Gatot Sugiharto, MD, Internist Faculty of Medicine, UWKS Lecture - 2010

Gatot Sugiharto, MD, Internist
Faculty of Medicine, UWKS

Lecture - 2010
1 GSH - Gastro - 2010
Dyspepsia
Epigastric fullness, discomfort, vague term (indigestion)
Dysphagia
Difficulty swallowing, feeling of food sticking in oesophagus
Odynophagia
Painful swallowing usually associated with dysphagia
Heartburn
Burning sensation retrosternally associated with reflux
Anorexia
Loss of appetite
Haematemesis
Vomiting blood (could be red or altered coffee ground)
Melena
Passing of black tarry, offensive stool (usually due to upper GI bleeding)
Haematochezia
Passing blood per rectum (PR bleeding)
Definition: Reflux of gastric contents (acid) into
oesophagus
Symptoms:
May be asymptomatic;
Heartburn +/- retrosternal chest pain
Regurgitation of gastric contents
Acidbrash, waterbrash (watery sensation in mouth)
Atypical chest pain
Nocturnal cough (exacerbation of asthma)
Dysphagia (long term symptoms)
Epidemiology : Common ~10-20% in West (5% in
Asia)
Exacerbated by: Obesity, caffeine, alcohol, smoking,
fatty meal, medication, pregnancy
(hormonal/anatomic)
Drugs known to lower LES pressure: calcium channel
blockers, beta-agonists, anti-cholinergic
medications, alphablockers, theophylline,
progesterone, morphine, dopamine and nitrates
Mechanism : GO junction incompetence
Due to transient LOS relaxation (tLOSR) (Common GERD)
Hypotensive LOS (More severe GERD)
Anatomical disturbance of LOS (Hiatus Hernia)
Complications
Esophageal complications: esophagitis, bleeding,
stricture, Barretts esophagus, adenocarcinoma
Extra-esophageal complications: Laryngitis, Laryngeal
carcinoma , Tracheal stenosis, Asthma, Aspiration
pneumonitis, Chronic cough, Dental erosion

GSH - Gastro - 2010 6
Diagnosis
Endoscopy gold standard for diagnosis
Barium Meal not used much may be helpful in diagnosis of hiatus
hernia
Manometry/pH studies useful to document reflux
PPI test
Management
Lifestyle- Cease exacerbators, weight reduction, posture
Medication :
Proton pump Inhibitor (omeprazole, pantoprazole, rabeprazole,
esomeprazole, lanzoprasole)
H2Blocker (ranitidin, cimetidin, famotidin
GI motility regulator ( primperan,domperidome, cisaprid)
Surgery- Hiatus hernia repair
GI 8
Can be caused by an infection or irritation of
the esophagus
Infection can occur because of bacteria,
viruses (herpes), fungi, and yeast (Candida)
A primary condition or secondary to
gastroesophageal reflux, hiatal hernia,
vomiting, surgery, medications, Lye,
Radiation
Symptoms: Dysphagia, Odynophagia, Heart
Burn (reflux), oral lesions (herpes)
GI 9
Tests:Barium esophagogram, acid perfusion
tests (Bernstein), culture, Esophagoscopy
with/without biopsy (gold standard)
Treatment depends on the specific cause
Complications: severe discomfort,
swallowing difficulty, malnutrition
/dehydration, scarring, Barrett's esophagus,
cancer

GI 10
Esophageal squamous epithelium replaced with metaplastic
columnar epithelium
Incidence up to 10%/lifetime
Usually men >55
GERD commonly present
Dx EGD with biopsy
Treatment:
Treat reflux aggressively PPI
Surveillance for dysplasia
No dysplasia q 3-5 years
Dysplasia confirm with expert pathologist/
GI specialist

GI 11
A diffuse motor disorder: incomplete relaxation of
the L.E.S and absence of peristalsis (this cardinal
finding sufficient to make a diagnosis of achalasia)
Symptoms: dysphagia, regurgitation, and the classic
x-ray finding of gradual tapering of distal esophagus
(birds beak)
Esophageal manometry (gold standard)
Treatment
Esophageal dilatation
Surgery
Botulinum toxin injections into L.E.S
GI 12
Common in aging persons, 7 to 10 % of adults >
50 years
Oropharyngeal dysphagia: dysfunctional
transfer from pharynx to esophagus
Stroke is the leading cause of oropharyngeal
dysphagia
Esophageal dysphagia: disordered peristaltic
motility(Neuromuscular Disorder) or
(Mechanical Obstruction)

