MODULE 1

. A 70 years old men, came to the emergency with chief complaint pain through
out the abdominal wall since 12 hours ago, from the pit of the stomach, then
spread to abdominal wall. History of patients suffering from rheumatism and
often taking pain medication for a long time. On physical examination the
abdomen appears bloated.

Hard word
-
Keyword
1. A man 70 years old
2. Pain in the entire abdominal wall since 12 hours ago
3. Initially from the pit of the stomach, then spread to the entire abdominal wall
4. History of suffering from rheumatism and taking anti-pain medication for a long time
5. On physical examination the abdomen appears bloated

Questions
1. Explain the anatomical structure and histology in the scenario?
2. Explain the pathomechanism of pain in the patient's stomach wall in the scenario?
3. Why can pain spread from the pit of the stomach to the abdominal wall?
4. Explain the types of acute abdominal pain?
5. how to reduce the pain that patients feel related to the scenario?
6. is there a relationship between drugs consumed for a long time and abdominal
pain that patients feel in the scenario?
7. what is the relationship between rheumatism and pain in the scenario?
8. what causes the patient's stomach to appear bloated?
 ANSWER

1. Explain the anatomical structure and histology in the scenario?

Cavum oris
Is a cavity that is limited by the lips (labium) and cheeks. Inside is a ginggiva, teeth
(dentes) and at the base of the cavum there are lingua (tongue). Adult humans have 32 teeth
found in the maxilla (maxilla) and in the mandible (mandible). On each side (left and right)
there are 2 incisors, 1 canine tooth, 2 premolar teeth, and 3 molar teeth. Teeth deciduas (milk
teeth) in children amounted to 20 pieces (left and right) and top-bottom 5 teeth. Teeth in
children are replaced by permanent premolar teeth. Which time and teeth that erupt can vary.
The top wall of the cavity is formed by the hard palate and soft palate.

Pharynx

As the first part of the tractus digestivus is pharynx. The cranial end of the pharynx
reaches the crania base, located dorsal choanae and in the ventral direction associated with
the oral cavity.
Pharynx can be divided into 3 parts, namely:
Nasopharynx, oropharynx, and laryngopharynx. The dorsal pharynx is protected by
six cervical vertebrae where between the bones and the pharynx there is a connective tissue
that allows the tube to move freely. On the dorsal larynx, the pharynx continues to become
the esophagus. The esophagus is made up of muscle tissue, in which the ventral walls and
dorsal walls meet and only open when passed by food. Pharynx has a relationship with cavum
oris, rice cavum, and larynx. Thus pharynx can be considered as a tube that has a dual
function, namely the passage of respiration air and food (from the oral cavity through the
pharynx to the esophagus). On the lateral wall of the nasopharynx there is an estuary of the
eustachian tube that connects the pharynx to the middle ear space so that the tympani
membrane gets the same air pressure on both surfaces.
Salivary Glands:
• Parotid glands
• Sublingualist glands
• Submaxillary gland

Oesophagus
Pharynx at the level of the cervical vertebra VI continues to become the esophagus.
At the same place, the larynx continues to become the trachea which is ventral to the
esophagus. The esophagus is a tube formed by muscle tissue with a length of approximately
10 inches (25 cm). The 2 inch cranial tip is located in the neck and the rest is inside the
thoracic cavity. In general it can be said that the location of the esophagus is at the median
linea, initially located in the ventral corpus vertebrae and dorsal trachea, the caudal to the
dorsal of the heart and ventral to the thoracal aorta. The caudal end of the esophagus turns to
the left, penetrates the diaphragm and enters the abdominal cavity and empties (continues) on
the stomach (ventriculus). The muscle tissue that forms the esophagus consists of an outer
layer in which the fibers are longitudinal and the inner layer is circular (circular), the
contraction of these muscle fibers produces peristaltic movements that push food (bolus)
towards the caudal (towards the anal).

Gastrer
Pharynx at the level of the cervical vertebra VI continues to become the esophagus.
At the same place, the larynx continues to become the trachea which is ventral to the
esophagus. The esophagus is a tube formed by muscle tissue with a length of approximately
10 inches (25 cm). The 2 inch cranial tip is located in the neck and the rest is inside the
thoracic cavity. In general it can be said that the location of the esophagus is at the median
linea, initially located in the ventral corpus vertebrae and dorsal trachea, the caudal to the
dorsal of the heart and ventral to the thoracal aorta. The caudal end of the esophagus turns to
the left, penetrates the diaphragm and enters the abdominal cavity and empties (continues) on
the stomach (ventriculus). The muscle tissue that forms the esophagus consists of an outer
layer in which the fibers are longitudinal and the inner layer is circular (circular), the
contraction of these muscle fibers produces peristaltic movements that push food (bolus)
towards the caudal (towards the anal).
Duodenum
It is the cranial end of the intestine tenue, about 25 cm in size. consists of 4 parts,
namely:
• Pars superior
• Pars descendens duodeni
• duodene pars horizontalis
• Pars ascendens duodeni
Jejunum and Ileum
Overall the length of the intestine tenue is 5-8 m
Intestinum Crassum
approximately 1.5 m long. consists of: cecum and vermiform process, colon, and
rectum.
Colon
consists of: ascendent colon, colon descendens, sigmoid colon, and ascendent colon
The rectum is the caudal (anal) part of the crassum intestine, the retroperitoneal location
Pancreas
is an exocrine and endocrine gland, peritonel location, consisting of caput, collum,
corpus, and cauda.
Lien

 Lymphoid organs (not organ digestivus)

