ANATOMY AND PHYSIOLOGY OF THE
STOMACH contents from the body of the stomach
The stomach is a J-shaped enlargement of
the GI tract found inferior to the diaphragm
which serves as a connection for the
esophagus and the duodenum of the small
intestine. It functions as a mixing chamber
and holding reservoir. Empty, it is about the
size of a large sausage but it is the most
elastic part of the GI tract and can
accommodate large quantities of food. In
the stomach (1) starch and triglyceride
digestion continues (2) protein digestion
begins (3) semisolid bolus is converted to a
liquid and (4) certain substances are
absorbed.
Four Main Regions of the Stomach
 The Cardia
 The Fundus
 The Body
 The Pyloric Part:
 Pyloric
 Antrum
 Pyloric Canal
 Pylorus
Mechanical and Chemical Digestion of the
Stomach
Propulsion: the act of moving gastric
down into the antrum.
Retropulsion: The act of returning the
gastric contents to the body of the stomach
since most food particles cannot fully pass
through the pyloric sphincter.
Chyme: The result of the continuous cycle
of propulsion and retropulsion that mixes
the gastric contents with gastric juices
which consequently makes it into a soupy
substance that is slowly able to pass
through the pyloric sphincter bit by bit
which is called the process of Gastric
Emptying.
In the fundus food is stored for an hour
wherein SALIVARY AMYLASE continues to
to digest food (carbohydrates) but once it
becomes chyme and is churned gastric
juices inactivates it and activates LINGUAL
LIPASE consequently which digests
trigylycerides into fatty acids and
diglycerides.
PARIETAL CELLS secrete HCL. PROTON
PUMPS actively transport H+ into the lumen
while bringing K+ into the cells and at the
same time Cl- and K+ diffuse out into the
lumen. CARBONIC ANHYDRASE Present in
parietal cells catalyzes the formation of
Carbonic Acid (H2CO3) from H2O and CO2.
Soon Carbonic acid will dissociate and will
be a ready source of H + for the proton
pumps which will generate bicarbonate ions
(HCO3-) that build up in the cytosol and is
consequently secreted in the capillaries for
alkalinity of the urine. Parietal cells also
secrete intrinsic factor needed for the
absorption of B12
Stimulation of HCL secretion is done
through the ff:
 1. Acetylcholine released by
parasympathetic neurons.
2. Gastrin secreted by G cells
3. Histamine released by Mast cells.
In the presence of Histamine at the H2
receptor, Ach and Gastrin stimulate parietal
cells to secrete more HCL.
PEPSIN secreted by CHIEF CELLS is the only
proteolytic enzyme in the stomach, it acts
by cutting peptide bonds in amino acids into
smaller peptide fragments. To regulate the
action of pepsin and to prevent the
proteolysis of the proteins of the stomach
pepsin is first produced in its inactive form
PEPSINOGEN and is only activated and goes
to work when it has come in contact with
HCl and also the stomach is protected by a
1-3 mm thick lining of alkaline mucus
secreted by surface mucuos cells and
mucous neck cells.
GASTRITIS
Is a condition wherein there is an
inflammation, irritation, or erosion of the
lining of the stomach.
There are two types of gastritis (1) ACUTE
GASTRITIS: One that occurs suddenly. And
(2) CHRONIC GASTRITIS: one that appears
slowly over time.
GENERAL SIGNS AND SYMPTOMS
 Gnawing or burning ache or pain in
the upper abdomen that may
become worse or better when
eating.
 Indigestion
 Nausea/Vomiting
 Feeling of fullness specifically in the
upper abdomen after eating.
GASTRIC LIPASE an enzyme in the stomach
that splits triglycerides in fat molecules into
fatty acids and monoglycerides.
SURFACE MUCOUS CELLS AND MUCOUS
NECK CELLS Secrete mucous for protection
from the acids secreted by the parietal cells.
Site of absorption of water, short chain fatty
acids and drugs.
Only a small amount of nutrients is
absorbed in the stomach because epithelial
cells are impermeable to most materials.
GASTRIC EMPTYING lasts for 2-4 hours. (1)
carbohydrate rich foods spend the least
time in the stomach. (2) protein rich foods
are retained much longer. (3) emptying is
slower after a fat laden meal containing
large amounts of triglycerides.
