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Group 18 Problem 1B

Thedi Darma Wijaya


405090120

LO 1: Anatomy, Histology,
Physiology, and Biochemical of
Upper GIT

Anatomy of Upper GIT

Cavum Oris; Oral


Or Buccal Cavity

The Palate (palatum)


forms the roof of the
mouth; it consists of two
portions
the hard palate in
front
the soft palate
behind.

The Teeth (dentes)

The deciduous teeth are twenty


in number:
four incisors, two canines, and four
molars, in each jaw.

The permanent teeth are thirtytwo in number:


four incisors, two canines, four
premolars, and six molars, in each
jaw.

The Salivary
Glands
Three large pairs
of salivary glands
communicate with
the mouth, and
pour their
secretion into its
cavity; they are
The parotid,
The
submaxillary,
The
sublingual.

The Esophagus
The esophagus or gullet is a
muscular canal, about 23 to
25 cm. long, extending from
the pharynx to the stomach.
There are 3 portions of
esophagus:
The cervical portion
The thoracic portion
The abdominal portion
It measures about 1.25 cm. in
length.
It is somewhat conical with its
base applied to the upper orifice of
the stomach, and is known as the
antrum cardiacum.

The Abdomen
a. Median plane.
b. Lateral planes.
c. Trans tubercular
plane.
d. Subcostal plane.
e. Transpyloric plane

The abdominal Regions

The Peritoneum

The Stomach

Muscular layers of stomach

The Duodenum
The Duodenum has received its name from being
about equal in length to the breadth of twelve
fingers (25 cm.)
The duodenum may be divided into four portions:
superior, descending, horizontal, and
ascending.

Histology of Upper GIT

The layers of GIT


a. Fibrous covering.
b. Divided fibers of longitudinal
muscular coat.
c. Circular muscular fibers.
d. Submucous or areolar layer.
e. Muscularis mucos.
f. Mucous membrane, with
vessels and part of a lymphoid
nodule.
g. Stratified epithelial lining.
h. Mucous gland.
i. Gland duct.

The oesophagus
The oesophagus has a stratified
squamous epithelial lining (SE)
which protects the oesophagus
from trauma
The submucosa (SM) secretes
mucus from mucous glands (MG)
which aid the passage of food
down the oesophagus.
The lumen of the oesophagus is
surrounded by layers of muscle
(M)- voluntary in the top third,
progressing to involuntary in the
bottom third- and food is propelled
into the stomach by waves of
peristalisis.

The Stomach
G- mucosa containing glandular
tissue:
parietal cells which secrete
hydrochloric acid
chief cells which secrete pepsin
enteroendocrine cells which secrete
regulatory hormones.

MM- muscularis mucosae


SM- submucosa
The stomach contains three layers
of involuntary smooth muscle :
OM- inner oblique muscle
CM- circular muscle
LM- outer longditudional muscle

The Small Intestine


The epithelial surface of the
plicae (P) is further folded
to form villi(V), the surface
of each villus is covered in
small microvilli to maximise
surface area- the area
available for absorption is
vast.
The vessels can be seen in
the submucosa (SM)
The double muscle layer
(M) moves food through the
intestine by peristalisis.

The large Intestine


The mucosa (M) is arranged into
tightly-packed straight tubular
glands (G) which consist of cells
specialised for water absorption
and mucus-secreting goblet cells to
aid the passage of faeces.
The large intestine also contains
areas of lymphoid tissue (L); these
can be found in the ileum too
(called Peyer's patches), and they
provide local immunological
protection.

Physiology & Biochemical of


Upper GIT

LO 2: Nausea & Vomiting


Patophysiology

Physiology of nausea and vomiting

The vomiting reflex is triggered by stimulation of chemoreceptors in the


upper GI tract and mechanoreceptors in the wall of the GI tract which are
activated by both contraction and distension of the gut as well as by physical
damage.
A coordinating center in the central nervous system controls the emetic
response. This center is located in the parvicellular reticular formation in the
lateral medullary region of the brain.
Afferent nerves to the vomiting center arise from abdominal splanchnic and
vagal nerves, vestibulo-labyrinthine receptors, the cerebral cortex and the
chemoreceptor trigger zone (CTZ).The CTZ lies adjacent in the area
postrema and contains chemoreceptors that sample both blood and
cerebrospinal fluid.
Direct links exist between the emetic center and the CTZ. The CTZ is
exposed to emetic stimuli of endogenous origin such as hormones
associated with pregnancy and to stimuli of exogenous origin such as drugs
(3).
The efferent branches of cranial nerves V, VII, and IX, as well as the vagus
nerve and sympathetic trunk produce the complex coordinated set of
muscular contractions, cardiovascular responses and reverse peristalsis
that characterizes vomiting

LO 3: Diseases in Upper GIT

GERD

GERD is one of the most prevalent


gastrointestinal disorders.
Population-based studies show that up to 15%
of individuals have heartburn and/or
regurgitation at least once a week, and 7%
have symptoms daily.
Symptoms are caused by backflow of gastric
acid and other gastric contents into the
esophagus due to incompetent barriers at the
gastroesophageal junction.