 Holotomy: the normal hypochondrium region
 Soft
 Intraperitoneal
 Vascular-reservoir of blood
Liver
The largest organ, sorrel, solid consistency
Holotomy: from the hypochondrium region dexter to the epigastric region
Intraperitoneal
Wrapped by Glissoni Capsules
Form of hemispherium
Consists of: dexter lobe, sinister lobe, qaudatus lobe & quadratus lobe
Diaphragmatica Facies & Visceral Facies

Porta hepatis
The entry and exit of structures to and from the liver:

 Veins Porta and its branches

 Ductus Cysticus, Ductus Hepaticus, Ductus Choledochus.
 A. Hepatica propria dextra et sinistra
 Lymph Lymph nodes & veins

Vesica Fellea
Muscular sac Consists of:

 Fundus
 Corpus
 Collum
Located between the dexter lobe & quadratus lobe. In the ventral Duodenum & Transverse
Colon
Abdominal muscles
Ventral abdominal muscles (ventero-lateral):
1. M. rectus abdominis
2. M. obliquus externus abdominis
3. M. obliquus internus abdominis
4. M. transversus abdominis
Dorsal abdominal muscles:
1. M. psoas major & minor
2. M. quadratus lumborum

Vasa Abdominis
• Abdominal aorta
• inferior Vena cava
• Veins portae hepatis
Vascularization and innervation
a. Arteriae

 A. pancreaticoduodenalis superior (A.gastroduodenalis branch)

 inferior A.pancreaticoduodenalis (A.mesenterica cranialis branch)
 A.pancreatica magna and A.pancretica caudalis and inferior A.lienalis branches
b. Venae
Venae who is in accordance with her arteries flows blood to the port system.
c. Lymphatic Flow
Lymph nodes are located along the arteries that bleed Pancreas. Efferent vessels
finally drain lymph fluid into the lymph nodes of the coeliaci and mesenteric superiores.
d. Innervation
Derived from the fibers of the sympathetic nerve (celiac ganglion) and parasympathetic
(vagus).
HISTOLOGY
2. Explain the pathomechanism of pain in the patient's stomach wall in the scenario?

A. Understanding Pain
Pain as a subjective sensory and emotional experience
not fun that is related to tissue damage acute nature that is felt in the events
where it occurs damage. Pain is a sensory pain and emotional experience that
is not fun related to actual and network damage potential.

B. Pain Classification
a. Duration Classification of Pain
1) Acute pain
Acute pain is pain that occurs after acute injury, disease, or surgical intervention and
has a fast process with intensity
which varies (mild to severe). Acute pain is short duration (approximately 6 months)
and will disappear without treatment after the damaged area has recovered.

2) Chronic pain
Chronic pain is a constant, intermittent pain that persists
over a period of time, this pain lasts long with
the intensity varies and usually lasts more than 6 months.

b. Pain Classification Based on Origin

1) Nociceptive pain
Nociceptive pain is pain caused by the activity or sensitivity of peripheral nociceptors
which are special responder that deliver naxious stimuli. This nociceptor pain can
occur because of the presence of a stimulus that affects the skin, bones, joints,
muscles, connective tissue, and others. This process goes through several stages,
which begins with stimulation, transduction, transmission, modulation, and
perception.
2) Neuropathic pain
Neuropathic pain is the result of an injury or abnormality that is acquired in peripheral
or central nerve structures, this pain is more difficult to treat.

c. Based on the source of pain, the pain is divided into:

1) Outside somatic pain
Pain whose stimulus comes from the skin, subcutaneous tissue and
mucous membrane. Pain is usually felt like burning, sharp and
localized.
2) Deep somatic pain
Dullness and not well localized due to stimulation of skeletal muscles, bones, joints,
connective tissue.
3) Visceral pain
Pain due to stimulation of visceral organs or organs that cover it (parietal pleura,
pericardium, peritoneum). This type of pain is divided into localized visceral pain,
localized parietal pain, visceral transfer pain and parietal pain over
 C. Pathomechanism Nociceptive Pain

Transduction. Is a change in pain stimulation (noxious stimuli) into electrical activity

in sensory nerve endings. Algesic substances such as
prostaglandin, serotonin, bradykinin, leukotriene, substance P, potassium,
histamine, lactic acid and others will activate or sensitize
pain receptors. Pain receptors are woven edges
free afferent fibers A-delta and C. These receptors are often found in the skin tissue,
periosteum, in the dental pulp and tissues
another body. Afferent nerve fibers A-delta and C are nerve fibers
sensory function has the function of continuing sensory pain from peripheral to
central to the central nervous system. Interaction between algesic substances and receptors
pain causes the formation of pain impulses. Transduction is
the process of pain stimulation is configured in forms that can be accessed by
brain. The transduction process starts when the nociceptor is the receptor
function to receive activated pain stimuli. Activation of this receptor
(nociceptors) is a form of response to a stimulus
come like network damage.
Transmission / Transmission. Transmission is a series of neural events that carry electrical
impulses through the nervous system to the area of the brain. The transmission process
involves afferent nerves formed from small to medium-diameter nerve fibers and large-
diameter ones. Afferent nerves will accuse the dorsal horn in the spinal cord. Furthermore
this transmission is continued through the contralateral spinalthalamic system through the
lateral ventral of the thalamus to the cerebral cortex.
Modulation / Modulation. The modulation process refers to neural activity in an effort to
control the nociceptor transmission line. The modulation process involves a complex neural
system. When pain impulses reach the nerve center, the transmission of pain impulses will be
controlled by the central nervous system and transmit these pain impulses to other parts of the
nervous system such as
cortex section. Furthermore this pain impulse will be transmitted through
descend nerves to the spine to modulate effectors.
Perception / Perception. Perception is a subjective process. This perception process is not
only related to physiological processes or anatomical processes, but also includes cognition
and memory. Therefore, psychological, emotional, and berhavioral (behavioral) factors also
appears as a response in perceiving the experience of the pain.
This process of perception is also what makes the pain a phenomenon
which involves multidimensional.

