MEDICAL SCHOOL Makassar, December 13, 2020

GASTROENTEROHEPATOLOGY BLOCK
INDONESIAN MUSLIM UNIVERSITY

PBL REPORT MODULE I

GASTROENTEROHEPATOLOGY BLOCK

TUTOR:

dr. Prema Hapsari Hidayati, Sp.PD

Arranged by :
Group: 5 B

Muhammad Nirwan Rusdy (11020170039)

Muh. Anugrah Ramadan L. (11020170117)
Ni'ma Haifa Amin (11020190136)
Nurul Indrifah (11020190141)
A. Fatika Sari Pangerang (11020190152)
Muh. Taqdir. S (11020190169)
Muhammad Naufal Nabil Almusawir (11020190170)
Chairul Fikri (11020190186)
St. Islamiati Rahmadini Husrin Putri (11020190193)
Wiwi (11020190206)
Nurika Sarah Madellu (11020190213)
 FOREWORD

Peace be upon you, and Allah's mercy and blessings. Praise be to Allah SWT.
who has given him grace and guidance so that we can compile a Module 1 Report
entitled Acute Abdominal Pain. Salawat and greetings may Allah SWT convey to
all of us, namely to the Prophet Rasulullah SAW who has become a role model
for us all, as well as our motivator in pursuing knowledge to this day.

With thanks Alhamdulillah, this report was finally completed. This report is
completeness for students in order to know and understand the material that has
been given. This report is also expected to be used by students in increasing their
knowledge.

On this occasion the compilers would like to express their appreciation and
gratitude to dr. Prema Hapsari Hidayati, Sp.PD who has guided us and has been
willing to take the time to become our tutor.

In preparing this report, we realize that it is still far from perfect and that
there are many deficiencies in terms of both the writing technique and the content
of the material. Therefore, with great humility, we look forward to his
constructive guidance and direction for the improvement of this report.

Finally, with all the limitations that exist, hopefully this report can benefit
all of us. Amen.

Makassar, December 13, 2020

Group 5B
SCENARIO 3

A 60 year old man, came to a general practitioner with a complaint of heartburn

since the last 2 days, pain that was felt to his back. Nausea, vomiting, there is a
frequency of 1 time containing food scraps, no blood. The patient also complained
of shortness of breath, no cough. The patient likes to eat spicy and oily food, a
history of smoking 1 pack per day. On examination, it was found that TB 165 BW
78kg, vital signs within normal limits, epigastric tenderness and right
hypochondrium.

A. DIFFICULT WORD
-Epigastric tenderness.
-Right hypochondrium.

B. KEY WORD
1. 60 years old man
2. Complaint of heartburn since the last 2 days
3. Pain that was felt to his back
4. Nausea, vomiting, there is a frequency of 1 time containing food
scraps, no blood
5. The patient also complained of shortness of breath, no cough
6. The patient likes to eat spicy and oily food, a history of smoking 1
pack per day
7. On examination, it was found that TB 165 BW 78kg, vital signs within
normal limits, epigastric tenderness and right hypochondrium

C. QUESTION
1. Explain the anatomy, histology in the scenario?
2. What is the patomechanism of the symptoms in the scenario?
3. What is the relationship between nausea and vormiting?
4. What are the risk factors in the scenario?
5. What precautions can be taken regarding this scenario?
6. What are the diagnostic step in the scenario?
7. What dd in the scenario?
8. How the management of disease based on dd?
9. Explain the Islamic perspective to the scenario?
D. ANSWER TO QUESTIONS
1. Explain the anatomy, histology in the scenario?
Answer:
Anatomy

 Epigastrium
Pancreatitis, duodenal ulcer, gastric ulcer, cholocystitis, pancreatic cancer,
hepatitis, intestinal obstruction, appendicitis (early symptoms), subfrenic abscess,
pneumonia, pulmonary embolism, myocardial infarction

 Right hypochondrium
Cholocystitis, cholangitis, hepatitis, pancreatitis, subfrenic abscess, peneumonia,
pulmonary embolipers, nyerimiocardial pain

 Left hypochondrium
Splenic pain due to lymphoma, viral infection. Absessubfrenicus, gastric ulcer,
pneumonia, pulmonary embolism, myocardial pain

 Periumbilical
Pancreatitis, pancreatic cancer, intestinal obstruction, aortic aneurysm, early
symptoms of appendicitis

 Lumbar
Kidney stones, pyelonephritis, perinephric abscess, Ca and Intuinal Colon

 Suprapubic
Diseases of the colon, appendicitis of the inguinal tract, left-sided
diverticulosis, salphingitis, cystitis, ovarian cysts, ectopic pregnancy.

I. Liver
Acute viral hepatitis
It is a systemic infection that predominantly attacks the liver
caused by one of five types of viruses, namely: hepatitis A virus,
hepatitis B virus, Hepatitis C virus, hepatitis C virus, hepatitis D
virus, and Hepatitis E.
Which is accompanied by symptoms of jaundice, weakness, loss of
appetite, pain and discomfort in the upper right quadrant of the
abdomen.

II. Gall bladder

Cholecystysis
Inflammation of the gallbladder is an acute inflammatory reaction
to the gallbladder wall accompanied by complaints of upper right
abdominal pain, tenderness, and fever.

III. Pancreas
Pancreatitis
Inflammation of the pancreas characterized by acute abdominal
pain in the epigastrium accompanied by an increase in enzymes in
the blood and urine

IV. Stomach
Gastritis
Inflammatory process of the mucosa and submucosa of the
stomach, characterized by pain and heat in the epigastrium

V. Appendix Vermiformis
Appendicitis
Inflammation that occurs in the appendix vermiformis and is the
cause of acute abdominal pain in the right lower quadrant, which is
most common in children and adults.
 Gastric Histology

The stomach is an enlarged segment of the digestive tract, whose

main function is to accommodate the food that has been eaten, turning it
into a tough pulp called chymus (chyme). The epithelium dividing these
three parts consists of thoracic cells that secrete mucus. The stomach
histologically can be divided into: cardia, corpus, fundus, and pylorus.

