Bahan Pemicu 2 Gastrointestinal Ivan Buntara

BAHAN PEMICU 2
GASTROINTESTINAL
Ivan Buntara
405120049
Learning Objective 1
Describes the anatomy, histology, physiology and biochemistry of stomach until
ileum; pancreas and gallbladder
ANATOMY OF STOMACH UNTIL ILEUM;
PANCREAS AND GALL BLADDER
STOMACH
• The stomach is a J-shaped, pouchlike organ, about 25-30 centimeters
long, which hangs inferior to the diaphragm in the upper left portion
of the abdominal cavity
• The stomach is divided into 4 parts
1. Cardia : surrounds the gastroesophageal sphincter
2. Fundus : is the rounded portion above and to the left of the cardia
3. The body : below the fundus is the large central portion of the stomach
4. Pylorus or Antrum : is the narrow inferior region that connects with the
duodenum of the small intestine via pyloric sphincter
• When there is no food in the stomach, the mucosa lies in large
folds called rugae, which are visible with the unaided eye
• The wider and more superior part of pyloric region, the pyloric
antrum narrows to form the pyloric canal, which terminates at the
pylorus
• The pylorus is continuous with the duodenum through the pyloric
valve or sphincter, which controls stomach emptying
• The convex lateral surface of the stomach is its greater curvature and
its concave medial surface is the lesser curvature
• Extending from these curvatures are two mesenteries, called omenta
 help tether the stomach to other digestive organs and the body
wall
• The lesser omentum runs from the liver to the lesser curvature of the
stomach, where it becomes continuous with the visceral peritoneum
covering the stomach
• The greater omentum drapes inferiorly from the greater curvature of
the stomach to cover the coils of the small intestine
• Then runs dorsally and superiorly, wrapping the spleen and the transverse
portion of the large intestine before blending with the mesocolon
• The greater omentum is riddled with fat deposits that give it the
appearance of a lacy apron
• Also contain large collections of lymph nodes
• The stomach is served by the autonomic nervous system
• Sympathetic fibers from thoracic splanchnic nerves are relayed through the
celiac plexus
• Parasympathetic fibers are supplied by the vagus nerve
• The arterial supply of the stomach is provided by branches (gastric &
splenic) of the celiac trunk
• The corresponding veins are part of the hepatic portal system and
ultimately drain into the hepatic portal vein
SMALL INTESTINE
• The small intestine extends from the pyloric valve of the stomach
to the ileocecal valve, where it joins the large intestine
• It is named for its small diameter (compared to that of the large
intestine), but perhaps it should be called the long intestine
• The small intestine takes up a large portion of the abdominal
cavity, averaging about 6 m (18 ft) in length
REGIONS OF SMALL INTESTINE
The small intestine has the following regions :
• Duodenum
• The first 25 cm (10 in.) contain distinctive glands that secrete mucus and also
receive the pancreatic secretions and the bile from the liver through a common
duct. Folds and villi are more numerous at the end than at the beginning
• Jejunum
• The next 1 m (3 ft) contains folds and villi, more at the beginning than at the end
• Ileum
• The last 2 m (6–7 ft) contain fewer folds and villi than the jejunum
• Nerve fibers serving the small intestine include
• Parasympathetic from the vagus
• Sympathetics from the thoracic splanchnic nerves
• Both relayed through the superior mesenteric plexus
• The arterial supply is primarily from the superior mesenteric artery
• The veins parallel the arteries and typically drain into the superior
mesenteric vein
• From there, the nutrient-rich venous blood from the small intestine
drains into the hepatic portal vein, which carries it to the liver
PANCREATIC ANATOMY
• Gland with both exocrine and endocrine functions
• 15-25 cm long
• 60-100 g
• Location: retro-peritoneum, 2nd lumbar vertebral level
• Extends in an oblique, transverse position
• Parts of pancreas: head (caput), neck (collum), body (corpus) and tail
(cauda)
Copyright (c) The McGraw-Hill Companies, Inc.

