal bleeding, Diverticular,
Vascular anomalies, Colorectal cancer, Infectious or o Palpitation
inflammatory colitis)
 Blood abnormality:
 Hemorrhoidas (most common cause of LGI bleeding)
 RBC count, Hb (hemoglobin), Hct (hematocrit)
 Bright red blood on surface of stool
 Early stage of bleeding: may appear normal, not diluted
 Confirmed by: anoscopy, flexible sigmoidoscopy by tissue fluid

 Colonic diverticulum (2nd most common)  Anemia occurs after 3-4 hrs, reaches peak at 24-72hrs

 Due to increase intraluminal pressure at the sites of natural 4) Fever
weakness in colonic wall
 Acute massive GI bleeding
 Confirmed by: colonoscopy
 Found within 24 hrs
 Vascular anomalies (Angiodysplasia, Dieulafoy lesions)
 <38.5℃

 Continuing for 3-5 days
 Colorectal neoplasm

 With occult blood loss, may be hematochezia 5) Azotemia

 Diagnosis: distal examination of rectum, endoscopy  blood urea nitrogen (BUN) ↑

Diagnosis & management of GI bleeding  As a result of breakdown of blood proteins by bacteria to
urea and reuptake of this from the gut
Step 1: GI bleeding recognition
 Starting from several hours after bleeding
1) GI bleeding manifestations  Peaking at 24-48 hrs
 Hematemesis (upper GI bleeding, differentiate from  Normalizing after 3-4 days
hemoptysis & nosebleeding)
6) Misleading factors for GI bleeding
 Hematochezia (lower GI bleeding, or vigorous upper GI
 Bleeding outside GI tract: nasopharynx
 Melena (shiny, blacky, sticky, tarry stool; typically
indicates upper GI bleeding; be aware of (-) occult blood)  Food or drugs

 Chronic occult bleeding (Detect by testing stool sample  Confirmatory testing is required
with McAb)
Step 2: Patient assessment (Bleeding amount & speed evaluation)
2) Hypovolemia or shock
1) Postural hypotension (10–20% volume loss)
 Symptoms: o Weakness o Cold (feet,
hands) 2) Resting Hypotension and tachycardia (30% loss volume)
o Giddiness
3) Syncope (rapid blood loss of as little as 10% volume)
4) Hematochezia (at least 1000 ml in the setting of upper GI  Reveal bleeding (even rate is low)
 Not specific (cannot specifically locate the source)
5) Red hematemesis and concomitant hematochezia

 massive brisk bleeding in the UGI tract

 with a 30% mortality before and during diagnostic Treatment
1) Emergent and intensive care

 Secure airway if needed to prevent
aspiration of blood (endotracheal intubation)

 Fluid resuscitation & Blood transfusion if
needed (for hypovelemia or hemorrhagic shock)

 Normal saline: until hypovolemia remit
Step 3: Resuscitation
 Tranfusion: type & cross CBC, paced RBC; until
1) Suggest hypovolemia or hemorrhagis shock (Syncope, intravascular volume is restored
Hypotension (BP↓), Pallor (face), Sweating, Tachycardia

2) Stabilization with airway management; IV fluids, or blood 2) Specific hemostasia therapy
transfusions is essential
 Causes and hemostasis
Step 4: The source of bleeding
 Nonvaciceal upper GI bleeding
1) Hematemesis/coffee-ground emesis /melena (more proximal
 Variceal bleeding
to UGI)
 Lower GI bleeding
2) Hematochezia (more distal colorectal lesion)
Non-variceal UGI bleeding (Four types of methods)
Step 5: The causes of bleeding (diagnostic)
 Medical management
1) History and physical examination
o PPIs
2) Endoscopy
 Prevent clot dissolution, allow healing of underlying lesion
 Upper GI endoscopy: examination of the esophagus,
stomach, and duodenum  Maintaining gastric pH above 6.0

 Colonoscopy: colon  High-dose PPIs: Omeprazole or pantoprazole
administration (80mg bolus injection followed by 8mg/h
 Double-balloon enteroscopy: Small intestine continuous infusion)

 Capsule endoscopy: Small intestine o Octreotide

 Intraoperative enteroscopy: Small intestine  Analogue of somatostatin: inhibitory neuropeptide

 Inhibits portal venous and arterial blood flow to stomach
3) Barium radiography and duodenum

 Upper GI barium x-rays have no role in acute bleeding  Reducing the risk of continued bleeding and need for
 Bleeding stopped for 3 days at least
 Not recommended for routine treatment of nonvariceal
4) Angiography upper GI bleeding