GENERAL DIAGNOSIS
TESTS FOR H.PYLORI it may be detected by
breath tests, blood tests, stool tests.
ENDOSCOPY the physician passes a tube
down the throat upto the small intestine of
the patient to check for signs of
inflammation.
X-RAY used to look for abnormalities in the
GI tract.
www.mayoclinic.org/diseases-
conditions/gastritis/diagnosis-
treatment/diagnosis/dxc-20319961
 ACUTE GASTRITIS
Acute gastritis is a term covering a broad
spectrum of entities that induce
inflammatory changes in the gastric
mucosa. Said inflammation may involve the
entire stomach (pangastritis) or a region of
 Use of drugs
 Alcohol
 Bile
 Ischemia
 Bacterial infections
 Viral infection
 Fungal infection
 Acute stress
 Radiation
 Allergy
 Food poisoning
 Direct trauma
The common mechanism of injury is an
imbalance between the aggressive and
defensive factors that maintain the integrity
of the stomach lining.
ACUTE EROSIVE GASTRITIS also called
reactive gastritis is commonly caused by the
exposure to NSAIDS, alcohol, cocaine ,
stress, radiation, bile reflux, ischemia all in
which cause the mucosa to have
hemorrhages, erosions, and ulcers. The MOI
of the NSAIDS is the reduction in the
prostaglandin synthesis.
BACTERIAL INFECTION H. pylori is the most
common C.A. it is usually asymptomatic but
in this case the bacteria imbed itself in the
mucous layer protected by UREASE. it lets
other toxins to be activated which cause IL
8 to be activated which will eventually
attract polymorphs and monocytes which
ultimately cause the gastritis
.  Bleeding from an erosion or ulcer
the stomach (antral gastritis) it has two
categories (1) EROSIVE (2) NONEROSIVE.
PATHOPYSIOLOGY
The following are the causes of acute
gastritis in patients:
TUBERCULOSIS is a rare cause of gastritis
since it mostly affects immunocompromised
patients and often is associated with
pulmonary and disseminated disease.
PHLEGMONOUS GASTRITIS caused by
numerous pathogens (strep. Staph. Proteus,
clostridium, Escherichia spp.) it occurs in
extremely debilitated patients who have
recently taken up (1) large intakes of
alcohol (2) has a concomitant URTI & (3)
AIDS. The disease commonly implies
infection of the deeper layers of the
stomach which mostly leads to gangrene.
VIRAL INFECTIONS the common CA is
Cytomegalovirus (CMV) which affects the
immunocompromised, those which have (1)
Cancer (2) Transplant patients (3) AIDS.
FUNGAL INFECTIONS also affect the
immunocompromised/immunossupressed
and is often caused by Candida albicans and
histoplasmosis. It usually affects an already
existing ulcer or an erosion bed which
causes bleeding or further erosions.
PARASITIC INFECTIONS (Anisakidosis)
caused by a nematode from contaminated
raw fish it causes gastric fold swelling,
erosions and ulcers.
COMPLICATIONS
 Gastric outlet obstruction due to
edema limiting the adequate transfer
of food from the stomach to the small
intestine.
 Dehydration from vomiting
 Renal insufficiency as a result of
dehydration.
TREATMENT
Surgical intervention is not necessary with
the exemption in the case of phlegmonous
gastritis.
 Treat underlying causes of the
disease.
 Administer fluids and electrolytes.
 Discontinue the drugs that are
causing gastritis.
 Give medications to fend off S/S
PHARMACOLOGICAL
ANTACIDS
Used for general prophylaxis.
ALUMINUM AND MAGNISUM HYDROXIDE:
Drug combination neutralizes gastric acidity
and increases pH of the stomach. Al ions
inhibit smooth-muscle contraction and
inhibit gastric emptying. These mixtures are
used to avoid bowel function changes.
H2 BLOCKERS: Acts as a competitive
inhibitor of histamine at its receptor.
Thereby decreasing gastric acid secretion.
PROTON PUMP INHIBITORS: can completely
inhibit acid secretion and is considered as
the most effective gastric acid blockers.
ANTIBIOTICS
To treat the H. Pylori infection there are
multiple regimens to choose from ranging
from dual therapy to quadruple therapy:
 Dual Therapy: PPI + Amoxicillin or
PPIqu + Clarithromycin
 Triple Therapy: PPI/Bismuth based
drug + clarithryomycin +
amoxicillin/metronidazole
 Quadruple Therapy: 2 antibiotics,
bismuth, antisecretory agent
AMOXICILLIN: interferes with cell wall
mucopeptides during active multiplication.
