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Algri Wijaya

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

Other input: tanpa rangsangan oral, cth: berpikir, melihat, membaui,


mendengar

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

GERD or acid reflux, is a condition in which the


liquid content of the stomach regurgitates (backs
up or refluxes) into the esophagus

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

Elevation of the upper body at night generally is recommended for all


patients with GERD

GERD Diet

* These foods should be avoided and include:


Chocolate, peppermint, alcohol & caffeinated drinks
* Fatty foods (which should be decreased) and smoking (which should
be stopped) also reduce the pressure in the sphincter and promote
reflux
* Chewing gum stimulates the production of more bicarbonatecontaining saliva and increases the rate of swallowing.

Antacids

Antacids neutralize the acid in the stomach so that there is no acid to


reflux
they do so for only a short period of time
The best way to take antacids, therefore, is approximately one hour
after meals or just before the symptoms of reflux begin after a meal.
Since the food from meals slows the emptying from the stomach, an
antacid taken after a meal stays in the stomach longer and is
effective longer

Histamin
Antagonist

The first medication developed for more effective and convenient


treatment of acid-related diseases, including GERD, was a histamine
antagonist, specifically cimetidine (Tagamet)
Histamine is an important chemical because it stimulates acid
production by the stomach

Treatment
Protein Pump
Inhibitor

The second type of drug developed specifically for acid-related


diseases, such as GERD, was a proton pump inhibitor (PPI),
specifically, omeprazole (Prilosec)
The advantage of a PPI over an H2 antagonist is that the PPI
shuts off acid production more completely and for a longer period
of time
Five different PPIs are approved for the treatment of GERD,
including omeprazole (Prilosec), lansoprazole (Prevacid),
rabeprazole (Aciphex), pantoprazole (Protonix), and esomeprazole
(Nexium). A fifth PPI product consists of a combination of
omeprazole and sodium bicarbonate (Zegerid). PPIs (except for
Zegarid) are best taken an hour before meals

Pro Motility Drug

Pro-motility drugs work by stimulating the muscles of the


gastrointestinal tract, including the esophagus, stomach, small
intestine, and/or colon. One pro-motility drug, metoclopramide
(Reglan)
Pro-motility drugs increase the pressure in the lower esophageal
sphincter and strengthen the contractions (peristalsis) of the
esophagus

Foam Barriers

Foam barriers are tablets that are composed of an antacid and a


foaming agent.
There is only one foam barrier, which is a combination of
aluminum hydroxide gel, magnesium trisilicate, and alginate
(Gaviscon).

Surgery

The surgical procedure that is done to prevent


reflux is technically known as fundoplication and is
called reflux surgery or anti-reflux 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.

Bile reflux Drugs

Etiology

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)

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

PEPTIC ULCER DISEASE

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

The majority of GUs can be attributed to either


H. pylori or NSAID-induced mucosal damage.
The majority of DUs can be attributed to H.
pylori

Campylobacter
pyloridis

It is S-shaped (~0.5 3 um in size)


and contains multiple sheathed
flagella.
Its ability to colonize the gastric
mucosa and produce mucosal injury.
a gram-negative microaerophilic
This rate of colonization increases
with age, with about 50% of
individuals age 50 being infected.

Figure 1: Helicobacter pylori invading epithelial


cells.

Campylobacter
pyloridis

Transmission of H. pylori occurs


from person to person, following
an oral-oral or fecal-oral route.

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

upper abdominal discomfort


Anorexia
slight nausea and vomiting
Weight loss
Dysphagia (caused by lesions of
the cardia)
iron-deficiency anemia
occult blood in the stool

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

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