Gastro Week 1

Gilbert S. Octavius 2014

 What’s missing in this slide
• GERD
• PUD
• Gastritis
• H. Pylori

There might be some mistakes in this slide

hence please do not trust the information below
100%
 Sources
• Harrison Gastroenterology 2nd edition
• Netter Gastroenterology
• Grey Anatomy
• Langman Embryology
• Yamada Textbook of Gastroenterology
• Slides from Lecture
• Sherwood
 Embryology of Esophagus
• 4 weeks old  the respiratory diverticulum
(lung bud) appears at the ventral wall of the
foregut at the border with the pharyngeal gut
• The tracheoesophageal septum gradually
partitions this diverticulum from the dorsal
part of the foregut
• It divides into two: the ventral portion is the
respiratory primordium and the dorsal part is
the esophagus
 Anatomy of Esophagus
• 40 cm; 3 parts: Cervical (C5-C7), thoracal (T1-
T10)and abdominal (T10 after hiatus to T11)
• Cervical constriction: due to cricoid cartilage at
the level of C5/6
• Thoracic constriction: due to aortic arch at the
level of T4/5
• Abdominal constriction: at oesophageal hiatus at
T10/11
• Upper 1/3  skeletal muscle, middle 1/3 
mixed, lower 1/3  smooth muscle
 Physiology of Deglutition
1. Oral stage (Voluntary)
• Initiated when a bolus is voluntarily forced
by the tongue and into the pharynx
• Stimulate the pharyngeal pressure
receptors  impulses to swallowing center in
the medulla oblongata
• All or none process (Initiated voluntarily)
 Physiology of Deglutition
2. Oropharyngeal stage
• Moving the bolus from the mouth through the pharynx
and into the esophagus
• Food is prevented to enter the trachea by:
a) Swallowing center temporarily inhibits the nearby
respiratory center
b) Uvula is elevated and lodges against the back of the throat
sealing off the nasal passage
c) Tongue is against the hard palate to keep food from
reentering the mouth during swallowing
d) Elevation of larynx and tight closure of glottis; contraction
of laryngeal muscles align the vocal folds in tight
apposition to each other thus sealing the glottis entrance
 Physiology of Deglution
a) The epiglottis folds backward down over the closed
glottis
b) Pharyngeal muscles contract to force bolus into the
esophagus
c) UES pharyngoesophageal sphincter, LES (smooth
muscle)  gastroesophageal sphincter
d) Except during a swallow, UES remains closed as a
result of neutrally induced contraction of the
sphincter’s circular skeletal muscle which prevents
large volumes of air from entering  excessive
eructation
• 1 second is taken for this stage
 Physiology of Degluttition
3. Esophageal stage
• Swallowing centre initiates primary peristaltic wave which takes
about 5-9 seconds to reach the lower end of esophagus and
innervated by vagus.
• Secondary peristaltic wave is initiated when there is a food lodge
that causes distension and hence stimulates mechanoreceptors &
intrinsic nerve plexus; involuntary. This effect is enhanced by saliva’s
lubrication
• Tertiary peristaltic waves  spasm contraction that is inefficient
(usually seen in elderly)
• LES stays tonically contracted by means of myogenic activity
• Contraction also increases during inspiration reducing the chance of
acidic gastric contents reflux
 Question 1
A 1-year-old baby is born pre-term with
polyhydramnios. After being given ASI, 1 hour
later he vomitted. What is your diagnosis?
A) Esophageal stenosis
B) Esophageal atresia
C) Duodenal atresia
D) Hypertrophic pyloric stenosis
E) Gastroparesis
 Esophageal Atresia
• Congenital, mother usually suffers a condition called
polyhydramnios (excessive amniotic fluid  the
stomach looks bigger than for supposed pregnancy
week)
• Associated with VACTERL (Vascular, anus, cardiac,
tracheoesophageal, renal and limb) malformations;
hence the alternative name tracheoesophageal fistula
– esophageal atresia (TEF-EA)
• 5 types, proximal pouch and distal fistula is most
common
• Clinical feature: Rapid onset of vomitting (in 1 – 2
hours)
 Question 2
Adi is a 55-year-old man that has a history of
GERD and dyspepsia for 20 years. He is not really
well controlled and now complaints of
progressive dysphagia. Upon endoscopy, what is
the most likely finding?
a) Barrett’s Metaplasia
b) Esophageal ca. sq type
c) Esophageal ca. adenoca type
d) What the hell is this
 Barrett’s Metaplasia
• Due to prolonged injury of esophagus to
caustic insult; most commonly acid reflux
(GERD)
• Columnar or intestinal metaplasia (Esophagus
is non-keratinized stratified squamous
epithelium)
• Predispose to Adenocarcinoma Cancer of the
Esophagus
 Esophageal cancer
• Usually barrett’s metaplasia is an early finding to
cancer
• Adeno ca type is usually caused by GERD (or due
to barrett’s metaplasia of any causes)
• Sq ca type is due to smoking and alcohol (to a
lesser extent)
• Clinical manifestation: solid food dysphagia won’t
present until >60% obstruction, progressive
dysphagia, pain in the chest, vomitting
• 55% of the cancer is found in the lower third of
esophagus
 Achalasia
• 2 hallmarks: aperistalsis and failure of
relaxation of LES
• X-ray: Rat rail or bird beak sign
• Clinical symptom: Solid food dysphagia AND
liquid dysphagia (usually most of the time)
• Aganglionosis in the myenteric plexus
(Auerbach’s)
Anatomy of Stomach
 Anatomy of Duodenum
• Superior
• Descending
• Inferior
• Ascending
Gastric Mixing & Emptying
 Factors Affecting the Rate of Gastric
Emptying
1. Factors in the stomach
• Main factor  Amount of chyme
• Stomach distension  increased gastric
motility through direct effect of stretch on
smooth muscle and through involvement of
the intrinsic plexuses, CN X and gastrin
• Degree of fluidity  The faster it becomes
fluid, the better
 Factors Affecting the Rate of Gastric
Emptying
2. Factors in the duodenum
• Delay the rate of emptying by reducing the strength of
antral peristalsis
• Presence of stimuli will trigger a neural or hormonal
response
• Neural response:
• By both short and long reflexes  Enterogastric reflex
• Hormonal response:
• GI hormones  Enterogastrones
• Inhibit antral contractions  Secretin (S cells) and CCK
(I cells) in the duodenal and jejunal mucosa
 Factors Affecting the Rate of Gastric
Emptying
4 important factors that affect emptying:
a) Fat
• High caloric density  most effective in delaying emptying
• TG strongly stimulates CCK (inhibits antral contractions and induces contraction of pyloric
sphincter)
b) Acid
• Unnneutralized acid may damage the duodenal mucosa and inactivate the pancreatic
enzymes
• Unneutralized acid induces secretin  slows emptying