Differential Diagnoses
Mechanical obstruction
Benign stricture (burn injury, web, GERD)
Malignant obstruction (SCC, Adenocarcinoma)
Neurological
Stroke
Achalasia
MND, Myaesthenia Gravis, Parkinsons
Functional
Management
Diagnosis specific and multifactorial
GI 14
A strong feeling of burning, squeezing pain
while swallowing
Dysphagia may or may not be present
May have symptoms of chest pain, food
stuck in the throat, or heaviness or pressure
in the neck or upper chest
May be caused by destruction of the
mucous membrane, infection, chemicals, or
motor disorders of the esophagus
GI 15
Manifestation :
Hematemesis and/or melena (black tarry stools)
Hematochezia (maroon or bright red blood per
rectum) when massive
Multiple etiologies PUD, Mallory-Weiss,
Variceal, Carcinoma
Diagnosis-clinical presentation : NG lavage
GI 17
Management
Endoscopic treatment
Thermal coagulation (heater probe, gold probe, BICAP)
Injective sclerotherapy (epinephrine)
Combination therapy commonly used for high risk causes i.e. active
bleeding
Endoclips
Antisecretory therapy
PPI : Omeprazole i.v. decreases rebleeding after endoscopic treatment
H
2
blockers disappointing results
Octreotide (somatostatin analoque) reduce rebleeding
50-100 mcg bolus, 25-50 mcq/hr for up to 3 days
Surgery

GI 18
25 percent (13 to 40 percent) of population
The most common cause of dyspepsia is
functional or nonulcer, dyspepsia (specific
etiology is not identified)
Management:
Endoscopy all patients
Trial of empiric antisecretory (PPI) drug therapy,
Testing for H. pylori infection followed by Tx if positive
1/3 - 1/2 spontaneous resolution of symptoms

Ulceration caused by acid/pepsin
Stomach, Oesophagus, Duodenum, Meckels diverticle
Symptoms
Often none
Gnawing abdo pain (epigastric)
Vomiting/nausea
Complications
Haemorrhage
Perforation/penetration
Gastric outlet obstruction
Aetiology
Helicobacter pylori
Up to 90% of DU and 75% of GU
NSAIDs (Non steroidal antiinflammatory drugs)
Physiological stress
Mechanism
Hp infection causing gastrin release and local
inflammation
Loss of mucosal defence, mucous, prostaglandins,
blood flow (NSAID)


Mucus and bicarbonate secretion
of epithelial cells
Surface membrane of mucosal
cells
PG E-1 and PG E-2
Diagnosis
Non-invasive diagnosis of Hp
Endoscopy
Barium Meal
Management
Complications
GI bleed, perforation
Healing the ulcer
Eradicate Hp
Treat with PPI
Prevent recurrence
Ensure eradication Hp
Longterm PPI prophylaxis if need NSAID (COX-2 selective?)
GI 24
Etiology
Gallstones 45%
Alcohol 35%
Others: Post ERCP, Tumor, Drugs, Anatomic variation,
Cystic Fibrosis
Symptoms
Acute upper abdominal pain steady
Hyperglicemic
Alcohol related 1-3 days after binge

GI 25
Diagnosis :
Amylase
Usually elevated for 3-5 days and >3x upper limits of
normal
Elevated in nonpancreatic processes (cirhosis, renal
failure, alcoholism, intestinal infarct, fallopian tubes)
Lipase
Elevation occur earlier and last longer than Amylase
ABD US/CT-ABD with contrast (R/O necrosis as
nonenhancing areas >3 cm in size