PANCREAS

PANCREAS
PANCREATIC DUCT
LOCATION OF GALLBLADDER
GALLBLADDER
AMPULLA OF VATER WITH CBD AND PANCREATIC DUCT
Ampulla of Vater
THE GALLBLADDER WITH BILIARY SYSTEM AND PANCREAS
HISTOLOGY OF STOMACH UNTIL ILEUM;
PANCREAS AND GALLBLADDER
ESOPHAGUS-GASTER JUNCTION
FUNDUS-TRANSVERSE SECTION
PYLORIC PART OF THE STOMACH-PYLORIC GLANDS
• In contrast to the gastric glands of the corpus and fundus of the stomach, the
tubules of the pyloric glands (pylorus = pars pylorica ventriculi) branch out
and form coils only deep in the mucous membrane
• The gastric foveolae are deeper than the foveolae in the mucous membrane
of the gastric corpus and fundus. The glandular tubules undulate considerably
and may therefore be sectioned in different planes relative to their axis
• The columnar surface epithelium also covers the funnel-shaped gastric
foveolae
• Pyloric glands exclusively consist of mucous cells
PYLORIC
PYLORIC-DUODENUM JUNCTION
SMALL INTESTINE-DUODENUM
• The tissue surface in the duodenum, as in the rest of the upper small intestine, shows
circular folds called plicae circulares or Kerckring’s folds. Circular folds form an
impressively articulated relief in the duodenum
• The surface of the Kerckring’s folds features intestinal villi in different shapes and sizes
(villi intestinales). They are 0.5–1.5mm high and about 0.15mm thick. Intestinal villi are
covered with a columnar epithelium (enterocytes, absorptive cells)
• Tubular canals extend from the cell surface at the bottom of the invaginations between
microvilli to the lamina muscularis mucosae. These are the intestinal glands of
Lieberkühn, also called crypts of Lieberkühn
• Brunner’s glands (duodenal glands) are characteristic of the duodenum. They are located
in the submucosal layer. The glands with their winding tubules remind of the pyloric
glands
DUODENUM
SMALL INTESTINE-JEJUNUM
• This longitudinal section of the jejunal wall from an adult human
shows six circular plicae (Kerckring’s folds)
• The villi of the small intestines are protrusions from the tunica
mucosa. Therefore, they consist of the surface epithelium, the
lamina propria mucosae and sporadic smooth muscle cells from
the lamina muscularis mucosae
• As the jejunum continues toward the ileum, the circular plicae
stand lower and become sparse
SMALL INTESTINE-ILEUM
• Compared with the adjacent small intestine, there is only little surface
enlargement in the ileum. This is the major difference between both
tissues. The circular plicae are lesser in height, and there are fewer and
fewer of them until they are completely absent
• In the process, the villi also become shorter and scarcer than in the
jejunum
• There are small crypts at the bottom of the spaces between the villi. The
development of the lymphoreticular organs in the form of lymphatic
nodules (noduli lymphatici aggregati)
PANCREATIC HORMONES, INSULIN AND GLUCAGON, REGULATE
METABOLISM

PANCREAS
Interlobular Ducts (D)
Septa (S)
Islets of Langerhans (I)
Secretory portions (Acini)
GALLBLADDER
PHYSIOLOGY OF STOMACH UNTIL ILEUM;
PANCREAS AND GALLBLADDER
STOMACH
• Specialized for accumulation of food
• Capable of considerable expansion (can hold 2-3L)
• Gastric juice converts food into semiliquid called chyme
• 4 Parts
• Cardia
• Fundus
• Body
• Pylorus
STOMACH
• Three main functions :
• Store ingested food until it can be emptied into small intestine
• Secretes hydrochloric acid (HCl) and enzymes that begin protein digestion
• Mixing movements convert pulverized food to chyme
STOMACH
Chapter 16 The Digestive System

Human Physiology by Lauralee Sherwood
©2007 Brooks/Cole-Thomson Learning
STOMACH
• Gastric mucosa has numerous openings called gastric pits
• 3 functionally different cell types compose glands
• Mucous cells
• Chief cells
• Parietal cells
STOMACH
GASTRIC MOTILITY
• Four aspects
• Filling
• Involves receptive relaxation
• Enhances stomach’s ability to accommodate the extra volume of food with little rise in
stomach pressure
• Triggered by act of eating
• Mediated by vagus nerve
• Storage
• Takes place in body of stomach
• Mixing
• Takes place in antrum of stomach
• Emptying
• Largely controlled by factors in duodenum

Sherwood L. Introduction to human physiology. 8th ed. United
States: Brooks/Cole-Cengage Learning; 2013.
GASTRIC SECRETION
• Gastric mucosal cells secrete gastric juice
• HCl and pepsinogen initiate protein digestion
• Intrinsic factor required for absorption of vitamin B12
• Mucus protects gastric mucosa from HCl
• Cell Types of Gastric Mucosa

• Parietal cells → HCl and Intrinsic Factor
• Chief cells → Pepsinogen
• G cells → Gastrin into the circulation
• Mucous neck cells → Mucus, HCO3-
HCl SECRETION
• Functions of HCl
• Activates pepsinogen to active enzyme pepsin and provides acid medium for
optimal pepsin activity
• Aids in breakdown of connective tissue and muscle fibers in foods
• Denatures protein
• Along with salivary lysozyme, kills most of the microorganisms ingested with
food