 Endoscopic methods
 Only if endoscopy has failed
o For patients with persistent or recurrent hemorrhage
 Blood rate at least (0.5-ml/min)
o Safer than emergency
5) Radionuclide scans
 Surgical o Vasopressin and analogues

o When endoscopy and medical therapy fail o Somatostatin and analogues

o Be used in patients with continued bleeding
o Thrombin cluster

 Angiographic

o Methods above are ineffective or unfeasible
Inflammatory Bowel Diseases (CD & UC)
o Angiography with embolization
Definition: inflammatory disease of GI tract
o Angiography with Vasopressin infusion

 Environmental factor

 Diet

 Smoking (bad for CD/good for UC)

 Mental factor : nervous, tired, mentaldepression, anxious ,
Variceal bleeding etc

 Medical therapy (Vasopressin & analogues - octreotide)  Genetic factor

 Endoscopic therapy  Positive family history for IBD

o Endoscopic sclerotherapy of varices  Genetic influences overlaped

o Endoscopic variceal band ligation  Multigenic

 Balloon tamponade  Immunological factors

o Endoscopic cannot control variceal hemorrhage  Lamina propria infiltrated with lymphocytes, macrophages,
other immune cells
 TIPS (Transjugular intrahepatic portosystemic shunt)
 Up-regulated immune genes in mucosa
 Surgery
 Specific antigen triggers for immune response
o Continuing to bleed
o Microbial pathogens
o Having more than one rebleeding episode
o Dietary antigen or nonpathogenic microbial agent
o Child’s cirrhosis
o Autoimmunity (autoimmune antigen on GI cells)
Ulcerative Colitis
 Monitoring varices by endoscopy every 3-6m until varices are
eradicated Definition: Ulcerative colitis is a chronic idiopathic
inflammation limited to the rectum and colon, up to now the
 Oral Beta-blocker therapy: to decrease cardiac output disease’s origin has not been cleared

Histological: Inflammation confined to mucosa and submucosa,
Lower GI bleeding
Distribution: Confined in colon (sigmoid), sometimes involve
 Endoscopic treatment rectum, terminal ileum, continuous

 Angiographic intervention Clinical characters: diarrhea, mucopurulent bloodystool,
abdominal pain
 Urgent surgery
 Medical therapy:
 Age: Peak age: 20-40 yrs old, Can occur in childhood or old  Severe cases: anorexia, nausea, vomit
 Signs
 Gender: equal
 tenderness in the left lower andomen

 obvious tenderness, intestinal pattern

 Muscle guarding, rebound tenderness, bowel sound↓
(toxic megacolon? perforation?)

Pathology External manifestation

 General characteristics:  Arthritis  Eye complications (1-2%)

 Diffuse, continuous  Osteoporosis  Thromboembolic
 Superficial mucosal or submucosal inflammation  Renal
complications  Hepatobiliary compications
 Large bowel (3%)

 Can begins in the rectum and extends to any contiguous  Dermatological manifestations (1%)
Systemic symptoms
 small intestine is seldom involved (terminal ileum)
 Severe and fulminant UC
 Macroscopic test: mucosal congestion, edema, erosion, ulcer.
 Accompanied by diarrhea
 Gland body is out of shape, disorganized, decreased
(atrophy)  Fever  Hypoproteinemia

 Goblet cell ↓, Paneth cell metaplasia  Weight loss  Electrolyte disturbance

 Inflammatory polyp  Weak  Nausea and vomiting

Clinical manifestation  Anemia  Night sweats

 Typically insidious rather than abrupt Classification
 Chronic, recurrent
 Initial onset
 Causes/aggravating factors: diet, tired, mental,
infection  Chronic recurrent (most common)
Clinical types:
 Diarrhea:  Chronic persistent

 mucopurulent bloodystool  Acute fulminant (seldom, severe,
 Increased or decreased stool frequency
 Mild:
 Abdominal pain:
 <4 bowel movements/day
 mild, moderate
 No fever, tachycardia
 left lower abdomen , lower abdomen , the whole
abdomen  ESR (Erythrocyte sedimentation
rate ):normal
 Paroxysmal; persistent, drastic →toxic megacolon?
 Bloodystool,anemia: no or mild
 pain---diarrhea---anesis
 Able to proceed with daily-life activities
 tenesmus

 Others

 abdominal distension
Symptomatic  Moderate:  Proctosigmoiditis or Left-sided colitis-40%
criteria for
severity of UC  4-6 stools/day  40% of UC cases

 Severity between the mild and severe  Intermediate syndrome presentation

 Severe: o Either constipation or diarrhea
(Accompanied by tenesmus,
 >6 stools/day bleeding)