2. What is the patomechanism of the symptoms in the scenario?

Vomiting activity is characterized by a vomiting cycle followed by a
strong excretion of gastric contents through the mouth. The diaphragm
drops, the breathing muscles contract (intercostal breathingmuscle) and
closed glottis. The esophagus dilates in response to decreased intrathoracic
pressure. The stomach temporarily remains atony filled with reflux
material from the small intestine. The abdominal muscles begin to contract
pressing on the stomach and pressing the stomach contents into the fundus
and lower esophagus.
In this phase the fundus can herniate into the thoracic cavity thereby
removing the anti-reflux barrier mechanism generated by abdominal
pressure on the LES.By relaxing the contraction of the stomach and
cessation of contraction of the respiratory muscles and the esophagus
 empties its contents back into the stomach. Several cycles of vomiting
occurred, becoming shorter, more rhythmic with high force so that the
esophagus did not have time to refill the hull.
The last contraction of the stomach in the cycle triggers the discharge of
the stomach, this event occurs when the esophagus is still full and is
associated with an elevated diaphragm which creates positive pressure in
the chest and abdominal cavities. This incident follows spinal flexion,
mouth wide open, elevation of the mole palate, relaxation of the upper
esophageal sphincter and spraying of stomach contents (vomiting).

Reference
http://spesialis1.ika.fk.unair.ac.id/wpcontent/uploads/2017/04/GE01_M
vomit.pdf

3. What is the relationship between nausea and vormiting?

Nausea is discomfort in the upper abdomen. Vomiting is an
unconscious push from the stomach and its excretion through the
esophagus to the mouth. Vomiting is usually accompanied by nausea but
nausea does not always lead to vomiting. One of the side effects that often
occur after anesthesia is nausea and vomiting.
Nausea and vomiting can be short-term and long-term. In the short
term nausea and vomiting are usually not harmful to the patient. But if it
has entered in the long term, usually nausea and vomiting can cause
dehydration so that the electrolyte balance is disturbed. This can be
dangerous for the patient. Most vomit is expelled by mouth, so the
stomach acid contained in vomit can damage tooth enamel. The negative
effects of digestive enzymes can also damage the gums.
The vomiting center receives afferent impulses from the CTZ
through direct or indirect stimulation of the gastrointestinal tract. In the
vomiting center area, there are many receptors that play a role in the
process of nausea and vomiting, and antiemetics generally work to inhibit
neurotransmitters at these receptors. Efferent impulses through the cranial
nerves V, VII, IX, X and XII to the gastrointestinal tract can cause nausea
and vomiting.
 Reference

R. Jusuf. General pathology, University of Indonesia Esa Unggul, 2019.

Indonesia

4. What are the risk factors in the scenario?

a. Psycho-Social Factors
Dyspepsia is closely related to psychological factors. role of stress
in triggering various diseases is often not realized by sufferers even
by their own imedical power. This also explains why some
diseases can find such progressive healing well is after this stress
factor is dealt with.
b. Drug user
A number of drugs can affect iepigastric disorders, nausea,
vomiting and heartburn. For example, the NSAIDs, such as aspirin,
ibuprofen, and naproxen, steroids, theophylline, digitalis, and
antibiotics.
c. Irregular Diet
Irregular eating patterns, especially if you rarely eat breakfast in
the morning days, including those at risk of dyspepsia. In the
morning, need calories a person is enough, so that if you do not eat
breakfast, the stomach will more acid production
d. Unhealty lifestyle
• Smoking. Water in cigarette smoke can weaken the binding
Lower Esophageal Spinter (LES), tie between the stomach
and throat, is so that the gas rises up to the esophagus
• Drink Alcohol. iAlcohol flexes the LES valve, so that i
causes reflux or reversal of stomach acid into the
esophagus. Alcohol also increases the production of
stomach acid.
• Drink coffee, tea or other drinks that contain caffeine.
Caffeine can relax the iLES, the valve between the stomach
and the throat, so that causes gas in the stomach to rise up
to the esophagus.
• Too often consuming foods that are oily and fatty. These
foods tend to slow down digestion, making food stay longer
in the stomach, which in turn increases the pressure the
occurrence of LES attenuation. If the iLES is weakened,
stomach acid will rise ike the esophagus.
e. Women are more at risk than men (man / women: 40.3% /
59.7%)
5. What precautions can be taken regarding this scenario?
a. Eat small portions, but often. Food should be chewed slowly before
being swallowed.
b. Try to avoid things that can trigger dyspepsia. For example spicy and
fatty foods or soft drinks, alcohol, or those containing caffeine.
c. Quit or don't smoke
d. Maintain an ideal body weight.
e. Regular exercise can help you lose excess body weight and maintain a
healthy body weight.
f. Overcoming stress and anxiety. You can do this with sports such as
yoga to ensure adequate sleep.
g. If there are other alternatives, replace the drugs that can irritate the
stomach. However, if not available, make sure that the drug is always
taken after eating (not on an empty stomach).

Reference https://www.halodoc.com/keseh/dispepsia

6. What are the diagnostic step in the scenario?

History

 Asking the location of the pain

The superior and inferior location of pain is not a good indicator of the
organs involved, but may suggest the origin of the foregut, middle gut
(midgut), or (hindgut). We can use the help "9 Region of the
Abdomen" to narrow down the differential diagnosis of acute
abdominal pain.