States: Brooks/Cole-Thomson Learning; 2007.
HCl SECRETION
• Parietal cells secrete HCl which converts inactive pepsinogen to
pepsin
1.Within cell, CO2 combines with H2O to form H+ and HCO3-

2.H+ secreted into lumen of stomach via H+-K+ ATPase (proton pump)
• Cl- follows H+ into the lumen by diffusing through Cl- channels
3.HCO3- absorbed into blood via a Cl--HCO3- exchanger
• Eventually HCO3- secreted back into GI tract by pancreas
PHASES OF GASTRIC SECRETION
• Cephalic phase
• Refers to increased secretion of HCl and pepsinogen that occurs in response
to stimuli acting in the head before food reaches stomach
• Gastric phase
• Begins when food actually reaches the stomach
• Presence of protein increases gastric secretions
• Intestinal phase
• Inhibitory phase
• Helps shut off flow of gastric juices as chyme begins to empty into small
intestine
REGULATION OF HCl SECRETION
• ACh
• Released from vagus nerve
• Binds to receptors on parietal cells
• Produces H+ secretion by parietal cells
• Histamine
• Released from mastlike cells in gastric mucosa
• Binds to H2 receptors on parietal cells
• Produces H+ secretion by parietal cells
• Gastrin
• Released into circulation by G cells of stomach antrum
• Binds to receptors on parietal cells
• Stimulates H+ secretion
GASTRIC MUCOSAL BARRIER
• Enables stomach to contain acid without injuring itself

SMALL INTESTINE
 The site where most digestion and absorbtion
take place
 Divided into 3 segments: duodenum, jejunum
and ileum
 Its motility includes
 Segmentation
 Migrating motility complex
SMALL INTESTINE
SEGMENTATION
 Oscillating, ring-like contraction of the circular smooth muscle
along the small intestine’s length
 Between the contracted segments are relaxed areas containing a
small bolus of chyme
 After a brief period of time → the contracted segments relax and
previously relaxed area contract
 The new contraction forces the chyme in a previously relaxed
segment → move in both direction into the now relaxed adjacent
segments. Shortly thereafter, the areas of contraction and
relaxation is alternate again
 In this way, the chyme is chopped, churned and thoroughly mixed
 Functions: mixing the chyme with digestive juices secreted in
small-intestine lumen; exposing the chyme to the absorbtive
surface of the small intestines mucosa
SEGMENTATION
 Initiated by pacemaker cells in small intestine
which produce basic electrical rhythm (BER)
 Circular smooth muscle responsiveness is
influenced by distension of intestine, gastrin,
and extrinsic nerve activity
 Functions
 Mixing chyme with digestive juices
secreted into small intestine lumen

 Exposing all chyme to absorptive surfaces
of small intestine mucosa

SEGMENTATION
http://arbl.cvmbs.colostate.edu/hbooks/pathphys/digestion/ba
sics/gi_motility.html
SEGMENTATION

MIGRATING MOTILITY COMPLEX
(MMC)
 When most meal has been absorbed →
segmentation cease; replaced between meals
by the migrating motility complex
 This between meal motility → weak,
repetitive peristaltic waves that move a short
distance down the intestine
 Each contraction → sweep any remnants of
the preceding meal, mucosal debris and
bacteria forward toward the colon
SECRETIONS
 Exocrine gland cells of small intestine mucosa
secrete about 1.5 liters of an aqueous salt and
mucus solution called succus entericus
 Functions: provides protection and
lubrication; provides plenty of H2O to
participate in the digestion of food
 No digestive enzymes are secreted in the
intestinal juice
DIGESTION
 Digestion within the small intestine lumen →
accomplished by pancreatic enzymes with fat
digestion being enhanced by bile secretion
 This digestion is completed by special hairlike
projections of luminal surface of small
intestine epithelial cell, microvilli
ABSORPTION
 All products of carbohydrate, protein and fat
digestion, as well as electrolytes, vitamin and
water → absorbed by small intestine
indiscriminately
 Only absorption calcium and iron is adjusted
by body needs
 Most absorption occurs in duodenum and
jejunum, very little in ileum (normally only
B12 and bile salt are absorbed by ileum)
PANCREAS
• Mixture of exocrine and endocrine tissue
• Elongated gland located behind and below the stomach
• Endocrine function
• Islets of Langerhans
• Found throughout pancreas
• Secrete insulin and glucagon
• Exocrine function
• Secretes pancreatic juice consisting of
• Pancreatic enzymes actively secreted by acinar cells that form the acini
• Aqueous alkaline solution actively secreted by duct cells that line pancreatic ducts