Risk Factor
Incompetence of the diaphragmatic crural
muscle, which surrounds the esophageal hiatus
in the diaphragm and functions as an external
LES, also predisposes to GERD.
Obesity is a risk factor for GERD.

Pathophysiology
Reflux occurs only when the gradient of pressure between the
LES and the stomach is lost.
It can be caused by a sustained or transient decrease in LES
tone.
Secondary causes of sustained LES incompetence include
scleroderma-like diseases, myopathy associated with chronic
intestinal pseudo-obstruction, pregnancy, smoking,
anticholinergic drugs, smooth-muscle relaxants ( -adrenergic
agents, aminophylline, nitrates, calcium channel blockers, and
phosphodiesterase inhibitors), surgical damage to the LES, and
esophagitis.

Pathophysiology
tLESR without associated esophageal contraction is
due to a vagovagal reflex in which LES relaxation is
elicited by gastric distention.
Increased episodes of tLESR are associated with
GERD.
Apart from incompetent barriers, gastric contents are
most likely to reflux
(1) when gastric volume is increased (after meals, in pyloric
obstruction, in gastric stasis, during acid hypersecretion
states),
(2) when gastric contents are near the gastroesophageal
junction (in recumbency, bending down, hiatal hernia), and
(3) when gastric pressure is increased (obesity, pregnancy,
ascites, tight clothes).

Clinical Features
Heartburn and regurgitation of sour material into the mouth are
the characteristic symptoms of GERD.
Angina-like or atypical chest pain occurs in some patients.
Persistent dysphagia suggests development of a peptic
stricture.
Most patients with peptic stricture have a history of several years of
heartburn preceding dysphagia.

Rapidly progressive dysphagia and weight loss may indicate


the development of adenocarcinoma in Barrett's esophagus.
Bleeding occurs due to mucosal erosions or Barrett's ulcer.
Extraesophageal manifestations : chronic cough, laryngitis, and
pharyngitis.
Recurrent pulmonary aspiration may cause or aggravate
chronic bronchitis, asthma, pulmonary fibrosis, chronic
obstructive pulmonary disease, or pneumonia.
Chronic sinusitis and dental decay have also been ascribed to
GERD.

Diagnosis
The diagnosis can be made by history alone in many cases.
A therapeutic trial with a PPI such as omeprazole, 40 mg bid for
1 week, provides support for the diagnosis of GERD.
The diagnostic approach to GERD can be divided into three
categories:
(1) documentation of mucosal injury,
by the use of barium swallow, esophagoscopy, and
mucosal biopsy
(2) documentation and quantitation of reflux
can be done by ambulatory long-term (2448 h)
esophageal pH recording
(3) definition of the pathophysiology.
indicated for management decisions such as antireflux
surgery

Treatment
The goals of treatment are to provide symptom relief,
heal erosive esophagitis, and prevent complications
Pharmacology
H2 receptor blocking agents (cimetidine, 300 mg qid;
ranitidine, 150 mg bid; famotidine, 20 mg bid; nizatidine, 150
mg bid) are effective in symptom relief.
PPIs are more effective and more commonly used.
The PPIs are comparably effective: omeprazole (20 mg/d),
lansoprazole (30 mg/d), pantoprazole (40 mg/d), esomeprazole (40
mg/d), or rabeprazole (20 mg/d) for 8 weeks can heal erosive
esophagitis in up to 90% of patients. The PPI should be taken 30 min
before breakfast.
SE: hypergastrinemia but does not increase the risk for carcinoid
tumors or gastrinomas. Vitamin B12 and calcium absorption may be
compromised

Treatment
Non Pharmacology
The management of mild cases includes weight reduction,
sleeping with the head of the bed elevated by about 46 in.
with blocks, and elimination of factors that increase
abdominal pressure.
Patients should not smoke and should avoid consuming fatty
foods, coffee, chocolate, alcohol, mint, orange juice, and
certain medications (such as anticholinergic drugs, calcium
channel blockers, and other smooth-muscle relaxants).
They should also avoid ingesting large quantities of fluids
with meals.
Patients who have an associated peptic stricture are treated
with endoscopic dilation to relieve dysphagia, and such
patients should be vigorously treated for reflux.
Esophagoscopy should also be performed in patients
suspected of other complications such as bleeding or
development of cancer.

