FAKULTAS KEDOKTERAN Makassar, 10 January 2020

BLOK GASTROENTEROHEPATOLOGI
UNIVERSITAS MUSLIM INDONESIA
LAPORAN TUTORIAL MODUL III
BLOK GASTROENTEROHEPATOLOGI

Kelompok: 3 A
Tutor : dr. Zulfahmidah
Disusun Oleh :
Muhammad Rafly Thio (11020180106)
Nurul Aisyah Palo (11020180112)
Muhammad Al-Qidham Alqifari (11020160087)
A. Zihni Amalia (11020160139)
Resti (11020180006)
Abdul Raqib Rahman (11020180013)
Nia Anggreni (11020180031)
Ulfa Namirah (11020180040)
Restika (11020180048)
Masyita Damayanti Machmud (11020180063)
Syafira Ananda Marendengi (11020180077)
Nur Fadillah (11020180083)
Rodiyah Mulyadi (11020180086)
 FOREWORD

Let’s thank Allah SWT by His grace and guidance so that this tutorial report can be
completed on time. Aamiin

We are aware that there are still many shortcomings in this tutorial report, therefore
constructive criticism and suggestions are always expected to spur us to create better works.
Finally, we would like to thank all those who expected to support our group to create:

1. Dr. dr. Shofiyah Latief, Sp.Rad as the Chief of the Gastroenterohepatology

System

2. dr. Ratih Natasha, Sp.M, M.Kes as the Secretary of the

Gastroenterohepatology System

3. dr. Zulfahmidah as a tutor

4. Friends who have supported and helped provide motivation in completing this
tutorial report.

May Allah SWT be able to provide in return for all good and sacrifice with an abundance of
mercy from Him. Aamiin ya Robbal A'lamiin.

Makassar, 10 January 2020

SCENARIO 1

A 60 Years old man came to the IRD Hospital brought by his family with complaints of
thin black stools experienced since yesterday, frequency 2 times with quite a lot of volume.
Abdominal pain is not felt, nausea is present, vomiting is not present. Patients often complain
of weakness and lack of appetite since teh last 1 month. Previous history of rheumatism and
hepatitis was experienced 10 years ago.

A. DIFFICULT WORD
-

B. KEYWORDS
1. A 60 years old man.
2. Complaints thin black stools since yesterday.
3. Frequency 2 times with quite a lot of volume.
4. Nausea is present.
5. Weakness and lack off appetite since the last 1 month.
6. Previous history of rheumatism and hepatitis was experinced 10 years ago

C. QUESTIONS
1. Explain the Mechanism of Defect!
2. Explain the patomechanism of black stool, weakness, and lack of appetite!
3. What are the relation between the previous disease and the symptomps?
4. Explain the Diagnosis steps based on scenario!
5. Explain the Differential Diagnoses based on scenario!
6. What kind of first treatment should be given based on scenario ?
7. Explain the Islamic perspective according to the scenario !
D. ANSWERS

1. Explain the Mechanism of Defect!

DEFECATION

Pictures 1. Defecation Mechanism

Factors that prevent continued fecal impulse are due to tonic contractions in:

a. Internal anal sphincter: circular smooth muscle of the anus.

b. External anal sphincter: voluntary striated muscles surrounding the internal

anal sphincter.

Reflexes Defecation

It is the reflex that causes defecation. Reflex mechanism:

• Intrinsic reflex (enteric SS): faeces → rectum → rectal wall distension →

afferent signal (myenteric plexus) → peristaltic motion in the descending colon,
sigmoid, and rectum → pushing faeces → peristaltic to the anal canal →
inhibition by the myenteric plexus → sphincal relaxation → sphincal relaxation
→ sphincal relaxation ani internus → if the external anal sphincter is in a state of
voluntary relaxation, DEFECTATION occurs.

To strengthen the stimulus for defecation, there are other reflexes that
strengthen the stimulus:

a) Parasympathetic reflexes: rectal nerve endings are stimulated → afferent

nerves → sacral segments of the spinal cord → efferents in the N. Pelvikus →
descending colon, sigmoid, rectum, anus → relaxation of the internal anal
sphincter → external anal sphincter voluntary relaxation → DEFECTATION.

b) Weak activation by taking a breath: downward movement of diaphragm →

abdominal muscle contraction → abdominal pressure increases → pushing stool
contents into the rectum.

Factors affecting defecation include:

- Age

- Diet

- liquid

-Psychological

-Lifestyle

- Medicine

- Pathological disorders, for example: enteritis

Anatomi

Pictures 2. Digestive System

Intestinum Tenue (small intestine)

Spanning from pylorus to junctura ileocaecalis. Consists of :

a) Duodenum

b) Jejenum

c) Ileum

Most of the digestion and absorption of food takes place in the intestine tenue.
Duodenum

Pictures 3. Duodenum

The shortest part of the intestine tenue is about 10 inches (25 cm) long and has
the shape of the letter C that surrounds the head of the pancreas. The duodenum
starts at the pylorus on the right and ends at the transition of the duodenojejunal
on the left. It is an important organ because it is a place of ductus choledochus
and ductus pancreatis.

I. Proximal pars: short (5 cm), located ventrolateral to the L1 corpus vertebrae, ie

superior pars.

II. Pars descendens: longer (7-10 cm), passing into the caudal parallel to the right
side of the L1-L3 vertebrae.

III. Horizontal Pars: 6-8 cm long and ventral across the L3 vertebra.

IV. Pars ascendens: short (5cm) and begin to the left of the L3 vertebra, then
cross into the cranial to the level of the cranial vertebra L2.
Vascularization

 Truncus celiacus and superior artery mesentrica du duodenal artery.

 The superior pancreaticoduodenale vein empties into the hepatic portal vein.

The inferior pancreaticoduodenale vein empties into the superior mesentrica vein.

Lymph flow

The duodenal lymph vessels follow the arteries and are accommodated by the
pancreoticoduodenal nodes lymphoidides along the arterial splenica and by the
pyloric lymphoid lymph node along the gastroduodenal artery.

Innervation

Derived from the sympathetic and parasympathetic nerves of the vagus and
sympathetic nerves through the coeliac plexus and mesentric plexus.

Jejenum and Ileum

Jejenum starts from the duodenojejunalis flexura, and the ileal intestine ends at
the ileocecal junction (the meeting of the ileum with the cecum). moves freely
and attaches to the posterior abdominal wall by means of a fan-shaped peritoneal
fold and is known as mesentrium.

 Difference between Jejenum and Ileum

 Pictures 4. Lower Digestive System

Vascularization

Blooded by A.mesentrica superior and the very bottom of the ileum blooded by
a.ileocolica.The veins correspond to the A.mesentrica superior branch and drain
their blood into the superior mesentrica vein.

Lymph flow

The jejenum and ileal lymph vessels cross between the mesentrium sheets to the
lymphoidei nodi mesentrici located:

a) Close to the intestine wall

b) Between arterial arcs

c) Along the proximal portion of the superior mesentrica arteriae.

Lymph vessels from the end of the ileum follow the ramus ilealis arteria
ileocolica to nodi lmphoidei iliocolici.

Innervation

Derived from the sympathetic nerve and parasympathetic (vagus nerve) superior
mesentricus plexus.

Intestinum Crassum (Large Intestine)

Spanning from the ileum to the anus, it consists of:

a) Caecum

b) Appendix versiformis

c) Colon ascendens

d) Colon transversum

e) Colon descendens

f) Sigmoid Colon

g) Rectum

h) Canalis analyst

The main function of Crassum is to absorb water and electrolytes and store
undigested material until it can be removed from the body as stool.

Caecum
 Pictures 5. Caecum

The first part of the intestine crassum and turn into colon ascendens.Located at
the border of the ileum and intestinum crassum.Is a dead-end pouch located on
the iliaca dextra fossa.Length 2.5 inches (6 cm) and entirely covered by
peritoneum.Easy to move even though it does not have mesentrium.

Vascularization

The anterior caecalis artery and posterior caecalis arteriae form a.ileocolica, a
superior mesentrica artery branch. The veins follow the corresponding arteriae
and drain their blood into the superior mesentrica vein.

Lymph flow and innervation

Walk through several nodi mesentrici and finally reach the nodi mesentrici
superiores.Nerve supply: originating from branches of the sympathetic and
parasympathetic nerves (vagus nerve) to form the superior mesentricus plexus.

Appendix Versimformis

In the form of a dead-end tube shaped like a worm and connected with the
caecum in the caudal ileosecal transition. It has muscles and contains a lot of
lymphoid tissue. Length varies from 3-5 inches (8-13 cm). The base is attached to
the posteromedial caecum surface, about 1 inch (2.5 cm) below the ileocaecalis
bed. The other part of the appendix is free, covered by the peritoneum, which
attaches to the lower layer of the mesestrium intestine tenue through its own short
mesentrium, messoappendix. Messoapendix contains arteries, appendicular veins
and nerves.
Appendix versiformis is located in the iliac region of dextra, and the base is
projected into the anterior abdominal wall at the lower third point of the line
connecting the anterior superior iliac spine and the umbilicus (McBurney's point).

Pictures 6. Caecum

Bleeding
Arteria appendicularis is a branch of the posterior caecalis artery. This artery runs
towards the end of the vermifomis appendix in the messoappendix. The
appendicular vein drains its blood into the posterior caecalis vein.

Lymph
Lymph vessels flow lymph fluid to one or two nodi located in the messoappendix
and from here flowed to the nodi mesenterici superiores.Nerve supply:
originating from the sympathetic and parasympathetic branches (vagus nerve) of
the superior mesentricus plexus.

Colon Ascendens

It passes from the cecum in the cranial direction on the right side of the
abdominal cavity into the liver, and turns left as the flexure coli dextra. the left
colon of the ascendens forms the paracolica fossa. The ascendent colon is usually
separated from the ventral abdominal wall by the intestine twists and omentum
majus.
 Pictures 7. Colon

Vascularization

The ileocolica artery and the arteria colica dextra, branches of the superior
mesentrica artery. The ileocolica vein and the venous colica dextra branch of the
superior mesentrica drain blood back from the colon ascendens.

Lymph vessels and innervation

Lymph vessels cross into the lymphoidei paracolici nodi and epicolici lymphoidei
nodi  nodi lymphoidei mesenterici superiores.

Innervation originates from the superior plexus mesentricus.

Colon Transversum

The largest intestine and car parts. This intestine section passes through the
abdomen from flexura colli dextra to flexura colli sinistra and here turns caudal
into colon descendens. Flexion colli sinistra is located in the caudal ren sinistra
and is connected diaphragm by phrenic ligamentum. colon tranversum
mobil.Radix mesentrii is located along the caudal edge of the pancreas and
continues with the peritoneum parietale next to the dorsal. Because this
mesentrium is for the car, the location of the colon can vary, and usually the
colon hangs down to the height of the umbilical ring. Can also reach the pelvis.
Vascularization

The transverse Colon artery is mainly through arterial colica media, superior
mesentric artery branches but also obtains blood from a.colica dextra and
sinistra.Channeling blood from the transverse colon occurs through the superior
mesentrica vein.