PANCREATIC ENZYMES
• Exocrine secretion is regulated by
• Secretin
• CCK
• Proteolytic enzymes
• Digest protein
• Trypsinogen - converted to active form trypsin
• Chymotrypsinogen – converted to active form chymotrysin
• Procarboxypeptidase – converted to active form carboxypeptidase
• Pancreatic amylase
• Converts polysaccharides into the disaccharide amylase
• Pancreatic lipase
• Only enzyme secreted throughout entire digestive system that can digest fat

• Bile
• Actively secreted by liver and actively diverted to gallbladder between meals
• Stored and concentrated in gallbladder
• Consists of
• Bile salts
• Cholesterol
• Lecithin
• Bilirubin
• After meal, bile enters duodenum

• Bile salts
• Derivatives of cholesterol
• Convert large fat globules into a liquid emulsion
• After participation in fat digestion and absorption, most are reabsorbed into the
blood

BIOCHEMISTRY OF STOMACH UNTIL
DUODENUM; PANCREAS AND GALLBLADDER
GASTRIC GLANDS AND SECRETION
PANCREAS SECRETION
CATEGORIES OF PANCREATIC ENZYMES
Pancreatic Enzymes Functions
Proteases Cleave peptide bonds
Nucleases Hydrolyze DNA/RNA
Elastases Break down proteins
Phospholipases Convert phospholipids into fatty acid
Lipases Convert TG to fatty acids + gliserol
Amylase Convert starch to maltose + glucose
ACTIVATION OF PANCREATIC
PROTEASES
Enterokinase
Trypsinogen Trypsin
Trypsinogen Trypsin
Chymotrypsinogen Chymotrypsin
Proelastase Elastase
Procarboxypeptidase Carboxypeptidase
BICARBONATE FUNCTIONS
1. Neutralize gastric acid emptied into the duodenum
2. Provide a favorable alkaline environment for optimal activity of
pancreatic enzymes
CONTROL OF PANCREATIC FUNCTIONS
• Bicarbonate secretion stimulated by secretin
• Secretin released in response to acid in duodenum
• Zymogen secretion stimulated by cholecystokinin (CCK)
• CCK released in response to fat/amino acids in duodenum
• Also under neural control (vagal/local reflexes) - triggered by arrival of
organic nutrients in duodenum
CONTROL OF PANCREATIC FUNCTIONS
FUNCTIONS OF BILE
• Emulsification of fats
• Increased absorption of lipids into enterocytes (include vitamin A, D,
E, K)
• Cholesterol excretion (only route)
• Excretion of breakdown products of hemoglobin (bilirubin)
• Netralization of acid
SMALL INTESTINE
• Digestive enzymes not secreted from small intestine → from pancreas
or found on enterocytes
• Except enterokinase secreted from duodenal mucosa
• Mucus/alkali secretions → mucosal protection
• Aqueous secretions
SMALL INTESTINE
• Function
• Lubricate and protect intestinal surface (IgA)
• Dilute digestive products
• Digest specific food substances
• (enzymes in enterocytes: peptidase, sucrase, etc )
REGULATION OF SMALL INTESTINAL
SECRETIONS
• Local stimuli
• The presence of chyme in the intestine
• Hormonal regulation
• Secretin
• CCK
• Neuronal regulation
• Vagus nerve – excitatory
• Sympathetic nerve - inhibitory
Describes about dyspepsia (definition, classification, etiology, pathophysiology,
clinical presentation, diagnosis, management, prognosis, complication and
prevention)
DYSPEPSIA
DYSPEPSIA
• Syndrome that consists of intermittent epigastric pain or discomfort,
nausea, bloating, vomiting, early satiation and flatus
• The symptoms characteristically develops after eating
DYSEPSIA ETIOLOGY
• Food or drug intolerance
• Functional dyspepsia
• Luminal GI tract dysfunction
• Helicobacter pylori infection
• Pancreas disease (pancreas carcinoma and pancreatitis)
• Other conditions (DM, thyroid disease, CKD, myocardial ischemia,
malignancy, gastric volvulus or paraesophageal hernia, pregnancy)
Harmon RC, Peura DA. Evaluation and management of
dyspepsia. Ther Adv Gastroenterol. 2010;3(2):87-98.
DIFFERENTIAL DIAGNOSIS OF DYSPEPSIA
COMPLAINTS
Vojvodic M, Young A, editors. Toronto notes 2014. Toronto:

Toronto Notes for Medical Students Inc.; 2014.
FUNCTIONAL DYSPEPSIA
• Symptoms thought to originate in gastroduodenal origin
• Absence of any organic, systemic or metabolic disease
Tack J, Talley NJ, Camilleri M, Holtmann G, Hu P, Malagelada J,

et al. Functional gastroduodenal disorders. Gastroenterology.
2006;130:1466-79.
THREE GROUPS OF FUNCTIONAL DYSPEPSIA
• Ulcer-like type → epigastric pain and nocturnal pain symptoms are
the more dominant symptoms
• Dismotility-like type → bloating, nausea, vomiting, fullness and early
satiety are the more dominant symptoms
• Non-specific dyspepsia → no dominant complaints
FUNCTIONAL DYSPEPSIA DIAGNOSTIC CRITERIA
(ROME III)
Rome III Diagnostic Criteria for Functional Gastrointestinal

Disorders
DIAGNOSIS FOR HELICOBACTER PYLORI
INFECTION
• Serology
• Cheap, acceptable for asymptomatic or pediatric patients
• Look for IgG antibody to H. pylori
• ELISA, Westernblot, complement fixation, immunofluorescent
• Urea Breath Test (UBT)
• Golden standard
• The patients swallow urea that contain carbon isotopes
• (+) → there is urease activity from the bacteria that produce carbon dioxide
and ammonia → the carbon dioxide detected from patient’s exhalation by
mass spectrometer
DIAGNOSIS FOR HELICOBACTER PYLORI
INFECTION
• Invasive examination → gastric mucosal biopsy
• Biopsy urease test (BUT)
REGIMENS FOR HELICOBACTER PYLORI
THERAPY
• Triple therapy :
• PPI + Amoxicillin + Clarithromycin
• PPI + Metronidazole + Clarithromycin
• PPI + Metronidazole + Tetracycline
Regiments given in 7 – 14 days
• Quadruple therapy :
• Colloidal bismuth subcitrate + PPI + Amoxicillin + Clarithromycin
• Colloidal bismuth subcitrate + PPI + Metronidazole + Clarithromycin
• Colloidal bismuth subcitrate + PPI + Metronidazole + Tetracycline
REGIMENS FOR HELICOBACTER PYLORI
THERAPY
Dosage :
• Proton pump inhibitor :
• Omeprazole 2 x 20 mg
• Lansoprazole 2 x 30 mg
• Rabeprazole 2 x 10 mg
• Esomeprazole 2 x 20 mg
• Amoxicillin 2 x 1 g/day
• Clarithromycin 2 x 500 mg/day
• Metronidazole 3 x 500 mg/day
• Tetracycline 4 x 250 mg/day
• Colloidal bismuth subcitrate 4 x 120 mg/day
MEDICAL NUTRITION THERAPY FOR
DYSPEPSIA PATIENTS
• Reduction of dietary fat intake
• Use of smaller meals
• Diets with low calories
• Achieve a healthy weight
• Limiting alcohol intake
• Mild exercise
• Behavioral management and emotional support
MEDICAL NUTRITION THERAPY FOR PEPTIC
ULCER PATIENTS
• Limit the consumption of alcohol, spices and caffeine-containing
foods or beverages
• Food combinations to inhibit the growth of Helicobacter pylori
• Increase the consumption of omega-3 and omega-6 fatty acids → may
have immune and cytoprotective effect
• Nutritionally complete diet + adequate dietary fiber
• Behavioral management : avoid tobacco products
PYLORIC STENOSIS
DEFINITION
• A narrowing of the pylorus, the opening from the stomach into the
small intestine
ETIOLOGY
• The cause of the thickening is unknown, although genetic factors may
play a role. Children of parents who had pyloric stenosis are more
likely to have this condition
• Pyloric stenosis occurs more often in boys than in girls, and is rare in
children older than 6 months. The condition is usually diagnosed by
the time a child is 6 months old
EPIDEMIOLOGY
• Pyloric stenosis is one of the most common conditions requiring
surgery in infants
• It is more common in boys than girls and usually affects children who
are born at full term
• It rarely occurs in premature infants
SIGN AND SYMPTOMS
• Vomiting is the first symptom in most children
• Vomiting may occur after every feeding or only after some feedings
• Vomiting usually starts around 3 weeks of age, but may start any time
between 1 week and 5 months of age
• Vomiting is forceful (projectile vomiting)
• The infant is hungry after vomiting and wants to feed again
• Other symptoms generally appear several weeks after birth
• Abdominal pain
• Belching
• Constant hunger
• Dehydration (gets worse with the severity of the vomiting)
• Failure to gain weight or weight loss
• Wave-like motion of the abdomen shortly after feeding and just before
vomiting occurs
DIFFERENTIAL DIAGNOSIS
• Enteritis
• Neonatal intestinal obstruction
• Intracranial birth injury
• Overfeeding
CLINICAL ASSESSMENT
• The condition is usually diagnosed before the baby is 6 months old
• A physical exam may reveal signs of dehydration. The infant may have
a swollen belly. The doctor may detect the abnormal pylorus, which
feels like an olive-shaped mass, when touching the stomach area
• An ultrasound of the abdomen may be the first imaging test
performed
• Other tests that may be done include:
• Barium x-ray  reveals a swollen stomach and narrowed pylorus
