A man aged 55 years, come to emergency unit with blood diarrhea complaints. Patients also complain of heartburn. A history of using medications for arthritic pain in the knee during the last 6 months. A history of suffering from the DM and irregular treatment.
3. A man aged 55 years, come to emergency unit with blood diarrhea
complaints. Patients also complain of heartburn. A history of using
medications for arthritic pain in the knee during the last 6 months.
A history of suffering from the DM and irregular treatment.
4. HEARTBURN
• Is retrosternal burning sensation in the area, which arise
suddenly and spread up to the neck ; perhaps with reflux
liquid into the mouth is often caused by gastroesophageal
reflux
DM
• Is a chronic metabolic disease or disorders with
multiple etiologies characterized by high blood sugar
levels accompanied by impired metabolism of
carbohydrates, lipids, and proteins as a result of
insufficiency of insulin function
( Kamus Kedokteran Dorland. Edisi 28. Hal 501)
( Kamus Kedokteran Dorland. Edisi 28. Hal 309)
5. A man aged 55
years
Blood diarrhea
complaints
Patients also
complain of
heartburn
A history of
using
medications for
arthritic pain in
the knee
Suffering from
the DM and
irregular
treatment
12. Digestive system Motility Secretion Digestion Absorpsi
Mouth and saliva Chew Saliva
Amilase
Mukus
Lisozim
Digestion of
carbohydrates begins
The food was not;
some drugs such as
nitroglycerin
Pharynx and
esophagus
Swallow Flawless - -
Stomach Relaxation
receptive;
peristalsis
Gastric juice
• HCl
• Pepsin mucus
• Intrinsic factor
Carbohydrate
digestion continues in
the corpus of the
stomach; protein
digestion begins in
the gastric antrum
The food was not;
some fat soluble
ingredients, such as
alcohol and aspirin
Pancreatic exocrine There is no Pancreatic digestive enzymes
•Trypsin, chymotrypsin,
karboksipeptidase
•Amylase
•Lipase
NaHCO3 liquid secretion of
the pancreas
These pancreatic
enzymes complete the
digestion in the
duodenum lumen
-
13.
14. • Heartburn is caused by a back-up of stomch acid into the esophagus. When
stomach acid comes into contact with the walls of the esophagus it often
causes a “burning” feeling.
• Certain foods and lifestyle choices can increase the back up of stomach
acid, making symptoms worse.
• The most common cause is due to the use of NSAIDs in the treatment of
artritisreumatoid and osteoartris. The use of NSAIDs (eg, aspirin,
piroxicam, ibuprofen, meloxicam, celecoxib, trisalicylate etc.), have a
direct effect on the gastric mucosa and causes the formation of ulcers. may
be caused because the destruction of one of the protective barrier in the
stomach.
15. NSAIDs can cause stomach ulcers through two ways:
a. Irritate the stomach epithelium directly
b. Through inhibiting the synthesis of prostaglandins.
However, the inhibition of prostaglandin synthesis is the dominant factor
that causes peptic ulcers by NSAIDs. Prostaglandins are compounds that
disentsis in the gastric mucosa that protects the body's physiological
functions such as renal function, homeostasis and gastric mucosa.
Based on the literature, the mechanisms involved still unknown but is
thought inhibited production of prostaglandins in the stomach so that the
protection of the gastric mucosa decreases and increases the risk of peptic
ulcers.
16.
17.
18. • The impact of the inhibition of COX- 1 is the reduction of prostaglandin synthesis so that the physiological
regeneration of the gastric mucosa becomes blocked.
• Long-term NSAID use cause local irritation of the gastric mucosa becomes longer and more intense. So the
gastric mucosa which originally was either be damaged or the gastric mucosa that is damaged can be
bleeding.
• Inhibition of COX-1 would result in a decrease in production tromboxan, followed by the extension of the
blood clotting time ease of bleeding.
• COX-2 inhibitor celecoxib, and other nimesulid experimentally not interfere with blood clotting. Along
with the growing process of vasoconstriction, increased blood clotting due to the more independent of
COX-1 pathway in synthesizing tromboxan will facilitate the occurrence of heart attack in users of
NSAIDs with inhibition of COX-2 which is highly selective.
• Inhibition of prostaglandin biosynthesis in the kidneys causing disruption of homeostasis. In patients with
hypovolemia, heart failure, hepatic cirrhosis, blood flow and filtration rate glomerolus Gijal will be
reduced, even acute renal failure can occur.
19.
20. • Diabetes Mellitus patients with decreased insulin levels. Insulin plays a
role in stimulating the synthesis of bone matrix and cartilage formation. In
addition, insulin is also very important in normal bone mineralization, and
stimulate the production of IGF-1 by the liver.
• The role of insulin on matrix synthesis, especially in osteoblast
differentiation and function of IGF-1 increases the number of cells that can
synthesize the bone matrix.
• IGF-1 stimulating the synthesis of collagen matrix and bone, stimulate the
replication of cells derived osteoblasts and decreased bone collagen
degradation.