 Obvious mucopurulent bloodystool o Colicky left lower quadrant pain is
more common than proctitis
 T>37.5℃, persist for 2 days at least;
o Extraintestinal symptom is also
 Pulse >90bpm common

 HB<100g/L ,ESR>30mm/h  Prognosis

 Fulminant o The proximal margin usually fixed

 >10 stools/day  Pancolitis or extensive colitis-30%

 Severe pain  Diagnosed when extends to transverse
or right colon
 Relentless tenesmus
 Presentation
 Rebound tenderness
o More likely presenting with diarrhea
 Distention with tympanic bowel
sounds o Diminished absorptive capacity of
 Prostration, high fever, hypotension
o Accompanied by rectal bleeding,
 Radiography: Mucosal edema,
Intramural air, Colonic dilation
o Diffused or localized cramping
Activity:  Period of onset (active) abdominal pain
 In remission(quiescent) o More likely having weight loss,
systemic or extraintestinal
 Proctitis (Rectitis)-30% symptoms, anemia
 Limited to distal 15-20cm of rectum

 The most common and mildest UC Complication
(25-30% of cases)
 Toxic megacolon: (most severe UC)
 Typical presentation:
 Diagnosed when inflammation extends from superficial
o Hematochezia mucosa into submucosa and muscular layers

o Constipated bowel movements  More common in extensive colitis but also in severe distal
o Systemic symptoms uncommon
 Manifestation: Fever, prostration, severe cramps,
abdominal distention and tenderness, etc.
o Extraintestinal symptoms can occur
 Prognosis: bad, perforation.
 Prognosis
 Canceritaion:
o Usually remains confined to rectum
 rectum ,colon
o Advance in 30-40%
 pancolitis

 juvenile-onset, chronic

 Other:
 Bleeding: 3% o Severe UC: Air-filled colon, Extralumenal gas under
 Perforation

 Intestinal obstruction: seldom
Differential diagnosis
 Chronic bacillary dysentery: dysentery bacillus (feces,
 History and physical examination culture)

 Laboratory investigations  Amoebiasis: entamoeba histolytica trophozoite

 Blood test  Schistosomiasis: contact history, schistosomeovum

o Leucocytosis (WBC ↑) o Hypoalbuminemia  Crohn’s disease

o Anemia (RBC ↓) o Electrolyte imbalance  Colorectal cancer: digital examination of the rectum
endoscopy, biopsy
o ESR elevation
 Irritable bowel syndrome: no pus or blood, no disorder of

 Fecal markers Treatment

o Fecal leukocytes-inflammatory diarrhea: mucus, pus, General measurement-drugs-surgical-medical management
blood; RBC, pyocyte, macrophage
 General measures
o Exclude infectious diarrhea
 Rest  Correct electrolyte
 Endoscopy disturbance
 Diet, Fasting
 Establish the diagnosis  Transfusion
 Nutrition
 Appearance  Transfuse albumin
Total parenteral
o Diffuse, continuous inflammation nutrition (TPN)  Antibiotics: infection

o Beginning in rectum, extending to different proximal  Drugs
 Sulfasalazine (SASP):
o Healthy colonic mucosa: Smooth and glistening
o It consist 5-ASA (anti inflammatory) & sulfapyridine
o Inflammatory mucosa: Edematous, erythematosus, (anti bacterial)
more granular, breaking apart the light reflection;
Mucosal granularity may be fine or coarse o Activated in colon, ineffective for small bowel

 Histology  Mesalamine:

 Histological features parallel the endoscopic appearance o 5-aminosalazine acid (5-ASA)

 Principle components o Active in small bowel if taken orally
o Disruption of glandular architecture o May active in colon if given suppositories or enema
o Inflammatory infiltrate Sulfasalazine & 5-ASA are primary therapy for mild-
moderately active UC
 Imaging studies
 Corticosteroids:
 Conventional barium radiography
o For acute cases, espacially for the severe and fulminant
o Largely been supplanted by endoscopy
o For mild, moderate cases failed to the treatment of
o Valuable in specific clinical situations sulfasalazine and 5-ASA.
 Plain abdominal radiograph o May be given as enemas (decrease systemic absorption,
“Budesonide”) or orally.
o Work better in UC than CD. Moderate:

o If unable to taper steroid, this is indication for o o High dose oral mesalamine (topical +
antimetabolite and/or infliximab Most likely to corticosteroid may help)
o Monitor: bone mineral density, ophtho exam, adrenal surgery o Corticosteroid (if above therapy fail)
insuff, glucose intolerance
o o Analogue or infliximab (if Repeatedly
 Immunomodulators (use in refractory case) At a higher risk relapse on corticosteroid taper)
for colorectal
Antimetabolites: Azathioprine and 6-mercaptopurine, cancer Severe:
o o Immediate evaluation & treatment
Calcineurin inhibitors: Cyclosporine and Tacrolimus Medical therapies (avoid proression to fulminant or toxic
decrease the state)
Anti-tumor factor agents risk
o Starts iv corticosterois
o Azathioprine and 6-MP:
o Combine with other therapies (Oral
 Azathioprine is prodrug conversed to 6- mesalamine, Topical mesalamine or
mercaptopurine. corticosteroids)

 Inhibits purine metabolism and DNA synthesis and o Nutritional assessment
repair, inhibiting cellular proliferation.
o Surgical consultation
o Cyclosporine and Tacrolimus :
Fulminant colitis and toxic megacolon:
 Inhibit calcineurin, required for activation of T
lymphocytes o Surgical emergency
 Cyclosporine:
o Broad spectrum antibiotics
Induction in UC
o Recuscitation
Severe steroid-refractory UC
o Supportive therapies
Concomitant steroids used in severe UC
Maintenance of o Agent used to induce remission is
Goal to bridge to AZA or 6-MP as maintenance remission often the one to initially try to
tx maintain remission

 Surgical o Oral mesalamine-based maintenance

o Indication: o Acute massive bleeding o Purine analogues maintenance

o Acute perforation
Crohn’s disease
o Severe cases threaten the life,failed to the
drug treatment. Definition: A chronic granulomatous inflammation that may
affect any portion of the GI tract, up to now the disease’s origin
 Medical management of UC has not been cleared.
Ulcerative o Masalamine suppositories Histological: Inflammation extends through intestinal wall from
proctitis mucosa to serosa, granulomatous.
o Topical corticosteroids
Distribution: Involving entire GI tract potentially (terminal ileum,
o Oral mesalamine proximal colon), skip lesions.

Ulcerative o Topical therapy (Mesalamine / Clinical characters: abdominal pain, diarrhea, abdominal mass,
proctisigmoiditis Corticosteroids) fistula, intestinal obstruction.

o Combination with oral agent Epidemiology: peak age (15-30), may occur in any age; equals
Pancolitis Mild: oral mesalamin agents (combine
with topical agent may help) Pathology (Focal, asymmetric, transmural inflammation of GI
 Patchier (focal, discontinuous) Fever

 Any segment of GI tract (From mouth to anus): 50% affect Malnutrition
terminal ileum and proximal right colon
o Weight loss
 Transmural nature: Complications of stenoses (strictures) and
fistulae Systemic symptoms o Anemia

 Histological Noncaseating granulomas-hallmark: But only o Hypoproteinemia
30%, not necessary for diagnosis
o Vitamin deficiency
Clinical manifestation
o Developmental delay
 Presentations determined by site, extent, severity, (preadolescence)
complications of intestine and extraintestinal disease.

 Usually chronic but can be acute Arthritis


Joint erythema
presentations Canker sore

 Symptoms: Eye complications

Thromboembolic complications
Abdominal pain (most common)
Hepatobiliary compications
o right lower abdomen ,
Periumbilical pain

o Intermittent onset Complication

o after meal ↑,after defecation or pass  Intestinal obstruction (most common)
gas ↓
 Intra-abdominal abscess (less common)
o Spasm? stenosis? obstruction?
perforation?  Fistulae  Toxic megacolon: seldom
Diarrhea  Malabsorption syndrome
Digestive system’s  Cholelithiasis
symptoms o Intermittent → chronic, persistent  Acute perforation, massive
bloodystool  Lithangiuria
o pasty stool, seldom with mucus
,pus, or blood  Canceration  Fatty liver

Abdominal mass (10-20%)
Obstruction sign & symptoms
o right lower abdomen, periumbilical
area  Depend on location of blockage: (Pyloric, Jejunal, Small, or
 Treatment:
o internal fistula→ diarrhea↑,
malnutrition↑ o Kept Nil by mouth o Medical therapy

o external fistula→ discharge stool, o Intravenous hydration o Surgery
o Nasogastric suctioning
Lesions around the anus
Abscesses and fistulae
o Perianal abscess, anal fissure ,etc.
 Abscesses  20% CD patients