TETRACYCLINE: Inhibits bacterial protein
synthesis by binding with 30s ribosomal
subunits.
CLARITHROMYCIN: Inhibits bacterial
growth, possibly by blocking dissociation of
peptidyl t-RNA ribosomes and causing
arrest of RNA-dependent protein synthesis.
METRONIDAZOLE: Inhibitor of nucleic acid
synthesis disrupting the DNA of microbial
cells.
ANTIDIARRHEAL AGENTS
Used in combinations with antibiotics and
proton pump inhibitors or H2 receptor
antagonists to eradicate H. pylori.
BISMUTH SUBSALICYLATE
NONPHARMACOLOGICAL
Patients should avoid the following:
 Alcohol
 Tobacco
 Acidic beverages, Carbonated
beverages, Fruit Juices
  NSAIDS
 High fat foods since it may cause
increased inflammation in the
stomach lining
Diet should include:
 Fiber rich diet
 Foods rich in flavonoids like apples,
celery, cranberries, onions, garlic,
and tea to stop the growth of H.
Pylori
emedicine.medscape.com/article/175909-
overview#a4
http://www.umm.edu/health/medical/alt
med/condition/gastritis
CHRONIC GASTRITIS
Chronic gastritis is a relatively minor
manifestation of disease that
predominantly manifest in other organs or
systematically.
PATHOPHYSIOLOGY
H pylori associated chronic gastritis once
H. pylori is present in the stomach it passes
through the mucous layer and becomes
established at the luminal surface of the
stomach causing an intense inflammatory
response in the underlying tissue. H pylori
causes the secretion of various cytokines
(TNF-a, IL-1B,6,7,8,12,17,18) which causes
more inflammation. Leukotriene levels are
also elevated and with all of these
functional changes will occur in the
stomach, parietal cells will be inhibited,
leading to reduced acid secretion and
when inflammation continues loss of
parietal cells will occur and the reduction in
acid secretion becomes permanent.
G cells and D cells who secrete gastrin and
somatostatin respectively are also affected
wherein in meals gastrin is overly
produced.
H. pylori causes 2 kinds of gastritis
 Antral predominant gastritis- this is
characterized by inflammation and
is mostly limited to the antum PUD
is commonly a predisposing factor.
 Multifocal atrophic gastritis – this
involves the corpus and gastric
antrum with loss of gastric glands.
INFECTIOUS GRANULOMATOUS GASTRITIS
tuberculosis or fungi may affect the
stomach and cause caseating granulomas
often found in immunosuppressed and H
pylori infected patients.
GASTRITIS IN PATIENTS WHO ARE
IMMUNOSUPPRESSED
CMV and HSV infections are commonly
observed. Common mycobacterial
infections are by Mycobacterium avium-
intracellulare
AUTOIMMUNE ATROPHIC GASTRITIS
It is associated with serum anti-parietal and
anti-Intrinsic Factor antibodies that causes
IF deficiency which ultimately leads to
pernicious anemia.
CHRONINC NONINFECTIOUS
GRANULOMATOUS GASTRITIS
Noninfectious diseases are the usual cause
of gastric granulomas these diseases are
CROHN DISEASE, SARCOIDOSIS and
ISOLATED GRANULOMATOUS GASTRITIS
LYMPHOCYTIC GASTRITIS is a type of CG
that is characterized by dense infiltration of
the surface and faveolar epithelium by T
lymphocytes. It is proposed to result from
intraluminal antigens. High anti H.Pylori
antibodies have also been found in patients
with lymphocytic gastritis however patients
are not deemed positive for H.Pylori.
EOSINOPHILIC GASTRITIS caused by
parasitic infections but in cases of children
it may occur from food allergies.
RADIATION GASTRITIS occurs 2-9 months
after initial radiotherapy. Small doses cause
reversible mucosal damage while higher
doses are irreversible which comes with
atrophy and ischemic related damage.
ISCHEMIC GASTRITIS arises from
atherosclerotic thrombi arising from the
celiac and superior mesenteric arteries.
TREATMENT
PHARMACOLOGICAL
Treatment of CG is aimed at a specific
etiologic agent but if CG is from a systemic
disease treatment is directed towards the
primary disease.