Pain from the structures of the forebut (esophageal, distal, stomach,

proximal duodenum, liver, biliary system, and pancreas) often presents as
pain in the middle area in the epigastrium.
 Pranceas pain often presents as pain in the midepigastrium or left
epigastric area with reffered pain to the back.
Pain from the middle intestine (small bowel, appendix, ascending colon,
and the proximal two-thirds of the transverse colon) is usually
periumbilical, although pain from the ileun (as in Crohn's ileitis) may
occur in the lower right quadrant.
Pain from the back gut organs (distal transverse colon, descending colon,
and sigmoid colon) is often present in the mid-lower abdomen between the
umbilicus and symphysis pubis.

 Ask about the timing of the pain

Abdominal pain can be sudden (seconds to minutes), rapidly progressive
(within 1-2 hours), or slow (within hours). Abdominal pain suddenly
indicates an emergency such as rupture of the abdominal aneurysm or
perforation of the peptic ulcer. Pain that occurs after vomiting often
indicates a medical illness, whereas pain preceding vomiting often
indicates surgical disease. Pain that persists for more than 6 hours after the
acute onset has a high likelihood of being surgical and the patient should
be treated.

 Ask for the intensity and ask the patient to describe the pain
The characteristics of the type and severity of pain can lead to a specific
diagnosis. Peptic ulcer pain is usually felt as a dull pain of mild to
moderate severity.
Intense pain with a sudden onset leading to mesenteric ischaemia or
perforation of the peptic ulcer.
Colic is episodic pain with pain-free intervals. This is often seen in renal
colic, but biliary colic is usually a constant pain, persistent, without pain-
free periods.
Pain of severe intensity and like tearing is common with aneurysm
dissection. Patients with postprandial pain, avoiding food, weight loss, and
atherosclerosis should be evaluated for possible mesenteric angina.

 Factors that Increase and Relieve Pain

Factors that aggravate and reduce pain can help determine the cause. Pain
relieved by antacids leading to peptic ulcers or esophagitis. Pain
aggravated by movement leads to peritonitis, whereas patients who are
constantly moving to find a comfortable position are commonly seen with
intestinal obstruction and renal colic. Patients with a retroperitoneal
process (such as pancreatitis) generally have pain relief by bending
 forward, and are exacerbated by sleeping on their backs. Pain that is
relieved by defection leads to colonic disorders.

Physical examination

 Inspection

Inspection is carried out by looking at the surface, contour and movement of the
abdominal wall. The inspection includes:

1. Skin: On the skin, look for scars, striae, dilated veins, and redness and
ecchymosis (can be seen in intraperitoneal or retroperitoneal bleeding)
2. Ecchymosis: Apart from suggesting intraperitoneal or retroperitoneal bleeding,
the presence of ecchymosis may also suggest another diagnosis. Gray Turner sign
is an ecchymosis which may be accompanied by a greenish color on the flank area
of the patientacute pancreatitiswith extraperitoneal hemorrhage that diffuses into
the subcutaneous tissue of the flank area. Cullen's sign is an ecchymosis that can
be accompanied by a bluish coloration on the skin of the periumbilical area due to
retroperitoneal or intraabdominal bleeding, such asinterrupted ectopic pregnancy

3. Umbilicus: In the umbilicus, it is necessary to pay attention to its contour and

location, and the presence or absence of inflammation or lumps, as in umbilical
hernia

4. Abdominal contours: Abdominal contours are defined as the surface (flat,

distended, protruding, or concave), the sides of the abdomen (presence or absence
of lumps or masses), symmetry of the abdominal wall, masses or organomegaly
that is prominent (eg hepatomegaly or splenomegaly)
5. Peristalsis: In very thin patients, the possibility of bowel peristalsis may be
seen, especially if there is obstruction
6. Pulsation: Aortic pulsation can also be seen in very thin patients. When seen in
the epigastric area, it can be said to be normal.
  Auscultation

Auscultation on examination of the abdomen provides mainly information

regarding bowel sounds. Different from other physical examinations, it is
advisable to carry out auscultation in the physical examination of the abdomen
because percussion and palpation maneuvers can stimulate or depress intestinal
peristalsis. Normal bowel sounds range from 5-34 beats / minute. Auscultation is
carried out for at least 2 minutes in each region, and at least in 1 region to
determine the conclusion of the patient's bowel sounds.

The presence of inflammation (egperitonitis), infection,paralytic ileus,

andobstructive ileuswill change the characteristics of bowel sounds. In certain
conditions, such as infection, borborygmi and hyperperistalsis may be heard. In
peristalsis of auscultation of the intestine, it is necessary to pay attention to the
frequency, duration, volume, and quality of bowel sounds.

On auscultation of the abdomen, a murmur-like sound may be found in the aorta,

iliac artery, and femoral artery. Murmurs can be heard especially in patients
withhypertension. Murmurs can also be heard in patients with arterial stenosis or
dilated arteries caused by aneurysms. The murmur of the renal artery, according to
its anatomical position, will be heard more from the back.

In the area of the liver and spleen, auscultation is necessary for friction rubs. This
can occur in patients with hepatoma, gonococcal infection of the liver area, and
splenic infarction.

 Percussion

Percussion is performed to see the distribution of intra-abdominal gas, possible

mass, as well as the size of the liver and spleen and other organs. Percussion is
performed on the four quadrants of the abdomen by looking at the tympanic and
deaf areas. The tympanic sound is caused by gas in the gastrointestinal tract, while
the sharp sound can be caused by the presence of fluid, mass or enlargement of
organs, or feces.

