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ALEXANDRA ADELINE
405090036
Learning Objective
7
Duodenum
Pylorus - flexura duodenojejunal turned
jejenum
long 25 cm
C-shaped surrounding the pancreatic caput
Divided parts: pars superior, pars descenden,
pars horizontalis (inferior), pars ascending
Pars superior duedeni
5 cm long
Vertebra L 1 is located as high as
Move freely on radiography is shaped like a triangle
with its base at the pylorus called fleeced duodeni
(duodenal cap)
Deep
inspiration &
epiglottis
closed
Ulcers 31-59
Varices 7-20
Mallory-Weiss tears 4-8
Gastroduodenal erosions 2-7
Erosive Esophagitis 1-13
Neoplasm 2-7
Vascular ectasia 0-6
No Source indentified 8-14
http://www.wrongdiagnosis.com/bookimages/10/5248.pn
MELENA
Definition
The passage of dark black, liquid, tarry,
metallic-smelling stools
- Prostaglandin - Acid-pepsin
- Mucous Gel environ-
Layer ment
- Bicarbonate - Mucosal
- Mucosal Blood Ischemia
Flow - H. Pylori
Infection
- NSAID
- Trauma
Peptic Ulcer
Physiologi :
1. Mucosal defense system can be envisioned asa
a three-level barrier composed of : preepithelial
, epithelial and subepithelial
2. Preepithelial have mucus-bicarbonate and
surface active phospholipids layer which serve
as a physicochemical barrier
3. Epithelial cells provide the next line of defense
through several factors, including mucus
production , epithelial cell ionic balance which
maintain intracellular pH and bicarbonate
production.
Peptic Ulcer
Physiologi :
4. If the pre-epthelial barrier were breached,
epithelial cells bordering a site of injury can
migrate to restore the damaged region
(restitution). This process requires blood flow ,
alkaline pH and growth hormone factor.
5. In the subepithelial an elaborate of
microvascular induced defense/repair system ,
providing HCO3 and supply adequate oxygen
to epithelial cells.
Peptic Ulcer
Physiology :
6. Prostaglandine play a central role in gastric
epithelial defense/repair which release mucosal
bicarbonate and mucus , inhibit parietal cell
secretion and maintaining mucosal blood flow and
epithelial cell restitution.
Peptic Ulcer
Pathophysiology :
1. NSAID and Mucosal Ischemia will reduce the
amount of mucous and bicarbonate which
trigger imbalance
2. Infection of H.Pylori induce mucosal injury
Peptic Ulcer
Esophagogastroduodenoscopy (EGD)
1. Examination of the lining of the esophagus,
stomach, and upper duodenum with a small camera.
2. Procedure :
a. Patient should be on fasting state for 6
- 12 hours before the EGD procedure
b. Patient will be given a sedative and
analgesic (painkiller)
c. Local anesthetic may be sprayed into
your mouth to surpress cough or gag
when endoscope is inserted
Peptic Ulcer
2. Procedure :
d. A mouth guard will be inserted to
protect your teeth and the
endoscope
e. Endoscope will go through your
esophagus to upper duodenum with
a small camera to locate the ulcer or
cancer.
Left Right :
1.1st degree
scar
2.2nd degree
scar
Left Right :
1. 1st degree
ulcer
2. 2nd degree
ulcer
Left Right :
1. 1st degree
healing
2. 2nd degree
healing
1st Degree Ulcer
(duodenum)
2nd Degree
Ulcer
(gaster)
Peptic Ulcer
Gastric Biopsy :
1. Gastric tissue biopsy is the removal of stomach
tissue for examination
2. Procedure :
a. Patient should be on fasting state for
6 - 12 hours before the biopsy
procedure
b. The gastric tissue biopsy sample is
removed during an upper endoscopy
Peptic Ulcer
2. Procedure :
c. Then in laboratory staining examines the tissue for
bacteria or other organism that cause the disease
d. Culture of H.Pylori will be stained by hematoxylin-
eosin , gram staining or The Wartin Starry Silver
for the best result (most sensitive).
Peptic Ulcer
Urease Test :
1. Urease test is the test to examine the bacteria
H.Pylori by the level of urease
2. There are 2 types of urease test :
a. Invasive :
Biopsy of the gastric epithelial cell to measure the
level of urease
b. Non-invasive (Urea Breath Test) :
Test to measure the level of urea in our breath after
taking a specific species of carbon
Peptic Ulcer
3. Procedure :
a. Invasive : same as gastric biposy
b. Non-invasive :
1. Patient drink an isotopically labeled urea acid which
dissolved in aqua (14C or 13C isotype)
2. Breath collection after 30 60 minutes
3. Breath sample are transferred to an empty canister
to be examined.
GERD
Gastroesophageal reflux disease (GERD) is a
condition in which food or liquid travels
backwards from the stomach to the
esophagus (the tube from the mouth to the
stomach).
This action can irritate the esophagus, causing
heartburn and other symptoms.
Gastroesophageal reflux is a common
condition that often occurs without symptoms
after meals.
Classification
Gastroesophageal
Reflux
Regurgitation
2 categories:
erosive (e.g, superficial erosions, deep
erosions, hemorrhagic erosions)
non-erosive (generally caused by
Helicobacter pylori)
Etiology
Bile reflux Drugs
NSAIDs, such as aspirin, ibuprofen, and naproxen
Cocaine
Iron
Colchicine, when at toxic levels, as in patients with
failing renal or hepatic function
Kayexalate
Chemotherapeutic agents, such as mitomycin C, 5-
fluoro-2-deoxyuridine, and floxuridine
Potent alcoholic beverages, such as whisky, vodka,
and gin
Bacterial infections
H pylori (most frequent)
H heilmanii (rare)
Streptococci (rare)
Etiology
Fungal infections
Candidiasis
Histoplasmosis
Phycomycosis
Parasitic infection (eg, anisakidosis)
Acute stress (shock)
Radiation
Allergy and food poisoning
Spicy food
Smoking
Viral infections (eg, CMV)
Sign and Symptoms
Acute gastritis may be entirely asymptomatic
Epigastric pain
Nausea
Vomiting
Hematemesis
Melena
Potentially fatal blood loss
Risk Factors
Acute gastritis is frequently associated
with:
Heavy use NSAID, particularly aspirin
Excessive alcohol consumption
Heavy smoking
Treatment with cancer chemotherapeutic drugs
Systemic infections (eg. Salmonellosis)
Severe stress (eg. Trauma, burns, surgery)
Ischemia and shock
Suicide attempts with acids and alkali
Mechanical trauma (eg. Nasogastric intubation)
Reflux of bilious material after distal
gastrectomy
Chronic Gastritis
Definition: the presence of chronic
inflammatory changes in the mucosa leading
eventually to mucosal atrophy and epithelial
metaplasia
Most individuals with the infection also have
the associated gastritis but are asymptomatic
Etiology
Autoimmune
Bacterial (H. Pylori)
Chemical (NSAIDs)
Chronic noninfectious granulomatous
gastritis
Lymphocytic gastritis
Eosinophilic gastritis
Ischemic gastritis
Radiation gastritis
Pathophisiology
Most important etiologic association is
chronic infection by the bacillus H. pylori
Gastritis develops as a result of the
combined influence of bacterial enzymes
and toxins and release of noxious
chemicals by the recruited neutrophils
Characterized by mononuclear cell
infiltration in the lamina propia with
intestinal metaplasia and frequently
proliferation of lymphoid tissue
Sign and Symptoms
Usually causes few or no symptoms
Upper abdominal discomfort
Nausea
Vomiting