GIT PROBLEM 2

NICYELA JILLIEN HARLENDEA

405150048
ANATOMY
GASTER

Sobotta Anatomy
GASTER
• Blood supply
• Lesser curvature: the right and left gastric arteries
• Greater curvature: the right and left gastroomental arteries
• Fundus and upper body: short and posterior gastric arteries.
• Nerve supply
• Parasympathetic: anterior and posterior vagal trunks
• Sympathetic: T6-T9 segments of the spinal cord
• Lymphatic drainage
• Superior 2/3: gastric lymph nodes
• Fundus and superior part of corpus: pancreaticosplenic lymph nodes
• Right inferior 2/3: pyloric lymph nodes
• Left greater curvature 1/3: pancreaticaduodenal lymph nodes
Moore Anatomy
DUODENUM

Sobotta Anatomy
DUODENUM
• Blood supply
• Duodenum proximal: superior pancreaticoduodenal artery
• Dudodenum distal: inferior pancreaticoduodenal artery
• Nerve supply
• The vagus
• Greater and lesser splanchnic nerves
• Lymphatic drainage
• Anterior: pancreaticoduodenal lymph nodes
• Posterior: superior mesenteric lymph nodes

Moore Anatomy
HISTOLOGY
GASTER
MUCOSA

SUBMUCOSA

MUSCULARIS EXTERNA

SEROSA
Junqueira Histology
GASTRIC GLAND CELLS
1.Mucous neck cells
2.Parietal cells
3.Chief cells
4.Enteroendocrine
cells

Junqueira Histology
SMALL INTESTINE
CELLS
1. Enterocytes cells
2. Goblet cells
3. Paneth cells
4. Enteroendocrine cells
5. M cells
PHYSIOLOGY
GASTRIC MOTILITY AND EMPTYING

FILLING

STORAGE

MIXING

EMPTYING

Sherwood Physiology
FACTORS REGULATING GASTRIC MOTILITY
AND EMPTYING

Sherwood Physiology
COMPOSITION OF GASTRIC JUICE

Sembulingam Physiology
SECRETORY FUNCTION

Sembulingam Physiology
REGULATION OF GASTRIC SECRETION

Sembulingam Physiology
VOMITING
ELEVATED
ROTATION OF
INTRACRANIAL
THE HEAD
PRESSURE

IRRITATION OR CHEMICAL
DISTENSION AGENTS

TACTILE
STIMULATION PSYCHOGENIC
OF THE BACK VOMITING VOMITING
OF THE THROAT

Sherwood Physiology
 VOMITING
TEMPORARY
ANTIPERISTALSIS DEEP INSPIRATION CESSATION OF CLOSURE OF GLOTTIS
BREATHING

COMPRESSION OF THE UPWARD AND

CONTRACTION OF
STOMACH BETWEEN ELEVATION OF SOFT FOWARD MOVEMENT
DIAPHRAGM AND
DIAPHRAGM AND PALATE OF LARYNX AND HYOID
ABDOMINAL MUSCLES
ABDOMINAL WALL BONE