Percussion in the infero-anterior part of the right arcus ribs can be found deaf due
to the presence of the liver, while on the left you will find tympanic in the gastric
area and splenic flexure.
 Percussion is performed by extending the middle finger of the left palm
(pleximeter) on the surface of the abdomen that wants to be percussed, with the
right middle finger flexed (percusor) while tapping repeatedly at the distal
interphalangeal joint on the pleximeter.

 Palpation

Palpation on physical examination of the abdomen consists of light and deep

palpation. Light palpation can assess the presence of tenderness, muscular
defenses, and masses in the superficial organs.

a. Light palpation is carried out in the following ways:

1. Place the palms of the hands with the fingers together and flat on the
abdominal wall
2. Apply light pressure to all four quadrants of the abdomen.
3. In this light palpation, it is necessary to identify organs and masses that are
superficial, as well as areas that experience tenderness.
4. If there is a defense, distinguish between voluntary resistance and
involuntary muscle spasm, as the presence of an involuntary spasm can lead to the
diagnosis of peritonitis.

b. Deep palpation was performed to depict the intra-abdominal mass and the
presence of organomegaly. This palpation is done by:

1. Use the surface of your palms, then apply emphasis on all four quadrants
2. If a mass is present, identify the location, size, shape, consistency, pain on
compression, pulse, and mass mobility
Carnett's signis a tenderness that is felt to increase when contracting the
abdominal wall muscles. This examination is carried out by asking the patient to
supine, then at the location that the patient predicts pain, pressure is applied while
asking the patient to lift both the legs and torso and head simultaneously. This will
make the abdominal wall muscles contract.
Often some intra-abdominal organs, such as the liver, kidneys, and intestines are
difficult to palpate, this is normal, especially in patients with thick abdominal
walls, for example, patients withobesitycentral

Pain in epigastric palpation can be caused bygastritis,acute cholecystitis, certain

defects (eg muscle diastasis), and pulsatile masses of abdominal aortic aneurysms.

Supporting investigation

 Laboratory examination
Initial examination includes complete peripheral blood count, electrolytes, kidney
function, liver function, amylase and urinalysis.

Blood types and blood cross-matches should be performed in patients requiring

surgery. Blood gas analysis is performed for peritonitis, pancreatitis, intestinal
ischemia, or hypotension for metabolic acidosis or hypoxemia.

 Radiologist
Plain radiographs can aid in the initial evaluation of a patient with acute
abdominal pain. Films taken should include chest radiographs in the upright and
lying position and plain radiographs of the abdomen in the upright position. Plain
radiographs can identify cases of bowel obstruction, viscus perforation (free
intraperitoneal air is best seen on an upright chest X-ray), air in the portal or
biliary system, classification (kidney stones, chronic pancreatitis, gallstones),
pneumatosis (air on the walls). intestines), or thickening of the intestinal wall.

- Abdominal radiograph may show loss of the normal psoas image

indicating intra-abdominal inflammatory processes. Chest X-ray may also
show pulmonary infiltrate, spontaneous pneumothorax, or sympathetic
pleural effusion (due to infection or irritation of the subdiaphragm). photo
done.
- Other tests include angiography for patients suspected of having
mesenteric ischemia, or upper gastrointestinal studies with contrast for
patients with possible perforation of peptic ulcers (using soluble water
contrast to avoid barium peritonitis). Lower gastrointestinal contrast
studies are useful in evaluating diagnostic as well as therapeutic suspicions
in suspected colonic volvulus. Endoscopy is more sensitive and specific
for mucosal abnormalities than contrast radiography.
- Ultrasonography (USG) is a non-invasive test that is useful for showing
biliary abnormalities including cholelithiasis, dilation of the ducts,
thickening of the gallbladder wall, and pericolesistic fluid. Ultrasound of
 the abdomen can also show acute appendicitis, abdominal masses,
hydronephrosis, pelvic inflammatory disease, and other conditions causing
abdominal pain.
- CT-scans can help diagnose pancreatic disease, aneurysms, abdominal
aorta, intraabdominal fluid collection, diverticulitis, intestinal obstruction,
appendicitis, and malignancy.
- MRCP can detect bile duct obstruction noninvasively with the same
sensitivity as ERCP.

Reference:

1. Reuben A.Examination of the abdomen. Clin Liver Dis. 2016; 7 (6): 143–50

2. bdullah M, Firmansyah MA. Diagnostic Approach and Management of Acute

Abdominal Pain. Acta Med Indones. 2012; 44 (4): 7.

3. Mealie CA, Manthey DE. Abdominal Exam. In: StatPearls. Treasure Island
(FL): StatPearls Publishing; 2019. Available
from:http://www.ncbi.nlm.nih.gov/books/NBK459220/

4. EIMeD PAPDI textbook (emergency in internal medicine).

7. What deferential diagnosis in the scenario?

1. Dyspepsia
a. Definition
Dyspepsia is a collection of symptoms or heartburn syndrome,
nausea, bloating, vomiting, feeling full or full quickly, belching is a
problem that is often found in daily practice. Clinical complaints can
persist for a certain time or may recur. Dyspepsia comes from Greek: duis
bad, and peptein to digest, which means indigestion. Complaints of
gastroesophageal reflux in the form of a burning sensation in Qieartburn's
chest and regurgitation of gastric acid are no longer included in the
dyspepsia syndrome, however these two clinical symptoms often overlap
and it is difficult to distinguish between dyspepsia and gastroesophageal
reflux disease (GERD) in dyspepsia patients who have not investigated.
The definition of dyspepsia is divided into two, namely:
1). Organic dyspepsia, if an organic disorder is known to be the cause.
Organic dyspepsia syndrome, there are obvious abnormalities of the body's
organs, such as ulcers / ulcers in the stomach or duodenum, cholecystitis,
and others.
2). Non-organic dyspepsia or functional dyspepsia, or non-ulcer dyspepsia
(DNU), if the cause is not clear.