21. • So that a decrease in insulin levels lead to production of IGF I declined
which is a growth factor that plays a role in the process of cartilage repair.
Thus, there is an imbalance between the formation and bone breakdown
which affects the risk of osteoarthritis.
• Therefore, to reduce the pain experienced or lowers blood glucose levels,
patients taking medications such as allopurinol rheumatic NSAIDs,
medicines urikosirik, indomesatisin, or colchicine and corticosteroids and
ACTH hormone drugs.
• The drugs can inhibit the secretion of prostaglandins in the intestine and
stomach that can cause erosion, ulceration and even perforation of the
organ so that it can cause bleeding issued through the mechanism of
vomiting and defecation mechanism.
22.
23. ETIOLOGY
PEPTIC ULCER
DISEASE
• Damage to the
mucosal or
submucosal layer
until the muscle
layer of the GI tract
due to the activity of
pepsin and
excessive stomach
acid
GASTRITIS
• The state of
inflammation or
inflammatory
process in the
gastric mucosa and
submucosa
ULCERATIVE
COLITIS
• A chronic inflammatory
disease of the intestine
(Inflammatory bowel
disease) causes
inflammation and ulcers
continuously on the
innermost layer of the
colon and rectum.
Ulcerative colitis rarely
affects the small
intestine.
DEFINITION
24. GEJALA
PEPTIC ULCER
DISEASE
• Helicobacter pylori
• The secretion of
bicarbonate
• Feature genetic
• Stress
• NSAIDs
GASTRITIS
• Drugs - NSAIDs, such as aspirin,
ibuprofen
• Potent alcoholic beverages
• Bacterial infections - H pylori (most
frequent)
• Viral infections (eg, CMV)
• Fungal infections - Candidiasis,
histoplasmosis, phycomycosis
• Parasitic infection (eg, anisakidosis)
• Acute stress (shock)
• Radiation
• Allergy and food poisoning
• Bile: The reflux of bile
• Ischemia
• Direct trauma
ULCERATIVE
COLITIS
• Etiology is unknown,
but the disease has a
multifactorial and
polygenic causes.
ETIOLOGY
25. GEJALA
PEPTIC ULCER
DISEASE
• The most common
symptom is burning pain
• The pain often occurs
between meals and
sometimes awakens
people from sleep.
• May last minutes to
hours
• Relieved by eating,
taking antacids or acid
blockers.
• include nausea,
vomiting and loss of
appetite and weight,
and bleeding.
GASTRITIS
• Heartburn, anorexia,
belching, nausea,
vomiting, bleeding and
hematemesis
ULCERATIVE
COLITIS
• The predominant
symptom is diarrhea,
which can be
associated with frank
blood in the stool.
• Other symptoms :
abdominal or rectal
pain, fever and weight
loss. Although
• Some patients may
complain of constipation
and rectal spasm.
CLINICAL MANIFESTATION
26. GEJALA
PEPTIC ULCER
DISEASE
• In 70 percent of patients it
occurs between the ages of
25 and 64 years
• Lifetime prevalence of PUD
in the United States is
~12% in men and 10% in
women.
• Moreover,an estimated
15,000 deaths per year
occur as a consequence of
complicated PUD.
GASTRITIS
• In developing countries the
prevalence of Helicobacter
pylori infection in adults is
90% whereas in children
pravelensi Helicobacter
Pylori infection is higher
ULCERATIVE
COLITIS
• Most common between 15
and 40 years of age,
• with a second peak in
incidence between 50 and
80 years.
• The disease affects men
and women at similar rates.
• Studies indicate a
decreased risk of ulcerative
colitis for current smokers,
however, former smokers
are at increased risk of
developing the disease.
EPIDEMIOLOGY
27. GEJALA
PEPTIC ULCER
DISEASE
• Injury atthe mucosa as a result of
the topical encounter with NSAIDs.
NSAIDs are weak acids that
remain in a nonionized lipophilic
form when found within the acid
environment of the stomach.
NSAIDs migrate across lipid
membranes of epithelial cells,
leading to cell injury once trapped
intracellularly in an ionized form.
• Topical NSAIDs can also alter the
surface mucous layer, permitting
back diffusion of H+ and pepsin,
leading to further epithelial cell
damage.
GASTRITIS
• Helicobacter pylori attached to the
gastric epithelium and destroy the
protective mucous layer, leaving
the epithelial area deforested
• Disrupt the gastric mucosal barrier
ULCERATIVE COLITIS
• There are three major hypotheses as to
these antigenic triggers. One hypothesis
is that these triggers are microbial
pathogens, as yet unidentified. According
to this theory, the immune response in
UC is an appropriate but ineffective
response to these pathogens. The
second hypothesis as to the antigenic
trigger in UC is that there is some
common dietary antigen or
nonpathogenic microbial agent to which
the patient mounts an abnormal immune
response. In UC, the immune cells of
the lamina propria are exposed to
numerous luminal antigens. These
luminal antigens are capable of triggering
immune responses. As a result, specific
immune responses to the etiological
agent may be overwhelmed by immune
responses to thousands of luminal
antigens that pass through the damaged
epithelium.