SIMULTANEOUS
RELAXATION OF LOWER FORCEFUL EXPULSION
ESOPHAGEAL OF GASTRIC CONTENTS
SPHINCTER Sembulingam Physiology
BIOCHEMICAL PROCESS
DYSPEPSIA
Dyspepsia-Definition
• Indigestion (dyspepsia) is a vague feeling of discomfort in the upper
belly or abdomen during or right after eating
• This may include:
• A feeling of heat, burning, or pain in the area between the navel and the
lower part of the breastbone
• A feeling of fullness that is bothersome and occurs soon after the meal begins
or when it is over
Etiology
• Indigestion may be triggered by:
• Drinking too much alcohol
• Eating spicy, fatty, or greasy foods
• Eating too much (overeating)
• Eating too fast
• Emotional stress or nervousness
• High-fiber foods
• Tobacco smoking
• Too much caffeine
• Other causes of indigestion are:
• Gallstones
• Gastritis (when the lining of the stomach becomes
inflamed or swollen)
• Swelling of the pancreas (pancreatitis)
• Ulcers (stomach or intestinal ulcer)
• Use of certain drugs such as antibiotics, aspirin, and
nonsteroidal anti-inflammatory drugs (NSAIDs)
Epidemiology
• It has been estimated that as many as 25% to 40% of adults will
experience dyspepsia in a given year
• Although most individuals who experience dyspepsia symptoms do
not seek medical attention, approximately 25% do seek treatment,
making the condition responsible for 4% to 5% of all primary care
physician visits
Signs and Symptoms
• Pain or discomfort in the upper abdomen
• Heartburn
• Bloating
• Belching
• Quickly feeling full after eating
• Feeling sick (nausea) or vomiting
Clinical Assessment
• Abdominal ultrasound
• Blood tests (depending on the suspected cause)
• Esophagogastroduodenoscopy (EGD )
• Upper GI and small bowel series
Treatment
• Changing the way you eat may relieve your symptoms
• Allow enough time for meals
• Chew food carefully and completely
• Avoid arguments during meals
• Avoid excitement or exercise right after a meal
• A calm environment and rest may help relieve stress-related indigestion
• Avoid aspirin and other NSAIDs. If you must take them, do so on a full
stomach
• Antacids may relieve indigestion
• Ranitidine and Omeprazole can relieve symptoms
Prognosis
• Indigestion is usually not a sign of a more serious health problem,
unless other symptoms also occur, such as weight loss or trouble
swallowing
• Indigestion is a common problem
GERD-Definition
• A condition that causes the upward movement of stomach content,
including acid, into the esophagus and sometimes into or out of the
mouth
Etiology
• A child's immature digestive system is usually to blame and most
infants grow out of GERD by the their first birthday
• In older children, the causes of GERD are often the same as those
seen in adults. Anything that causes the muscular valve between the
stomach and esophagus (the lower esophageal sphincter, or LES) to
relax, or anything that increases the pressure below the LES, can
cause GERD
• Certain factors also may contribute to GERD, including
obesity, overeating, eating spicy or fried foods,
drinking caffeine, and specific medications
Pathophysiology
• The best defined subset of GERD patients have esophagitis
• Esophagitis occurs when refluxed gastric acid and pepsin  necrosis
of the esophageal mucosa  erosions and ulcers
• Restricting reflux depends on the anatomic and physiologic integrity
of the esophagogastric junction
• Mechanisms of esophagogastric junction
incompetence are recognized
• Transient LES relaxations (a vagovagal reflex in which LES
relaxation is elicited by gastric distention)
• LES hypotension
• Anatomic distortion of the esophagogastric junction
inclusive of hiatus hernia
• Factors tending to exacerbate reflux regardless of
mechanism are
• Abdominal obesity, pregnancy, gastric hypersecretory
states, delayed gastric emptying, disruption of esophageal
peristalsis, and gluttony
• After acid reflux, peristalsis returns the refluxed fluid to
the stomach and acid clearance is completed by titration
of the residual acid by bicarbonate contained in
swallowed saliva
• Consequently, two causes of prolonged acid clearance are
impaired peristalsis and reduced salivation
Signs and Symptoms
• The most common symptoms of gastroesophageal reflux in infants
and children are
• Frequent or recurrent vomiting.
• Frequent or persistent cough or wheezing.
• Refusing to eat or difficulty eating (choking or gagging with feeding)