b. Epidemiology

Based on research in the general population, the prevalence of

dyspepsia ranges from 12-45% with a mean estimate of 25%. The
incidence of dyspepsia per year is estimated to be between 1-11.5%. There
is no epidemiological data in Indonesia yet. The prevalence of dyspepsia is
mediated by factors: gender, age, body mass index, smoking, alcohol
consumption and psychology, where these psychological factors have a
strong correlation with dyspepsia complaints, while demographic and
environmental factors have weak correlation. Complaints of dyspepsia are
experienced for a certain time and are chronic in nature and can have an
impact on the quality of life of the sufferer and the economic burden
directly or indirectly. Research in the UK the indirect costs of this
complaint reached 1 billion Pounds Sterling,

c. Pathophysiology

Various theories have been proposed to explain the pathogenesis of

dyspepsia. In functional dyspepsia according to the criteria for the absence
of organic abnormalities in the upper gastrointestinal tract, the theory
varies greatly. The gastric acid hypothesis explains that an increase in
stomach acid or an increase in the sensitivity of the gastric mucosa to
stomach acid is responsible for the occurrence of dyspepsia complaints.
Hypotheses of motor dysfunction such as gastroesophageal reflux,
gastyoparesis, small bowel dysmotility and biliary dysentery cause
dyspepsia. Various neurotransmitters and polypeptide hormones are
involved in the regularity of gastric motility. In addition, there are also
visceral and psychosomatic hypersensitivity hypotheses.

-Secretion of Stomach Acid

Basal and peak gastric acid secretion in dyspepsia patients

associated with various patient complaints, in functional dyspepsia
patients did not differ significantly from the normal population. It is
suspected that there is an increase in the sensitivity of the gastric
mucosa to acids which cause discomfort in the stomach. In the case of
functional dyspepsia with H. pylori infection, it will increase gastrin
secretion so that the parietal cell mass produces more gastric acid (see
table 1). Research by conducting acid instillation of the gastric mucosa
in functional dyspepsia cases failed to show an increase in dyspepsia
symptoms.

- Motility and gastric accommodation abnormalities

Basically, motility is a propulsion / peristalsis movement which is

influenced by the regulation of the enteric nervous system through
various neurotransmitters. Various conditions can affect this motility
(both hyper, hypo and dysmotility) with various manifestations of
visceral perception (complaints of abdominal pain, etc.). The issue of
this area becomes prominent in functional gastrointestinal disorders
where there is no finding of structural organic lesions. Many reported
disorders of gastric motor function are the basis for this dyspepsia.
Gastrointestinal dysmotility is a complex condition that involves the
electrical activity of smooth muscles, changes in intestinal intraluminal
pressure and passage of intestinal contents. There has not been a single
supporting examination that can completely describe this motility state.
In 30-40% of cases of functional dyspepsia there is disturbance of
MMC phase III, impaired coordination of antroduodenal contraction /
peristalsis, and delayed gastric emptying time for solid foods. The
presence of a low excitability threshold or sensitive perception can be
assessed from trials of balloon distension in the stomach, where a lower
volume is required than in control cases to induce the perception of
bloating. The cause of the motility disorder is not clear, it may be
hormonal, stress, or others. where it takes a lower volume than case
controls to induce the perception of bloating. The cause of the motility
disorder is not clear, it may be hormonal, stress, or others. where it
takes a lower volume than case controls to induce the perception of
 bloating. The cause of the motility disorder is not clear, it may be
hormonal, stress, or others.

- Diet and Environment

Patients reported various types of food as triggering attacks,

including fruits, pickles, coffee, alcohol, fatty foods, and others. But in
research it is difficult to prove that these factors apply to everyone, and
so does a person's diet.

- Visceral Sensory Disorders

More than 50% of patients with functional dyspepsia show

sensitivity to gastric or intestinal distension, therefore it may be due to:
slightly irritating foods such as spicy food, air distension, impaired
intestinal gastric contractions or premature distension of the
postprandial antrum can induce pain in this area.

d. Diagnosis

To make a diagnosis of functional dyspepsia, a good history, accurate

physical examination, accompanied by supporting tests is needed to
exclude organic / structural / metabolic diseases. There are additional
threatening complaints (alarm symptoms) in dyspepsia such as age more
than 55 years with new onset, history of peptic ulcer, family history of
upper gastrointestinal cancer, weight loss, bleeding, progressive
dysphagia, odynophagia, anemia, persistent vomiting, jaundice, palpable
abdominal mass or lymphadenopathy.

- Laboratory: more emphasis is placed on eliminating other organic

causes such as chronic pancreatitis, diabetes mellitus and others
among others. In functional dyspepsia, laboratory results are
usually within normal limits.
- Endoscopy (esophagogastro-duodenoscopy): In accordance with
the definition that in functional dyspepsia, the endoscopic image is
normal or very nonspecific.
- Gastric emptying time: 30-50% of functional dyspepsia patients
experience a delay in the solid phase, this delay in gastric
emptying has no correlation with dyspepsia complaints.
- Ultrasonography (USG): in several centers in Europe USG is used
to assess the time of gastric emptying by measuring the proximal
 size of the stomach, in dyspepsia patients it is smaller than in non-
dyspepsia.