H PYLORI THERAPIES
Triple therapies: FDA approved and yield
the best results Triple therapies are the
therapies of choice for the treatment of CG
caused by H. Pylori.
 30 mg lansoprazole/20 mg
Omeprazole/400 mg ranitidine
bismuth citrate + Clarithromycin 500
mg + Amoxicillin 1000
mg/Metronidazole 500 mg all twice
daily.
Quadruple therapies:
 PPI(lanso 30mg/omep20mg)(bid) +
Tetracycline 500 mg (qid) + Bismuth
Subsalicylate 120 mg (qid) +
Metronidazole 500 mg (tid)
Therapy normaly lasts for 7-14 days and
evaluate for complete eradication 4 weeks
after beginning of therapy. This can be done
through urea breath test or stool antigen
test.
ANTIBIOTICS
Amoxicillin: Acid stable semisynthetic
penicillin
Clarithromycin: Macrolide that binds to
bacterial ribosomes and disrupts protein
synthesis.
Tetracycline: Inhibits bacterial protein
synthesis by binding with the 30 s
Ribosomal subunit.
Metronidazole: Inhibitor of nucleic acid
synthesis disrupting the DNA of microbial
cells.
PROTON PUMP INHIBITORS
Decreases gastric acid secretion by
inhibiting the parietal cell H/K atp pump at
the secretory surface of gastric parietal
cells.
GASTROINTESTINAL AGENTS
emedicine.medscape.com/article/176156-
overview#a3
NONPHARMACOLOGICAL
DIET:
 Foods containing flavonoids like
apples, celery, cranberries, onions,
 garlic, and tea to inhibit the growth
of H. pylori
 Antioxidant rich food such as
blueberries, cherries, tomatoes,
squash, bell peppers
 Foods high in B vitamins and
Calcium such as beans, whole grains,
dark leafy greens.
 Avoid refined foods such as white
bread, pasta and sugar
 Lean meat, cold water fish, tofu or
beans
 Opt for healthy ois like Olive oil
 Reduce or eliminate trans fatty acids
found in commercially baked goods
such as cookies, crackers, cakes,
French fries, onion rings, donuts,
processed foods and margarine.
 Avoid acidic, carbonated, sweet
alcoholic drinks.
 Water consumption of 1-2 liters per
day
EXERCISE:
 30 Minutes daily 5 days a week.
www.umm.edu/health/medical/altmed/con
dition/gastritis
GASTROPARESIS
ANATOMY AND PHYSIOLOGY
The major digestive functions of the
stomach are as follows:
1. Storage of large amounts of
food.
PATIENT EDUCATION
Explain the disease to the patient
encourage cessation of smoking and
alcohol consumption and warn the patients
of the potential effects of noxious drugs
and chemical agents.
HOW DO YOU DIFFER ACUTE GASTRITIS
FROM CHRONIC GASTRITIS?
 AG is erosive and hemorrhagic but
CG is not
 NSAIDS and Alcohol are the common
causes of AG while autoimmunity
and H pylori are the common causes
of CG
 Endoscopically inflammatory
changes are seen only in AG
 Neutrophils are the predominant
inflammatory cell in AG while
lympho-plasmatic infiltration is seen
in CG
2. Mixing, mechanical and
enzymatic breakdown of larger
particles into smaller particles
(< 2 mm), known as chyme.
3. Slow delivery of chyme to
the duodenum at a rate not to
 exceed the digestive and
absorptive capacity of the
small intestine.  Gastric
emptiying
OVERVIEW
 Gastroparesis (gastric stasis) is
a condition that affects the
normal spontaneous
movement of the muscles
(motility) in your stomach
 your stomach's motility is
slowed down or doesn't work
at all, preventing your stomach
from emptying properly.   Abdominal pain
CAUSE
 It's not always clear what leads
to gastroparesis. But in many
cases, gastroparesis is believed
to be caused by damage to the
vagus nerve that controls the
stomach muscles.
 The vagus nerve can be
damaged by diseases, such as
diabetes, or by surgery to the
stomach or small intestine.