Inflammation is a tissue response to destructive physical or chemical stimuli. This stimulation

causes the release of inflammatory mediators such as histamine, serotonin, bradykinin, and
prostaglandins which cause inflammatory reactions in the form of heat, pain, redness,
swelling and accompanied by impaired function. Cell damage associated with inflammation
affects the membranes of cell membranes that cause leukocytes to secrete lysosomal enzymes
and arachidonic acid. Arachidonic acid metabolism produces prostaglandins-prostaglandins
which have effects on blood vessels, nerve endings, and on cells involved in
inflammation. The process of inflammation is actually wrong
a self-defense mechanism from the body against foreign objects, but if this process continues
continuously (chronic) it will damage the tissue.
Cyclooxygenase (COX) enzyme is an enzyme that catalyzes
prostaglandin synthesis of arachidonic acid. NSAID drugs block action from
COX enzymes that reduce the production of prostaglandin mediators, where this is
produce both positive and positive effects (analgesia, anti-inflammatory)
or negative (gastric ulcer, decreased renal perfusion and bleeding). COX activities are
associated with two isoenzymes, namely ubiquitously and
constitutive which is expressed as COX-1 and which is induced by COX-2 inflammation.
COX-1 is mainly found in the gastric mucosa, renal parenchyma and platelets. This enzyme
is important in homeostatic processes such as platelet aggregation, the integrity of the
gastrointestinal mucosa and kidney function. Conversely, COX 2 is inducible and is
expressed primarily in places of trauma (brain and kidney) and causes inflammation, fever,
pain and cardiogenesis. Transient COX-2 regulation in the spinal cord in response to
inflammation may be important in central sensitization.

D. Abdomen pain Visceralis

Visceral pain is pain due to stimulation of visceral organs or membranes that cover it (parietal
pleura, pericardium, peritoneum). This type of pain is subdivided into localized visceral pain,
localized parietal pain, visceral transfer pain and parietal pain. The location of origin of
visceral pain is difficult to determine because the number of receptors is only small. Often
accompanied by involvement of the autonomic nervous system in the presence of nausea,
sweating and changes in blood pressure. Adequate stimulation is strain, spasm or excessive
wrinkling of smooth muscle, ischemia and chemistry. Usually visceral pain is also
accompanied by muscle wrinkles that are near the affected visceral. It aims to protect the
visceral pain. Visceral pain is transmitted by type C nerve fibers. Occurs when there is
stimulation of the organs / structures in the abdominal cavity. Visceral peritoneum covering
the abdominal organs is innervated by the autonomic nervous system and insensitive to
palpation or cutting. So that the incision / suture in the intestine can be done without being
felt by the patient. However, if an organ pull / strain or excessive muscle contraction causes
ischemia (eg, colic or inflammation, pain will arise). This pain cannot be shown exactly
where the pain is.
Typical pattern with embryonal innervation of the organs involved. The gastrointestinal tract
originating from the front intestine (foregut), which is the stomach, duodenum, hepatobiliary
system and pancreas causes pain in the pit of the stomach (epigastrium). The gastrointestinal
tract (midgut), which is the small intestine to the middle of the transverse colon, causes pain
around the umbilicus. The gastrointestinal tract of the back of the intestine (hindgut), which is
mid-colon to the sigmoid colon causes pain in the lower abdomen. Likewise, pain from the
bladder and rectosigmoid. Because it is not accompanied by peritoneal excitement, this pain
is not affected by movement, so the patient can usually move actively. The cause:

a. Chemical stimuli. At one point, the damaged material coming out of the gastrointestinal
tract enters the peritoneal cavity. For example, proteolytic acid in gastric juice can often come
out of a torn stomach or duodenic ulcer. This sap then causes the digestion of the peritoneum
(the serous membrane coated with the visceral abdominopelvis wall), which stimulates a very
broad area of pain fibers. The pain that arises is usually very great.

b. Ischemia. Ischemia or blockage of the arteries flowing to the muscles that are actively
working causes visceral pain in the same way as the onset of pain in other tissues, perhaps
due to the formation of acidic metabolic end products or products produced by degenerative
tissues such as bradykinin, proteolytic enzymes ( protein breaking enzymes) or other
ingredients that stimulate the ends of pain fibers.

c. Hollow viscus spasm. Often the pain that arises from a spastic viscus (spasm: involuntary
smooth muscle contraction) is triggered in the form of cramps with pain that intensify and
then disappear. Viscus is a cavity in the abdomen. This process continues repeatedly, arising
every few minutes. The onset of the repetitive cycle is caused by repetition of smooth muscle
contractions. For example, this cramping state will arise every time a peristaltic wave spreads
through the spastic intestine. Cramp type pain often occurs in appendicitis, gastroenteritis,
constipation, menstruation, labor, gallbladder abnormalities or ureteral obstruction.

d. Excessive distention of the hollow viscus. Hollow viscus when overfilled will also cause
pain, this may be caused by the tissue itself being too stretched. Excessive distension can also
constrict the blood vessels that surround the organ of the viscera or through the organ walls of
the viscera, so it may stimulate the onset of pain ischemia.

e. Viscera that is not sensitive. A small part of the viscera organ area is almost completely
insensitive to any type of pain. This area includes the area of the liver parenchyma and
pulmonary alveoli. Apparently, the liver capsule is very sensitive to direct trauma and
stretching, and the bile duct is also sensitive to pain.