Peptic Ulcer Disease

Definition
Burning epigastric pain exacerbated by fasting
and improved with meals is a symptom complex
associated with peptic ulcer disease (PUD).
An ulcer is defined as disruption of the mucosal
integrity of the stomach and/or duodenum
leading to a local defect or excavation due to
active inflammation.
Ulcers are defined as breaks in the mucosal
surface >5 mm in size, with depth to the
submucosa.
Ulcers occur within the stomach and/or
duodenum and are often chronic in nature

Epidemiology
Duodenal Ulcers
DUs are estimated to occur in 615% of the Western
population.
The death rates, need for surgery, and physician visits have
decreased by >50% over the past 30 years.
The reason for the reduction in the frequency of DUs is likely
related to the decreasing frequency of Helicobacter pylori.
Eradication of H. pylori has greatly reduced these recurrence
rates.
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 and are less common
than DUs, perhaps due to the higher likelihood of GUs being
silent and presenting only after a complication develops..

Pathology
Duodenal Ulcers
DUs occur most often in the first portion of duodenum (>95%),
with ~90% located within 3 cm of the pylorus.
They are usually 1 cm in diameter but can occasionally reach
36 cm (giant ulcer).
Ulcers are sharply demarcated, with depth at times reaching
the muscularis propria.
The base of the ulcer often consists of a zone of eosinophilic
necrosis with surrounding fibrosis.
Gastric Ulcers
In contrast to DUs, GUs can represent a malignancy.
Benign GUs are most often found distal to the junction between
the antrum and the acid secretory mucosa.
Benign GUs associated with H. pylori are also associated with
antral gastritis.

Pathophysiology
Duodenal Ulcers
H. pylori and NSAID-induced injury account for the majority of
DUs.
Many acid secretory abnormalities have been described in DU
patients.
Bicarbonate secretion is significantly decreased in the
duodenal bulb of patients with an active DU as compared to
control subjects.
H. pylori infection may also play a role in this process

Pathophysiology
Gastric Ulcers
GUs that occur in the prepyloric area or those in the
body associated with a DU or a duodenal scar are
similar in pathogenesis to DUs.
Gastric acid output (basal and stimulated) tends to be
normal or decreased in GU patients.
When GUs develop in the presence of minimal acid
levels, impairment of mucosal defense factors may be
present.
Abnormalities in resting and stimulated pyloric
sphincter pressure with a concomitant increase in
duodenal gastric reflux have been implicated in some
GU patients.

Pathophysiology
H. pylori and Acid Peptic Disorders
Gastric infection with the bacterium H. pylori
accounts for the majority of PUD. This
organism also plays a role in the development
of gastric mucosal-associated lymphoid tissue
(MALT) lymphoma and gastric adenocarcinoma

Clinical Features
Epigastric pain described as a burning or gnawing
discomfort can be present in both DU and GU
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.
The pain pattern in GU patients may be different from
that in DU patients, where discomfort may actually be
precipitated by food.
Nausea and weight loss occur more commonly in GU
patients.
Dyspepsia.

Physical Examination
Epigastric tenderness is the most frequent
finding in patients with GU or DU.
Physical examination is critically important for
discovering evidence of ulcer complication.
Tachycardia and orthostasis suggest
dehydration secondary to vomiting or active
gastrointestinal blood loss.
A severely tender, boardlike abdomen suggests
a perforation.
Presence of a succussion splash indicates
retained fluid in the stomach, suggesting gastric
outlet obstruction.

Drugs Used in the Treatment of Peptic Ulcer Disease


Drug Type/Mechanism

Examples

Dose

Mylanta, Maalox, Tums,


Gaviscon

100140 meq/L 1 and 3 h after


meals and hs

Acid-suppressing drugs
Antacids

H2 receptor antagonists Cimetidine


Ranitidine
Famotidine
Nizatidine

400 mg bid
300 mg hs
40 mg hs
300 mg hs

Proton pump inhibitors

Omeprazole
Lansoprazole
Rabeprazole
Pantoprazole
Esomeprazole

20 mg/d
30 mg/d
20 mg/d
40 mg/d
20 mg/d

Sucralfate

1 g qid

Prostaglandin
analogue

Misoprostol

200

Bismuth-containing
compounds

Bismuth subsalicylate
(BSS)

See anti-H. pylori regimens (Table


287-4)

Mucosal protective
agents
Sucralfate

g qid

www. Theodora.com/anatomy
Harrison
Anatomi Abdomen
Medscape.com