VAGUS NERVE: signaling the
muscles in your stomach to
contract and push food into
the small intestine
SYMPTOMS
 Vomiting
 Nausea
 A feeling of fullness after
eating just a few bites
 Vomiting undigested food
eaten a few hours earlier
 Acid reflux
 Abdominal bloating
 Changes in blood sugar levels
 Lack of appetite
 Weight loss and malnutrition
RISK FACTORS
 Diabetes
 Abdominal or esophageal
surgery
 Infection, usually a virus
 Certain medications that slow
the rate of stomach emptying,
such as narcotic pain
medications
 Scleroderma (a connective
tissue disease)
 Nervous system diseases, such
as Parkinson's disease or
multiple sclerosis
 Hypothyroidism (low thyroid)
COMPLICATIONS
 Severe dehydration: Ongoing
vomiting can cause dehydration
 Malnutrition: Poor appetite
 unable to absorb enough nutrients  erythromycin
due to vomiting  domperidone
 Undigested food that hardens  Medications to control nausea
and remains in your stomach: and vomiting
Bezoars can cause nausea and
 prochlorperazine
vomiting and may be life-
threatening if they prevent food  diphenhydramine
from passing into your small  ondansetron
intestine  METOCLOPRAMIDE
 Unpredictable blood sugar o increases muscle
changes: frequent changes in the contractions in the upper
rate and amount of food passing digestive tract
into the small bowel can cause o speeds up the rate at which
erratic changes in blood sugar levels
the stomach empties into
 Decreased quality of life
the intestines
DIAGNOSIS
o Side Effects: High doses or
 Gastric emptying study
o This is the most important long-term use of
test used in making a metoclopramide can cause
diagnosis of gastroparesis a serious movement
 Upper gastrointestinal (GI) disorder that may not be
endoscopy reversible (uncontrollable
o This procedure is used to muscle movements of your
visually examine your upper lips, tongue, eyes, face,
digestive system arms, or legs)
 Ultrasound o Contraindications:
o Ultrasound can help
 bleeding or blockage in
diagnose whether problems
with your gallbladder or your
your stomach or
kidneys could be causing intestines;
your symptoms  a perforation (hole) in
 Upper gastrointestinal series your stomach or
o This is a series of X-rays in intestines;
which you drink a white,  epilepsy or other seizure
chalky liquid (barium) that disorder; or
coats the digestive system to
 an adrenal gland tumor
help abnormalities show up.
PHARMACOLOGIC MANAGEMENT (pheochromocytoma)
 Medications to stimulate the  Parkinson’s Disease
stomach muscles o Drug interaction:
 metoclopramide  acidic drugs
 ERYTHROMYCIN
o used for the treatment of
gastroparesis and other GI
hypo-motility disorders off-
label.
o stimulates motilin
receptors in the GI tract =
increased motility
o Side Effects: potential to
induce abdominal cramps
diarrhea and nausea, and to
slow small-intestinal transit
o Drug Interactions:
 Theophylline
 increase in serum
theophylline levels
and potential
theophylline
toxicity
 Verapamil
 Hypotension,
bradyarrhythmias,
and lactic acidosis
 Digoxin
 elevated digoxin
serum levels
 DOMPERIDONE
o speeds gastrointestinal
peristalsis, causes prolactin
release, and is used as
antiemetic and tool in the
study of dopaminergic
mechanisms.  o The neurotransmitters
o Side Effects:  headache,
dizziness, dry mouth,
nervousness, flushing, or
irritability
o  Drug Interaction: may
affect the absorption and
action of other medications
 PROCHLOPERAZINE
o  Dopamine blockade in the
chemoreceptor trigger zone. It
is more likely than
chlorpromazine to cause
extrapyramidal disorders
o Side Effects: Drowsiness,
dizziness, lightheadedness,
blurred vision, constipation,
or dry mouth may occur.
o Contraindication: Do not use in
comatose states or in the
presence of large amounts of
central nervous system
depressants (alcohol,
barbiturates, narcotics, etc.).
o Drug Interaction:
 Potentiates CNS
depression with alcohol,
other CNS depressants.
Potentiates α-blockers.
