PLENARY

TUTORIAL 5
GASTROINTESTINAL DISEASE

10
B

Amalia Savira
Aisyah Marwa Bilqis
M Fadila Arie Novard
Mirza Nuring
Nabila Jasmine

Nugra Daary Razsky G

Rezky Fajriani Anugra
Ririn Lausarina
Srikitta Daniella
Yeni Novi Yanti

Skenario Modul 5- Ada

Apa di Kampung Pak
Umar ?

Kampung pak umar heboh karena sehabis pesta selamatan di kelurahan , banyak
warga yang mengalami muntah-muntah dan diare setelah makan ikan bakar yang
disuguhkan panitia. Termasuk yang mengalami adalah pak Umar dan istrinya,
mereka terlihat letih , mata cekung tetapi masih mau minum. Setelah dibawa ke
puskesmas, mereka diberikan oralit dan boleh pulang.
Satu minggu sebelumnya, anak mereka yang berusia empat tahun mengalami
diare bercampur lender. Anak tersebut sudah dibawa ke RS, berdasarkan hasil
pemeriksaan dokterdidapatkan hiponatremia. Menurut dokter, anak Pak Umar
mengalami diare akibat infeksi karena mengkonsumsi makanan yang
terkontaminasi. Terhadap anak Pak Umar dilakukan upaya rehidrasi dengan
memberikan cairan kristaloid intravena, dan juga pemeriksaan analisis gas darah
karena berisiko asidosis metabolic. Dokter juga menasehati agar pak Umar
memelihara kebersihan lingkungan dan tidak membiarkan anak jajan sembarangan.
Pak Umar prihatin dengan kejadian yang menimpa keluarganya. Dulu waktu kecil
anaknya juga pernah mengalami diare ketika diberikan susu formula, dokter
mengatakan bahwa penyakit ini disebut intoleransi laktosa. Ternyata banyak hal
yang dapat menimbulkan diare.
Bagaimana anda menjelaskan apa yang terjadi pada keluarga Pak Umar?

Step I - V

Step I
Oralit = oral rehidration with mixture of NaCl,
KCl, anhydrous glucose, and sodium bicarbonate
Crystalloid fluids = ions with low molecular
weight
Blood gas analysis = test measuring the acidity
(pH) and the levels of O2 and CO2 in the blood
from an artery
Metabolic acidosis = condition when the
chemical in the blood is unbalanced, making the
body more acidic
Lactose intolerance = condition when the body
cannot fully digest lactose

Step II
1. Why do people vomit and have diarrhea
after eating the fish?
2. Why do the couple look tired, have
sunken eyes, but are still willing to drink?
3. Why are they given the oralit and able
to go home?
4. Why did the kid have diarrhea with
mucus?

5. How is the interpretation of doctor's

examination?
6. Why was he given crystalloid fluids and
having blood gas analysis?
7. How does metabolic acidosis occur?

Step III
1. - Contamination of bacteria
(campylobacter, salmonella, e. coli), virus
(norovirus, rotavirus), paracites
(entamoeba hystolitica, giardia)
- Specific kinds of fish are sometimes
poisonous
2. Undernourished, dehidration
3. Mild dehidration and unbalanced level
of electrolytes

4. Infection caused by amoeba or bacteria

(shigella dysenteriae) which kill cells and
make the symptom arises
5. - Severe dehidration = loss of fluid >
10% of body mass
- Oliguria = urine < 400 ml / day
- Hypoglicemia = blood sugar < 50
mg/dL
- Hypocalemia = blood potassium < 3.8
mEq/L

6. Crystalloid fluids has alkaloid quality;

given to patients with metabolic acidosis,
urine alkalization
7. Excessive production of acid or lack of
excretion by kidney

Step IV
Keracuna
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Makanan
infeks
i
Malabsorb
si
Intoleransi
Penyeba
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Lain
La

komplik
asi

DIAR
E

Dehidra
si
Ketidakseimb
angan
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DIAGNOSI
S

