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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
Esophagitis
Distal esophagus
Complication
Differential diagnosis
Carcinoma of esophagus
Asthma
Treatment
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
Characteristics
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
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
Epidemiology
H. pylori pathophysiology
Complication
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)
Staging
Clinical findings
Anorexia Vomiting
Epigastri Hematem
c pain esis Treatment
2) Drugs therapy
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
Epidemiology
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
Hp → gastrin↑, acid↑.
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)
Major cause Duration of therapy: the first week and the first month of
therapy
Hp (helicobacter pylori)
Dose and duration of action and use of multiple NSAIDs
NSAIDs (nonsteroidal anti-inflammatory
Dyspepsia
drugs)
Cotherapy with corticosteroids
Mechanism
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
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
Sign
Chronic: recurrent, weeks, months, years o Precisely identification of exact time the pain began
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
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:
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,
Ag-test)
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
Definition: any bleeding that stars in GI tract, which extends from 3. Acute Gastropathy (Acute mocosa lesions)
mouth to anus.
Involve gastric body & fundus
Classification
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
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
10-15mmHg)
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
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)
hemorrhage)
Not specific (cannot specifically locate the source)
5) Red hematemesis and concomitant hematochezia
Upper GI barium x-rays have no role in acute bleeding Reducing the risk of continued bleeding and need for
surgery
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
Angiographic
Environmental factor
Diet
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)
Prevention:
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
Can begins in the rectum and extends to any contiguous Dermatological manifestations (1%)
colon
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
Others
abdominal distension
Symptomatic Moderate: Proctosigmoiditis or Left-sided colitis-40%
criteria for
severity of UC 4-6 stools/day 40% of UC cases
o Constipated bowel movements More common in extensive colitis but also in severe distal
colitis
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
Distribution:
rectum ,colon
o Advance in 30-40%
pancolitis
juvenile-onset, chronic
Other:
Bleeding: 3% o Severe UC: Air-filled colon, Extralumenal gas under
diaphragm
Perforation
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
organs
Histology Mesalamine:
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)
undergo
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:
methotrexate
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)
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
(M/F)
Pancolitis Mild: oral mesalamin agents (combine
with topical agent may help) Pathology (Focal, asymmetric, transmural inflammation of GI
tract)
Patchier (focal, discontinuous) Fever
Acropachy
Joint erythema
Extraintestinal
presentations Canker sore
Thromboembolic complications
Abdominal pain (most common)
Hepatobiliary compications
o right lower abdomen ,
Periumbilical pain
Intraabdominal abscesses:
Any more and more obvious
o Pain, fever, chills, rigors
CT enterography
Differential diagnosis
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
Electrolyte disturbances
Hypoalbuminemia
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
Laboratory abnormalities
Hypoalbuminemia
Normal intestinal movement
Low serum cholesterol
Hypocalcemia
Secretory condition
Watery diarrhea
Causes
cholera
Inflamatory condition
IBD
Other symptoms
Motility disorders
IBS
Hyperthyroidism
Surgery
Chronic inflamation
Protozoans giardia
Entamoeba histolytica
Cyclospora
Intestinal nematodes