May potentiate
phenytoin; monitor for
toxicity. Hypotension
potentiated with thiazide
diuretics. Antagonized by
anticholinergics
 DIPHENHYDRAMINE
implicated in the control of
nausea
and vomiting include acetylchol
 ine, dopamine, histamine (H-1
receptor), substance P (NK-1
receptor), and serotonin (5-
HT3 receptor)
o also a potent antimuscarinic
o Side Effects:
 dizziness, drowsiness,
loss of coordination;
 dry mouth, nose, or
throat;
 constipation, upset
stomach;
 dry eyes, blurred vision;
or.
 day-time drowsiness or
"hangover" feeling after
night-time use.
o Drug Interactions:
 alcohol
 anticholinergics (e.g.,
benztropine, oxybutynin)
 antihistamines (e.g.,
brompheniramine,
chlorpheniramine)
 barbiturates (e.g.,
phenobarbital,
butalbital)
 benzodiazepines (e.g.,
diazepam, lorazepam,
oxazepam)
 muscle relaxants (e.g.,
cyclobenzaprine)
 opioid medications (e.g.,
codeine, morphine)
 other medications that
cause drowsiness (e.g.,
chlorpromazine,
gabapentin, loxapine,
mirtazapine, quetiapine,
zopiclone, droperidol)
NON- PHARMACOLOGIC
MANAGEMENT
 Mild gastroparesis: may be
managed by proper nutrition
and weight maintenance
 Moderate to severe
gastroparesis: symptoms may
require medication therapy in
addition to dietary and lifestyle
modifications
 Refractory patients:
Percutaneous endoscopic
gastrostomy (PEG) tube
placement, parenteral
nutrition, or gastric electrical
stimulation
 Dietary Modification:
o avoidance of foods
causing GI intolerance
o avoid solid, high-fiber,
and fatty foods
o advise to eat multiple,
small meals throughout
the day
o cook or puree food until
softened, and chew
thoroughly when eating
o light exercise 
o moderate-to-severe
gastroparesis: thick or
thin liquids may be
recommended
 (supplemental nutritional drinks)

PEPTIC ULCER DISEASE

Refers to a group of ulcerative disorders of
the upper gastro intestinal tract that Chief cells secrete:
requires acid and pepsin for their formation  Pepsinogen- the inactive precursor of
The most common sites are the stomach pepsin
and duodenum:
Gastric ulcer- stomach *Pepsin- an important cofactor that plays
Duodenal ulcer- duodenum an important role in the proteolytic activity
Pathophysiology involved in ulcer formation.
 Peptic ulcer involves the distal stomach - activated by acid pH (1.8-3.5),
or proximal duodenum inactivated reversibly at pH 4 and
irreversibly destroyed at pH 7
 The ulcer results from digestion of the Enterochromaffin cells secrete:
mucosa by acid gastric juice  Histamine- acts with the parietal cells
to secrete more acid
 Persons who secrete large volumes of
acidic gastric juice are prone to ulcers Fabiolar cells- produces mucus which
protect epithelial cells from the effects of
 The initial event is probably a small, gastric acid and pepsin
superficial erosion of the gastric or G cell-located in the gastric antrum
duodenal mucosa It secretes:
 Gastric acid and pepsin begin to digest  Gastrin- interact with the parietal cell
the deeper tissues, which have been to produce more H+
denuded of covering epithelium D cell-located in the gastric antrum
 Attempts at healing in the presence of It secretes:
continuing digestion eventually lead to  Somatostatin- inhibits the parietal cells
considerable scarring at the base of the from producing H+
ulcer Aggressive factors Protective
 Clinically, ulcers produce pain that is factors
usually relieved by ingestion of food or HCl Mucus
antacids that neutralize the gastric acid Pepsin Production
Alcohol Somatostatin
Parietal cells secrete: Nicotine
 Gastric acid- contain receptors for Gastrin
histamine, gastrin, and acetylcholine Ulcerogenic drugs
-NSAIDs
H.pylori
PUD results from an imbalance between
aggressive factors(acid secretion) and
protective factors(mucosal defense)
Duodenal Ulcer
 Duodenal ulcer is an ulcer in the wall of
the duodenum, rarely malignant,
extending into the muscularis mucosa.
