Professional Documents
Culture Documents
Group 06 Case 1a
Group 06 Case 1a
NIM
Occupation
Adelia Melanti
405070017
Member
Adrian Hartanto L
405070039
Member
405070078
Member
405070092
Member
Dian Natalia
405070097
Secretary
Anthony Kane B
405070098
Scriber
Devi Regina
405070099
Member
Agnes Santoso
405070100
Member
Clement Drew
405070104
Member
Risma Kamilah
405070121
Member
Christiani
405070161
Leader
Tutor: dr Susilodinata
Group 6
SECRETION
DIGESTION
ABSORPTION
Saliva
Amylase
Mucus
Lysozyme
Carbohydrate digestion
begins
No foodstuffs; a few
medicationsfor example,
nitroglycerin
None
Mucus
None
Gastric Juice
HCl
Pepsin
Mucus
Intrinsic factor
Carbohydrate digestion
No foodstuff; a few lipid
continues in body of
soluble substances, such as
stomach; protein digestion
alcohol and aspirin
begins in antrum of stomach
Pancreatic digestive
enzymes
Trypsin, chymotrypsin,
carboxypeptidase
Amilase
Lipase
Pancreatic aqueous
NaHCO3 secretion
Not applicable
SECRETION
DIGESTION
Bile
Bile salts
Alkaline secretion
Bilirubin
Succus entericus
Mucus
Salt
(Small intestine enzymes
are not secreted but
function within the brush
border membrane --disaccharidases and
aminopeptidases)
None
Mucus
ABSORPTION
Nausea
Discomfort characterized by a loss of
appetite and the sensation of impending
vomiting, Its causes include local irritation
of the GI tract, a systemic disease brain
disease or injury, overexcretion, oe the
effect of medication or drug overdosage
Gastrointestinal Bleeding
May present in five ways :
Hematemesis : vomitus of red blood or coffeegrounds material blood
Melena : black, tarry, foul smelly stoul
Hematoschezia : passage bright red or maroon from
rectum
Occult GI bleeding : may be identified in the absence
of overt bleeding by fecal occult blood test or the
presence of iron deficiency.
Symptoms of bood loss or anemia : syncope, angina
or dypsnea
Hematemesis
is the vomiting of blood, which
may be obviously red or have an
appearance similar to coffee
grounds.
Bleeding ulcer in the stomach,
first part of the small intestine, or
esophagus
Bleeding esophageal varices or
stomach varices
gastroenteritis
esophagitis
Gastritis
Irritation or erosion of the lining
of the esophagus or stomach
Swallowing blood (for example,
swallowed after a nosebleed)
Tumors of the stomach or
esophagus
Melena
is the passage of black, tarry
stools
Gastritis
Esophageal Varices
Bleeding Ulcers
NSAIDs
Mallory-Weiss Tear
Hematochezia
is the passage of fresh
blood per anus, usually
in or with stools.
hemorroids
diverticulosis
Colorectal cancer
enterocolitis
inflammantory bowel
disease
Hematemesis
Melena
Hematochezia
Hypovolemia
2. Lower intestinal
1. Hematochezia
2. Symptoms of arteriovenous malformations,
diverticulosis, cancer, hemorrhoids, inflammatory
bowel disease, ischemic colitis
ESOPHAGITIS
is a general term for any
inflammation, irritation, or swelling of
the esophagus.
Risk Factor
Excessive vomiting
Medications such as aspirin, ibuprofen,
potassium, alendronate, tetracycline, and
doxycycline
Vitamin C supplements
Surgery or radiation to the chest (for
example, treatment for lung cancer)
Etiology
Esophagitis is frequently caused by the backflow of
acid-containing fluid from the stomach to the
esophagus, a condition called gastroesophageal
reflux.
An autoimmune disorder called eosinophilic
esophagitis also causes this condition.
Persons with weakened immune systems due to HIV
and certain medications (such as corticosteroids)
may develop infections that lead to esophagitis.
Esophageal infection may be due to fungi, yeast
(especially Candida infections), or viruses such as
herpes or cytomegalovirus.