GI 26
Management
Early ERCP for gallstone pancreatitis elective cholecystectomy
prior to hospital discharge
Pain control Meperdine, Morphine or Fentanyl
Prophylactic antibiotics reduce mortality in severe necrotizing
pancreatitis
Imipenem, fluoroquinolones
Enteral Feeds
Considered safe
May reduce complications
High protein, low fat (Peptamen)
Start slow
100-300 cc fluids q 4hr day 1
Same volume add nutrients day 2
GI 28
Most common etiology alcohol
Diagnosis based on clinical criteria in the
setting or recurrent abdominal pain assisting by
imaging
Pain: epigastirc, radiates to back postprandial
Pancreatic insufficiency: 90% of pancreas usually
destroyed. Loose, greasy, foul smelling stools that are
difficult to flush. Diabetes is usually insulin requiring
Amylase/Lipase commonly normal
Imaging U.S., CT Scan, MRI, ERCP, Endoscopic U.S., Plain
films
GI 29
Defined as watery or liquid stools, usually with
increases in daily frequency and in total stool weight
(>200 g per day)
More than 3 times per day, less than 14 days,
usually spontaneously resolves
Etiology : Bacterial, viral, parasitic, non-
infectious
Mechanism : impaired balance between resorption
and secretion in the intestinal wall which leads to
the increased wateriness of the feces

Non
inflamatory
diarrhea
Agent Inflamatory
diarrhea
Agent
Viral Norwalk virus, Norwalk
like virus, Rotavirus
Viral Cytomegalovirus
Protozoal Giardia lamblia,
Cryptosporidium
Protozoal Entamoeba hystolytica
Bacterial Preformed enterotoxin :
Staphylococcus aureus,
Bacillus cereus,
Clostridium perfringens
Bacterial Cytotoxin production :
Enterohemorrhagic E.coli
(EHEC), Vibrio parahemolity-
cus, Clostridium difficile
Enterotoxin production :
ETEC, Vibrio cholerae
Mucosal infection : Shigella,
Campylobacter jejuni, Salmo-
nella, Enteroinvasive E.coli
(EIEC), Aeromonas, Plesio-
monas, Yersinia enterocolica,
Chlamydia, Neisseria Go,
Listeria monocytogenes
Empirical AB (while awaiting culture) based on : Fecal leukocyte (+), Bloody diarrhea, abd pain,
dehidration, > stools/24h, immunocompromized, elderly
GI 31
With fever and blood (invasive pathogen)
inflammatory diarrhea
Shigella, Campylobacter, Salmonella
Leukocytes in feces, fecal culture(+)
Tx : Antimicrobials for persistent shigella,
salmonella or campylobacter infections
especially: immunocompromised px
No fever or blood (Non-invasive pathogens) non
inflammatory diarrhea
No leukocytes in feces, fecal culture (low yield)
Etiology :
Enterotoxic E.coli (ETEC) , Giardia, Rotavirus, Norwalk,
Parasites
Traveler's diarrhea (85% of cases)
Tx :
Correct dehydration, spontaneous recovery except treat
parasite infection
Most viral and bacterial causes of diarrhea resolve without
treatment, antibiotics may prolong or worsen diarrhea

GI 33
Lasts for more than 2 weeks
Infectious:
Parasites Cryptosporidium, Cyclospora, Entamoeba,
Giardia,microsporidia
Bacteria : Campylobacter, Clostridium difficile, E.coli, Listeria,
Salmonella, Shigella,
Viral : HIV, rotavirus, Norwalk
Non Infectious :drugs, crohns disease, endocrine diseases,
food additives (sorbitol, fructose, and others), food allergies, GI
surgery or radiation, tumors, intestinal ischemia, lactose,
caffeine, ethanol
GI 34
Usually related to functional disorders like irritable
bowel syndrome (IBS), celiac disease, or inflammatory
bowel disease (IBD)
Should consider testing if patients are febrile or have
bloody stool
Avoid antimotility agents in bloody diarrhea
especially when caused by E. coli . (risk of hemolytic-
uremic syndrome)
Endoscopy more specific than radiographic studies in
detecting the etiology of chronic diarrhea