Lymph flow and innervation

Lymph from the colon tranversum is channeled to the lymphoidei colicii medii
nodi which is accommodated by the node lymphodei mesentrici superiores.The
nerve originates from the superior mesentricus plexus and follows the a.colica
dextra. Which follows the a.colica sinistra plexus mesentricus inferior.

Colon Descendens

Retroperitoneal crossing from flexura colli sinistra to the iliaca sinistra fossa and
here is called the sigmoideum. The peritoneum covers the ventral and lateral sides
and fixes it on the dorsal abdominal wall.

Vascularization

Blooded by a.colica sinistra and a.sigmodae which are branches of a.mesentrica

inferior.Vena follows the appropriate arteries and empties into the inferior
mesentrica vein.

Innervation and lymphatic flow

Lymph fluid is channeled to the lymphoidei colici nodi and mesentrici inferiores
nodi located at the base of A.Mesentrica inferior.Nerve-sympathetic and
parasympathetic nerves nervi sphlancini pelvici through the inferior mesentricus
plexus.
Sigmoid Colon

S-shaped intestinal meshes. Connecting the colon descendens with the rectum.
Extends from the edge of the pelvis to the third sacrum segment, to switch to a
rectum. Finally the taenia coli shows the beginning of the rectum. The sigmoid
colon has a long mesentrium and is known as the sigmoideum mesocolon. .

Blooded by Arteriae sigmoidae branch of the inferior mesentrica artery. Inferior

mesentrica veins carry blood back from the sigmoid colon and
descendens.Lymph vessels to nodi lymohoideii colici medii - superior mesentrici
nodi

The innervation of sympathy originates from the lumbar truncus symphateticus

and the superior hypogastric plexus along the inferior a.mesentrica branches.
Parasympathetic nerves originate from Darinervi splanchini pelvici.

Rectum

The final part of the intestinum crassum is fixed. The caudal direction becomes
the analyst canal.Approximately 12 cm - 15 cm long with 2.5 cm empty
appearance. Rectum has the ability to be dilatasis to 7.5 cm.

Canalis Analyst

The anal canal is the final part of the intestinum crassum, which is 2.5 cm to 4 cm
long. starting from the flexura parinealis recti. Usually the analyst canal is closed
and only opens at the time of defecation (defecation).

Histologi Lower Gasrtointestinal Tract

DUODENUM

Mucosal tunica: a cylindrical epithelium having a microvilli and between the

villi there is an intestinal gland or kel. Lieberkuhn. At the base of the gland there
are paneth cells. Inside the cytoplasm there are rough red granules.
Submucosal tunica: filled kel .runner. The mucosal + submucosal worlds form the
krenkingi circular plica. Many of the intestinal veins and meissner plexus can be
found here.

Layer muscular tunica: circular and longitudinal, there is the auerbach nerve
plexus.

Adventist tunica: a rare connective tissue.

Pictures 8.
Histology Structure of Duodenum

Ileum

Pictures 9. Histology Structure of Ileum

-Mucosal tunica: in the lamina propria there are groups of lymphatic nodules that
form a special building called pey spots. This lymphatic nodule group is often
seen extending into the submucosa so that it often makes the muscularis mucosa
beheaded.

-Submucosal tunica: consisting of a sparse tissue with a meissner plexus in it.

Here there are no glands. Circular kerchini appear shorter than those found in the
duodenum and yeyenum.

-Muscular tunica: the structure is the same as the duodenum and yeyenum

-Serous tunica: consisting of a rare jar.

JEJENUM

Pictures 10. Histology Structure of Jejenum

Vermiforfis Appendix

-Tunica Mucosa: a cylindrical layer of epithelium, which has no villus that is only
keleberkuhn only. There are many lymphatic nodules in the lamina propria,
which surround the walls. The mucosal muscularis can be found too.
-Submucosal Tunica: jar. Bonding is rare without kel. And there are many
lymphocyte powders originating from lamina propria.

Pictures 11. Histology Structure of Appendix

Colon

-Tunica Mucosa: cylindrical epithelium, having no villus. And there are many
lymphatic nodules in the lamina propria. Forming a series of lip.length (rectal
column morgagni)

-Submucosal tunica: consisting of a scarred tissue of the meissner plexus.

-Tunica muscularis: circular arrangement as usual, longitudinally does not have

the same thickness around the circumference of the wall.
 Pictures 12.
Histology Structure
of Colon

Rectum-anus

-Mucosal tunica: a
change in the type of
epithelium from a
cylindrical epithelium with goblet cells to a layered epithelium without a layer of
horn. Classify lymphatic nodules found in this layer. Cryptus is no longer visible
in the anus.

-Tunica muscularis Mucosa: not found in the anal region, lamina propria is
replaced by the dermis and an apocrine gland called the circumanal gland is
found.

-Submucosal tunica: a rare connective tissue of lamina propria at its site of

contact with the anus and eventually replaced by the dermis and hypodermis.

-Tunica Muskularis: circular to the thickened rectal region to form a circular

muscle, namely the M. internal sphincter ani.

-Tunika Adventisia: connective tissue is rare.

 Pictures 13. Histology Structure of Rectum-Anus

PHYSIOLOGY OF DIGESTIVE CHANNELS

Small intestinal motility only slightly develops before 28 weeks' gestation.

Irregular gastric contractions are first discovered at the beginning of the 26th
week of pregnancy.

Gastrointestinal motility can begin to be measured at 28 to 30 weeks' gestation,

although not yet enter the enteral diet. The small intestine shows an irregular
motility pattern between 27 and 30 weeks 'gestation, and becomes a more mature
pattern at 33 to 34 weeks' gestation where there is a complex of myoelectric
migration. Gastroanal transit ranges from 8 to 96 hours in preterm infants while in
adults 4 to 12 hours.

Increased coordination and contraction strength of the gastric and small intestine
began to be obtained at 30 weeks gestation. At 36 weeks gestation the fetal
gastrointestinal motility pattern starts to resemble the baby's intestinal motility
pattern which is already quite months, now the movement of sucking and
swallowing has been regular, the fetus swallows amnionic fluid about 450 mL /
day in the third trimester.

The motility of the gastrointestinal organs is regulated by input from myogenic,

neural and neuroendocrine either during fasting or during digestion. Here are
some of the factors that affect gastrointestinal motility including electrical activity
of the smooth muscle of the gastrointestinal and calcium ions, potassium and
muscle contraction, the nervous system and neurotransmitters and hormones
secreted by enteric neurons that affect the gastrointestinal motility.

The ratio of intra and extracellular potassium is a determinant of the electrical

potential in cell membranes. this plays a role in the potential generation of nerve
and muscle tissue. In hypokalaemia, neuromuscular excitability can occur
(hyporeflexia or paralysis, decreased peristalsis or ileus).

The gastrointestinal tract has a nervous system called the enteric nervous system,
all located in the intestinal wall, starting from the esophagus esamagus to the
anus. This system mainly regulates gastrointestinal movements and secretions.

Defecation Physiology

The defecation process begins with the mass movement of the descending large
intestine which pushes stool into the rectum. Mass movement arises +/- 15
minutes after eating and only occurs a few times a day. The presence of stool in
the stool in the rectum causes rectal stretching and stool pushing towards the anal
sphincter.

Defecation reflexes

The defecation reflex arises when the stool enters the rectum, then stretching the
rectum further gives rise to sensory stimulation of the intestinal and pelvic walls,
giving rise to peristalsis in the descending, sigmoid and rectal large intestine,
pushing the stool towards the anus. Rectal distension creates impulses in
ascending sensory fibers which are then carried to the cortex which raises
awareness about distension. Meanwhile a temporary contraction of the external
anal sphincter luric muscle, puborectal sling (part of the levator ani muscle). Thus
there is a reflex called inflation reflex.

Delivery of distal nerve impulses through the myenteric plexus in the caudal
portion of the rectal wall will cause reflexes of smooth muscle inhibition of the
internal anal sphincter muscle. This event is called a rectoscopic relaxation reflex.

The relaxation of the internal anal sphincter occurs proportionally to the volume
and velocity of rectal distension. This condition is followed by inhibition of the
external anal sphincter, which involves the reflex pathway and cortical
facilitation. Puborectal reflexes will result in widening of the anorectal angle
(normal 60 - 105o to 140o) causing the anal canal to be obstructed. Increased
abdominal pressure is associated with peristalsis in the abdominal wall, causing
fecal discharge resulting in rectal emptying.

After the stool comes out, then the closure reflexes occur immediately, this
activity occurs very quickly, namely the return of the pelvic floor muscles,
anorectal angle and sphincter tone to its original position.

Physiology of defecation in infants

In infants the development of anorectal function and structure increases with age.
The rectum increases in length accompanied by the growth of rectal valve and
anorectal angle. There is time variation in the development of rectoanal inhibitor
reflexes. In voluntary control, rectal distension will quickly cause loss of
electrical activity and tone of the external anal sphincter.

Defecation in newborns begins with the release of meconeum. Meconeum is

black, thick, sticky stool which is a mixture of intestinal glandular secretions and
amniotic fluid. Under normal circumstances, the meconeum will come out in the
first 36-48 hours after birth 2-3 times per day.
 More gram positive normal intestinal microflora in breast milk than gram
negative. In infants less months often have a hard stool or low frequency of
defecation. In babies who get formula milk have more solid stool compared to
those who get breast milk.

REFERENCE:

Kapita Selekta Kedokteran, Edisi ketiga, Jilid 2, editor: Mansjoer, Arif,

Suprohalta, waedhani, FK-UI, Media Aesculapies, Jakarta 2015.

Pieter,John:Sjamsuhidayat,R And De Jong ,WIM,Bab 31:Lmabung and

Duodenum,Buku ajar ilmu bedah,edisi 2 ,EGS:Jakarta,2014.Hal.541-59

2. Explain the patomecanism of black stool, weakness, and lack of appetite!

BLACK STOOL/MELENA MECHANISM

The presence of gastrointestinal bleeding of the upper part such as esophageal

disorders (varicose veins, esophagitis, malignancy), Gastric and duodenal
disorders (peptic ulcers, duodenal ulcer and malignancy, blood diseases
(leukemia, purpura, thrombocytopenia) and the use of ulcerogenic drugs
(salicylates, corticosteroids, and alcohol) In failing Hepar chronic cirrhosis, cell
death in Hepar resulted in an increase of the port vein pressure. Consequently, a
collateral channel is formed in the esophageal and rectum submucosa and on the
anterior abdominal wall to divert the blood from the splenic circulation away
from Hepar.

With increasing pressure in this vein, the vein expands and enlarges (dilation)
by the blood (called Varicose veins). Varicose veins may rupture, causing
gastrointestinal bleeding. Furthermore, it may result in sudden blood loss,
decreased venous backflow to the heart, and decreased cardiac rainfall. If the
bleeding becomes excessive, it will result in decreased tissue perfusion. In
respond to the decline in cardiac precipitation, the body will conduct a
compensation mechanism to try to maintain perfusion. This mechanism
stimulates the main signs and symptoms seen at the time of the initial assessment.