c) Hypertonicity
• Protein and starch is broken down, releasing amino acids and glucose.
• If their absorption doesn’t keep pace with the breaking down, large numbers of molecules
remain in the chyme and increase the osmolarity of the duodenal contents
• Large volumes of water entering the intestine from the plasma lead to intestinal distension
and more important, circulatory disturbances result because of reduction in plasma volume

d) Distension
• Too much chyme in the duodenum inhibits the emptying of even more gastric contents
• High carbohydrate foods are emptied more quickly than fat or protein is
 Factors Affecting the Rate of Gastric
Emptying
3. Emotion
• Sadness and fear decrease motility
• Anger and aggression increases motility
• Intense pain inhibits motility in all GI tract
 due to increased SNS activity
Gastric Secretions
 HCl Secretion
• The parietal cell, also known as the oxyntic cell, is usually
found in the neck, or isthmus, or in the oxyntic gland.
• The resting, or unstimulated, parietal cell has prominent
cytoplasmic tubulovesicles and intracellular canaliculi
containing short microvilli along its apical surface
• H+,K+-ATPase is expressed in the tubulovesicle membrane;
upon cell stimulation, this membrane, along with apical
membranes, transforms into a dense network of apical
intracellular canaliculi containing long microvilli.
• Acid secretion, a process requiring high energy, occurs at
the apical canalicular surface. Numerous mitochondria (30–
40% of total cell volume) generate the energy required for
secretion
Stimulation & Inhibition of Gastric
Secretion
Gastric Mucosal Barrier
 Digestion in Stomach
• Little protein digestion occurs here but in the
centre of the mass carbohydrate digestion still
occurs due to salivary amylase
• Alcohol and aspirin
 Dyspepsia
• Rome III Criteria:
a) Early satiation
b) Postprandial fullness
c) Epigastric burning
d) Epigastric pain