• Heartburn, gas, abdominal pain, or colicky behavior (frequent crying and
fussiness) associated with feeding
• Regurgitation and re-swallowing.
• Complaining of a sour taste in their mouth
• Other problems seen in young children and infants
that may be blamed on GERD include:
• Colic
• Poor growth
• Breathing problems or wheezing
• Recurrent pneumonia
Differential Diagnosis
• Pyloric stenosis
• Hiatal hernia
• Tracheoesophageal fistula
Clinical Assessment
• Barium swallow or upper GI series
This is a special X-ray test that uses barium to highlight the
esophagus, stomach, and upper part of the small intestine. This test
may identify any obstructions or narrowing in these areas
• pH probe
During the test, your child is asked to swallow a long, thin tube with a
probe at the tip that will stay in the esophagus for 24 hours. The tip is
positioned, usually at the lower part of the esophagus, and measures
levels of stomach acids. It also helps determine if breathing problems
are the result of reflux
• Upper GI endoscopy
This is done using an endoscope (a thin, flexible,
lighted tube and camera) that allows the doctor to
look directly inside the esophagus, stomach, and
upper part of the small intestine
• Gastric emptying study
Some people with GERD have a slow emptying of the
stomach that may be contributing to the reflux of
acid. During this test, your child drinks milk or eats
food mixed with a radioactive chemical. This chemical
is followed through the gastrointestinal tract using a
special camera
Treatment
• For babies
• Elevate the head of the baby's crib or bassinet.
• Hold the baby upright for 30 minutes after a feeding
• Thicken bottle feedings with cereal (do not do this without your doctor's
approval)
• Feed your baby smaller amounts of food more often
• Try solid food (with your doctor's approval)
• For older children
• Elevate the head of the child's bed
• Keep the child upright for at least two hours after eating
• Serve several small meals throughout the day, rather than
three large meals
• Make sure your child is not overeating
• Limit foods and beverages that seem to worsen your child's
reflux such as high fat, fried or spicy foods and caffeine
• Encourage your child to get regular exercise
• Drugs to decrease stomach acid
• Antacids
• Histamine-2 blockers
• Proton-pump inhibitors
• Drugs to lessen gas
• Simethicone
• Gaviscon
• Surgery isn't often needed to treat acid reflux in
babies and kids. When it is necessary, the Nissen
fundoplication is the most often performed surgery.
During this procedure, the top part of the stomach is
wrapped around the esophagus forming a cuff that
contracts and closes off the esophagus whenever the
stomach contracts -- preventing reflux
Complications
• Chronic esophagitis (bleeding and stricture)
• Barrett's metaplasia
• Esophageal adenocarcinoma
GASTRITIS
• The term gastritis should be reserved for histologically documented
inflammation of the gastric mucosa
Gastritis
• Gastritis occurs when the lining of the stomach becomes inflamed or
swollen.
• Gastritis can last for only a short time (acute gastritis). It may also
linger for months to years (chronic gastritis).
• Causes
• The most common causes of gastritis are:
• Certain medicines, such as aspirin, ibuprofen, or naproxen
• Heavy alcohol drinking
• Infection of the stomach with a bacteria called Helicobacter pylori
• Less common causes are:
• Autoimmune disorders (such as pernicious anemia)
• Backflow of bile into the stomach (bile reflux)
• Cocaine abuse
• Eating or drinking caustic or corrosive substances (such as poisons)
• Extreme stress
• Viral infection, such as cytomegalovirus and herpes simplex virus
(more often occurs in people with a weak immune system)
• Trauma or a severe, sudden illness such as major surgery, kidney
failure, or being placed on a breathing machine may cause gastritis.
• Symptoms
• Many people with gastritis do not have any
symptoms.
• Symptoms you may notice are:
• Loss of appetite
• Nausea and vomiting
• Pain in the upper part of the belly or abdomen
• If gastritis is causing bleeding from the lining of the
stomach, symptoms may include:
• Black stools
• Vomiting blood or coffee-ground like material
• Exams and Tests
• Tests that may be needed are:
• Complete blood count (CBC) to check for anemia or low blood count
• Examination of the stomach with an endoscope (esophagogastroduodenoscopy or EGD)
• H. pylori tests