Pathophysiology
Reflux esophagitis develops when gastric contents are
passively regurgitated into the esophagus. Reflux
happens commonly and does not cause major harm
because natural peristalsis of the esophagus clears the
refluxate back to the stomach.
In others, where acid reflux from the stomach is
persistent, the result is damage to the esophagus
causing symptoms and macroscopic changes.
Gastric acid, pepsin, and bile irritate the squamous
epithelium, leading to inflammation, erosion, and
ulceration of the esophageal mucosa.
Symptoms
Difficulty swallowing
Painful swallowing
Heartburn (acid reflux)
Oral lesions (herpes)
Examination
Endoscopy
Upper GI x-ray with barium
Biopsy
Treatment
Treatment depends on the specific cause.
Reflux disease may require medications to
reduce acid. Infections will require
antibiotics.
Complication
severe discomfort
swallowing difficulty to the extent of causing
malnutrition or dehydration
eventual scarring of the esophagus. This
scarring may lead to a stricture of the
esophagus, and food or medications may
not be able to pass through to the
stomach.
Differential Diagnoses
Acute Coronary Syndrome
Cholecystitis and Biliary Colic
Esophageal Perforation, Rupture and
Tears
Foreign Bodies, Gastrointestinal
Gastritis and Peptic Ulcer Disease
Myocardial Infarction
Barrets Esophagus
Barrets Esophagus is one of the disease
that happens because of recurrent exposure
from gastric HCl.
Normally, the epithel that forms the
esophagus mucosae is the non keratinized
stratified squamous type, but in barrets
disease, the HCl which keep on injuring the
epithel, the mucosae undergoes metaplasia.
Esophageal Varices
Is an abnormally enlarged
veins in the lower part of your esophagus.
Etiology
liver disease (portal hypertension)
Pathophysiology
The portal vein carries blood from the intestine to the
liver.
Increased pressure causes the veins to balloon outward.
The vessels may break open (rupture). Any cause of
chronic liver disease can cause bleeding varices.
Normally, blood from your intestine, spleen and pancreas
enters your liver through a large blood vessel called the
portal vein. But if scar tissue blocks circulation through
your liver, the blood backs up, leading to increased
pressure within the portal vein (portal hypertension). This
forces blood into smaller veins in your esophagus,
stomach and occasionally your rectum. The excess
blood causes these fragile, thin-walled veins to balloon
outward and sometimes to rupture and bleed. Once
varices develop, they continue to grow larger.
Esophageal Varices
2 complementary strategic guide therapy
of bleeding varices :
local treatment of the bleeding vessel :
endoscopy sclerotherapy, endoscopic band
ligand, and baloon tamponade with a
Sengstaken-Blackmore tube,
and treatment of the underlying portal
hypertension (pharmacology therapy)
Symptoms
Vomiting blood
Black, tarry or bloody stools
Decreased urination from unusually low
blood pressure
Excessive thirst
Lightheadedness
Shock, in severe cases
Risk Factor
Male : female = 2-4:1.
Age = 40 50 years old, but the age
range is quite wide.
Pathophysiology
Symptoms
Esophageal bleeding
Vomiting
Severe retching
Vomiting blood (bright red)
Melena
Pallor
Tachycardia
Hiccups
Examination
Fiber-optic endoscopy
(esophagogastroduodenoscopy confirms
Mallory-Weiss syndrome by identifying
esophageal tears. Recent tears appear as
erythematous longitudinal cracks in the
mucosa; older tears appear as raised
white streaks surrounded by erythema.
Treatment
proton pump inhibitors or histamine-2
receptor antagonists to help decrease acidity
blood transfusions if blood loss is great
endoscopy with electrocoagulation or heater
probe for hemostasis
transcatheter embolization or thrombus
formation with an autologous blood clot or
other hemostatic material (such as a
shredded adsorbable gelatin sponge)
surgery to suture each esophageal laceration.