TATALAKSA
NA
PROGNOSIS

Derajat
Dehidrasi

Analisis gas
darah, dll

Rehidrasi,dll

Step V
Students are able to:
1. Explain about diarrhea
2. Explain about malabsorption
3. Explain about food intoxication
4. Explain about imbalance of liquid,
electrolytes, and acidity in the body due
to diarrhea

Learning
Objective 1
DIARRHEA

DIARRHEA

Definitions
Defecation with liquid or semi-liquid stool
(contains water of 200 ml / 24 hours)
Watery defecation with frequency of more
than 3 times a day
May or may not contain mucus or blood

Classification
Based on:
1. Time
. Acute
. Chronic
. Persistent
2. Patophysiological Mechanism
. Osmotic
. Secretory

3. Infectious Causal
. Infective
. Non invective
4. Organical Causal
. Organic
. Non organic (functional)

ACUTE DIARRHEA
Less than 15 days
Or
Less than 14 days (WGO, 2005)

Etiology (WGO Global Guidelines, 2005)

1. Infection
. Bacteries: Shigella sp, pathogenic E.coli,
Salmonella sp, Vibrio cholera, Yersinia
entero colytica, Compylobacter jejuni,
V.parahaemoliticus, V.NAG., Staphylococcus
aureus,
Streptococcus,
Klebsiella,
Pseudomonas, Aeromonas, Proteus, etc.
. Viruses: Rotavirus, Adenovirus, Norwalk
virus, Norwalk like virus, Cytomegalovirus
(CMV), echovirus.

 Parasites
(protozoa):
histolytica,
Giardia
Cryptosporidium parvum,
coli.

Entemoeba
lamblia,
Balantidium

Invasive: EIEC, Salmonella, Shigella,

Yersinia, C. Perferingens type C, E.
Hystolitica, G. Lamblia
Non invasive: V. Cholerae eltor, ETEC, C.
perferingens

2. Non Infection
Immunodeficiency
Medicines , antibiotics, corticosteroids
Certain
treatments
(Gastrectomy,
gastroenteroctomy, radiation terapy)
Others:
Synd.
Zollinger-Ellison,
autonomic neurophaty

Pathophysiology
1. Osmotic
2. Secretory
3. Bile acid, fat malabsorption
4. Electrolyte transport system defects
5. Abnormality of motility and transit time
6. Abnormality of permeability
7. Infection

Diagnosis

Treatments
1. Rehydration
. Oral (Oralit)
. IV (RL 50-200ml/kgBB/24h)
2. Diet
3. Anti-Diarrhea Medication
. Anti-Motility: Loperamide, Difenoxilat
. Stool hardener: Antapulgite
. Anti-Secretory: Hidrase

4. Antimicrobial
Only recommended for invasive diarrhea,
traveler's
diarrhea,
or
immunosuppressive
. Kuinolon: Siprofloxaxine
. Kotrimoxazol:
Trimetoprim/Sulfametoxazol

CHRONIC DIARRHEA
More than 14 days

Etiology
Based on:
1. Patophysiology
. Osmotic
. Secretory
. Bile acid, fat malabsorption
. Electrolyte transport system defects
. Abnormality of motility and transit time
. Abnormality of permeability
. Fluid exudation

2. Location or Organs Abnormality

. Pancreas (Cistic fibrosis, PEM, chronic
pancreatitis, enzyme deficiency)
. Hepatobilier (bile atresia, obstructive
icteric,
chronic
hepatitis,
hepar
cirrhosis)
. Bowel

3. Stool characteristics
. Fatty stool / steatorrhoea
. Bloody stool
. Non fatty or bloody stool (watery and
semisolid)

4. Powell DWs
. Steatorrhoea
. Watery stool with respons to fasting
. Watery stool with respons or no respon
to fasting
. Watery stool with no respon to fasting
. Inflamatory diarrhea