PATOGENESIS
28. GEJALA
PEPTIC ULCER
DISEASE
• Antacids
• Diet
• Anticholinergic
• Inhibiting H2 (cimetidine,
ranitidine, famotidine)
• Anti-microbial therapy
• antibacterial
• Surgery: vagotomi, antrektomi,
gastrectomy
GASTRITIS
• Antacids, such as aspirin, sodium
bicarbonate, and citric acid (Alka-
Seltzer); alumina and magnesia
(Maalox); and calcium carbonate
and magnesia (Rolaids). Antacids
relieve mild heartburn or
dyspepsia by neutralizing acid in
the stomach.
• Histamine 2 (H2) blockers, such
as famotidine and ranitidine. H2
blockers decrease acid
production.
• Proton pump inhibitors (PPIs),
such as omeprazole,
lansoprazole, pantoprazole. PPIs
decrease acid production more
effectively than H2 blockers.
ULCERATIVE
COLITIS
• Diet and supportive therapy
• The choice of drugs depending
on the degree of disease. In mild
to moderate cases can be
administered 5-ASA
(aminosalicylic acid) whereas in
the case of complicated joints
(arthritis) can be administered
orally at a dose sulfasalazine
gradually.
• Surgery. Surgical indications
necessary if found no cases of
drug response (cyclosporine) or
cases with life-threatening
complications, such as
megacolon, perforation, ileus
obstruction / paralytic ileus, and
intestinal bleeding extensively.
MANAGEMENT
29. GEJALA
PEPTIC ULCER
DISEASE
• Pola Healthy living
and adequate rest,
avoid excessive
stress
• Quit smoking
• Modification of diet
GASTRITIS
• Set the feeding
schedule
• Avoid greasy foods,
sour and spicy
• Reduce alcohol
• Control stress
ULCERATIVE
COLITIS
• Psychotherapy is
sometimes
necessary to
prevent
psychological
stress. Avoid
cigarettes and set
the pattern for a
healthier life
• A special diet is not
required, it may be
necessary to avoid
cabbage and
onions because
PREVENTION
30. GEJALA
PEPTIC ULCER
DISEASE
• If the underlying cause of
peptic ulcer is resolved, it
will provide a good
prognosis.
• Most people recover with
treatment of H. pylori
infection, avoid taking
NSAIDs and anti sekretorus
in the stomach.
• Treatment with H.pylori
infection will change the
scientific history of the
disease by lowering the
incidence of this disease.
GASTRITIS
• If the underlying cause of
gastritis is resolved, it will
provide a good prognosis
• Many are cured with
therapy Helicobacter and
avoid NSAIDs
ULCERATIVE
COLITIS
• Pretty much reported
remisis spontaneous and in
the long term. Prognosis
influenced by the presence
or absence of complications
or the level of response to
conservative treatment.
PROGNOSIS
33. PHYSICAL FEATURES OF DIAGNOSTIC
LABORATORY
Complete blood cell (CBC)
Liver and kidney function tests
Gallbladder and pancreatic
function tests
Stool for blood
36. A HISTORY FROM IMAM MUSLIM IN HIS SHAHIH (NO. 2032) :
Told us yahya bin yahya, abu mu’awiya preach to us from Hisham ibn Urwah from
Abdurrahman bin Sa’d of Ka’b bin Malik of a fatrher who said, “ The messenger
sallalahu ‘alaihi wa sallam was eaten by using three fingers, and licking the finger,
before bringing it down”
َعُم ُوبَأ اَنَرَب ْخَأ ،ىَي ْحَي ُْنب ىَي ْحَي اَنَثَّدَحَع ْنَع ،َة َو ُْرع ِْنب ِامَشِه ْنَع ،َةَيِاوِدْب
،ٍكِلاَم ِْنب ِبْعَك ِْنبا ِنَع ،ٍدْعَس ِْنب ِنَم ْحَّالرَلاَق ،ِهيِبَأ ْنَع:«ُلُوسَر َانَك
ِث ََلَثِب ُلُكْأَي َمَّلَس َو ِهْيَلَع ُهللا ىَّلَص ِهللاَأ َلْبَق َُُدَي َُُعْلَي َو ،ََِابَصَأاَهَحَسْمَي ْن »
37. THERE IS A HISTORY OF ABU HASAN BIN AL-MURQI IN SYAMAILNYA AS MENTIONED IN AL-
IHYA TAKHRIJ WORK OF AL-IRAQI (1/432)
ُيْال ركبته ىَلَع استوفز امَعَّالط ىَلَع قعد ذاِإ َانَكىَنُْميْال امَقأ َو ىَرْس
“That (the prophet shallalahu ‘alaihi wassalamu) when he sat down to eat
his knees left and uphold the right food”