 Intraabdominal abscesses:
Any more and more obvious
o Pain, fever, chills, rigors

o Abdominal-pelvic CT scan or ultrasound  Histology

o Drainage-surgical resection  Reflecting the gross pattern of focal and asymmetric
intestinal involvement
 Fistulae  20-40% patients
 Aphthous ulcer: Minute erosions overlying lymphoid
 Any portion of the bowel affected by CD aggregates

 Medical therapy  Crypt abscesses

Surgery  Noncaseating granulomas

 Imaging studies (complementary in CD diagnosis)

 Air-contrast radiography: Mucosal detail, colonic
distensibility, and strictures

 CT scan: Urgent conditions, Extralumenal complications
(Abscess, Obstruction)

 CT enterography

Differential diagnosis
 Enterophthisis
 History and physical examination
 Malignant lymphoma of small intestine
 Laboratory investigations
 Acute appendicitis
Blood test Stool examination
 UC (ulcerative colitis)
 Anemia (RBC↓)  Fecal leukocytes, OBT
 Leukocytosis (WBC↑)
 Stool volume↑:
 Thrombocytosis (PLT↑) Malabsorption syndrome

 Elevated erythrocyte  Fecal fat ↑:
sedimentation rates (ESR↑) Malabsorption syndrome

 Elevated C-reactive protein

 Electrolyte disturbances

 Hypoalbuminemia

 Endoscopy (complementary in CD diagnosis)

Colonoscopy–Wireless capsule endoscopy–upper GI Treatment
General measurement-drugs-surgical-medical management
 Rectal sparing areas of active disease
interspersed with normal mucosa
 General measures
 Sharp, punched-out ulcerations surrounded
 Rest  Correct electrolyte
by normal mucosa
 Diet, Fasting
 Cobblestoning or nodular mucosa intersected
 Transfusion
by crossing linear ulcerations
 Nutrition
therapy  Transfuse albumin
 Drugs  Volume of stool: 200-300g/d

 Sulfasalazine (SASP)  Frequency: 1 or 2-3 times a day

 Mesalamine Diarrhea
 Corticosteroids  Volume: > 200g/d
 Immunomodulators (use in refractory cases)  Frequency: > 3 times a day
o Methotrexate
Chronic diarrhea
o Cyclosporine and Tacrolimus
 Duration: above two months
o Infliximab (Remicade) (antibody to TNF-a) is used in
severe CD. Etiology

 Antibiotics (metronidazole)  Osmotic diarrhea  Inflammatory
 Malabsorptive
 Surgical-Indication
conditions  Motility disorders
 Complete intestinal obstruction  Secretory conditions  Chronic infections

 Fistula Osmotic diarrhea

 Abscess  Fecal osmolality = Serum osmolality

 Acute perforation  Increased osmotic gap

 Massive bleeding uncontrolled  diarrhea is caused by ingestion or malabsorption of an
osmotically active substance
 Medical management of CD
 Common reasons
 Same as UC management  lactase deficiency

 Two stages of therapy (Induction, Maintenance)  laxative abuse

Mild to moderate Moderate to severe Fistulous CD Malabsorptive condition
CD disease
 Major cause:
First-line therapy Steroids Combined medical
and surgical  Small intestinal mucosal  Small intestinal bacterial
 Mesalamine  Budesonide approach diseases overgrowth
 Prenisone  Antibiotics  Intestinal resections  Pancreatic insufficiency
 Antibiotics
Anti-TNF  Drainage  Lymphatic obstruction
Failed to first-line
thrapy  Infliximab  Azathioprine  Hallmark of malabsorption

 Budesonide  Adalimumab  Methotrexate  Weight loss

 Azathioprine  Infliximab  Osmotic diarrhea

 Methotrexate  Nutritional deficiencies

 Laboratory abnormalities

 Anemia (microcytic or macrocytic, vitamins or minerals
Diarrhea deficiencies)

 Hypoalbuminemia
Normal intestinal movement
 Low serum cholesterol

 Hypocalcemia

 Prolonged prothrombin time

Secretory condition

 Watery diarrhea

 large volume but normal osmotic gap

 dehydration and electrolyte imbalance

 Causes

 endocrine tumors (pancreatic carcinoma, gastrinoma)

 bile salt malabsorption

 cholera

Inflamatory condition


 Crohn’s disease, ulcerative colitis

 Other symptoms

 abdominal pain, fever, weight loss, hematochezia

Motility disorders


 Hyperthyroidism

 Surgery

Chronic inflamation

 Protozoans giardia

 Entamoeba histolytica

 Cyclospora

 Intestinal nematodes

 AIDS: microsporida, cryptosporidium, cytomegalovirus,
isospora belli, cyclospora, mycobacterium avium complex