2. Pancreatitis
a. Definition
Chronic pancreatitis is defined as a chronic, continuous
inflammatory process of the pancreas, characterized by irreversible
morphological changes.

b. Epidemiology
Hospital data (RS) in the United States get 87,000 chronic
pancreatitis patients a year. Hospital patient data in several cities in the
world show a similar prevalence. Marseille 3.1 per 1000 hospital
treatments, Cape Town 4.4 per 1000 hospital treatments, Sao Paulo 4.9
per 1000 hospital treatments and Mexico City 4.4 per 1000 hospital
treatments. The incidence of chronic pancreatitis from 1945-1985
appears to be increasing. Chronic pancreatitis treatment for blacks is 3
times higher than for whites in the United States. In population studies,
men were affected more than women (6.7 versus 3.2
per 100,000 population).

c. Pathophysiology
Pancreatic fiorogenesis is this typical response to damage. This
fibrogenesis includes the complex role of growth factors, cytokines
and chemokines, which lead to deposition of the extra-cellular matrix
and proliferation of fibroblasts. In pancreatic damage, local expression
and release of transforming growth factor beta (TGF-beta) stimulates
the growth of mesenchymal cells and stimulates the synthesis of
extracellular matrix proteins such as collagen, fibronectin and
proteoglycans. Research evidence suggests that certain chemokines are
affected at the initiation and perpetuation stages of chronic
pancreatitis.
The occurrence of chronic pancreatitis is usually a metabolic
disorder. Some of the pathogenesis of chronic pancreatitis include:
- Intraductal obstruction, eg ethanol (ETOH) intoxication, stones,
tumors.
- Toxins and direct toxic metabolites that stimulate pancreatic aciner
cells to release cytokines that stimulate stellate cells to produce
collagen and cause fibrosis, such as ETOH and tropical spruce.
- Oxidative stress, eg idiopathic pancreatitis
 - Necrosis-fibrosis: recurrent acute pancreatitis that resolves with
fibrosis.
- Ischemia
- Autoimmune disorders: chronic pancreatitis is associated with
autoimmune diseases including Sjogren's syndrome, primary
biliary cirrhosis (PBC), and renal tubular acidosis (renal tubular
acidosis, RTA).

d. Clinical Manifestations
The most common symptoms are chronic abdominal pain (epigas-
trium) and / or symptoms of pancreatic endocrine and exocrine
dysfunction (chronic diarrhea) (steatorrhoea), distention / typical
bloating and weight loss). Jaundice can arise as a result of biliary tract
stenosis in the acute exacerbation phase of chronic pancreatitis.

e. Etiology

The causes of chronic pancreatitis are quite diverse, including:

- Intraductal obstruction into alcohol (ethanol = ETOH) c (chronic

alcoholic pancreatitis), stones / tumors of the pancreatic tract
- Toxic substances and toxic metabolites
- Idiopathic
- Autoimmune disorders
- Hereditary pancreatitis
- Cystic Fibrosis of the pancreas
- Congenital abnormalities
- Acquired obstructive chronic pancreatitis
- Hyperlipidemia (usual types I and V)
- Hypercalcemia
- Nutritional or tropical.
- Medicines
- Pancreatic fluid flow obstruction
- Chronic tropical pancreatitis (mostly in tropical countries
and growing).
f. Diagnosis
Diagnosis is made based on history, physical examination, and
investigations. The history shows that the patient has chronic
abdominal pain, chronic diarrhea (steatorrhoea) and weight loss.
Physical examination is not unique, except that at the time of the
attack, the patient chooses certain positions to relieve stomach pain,
 including sleeping on his left side, bending the vertebrae and pulling
the knees over the chest. Sometimes the epigastrium feels bloated and
painful or the mass indicates a pseudocyst or a period of abdominal
inflammation.
Patients with severe acute pancreatitis with steatorrhoea exhibit
reduced subcutaneous fat, malnutrition, and a deep supraclavicular
fossa. Investigations show normal or slightly elevated levels of
pancreatic enzymes and atrophic fibrosis of the pancreatic gland
accompanied by dilation of the pancreatic duct and pancreatic
calcification. The results of conventional investigations in early stage
chronic pancreatitis can still be normal, where inflammatory changes
can be seen through histological examination.
The differential diagnosis of chronic pancreatitis includes ampulla
cancer, cholangitis, cholecystitis. Crohn's disease, chronic gastritis,
intestinal perforation of the mesenteric artery, myocardial infarction,
pancreatic cancer, peptic ulcer and pneumonia.
Routine supporting examinations that are needed include
examination of peripheral blood (hemoglobin, leukocytes), serum
amylase and lipase, blood sugar, levels of tryglyceride, and serum
calcium.
Radiological examinations include ultrasound (USG), abdominal
CT-scan, abdominal MRI, Endosonography, Magnetic resonance
cholangiopancreatagraphy (MRCP), Endoscopic Retragrade
cholangiopancreatagraphy (ERCP).

3. Pepticus Ulcer
a. Definition
Peptic ulcer patients generally present with heartburn, bloating, and
nausea. In more severe conditions, where a perforation has occurred, the
patient may complain of vomiting blood, black bowel movements, and
symptoms of peritonitis. The diagnosis is confirmed by carrying out an
endoscopy
The main treatment of peptic ulcer is lifestyle and pharmacological
therapy which aims to reduce stomach acid and treat H.pylori infection.
The recommended regimen is triple therapy using a proton pump inhibitor
(PPI) or H2 blocker (H2 blocker), and two antibiotics, for example a
regimen.omeprazole,amoxicillin, andclarithromycin

Peptic ulcer is injury to the peptic acid in the mucosa of the gastrointestinal tract,
which can cause damage to the submucosa lining. Peptic ulcers generally affect
the stomach and proximal duodenum. The most common cause of peptic ulcer is
Helicobacter pylori infection. Other causes include consumption of nonsteroidal
anti-inflammatory drugs (NSAIDs) and conditions that cause hypersecretory
stomach acid, such as food consumption and stress.

b. Etiology
The etiology of peptic ulcer is damage to the mucosa of the
gastrointestinal tract, generally the stomach and proximal duodenum. This
damage is influenced by several risk factors such as Helicobacter pylori
infection, consumption of nonsteroidal antiinflammatory drugs (NSAIDs),
stress, smoking, and chronic alcohol consumption.

c. Risk Factors
A systematic review reports the risk factors associated with the
appearance of peptic ulcers, their recurrence, and mortality.