Complication
Gastrointestinal bleeding
Peritonitis
Abdominal pain
Differential Diagnosis
Boerhaave Syndrome
Esophagitis
Gastric Ulcers
Ulcers :
defined as a break in the mucosal surface >5
mm in size, with depth to the submucosa
Predisposing Factors
Ulcers are more common in :
Smokers
amount of hydrochloric acid in the stomach
the bicarbonate content of pancreatic secretions
degree of acid neutralization
NSAIDs users.
Etiology of PUD
Normal
Increased Attack
Hyperacidity
Weak defense
Helicobacter pylori*
Etiology
3 major causes of peptic ulcer disease:
1. infection with Helicobacter pylori,
2. use of nonsteroidal anti-inflammatory drugs
(NSAIDs), and
3. pathologic hypersecretory states such as
Zollinger-Ellison syndrome.
Infection
Drug/toxin
CMV
HSV
Helicobacter heilmanni
Biphosphonates
Chemotherapy
Clopidogrel
Crack cocaine
Glucocorticoids (when combined with NSAID)
Mycophenolate mofetil
Potassium chloride
Miscellaneous
PUD - Diagnosis
Endoscopy
Barium meal contrast x-ray
Biopsy bacteria & malignancy
H.Pylori:
Endoscopy cytology
Biopsy Special stains
Culture - difficult
Urease Breath test.
Complications:
Bleeding Chronic-IDA, Acute, Massive
Fibrosis, Stricture obstruction pyloric
stenosis.
Perforation Peritonitis- emergency.
Gastric carcinoma. (not duodenal ca)
2 Types
DUODENAL ULCER
A duodenal ulcer is a
particular type of peptic
ulcer (stomach ulcer) that
afflicts the lining of the
duodenum
GASTRIC ULCER
Ulceration of the
GASTRIC MUCOSA due
to contact with GASTRIC
JUICE.
It is often associated with
HELICOBACTER PYLORI
infection or consumption of
nonsteroidal antiinflammatory drugs
(NSAIDS).
Epidemiology
Sex :
Male-to-female ratio is approximately 2:1
Age :
Duodenal ulcers usually occur in those aged
25-75 years.
Gastric ulcer prevalence peaks in those aged
55-65 years.
ETIOLOGY
DUODENAL ULCER
Excess stomach acid
Helicobacter pylori
bacteria
See underlying conditions
of peptic ulcers
The most common cause
of such damage is
infection of the stomach
with a bacterium called
Helicobacter pylori
(H.pylori)
GASTRIC ULCER
Pathology
Duodenal ulcers :
Occur in the first portion of duodenum (>95%)
Located within 3 cm of the pylorus
Ussualy 1 cm in diameter but can occasionaly 3-6
cm (giant ulcers)
Ulcers sharply demarcated, with dept at time reaching
the muscularis propia
The base of the ulcer often consist of a zone of
eosinophilic necrosis with surounding fibrosis
Malignant DUS rare extremely
Phatology
Gastric ulcers :
GUs can represent a malignancy
Benign GUs are most often found distal to the junction
between the and the acid secretory mucosa (quite rare
in the gastric fundus)
Associated with H.pylori are also associated with
antral gastritis.
In contras, NSAID-related GUs are not accompanied
by chronic active gastritis but may instead have
evidence of a chemical-gastropathy, typified by
foveolar hyperplasia, edema of lamina propia and
ephitel regeneration in the absence of H.pylori.
Extension of smooth muscle fibers into upper portion
of mucosa may also occur
Pathophysiology
Duodenal ulcers :
H.pylori and NSAID induced injury account of the
majority of DUs
Many acid secretory abnormalities have been
describes in DU patient.
Of these, average basal and nokturnal gastric acid
secretion appears to be increased in DU patient as
compared as control;however, the level of overlap
between DU patient and control subject is substantial
Bicarbonate secretion is significantly decreasedin the
duodenal bulb of patient with an active DU as
compare to control subject. H.pylori infection may
also play role in this process.
