Get that

cow milk
away from
me,
please.

Kelompok 11

GROUP 11
No

Nama

NIM

Peran

Edward Adisaputra Atmodjo

405070139

Leader

Elly

405070081

Secretary

Kristian Wongso

405070136

Scriber

Reinecia

405070038

Member

Hasri Larasati Utami

405070067

Member

Melisa

405070079

Member

Daria Putri Roman

405070087

Member

Julian

405070095

Member

Marcella Dian

405070096

Member

10

Luki

405070107

Member

11

Yuliana

405070135

Member

12

Christie Cindy R

405070137

Member

Fasilitator : Dr. Hendra

Case 1B
Get That Cow Milk Away From Me,
You
receive a call from Mrs. Melati, mother of Rosa, a
Please!!

previously healthy 2-month-old girl. For the past 3 days,

Rosa developed an occult bleeding and mucous in the
stool accompanied by a moderate degree of emesis.
However, her temperature hasnt increased, no
abdominal cramping or colic, but today she seems a bit
pale and more irritable.
Unfortunately, Mrs. Melati didnt breastfeed Rosa about
a week ago, and give her regular cow milk formula.
While you are discussing her family history, Mrs. Melati
reports that Rosas brother and sister are having food
allergy, and her 6 years old brother is asthmatic as well
as his father. The mother assumed that he has the
same dairy product allergy like his 3 years old sister.
You tell her to bring him for further diagnostic
investigation and call the lactation clinic for a
counseling appointment in order to return to exclusive
breastfeeding.

LO
Explaining mechanism and etiology of occult bleeding
in infant
Explaining mechanism and etiology of emesis in
infant
Explaining mechanism and etiology of mucous in the
stool in infant
Explaining the most likely diagnosis (differential
diagnosis)
Explaining further diagnostic investigations to confirm
the diagnosis
Explaining predisposing factors
Explaining complications associated with the disease
Explaining treatment of the case
Explaining education for patients mother

1. Salivary glands
2. Parotid
3. Submandibularis (lower jaw)
4. Sublingualis (under the tongue)
5. oral cavity.
6. Soft palate / pharynx
7. Tongue
8. Throat / esophagus
9. Pancreas
10. Stomach
11. Pancreatic duct
12. Hearts
13. Gall bladder
14. Duodenum (Duodenal)
15. Bile ducts
16. Large intestine / colon
17. Flat colon (transverse)
18. Colon up (ascending)
19. Colon down (descending)
20. Small intestine (ileum)
21. Cecum
22. Appendix
23. Axis intestine / rectum
24. anus

Emesis

Function
Vomiting, as a basic physiologic
protective mechanism, limits the
possibility of damage from ingested
noxious agents by emptying the
contents of the stomach and portions
of the small intestine.
Nausea and vomiting may represent a
total-body response to drug therapy,
including overdosage, cumulative
effects, toxicity, and side effects.

Mechanism
Vomiting involves two functionally
distinct medullary centers:
the vomiting center
in the dorsal portion of the reticular formation of
the medulla near the sensory nuclei of the vagus.

the chemoreceptor trigger zone.

in a small area on the floor of the fourth ventricle,
where it is exposed to both blood and
cerebrospinal fluid. It is thought to mediate the
emetic effects of blood-borne drugs and toxins.
responds to numerous chemicals and hormones,
including dopaminergic, a2-adrenergic, and opioid
agonists, and cardiac glycosides, cytotoxins, and
CuSO4.

Receptors and neurotransmitters involved in

mediating vomiting
Structures

Receptors

Agonist

Antagonist

Area postrema

D2

Apomorphine

Antidopaminergic
drugs

CTZ
Vestibular nuclei

L-DOPA
M, H1

N. tractus solitarius

Cholinomimetics

Scopolamine

Histamine

Dramamine

Vomiting center

Cholinomimetics
(e.g., physostigmine)

Scopolamine

Vagal sensory
nerveendings

5-HT3

Serotonin

Ondansetron
Granisetron
Tropisetron

Treatment

Anticholinergics
The only anticholinergic to have been shown to have any
antiemetic quality is hyoscine. It may be of use in patients for
whom the main stimulus is vestibular (that is, nausea and vomiting
caused by movement or ear, nose, and throat surgery). Its main
use, however, is now in palliative care where it is used to dry upper
airway secretions and ease breathing at the end of life.

Antihistamines
Several drugs inhibit the action of histamine at the H 1synaptic
pathways, which are predominantly involved in signalling from the
vestibular centre, but only cyclizine is used to treat postoperative
nausea and vomiting. Has few side effects. Common mild side
effects are a consequence of its antimuscarinic actions and include
sedation and dry mouth.

