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405070108
PHYSIOLOGY OF
DIGESTIVE TRACT
MOUTH
Saliva:
-Glands: parotid, sublingual
& submandibular
-Minor gland: Buccal
-99.5% H2O, 0.5% protein
(amylase, mucus, lysozyme,
& electrolyte)
Functions:
-Amylase:polisaccharide
dissacharide
-Mucus: lubrication, foodcondensing
-articulation
-Hygiene
-HCO3- netralizing acid from
foods + bacteria prevent
caries
Vomiting
Vomiting is abnormal emptying of stomach and
upper part of intestine via esophagus through
mouth.
Causes:
1. Irritation in GIT
2. Mechanical stimulation of pharynx
3. Pregnancy
4. Alcohol
5. Stimulation of labyrinth of ear eg sea sickeness,
mountain sickeness
6. Acute GI infection
7. Metabolic disorders
8.Increase Intracranial Pressure
Pathophysiol
ogy of
Emesis
Emesis mechanism
Emesis mechanism
Complications of Emesis
Excessive or repeated vomiting can cause dehydration
and may lead to severe disturbances in the electrolyte
and acid-base balance in the body.
Dehydration due to loss of water from the GI tract.
Hypokalaemia due to loss of the potassium ions in GI
secretions
Hypochloremia due to loss of chloride ions in the
vomitus
Alkalosis - due to loss of H+ ions in the vomitus
Aspiration syndrome
Malnutrition and failure to thrive
Peptic oesophagitis
Mallory-Weiss tear
erosions to the esophagus or small tears in the
esophageal mucosa
GERD
Gastroesophageal reflux (GER) is a common, selflimited process in infants that usually resolves by
six to 12 months of age. The prevalence of GER
peaks between 1 ~ 4 mo of age
If complications develop or regurgitation persists, GER is
considered pathologic (considered as gastroesophageal
reflux disease, GERD) rather than merely developmental
& deserves further evaluation & treatment
Classifying GERD
Gastroesophageal
Reflux
Physiological
Gastroesophageal Reflux GER
Primary GERD:
Motility problem
Affecting lower
Esophageal sphincter
Gastroesophageal Reflux
Disease GERD
(Symptomatic)
Secondary GERD:
External factor causing
transient relaxations of
lower Esophageal sphincter
(eg. Food allergy)
Examination
Endoscopy
Biopsies
X-rays
Examination of the throat and larynx
Esophageal acid testing
Acid perfusion test
Treatment
Treatment
Life style
modification
GERD Diet
Antacids
Histamin
Antagonist
Treatment
Protein Pump
Inhibitor
Foam Barriers
Surgery
What is Gastritis?
An inflammation, irritation or erosion
of the stomach lining. Can be of
acute or a chronic complaint.
Acute gastritis often due to chemical
injury (alcohol/drugs)
Chronic gastritis: H. Pylori infection,
chemical, autoimmune.
Etiology
Etiology
Fungal infections
Candidiasis
Histoplasmosis
Phycomycosis
Acute Gastritis
Acute gastritis can be broken down
into 2 categories:
erosive (eg, superficial erosions, deep
erosions, hemorrhagic erosions)
nonerosive (generally caused by
Helicobacter pylori).
Erosive Gastritis
Acute erosive gastritis can result from
the exposure to a variety of agents or
factors. This is referred to as reactive
gastritis.
These agents/factors include
nonsteroidal anti-inflammatory
medications (NSAIDs), alcohol, cocaine,
stress, radiation, bile reflux, and
ischemia.
This results from oral or systemic
administration of these agents either in
therapeutic doses or in
supratherapeutic doses.
Chronic Gastritis
Autoimmune
Bacterial (H. Pylori)
Chemical (NSAIDs)
Chronic noninfectious granulomatous
gastritis
Lymphocytic gastritis
Eosinophilic gastritis
Ischemic gastritis
Radiation gastritis
Definition
Peptic ulcers are defects in the gastric or
duodenal mucosa that extend through the
muscularis mucosa
Peptic ulcer disease (PUD) is one of the most
common diseases affecting the
gastrointestinal (GI) tract.
It causes inflammatory injuries in the gastric
or duodenal mucosa, with extension beyond
the submucosa into the muscularis mucosa.
Epidemiology
The incidence of DUs declined
steadily from 1960 to 1980 and
has remained stable since then.
Gastric Ulcers GUs tend to occur
later in life than duodenal lesions,
with a peak incidence reported in
the sixth decade.
More than half of GUs occur in
males
Etiology
H. pylori infection
Predominant cause
NSAIDs
Cigarette smoking
Genetic predisposition
blood group O
Psychological stress
Campylobacter
pyloridis
Campylobacter
pyloridis
PATHOPHYSIOLOGY H.
pylori
PATHOPHYSIOLOGY
NSAIDs
PATHOPHYSIOLOGY
NSAIDs
CLINICAL FEATURES
Epigastric pain can be present in both DU and GU.
Pain pattern in DU occurs 90 min to 3 h after a
meal and is frequently relieved by antacids or
food.
Pain that awakes the patient from sleep (between
midnight and 3 A.M.) is the most discriminating
symptom, with two-thirds of DU patients
describing this complaint.
GU discomfort may actually be precipitated by
food.
Nausea and weight loss occur more commonly in
GU patients.
Hematemesis
CLINICAL FEATURES
Other symptoms are :
losing weight
not feeling like eating
having pain while eating
feeling sick to your stomach
vomiting
Related Complications
Gastrointestinal Bleeding
Perforation
Gastric Outlet Obstruction
Treatment
GASTRIC ADENOCARCINOMA
Epidemiology
Gastric cancer incidence has
decreased worldwide but remains high
in Japan, China, Chile, and Ireland.
The risk of gastric cancer is greater
among lower socioeconomic classes.
Etiology
PATHOPHYSIOLOGY
Gastric carcinomas spread by direct
extension through the gastric wall to
the perigastric tissues, occasionally
adhering to adjacent organs such as
the pancreas, colon, or liver.
The disease also spreads via lymphatics
or by seeding of peritoneal surfaces.
The liver is the most common site for
hematogenous spread of tumor.
Clinical Features
TREATMENT
Gastrectomy
subtotal gastrectomy is the
treatment of choice for patients with
distal carcinomas, total or near-total
gastrectomies are required for more
proximal tumors.
chemotherapy combined with
radiation therapy has been shown to
reduce the recurrence rate and
prolong survival