The nature of visceral pain is:

a. Pain relief. Occurs if an innervation segment serves> 1 area, for example, innervation of
the diaphragm originating from the neck region C 3-5 moves downward in the embryonal
period, so stimulation of the diaphragm by bleeding / inflammation will be felt in the joint.

b. Radiation Pain. Pain spreads in the same system / anatomical pathway, for example,
ureteric colic or renal colicky colic, usually felt up to the external genitals (labium major
(female) or testicles). Sometimes it is difficult to distinguish from pain over.

c. Projection Pain. Caused due to sensory nerve stimulation nerve injury / inflammation.

d. Continuous Pain.
As a result of stimulation of the parietal peritoneum which is continuous, for example, in an
inflammatory reaction. On examination of patients with peritonitis, local pain was found.
Abdominal wall muscles show the muscular defect reflexively protects the inflamed part and
avoids local movements or pressures.
e. Colic pain.
Visceral pain due to spasm of hollow smooth muscle and usually caused by the obstruction of
passages in these organs (intestinal obstruction, ureteric stones, gallstones, increased
intraluminer pressure). Pain arises from hypoxia which is experienced by the canal wall
tissue. Because these contractions pause, colic is felt to be lost. The initial phase of intestinal
wall bleeding disorders is also colic pain. Usually accompanied by feelings of nausea and
even vomiting. During an attack, the patient is very nervous, sometimes rolling around in bed
or on the road. Triassic colic, a distinctive sign that consists of an attack of abdominal pain
accompanied by nausea or vomiting accompanied by forced motion.

f. Ischemic Pain.
Severe pain, persistent, and not receding. It is a sign that the tissue is threatened with
necrosis. Furthermore, there are signs of general intoxication such as tachycardia,
deterioration of the general condition, and shock due to resorption of toxins from necrotic
tissue.

E. Somatic Abdomen Pain

Very localized pain can originate from the parietal peritoneum (somatic pain). Parietal pain is
mediated by delta C and A nerve fibers, which are responsible for the transmission of very
acute, sharp, more localized pain sensations. Direct irritation of the somatic parietal
peritoneum (especially the upper and anterior) by pus, urine or gastrointestinal secret leads to
a very localized pain state. Colic pain is a loss of pain (coming and goes in waves) that shows
an obstruction of a hollow organ (lumen), a muscle-walled organ (intestine, bile, bile duct,
ureter). Burning: usually indicates due to acidic effects and is associated with the stomach,
duodenum or distal part of the esophagus.
a. Renal colic: colic pain in the renal angle, which is painful when pressed, radiates to the
pelvis / scrotum / labia.

b. Bladder pain: severe diffuse pain in the suprapubic region

c. Prostate pain: blunt pain that is felt in the lower abdomen, rectum, perineum or anterior
thigh

d. Urethral pain: varies greatly from discomfort to severe sharp pain that is felt at the end of
the urethra (penis tip in men) and is more painful when micturition.

e. Small bowel obstruction: central colic pain associated with vomiting, distension and
constipation
f. Colonic pain: sometimes pain can be temporarily reduced by defecation or flatus

g. Intestinal ischemic: blunt, severe, constant / constant, right upper / central quadrant
abdominal pain which increases when eating

h. Gallbladder pain: severe, constant / upper right, epigastric right quadrant pain and often
worsens after eating fatty foods (fatty foods)

i. Pancreatic pain: epigastrium, radiating to the back, improving when sitting and leaning
forward.
j. Peptic ulcer pain: blunt, burning pain in the epigastrium. Typical night episodes, wake the
patient from sleep. It is exacerbated by eating and sometimes sometimes reduced by drinking
milk or antacids.

3. Why pain can spread from the pit of the stomach to the abdominal wall ?

Jawab :

The splanchnic and the cerebrospinal are the two neural pathways available for transmission
of abdominal pain. Pacinian corpuscles and free nerve endings in the walls of the viscera are
the splanchnic afferent nerve receptors. They are sensitive only to stretch and spasm. By
contrast, receptors of the cerebrospinal nerves are sensitive to pressure, friction, cutting,
burning, and any other stimulus that can be appreciated by skin. In the dorsal root ganglia the
splanchnic and cerebrospinal cell bodies are side by side. Their proximal fibers also terminate
in close proximity within the spinal cord. The close relationship of these anatomic pathways
may account for the fact that severe visceral pain, such as rapid distention of a viscus, may
"spill over" into somatic segments (viscerosensory and visceromotor reflexes) in the absence
of somatic nerve irritation. Understanding of "spillover" pain is essential for accurate
diagnosis of abdominal pain.

Since the embryonic gut and its appendages arise as midline organs, their splanchnic
innervation is bilateral, and accordingly, visceral pain is perceived in the midline.
Cerebrospinal nerves to the parietal peritoneum (T6 through T12) have the same segmental
arrangement as the lower thoracic dermatomes. There are no nerve fibers in the visceral
peritoneum.

Upper abdominal organs have anatomic features that make pain patterns emanating from them far
more complex than those of the appendix. Painful lesions of the gastroesophageal junction, the fundus
and lesser curvature of the stomach, the biliary tract, and proximal portions of the duodenum
commonly produce pain in the interscapular zone corresponding to the sixth thoracic segment, since
the somatic innervation of the lesser omentum is supplied by that thoracic nerve. Pancreatic pain is
often perceived in the same location one segment lower.