If blood volume is not replaced, decreased tissue perfusion results in cellular

dysfunction. The cells will turn into metabolism anaerobic and lactic acid form,
decreased blood flow will give effect on the channel of the body system and
without adequate oxygen supply the system will suffer failure.

Varises esophagus,ulkus peptikum,sirosis hepatis,Ca

esophagus,Gastritis erosif.

Ruptured Gastrointestinal Blood Vessels

Gastrointestinal Bleeding

MELENA

Pictures 14. Black Stool Mechanism

Nausea mechanism:

Nause Vomitting is caused by various stimulations in the vomiting center in

dimedulla oblongata. The vomiting center receives afferent impulses from CTZ
through cross stimulation or indirectly in the digestive tract. In the vomit region
there are many receptors that play a role in

the process of nausea and vomiting, and antiemetics generally work to inhibit
neurotransmitters at the receptor. Efferent impulses through cranial nerves V, VII,
IX, X and XII towards gastrointestinal channeling can cause nausea and
vomiting.

In our body there is inflammation of the stomach because we eat foods containing
alcohol, aspirin, steroids, and caffeine, causing irritation to the stomach and cause
inflammation in the stomach caused by high stomach acid. After inflammation of
the stomach, the body will stimulate expenditure of substances which is called an
active vase that causes capillary permeability of the arteries to rise. Causing the
stomach to become edema (swelling) and stimulate the voltage receptors and
stimulate the hypothalamus for nausea. As a result of electrical disturbances and
gastric crossing will cause permanent dyspepsia and nausea. If the disorder
intensified, through the vagus nerve can stimulate vomiting.

Pictures 15. Mechanism of Nausea

Decreased appetite:
 Pictures 16. Mechanism of the Decreased Appetite

Il-1 is responsible for other symptoms such as the onset of drowsiness / sleep,
appetite suppression, and decreased albumin and tranferin synthesis. Decreased
appetite is a result of the collaboration of IL-1 and TFN-α. Both will increase the
expression of leptin by adipose cells. In the Medial Hypothalamus section, Leptin
activates Anorectic nerve cells which will

release neuropeptide which suppresses appetite (POMC, CRH and CART). At the
same time, Leptin will inhibit another group of nerve cells that are sensitive to
Leptin called Orexigenic which will release neuropeptides that regulate appetite
(NPY and AGRP).

Both groups of nerve cells that are sensitive to leptinini will send appetite
suppression signals to key nerve cells in the lateral portion of the hypothalamus
controlling habits including eating habits. Increased circulation of leptin causes
negative feedback to ventromedial hypothalamus which results in decreased food
intake.

References:

Djumhana A. 2011. Acute bleeding of the upper gastrointestinal tract. Bandung:

Pustaka Unpad.

Alfiani SQ. Jurnal KTI Nause & Vomiting. Eprints Undip.

Mutiara Indah Sari. Regulasi Sistem Saraf Pada Nafsu Makan. 2007

3. What are the relation between the previous disease and the symptoms?

RHEUMATIC HISTORY

The main pathophysiology of damage to the stomach and duodenum due to the
use of NSAIDs is the physiochemical disturbance of the defense of the gastric
mucosa and systemic inhibition of the protective mucosa of the stomach through
inhibition of the activity of cyclooxygenase (COX) of the gastric mucosa.
Nonsteroidal anti-inflammatory drugs (NSAIDs) can inhibit prostaglandin
synthesis (PG) which is a inflammatory mediator and reduce the sign of
inflammation. Nonetheless, prostaglandins, especially prostaglandin E, are
actually protective substances for upper gastrointestinal mucosa. Barriers to PG
synthesis will reduce mucosal resistance, with the effect of acute lesions of the
gastric mucosa in mild to severe forms. Non-steroidal anti-inflammatory drugs
damage the gastric mucosa through two main mechanisms namely topical and
systemic. Topical mucosal damage occurs because NSAIDs are lipophilic and
acidic, making it easier to trap hydrogen ions into the mucosa and cause
ulceration. The systemic effect of NSAIDs is more important, namely damage to
the gastric mucosa due to decreased prostaglandin production.

Prostaglandin is a cytoprotection substance that is very important for the gastric

mucosa. Cytoprotection is done by maintaining blood flow to the mucosa and
increasing mucosal secretion and bicarbonate ions. Prostaglandins strengthen the
barrier of the gastric mucosa by increasing the levels of gastric mucosa
phospholipids, so that the hydrophobicity of the mucosal surfaces increases,
which in turn reduces the diffusion backward of hydrogen ions. Clinical
manifestations of gastritis vary from asymptomatic, mild symptoms with the most
common manifestations of heartburn, dyspepsia, abdominal discomfort and
nausea, to severe symptoms such as peptic ulceration, bleeding, and perforation.
decreased appetite, flatulence and feeling full in the stomach, vomiting, nausea
and belching. If there is active bleeding, hematemesis and melena can occur.

The history that needs to be asked is a history of chronic liver disease, a history of
dyspepsia, a history of taking NSAIDs, rheumatic drugs, alcohol, herbs,
medicines for heart disease, medications for stroke. Then asked for a history of
kidney disease, a history of lung disease and the presence of bleeding elsewhere.
A history of vomiting before the occurrence of hematemesis strongly supports the
possibility of Mallory Weiss syndrome.

In the first physical examination to be performed is the ABC assessment, patients

with massive hematemesis can experience aspiration or airway obstruction, this is
often common in elderly patients and patients who experience decreased
consciousness.

HEPATITICAL HISTORY

Acute viral hepatitis is a systemic infection that predominantly attacks the liver.
Almost all cases of acute viral hepatitis are caused by one of five types of viruses,
namely: hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus
(HCV), hepatitis D virus (HDV) and hepatitis E virus (HEV) . Based on the
scenario, there may be a history of hepatitis from hepatitis B or hepatitis C,
because there is a history of rheumatism, so it is possible for patients to have been
given intravenous medication with a hepatitis virus needle. This if it lasts a long
time and is not treated it will turn into chronic hepatitis. In patients with hepatitis
who are unable to maintain the condition of the liver will continue to become
chronic hepatitis sufferers, and if the condition continues to worsen there will be a
kind of large pimples on the liver / nodules, which is a characteristic of cirrhosis.
Cirrhosis of the liver can be said as follows: A state of disorganization diffused
from normal liver structures due to regenerative nodules surrounded by fibrotic
tissue.

Clinical manifestations of cirrhosis of the liver include Portal Obstruction and

Ascites. Late manifestations are partly due to chronic liver failure and partly by
portal circulation obstruction. All blood from digestive organs will practically
gather in the portal vein and be carried to the liver. Because the cirotic liver does
not allow free passage of blood, the blood flow will return to the spleen and
gastrointestinal tract with the consequence that these organs become chronic
passive congestive sites, in other words both organs will be filled with blood and
thus not can work well. Patients with this condition tend to suffer from chronic
dyspepsia and constipation or diarrhea. The patient's body weight gradually
decreases.

Obstruction of blood flow through the liver that occurs due to fibrotic changes
also results in the formation of collateral blood vessels in the gastrointestinal
system and blood flow from blood vessels with lower pressure. As a result,
patients with cirrhosis often show prominent abdominal blood vessel distension
and are seen on abdominal inspection (head of the medusa), and blood vessel
distension throughout the gastrointestinal tract. The esophagus, stomach and
lower rectum are areas that often experience the formation of collateral blood
vessels. This blood vessel distension forms varices or hemorrhoids depending on
its location.

Because its function is not to bear high blood volume and pressure due to
cirrhosis, these blood vessels can rupture and cause bleeding. Therefore, the
assessment must include observations to find out the real and hidden bleeding
from the gastrointestinal tract. Approximately 25% will experience mild
hematemesis, the rest will experience massive hemorrhage from rupture of
varicose veins in the stomach and esophagus. This is what causes upper
gastrointestinal bleeding that causes melena.

References:

http://juke.kedokteran.unila.ac.id/index.php/majority/article/download/917/731
https://simdos.unud.ac.id/uploads/file_penelitian_1_dir/aafa43ca8f7914ac9fde6a5d1
9ff3094.pdf

Sanityoso, A. Hepatitis Virus Akut. Buku Ajar Ilmu Penyakit Dalam Jilid I Edisi
V. Jakarta. Departemen Ilmu Penyakit Dalam Fakultas Kedokteran Universitas
Indonesia; 2009
 Bashar Sharma, Savio John, June 3, 2019. hepatic cirrhois

www.ncbi.nlm.nih.gov

4. Explain the Diagnosis steps based on scenario!

ANAMNESIS

 Degree of awareness
 The degree of pain
 Nutritional status
 identity
• Name
• age
• Address
• Profession

1. Current Disease History

 Location of Pain
If necessary, patients are asked to show with their hands where the most
painful and where the spread.

 Onset
When did the onset of illness begin and or how long has it lasted. Arise
suddenly or slowly.

 The nature of pain

Sharp (obvious) pain such as burning, burning, stinging, sliced, punctured,
indicates inflammation of the organ. Pain that is dull (dull) such as
squeezing, cramps, colic, something that moves usually shows the process
 in hollow organs (digestive tract, bile). Pain that is not typical indicates
solid organs (liver, pancreas).

 Factors that aggravate complaints

Like physical activity, eating, certain circumstances or positions.

 Factors that alleviate complaints

Efforts are given by patients who can ease pain, for example drugs, certain
positions.

 Complaints that accompany

 Abdominal pain (-)
 Nausea (+)
 Gag (-)
 Limp (+)
 Decreased appetite

2. Previous medical history

3. History of habits

4. Past medical history: Rheumatism and Hepatitis (10 years ago)

5. Family history (-)

PHYSICAL EXAMINATION

Stomach inspection

A. Skin.

Inspection of lesions on the surface of the abdominal skin that correspond to

lesions of certain diseases. For example:
1) Icterus in hepatitis

2) Rose spots on typhoid fever

Contact if there are dilated vessels on the surface of the stomach. Usually
because of the dam process. Determine the direction of flow of the dilated veins.
If a vein is obtained above the umbilicus, if it flows upward, there may be portal
hypertension. If the flow is down then choose one of the dams in the superior
vena cava. If a widening of the umbilicus veins is obtained, if blood flow is down
then use the portal hypertension, release if the flow is up then place the dam on
the lower vena cava. In the portal of the dam that causes hypertension, can be
found caput medusae, is a widening of the veins that run fast radiating from the
lower and upper lateral umbilicus. The image of the medusa head is rarely
obtained.

b. Umbilicus

What if not, whether it's normal or not, maybe just a coughing process or
an increase in pressure in the abdominal cavity. Large bulges can be caused by
umbilical hernia when released with a consistency that is difficult to use
malignancy.
c. Abdominal wall movement

Normal abdominal wall movements, regular breathing and free

movement. If the wall of the abdominal wall is delayed when breathing, it can be
caused by:

1) If part of it is too late it can be caused by the process of inflammation of the

organs involved depending on the location of the organ.