• Blood chemistry panel  often reveals an electrolyte imbalance
TREATMENT
• Treatment for pyloric stenosis involves surgery to split the
overdeveloped muscles
• Balloon dilation does not work as well as surgery, but may be
considered for infants when the risk of general anesthesia is high
COMPLICATIONS
• Failure for the baby to gain weight
PROGNOSIS
• Surgery usually provides complete relief of symptoms. The infant can
usually tolerate small, frequent feedings several hours after surgery
HIATAL HERNIA
DEFINITION
• A condition in which a portion of the stomach protrudes upward into
the chest through an opening in the diaphragm (the sheet of muscle
used in breathing that separates the chest from the abdomen)
• Stomach content is coming out of the stomach into the esophagus for
an extended period of time
• Hiatal hernia is usually associated with gastroesophageal reflux in
infants
• Regurgitation of gastric acid from the stomach into the esophagus can
result from this condition
ETIOLOGY
• The cause is unknown but may be the result of a weakening of the
supporting tissue
• Obesity and smoking may be risk factors in adults
• Children often have this condition present at birth (congenital)
CLASSIFICATION
• Type I
• Sliding hiatal hernia comprising at least 95% of the overall total
• Gastroesophageal junction and gastric cardia slide upward as a result of
weakening of the phrenoesophageal ligament attaching the gastroesophageal
junction to the diaphragm at the hiatus
• Type II, III, IV
• Paraesophageal hernia
• The herniation into the mediastinum includes a visceral structure other
than the gastric cardia
• Type II : the gastric fundus also herniates with the distinction being that
in type II, the gastroesophageal junction remains fixed at the hiatus
• Type III : mixed sliding/paraesophageal hernia
• Type IV : viscera other than the stomach herniate into the mediastinum,
most commonly the colon
SIGN AND SYMPTOMS
• Swallowing difficulty
• Aspiration pneumonia
• Apnea
• Asthma
• Hoarseness
• Gastric or esophageal dysmotility may also contribute to symptoms
• Chest pain
• Belching
CLINICAL ASSESSMENT
• Barium swallow X-ray
• EGD (esophagogastroduodenoscopy)
• External esophageal pH monitoring
• Gastric emptying scan
TREATMENT
• The goals of treatment are to relieve symptoms and prevent
complications
• Medical therapy is aimed at reducing regurgitation of stomach
contents into the esophagus (gastroesophageal reflux)
• Medications that neutralize stomach acidity, or that strengthen the
lower esophageal sphincter, may be prescribed
• Medications that improve esophagus and gastric motility may be used
• Failure to control the symptoms by general or medical measures, or
the onset of complications, may require surgical repair of the hernia
COMPLICATIONS
• Slow bleeding and iron deficiency anemia (esophagitis)
• Pulmonary (lung) aspiration
• Stricture of the esophagus
PROGNOSIS
• Most symptoms are alleviated with treatment
TRACHEOESOPHAGEAL FISTULA
DEFINITION
• An abnormal connection in one or more places between the
esophagus (the tube that leads from the throat to the stomach) and
the trachea (the tube that leads from the throat to the windpipe and
lungs)
• When a baby with a TE fistula swallows, the liquid can pass through
the abnormal connection between the esophagus and the trachea.
When this happens, liquid gets into the baby's lungs. This can cause
pneumonia and other problems
EPIDEMIOLOGY
• About one in 4,000 babies in the United States is born with these
problems
• A common congenital anomaly with an incidence of 1 case in 2000-
4000 live births
PATHOPHYSIOLOGY
• As a fetus is growing and developing in its mother's uterus before
birth, different organ systems are developing and maturing
• The trachea and the esophagus begin developing as one single tube
• At about four to eight weeks after conception, a wall forms between
the fetus' esophagus and trachea to separate them into two distinct
tubes
• If this wall does not form properly, TE fistula and/or esophageal
atresia can occur
SIGNS AND SYMPTOMS
• Frothy white bubbles in the mouth
• Coughing or choking when feeding
• Vomiting
• Blue color of the skin, especially when the baby is feeding
• Difficulty breathing
• Very round, full abdomen
CLINICAL ASSESSMENT
• Along with a physical examination and medical history, imaging
studies are usually done to evaluate whether a baby has TE fistula
and/or esophageal atresia
• X-rays are taken to look at the chest and abdomen
Describes about GERD
GASTROESOPHAGEAL REFLUX DISEASE (GERD)
• Condition which the stomach contents (solid or liquid) leak backwards
from the stomach into the esophagus (the tube from the mouth to
the stomach)