Diagnosis
1. Anamnesis
. Time and frequency
. Stool
. Other complaints
. Medicines
. Foods / drinks

2. Physical Examination
3. Stool
. Macroscopic
. Microscopic
. pH
4. Laboratory
. Blood
. Serology
. Urine

5. Other
. BNO (foto polos abdomen)
. Barium enema
. Sigmoidoskopi

Diarrhae In Child

ACUTE

Defenition
Defecation in infant or child that more than
3 times a day, with a feses consistention
change to more watery with or without
mucous and blood less than 1 week

Epidemiology
World
6million childs a year are dead because
of diarrhae and most of them are from
development country.
Riskesdas 2007
42% in baby
25,2% in childs (1-4 yo)

Etiology

Bactery
Anatomy Deffect
Escherichia coli
Shigella
Malabsorbsion
Campylobacter jejuni

Endocrinopaty
Virus
Rotavirus
Parasit
Cryptosporidium

Neoplasm
Etc.

Risk Factor

Age
Genetic
Environment
Poor sanitation
Poor of food higiene
Malnutrition
Imunodeficient
Decrease of gastric acid
Decrease of bowl motility
Etc.

Pathogenesis

Clinical Manifestation
Gastrointestinal manifestation
Neurologis manifestation
Systemic manifestation

Diagnoses
ANAMNESIS
When the first symtomp is
Diarrhae after the specific kondition
Onset
Frequention
The look of feces
Ekstraintestinal symtomps
History of antibiotical uses

Clinical Examination
General kondition
Dehidration status
Abdominal examination
Weight decrease symtomps
Growth curve
Radiology
Kongenital malformation
Intestinal bowl disease
Hirchsprung

Therapy

PERSISTEN & CHRONIC

Defenition
Chronic diarrhea is an episode of diarhea
more than 2 weeks, if there is same
condition with decrease of body weight or
hard to increase body weight, its called
persistent diarrhea.

Epidemiology
3-20% of all diarrhae in baby
In developmental countries 7-15% in every
year
Indonesia, 0,1% and most of that are attact
6-11yo baby

Etiology
Bad therapy of acute diarrhae
Cow's milk protein intolerance
Celiac disease
Cystic fibrosis

Pathogenesis

Clinical Manifestation
Watery diarrhae
Decrease of epetit
Nausea and fomittus
Fever
Mucus in feces
Flu symtomps
Etc.

Diagnoses
ANAMNESIS
When the first symtomp is
Diarrhae after the specific kondition
Onset
Frequention
The look of feces
Ekstraintestinal symtomps
History of antibiotical uses

Clinical Examination
General kondition
Dehidration status
Abdominal examination
Weight decrease symtomps
Growth curve
Radiology
Kongenital malformation
Intestinal bowl disease
Hirchsprung

Therapy
First aid, resusitasi, and stabilisation
Nutritional therapy
Farmako therapy
Follow up

Learning
Objective 2
MALABSORPTION

Preliminary
DEFINITION
A situation where an interruption in the process of digestion
and absorption of nutrients, so that nutrients can not enter
the intestinal mucosa
ETIOLOGY
gastroenteritis, BBLR
cystic fibrosis, celiac
jejunal mucosa abnormalities Infection, drugs, radiation
exocrine pancreatic enzyme insufficiency, bile acids
bowel resection

Carbohydrate Malabsorption
4 processes :
Starch
Polysaccharides
Disaccharides
monosaccharides

Lactose Intolerance
Lactose glucose + galactose
The only carbohydrates in the milk of mammals
ASI : 7%
Cows milk : 4%
sea lions milk : Benefits :
- Energy sources
- Calcium Absorption
Classification
PRIMER ( genetic )
SECONDARY ( acquired )