Pathophysiology
Gastric ulcers :
Gastric acid output (basal and stimulated) tends to be
normal or decreased in GU patient
When GUs develop in the presence minimal acid
levels, impairment of mucosal defense factors may be
present
Abnormalities in resting anf stimulated pyloric
sphincter increase duodenal gastric reflux have been
implicated some GU patients
Delayed gastric emptying of solids has been
described in GU patients but has not been reported
consistely.
SYMPTOMs
GASTRIC ULCERS
DUODENAL ULCERS
1. Abdominal pain
2. Abdominal pain at night
3.
4.
5.
6.
7.
8.
9.
1.
Complications
DUODENAL ULCER
Bleeding internally
Perforation of the intestine
and peritonitis
Bowel obstruction
Pancreatitis, acute
Gastrointestinal perforation
Hypovolaemic shock
Abdominal pain
Gastroduodenal ulcers
GASTRIC ULCER
Chronic blood loss, iron
deficiency anaemia
Bleeding from the ulcer
Perforation (hole) in the
stomach
Blockage in the stomach
that prevents movement
of stomach contents
Malignancy
Differential Diagnosis
NUD (Non Ulcer Dyspepsia) also known
as functional dyspepsia or essential
dyspepsia
Proximal gastrointestinal tumors
Gastroesophageal reflux
Vascular disease
Pacreaticobiliary disease
Gastroduodenal Crohn disease
Gastritis
Inflammation of the gastric
mucosa caused by any of several conditions, including
infection (Helicobacter pylori), drugs (NSAIDs, alcohol),
stress, and autoimmune phenomena (atrophic gastritis).
Etiology
The most common are:
Alcohol
Erosion (loss) of the protective layer of the stomach lining
Infection of the stomach with Helicobacter pylori bacteria
Medications such as aspirin or other nonsteroidal antiinflammatory drugs (NSAIDs)
Smoking
Less common causes are:
Autoimmune disorders (such as pernicious anemia)
Backflow of bile into the stomach (bile reflux)
Eating or drinking caustic or corrosive substances (such as
poisons)
Excess gastric acid secretion (such as from stress)
Viral infection, especially in people with a weak immune system
Symptoms
Diagnosis
Upper endoscopy
Blood tests
Fecal occult blood test (stool test
Treatment
Mediacation
1.H2-blockers :
cimetidine (Tagamet), famotidine (Pepcid),niza
tidine (Axid), ranitidine (Zantac).
2.Proton pump inhibitors (PPIs) :
lansoprazole (Prevacid),omeprazole (Prilosec,
Losec).
3.Coating agents:
Sucralfate (Carafate), Misoprostol (Cytotec)
4.Antacids
5.Antibiotic
6.Antiemetic
Prevention
Avoid substances that trigger gastritis symptoms:
1. Cigarette smoking
2. Coffee and other beverages that contains caffein (cola,
tea)
3. Alcohol
4. Aspirin (use coated aspirin if you must take aspirin)
5. NSAIDs such as ibuprofen (Motrin, Advil) or naproxen
(Naprosyn)
Differential Diagnosis
Complications
Malignancy
Hemorrhage
Perforation
Obstruction
Prognosis
The prognosis is excellent. Most patients
are cured when the cause has been
identified and treated appropriately.
Conclusion
Based on the signs and symptoms
Mrs.Doubtfire, shows upper
gastrointestinal bleeding.
She probably experiencing peptic ulcer
disease.
To make a firm diagnosis, the patient have
to take further examination.
Suggestion
Mrs.Doubtfire has to avoid eating sour and
spicy food, drinking beverages that
contains caffein and alcohol.
References
Price, Sylvia A., Wilson, Lorraine M. Patofisiologi
vol 1. Ed 6. Jakarta : EGC, 2006.
Fauci, Braunwald, Kasper, dkk. Harrisons
Principles of Internal Medicine vol II. Ed
17.United Stated : mcGraw-Hills, 2008.
Sherwood, Lauralee. Physiology from Cells to
Systems. Ed 6. United Stated : Thomson Higher
Education, 2007.
Reid Robin, Roberts Fiona. Pathology Illustrated
6th ed. London: Elsevier, 2005.