 Practically all duodenal ulcers occur in
the duodenal bulb
location, socio-economic condition,
ethnicity and age
NSAIDs
 Approximately 25% of patients on long-
term treatment with NSAIDs develop
a peptic ulcer(ulceration of the stomach
or duodenum)
 Cause superficial mucosal damage
consisting of intramucosal hemorrhage
within minutes of ingestion

 Duodenal ulcers are usually round or  NSAID- induced ulcers are dose-
oval and less than 1 cm in diameter but dependent
may be larger and irregular in shape  NSAID- induced ulcer and GI
 Both chronic and recurrent complication are increased with the use
of multiple NSAIDs or with the
concomitant use of:
Gastric Ulcer
 Benign Gastric ulcers are similar to Low dose aspirin
duodenal ulcers histologically but are Oral biphosphonates
deep and usually exhibit more Corticosteroids
extensive gastritis surrounding the Anticoagulants
ulcer crater SSRIs
Antiplatelets
 Caused primarily by the breakdown of How do NSAIDs work and how do they
the mucosal barrier and subsequent cause stomach problems?
back-diffusion of acid across the gastric Certain prostaglandins are important in
mucosa protecting the stomach lining from the
corrosive effects of stomach acid as well as
playing a role in maintaining the natural,
Etiology healthy condition of the stomach lining.
Helicobacter Pylori These protective prostaglandins are
 Spiral shaped, Gram-negative produced by an enzyme called Cox-1. By
flagellated, urease-producing organism blocking the Cox-1 enzyme and disrupting
the production of prostaglandins in the
 Injures the mucosa and initiates the
stomach, NSAIDs can cause ulcers and
mucosal erosion that eventually
bleeding. 
develops into a chronic ulcer
Other causes:
 Can be trasmitted via: Smoking
Physiological Stress
Oral- oral Dietary Factors
Fecal- oral
 Prevalence varies by geographic
Signs and Symptoms: recurrence and reduce ulcer- related
General: complication
Mild epigastric pain or acute life Pharmacologic
threatening upper gastrointestinal Cause: H. pylori
complications  Triple therapy- 10-14 days
Symptoms:
Duodenal ulcer PPI (omeprazole) once or twice daily
Pain- 40 minutes to 3 hours after eating Clarithromycin 500 mg bid
Relieved with food Amoxicillin 1g bid or
Nocturnal pain- usually awakens the patient Metronidazole 500 mg once a day
during sleep (between 12 am-3am)  Quadruple therapy
Gastric ulcer PPI or H2 antagonist once or twice daily
Pain with food Bismuth Subsalicylate 525 mg qid
Nausea and weight loss Metronidazole 250- 500 mg qid
Signs: Tetracycline 500 mg qid
Weight loss associated with nausea,
vomiting, and anorexia
Cause: NSAID
Diagnosis/ Evaluation:  Stop using NSAID, if possible
Laboratory Tests:
Gastric acid secretory studies If not,
Stool hemoccult test  Misoprostol cotherapy
Tests for H. Pylori:
 Endoscopic tests  PPI cotherapy

Histology- gold standard to determine  H2 receptor antagonist cotherapy

active H. pylori infection
Culture-enables sensitivity testing to
determine appropriate treatment
 Non endoscopic
Urea breath test
Fecal antigen test
Diagnostic Tests:
Fiberoptic upper endoscopy- detects more
than 90% of peptic ulcers and permits direct
inspection, biopsy, visualization of
superficial erosions, and sites of active
bleeding
Treatment:
Desired Outcome: relieving ulcer pain,
healing the ulcer, preventing ulcer
 Selective COX 2 inhibitors
Non Pharmacologic
 Surgery is rare, but it is needed
sometimes to treat: Ulcers that don't
heal (intractable peptic ulcers). Life-
threatening complications of an ulcer,
such as severe bleeding, perforation, or
obstruction.
 Diet modification
Avoid foods and beverages that cause
dyspepesia or that exacerbate ulcer
symptoms such as: spicy foods and caffeine
 Stress management

 Management of Alcohol use

 Management of smoking habits

STOMACH CANCER
 Bleeding in the stomach from
rd
Is the 3 most common cause of cancer esophageal varices
related death in the world. Since it is often  Intrahepatic jaundice caused by
diagnosed in advanced stages wherein hepatomegaly
treatment can no longer serve as cure for  Extrahepatic jaundice
the patient.  Inanition from starvation or cachexia
of tumor origin
SIGNS AND SYMPTOMS
DIAGNOSIS
Early gastric cancer has no associated
symptoms, it is often diagnosed through  CBC: To identify anemia.
accidental complaints. All physical signs and  Electrolyte panels
associated symptoms of SC reflect advanced  Liver function tests
stages.  Tumor markers: CEA and CA19-9
 Imaging studies:
 Indigestion  Esophagogastroduodenoscopy
 Nausea and Vomiting (EGD) : Evaluates gastric wall and
 Dysphagia lymph node involvement.