2) If the entire abdomen appears to be lagging behind in movements usually due

to generalized peritonitis.
3) Movement in the epigastric region corresponding to cardiac pulsation is found
in the right lungs.

4) In thin people often seen abdominal aortic pulsation.

5) Sometimes seen intestinal movement which is a moving mass is found in the

obstructive ileus.

d. Abdominal shape

1. If the stomach is enlarged and symmetrical, it is caused by:

a. Overweight

b. Ascites

c. Stockpiling of air in the intestine

2. If the enlargement of the abdomen is not symmetrical, chances are:

a. Pregnancy

b. Tumors in the abdominal cavity

3. Local enlargement can be caused by enlarged liver, spleen or tumors.

4. Concave stomach shape can be obtained on:

a. Thin people

b. Meningitis TB

Abdominal auscultation
The purpose of auscultation of the abdomen is to determine:
1. The presence or absence of intestinal peristaltic
The normal sound heard is caused by the movement of water and idara in
the intestinal lumen. If there is a blockage in the intestinal lumen. If there is an
intestinal obstruction, a high-pitched and loud metallic sound will be heard. This
increase in sound is also known as borborigmie. In paralytic ileus states weaken
or disappear.
2. Fluid movement
Fluid can be heard for example in stenosa pyloris movements. The sound of fluid
in the epigastrium after the patient drinks liquid, when the pylorus rocked while
listening with a stethoscope in the epigastric region. This sound is called
succution flash.
3. Noisy blood vessels
Vascular sounds that arise can be clearly audible noise in the aortic aneurysma or
in hepatomas that can be heard in certain places =. In portal hypertension, there
may be a "venous hum" venous noise that is located between the epigastrium and
the umbilicus.

Palpate the abdomen

Palpate with both hands ie the left hand is placed at the bottom of the right
or left hip and lifts the patient's waist up. The right hand palpates the upper
abdomen. In this way the lat-tool in the abdominal cavity is more easily palpated.
This way of palpation is called bimanual palpation. When abdominal palpation
should be noted:
a) Is there a wall of the abdominal wall and if there is in which region. The
existence of tension in the abdominal wall is a reaction of the abdominal wall to
protect the area underneath. This symptom is called defance musculair. In
general, areas that show tenderness will strain the abdominal wall. Defender
musculair is found in:
1. Local; in acute cholecystisisl, acute appendicitis
2. Comprehensive; in generalist peritonitis.
3. Pressure pain
 Abdominal tenderness indicates the process of inflammation under the
abdominal wall, both in the peritoneum and in the organs in the abdominal cavity.
Localization of tenderness is important to determine diseased organs such as
tenderness in the right hypocondrium, usually caused by cholisistisis or acute
hepatitis.
4. Hyperastesia
By palpating with a small touch on the surface of the stomach,
the sufferer feels extreme pain. This is determined in patients with
peritonitis, post herpetic neuralgia.
5. Enlargement of the abdominal cavity
a. Palpate the liver
b. Palpate the gallbladder
c. Renal palpation
d. Palpation of the spleen
e. Palpation of the bladder
f. Gastric palpation
g. Palpate the tumor

Abdominal Percussion
Useful for assessing the results of palpation and percussion examination
with percussion can be known:
a. Enlargement of the organs (when the liver and spleen enlarges in the
percussion).
b. The existence of free air when in this area sounds tympani then there is free air
in the abdominal cavity due to intestinal perforation
c. Free fluid or percutaneous ascents there are three ways depending on the
amount of liquid:
1.Percussion fluid sites are percussion in areas containing dull sounds and
then the patient is instructed to lie down then fluid will collect on the left and
right sides of the abdomen (lowest area). Percussion in both places will sound
deaf and then the patient is told to tilt to one side, the percussion sound of Peke
on one of the highest sides will change to tympani.
2. Percussion of many ascitic fluids. The examiner's hand is placed on one
side of the abdomen, the other hand taps the abdominal wall, there will be waves
of fluid felt on the hand on the opposite side. To differentiate from large ovarian
tumors, the surface of convex ovarian tumor fluid is convex in patients with
concave surface concave.
3. For small amounts of liquid. Percussion is done by asking the patient to
lie on his stomach or menungging position. After a while percussion in the lowest
area, if there is liquid it will sound deaf. You can also use a stethoscope in the
lowest area. By performing percussion on the side of the abdomen, there will be a
difference in sound through the stethoscope if the stethoscope is moved through
the abdomen to the other side (puddle sign).
d. The phenomenon of a chessboard
In the abdominal wall percussion found tympani sound and deaf alternating
conditions are found in tuberculous peritonitis.

SUPPORTING INVESTIGATION
A. Radiology
1. Barium Meal Double-contrastditional defect, primary tumor mucosal
irregularity or tumor spread to the esophagus / duodenum.
2. Abdominal ultrasonography -> to detect liver metastases.
3. Colon check loop
It is a radiological examination of the colon by using retrograde contrast
media in patients.
Patient's position: AP, AP with contrast, lateral photo with contrast.
Kotras: BaSO4 as a contrast medium.
Note the position of the contrast to where and pay attention to the mucosa,
henstrasi, incisura, lumen colon (whether there is a filling defect or additional
shadow)
 Pictures 17. Radiology
Image

4. Intravenous pyelography

This is a photo after injection of contrast at 3, 5, 15, 45 minutes, and if

necessary 60. At the 3rd minute photo check the position of the kidney, where the
left kidney is higher than the right with an
upper limit as high as T12 or L1. Check
the renal border to see indentation or
mass. Then look at the state of the
pelviokalises system to see calix
cupping and see dilation.

Pictures 18.Contrast: ioversol and iopamidol.

 5. Inspection of BNO - IVP
A radiographic examination and urinary tract (renal, ureter, vesica
urinaria, and urethra) with intravenous positive contrast injection.
Patient's position: AP

Pictures 19. Contrast: iodine

B. LABORATORY
EXAMINATION
1. Routine blood
a. Hemoglobin / HB
To detect anemia or kidney disease.
b. Hematocrit / HT
Measuring the concentration of red blood cells in the blood
2. Blood chemistry
a. SGPT (serum pneumatic piruvik transaminase)
Used to detect hapatocellular damage.
b. Albumin
 It was conducted to detect the ability of albumin synthesized by the
liver which aims to determine the presence of liver disorders or kidney
failure.
c. Bilirubin
Bilirubin examination is carried out to detect bilirubun levels. Direct
bilirubin is used to detect obstructive jaundice by hepatitis neoplasms.
Indirect bilirubin is done to detect anemia or malaria.
3. Endoscopy and Biopsy
Endoscopy is recommended to evaluate the symptoms caused by
abnormalities in organs. The disorder can be an infection, inflammation, or
cancer. Through the endoscopy procedure, doctors are also assisted to take
tissue samples (biopsy). Some symptoms that may require endoscopy to
support the diagnosis include:
Complaints of the digestive tract, such as bowel movements or blood
vomiting, diarrhea or continuous vomiting, abdominal pain, weight loss,
dysphagia, and heartburn.
Coughing up blood or chronic coughing.
Urinary complaints, such as urinating blood or bedwetting.

Referensi :

Bickley, Lynn S., Peter G. Szilagyi, and Barbara Bates. Bates' guide to physical
examination and history taking. Lippincott Williams & Wilkins, 2009.

Mansjoer, Arif, and Kupusji Triyanti. "Kapita selekta kedokteran." Jakarta:

Media Aesculapius (2000): 86-92.

5. Explain the Diferential Diagnoses based on scenario!

1. Hepatic Cirrhosis
Introduction

Cirrhosis is characterized by fibrosis and nodule formation of the liver, secondary

to a chronic injury, which leads to alteration of the normal lobular organization of
the liver. Various insults can injure the liver, including viral infections, toxins,
hereditary conditions, or autoimmune processes. With each injury, the liver forms
scar tissue (fibrosis), initially without losing its function. After a long-standing
injury, most of the liver tissue gets fibrosed, leading to loss of function and the
development of cirrhosis.

Etiology

Chronic liver diseases usually progress to cirrhosis. In the developed world, the
most common causes of cirrhosis are hepatitis C virus (HCV), alcoholic liver
disease, and nonalcoholic steatohepatitis (NASH). while hepatitis B virus (HBV)
and HCV are the most common causes in the developing world. Other causes of
cirrhosis include autoimmune hepatitis, primary biliary cholangitis, primary
sclerosing cholangitis, hemochromatosis, Wilson disease, alpha-1 antitrypsin
deficiency, Budd-Chiari syndrome, drug-induced liver cirrhosis, and chronic
right-sided heart failure. Cryptogenic cirrhosis is defined as cirrhosis of unclear
etiology.
Epidemiology

The worldwide prevalence of cirrhosis is unknown; however, in the United

States, it has been estimated to be between 0.15% and 0.27%.
Pathophysiology

Multiple cells play a role in liver cirrhosis including hepatocytes and sinusoidal
lining cells such as hepatic stellate cells (HSCs), sinusoidal endothelial cells
(SECs) and Kupffer cells (KCs). HSCs form a part of the wall of the liver
sinusoids, and their function is to store vitamin A. When these cells are exposed
to inflammatory cytokines, they get activated, transform into myofibroblasts, and
start depositing collagen which results in fibrosis. SECs form the endothelial
lining and are characterized by the fenestrations they make in the wall that allow
the exchange of fluid and nutrients between the sinusoids and the hepatocytes [4].
Defenestration of the sinusoidal wall can happen secondary to chronic alcohol use
and can promote perisinusoidal fibrosis. KCs are satellite macrophages that line
the wall of the sinusoids as well. Studies mainly from animal models have shown
that they play a role in liver fibrosis by releasing harmful mediators when
exposed to injurious agents and acting as antigen presenting cells for viruses.
Hepatocytes also are involved in the pathogenesis of cirrhosis, as damaged
hepatocytes release reactive oxygen species and inflammatory mediators that can
promote activating HSCs and liver fibrosis.
The major cause of morbidity and mortality in cirrhotic patients is the
development of portal hypertension and hyperdynamic circulation. Portal
hypertension develops secondary to fibrosis and vasoregulatory changes, both
intrahepatically and systematically, leading to collateral circulation formation and
hyperdynamic circulation.

