Pemicu 4 KGD

405130159
Upper GIT bleeding
= Manifestation are variations, from massive hemmoragic life-threatening until smooth
one even we doesn’t recognizing.
Classification
- Hematemesis  “bloody vomit”, showing upper GIT bleeding at Proximal Lig. Treitz
- Melena  “dark-bloody stool”, showing blood bonding w/ HCl that came from
gaster.

Epidemiology at Indonesia
= Rupture varises gastroesofagus (60%), Gastritis Erosive (30%), Peptic Ulcer (10%).
 High mortality: 60% varises rupture are died.

Sign and Symptom

- Bloddy-dark vomit looks like a coffee (hematemesis)
- Bloddy- dark stool looks like an asphalt (melena)
- W/ or w/o co-morbid as chronic hepatic / respiratory/ heart disease/ kidney problem
- Recall last 24h consumption that related (alcohol, coffee, NSAID,etc)
- History of recurrent hematemesis  DD/: Mallory Wiess Syndrome

Risk Factor: - NSAID abuse

- Cirrhosis Hepatic
Physical Examination
- examination of hemodynamic value (blood circulation)
- evaluation total blood-lost
- Chronic hepatic stigmata founding, abdominal mass / pain, peritonitis sign
- Looks for heart / respiration / rheumatoid disorder
- Rectal Touché
- Aspirated evaluation at NGT  white: not acctive / red maroon: active hemorrhagic

Diagnostic Tools: CBC and CXR. Diagnosis: Firm based on anamnesis, P-E & founding
 DD/: Hemoptisis , Hematokezia

Treatment
1) Stability of hemodynamic  (IV), O2 line, urine catheterization (volume), Vital sign
2) NGT  gastric flushing to made easier endoscopy
3) Bed-rest
4) Supplementation  H2 inhb / PPI medication, Sulfractate, Antacid, Vit. K (hepar)

Referring to better health provider

- Well suspicious was a rupture of varices esofagus
- Bleeding unstop with first line treatment
- In badly anemic condition
LO 1

PEPTIC ULCER
 Peptic Ulcer
• Peptic ulcer is the break of gastric mucosa due to
the corrosive action of pepsin and hydrochloric acid
on the mucosa of the upper gastrointestinal tract.
• Signs are abdominal discomfort, pain (burning builds
up for 1-2 hours, gradually decreases), or nausea.
• Gastric ulcer pain is aggravated by meals, whereas
the pain of duodenal ulcers is relieved by meals.
• Patients with gastric ulcer usually avoids food and
loses weight.
http://www.hopkinsmedicine.org/gastroenterology_hepatology/_pdfs/esophag
us_stomach/peptic_ulcer_disease.pdf
• H.pylori  colonizes in human stomach
• NSAIDS  acidic  diminishing the
hydrophobicity of gastric mucus  gastric acid
& pepsin may injure the epithelium
• NSAIDS  decreases the synthesis of mucosal
prostaglandin
RADIOLOGI (barium X-ray)
 Laboratory Test
• Indication:
- Refractory patients (not healed after 8 weeks of
therapy)
- Recurrent disease
• Serum gastrin and serum calcium (screening for
gastrinoma and multiple endocrine neoplasia/MEN)
• Gastric acid analysis  determine whether the ulcer
is caused by gastric acid hypersecretion (basal acid
output >10 mEq/hr) or decreased mucosal protection
• Gold standard for diagnosis of H.pylori :
endoscopic biopsy
• Urea breath test (UBT)  simple and non-
invasive  H.pylori infection
• H. pylori-positive  IgG and IgA ELISA test levels
are slightly higher
• Esophagogastroduodenoscopy (EGD)  most
direct and accurate method in diagnosing peptic
ulcer
 Medical Therapy
1. Reduce gastric acidity  inhibits or neutralize
acid secretion  antacids, histamin H2-
receptors (cimetidine, ranitidine, famotidine,
nizatidine), PPI (proton pump inhibitors)
• Gold standard in treating peptic ulcer : PPI
(omeprazole, lansoprazole, pantoprazole,
rabeprazole, esomeprazole)
• PPI  prevents NSAID-associated
gastroduodenal ulcers
 Medical Therapy
2. Coat ulcer craters to prevent acid and pepsin from
penetrating to the ulcer base  sucralfate
• Sucralfate  stimulates prostaglandin  promotes
to improve mucosal integrity and enhance epithelial
regeneration