Steroids
Steroids such as dexamethasone may be given preoperatively as
prophylaxis in patients with a high risk of nausea and vomiting.
Steroids act by reducing inflammatory oedema and altering central
and peripheral responsiveness to proemetic compounds such as
anaesthetics and analgesics.They can also be used as a last line
rescue treatment.

Dopamine antagonists
These pharmaceuticals, for example prochlorperazine, haloperidol, and
metoclopramide, have been used as antiemetics for many years. They
work by inhibiting the activity of dopamine at the D 2receptor in the
chemoreceptor trigger zone, thereby limiting the emetic input to the
medullary vomiting centre.
Certain other antipsychotics, especially haloperidol, are often used in
palliative care to treat nausea and vomiting caused by malignancy. Low
doses of haloperidol, such as 1 mg once a day, are effective and are the
treatment of choice for nausea and vomiting caused by intestinal
obstruction.
Metoclopramide closely resembles the phenothiazines but has a limited
role as an antiemetic for postoperative nausea and vomiting. It is
effective in certain settings, such as emesis associated with hepatic
disease, but has been shown to be ineffective in many trials for the
treatment of postoperative nausea and vomiting and should not be
considered without senior input. Because it also increases gastrointestinal
motility, it should never be considered in patients where bowel
obstruction is possible.

Serotonin antagonists
Ondansetron, granitetron, and tropisetron inhibit the action of serotonin
at the 5-hydroxytryptamine 3 (5-HT3) receptor in the small bowel, vagus
nerve, and chemoreceptor trigger zone. They therefore decrease afferent
visceral and chemoreceptor trigger zone stimulation of the medullary
vomiting centre. These drugs were developed for use with chemotherapy
and have been shown in trials to be the most effective of the currently
available agents for both prevention and treatment of postoperative
nausea and vomiting.

Diagnostic Tests and Clinical Suspicion for Patients with Nausea and Vomiting
Test
Complete blood count
Electrolytes
Erythrocyte sedimentation rate
Pancreatic/liver enzymes
Pregnancy test
Protein/albumin
Specific toxins
Thyroid-stimulating hormone

Clinical suspicion
Laboratory tests
Leukocytosis in an inflammatory process, microcytic anemia from a
mucosal process
Consequences of nausea and vomiting (e.g., acidosis, alkalosis, azotemia,
hypokalemia)
Inflammatory process
For patients with upper abdominal pain or jaundice
For any female of childbearing age
Chronic organic illness or malnutrition
Ingestion or use of potentially toxic medications
For patients with signs of thyroid toxicity or unexplained nausea and
vomiting

Radiographic testing
Supine and upright abdominal radiography
Mechanical obstruction
Further testing
Esophagogastroduodenoscopy
Mucosal lesions (ulcers), proximal mechanical obstruction
Upper gastrointestinal radiography with barium
Mucosal lesions and higher-grade obstructions; evaluates for proximal
contrast media
lesions
Small bowel follow-through
Mucosal lesions and higher-grade obstructions; evaluates the small bowel
to the terminal ileum
Enteroclysis
Small mucosal lesions, small bowel obstructions, small bowel cancer
Computed tomography with oral and
Obstruction, optimal technique to localize other abdominal pathology
intravenous contrast media
Gastric emptying scintigraphy
Gastroparesis (suggestive)
Cutaneous electrogastrography
Gastric dysrhythmias
Antroduodenal manometry
Primary or diffuse motor disorders
Abdominal ultrasonography
Right upper quadrant pain associated with gallbladder, hepatic, or
pancreatic dysfunction
Magnetic resonance imaging of the brain
Intracranial mass or lesion

Complication
Excessive vomiting can lead to large
losses from the stomach of the water
and salts that normally would be
absorbed in the small intestine. This
can result in severe dehydration,
upset the bodys salt balance, and
produce circulatory problems due to
a decrease in plasma volume.
The loss of acid from vomiting results
in a metabolic alkalosis.

Occult Bleeding

Occult bleeding
The digestive or gastrointestinal (GI)
tract includes the esophagus, stomach,
small intestine, large intestine or colon,
rectum, and anus. Bleeding can come
from one or more of these areas, that
is, from a small area such as an ulcer
on the lining of the stomach or from a
large surface such as an inflammation
of the colon. Bleeding can sometimes
occur without the person noticing it.
This type of bleeding is called occult or
hidden. Fortunately, simple tests can
detect occult blood in the stool.