 Postprandial fullness  Double contrast upper GI series and
 Loss of appetite barium swallows: Helpful in cases
 Melena or Pallor from anemia when obstructive symptoms or
 Hematemesis bulky proximal tumors are present in
 Weightloss which the endoscope cannot
 Palpable enlarged stomach with examine.
succession splash  Chest radiography: to evaluate
 Enlarged Lymph nodes metastatic lesions
 CT scanning or MRI of the chest,
COMPLICATIONS abdomen and pelvis: to assess the
local disease process and evaluate
 Pathologic peritoneal and pleural potential areas of spread.
effusions  Endoscopic ultrasonography (EUS):
 Obstruction of the gastric outlet, staging tool for more precise pre-
gastroesophageal junction or small operative assessment of the tumor
bowel stage.
 Biopsy
  Surgery
PATHOPHYSIOLOGY removal of the tumor and some
surrounding healthy tissue during an
Three oncogenic pathways that interact operation. The type of surgery used
with each are said to be cause of stomach depends on the stage of the cancer 
cancer.  For a very early stage (T1a)
 Proliferation cancer: endoscopic mucosal
 NF-kappaB resection- removal of the tumor
 Wnt/beta-catenin pathways with an endoscope

emedicine.medscape.com/article/278744-
overview#a5

PHARMACOLOGIC TREATMENT

Targeted drugs
Targeted therapy uses drugs that attack
specific abnormalities within cancer
cells or that direct your immune system
to kill cancer cells (immunotherapy).
Targeted drugs used to treat stomach
cancer include:
 Trastuzumab (Herceptin) for
stomach cancer cells that produce
too much HER2
 Ramucirumab (Cyramza) for
advanced stomach cancer that 
hasn't responded to other
treatments
 Imatinib (Gleevec) for a rare form of
stomach cancer called
gastrointestinal stromal tumor
 Sunitinib (Sutent) for
gastrointestinal stromal tumors
Stage 0 or 1: subtotal or partial
 Regorafenib (Stivarga) for gastrectomy- remove the part of
gastrointestinal stromal tumors the stomach with cancer and
nearby lymph nodes
NON-PHARMACOLOGIC
 o Reduce your risk of infection.
o Follow a nutritious diet.
o Participate in a reasonable
level of exercise.
o Rest when tired.
o Seek support.



Reduce Your Risk of

 Later stages: total gastrectomy-
removal of all of the stomach.
surgeon attaches the esophagus
directly to the small intestine
 Radiation Therapy
use of high-energy x-rays or other
particles to destroy cancer cells. This
may be used before surgery to
shrink the size of the tumor or after
surgery to destroy any remaining
cancer cells
o Side Effects: fatigue, mild
skin reactions, upset
stomach, and loose bowel
movements
 General Guidelines
o Stop smoking.
o Stop drinking alcohol.
Infection
To decrease your risk of
infection, avoid exposure to
bacteria and viruses:
 Try to avoid crowds,
especially during cold
and flu season.
 Ask your doctor
about immunization
against the flu and
pneumonia.
 Wash your hands
thoroughly and often.
Hand washing is the
most effective
method of decreasing
the chance of
catching colds and flu.
You may wish to carry
hand sanitizer with
you for occasions
when washing is not
convenient.

 Lifestyle changes:
o Strengthening your body so
that you can withstand some
of the rigors of treatment
o Optimizing the function of
your immune system to aid
in the fight against cancer
o Improving your emotional
outlook, so you can enjoy life
 to the fullest, even during
treatment for stomach
cancer
o Making healthful choices
that will help you avoid other
medical problems that could
complicate your health
- After gastrectomy, the patient will only be
able to eat a small amount of food at a
time.
- A common side effect is a group of
symptoms known as dumping syndrome,
which includes cramps, nausea, diarrhea,
and dizziness after eating
Dumping Syndrome- This happens
when food enters the small intestine
too fast
- Patients who have had their entire
stomach removed may need regular
supplements of vitamin D, Calcium, Iron and
injections of vitamin B12
After Surgery:
 Plan to have smaller, more frequent
meals
 Drink liquids before or after meals
 Cut down on very sweet foods