Lactose is not absorbed

attractive water
Colon
Gas
Absorbed

Water

Lactic Acid
Colonic Salvage
Osmotic diarrhea, lactic acid

Lactose

CLINICAL MANIFESTATION
o Increased intestinal peristalsis
oNauseous, vomit
oPH decrease in stool
oKThe water content of stools increases
oAbdominal bloating and pain
oBreath smelled sour
DIAGNOSIS
1.Lactose tolerance test
2.stool examination
3.Breath hydrogen test
4.Barium meal
5.A biopsy of the small intestine mucosa

TREATMENT
- Low-lactose milk SECONDARY
- Lactose-free milk PRIMER

FAT MALABSORPTION
Impaired absorption of fat in the intestine,
causing spending excessive fat in the stool
type :
A. pancreatic: declining production of lipase
B. Hepatic: decreased production of bile salts
C. Enteric : small intestinal mucosal damage
D. Lymphatic: decreased function of the lymph
channels

Protein
Malabsorption

 Deficiency enterokinase
Cystinuria
Hartnup disease
Blue diaper syndrome

Deficiency enterokinase
Enterokinase is an enzyme that activates
trypsinogen to trypsin.
This enzyme is produced in the proximal of
the small intestine.
Symptoms :

Diarrhea
Steatore
Hypoproteinemia
Anemia

Therapy : dietary protein + pancreatic extract

Hartnup disease
Inherited autosomal recessive
Symptoms : rash pellagra,
photosensitivity, cerebral ataxia
Pathophysiology : disturbance in renal
tubular resorption and absorption in
intestine aminosiduria, triptofanuria,
and indikanuria (typical)
Therapy : nicotinamide peroral

Blue diaper syndrome

Tryptophan malabsorption
Pathophysiology : tryptophan is not
absorped enter the colon converted by
bacteria into indole transferred to
liver oxidized and conjugated into
indikanexcreted through urine blue
diaper

Cobalamin malabsorption
Etiopathophysiology :
Congenital anomalies disturb the assimilation of
vitamin B12
Resection or dysfunction terminal ileum
Juvenile pernicious anemia production of
intrinsic factor is not good megaloblastic anemia
Deficiency of transcobalamin II failed transport
megaloblastic anemia, diarrhea, vomitting

Therapy : injection cobalamin 100 g/week

for def. transcobalamin II or 100 g/month for
other.

Learning
Objective 3
INTOXICATION

Intoxication
Defenition :
Toxin is a substance which when entered via the
oral , inhalation , and injection and absorption
through the skin , or used against a living
organism with a relatively small dose will ruin
lives and seriously interfere with the function of
one or more organ or tissue ( sartono 2001: 1 )

Etiology
There are several kinds of poisoning causes , and the
consequences can range from mild to severe . in
general a lot happens due to:
1. Microbe
Escherichia coli pathogen
Staphilococcus aureus
Salmonella
Bacillus parahemolyticus
Clostridium botulisme
Streptococcus

2. Chemical material
class of organophosphate pesticides
organo sulfates and carbonates
3. Toxin
mushrooms
poisoning the cassava
tempeh Bongkrek
spinach toxic

Pathogenesis
Poisoning can be caused by several things
including : factors chemicals , microbes , toxins .
These causes can affect systemic vascular. Usually
as a result of lead poisoning are nausea , vomiting ,
diarrhea , flatulence , respiratory disorders , blood
circulation disorders and liver damage .
Nausea and vomiting occur because irritation of
the stomach so that the stomach increases HCl.
Foods that contain toxic chemicals can inhibit the
enzyme acetylcholinesterase body .