Four ways LGI bleeding can be

revealed in
(1) hematochezia, that is, the passage of bright red blood
per rectum, either isolated or mixed with stools,
indicating an origin low in the gastrointestinal tract, most
commonly the colon.
(2) melena, that is, the passage per rectum of black, tarry,
and foul-smelling stools, indicating a source of bleeding
from above the ileocecal valve. Melena can also be seen
in cases of bleeding from the proximal large bowel
provided that the colonic transit time is slow;
(3) occult gastrointestinal bleeding, with symptoms limited
to pallor or fatigue, detected by discovery of iron
deficiency or iron deficiency anemia or by testing for the
presence of fecal blood;
(4) symptoms of severe blood loss such as malaise,
tachycardia, or even profound shock without any
objective sign of bleeding.

Commont cause
Eshopagus

Small intestine

inflammation (esophagitis)
enlarged veins (varices)
tear (Mallory-Weiss syndrome)
cancer
liver disease

duodenal ulcer
inflammation (irritable bowel
disease)
cancer

Stomach

Large intestine and rectum

ulcers
inflammation (gastritis)
cancer

hemorrhoids
infections
inflammation (ulcerative
colitis)
colorectal polyps
colorectal cancer
diverticular disease

Mucous in the stool

Mucous in the stool

The mucus in the stool because where there's mucus,

there's inflammation and probably colitis. The colitis can be
due to a bacterial infection such as Salmonella, Shigella,
Campylobacter,

or

Clostridium

difficile.

Hirschsprung's

disease is another possibility because it can present as

colitis.

But the most probable explanation is allergic colitis.

In working up suspected colitis, it recommended to take

Hemoccult test, an abdominal radiograph (kidney, ureter,
and bladder), and culturing the stool for C. difficile.

Mucous in the stool

The mechanism that causes allergic colitis in breast-fed

children is not well understood.

One hypothesis is that mothers who eat dairy pass milk

protein antigens into their breast milk. Radioimmunoassay
studies demonstrate this phenomenon by showing that "you
can actually see cows' milk antigens in mother's milk."

However, the theory falls short in explaining how the

peptide is absorbed and deposited into the breast milk.

Another explanation is that cytokines in mother's milk are

mediating the allergy.

Food alergic

Cows milk Protein

Intolerance
Cows milk protein intolerance is a
heterogeneous disorder. The most common
antigen in cows milk are alpha lactoglobulin,
casein, alpha lactalbumin, bovine serum albumin,
bovine alpha globulin.
The quantity of cows milk required to produce an
adverse reaction varies. Most cows milk formulafed infants with cows milk protein intolerance
develop symptoms in the first 3 months of life.
The age of onset of the first symptoms in breastfed babies depends on the age at which cows
milk is first introduced.
Prevalence studies of intolerance to cows milk
protein vary from 1, 9 to 7, 5%.

Cows milk Protein

Intolerance
Cows milk protein intolerance often lasts
only a few months, and in many cases it
has disappeared completely by the age
of 12 months, hence the need for milk
challenge at the age of 12 months in
patients who were diagnosed in infancy.
Most children become tolerant to cows
milk protein by the age of 3 years,
although some degree of intolerance
persists, occasionally into adult life, in a
small number of patients.

Cows milk Protein

Intolerance
Symptoms of cows milk protein intolerance
Vomiting is a common immediate symptom.
Frequent loose stools occur in 25-75% of patients. In
an uncommon but florid picture, infants can present
with heavily bloodstained loose stools, sometimes
accompanied by mucus, giving rise to the clinical
description of food allergic colitis. Malabsorption
may mimic celiac disease with bulky fatty stools,
abdominal distention and poor weight gain, and
protein losing enteropathy may be an associated
feature. In such cases a jejunal biopsy usually shows
some degree of villous atrophy. Acute abdominal
pain (often but not always accompanied by vomiting
or loose stools) can be striking symptom.

Cows milk Protein

Intolerance
Discomfort, crying or irritability are common
and major features of cows milk protein
intolerance in infancy, but it is not clear
whether this represents painful
hyperperistaltis of the gut or discomfort
associated with vomiting or other symptoms.
They may occur in conjunction with other
symptoms, particularly gastrointestinal
symptoms, or they may occur alone. These
symptoms usually commence within an hour
of cows milk protein ingestion.

Cows milk Protein

Intolerance
Clues to the diagnosis or cows milk protein
intolerance in the history
Symptoms occur, or are made worse, soon after
ingestion of cows milk protein. Multiple affected
systems (e.g. gut, chest and skin) make the diagnosis
more likely; single symptoms make it most unlikely.
Symptoms date from the time, or soon after the time,
that breast-feeding was stopped or cows milk protein
was first introduced into the diet. (feeding changes often
coincide with the onset of atopic disease, and do not
prove a cause and effect relationship).
A family history of cows milk protein intolerance.
The presence of severe atopic disease in an infant under
the age of 12 months.
The observation that spilling cows milk onto noneczematous skin causes an urticarial rash.