• A + B = PDS; C + D = EPS (Next slide)

• C & D must not be caused by any organic diseases
Classification of Dyspepsia &
Treatment
 Diagnosis
• Test & Treat approach  H. pylori
• Lifestyle
• Endoscopy (look at the indications in next
slides)
 Question 3
A baby was just born with no complications.
After 10 hours of ingesting milk, he vomits. The
vomit is non-bilious with most of the milk being
vomitted. There is no blood and other
symptoms are observed. Your diagnosis?
a) Duodenal Atresia
b) Hypertrophic Pyloric Stenosis
c) Gastroparesis
d) Jejunal Atresia
 Duodenal Atresia
• 80%  distal to ampulla of Vater
• More prolonged vomit compared to
esophageal atresia
• Bilious vomit due to bile secretion
• Double bubble sign on x-ray
 Gastroparesis
• The presenting symptom of gastroparesis may be
bloating, abdominal pain or distention, nausea, or
vomiting.
• The patient may report a history of continued
postprandial fullness.
• Nausea can be persistent and unexplained as the initial
symptom.
• Vomiting may or may not accompany the nausea.
• Vomitting is 10-15 hours after food ingestion; the food
that goes in and out of the mouth is the same
• There is a lot of causes, but amongst other identifiable
etiologies think of DM
 Hypertrophic Pyloric Stenosis
• The classic infant presentation is vomiting that occurs
in the second to sixth weeks of life.
• Vomiting increases in frequency and severity and is
characterized early as occurring suddenly with great
force (projectile vomiting).
• The infant cries, indicating hunger. Because less food
is able to pass the pylorus, the infant becomes
dehydrated and loses weight.
• On examination of the infant, the classic “olive” might
be felt in the area of the pylorus, and strong peristaltic
movements in the stomach may be observed on
inspection of the abdomen.
• USG  Classic „doughnut‟ sign of around 3mm
 Question 4
What is the most common type of gastric
cancer?
a) MALT-lymphoma
b) Sq. ca
c) Adeno. Ca
d) Linitis plastica
 Gastric Cancer
• Disease of the elderly
• RF: age, smoking, GU, H-pylori
• Protective factor: DU
• Clinical symptoms: Nothing specific (Epigastric
pain, dyspepsia-like symptoms); Presence of
virchow node might be more specific
• Most common type: Adenoca
• Whole gastric cancer (exo- and endophytic type) :
linitis plastica  Bottle-neck sign
Anatomy of Abdominal Wall
9 Layers of Abdominal Wall
 Question 5
A surgeon is going to cut the abdominal muscle
in between the xiphoid processus and umbilicus.
Which muscle is he going to cut first?
a) Transversus abdominis
b) EOM
c) EOM & IOM
d) IOM
e) Transversus abdominis and IOM
Abdominal Wall
Abdominal Wall
Peritoneum
 Intraperitoneal, Retroperitoneal &
Secondarily Retroperitoneal Organs
 Peritoneum
• Can be used for dialysis (peritoneal dialysis)
• Helps spread infection
• In females, the peritoneum is connected to
the pelvic areas
 Omentum
• The omenta consist of two layers of
peritoneum, which pass from the stomach and
the first part of the duodenum to other
viscera
• Two parts: greater omentum and lesser
omentum
• Helps to contain an infection
Greater and Lesser Omentum
 Mesenteries
Mesenteries are peritoneal folds that attach
viscera to the posterior abdominal wall. They
allow some movement and provide a conduit for
vessels, nerves, and lymphatics to reach the
viscera
• Peritoneal ligaments consist of two layers of
peritoneum that connect two organs to each
other or attach an organ to the body wall, and
may form part of an omentum
• Eg: Splenorenal & Gastrophrenic ligaments