Abdominal pain associated with altered stools
(diarrhea or constipation)
No organic cause identifiable
Epidemiology
Very common ~10% Western population
Up to 50% of visits to gastroenterology
Diagnosis
Diagnostic criteria somewhat helpful
Rome III criteria
Recurrent Abdo pain for 3 days in the last 3 months with 2 of:
Improvement with defecation
Onset associated with change in stool frequency
Onset associated with change in stool form
Symptoms include
Bloating, flatus, mucous in stool
Exacerbated by stress
Investigation
If typical syndrome in young (<50) patient probably
normal
If alarm symptoms present (GI bleeding, anemia, age
>50, abnormal laboratory tests) Need to exclude:
In young: Coeliac disease and IBD
In edlerly: Colorectal cancer, Coeliac disease, IBD
Management
Supportive, Reassurance and explanation
Symptomatic
Analgaesia (antispasmodic)
Dietary
Psychological
Counselling
Antidepressants
Aetiology
Probable polygenic disease
Environmental (gut infection)
Immunological
Symptoms
Can be varied depending on site
Often: Diarrhea, abdominal pain, hematochezia, PR
mucous
Nutritional disorders
Iron deficiency, Vitamin B12 deficiency, Folate deficiency etc
Extraintestinal manifestations
Arthritis, Uveitis, Skin changes, Primary Sclerosing Cholangitis
Crohns Disease
Pathology throughout GI tract
Often skip lesions with intervening normal gut
Transmural inflammation and fistulous disease
Ulcerative Colitis
Localised to the colon and rectum
Mucosal inflammation characteristic
Usually contiguous disease
Occasionally difficult to distinguish the two
Indeterminate Colitis
Epidemiology
Incidence in Western countries up to 14/100,000
Prevalence in West up to 240/100,000


Medical
Nutritional replacement
Oral 5-aminosalicylates
Sulphasalazine, Mesalazine
Antibiotics
Corticosteroids (oral/IV)
Immunomodulators
Azathioprine, Methotrexate
Anti-TNF antibodies
Infliximab, Adalumimab

Surgical
Resection of bowel
Abscess drainage
Fistula repair
Strictureoplasty

Medical
Nutritional replacement
Topical 5-ASA (suppositoria)
Oral 5-aminosalicylates
Sulphasalazine, Mesalazine
Antibiotics
Corticosteroids (oral/IV)
Immunomodulators
Azathioprine, Cyclosporine
Anti-TNF antibodies
Infliximab, Adalumimab
Surgical
Resection of bowel
Abscess drainage

GI 45
Less than three stools per week
Patophysiology : excess absorption of water from
slow passage in the colon
Possible causes, motility disorder and pelvic floor
disorder, endocrine disorder
Older people, not a result of aging but chronic
illnesses, diet, neurologic and psychiatric,
medicines, lack of exercise
In infancy and childhood most constipation is
functional rather than organic

GI 46
Most common cause inadequate fiber content
No spesific tests are usefull
Organic, metabolic, endocrine disease need to be
excluded
Treatment of constipation is symptomatic
Eat regular, eight (8-oz) glasses of water daily,
regular exercise, move bowels when urged
Best Tx, a diet rich in fiber (30 - 35 grams daily)
Avoid stimulant laxatives, a suppository or gentle
enema is better

Esophagus
Inflammation (esophagitis)
Enlarged veins (varices)
tear (Mallory-Weiss
syndrome)
Cancer
Stomach
Peptic ulcers
Inflammation (gastritis)
Cancer

Small Intestine
Duodenal ulcer
Inflammation (inflammatory
bowel disease)
Angiodysplasia
Large Intestine and Rectum
Hemorrhoids
Infections
Inflammation (IBD)
Colorectal polyps
Colorectal cancer
Diverticular disease

A. Melena. Passage of black, tarry stools secondary to GI bleeding
with intestinal transit time allowing for the digestion of
hemoglobin.
1. May be of upper or lower GI origin
2. Black, tarry stools can be the result of ingested iron, licorice, or
bismuth but the stool will be guaiac negative.
A. Hematochezia. Bright red blood per rectum.
1. Can be secondary to anal disease (hemorrhoids, rectal fissure).
2. May be secondary to a bleeding diverticulum, other colonic
disease such as angiodysplasia, Crohns disease, ulcerative colitis,
carcinoma (very rarely causes gross bleeding), dysentery
(especially amebiasis, campylobacter, shigella, or other invasive
organisms).
3. Ingestion of beets may simulate hematochezia.