The stomach is so situated that portions of its surface are in contact with the diaphragm, the
gastrohepatic ligament, the lesser sac, the pancreas, the parietal peritoneum, the splenic hilus, the
gastrocolic ligament, the transverse mesocolon, and the transverse colon. Inflammatory or neoplastic
lesions of the stomach that involve any of these surfaces may irritate somatic nerves from several
different spinal segments. Accordingly, pain may be localized by the patient to the supraclavicular
fossa from phrenic nerve stimuli, the interscapular region from irritation of T6 through T8, or even the
lumbar region from involvement of the T12 through L1 spinal cord segments.

Similarly to the stomach, the duodenum is in anatomic relationship to a number of somatic

cerebrospinal nerve roots. As a result, perforating ulcer pain can be appreciated in the interscapular
zone, the right subcostal region, and the right lower quadrant depending on which somatic nerves are
involved in the pathologic process. Retroperitoneal perforation of the duodenum from blunt
abdominal trauma may cause irritation of the genitofemoral nerve from leaking duodenal contents
resulting in pain in the right testicle or labia.

Pain from the gall bladder and biliary tract may have bilateral localization because they arise from
outbudding of the midline gut and have bilateral splanchnic innervation. If the inflammatory process
of acute suppurative cholecystitis involves the parietal peritoneum of the right upper quadrant,
somatic pain with its usual local manifestations and referred pain along the involved cerebrospinal
nerve to the tip of the scapula (T8) may be present. Involvement of the parietal peritoneum in the right
upper quadrant from suppuration of the gall bladder is not a very common event, as the greater
omentum (which has no somatic sensory innervation) often surrounds the inflamed gall bladder as a
buffer between the inflammatory process and the parietes.

Pathologic conditions that arise from the pancreas are responsible for a broad spectrum of pain-
producing syndromes. In addition, extrinsic lesions (e.g., penetrating duodenal ulcer) are frequently
involved in the production of pain from the pancreas. Further, disruption of the integrity of the gland
by pancreatitis permits the extravasation of enzymes that spread to many different intra-abdominal
locations that may involve somatic spinal pathways from the phrenic nerve to the lumbosacral plexus.

The small intestine, like the rest of the midgut, produces upper midline, periumbilical visceral pain in
response to distention or stretch. The foregut and hindgut are far less sensitive to stretch or distention.
Pain from these portions of the intestinal tract, the stomach and duodenum from the former and the
descending colon and rectum from the latter, is more often initiated by inflammatory lesions than
from distention.

Experimental studies of the production of pain from the gastrointestinal tract in humans by inflation of
balloons at various locations within the lumen of the gut should be interpreted very cautiously, as they
bear little or no resemblance to actual pathologic conditions that produce pain in humans. The most
valid observations concerning the origins of abdominal pain come from surgeons who have the
advantage of prompt inspection of the site of pathology within the abdomen and the opportunity to
compare these findings on the spot with the patient's perception of the abdominal pain.

The skin, subcutaneous tissues, fascia, muscle, and parietal peritoneum of the abdominal wall are
richly supplied with somatic nerves from T6 through T12. Pain in the abdominal wall can result from
neuromas in scars from previous laparotomies, such medical conditions as acute porphyria, or from
herpes zoster. In addition, pain from trauma to the abdominal wall from blunt injury must be carefully
identified to rule out abdominal pain originating from an intraperitoneal injury.

The ureters are second only to the pancreas as a source of abdominal pain caused by structures in the
retroperitoneum. The renal pelvis is sensitive to distention, and the ureters are richly supplied with
nerves from T10 through T12. Ureteral pain is ipsilateral, severe, and cramping in nature (renal colic).
It is usually of such severity and located in the flank that the diagnosis is difficult to confuse with
other abdominal catastrophies. Pain in the testicle or labia (T10) may on occasion confuse the
diagnosis of renal colic with retrocecal appendicitis. The presence of red blood cells in the urinalysis
may help solve this diagnostic dilemma.

Since the lower intercostal nerves also provide the parietal pleura and periphery of the diaphragm with
sensory (somatic) innervation, as well as the abdominal wall and anterior peritoneal parietes, it is
understandable that inflammatory processes that involve the parietal pleura innervated by these
nerves may also be manifested by abdominal pain. Needless to say, an appendectomy is poor therapy
for right lower lobar pneumonia that has produced reflex abdominal wall pain in the right lower
quadrant.

Pericarditis, myocardial infarction, and pulmonary infarction may also cause inflammatory lesions
that involve the parietal diaphragmatic or thoracic pleura, producing referred abdominal pain that
may be misdiagnosed as a primary intraperitoneal disorder

4. Explain the types of acute abdominal pain?

 kinds of abdominal pain :
 Abdominal pain by type
Abdominal pain can be either visceral pain or somatic pain, and can originate from various
processes in various organs in the abdominal cavity or outside the abdominal cavity, for
example in the chest cavity.
a. Visceral pain
Visceral pain occurs when there are stimuli in organs or structures in the abdominal cavity,
for example due to injury or inflammation. The viserale peritoneum covering the abdominal
organs is innervated by the autonomic nervous system and is not sensitive to touching, or
cutting. Thus the incision or suturing of the intestine can be carried out without being felt by
the patient. However, if done by pulling, stretching or excessive contraction of the muscles
that causes ischemia, such as in colic or inflammation can cause pain. Patients who
experience visceral pain usually cannot show the exact location of pain so that usually he
uses the entire palm of his hand to point to the painful area.
Visceral pain shows a characteristic pattern according to the embryonal innervation of the
organ in question. The gastrointestinal tract originating from the front intestine (foregut),
namely the stomach, duodenum, hepatobiliary system and pancreas causes pain in the pit of
the stomach or epigastrium. The gastrointestinal tract originating from the middle intestine
(midgut), namely the small intestine and the large intestine to the middle of the transverse
colon causes pain around the umbilicus. The other gastrointestinal tract, which is midway
through the transverse colon to the sigmoid colon originating from the back intestine
(hindgut), causes pain in the lower abdomen. Likewise, pain from the bladder and
rectosigmoid (see Figure 2.1A). Because it is not accompanied by peritoneal stimulation, this
pain is not affected by movement so that the patient can usually actively move.