 Question 6
Which of the following patient deserves an
emergency endoscopy?
a) A 20 year old woman presenting with sudden
onset of epigastric pain
b) A 45 year old man that has GERD but can’t be
managed on PPI
c) A 55 year old man that has new-onset of
dyspepsia
d) A 60 year old man that presents with epigastric
pain
Indications for Endoscopy
Pharmacology
 Antacids
• Weak bases that react with gastric
hydrochloric acid to form a salt and water.
• Na bicarbonate (NaHCO3) reacts rapidly with
HCl.
• NaHCO3 + HCl  CO2 + NaCl + H2O
• CO2  gastric distention & belching.
• NaCl  fluid retention.
• NaHCO3 metabolic alkalosis
 Antacids
• Calcium carbonate (CaCOOH) less soluble, reacts
slowly.
• CaCOOH + HCL  CO2 + CaCl2 + H2O
• Belching or metabolic alkalosis.
• Other benefits : bone mineralization.
• Excessive doses + calcium-containing dairy
products can lead to hypercalcemia, renal
insufficiency, and metabolic alkalosis (milk-alkali
syndrome)
 Antacids
• Aluminium Hydroxide & Magnesium
Hydroxide
• React slowly with HCl  magnesium chloride
or aluminum chloride and water.
• No gas is generated, belching does not occur.
• Metabolic alkalosis is also uncommon because
of the efficiency of the neutralization reaction.
 Antacids
• 30 min when taken in empty stomach
• 2 hrs when taken after a meal
• Al  Constipation, Mg  Diarrhea
 H2RAS (-ine)
• Blocks the H2R receptor
• Most potent  Famotidine
• Cimetidine causes gynecomastia, galactorrhea
(as it is antiandrogenic & increases prolactin
level)
 PPI (-zole)
• Irreversible inhibitor of H+ K+ ATPase
• Since it requires acid for activation - given 1 hr
before meals
• Other acid suppressing agents can not
coadministered
 Mucosal Protective Agent
1) Sucralfate
• Salt of sucrose complexed to sulfated
aluminium hydroxide
• In acidic pH polymerizes to viscous gel that
adheres to ulcer crater & stimulates mucosal
prostaglandin
• Taken on empty stomach 1 hr. before meals
• Concurrent antacids, H2 antagonist avoided (
as it needs acid for activation )
 Mucosal Protective Agent
2) Misoprostol
• PGE1 analogue
• Modest acid inhibition  Stimulate mucus &
bicarbonate secretion
• Enhance mucosal blood flow
• Approved for prevention of NSAID induced ulcer
• Side effect : Diarrhea & cramping abd. pain – 20
%
 Mucosal Protective Agent
3) Bismuth Colloidal Compound
• Coats ulcer, stimulates mucus & bicarbonate
secretion
• Direct antimicrobial activity against H.pylori
• May cause blackening of stools & tongue
• Not used for long periods – bismuth toxicity
Drugs for Pregnancy
Antacids & Sucralfate
 Eradication of H.Pylori
• First line (triple therapy)  Omeprazole /
Lansoprazole, Clarithromycin, Amoxycillin /
Metronidazole
• Second line (Quadruple therapy) 
Omeprazole / Lansoprazole, Bismuth
subsalycilate, Metronidazole, Tetracycline
• Taken for 10-14 days then re-assess
Patophysiology of Vomitting
 Serotonin 5 HT3 Antagonist (-setron)
• Even though 5 HT3 receptors are present in
vomiting centre & CTZ, the antiemetic action is
restricted to emesis caused by vagal stimulation.
• Indications: Chemotherapy induced nausea &
vomiting – given 30 min. before chemotherapy,
postoperative & postradiation nausea & vomiting
• All three drugs cause prolongation of QT interval,
but more pronounced with dolasetron
 Dopamine D2 Antagonist
• Antagonise D2 receptors in CTZ
• Domperidone & Metoclopramide
• Both drugs are also prokinetic agents due to
their 5 HT4 agonist activity.
• Metoclopramide crosses BBB but
domperidone can not