Intrahepatically, SECs synthesize both nitric oxide (NO) and endothelin-1 (ET-1)
which act on HSCs, causing relaxation or contraction of the sinusoids,
respectively, and controlling sinusoidal blood flow. In patients with cirrhosis,
there is an increase in ET-1 production as well as an increase in the sensitivity of
its receptors with a decrease in NO production. This leads to increased
intrahepatic vasoconstriction and resistance, initiating portal hypertension.
Vascular remodeling mediated by the contractile effects of HSCs in the sinusoids
augments the increase in vascular resistance. To compensate for this increase in
intrahepatic pressure, collateral circulation is formed.
In systemic and splanchnic circulation, the opposite effect happens, with an
increase in the production of NO leading to systemic and splanchnic vasodilation
and decreased systemic vascular resistance. This promotes the activation of the
renin-angiotensin-aldosterone system (RAAS), leading to sodium and water
retention and resulting in a hyperdynamic circulation. Thus, in cirrhosis with
portal hypertension, there is depletion of vasodilators (predominantly NO)
intrahepatically but an excess of NO extrahepatically in the splanchnic and
systemic circulation, which lead to sinusoidal vasoconstriction and splanchnic
(systemic) vasodilation. The collaterals also contribute to the hyperdynamic
circulation by increasing the venous return to the heart.
Histopathology

Cirrhosis is classified based on morphology or etiology.

Morphology Classification
Morphologically, cirrhosis is (1) micronodular, (2) macronodular, or (3) mixed.
This classification is not as clinically useful as etiologic classification.
1. Micronodular cirrhosis (uniform nodules less than 3 mm in diameter):
Cirrhosis due to alcohol, hemochromatosis, hepatic venous outflow obstruction,
chronic biliary obstruction, jejunoileal bypass, and Indian childhood cirrhosis.

2. Macronodular cirrhosis (irregular nodules with a variation greater than 3 mm

in diameter): Cirrhosis due to hepatitis B and C, alpha-1 antitrypsin deficiency,
and primary biliary cholangitis.

3. Mixed cirrhosis (when features of both micronodular and macronodular

cirrhosis are present): Usually micronodular cirrhosis progresses into
macronodular cirrhosis over time.

Etiology Classification
Based on the cause of cirrhosis which is sub-classified as follows:
1. Viral - hepatitis B, C, and D

2. Toxins - alcohol, drugs

3. Autoimmune - autoimmune hepatitis

4. Cholestatic - primary biliary cholangitis, primary sclerosing cholangitis

5. Vascular - Budd-Chiari syndrome, sinusoidal obstruction syndrome, cardiac
cirrhosis

6. Metabolic - hemochromatosis, NASH, Wilson disease, alpha-1 antitrypsin

deficiency, cryptogenic cirrhosis.

History and Physical

Patients with cirrhosis can be asymptomatic or symptomatic, depending on

whether their cirrhosis is clinically compensated or decompensated. In
compensated cirrhosis, patients are usually asymptomatic, and their disease is
detected incidentally by labs, physical exam, or imaging. One of the common
findings is mild to moderate elevation in aminotransferases or gamma glutamyl
transpeptidase with possible enlarged liver or spleen on exam. On the other hand,
patients with decompensated cirrhosis usually present with a wide range of signs
and symptoms arising from a combination of liver dysfunction and portal
hypertension. The diagnosis of ascites, jaundice, hepatic encephalopathy, variceal
bleeding, or hepatocellular carcinoma in a patient with cirrhosis signifies the
transition from a compensated to a decompensated phase of cirrhosis. Other
complications of cirrhosis include spontaneous bacterial peritonitis and a
hepatorenal syndrome which occur in patients who have ascites.
Multiple Organs Affected
Gastrointestinal:
Portal hypertension can cause ascites, hepatosplenomegaly and prominence of the
periumbilical abdominal veins resulting in caput medusa. Esophageal varices are
another complication of cirrhosis secondary to increased blood flow in the
collateral circulation, with a mortality rate of at least 20% at six weeks after a
bleeding episode. Patients with alcoholic cirrhosis are at increased risk of small
bowel bacterial overgrowth and chronic pancreatitis, and patients with chronic
liver disease have a higher rate of gallstones formation.
Hematologic:
Anemia can occur due to folate deficiency, hemolytic anemia (spur cell anemia in
severe alcoholic liver disease), and hypersplenism. There can be pancytopenia
due to hypersplenism in portal hypertension, impaired coagulation, disseminated
intravascular coagulation, and hemosiderosis in patients with cirrhosis due to
different causes.
Renal:
Patients with cirrhosis are prone to develop hepatorenal syndrome secondary to
systemic hypotension and renal vasoconstriction, causing the underfilling
phenomenon. Splanchnic vasodilation in cirrhosis leads to decreased effective
blood flow to the kidneys, which activates the RAAS system, leading to retention
of sodium and water and renal vascular constriction. However, this effect is not
enough to overcome the systemic vasodilation caused by cirrhosis, leading to
renal hypoperfusion and worsened by renal vasoconstriction with the end point of
renal failure.

Pulmonary:
Manifestations of cirrhosis include hepatopulmonary syndrome, portopulmonary
hypertension, hepatic hydrothorax, decreased oxygen saturation, ventilation-
perfusion mismatch, reduced pulmonary diffusion capacity, and hyperventilation.
Skin:
Spider nevi (central arterioles surrounded by multiple smaller vessels that look
like a spider, hence the name) are seen in patients with cirrhosis secondary to
hyperestrogenemia. Liver dysfunction leads to a sex hormone imbalance, causing
increased estrogen to free testosterone ratio and the formation of spider nevi.
Palmer erythema is another skin finding that is seen in cirrhosis and is also
secondary to hyperestrogenemia. Jaundice is a yellowish discoloration of the skin
and mucous membranes that is seen when the serum bilirubin is greater than 3
mg/dL and in decompensated cirrhosis.
Endocrine:
Patients with alcoholic liver cirrhosis can develop hypogonadism and
gynecomastia. The pathophysiology is multifactorial, mainly due to
hypersensitivity of estrogen and androgen receptors seen in cirrhotic patients.
Hypothalamic pituitary dysfunction has also been implicated in the development
of these conditions. Hypogonadism can lead to decreased libido and impotence in
males with loss of secondary sexual characteristics and feminization. Women can
develop amenorrhea and irregular menstrual bleeding as well as infertility.
Nail changes:
Clubbing, hypertrophic osteoarthropathy, and the Dupuytren contracture are seen.
Other nail changes include azure lunules (Wilson disease), Terry nails and
Muercke nails.
Others:
Fetor hepaticus (sweet musty breath smell due to high levels of dimethyl sulfide
and ketones in the blood) and asterixis (flapping tremor when the arms are
extended and the hands are dorsiflexed) are both features of hepatic
encephalopathy that can be seen in cirrhosis. Cirrhosis can lead to a
hyperdynamic circulation, reduction in lean muscle mass, muscle cramps, and
umbilical herniation.
Physical examination in patients with cirrhosis may reveal stigmata of chronic
liver disease (spider telangiectasias, palmar erythema, Dupuytren's contractures,
gynecomastia, testicular atrophy), signs of portal hypertension (ascites,
splenomegaly, caput medusae, Cruveilhier-Baumgarten murmur- epigastric
venous hum), signs of hepatic encephalopathy (confusion, asterixis and fetor
hepaticus), and other features such as jaundice, bilateral parotid enlargement, and
scant chest/axillary hair.
Evaluation

Lab Findings
Aminotransferases are usually mildly to moderately elevated with aspartate
aminotransferase (AST) greater than alanine aminotransferase (ALT); however,
normal levels do not exclude cirrhosis. In most forms of chronic hepatitis (except
alcoholic hepatitis), the AST/ALT ratio is less than one. As chronic hepatitis
progresses to cirrhosis, there is a reversal of this AST/ALT ratio. Alkaline
phosphatase (ALP), 5'- nucleotidase, and gamma glutamyl transferase (GGT) are
elevated in cholestatic disorders. Prothrombin time (PT) is elevated due to
coagulation factor defects as well as bilirubin, while albumin is low as it is
synthesized by the liver and the liver's functional capacity goes down. Thus
serum albumin and PT are true indicators of synthetic hepatic function.
Normochromic anemia is seen; however, macrocytic anemia can be seen in
alcoholic liver cirrhosis. Leukopenia and thrombocytopenia are also seen
secondary to sequestration by the enlarged spleen as well as alcohol suppression
effect on the bone marrow. Immunoglobulins, especially the gamma fraction, are
usually elevated due to impaired clearance by the liver.
Specific Labs to Investigate Newly Diagnosed Cirrhosis
Serology and PCR techniques for viral hepatitis and autoimmune antibodies (anti-
nuclear antibodies [ANA], anti-smooth muscle antibodies (ASMA), anti-liver-
kidney microsomal antibodies type 1 (ALKM-1) and serum IgG
immunoglobulins) for autoimmune hepatitis and anti-mitochondrial antibody for
primary biliary cholangitis may be ordered. Ferritin and transferrin saturation for
hemochromatosis, ceruloplasmin and urinary copper for Wilson disease, Alpha 1-
antitrypsin level and protease inhibitor phenotype for Alpha 1-antitrypsin
deficiency, and serum alpha fetoprotein for hepatocellular carcinoma (HCC) are
other useful tests.
Imaging and Liver Biopsy
A number of imaging modalities are used alongside with labs to help in the
diagnosis of cirrhosis. These include ultrasound, CT, MRI, and transient
elastography (fibroscan).
Ultrasonography is a cheap, noninvasive, and available modality for the
evaluation of cirrhosis. It can detect nodularity and increased echogenicity of the
liver, which are seen in cirrhosis; however, it is nonspecific as these findings can
be seen in fatty liver as well. It can also determine the ratio of the caudate lobe
width to right lobe width which usually increases in cirrhosis. Moreover, it is a
useful screening tool for HCC in cirrhotic patients. Duplex Doppler
ultrasonography helps to assess the patency of hepatic, portal, and mesenteric
veins.
CT and MRI with contrast can be used to detect HCC and vascular lesions, with
MRI being superior to CT. MRI also can be used to detect the level of iron and fat
deposition in the liver for hemochromatosis and steatosis, and biliary obstruction
if an MRC (magnetic resonance cholangiography) is obtained. MRI, however, is
expensive and not readily available.
Transient elastography (fibroscan) is a noninvasive method that uses high
velocity ultrasound waves to measure liver stiffness which correlates with
fibrosis. In cirrhosis, a colloid liver spleen scan using technetium-99m sulfur
colloid may show increased uptake of colloid in the bone marrow and spleen
when compared to the liver. Presence of varices in the esophagus or stomach on
esophagogastroduodenoscopy (EGD) suggests portal hypertension.
Liver biopsy is the gold standard for diagnosing cirrhosis as well as assessing the
degree of inflammation (grade) and fibrosis (stage) of the disease. Nevertheless, it
can miss the diagnosis at times due to sampling errors. The diagnosis of cirrhosis
by biopsy requires the presence of fibrosis and nodules. The nodular pattern can
be micronodular, macronodular, or mixed with the micronodular pattern
representing an independent risk factor of elevated hepatic venous pressure
gradient (HVPG) and a more severe disease.
Noninvasive tests using direct and indirect serum markers are being used to detect
patients with significant fibrosis/cirrhosis from patients with no/mild fibrosis.
Examples are AST to platelet ratio index (APRI), Fibrosis-4 (FIB-4), FibroTest-
ActiTest, and Fibrosure.
Treatment / Management