Under normal circumstances this enzin works to

hydrolyze the arachnoid . When the concentration
of toxins morehigh , then the accumulation of
arachnoid in certain places, causing symptoms of
excessive stimulation , which will cause effects
muscarinic , nicotinic , and depression central
nervous system.

clinical symptoms
1. The most prominent symptom
- Abnormalities in visual acuity
- Hyperactivity salivary glands and sweat
- Digestive tract disorders
- Difficulty breathing
2. mild poisoning
- anorexia
- Headache
- Weakness
- fear
- Tremor of the tongue and eyelids
- Pupil miosis

3. moderately poisoned
- nausea
- Vomiting
-kejang and stomach cramps
- hypersalivary
- bradycardia
4. severe poisoning
- diarrhea
- Light reaction is negative
- out of breath
- cyanosis
- Pulmonary edema
- Urinary incontinence of urine and feces
- kovulsi
- coma
- Blockade of heart that could eventually died

management
1. emergency action
- Airway: free the airway, if necessary to do the incubation
- Breathing: give artificial respiration, if the patient is not breathing or breathing spontaneously
inadequate
- Circulation: post infusion when the state of emergency and repair tissue perfusion
2. resuscitation
5% dextrose infusion at a speed of 15-20
3. The identification of the cause
4. reduce the absorption
to induce vomiting, gastric drain, absorb toxins with activated carbon and colon cleansing
5. increase the eliminations
can be done with a base or acid diuresis, multiple doses of activated carbon, dialysis, and hemoperfus.

according to the level for toxicity

1.mild poisoning regular poisoning
bed rest, drinking the ORS, and give norit, and if necessary,
provide antiemetic and antidiarrheal
2. severe poisoning
- stabilization
includes the acquisition of the airway, improvement of the
respiratory function, improved circulation with an infusion of
RL to overcome the shock, followed by oral therapy, if
necessary immediately refer to hospital

Besides, there are some actions that need to be

done on a case of food poisoning
1. check all people who ate
- Note the time of the occurrence of symptoms
- Materials vomit, blood, feces, send it to the lab
2. inspection of food and beverages
- Record and send samples to the laboratory mkanana
and beverages (include label)
3. examination of how contamination
- Check the proper way of cooking and presentation

Learning
Objective 4
imbalance of liquid, electrolytes, and
acidity in the body due to diarrhea

Electrolytes balance
disorder
A. Hyponatremia
.Na < 135 mEq/L. Severe <120 mEq/L
.Acute hyponatremia : < 48 hours, convulsions and
somnolen
.Chronic : > 48 hours, faint.
.Etiology :
1. Hyponatremia hipovolemik
Na urin > 20 mmol/L : over diuretik,
deff.mineralokortikoid, ketonuria,
Na urin < 10 mmol/L : vomitus, diarrhea,
pancreatitis

2. Hyponatremia euvolemik : Deff. Glucocorticoid,

hypotyroid
3. Hyponatremia hipervolemik :
Na urin > 20mmol/L : acute renal disorder
Na urin < 10 mmol/L : Nefrotic syndrome, sirosis
Clinical manifestation
Light : nausea, vomit, letargy, disorientation
Severe : convulsion, cerebral enema, koma
Diagnosis
anamnesis : vomitus-history, diuretik or manitol
used, adrenal insufficiency
Exam : Na serum level

Treatment
1. Hyponatremia asymptomatik : IV NaCl 0,9 %
with < 0.5 mEq/L/hour
2. Acute Hyponatremia : NaCl 3%. Increase
concentration of Na 5 mEq/L in one hour, after
that increase concentration 1 mEq/L in one hour
until 130 mEq/L
3. Chronic hyponatremia : Correction 0,5-1
mEq/L/hour. Total correction 10-12 mEq/24 hour.

Formula of Na correction :
Na = 0,5 x BB (kg) x (target Na - initial Na
concentration)

B. Hypernatremia
.Na : >145 mEq/L
.Etiology
1. Fluid deficit : osmotic and secretorik diarrhea,
elevated levels of IWL because fever, physical
activities, burn injured, osmotic diuresis in
hyperglicemia, non osmotic diuresis in diabetes
insipidus.
2. Increasing Na intake : IV NaCl hypertonic, IV
NaHCo3, increasing salt intake
.Clinical Manifestations
.Fluid secretion from cell to tissue, including brain
neuron causing mental status disorientation,
spasm, consciousness decline, polyuria, thirsty.