• Stool test to check for small amounts of blood in the stools, which may be a sign of bleeding in
the stomach
• Treatment
• Treatment depends on what is causing the problem. Some of the causes will disappear over
time.
• You may need to stop taking aspirin, ibuprofen, naproxen, or other medicines that may be
causing gastritis. Always talk to your doctor before stopping any medicine.
• You may use other over-the-counter and prescription drugs that decrease the amount of acid
in the stomach, such as:
• Antacids
• H2 antagonists: famotidine (Pepsid), cimetidine (Tagamet), ranitidine (Zantac), and nizatidine
(Axid)
• Proton pump inhibitors (PPIs) -- omeprazole (Prilosec), esomeprazole (Nexium), iansoprazole
(Prevacid), rabeprazole (AcipHex), and pantoprazole (Protonix)
• Antacids may be used to treat chronic gastritis caused by infection with Helicobacter pylori
bacteria.
• Outlook (Prognosis)
• The outlook depends on the cause, but is often very good.
• Possible Complications
• Blood loss and increased risk of gastric cancer can occur.
• When to Contact a Medical Professional
• Call your health care provider if you develop:
• Pain in the upper part of the belly or abdomen that does not go away
• Black or tarry stools
• Vomiting blood or coffee-ground-like material
• Prevention
• Avoid long-term use of substances that can irritate your stomach such as aspirin, anti-
inflammatory drugs, or alcohol.
PEPTIC ULCER DISEASE
PEPTIC ULCER DISEASE
• PUD encompasses both gastric and duodenal ulcers.
• Ulcers are defined as breaks in the mucosal surface >5 mm in size,
with depth to the submucosa.
• Duodenal ulcers and gastric ulcers have many common features in
terms of pathogenesis, diagnosis, and treatment, but several factors
distinguish them from one another.
CLINICAL FEATURES
Clinical Features
Abdominal pain
Epigastric pain (burning sensation)
Aching sensation (can occur)
Hunger pain (can occur)
Epigastric tenderness
In Duodenal Ulcer patient, the pain occurs 90 min to
3h after a meal
Nausea and weight loss occur more commonly in
Gastric Ulcer patients
Pain that awakes the patient from sleep (between
midnight and 3 A.M.) is the most discriminating
symptom, with two-thirds of DU patients
Patients with NSAID-induced mucosal disease can
present with a complication (bleeding, perforation,
and obstruction) without antecedent symptoms
Tarry stools or coffee-ground emesis indicate bleeding
GASTRIC ULCER
• The majority of GUs can be attributed to either H. pylori or NSAID-
induced mucosal damage.
• Gastric acid output tends to be normal or decreased in GU patients
• Abnormalities in resting and stimulated pyloric sphincter pressure
with a increase in duodenal gastric reflux have been implicated in
some GU patients.
DUODENAL ULCER
• 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 3–6 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
• H. pylori and NSAID-induced injury account for the majority of DUs.
• Nocturnal gastric acid secretion appears to be increased in DU patients
• Bicarbonate secretion is significantly decreased in the duodenal bulb
NSAID ULCER
• Prostaglandins play a critical role in maintaining gastro- duodenal mucosal integrity and
repair. It therefore follows that interruption of prostaglandin synthesis can impair
mucosal defense and repair, thus facilitating mucosal injury via a systemic mechanism.A
summary of the pathogenetic pathways by which systemically administered NSAIDs may
lead to mucosal injury is shown in Fig. 14-9.
• Injury to the mucosa also occurs as a result of the topical encounter with NSAIDs. Aspirin
and many NSAIDs are weak acids that remain in a nonionized lipophilic form when found
within the acid environ- ment of the stomach. Under these conditions, NSAIDs migrate
across lipid membranes of epithelial cells, lead- ing to cell injury once trapped
intracellularly in an ion- ized form. Topical NSAIDs can also alter the surface mucous layer,
permitting back diffusion of H+ and pepsin, leading to further epithelial cell damage.
More- over, enteric-coated or buffered preparations are also associated with risk of
peptic ulceration.
• The interplay between H. pylori and NSAIDs in the pathogenesis of PUD is complex.
Meta-analysis supports the conclusion that each of these aggressive factors are
independent and synergistic risk factors for PUD and its complications, such as
gastrointestinal bleeding.
HELICOBACTER PYLORI RELATED ULCER
FUNCTIONAL DYSPEPSIA
GERD