Damage to the liver is permanent. Nevertheless, further injury to the liver should
be avoided to halt the progression of the disease. General management to prevent
chronic liver disease includes avoidance of alcohol, vaccination for HBV and
HCV, good nutrition with a balanced diet, weight reduction, and early treatment
of precipitating factors like dehydration, hypotension, and infections. This is
achieved by routine monitoring of volume status, kidney function, varices
development, and progression to HCC.
Specific therapy usually targets the etiology including antiviral medications in
viral hepatitis, steroids and immunosuppressant agents in autoimmune hepatitis,
ursodeoxycholic acid and obeticholic acid in primary biliary cholangitis, copper
chelation in Wilson disease, and iron chelation and phlebotomy in
hemochromatosis. Weight loss of at least 7% is beneficial in NASH, and alcohol
abstinence is crucial in alcoholic cirrhosis.
Prognosis

Predictive models for the prognosis of cirrhosis estimate the ten-year survival in
patients with compensated cirrhosis at 47%, but this drops to 16% once a
decompensating event occurs. The Child-Turcotte-Pugh (CTP) scoring or
classification uses serum albumin, bilirubin, PT, ascites, and hepatic
encephalopathy to classify patients with cirrhosis into classes A, B, and C. One-
and two-year survival rates for these classes are 100% and 85% (A), 80% and
60% (B), and 45% and 35% (C). The model for end-stage liver disease (MELD)
score is another model used to predict the short-term mortality of patients with
cirrhosis. It uses serum bilirubin, creatinine, and INR to predict the mortality
within the next three months. Based on the MELD score (more recently the
MELDNa score), the priority of organ allocation for liver transplantation for
patients with cirrhosis is adjudicated in the US.
Liver transplantation is indicated in decompensated cirrhosis that does not
respond to medical treatment. The one-year and five-year survival rates after liver
transplantation are approximately 85% and 72%, respectively. Recurrence of the
underlying liver disease can occur after a transplant. Long-term side effects of
immunosuppressant drugs is another cause of morbidity in transplant patients.
Pearls and Other Issues
Hepatocellular Carcinoma
HCC is the most common primary cancer in the liver, and its incidence is
increasing. Cirrhosis secondary to HBV and HCV are the most common risk
factors. Routine monitoring of cirrhotic patients for development of HCC is
recommended, with at least six monthly screenings using abdominal
ultrasonography.
Enhancing Healthcare Team Outcomes

Treatment and Prevention liver cirrhosis is best done by an interprofessional team

that includes a hepatologist, gastroenterologist, liver surgeon, pathologist
infectious disease specialist, nurse practitioner, primary care provider and the
internist. All healthcare workers should follow patients with liver dysfunction
from any cause because it can quickly become irreversible. Liver cirrhosis is
associated with many systemic complications that can cause death. Liver
transplant is not always an option because of the shortage of donors.

Pictures 20. Cirrhosis Image

2. Peptic ulcer

1) Definition
Peptic ulcer is a round or semi-round / oval picture on the surface of the gastric
mucosa so that the continuity of the gastric mucosa is broken in the ulcer region.
Peptic ulcer is also called gastric, duodenal or esophageal ulcer, depending on its
location.

Peptic ulcer is a break in the continuity of the gastric mucosa that extends below
the epithelium. Mucosal damage that does not extend below the epithelium is
called erosion, although it is often considered an "ulcer" (for example, a stress
ulcer). By definition, peptic ulcer can be located in any part of the
gastrointestinal tract affected by gastric acid sap, namely the esophagus, stomach,
duodenum, and after gastroenterostomy, also jejenum.

Peptic ulcer is mucous membrane damage due to psychosomatic factors, toxins,

or Streptococcus germs. Psychosomatic factors (eg fear, anxiety, fatigue,
excessive desire) can stimulate excessive HCL secretion. HCL will damage the
gastric mucous membranes. Peptic ulcer is also called mag disease.

Duodenal ulcer, the most common type of peptic ulcer, occurs in the duodenum,
which is the first few centimeters of the small intestine, just below the stomach.

Gastric ulcers are less common, usually occurring along the upper arch of the
stomach. If a part of the stomach has been removed, marginal ulcers can occur,
in the area where the remaining stomach has been connected to the intestine.

2) Etiology

A common cause of peptic ulceration is an imbalance between gastric fluid

secretion and the degree of protection provided by the gastroduodenal mucosal
barrier and neutralization of gastric acid by deudenum fluid.

Specific causes include:

a. H. pylori bacterial infection

In the last five years, it was found that at least 75% of peptic ulcer patients had
chronic infections in the latter part of the gastric mucosa, and the duodenal
mucosa by H. pylori bacteria. Once the patient is infected, the infection can last a
lifetime unless the bacteria are eradicated with antibacterial treatment.
Furthermore, bacteria are able to penetrate the mucosal barrier, both with their
own physical ability to penetrate the barrier and by releasing digestive enzymes
that melt the barrier. As a result, the strong digestive acid secreted by the
stomach can penetrate into the epithelium tissue and digest the epithelium, even
the surrounding tissues. This condition leads to the condition of peptic ulcer.

b. Increased acid secretion

In most patients who suffer from peptic ulcer in the early part of the duodenum,
the amount of gastric acid secretion is greater than normal, often even doubling
from normal. Although half of this increase in acid might be caused by bacterial
infection, animal trials added evidence of excessive stimulation of nerve acid
secretion by nerves in humans with peptic ulcer leading to excessive secretion of
gastric fluid (Guyton, 1996). Predisposing an increase in acid secretion include
psychogenic factors such as when experiencing depression or anxiety and
smoking.

c. Consumption of medicines

Drugs such as NSAIDs / nonsteroidal anti-inflammatory drugs such as

indomethacin, ibuprofen, salicylic acid have a cyclo-oxygenase inhibitory effect
thereby inhibiting prostaglandin synthesis from arachidonic acid systemically
including gastric epithelium and duodenum. On the other hand, this also
decreases HCO3 secretion - thereby weakening mucosal protection. Another
effect of this drug is to damage the local mucosa through non-ionic diffusion into
mucosal cells. This drug also impacts on platelet aggregation so that it will
increase the danger of ulcer bleeding

d. Physical stress
 Physical stress caused by shock, burns, sepsis, trauma, surgery, respiratory
failure, kidney failure, and damage to the central nervous system (Lewis, 2000).
If this physical stress condition continues, then epithelial damage will spread and
the condition of peptic ulcer becomes more severe.

e. Gastrointestinal reflux

Gastric intestinal reflux with abundant bile salts and pancreatic enzymes that fill
the mucosal surface can predispose to mucosal epithelial damage.

3) Clinical Manifestations

Ulcer symptoms can disappear for days, weeks or months and can even disappear
only until they appear again, often without an identifiable cause. Many
individuals experience symptoms of ulcers, and 20-30% experience perforation or
hemorrhage without any preceding manifestations.

a) Pain

Usually patients with ulcers complain of blunt pain, such as puncture or a

burning sensation in the middle epigastrium or in the back. It is believed that
pain occurs when stomach and duodenal acid content increase causing erosion
and stimulating the exposed nerve endings. Another theory suggests that contact
of the lesion with acid stimulates the local reflex mechanism that begins
contracting the surrounding smooth muscle. Pain usually goes away by eating,
because eating neutralizes acid or by using alkalis, but if the stomach is empty or
alkaline is not used again the pain arises. Sharp local tenderness can be relieved
by applying gentle pressure on the epigastrium or just to the right of the midline.
Some symptoms decrease by applying local pressure to the epigastrium.

b) Pirosis (epigastric pain)

 Some patients experience a burning sensation in the esophagus and stomach,
which rises to the mouth, sometimes accompanied by acid eructation. Eructation
or belching is common when the patient's stomach is empty.

c) Vomiting

Although rare in uncomplicated duodenal ulcers, vomiting can be a symptom of

peptic ulcer. This is related to the formation of scar tissue or acute swelling of
the mucous membrane that is inflamed around it in acute ulcers. Vomiting can
occur or is not preceded by nausea, usually after severe pain that is relieved by
ejection of stomach acid content.

d) Constipation and bleeding

Constipation can occur in ulcer patients, possibly as a result of diet and

medication. Patients can also present with gastrointestinal bleeding. A small
proportion of patients who experience acute ulcers have no previous complaints,
but they show symptoms afterwards.

4) Pathophysiology

Peptic ulceration occurs in the gastroduodenal mucosa because this tissue cannot
withstand the action of gastrointestinal acid (hydrochloric acid and pepsin).
Erosion occurs due to an increase in the concentration and action of peptin acid,
or with regard to a decrease in the normal defense of the mucosa. Damaged
mucosa cannot secrete mucus which acts sufficiently as a barrier against
hydrochloric acid.

Gastric secretion occurs in 3 similar phases:

a. Cephalic

This first phase begins with stimuli such as sight, smell or taste of food acting on
cerebral cortical receptors which in turn stimulates the vagal nerve. In essence,
foods that don't cause appetite cause little effect on gastric secretion. This is what
causes frequent conventional food given to patients with peptic ulcer. At present
many gastroenterologists agree that the filtered diet has a significant effect on
gastric acidity or ulcer healing. However, excessive vagal activity during the
night when the stomach is empty is a significant irritant.

b. Gastric phase

In this phase stomach acid is released as a result of chemical and mechanical

stimulation of the stomach wall receptors. Vagal reflexes cause acid secretion in
response to gastric distension by food.

c. Intestinal phase

Food in the small intestine causes the release of hormones (considered to be

gastrin) which in turn stimulates gastric acid secretion. In humans, gastric
secretion is a mixture of mucocolisaccharides and mucoproteins that are secreted
continuously through the mucosal glands. This mucus absorbs pepsin and
protects the mucosa against acids. Hydrochloric acid is secreted continuously,
but the secretion increases due to neurogenic and hormonal mechanisms that start
from the stimulation of the stomach and intestine.

5) Diagnosis

The most important criterion in the diagnosis of duodenal ulcer is the typical pain
that is lost by food. The history is not as informative as in patients with peptic
ulcers, because the symptoms of unpleasant epigastrum are more common. It is
usually not possible to distinguish between gastric and duodenal ulcers only from
the history. The diagnosis of peptic ulcer is usually confirmed by barium
radiogram examination. If barium radiography fails to prove the presence of
ulcers in the stomach or duodenum but the symptoms persist, then there are
indications for endoscopic examination. Estimation of serum gastrin levels can
be done if gastric carcinoma or Zolliger-Ellison syndrome is suspected. The
diagnosis of gastric ulcer is made based on clinical observation, results of
radiological and endoscopic examination, accompanied by biopsy for
histopathological examination, CLO (Campylobacter Like Organism) test, and
Helicobacter pylori culture. Clinically patients complain of heartburn sometimes
radiating to the waist accompanied by nausea and vomiting.

a. Radiology: Visible image of a niche or crater.

b. Endoscopy: Visible gastric ulcer with regular margins, smooth mucosa,

radiation folds out from the ulcer's edge regularly.

c. Biopsy results: Did not show any malignancy

d. CLO (Compylobacter LikeOrganism) / PA (Pyloric Antrum) test:

To indicate whether there is Helicobacter pylori infection in order to eradicate

germs.

e. Endoscopic examination of the food channel facilitates the precise diagnosis

of duodenal ulcer. Endoscopy is not necessary for the diagnosis of duodeum
ulcer if it has been identified by barium radiographic examination. However,
endoscopy may be of greatest value:

(1) in detecting a duodenal ulcer suspected in the absence of an ulcer that can be
shown radiographically,

(2) in patients with radiographic deformity and uncertainty regarding ulcer

activity,

(3) in recognizing ulcers that are too small or too shallow to be recognized by x-
rays and (4) in recognizing (or eliminating), ulcers as an active source of bleeding
in food channels. Endoscopy allows visualization and photographic
documentation of the nature of the ulcer, its size, shape and location and can
provide a basis / reference base for the assessment of ulcer healing.