Treatment
Water correction in 48-72 hour to prevent
neurologic complications
This correction based on calculation of
ongoing water loss (OWL) and insensible
water loss (IWL) by using hypotonic fluid
( NaCl 0,45% and dextrose 5% ), max
correction 15 mEq/L/day

C. Hypokalemia
.K : <3.5 mEq/L
.Etiology
1. Decreasing of intake : starving
2. Redistribution to the cell : metabolic alkalosis, insulin
used, hipotermia, hypokalemia
3. Increasing of excretion : diarrhea, sweat, diuretic,
hiperaldosteronisme, cushing syndrome
. Clinical manifestation
.Light (K+=3-3,5 mEq/L) : asymptomatic
.Mild (K+=2-3 mEq/L) : mialgia, weak, constipation,
muscle necrotic, EKG T inversi, ST segment
depression, long PR interval
.Severe (K+=<2 mEq/L) : respirations muscle weakness

Treatment
1. KCl. Oral, every tablet contains ion
potassium 20 mEq
2. KPO4/potassium phosphate for
hypokalemia with phosphate-loosing
3. KHCO3/ potassium bicarbonate for
hypokalemia with metabolic acidosis
.40-60 mEq KCl (2-3 tablet) can increase
potassium level about 1-1,5 mEq/L. 135160 mEq can increase potassium level
about 2,5-3,5 mEq/L

D. Hyperkalemia
.K+= >5 mEq/L
.Etiology :
1. K-loose from intracellular space
2. Decreasing of K+ excretion by renal
.Clinical manifestation
.Muscle weakness
.Hipoventilation
.Metabolic acidosis caused by hiperkalemia
blocked NH3 absorption, so H+ excretion is
decreasing
.Cardiotoxic

Treatment
Ca glukonas, diuretik

ACID-BASE DISORDERS

 pH normal body fluids is 7.35 - 7.45

 plasma pH may be affected by a change

in either the [bicarbonate] or the PCO2

when the primary change is in the

PCO2, the disturbances is called
respiratory
when it is [bicarbonate], it is
called metabolic

Metabolic Acidosis
acid
or base
/ - from the body fluid
compensation : increasing alveolar
ventilation and decreasing pCO2
clinical features:

aritmia
artery dilated
hypotension
pulmo edema

 diarrhea --> many lose HCO3- --> Clcompensate the fluid volume
Cl- more absorbed than Na+ -->
hyperchloremia
diarrhea --> decreasing the exstracellular
fluid --> Cl- stay inside
so, diarrhea can cause metabolic acidosis
with hyperchloremia

 management
natrium bicarbonat if [HCO3-] < 5mmol/L
bicarbonat must be added to the hypotonic
solution and during 1 hour
acute watery diarrhea --> HCO3 in feces can
reach 40mEq/l --> intermediate metabolic
acidosis --> needed HCO3 (intravena)
but, don't forget to measuring K+ level in
serum before.

Metabolic Alkalosis
base increased or loss of acid
may cause : hypoxia, SSP changed,
irritable of the muscle, aritmia
clinical features

letargi
irritable
convulsions
confused
shortness of breath --> for reduced the CO2

 etiology : antassid, vomiting (it will loose

Cl too)
Cl level in urin --> <20mEq/L
Management

treat the main cause

Cl --> stimulate the kidney for removing
excess of base
severe alkalosis --> hidrochloride acid
for the case like vomiting, nasogastric
aspiration --> Nacl 1-2mEq/kg per day is
recommended

Respiratory Acidosis
increasing of pCO2 and decreasing of
plasma pH rapidly
not because of gastrointestinal disease
but may be happen because airway
osbtruction
management --> for the main cause
alkali is not necessary

Respiratory Alkalosis
decreasing of pCO2 because
hyperventilation
the gastrointestinal desease doesn't
cause this condition

THANKYOU FOR YOUR

ATTENTION

QUESTION