b. Somatic pain
Somatic pain occurs due to stimulation in the part that is innervated by the peripheral nerve,
such as strain on the parietal peritoneum, and injury to the abdominal wall. Pain is felt like
being pierced or slashed, and the patient can correctly pinpoint the location of the pain with
his finger. These stimuli that cause pain can be palpation, pressure, excitatory chemistry or
inflammation processes.
Table 2.1. Sensory innervation of the abdominal organs

Organ or structure nerve Level of innervation

the middle part of the N. phrenic C3-5
diaphragm
Edge of diaphragm, stomach, Seliakus plexus Th 6-9
pancreas, gallbladder, small
intestine
Appendix, proximal colon, Mesenteric plexus Th 10-11
and pelvic organs
Kolon distal, rektum, ginjal, N. caudal splanknikus Th 11-L1
ureter, dan testis
Bladder, rectosigmoid Hypogastric plexus S2-S4
Friction between the inflamed viscerals will cause peritoneal excitement and cause pain.
Inflammation itself or friction between the two peritoneums can cause changes in pain
intensity. This friction causes contralateral pain in acute appendicitis. Every movement of the
sufferer, whether in the form of body movements or deep breath movements or coughing,
will add to the pain so that patients with severe stomach accompanied by stimulation of the
peritoneum try not to move, breathe shallow and hold the stone.
Table 2.2. Location of somatic pain

location organ
Upper right abdomen Gallbladder , liver, duodenum, pancreas,
colon, lung, myocardium
Epigastrium Stomach , pancreas, duodenum, lung,
colon
Upper left abdomen spleen , colon, kidney, pancreas, lung
Lower right abdomen Appendix , adnexa , cecum, ileum, ureter
Lower left abdomen (Colon , adnexa , Colon , adnexa , ureter
ureter
Suprapubic bladder , uterus, small intestine
Periumbilikal small intestine
Waist / back pancreas , aorta, kidney
Shoulder diaphragm

5. How to reduce the pain that patients feel related to the scenario?
Non-pharmacological methods
Includes such techniques as superficial heat and cold, massage, relaxation, imagery,
prayer/spiritual practices, pressure or vibration, and therapeutic communication.
Consider Non-Pharmacological Management
NON-PHARMACOLOGICAL MANAGEMENT
Combine pharmacological methods with non-pharmacological methods to achieve effective
pain management and:
• Institute educational and psycho-educational interventions as part of the overall plan
of treatment for pain management;
• Implement educational and psychosocial interventions that facilitate coping of the
patient and family early in
the course of treatment;
• Non-pharmacological methods of treatmentshould notsubstitute for adequate
pharmacological management. Any
potential contraindications to non-pharmacological methods should be considered prior to
application. Selection of non-pharmacological methods should be based on individual
preference, and may include strategies such as:
  Superficial heat and cold;
 Massage;
 Relaxation;
 Imagery;
 Prayer/spiritual practices;
 Pressure/vibration;
 Music
 Cognitive /behavioral therapy
 Consult the Child Life Worker who can assist with distraction during painful
procedures
 Parental/family involvement with a child’s pain
 Positioning infants is an effective pain control technique (i.e. swaddling, cuddling)
 Sucrose is effective in controlling behavioural responses to pain in infants up to one
year.