6) Complications
 Most ulcers can be cured without further complications. But in some cases,
peptic ulcer can cause complications that can be fatal, such as penetration,
perforation, bleeding and blockage.

1) Penetration

           An ulcer can penetrate the muscular wall of the stomach or duodenum and
reach other adjacent organs, such as the liver or pancreas. This will cause severe
sharp pain and persistence, which can be felt outside the affected area (for
example in the back, because duodenal ulcers have penetrated the pancreas). Pain
will increase if the patient changes his position. If drug administration is not
successful in overcoming this situation, surgery may be needed.

2) Perforation

            Ulcers on the front surface of the duodenum or (more rarely) in the
stomach can penetrate the walls and form open holes into the abdominal cavity.
Pain is felt suddenly, very intense and continuous, and immediately spreads
throughout the stomach. Patients can also feel pain in one or both shoulders,
which will get worse if the patient sighs deeply. Changes in position will worsen
the pain so that patients often try to lie still. When pressed, the stomach feels
pain. Fever indicates an infection in the stomach. If not resolved immediately
shock can occur. This situation requires immediate surgical treatment and
administration of intravenous antibiotics.

3) Bleeding

Bleeding is the most common complication. Symptoms of bleeding due to ulcers

are:

a. vomiting fresh blood or reddish-brown lumps that come from partially

digested food, which resembles coffee deposits

b. Blackish stool or bloody stool.

 With endoscopy, ulcer cautery can be performed. If the source of bleeding
cannot be found and the bleeding is not great, treatment with H2-antagonists and
antacids is given. Patients are also fasted and infused, so that the digestive tract
can rest. If the bleeding is severe or persistent, endoscopy can be injected with
materials that can cause clots. If this fails, surgery is required.

4) Blockage.

Swelling or inflamed tissue around the ulcer or scar tissue due to a previous
ulcer, can narrow the hole in the end of the stomach or narrow the duodenum.
Sufferers will experience repeated vomiting, and often vomit large amounts of
food eaten several hours before.

Other symptoms are fullness in the stomach, flatulence and decreased appetite.
Prolonged vomiting can cause weight loss, dehydration and mineral imbalances.
Overcoming ulcers can reduce blockages, but severe blockages require
endoscopic or surgical procedures.

The goal of treatment for peptic ulcer is to eliminate complaints / symptoms of

patients, cure ulcers, prevent relapses and prevent complications. Broadly
speaking, peptic ulcer treatment is eradication of H. Pylori bacteria and
treatment / prevention of NSAID gastropathy (Tarigan, 2001). At present, the
emphasis of treatment is aimed at the broad role of Helicobacter pylori infection
as a cause of peptic ulcer. Eradication of Helicobacter pylori infection can be
done according to antibiotic treatment. Ulcer patients should stop treatment with
NSAIDs or if this cannot be done long-acting prostaglandin agonists, such as
misoprostol. In providing therapy for acute peptic ulcers are generally similar to
patients with chronic peptic ulcers. If you find patients with severe complaints,
then you should be treated in hospital, and need to rest for several weeks.

7. Patients with mild complaints can generally be done with outpatient treatment.
Broadly speaking, the management of patients with peptic ulcer is as follows:
a.Non - Pharmacology

1) Rest

In general, ulcer patients are recommended outpatient treatment, if it is less

successful or there are new complications recommended hospitalization. Healing
will be faster with hospitalization although the mechanism is unclear, possibly by
increased rest hours, reduced bile reflux, stress and analgesic use. Stress and
anxiety play a role in increasing gastric acid and ulcer disease.

2) Diet

Soft foods especially filtered porridge, foods containing milk are no better than
ordinary foods, because refined foods will stimulate acid expenditure. Chili,
stimulating foods, foods containing acid can cause pain in some patients with
ulcers and non-ulcer dyspepsia, although the link has not been proven yet.

3) Never smoke

Smoking prevents chronic gastric ulcer healing, inhibits pancreatic bicarbonate

secretion, increases acidity of the duodenal bulb, increases duogenogastric reflux
due to relaxation of the pyloric sphincter while increasing recurrence of ulcers.

Alcohol has not been proven to have a detrimental effect. Acidic orange juice,
coca-cola, beer, coffee do not have an ulcerogenic effect on the gastric mucosa
but can increase acid secretion and are not yet clear to prevent ulcer healing and
should not be taken on an empty stomach.

Pharmacology

1) H2 Receptor Antagonists

H2 receptor antagonists reduce gastric acid secretion by competing with

histamine to bind to H2 receptors on gastric pariental cells. When histamine
binds to H2, acid will be produced. By blocking the binding site between
histamine and the receptor replaced by these drugs, acid will not be produced.
Side effects of this class of drugs are diarrhea, headache, drowsiness, lethargy,
pain in the muscles and constipation

The ability of H2 receptor antagonists to reduce gastric acid in addition to low

toxicity is an advance in the treatment of disease. Results from several clinical
trials show these drugs can effectively preserve symptoms during acute episodes
and speed healing of duodenal ulcers.

2) PPI (Proton Pump Inhibitor)

The mechanism of action of PPI is to block the work of the enzyme KH ATPase
which will break down the KH ATP will produce energy used to remove acid
from the canaliculi and pariental into the gastric lumen. Long can cause an
increase in blood gastin and can cause carcinoid tumors in mice. In humans it has
not been proven that its safety is impaired in long-term use (Tarigan, 2001).
Proton pump inhibitors are metabolized in the liver and eliminated in the kidneys.
With the exception of patients with severe liver dysfunction, without adjusting the
dose in liver disease and kidney disease. Doses of Omeprazole 20-40 mg / day,
Lansoprazol 15-30 mg / day, Rabeprazol 20 mg / day, Pantoprazol 40 mg / day
and Esomeprazole 20-40 mg / day. Proton pump inhibitors have a very large
effect on acid production. Omeprazole also selectively inhibits carbonate
anhydrous mucosal gastric, which may contribute to its acid suspension (Parischa
and Hoogerwefh, 2008). Side effects of this class of drugs are rare, including
headaches, diarrhea, constipation, vomiting, and red rashes on the skin. Pregnant
and nursing mothers should avoid using PPI.

3) Sulkrafat

In the condition of acid damage, the hydrolysis of mucosal protein mediated by

pepsin also contributes to the erosion and ulceration of the mucosa. This protein
can be inhibited by sulfated polysaccharides. Besides inhibiting the hydrolysis of
mucosal proteins by pepsin, sulcrafate also has an additional cytoprotective
effect, namely stimulation of local production of prostagladin and epidermal
growth factors (Parischa and Hoogerwefh, 2008). Sulkrafat dose 1gram 4x daily
or 2gram 2x daily. Side effects that are often reported are constipation, nausea
and dry mouth

c. Therapy caused by NSAIDs

Antagonistic receptor H2 therapy or PPI can provide a fast response if NSAID

use in peptic ulcer patients is stopped. The use of NSAID drugs in the long term
can cause injury to the gastric mucosa, dyspepsia, and bleeding in the stomach. If
NSAID use is stopped, standard antagonist receptor H2 regimen or PPI or
sucralfate therapy is given. But if NSAID use is continued, then NSAIDs can be
replaced with selective COX-2 inhibitors and combined with misoprostol or PPI.
Misoprostol can suppress gastric acid secretion, increase mucus, bicarbonate
secretion and increase mucosal blood flow as well as mucosal defense and repair.
But the suppressive effect of gastric acid secretion on misoprostol is less strong
compared to H2 receptor antagonist. PPI is the right choice for NSAID use
compared to H2 receptor antagonists and sucralfate, because besides being able to
suppress acid secretion, PPI can also prevent recurrence of peptic ulcer

d. Operation action

There are two goals of surgical therapy in peptic ulcers, namely:

1) To suppress aggressive factors (acids and pepsin) against the pathogenesis of

peptic ulcer. 2) To remove the most resistant place in the antrum, and correct
stasis in the stomach. Surgical therapy is needed if there are indications such as
the following:

1) The ulcer has perforated or penetrated.

2) Frequent bleeding
 3) Difficult to cure with pharmacological therapy (therapeutic failure)

4) Patients older than 60 years

5) Active bleeding that cannot be controlled with endoscopic therapy. Surgical

treatment is often needed for acute peptic ulcers with initial bleeding for 48 hours.

8. Prognosis

Patients with peptic ulcer have a risk of 5% in their lives to experience

perforation. The risk of perforation in peptic ulceration due to consumption of
nonsteroidal anti-inflammatory drugs (NSAIDs) ranges from 0.3% per patient
year, and the incidence of obstruction is 0.1% per patient year.

A study showed that peptic ulcer perforation patients had a mortality of 8.9% in
patients aged <65 years. This mortality rate increases with age and can reach
44.6% in patients over 80 years of age.

- Medical therapy alone gives a cure> 85%.

- If not treated, ulcer disease can cause gastric outlet obstruction as a result of
chronic inflammation and stomach tissue.
- There is a risk of malignant transformation in gastric ulcers.

3. Oesophageal Varices
1) Definition
Esophageal varices are distension of submucosal veins projected into the
esophageal lumen in patients with portal hypertension. Portal hypertension
is an increase in portal blood flow pressure of more than 10 mmHg that
persists, whereas pressure under normal conditions is around 5-10 mmHg.
Portal hypertension is most often caused by cirrhosis of the liver. About
50% of patients with liver cirrhosis will develop esophageal varices, and
 one third of patients with varicose veins will have serious bleeding from
their varicose veins in their lives.
2) Epydemyologi
Varicose veins most commonly occur in a few centimeters of the distal
esophagus although varicose veins can form anywhere along the
gastrointestinal tract. About 50% of patients with cirrhosis will develop
gastroesophageal varices and about 30-70% will develop esophageal
varices (Table 1). About 4–30% of patients with small varicose veins will
become large varicose veins each year and therefore have a risk of bleeding.
3) Etylogy
The etiology of esophageal varices and portal hypertension are diseases that
can affect portal blood flow. This etiology can be classified as prehepatic,
intrahepatic, and post-hepatic.