Risk Factors for Peptic Ulcer

Risk factors associated with peptic ulcers include:

 Pylori infection
 Medication: NSAIDs, aspirin
 Male gender
 Increasing age
 The presence of comorbidities:generalized anxiety
disorder,schizophrenia,chronic obstructive pulmonary disease
 Chronic alcoholism
  Smoke
Risk Factors for Peptic Ulcer Recurrence

Risk factors associated with recurrent peptic ulcer include:

 Increasing age

 Medication: NSAIDs, aspirin, anticoagulants, immunosuppressants,

corticosteroids (for example:prednisone)
 Pylori infection
 Ulcer size> 1 cm

 Forrest class I (peptic ulcer with active bleeding), and II (peptic ulcer with
a history of bleeding in the near future)

 Zollinger-Ellison syndrome

Peptic Ulcer Mortality Risk Factors

Risk factors associated with peptic ulcer mortality include:

 Increasing age

 Comorbidity

 Use of steroids

 Clinical conditions: shock, low Hb level on admission, low blood pressure,

delay in treatment

 Forrest Class I-II

 Recurrence of complications

d. Epidemiology

The epidemiology of peptic ulcer is reported to be 10% in the

United States. National epidemiological data in Indonesia are not yet
available.
 Globaly The epidemiology of peptic ulcer in the United States is
reported to be 10%. A study in Iran reported that the prevalence of
peptic ulcer was 8.20%, whereas the prevalence of gastric ulcer was
3.26% and duodenal ulcer was 4.94%. Another study in Sweden
showed that the prevalence of gastric ulcers was 2.0%.

The pathophysiology of peptic ulcer is an imbalance between the

protective factors of the gastric mucosa and the destructive factors,
resulting in mucosal damage that causes ulcers in the gastrointestinal
tract. Protective factors include mucus, bicarbonate, prostaglandins,
epithelial cells, mucosal progenitor cells, and mucosal blood flow.
Destructive factors include the use of nonsteroidal anti-inflammatory
drugs (NSAIDs), Helicobacter pylori, stomach acid, and pepsin.

H. pylori infectionH. pylori infection is the most common cause

of peptic ulcers. The mechanism of mucosal damage by H. pylori
bacteria is a complex process, but basically H. pylori bacteria contain
urease enzymes which are capable of producing ammonia (NH3) from
urea. Ammonia will react with stomach acid (HCl) to form
monochloramine (NH2Cl).

e. Signs and symptoms

The main symptom of a peptic ulcer is abdominal pain. This pain

occurs due to irritation of stomach acid that soaks the wound. Usually, the
pain appears at night and gets worse on an empty stomach. In more severe
conditions, the pain you feel can spread to the neck, navel, and back. Other
symptoms of peptic ulcer include: heartburn, lack of appetite, nausea, and
indigestion.

f. Diagnosis

The diagnosis of peptic ulcers is based on a physical examination /

history and other examinations. Among them are endoscopy
(gastrocopy), radiological examinations (X-rays or CT scan), and tests
to confirm the presence of H. pylori bacteria (for example, by
examining blood, stool, or breathing tests) . After the diagnosis is
determined, the doctor will determine the steps of treatment based on
the cause. However, in general, the goal of peptic ulcer treatment is to
destroy the H. pylori bacteria and reduce the consumption of non-
steroidal anti-inflammatory drugs.

History: Patients with peptic ulcers generally present with epigastric

abdominal pain, such as burning or discomfort. Pain can appear
immediately after eating or several hours afterward. Other symptoms
that can appear are bloating, abdominal distension, nausea, and weight
loss.

EDUCATION:

Education that can be done to prevent peptic ulcers includes diet

education, stress management, and lifestyle modification.

Patient Education, Since H.pylori infection is the most common

cause of peptic ulcer, infection prevention is an important element.
Nutrition is an aspect that must also be considered to create a good
atmosphere for the stomach.

Apart from administering drugs, surgery is sometimes necessary.

Especially if the peptic ulcer has caused a hole in the stomach wall or
serious bleeding that cannot be treated with endoscopy. To help the
healing process and avoid more severe symptoms, here are some
things people with peptic ulcer can do:

 Quit smoking and limit your intake of liquor, tea and coffee.

 Avoid eating spicy or fatty foods.

 Increase consumption of foods that contain probiotics (such as
yogurt).
  Increase your consumption of fruits, vegetables and whole
grains.
 Get enough rest and control the stress you experience.

Although rare, peptic ulcers can cause serious complications. Some

of the complications that may occur if peptic ulcer is not treated
promptly are: bleeding in the stomach, peritonitis (inflammation of
the thin lining of the inner wall of the stomach), obstruction of the
movement of food in the digestive system, and gastric cancer.