6. is there a relationship between drugs consumed for a long time and abdominal pain
that patients feel in the scenario?
Nonsteroidal anti-inflammatory drugs (NSAIDs) can dam- age the gastrointestinal
tract, causing widespread morbidity and mortality. Although mechanisms of damage involve
the activities of prostaglandin-endoperoxide syn- thase 1 (PTGS1 or cyclooxygenase [COX]
1) and PTGS1 (COX2), other factors are involved. We review the mecha- nisms of
gastrointestinal damage induction by NSAIDs via COX-mediated and COX-independent
processes. NSAIDs interact with phospholipids and uncouple mitochondrial oxidative
phosphorylation, which initiates biochemical changes that impair function of the
gastrointestinal barrier. The resulting increase in intestinal permeability leads to low-grade
inflammation. NSAID inhibition of COX enzymes, along with luminal aggressors, results in
ero- sions and ulcers, with potential complications of bleeding, protein loss, stricture
formation, and perforation. We propose a model for NSAID-induced damage to the
gastrointestinal tract that includes these complex, inter- acting, and inter-dependent factors.
This model highlights the obstacles for the development of safer NSAIDs.
There have been many studies of the pathogenesis of NSAID-induced gastrointestinal
damage. NSAIDs inhibit prostaglandin-endoperoxide synthase 1 (PTGS1 or cyclo-
oxygenase [COX] 1) and COX2, which were believed to mediate the gastrointestinal damage.
NSAID-induced decreases in mucosal levels of prostaglandins (driven by inhibition of
COX1) correlate with gastric and small bowel damage, which can be attenuated by
administration of exogenous prostaglandins.Because COX2 is not constitutively expressed in
the gastrointestinal tract, COX2 selective inhibitors are perceived as safer than conventional
NSAIDs.Proposed mechanisms of damage to the stomach involve prostaglandin-mediated
increased gastric acid secretion, decreased mucus and bicarbonate secretion, decreased cell
proliferation, and decreased mucosal blood flow.These are all actions that are detrimental to
mucosal defense and healing, but the observed changes were only modest and the damage
seemed to lack an initiative action. Furthermore, decreased mucosal pros- taglandins have
been found to be less important in the pathogenesis of small bowel damage.
Further studies found that gastric and small bowel mucosal prostaglandins could be decreased
by 95% - 98% without mucosal damage,and confirmed in COX1- knockout mice. Short-term
loss or inhibition of COX2 does not cause damage, but small bowel damage is evident in
mice and humans exposed to NSAIDs for long periods of time. Dual inhibition of COX1 and
COX2 causes gastric and small bowel lesions, albeit somewhat less severe than the lesions
caused by conventional acidic NSAIDs.
The 3-dimensional structure of the COX enzymes reveals the active site of both COX
isoforms to be at the end of a hydrophobic channel. NSAIDs inhibit the enzyme by block- ing
the entrance of arachidonic acid to this channel and thereby denying substrate access to the
active site.The COX1 and 2 channels differ. Conventional NSAIDs have access to both
channels and form an ionic bond via their carboxyl or enolic group. The COX1 channel is
smaller than the channel in COX2 and does not accommodate COX2- selective agents, but a
side pocket in the COX2 enzyme has a polar binding site for the aryl sulfonamide and sulfone
moieties of the COX2-selective agents.
The most damaging consequence of decreased prostaglandin production with COX inhibition
could be the effects on the microcirculation. Regulation and maintenance of the intestinal
microcirculation is complex, involving several interacting biochemical mech- anisms. The
most relevant mediators are prostaglandins, leukotrienes, nitric oxide, and hydrogen sulfide.
NSAID- induced prevention of physiological compensatory increases in blood flow (leading
to tissue hypoxia) after injury is well described. The effects of nitric oxide and hydrogen
sulfide are remarkably similar to that of pros- taglandins, namely increased microvascular
blood flow, increased mucus secretion, and a modest decrease of gastric acid
secretion.Targeting these processes with nitric oxide donors, such as nitroglycerine,
nitroprusside, nitric-oxide NSAIDs, and hydrogen sulfite NSAIDs can reduce the
gastrointestinal damage due to NSAIDs in laboratory animals. Presumably these effects
counteract the reduced microvascular blood flow consequent to NSAID-induced decreased
prostaglan- dins. Proof-of-concept endoscopic studies of healthy volunteers found that nitric
oxide donors and NSAIDs reduced gastroduodenal damage compared with NSAIDs, but the
results of a llonger-term clinical trial did not show statistically significant differences.
Another vascular effect of NSAIDs involves NSAID- induced expression of neutrophil
adhesion molecules within the endothelium (common to most intestinal inflammatory
conditions).Neutrophil accumulation could mechanically compromise microvascular blood
flow. Nitric oxide and hydrogen sulfite are, like prosta- glandins, inhibitors of leukocyte
adhesion to the vascular endothelium.
However, vascular effects are probably not the primary or initiating event in NSAID-induced
gastrointestinal damage. The effects on the vasculature cannot account for the selective
localization of the macroscopic damage within the gastrointestinal tract or the mesenteric
rather than the anti-mesenteric location of small bowel ulcers. The damage also differs
macroscopically and microscopically from ischemic damage. The suggestion that neutrophil
adhesion to the vessel wall (a COX2- mediated effect) is a primary event in the damage is
difficult to reconcile with the fact that COX2 is not constitutively expressed in the
gastrointestinal tract. Furthermore, neutrophil adhesion to the intestinal vessel wall does not
automatically indicate damage, as neutrophils require a chemoattractant for activation-
degranulation and, hence, damage.
7. What is the relationship between rheumatism and pain in the scenario?
Nonsteroidal anti-inflammatory drugs (NSAIDs) can dam- age the gastrointestinal
tract, causing widespread morbidity and mortality. Although mechanisms of damage involve
the activities of prostaglandin-endoperoxide syn- thase 1 (PTGS1 or cyclooxygenase [COX]
1) and PTGS1 (COX2), other factors are involved. We review the mecha- nisms of
gastrointestinal damage induction by NSAIDs via COX-mediated and COX-independent
processes. NSAIDs interact with phospholipids and uncouple mitochondrial oxidative
phosphorylation, which initiates biochemical changes that impair function of the
gastrointestinal barrier. The resulting increase in intestinal permeability leads to low-grade
inflammation. NSAID inhibition of COX enzymes, along with luminal aggressors, results in
ero- sions and ulcers, with potential complications of bleeding, protein loss, stricture
formation, and perforation. We propose a model for NSAID-induced damage to the
gastrointestinal tract that includes these complex, inter- acting, and inter-dependent factors.
This model highlights the obstacles for the development of safer NSAIDs.
There have been many studies of the pathogenesis of NSAID-induced gastrointestinal
damage. NSAIDs inhibit prostaglandin-endoperoxide synthase 1 (PTGS1 or cyclo-
oxygenase [COX] 1) and COX2, which were believed to mediate the gastrointestinal damage.
NSAID-induced decreases in mucosal levels of prostaglandins (driven by inhibition of
COX1) correlate with gastric and small bowel damage, which can be attenuated by
administration of exogenous prostaglandins.Because COX2 is not constitutively expressed in
the gastrointestinal tract, COX2 selective inhibitors are perceived as safer than conventional
NSAIDs.Proposed mechanisms of damage to the stomach involve prostaglandin-mediated
increased gastric acid secretion, decreased mucus and bicarbonate secretion, decreased cell
proliferation, and decreased mucosal blood flow.These are all actions that are detrimental to
mucosal defense and healing, but the observed changes were only modest and the damage
seemed to lack an initiative action. Furthermore, decreased mucosal pros- taglandins have
been found to be less important in the pathogenesis of small bowel damage.
Further studies found that gastric and small bowel mucosal prostaglandins could be decreased
by 95% - 98% without mucosal damage,and confirmed in COX1- knockout mice. Short-term
loss or inhibition of COX2 does not cause damage, but small bowel damage is evident in
mice and humans exposed to NSAIDs for long periods of time. Dual inhibition of COX1 and
COX2 causes gastric and small bowel lesions, albeit somewhat less severe than the lesions
caused by conventional acidic NSAIDs.
The 3-dimensional structure of the COX enzymes reveals the active site of both COX
isoforms to be at the end of a hydrophobic channel. NSAIDs inhibit the enzyme by block- ing
the entrance of arachidonic acid to this channel and thereby denying substrate access to the
active site.The COX1 and 2 channels differ. Conventional NSAIDs have access to both
channels and form an ionic bond via their carboxyl or enolic group. The COX1 channel is
smaller than the channel in COX2 and does not accommodate COX2- selective agents, but a
side pocket in the COX2 enzyme has a polar binding site for the aryl sulfonamide and sulfone
moieties of the COX2-selective agents.
The most damaging consequence of decreased prostaglandin production with COX inhibition
could be the effects on the microcirculation. Regulation and maintenance of the intestinal
microcirculation is complex, involving several interacting biochemical mech- anisms. The
most relevant mediators are prostaglandins, leukotrienes, nitric oxide, and hydrogen sulfide.
NSAID- induced prevention of physiological compensatory increases in blood flow (leading
to tissue hypoxia) after injury is well described. The effects of nitric oxide and hydrogen
sulfide are remarkably similar to that of pros- taglandins, namely increased microvascular
blood flow, increased mucus secretion, and a modest decrease of gastric acid
secretion.Targeting these processes with nitric oxide donors, such as nitroglycerine,
nitroprusside, nitric-oxide NSAIDs, and hydrogen sulfite NSAIDs can reduce the
gastrointestinal damage due to NSAIDs in laboratory animals. Presumably these effects
counteract the reduced microvascular blood flow consequent to NSAID-induced decreased
prostaglan- dins. Proof-of-concept endoscopic studies of healthy volunteers found that nitric
oxide donors and NSAIDs reduced gastroduodenal damage compared with NSAIDs, but the
results of a llonger-term clinical trial did not show statistically significant differences.
Another vascular effect of NSAIDs involves NSAID- induced expression of neutrophil
adhesion molecules within the endothelium (common to most intestinal inflammatory
conditions).Neutrophil accumulation could mechanically compromise microvascular blood
flow. Nitric oxide and hydrogen sulfite are, like prosta- glandins, inhibitors of leukocyte
adhesion to the vascular endothelium.
However, vascular effects are probably not the primary or initiating event in NSAID-induced
gastrointestinal damage. The effects on the vasculature cannot account for the selective
localization of the macroscopic damage within the gastrointestinal tract or the mesenteric
rather than the anti-mesenteric location of small bowel ulcers. The damage also differs
macroscopically and microscopically from ischemic damage. The suggestion that neutrophil
adhesion to the vessel wall (a COX2- mediated effect) is a primary event in the damage is
difficult to reconcile with the fact that COX2 is not constitutively expressed in the
gastrointestinal tract. Furthermore, neutrophil adhesion to the intestinal vessel wall does not
automatically indicate damage, as neutrophils require a chemoattractant for activation-
degranulation and, hence, damage.