Prehepatik intrahepatik Pascahepatik

 Plenic venous  Congenital hepatic  Sindroma Budd-Chiari
thrombosis crisis  Inferior vena caval
 Portal venous  Idiopathic portal thrombosis
thrombosis hypertension  Constructive
 Extrinsic  Tuberculosis pericarditis
compression in the  Schistosomiasis  Venocclusive liver
portal vein  Primary biliary disease
cirrhosis
 Alcoholic cirrhosis
 Hepatitis B virus
cirrhosis
 Hepatitis C virus
cirrhosis
 Wilson's disease
 Alpha-1 antitrypsin
deficiency
 Chronic active
hepatitis
 Fulminant hepatitis

4) Pathophysiology
Cirrhosis is the final phase of chronic liver disease which most often causes
portal hypertension. Portal venous pressure is the result of intrahepatic
vascular resistance and blood flow in the portal bed. In cirrhosis, both
intrahepatic vascular resistance and portal flow both increase.
If there is obstruction of portal venous blood flow, whatever the cause, it
will cause an increase in portal venous pressure. High portal venous
pressure is the cause of the formation of portosystemic collateral, although
other factors such as active angiogenesis can also be the cause. However,
the presence of this collateral cannot reduce portal hypertension due to high
resistance and increased portal venous flow. This portosystemic collateral is
formed by the opening and dilatation of the vascular duct that connects the
superior and inferior portal venous and vena cava systems. Collateral flow
through the plexus of the esophageal veins causes the formation of
esophageal varices that connect the blood flow between the portal vein and
the vena cava.
The esophageal venous plexus receives blood from the gastric vein sinastra,
branches of the esophageal vein, short gastric vein / brevis (via the splenic
vein), and will drain blood into the azigos vein and hemiazigos. Whereas
the gastric vein sinistra receives blood flow from the blocked portal vein
into the liver.
The portal vein system has no valves, so resistance at each level between
the right side of the heart and splenic blood vessels will cause retrograde
blood flow and increased pressure transmission. Anastomosis that connects
the portal vein with the systemic circulation can be enlarged so that blood
flow can avoid (bypassing) the obstruction site so that it can directly enter
the systemic circulation.
Portal hypertension is best measured indirectly by using wedge hepatic
venous pressure (WHVP). A difference in pressure between the portal and
systemic circulation (hepatic venous pressure gradient, HVPG) of 10-12
mmHg is required for the formation of varicose veins. Normal HVPG is
 around 5-10 mmHg. Single measurements are useful for determining the
prognosis of compensatory or non-compensatory cirrhosis, while repeated
measurements are useful for monitoring the response of drug therapy and
progression of liver disease.
If the pressure on the vascular wall is very high, rupture of varicose can
occur. The possibility of rupture of varicose veins and the occurrence of
bleeding will increase in proportion to the increase in size or diameter of
varicose veins and the increase in varicose pressure, which is also
proportional to HVPG. Conversely, varicose bleeding does not occur if the
HVPG is below 12 mmHg. The risk of rebleeding decreases significantly
with a decrease in HVPG of more than 20% from the baseline. Patients with
decreased HVPG to <12 mmHg, or at least 20% from the baseline, have a
lower likelihood of recurring varicose bleeding, and also have a lower risk
of ascites, bacterial peritonitis and death.

5) Diagnoses
Esophageal varices usually do not give symptoms if the varicose veins have
not broken, that is, if there is no bleeding. Therefore, if the diagnosis of
cirrhosis has been established the diagnosis should be done through an
examination of esophagogastroduodenoscopy (EGD) which is the gold
standard for determining the presence or absence of esophageal varices. In
patients with compensated cirrhosis and no varicose veins, repeat EGD
every 2-3 years, whereas if there are small varicose veins, then EGD
examination is repeated every 1-2 years.
If the gold standard is not workable or is not available, another possible
diagnostic step is to use Doppler ultrasound from blood circulation (not
endoscopic ultrasound). Other alternative examinations are radiographic
examination by swallowing barium from the esophagus and stomach, and
portal vein angiography and manometry.
 During these tests, it is important to assess the location (esophagus or
stomach) and the size of varicose veins, signs of imminent bleeding, first
bleeding or recurrent bleeding, and if possible to find out the cause and
severity of liver disease.
Esophageal varices usually start from the distal esophagus and will extend
to the proximal esophagus if further. Following are the degrees of
esophageal varices based on endoscopic features.

Picture 21. The Degree of Esophageal Varices

6) Threatment
Pharmacological Therapy
The principle of pharmacotherapy is to reduce portal and intravenous
venous pressure. There are only two pharmacotherapies recommended for
oesophageal varices bleeding: vasopressin and lepressin.
Endoscopic Therapy
Endoscopic therapy is carried out in cases of varicose bleeding, especially
in an effort to achieve homeostasis. Endoscopic findings are also useful as
an indicator of the prognosis of the risk of rebleeding. The endoscopic
technique used to achieve homeostasis is to quickly cut off collateral blood
flow such as ligation or sclerotherapy due to thrombosis. Endoscopy can be
 performed on patients with esophageal varices before the first bleeding
occurs, when the bleeding takes place and after the first bleeding occurs.
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
A way to reduce the resistance of the portal flow by shunting (cutting) the
flow through the liver. The principle is to connect the hepatic vein with the
intrahepatic portal vein branch. The puncture needle is inserted into the
right hepatic vein through a jugular catheter. Subsequently, intra-hepatic
portal vein branches are punctured, the holes are widened and then fixed by
expanding stents (Figure 12). This is another last resort for bleeding that
does not stop or fails with pharmacotherapy, ligation or sclerotherapy.
7) Prognosis
In patients with esophageal varices, about 30% will experience bleeding in
the first year after diagnosis. The mortality rate due to bleeding episodes
depends on the severity of the underlying liver disease.
Deaths due to bleeding range from <10% in cirrhosis patients with
compensatory Child-Pugh A classification to> 70% in cirrhosis patients
with Child-Pugh C. The risk of high rebleeding reaches 80% within 1 year.
In patients with HVPG> 20% mmHg within 24 hours in varicose
hemorrhage, when compared with patients whose pressure is lower, have a
higher risk for the risk of rebleeding in the first week or fail to control
bleeding, and have a higher mortality in 1 year.
In patients who are not treated, about 60% will re-bleed and continue for 1-
2 years.

References:

Bashar Sharma, Savio John, June 3, 2019. hepatic cirrhois

www.ncbi.nlm.nih.gov
 Misnadiarly. 2015. Knowing Gastrointestinal Disease: Gastritis (Dyspepsia or
ulcer), Mycobacteria Infection in Gastrointestinal Ulcers. Jakarta: Torch Popular
Library.

Priyanto, Agus & Lestari, Sri. 2008. Gastrointestinal Endoscopy. Jakarta: Salemba
Medika

Netiana dkk. Varises Esofagus. Departemen Ilmu Kesehatan Telinga Hidung

Tenggorok Bedah Kepala dan Leher. Fakultas Kedokteran Universitas Airlangga

6. What Kind of first treatment should be given based on scenario?

a) Non Pharmacology
1. Rest
• Bed rest
• Fasting until the bleeding stops
• Blood transfusion of Hb> 10gr%
• Liquid + electrolyte / resuscitation infusion
In principle, the resuscitation process is the same as SCBA bleeding or
other acute bleeding, namely correction of intravascular volume and
hemodynamic stabilization. Installation of intravenous lines on large
vessels must be done (not on small vein vessels

2. Diet
• Parent's nutrition
• After improving the diet, porridge often and gradually become plain rice.

b) Pharmacology
• Endoscopy
 On moderate to severe scale bleeding, hematochezia can cause low blood
pressure, push, to shock. Patients with these symptoms should be given
fluids immediately through infusion and blood transfusion.
Then to stop the bleeding, the doctor will run an endoscope. Besides being
used to determine the cause and location of bleeding, endoscopy can also be
used to treat bleeding through the following methods:
- Electrocautery. The procedure uses an electric current to drain blood or
cause bleeding.
- ribbon ligation. This procedure is done by binding to swollen
hemorrhoids or esophageal varices. This action will inhibit blood flow
which causes bleeding.
- Intravariceal endoscopic cyanoacrylate injection. In this procedure, the
doctor will inject a special substance, namely cyanoacrylate, in the area
that addresses bleeding. Cyanoacrylate is a synthetic adhesive that can
be removed bleeding.

• Give Antibiotic

• Give antimicrobial drugs

Prevention

To reduce the risk of infection, people should wash their hands regularly with
soap and water, especially before and after using the bathroom and preparing
food.

This can reduce the frequency of Shigella infections and other types of
diarrhea by up to 35 percent.

Other steps to take when the risk is higher, for example, when traveling,
include:

 Only drink reliably sourced water, such as bottled water

 Watch the bottle being opened, and clean the top of the rim before
drinking

 Make sure food is thoroughly cooked

It is best to use purified water to clean the teeth, and avoid ice cubes, as
the source of the water may be unknown.
 References :

Pickering LK. Buku Ajar Pediatri Rudolph Vol 1 Bab Infeksi Bakteri dan
Virus: Infeksi Salmonella, Shigella dan E. Coli Enterik 663- 708

Offit PA. Buku Ajar Pediatri Rudolph Vol 1 Bab Infeksi Bakteri dan Virus:
Gastroenteritis Virus. 719-720

Permatasari, DCI. 2013. Tatalaksana Hematokezia. Sumatera Utara: USU.

repository.usu.ac.id

7. Explain the islamic perspective according to the scenario !

Imam An-Nawawi, Al-Adzkar

َ ‫ت ال َّشافِي اَل َشاف َِي إاَّل أَ ْن‬

‫ت شِ َفا ًء اَل‬ َ ْ‫ب ْال َبأ‬
َ ‫س ا ْشفِ أَ ْن‬ ِ ‫اس أَ ْذ ِه‬
ِ ‫اللَّ ُه َّم َربَّ ال َّن‬
‫ي َُغا ِد ُر َس ْقمًا‬
Means :
“My Lord, the Lord of human, spare me sickness. Give me a cure because you’re
a healer. Nothing can cure a disease except you give with a healing that leaves no
pain”

Al-qur’an Surah An-Nur: 26

َ ‫ا ُء َواَل ي ُْظلَم‬BBBBBBB‫ز ِّكي َمنْ َي َش‬BBBBBBBُ
‫ون َفتِياًل‬BBBBBBBُ َ ‫بَل هَّللا ُ ي‬
ِ ۚ ‫ ُه ْم‬BBBBBBB‫ون أَ ْنفُ َس‬ َ ‫تَر إِلَى الَّذ‬
َ ‫ِين ي َُز ُّك‬ َ ‫أَلَ ْم‬

“Do you not pay attention to people who consider themselves clean ?. Actually
God cleanses who He wants and they don't persecute one bit”
References:

Damaskus: Darul Mallah, 1971 M/1391 H], halaman 113.

Al-qur’an Surah An-Nur: 26