ETIOLOGY OF GERD
• Inappropriate transient relaxations of lower esophageal sphincter
(LES) → most common
• Low basal LES tone (especially in scleroderma)
• Contributing factors : delayed esophageal clearance, delayed gastric
emptying, increased intra-abdominal pressure
• Acid hypersecretion (rare): Zollinger-Ellison syndrome or gastrinoma
(gastrin-secreting tumour)

SIGN AND SYMPTOMS OF GERD

DIAGNOSIS OF GERD
• Based on symptom history and relief following a trial of
pharmacotherapy (proton pump inhibitor (PPI): symptom relief 80%
sensitive for reflux)
• Gastroscopy; indications :
• Heartburn accompanied by red-flags (bleeding, weight loss, etc.)
• Persistent reflux symptoms or previous severe corrosive esophagitis after trial
therapy
• History of esophageal stricture with persistent dysphagia

DIAGNOSIS OF GERD
• Esophageal manometry (study of esophageal motility) → to diagnose
abnormal peristalsis and/or decreased LES tone, but cannot detect
presence of reflux; indicated before surgical fundoplication (wrapping
of gastric fundus around the lower end of the esophagus)
• 24 hours pH monitoring: most accurate test, but rarely required or
performed. Most useful if PPIs do not improve symptoms

MANAGEMENT OF GERD
• PPIs → the most effective therapy and usually need to be continued
as maintenance therapy
• Antacids (Mg(OH)2, Al(OH)3, alginate)
• H2-blockers or PPIs can be used for NERD
• Diet helps symptoms, not the disease; avoid alcohol, coffee, spices,
tomatoes and citrus juices
• Lifestyle changes are weight loss (if obese) and elevating the head of
bed (if nocturnal symptoms)

COMPLICATIONS OF GERD
• Esophageal stricture disease → can lead to dysphagia (solids)
• Ulcer
• Bleeding
• Barrett’s esophagus and esophageal adenocarcinoma