8. what causes the patient's stomach to appear bloated?

Bloating is divided into 2 parts, namely:

a. Continuous, usually due to the mass or enlargement of orgasm in the abdomen such
as tumors, fluid (ascites), or fat tissue (overweight).
b. Temporary / intermittent, which is associated with increased gas or fluid in the
stomach, small intestine and large intestine.
Mechanism and Causes of Bloating Stomach
a. Excessive gas production, usually caused by bacteria, through 3 mechanisms. First,
the amount of gas produced by each individual is not the same because there are
certain bacteria that produce many gases while others do not. Second, foods that are
difficult to digest and absorb in the small intestine cause large amounts of food to
reach the large intestine so that the food that must be digested by bacteria will
increase and the resulting gas increases. Examples are in abnormalities of lactose
intolerance, pancreatic obstruction, and bile ducts. Thirdly, because of certain
conditions bacteria grow and develop in small intestine where it is usually supposed
to be in the large intestine. Usually this potentially increases flatus (farting).
b. Mechanical blockage. Blockage can occur along the stomach to the rectum, if it is
temporary it can cause temporary bloating. An example is the scarring in the gastric
valve which can interfere with the flow from the stomach to the intestine. After
eating food with the air swallowed, then after 1-2 hours the stomach expels acid and
liquid and mixes with food to help digestion. If there is an incomplete blockage
eating and digestion can enter the intestine and can overcome bloating. In addition,
the condition of stool that is too hard can also be a plug that can worsen bloating.
c. Functional blockage. What is meant by functional blockage is the result of weakness
that occurs in the muscles of the stomach and intestines so that the movement of the
digestive tract is not good which causes the movement of food to become slow and
 cause bloating. This can occur in gastroparesis, Irritable Bowel Syndrome (IBS) and
Hirschprung's. Besides food factors such as fat will also slow down the movement of
food, gas, and fluids into the lower digestive tract which also results in bloating.
Fiber used to treat constipation can also cause bloating without an increase in the
amount of gas, but the presence of bloating is caused by slow gas flow to the small
intestine due to fiber.
d. Gastrointestinal hypersensitivity. Some people have hypersensitivity to bloating,
they feel bloated even though the amount of food, gas, and fluid in the
gastrointestinal tract is within normal limits, usually when consuming foods that
contain fat.