REFERENCES:

 Malfertheiner P, Chan FK, McColl KE. Peptic ulcer disease. The Lancet,
2009. 374 (9699): 1449–1461. doi: 10.1016 / s0140-6736 (09) 60938-7
 Lanas A, Chan FKL. Peptic Ulcer Disease. Lancet, 2017. 390: 613-24.
 Mustafa M, Menon J, Muiandy RK, et al. Risk factors, diagnosis, and
management of peptic ulcer disease. IOSR J of Dental and Med Sci, 2015. 14
(7): 40-46.
 J. Fashner, AC Gitu. Diagnosis and Treatment of Peptic Ulcer Disease and H.
pylori Infection. Am Fam Phys, 2015.91 (4): 236-242.
 Rani, Aziz. Simadribata, Marcellus. Fahrial, Syam. 2011. Textbook of
Gastroenterology. Ed1. Jakarta: Internal Publishing. 131-142
 Reference: Setiati, S.dkk. 2014. Internal medicine textbook. Volume I (IV).
Jakarta: Interna Publishing

8. How the management of disease based on differential diagnosis?

1. Management of Dyspepsia
-The patient is less than 45 years old
o Acid suppression therapy
The administration of Proton pump inhibitor / PPI
drugs is not useful in dyspepsia syndromes in the absence
of organic disorders in the stomach (eg ulcers).
o Early endoscopy (early endoscopy):
Several studies have shown that early endoscopy
may be more effective than emperic therapy, although from
 the aspect of cost effectiveness it is not better than
empirical therapy.
o Hpylon test and treat (H.pylori test and treat):
This strategy was applied to all patients who
presented a positive non-invasive H.pylori test and had
persistent complaints even though the test results were
negative. The noninvasive H. pylori test is more effective
than the endoscopic examination. This strategy includes the
eradication of H. pylori in all dyspepsia, even in dyspepsia
patients without ulcer therapy. This strategy has advantages
and disadvantages.
Advantages:
• Improvement of complaints in a small population of
functional dyspepsia patients
• Prevent the risk of ulcers in the day and day.
• Eliminates risk factors for gastric cancer.
• Eliminates interactions between infection and possible
long-term PPI use g
Disadvantages / disadvantages:
• The widespread use of antibiotics creates the potential for
resistance to develop
• Increased cases of reflux esophagitis

- Patients over 45 years of age

Guidelines that apply to dyspepsia patients aged over 45
years, early endoscopy is recommended. Even new cases of
dyspepsia are recommended for endoscopy, although existing
research reports show no benefit of early endoscopy. As for the test
and treat H.pylori as aged under 55 years.

- Functional dyspecia patients

2. Management of Pancreatitis
The management goals of chronic pancreatitis are:
- improve a lifestyle that can exacerbate the course of chronic
pancreatitis.
- gives the pancreas a chance to heal itself.
- determine and treat the cause of abdominal pain.
- detect pancreatic exocrine insufficiency disorders
- improve digestive and absorption disorders. diagnose and treat
endocrine insufficiency.

In general, the management of chronic pancreatitis consists of:

1) Medical:
Nonpharmacologic:
o Low fat nutrition high in protein and carbohydrates is
recommended and does not interfere with pancreatic
function.
o Improve your lifestyle, for example, stop drinking alcohol,
cigarettes.

Pharmacologic:

o Analgesics: paracetamol, tramadol, codeine or non-steroidal

anti-inflammatory drugs (NSAIDs).
o Anti-oxidants: still controversial.
o Fat soluble vitamins (A, D, E, K) and B12 are given to patients
with chronic pancreatitis with deficiency of these vitamins.
o Supplementation pancreatic enzymes: trypanzymes, vitazymes,
pancreoflat, and so on.
o Hormones: somatostatin or octreotide can be given.
Antidepressants: for depressed people can be given
amitriptyline hydrochloride.
2) Minimally invasive: ERCP, sphincterotomy, stone extraction,
insertion of a pancreatic stent. Percutaneous drainage (PTBD),
CBD stent, pseudocyst drainage with EUS etc.
3) Surgery: Surgery is performed when there are complications such
as infected pseudocysts, abscesses, fistulas, ascites, common
hepatic duct obstruction, duodenal stenosis with pyloric
obstruction, and varicose bleeding due to splenic vein thrombosis.
 3. Peptic Ulcer Management
MANAGEMENT:
The management of peptic ulcer depends on the condition of the
patient at presentation. Patients with bleeding or perforation
require emergency treatment with stabilization, endoscopy, or
surgery. Patients who do not have an emergency are managed
withtriple therapyfor eradicationH.pylori,and given a lowering of
stomach acid.

Management of Bleeding and Perforation

Patients with peptic ulcer who present with bleeding or are
suspected of having perforation, should be given emergency
management first. Once the patient is stable, tests can be performed
to determine if this has occurredperitonitisor not, and whether
operative action is needed or not

REFERENCES:

 Malfertheiner P, Chan FK, McColl KE. Peptic ulcer disease. The Lancet,
2009. 374 (9699): 1449–1461. doi: 10.1016 / s0140-6736 (09) 60938-7
 Lanas A, Chan FKL. Peptic Ulcer Disease. Lancet, 2017. 390: 613-24.
 Mustafa M, Menon J, Muiandy RK, et al. Risk factors, diagnosis, and
management of peptic ulcer disease. IOSR J of Dental and Med Sci, 2015. 14
(7): 40-46.
 J. Fashner, AC Gitu. Diagnosis and Treatment of Peptic Ulcer Disease and H.
pylori Infection. Am Fam Phys, 2015.91 (4): 236-242.
 Rani, Aziz. Simadribata, Marcellus. Fahrial, Syam. 2011. Textbook of
Gastroenterology. Ed1. Jakarta: Internal Publishing. 131-142
 Setiati, S.dkk. 2014. Internal medicine textbook. Volume I (IV). Jakarta:
Interna Publishing
9. Explain the Islamic perspective to the scenario?

From Karimah Al-Miqdad ibn Ma'di Kariba radhiyallahu 'anhu, he said, "I
heard the Prophet sallallaahu' alaihi wasallam say,
"Adam's children and grandchildren did not fill a container / vessel that
was worse than his stomach, actually just a few mouthfuls was enough to
strengthen his ribs. Even if he had to fill it, then 1/3 for food, 1/3 for
drinks, and 1/3 for breathing. "