MEDICAL NUTRITION THERAPY FOR GERD
PATIENTS
• Avoid large, high-fat meals prior to going to bed → delay gastric
emptying, prolong acid secretion
• Lifestyle modification :
• Change in dietary practices
• Weight loss (if overweight)
• Smoking cessation
• Elevation of the head of the bed
• Avoid alcohol, wine
MEDICAL NUTRITION THERAPY FOR GERD
PATIENTS
• Limiting or avoiding aggravating foods or beverages :
• Caffeine (chocolate, coffee, tea)
• Onions
• Peppermint (may lower LES pressure)
• Spices
• Citrus food
• Carbonated beverages
NUTRITION CARE GUIDELINES FOR REDUCING
GASTROESOPHAGEAL REFLUX AND ESOPHAGITIS
• Avoid large, high-fat meals
• Avoid eating at least 3 to 4 hours before lying down
• Avoid smoking
• Avoid alcoholic beverages
• Avoid caffeine-containing food
Krenitsky JS, Decher N. Medical nutrition therapy for upper gastrointestinal tract
disorders. In Mahan LK, Stump SE, Raymond JL, editors. Krause’s food and nutrition
care process (chapter 28). 13th ed. St Louis: Saunders; 2012: p. 592-608.
NUTRITION CARE GUIDELINES FOR REDUCING
GASTROESOPHAGEAL REFLUX AND ESOPHAGITIS
• Stay upright and avoid vigorous activity soon after eating
• Avoid tight-fitting clothing, especially after a meal
• Consume a healthy, nutritionally complete diet with adequate fiber
• Avoid acidic and highly spiced foods when inflammation exists
• Lose weight if overweight
Krenitsky JS, Decher N. Medical nutrition therapy for upper gastrointestinal tract
disorders. In Mahan LK, Stump SE, Raymond JL, editors. Krause’s food and nutrition
care process (chapter 28). 13th ed. St Louis: Saunders; 2012: p. 592-608.
Describes the physiology and pathophysiology of bloating, vomiting and alarm
symptoms
ALARM SYMPTOMS
• Age older than 55 with new-onset dyspepsia
• Unintended weight loss
• Persistent/continuous vomiting
• Progressive dysphagia
• Odynophagia
• Unexplained anemia or iron deficiency
• Jaundice
ALARM SYMPTOMS
• Palpable abdominal mass or lymphadenopathy
• Hematemesis, melena, hematochezia (chronic GI bleeding)
• Anorexia
• Family history of upper GI cancer
• Previous gastric surgery
• Suspicious barium meal
VOMITING (EMESIS)
• Forceful expulsion of gastric contents through the mouth
• Not accomplished by reverse peristalsis
• The force for expulsion comes from :
• The diaphragm
• The abdominal muscles
• Coordinated by vomiting center in the medulla of brain stem
VOMITING (EMESIS)
1. Deep inspiration, closure of glottis
2. Contracting diaphragm + abdominal muscles → the intra-abdominal
pressure ↑
3. Flaccid stomach is squeezed
4. Gastric contents forced upward through relaxed sphincters till
mouth
CAUSES OF VOMITING (EMESIS)
• Tactile (touch) stimulation of the back of the throat
• Irritation or distention of stomach and duodenum
• Elevated intracranial pressure (e.g. cerebral hemorrhage)
• Rotation or acceleration of the head → dizziness
• Chemical agents (drugs, noxious substances)
• Psychogenic (emotional factors)
EFFECTS OF VOMITING (EMESIS)
• Reduction in plasma volume → dehydration, circulatory problems
• Loss of acid → metabolic alkalosis
REFERENCES
• Netter FH. Atlas of human anatomy. 6th ed. Philadelphia: Saunders Elsevier;
2014.
• Eroschenko VP. Atlas histologi diFiore: dengan korelasi fungsional. Ed 11.
Jakarta: EGC; 2008.
• Sherwood L. Introduction to human physiology. 5th ed. United States:
Brooks/Cole-Thomson Learning; 2007.
• Sherwood L. Introduction to human physiology. 8th ed. United States:
Brooks/Cole-Cengage Learning; 2013.
• Rome III Diagnostic Criteria for Functional Gastrointestinal Disorders.
REFERENCES
• Tack J, Talley NJ, Camilleri M, Holtmann G, Hu P, Malagelada J, et al.
Functional gastroduodenal disorders. Gastroenterology. 2006;130:1466-79.
• Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, editor. Buku ajar
ilmu penyakit dalam. Edisi 5. Jilid I. Jakarta: Pusat Penerbitan Ilmu Penyakit
Dalam FKUI; 2008.
• Rani AA, Simadibrata M, Syam AF, editors. Buku ajar gastroenterologi. Edisi
1. Jakarta: Pusat Penerbitan Ilmu Penyakit Dalam; 2011.
• Krenitsky JS, Decher N. Medical nutrition therapy for upper gastrointestinal
tract disorders. In Mahan LK, Stump SE, Raymond JL, editors. Krause’s food
and nutrition care process (chapter 28). 13th ed. St Louis: Saunders; 2012:
p. 592-608.
REFERENCES
• Harmon RC, Peura DA. Evaluation and management of dyspepsia. Ther Adv
Gastroenterol. 2010;3(2):87-98.
• Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto Notes
for Medical Students Inc.; 2014.
• Papadakis MA, McPhee S, Rabow MW, editors. Current medical diagnosis
and treatment. 52nd ed. New York: The McGraw-Hill Companies Inc.; 2013.

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Chapter 16 The Digestive System

Chapter 16 The Digestive System

• Cell Types of Gastric Mucosa

Sherwood L. Introduction to human physiology. 5th ed. United

1.Within cell, CO2 combines with H2O to form H+ and HCO3-

Chapter 16 The Digestive System

secreted into small intestine lumen

of small intestine mucosa

Sherwood L. Introduction to human physiology. 8th ed. United

Chapter 16 The Digestive System

Chapter 16 The Digestive System

Chapter 16 The Digestive System

Chapter 16 The Digestive System

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Tack J, Talley NJ, Camilleri M, Holtmann G, Hu P, Malagelada J,

Rome III Diagnostic Criteria for Functional Gastrointestinal

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Vojvodic M, Young A, editors. Toronto notes 2014. Toronto:

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto:

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto:

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto:

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto:

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto:

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