3. Provide a prostaglandin analog  misoprostol 

increases mucosal resistance & inhibits acid secretion,
prophylaxis of NSAID-induced mucosal injury
 Complications
• Hemorrhage
• Perforation
• Gastric outlet obstruction

 Major indications for surgical intervention

 Gastrointestinal Hemorrhage
• Hemorrhage from ulcers stops spontaneously
(75-80%)
• Endoscopic therapy 
to seal the feeding
vessel
 Penetration
• Pancreas, bile ducts, liver, small or large
intestine. Most common : pancreas
 Perforation
• 2 types of perforation :
- Free perforation : gastric contents spill into
abdominal cavity  peritoneal contamination
by gastric, pancreatic, and biliary juices  acute
abdomen
- Contained perforation the ulcer produces a
full-thickness hole in the duodenum or
stomach, but the omentum or other adjacent
organs prevent peritoneal contamination.
 Perforation
• Mostly in older patients on chronic NSAID
therapy
• Initial symptoms : severe abdominal pain,
worse in the epigastrium, nausea, vomiting,
typically the patient is acutely and severely ill
LO 2

INFECTIOUS DIARRHEA
 Infectious Diarrhea
• Diarrhea : an alteration in a normal bowel
movement characterized by an increase in the
water content, volume, or frequency of stools.
• Infectious diarrhea : diarrhea due to an
infectious etiology, often accompanied by
symptoms of nausea, vomiting, or abdominal
cramps.
LO 3

ISCHEMIC COLITIS
Sign and Symptoms
LO 4

DIVERTICULAR DISEASE
 Diverticular Disease
• Consists of :
- Diverticulosis : the presence of diverticula
within the colon
- Diverticulitis : inflammation of a diverticulum
- Diverticular bleeding
 Diverticulitis
• Diagnosis : left lower quadrant pain, rebound
tenderness (peritoneal involvement), fever,
leukocytosis
• Examination : abdominal tenderness or a mass
• CT :
- Thickening of the bowel wall
- Streaky mesenteric fat
- Associated abscess
Treatment
Treatment
LO 5

ANAL FISSURE
 Anal Fissure
• A small tear or cut in the skin lining the anus
which can cause pain and/or bleeding.
• Typical symptoms : extreme pain during
defecation and red blood streaking the stool
• Acute fissure  altered bowel habits or passing a
hard, dry bowel movement
• Chronic fissure  poor bowel habits, overly tight
or spastic anal sphincter muscles, scarring or an
underlying medical problem
 Treatment
• Bowel habits  improved by changing to a
high fiber diet, adding fiber supplements,
using stool softeners when needed, drinking
plenty of fluids
• Topical nitrate (eg. Glyceryl trinitrate 0.2%
ointment)  fissure has been present at least
3 weeks  increases blood flow to the anus
and reduces pain on defecation
 Treatment
• Topical calcium channel blockers (topical
diltiazem 2%)  only if the use of topical
nitrates has not improved symptoms
• Botulinum toxin injected into the internal anal
sphincter  paralyses the sphincter for several
months
• Surgery  open lateral sphincterotomy, closed
lateral sphincterotomy, posterior midline
sphincterotomy
LO 6

ANGIODYSPLASIA
 Angiodysplasia
• The finding of abnormal, ectatic, dilated,
tortuous and usually small (<10mm) blood
vessels visualised within the mucosal and
submucosal layers of the gut