A. Laboratory studies should include CBC and platelets, PT/PTT,
electrolytes, BUN/creatinine (GI bleeders will frequently have
elevated BUN secondary to the increased ingestion of
nitrogen from digested blood). Blood type and crossmatch
for tranfusion
B. Physical examination often reveals hyperactive bowel sounds
secondary to intraluminal blood. If an acute abdomen is
present, consider CXR and an upright abdominal film to look
for free air.
C. Endoscopy may be done acutely for upper GI bleeding to help
define the source and treat endoscopically if able.
D. Angiography or nuclear medicine studies can be useful to
localize lower GI bleeding.

1. Start IV fluid resuscitation and manage shock
2. Work-up may include colonoscopy, barium enema,
selective angiography, and radionuclide bleeding studies.
3. A recent study shows a role for urgent therapeutic
colonoscopy with epinephrine injection or bipolar
coagulation in patients with severe hematochezia and
diverticulosis.
4. A surgical consultation should be obtained in case
operative intervention is needed.
5. Most causes of lower GI bleeding are initially self limited.

GI 53
Definition : positive fecal occult blood test without
visible blood
More commonly a bleeding source in the upper GI
tract (29 to 56 percent) than in the lower
gastrointestinal tract (20 to 30 percent)
Colonoscopy and upper endoscopy remain the
major investigative methods
GI 54
Bleeding of unknown origin that persists or recurs after
negative endoscopic evaluation
Requires evaluation of the small bowel, may require
repeat upper and lower endoscopy
Biopsy to detect celiac sprue, a cause of IDA
Push Enteroscopy, Enteroclysis, Radioisotope bleeding
scans (high false-positives)
Angiography can identify highly vascular nonbleeding
lesions such as angiodysplasia and neoplasms
Wireless capsule endoscopy for small bowel lesions
(Given Imaging)

GI 55
Most frequent causes of anorectal bleeding
are hemorrhoids, fissures and polyps
High index of suspicion for cancer
Evaluation of bright red blood per rectum
<40 and obvious source no additional evaluation
40-50 sigmoidoscopy
>50 colonsocopy

GI 57
Pruritus ani is more likely to represent a chronic
itch/scratch cycle than infection
Any pruritic lesion that persists after adequate
treatment should be biopsied
Anal pain with fever and inability to void signals
perineal sepsis and is an emergency
Biopsy all "warts" before ablative treatment
Verrucous carcinoma can appear to be a wart
Cancer can coexist with benign lesions, so
complete assessment is necessary
Epidemiology
Second most common solid cancer globally
Risk related to Age and family history
Genetic risk
FAP
HNPCC (Lynch Syndrome)
Juvenile Polyposis
Environmental factors
Alcohol, obesity, Diabetes

Symptoms : Often none
Altered bowel habit, Hematochezia, LOW, Malaise, Iron
deficiency anaemia
Investigation
Colonoscopy
Barium Enema/CT colography
Management
Resection
Surveillance
Immune mediated disease due to allergy to
dietary gluten (protein in wheat, rye, barley)
Pathology
Exposure to gluten causes damage to small
intestine leading to malabsorption
Strong genetic association with HLA-DQ2 HLA-
DQ8
Environmental factors important
Prevalence 1:100

Symptoms
GI: diarrhoea, bloating, mouth ulcers, IBS type
Anaemia, Osteoporosis, lethargy Chronic fatigue
Thyroid disease, Type 1 DM
Migraines
Infertility
Abnormal liver function
Arthralgia
Asymptomatic
Diagnosis/Investigation
Coeliac serology Tissue Transglutaminase ab
Endoscopy with small bowel biopsy
Establish diagnosis and assess disease
Therapeutic trial
Improvement on gluten free diet
Important in paediatric setting but helpful for adult
Therapy
Lifelong gluten free diet
Dietician important

Gatot Sugiharto, MD, Internist Faculty of Medicine, UWKS Lecture - 2010

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