Cows milk Protein

Intolerance
Making the diagnosis of cows milk protein
intolerance
Most patients whose symptoms commence within an
hour if cows milk ingestion have a positive skin
prick test, but most of those whose symptoms occur
more slowly have negative skin prick test. As is the
case with more other examples of food intolerance,
skin prick test and RAST (radioallergosorbent
testing) are unhelpful because of the high incidence
of false positive and false negative results. A jejunal
biopsy is unnecessary because it cannot replace the
need for milk elimination and challenge, and the
histological changes seen in the small intestine are
not diagnostic for cows milk protein intolerance.

Cows milk Protein

Intolerance
The procedure required to diagnose cows milk
protein intolerance is :
A period of avoidance (2 days for those with symptoms
occuring within an hour of milk ingestion : 14-28 days for
those woth delayed-onset symptoms) causing loss symptoms
Recurrence of symptoms on reintroduction of cows milk
protein
Loss of symptoms after second withdrawal of cows milk
protein
Continued abatement of symptoms with continued avoidance
of cows milk protein

This strategy must be accompanied by regular

attempts to introduce cows milk protein, for example
yearly, to see if the patient has grown out of the
intolerance.

Lactose
Intolerance

Lactose Intolerance
Also called lactase deficiency
unable to fully digest the milk sugar
(lactose) in dairy products.

Who is at risk for lactose

intolerance?
Lactose intolerance is a common condition that is
more likely to occur in adulthood, with a higher
incidence in older adults. Some ethnic and racial
populations are more affected than others,
including African Americans, Hispanic Americans,
American Indians, and Asian Americans. The
condition is least common among Americans of
northern European descent.
Infants born prematurely are more likely to have
lactase deficiency because an infants lactase
levels do not increase until the third trimester of
pregnancy.

causes lactose
intolerance
The cause of lactose intolerance is best explained by
describing how a person develops lactase deficiency.
Primary lactase deficiency develops over time and begins
after about age 2 when the body begins to produce less
lactase. Most children who have lactase deficiency do not
experience symptoms of lactose intolerance until late
adolescence or adulthood.
Researchers have identified a possible genetic link to primary
lactase deficiency. Some people inherit a gene from their
parents that makes it likely they will develop primary lactase
deficiency. This discovery may be useful in developing future
genetic tests to identify people at risk for lactose intolerance.
Secondary lactase deficiency results from injury to the small
intestine that occurs with severe diarrheal illness, celiac
disease, Crohns disease, or chemotherapy. This type of
lactase deficiency can occur at any age but is more common
in infancy.

 Two tests are commonly used to measure the

digestion of lactose.
Hydrogen Breath Test. The person drinks a
lactose-loaded beverage and then the breath is
analyzed at regular intervals to measure the amount
of hydrogen. Normally, very little hydrogen is
detectable in the breath, but undigested lactose
produces high levels of hydrogen. Smoking and
some foods and medications may affect the
accuracy of the results. People should check with
their doctor about foods and medications that may
interfere with test results.
Stool Acidity Test. The stool acidity test is used for
infants and young children to measure the amount
of acid in the stool. Undigested lactose creates lactic
acid and other fatty acids that can be detected in a
stool sample. Glucose may also be present in the
stool as a result of undigested lactose.

Symptoms
Diarrhea the most common
symptom
Nausea
Abdominal cramps
Bloating
Gas

3 types of lactose
intolerance

Normal result of aging for some people (primary

lactose intolerance)
Result of illness or injury (secondary lactose
intolerance)
small intestine decreases lactase production after an
illness, surgery or injury to your small intestine.
It can occur as a result of intestinal diseases, such as
celiac disease, gastroenteritis or an inflammatory bowel
disease like Crohn's disease.
Condition you're born with (congenital lactose
intolerance)

Milk Allergy

Clinical Types of Milk

Allergic Reactions
Type 1
Symptoms start within minutes of intake
of small volumes of CM.
Mainly causes skin problems, eczema or
urticaria (hives). May have respiratory
(runny nose, wheezy chest) or gastrointestinal (vomiting and diarrhoea)
symptoms.

 Type 2
Symptoms start several hours after intake of
modest volumes of CM
Mostly symptoms of vomiting and diarrhoea.

Type 3
Symptoms develop after more than 20
hours, or even days after intake of large
volumes of CM.
Symptoms include diarrhoea, with or
without respiratory or skin reactions.

Preventive Education
Goat's milk, rice milk, or almond milks
are not safe and are not
recommended for infants.
People with lactosa intolerance should
know about food high lactosa,ex :
Bread and other baked goods,
Processed breakfast cereals , Instant
potatoes, soups, and breakfast drinks ,
Margarine , Lunch meats (except those
that are kosher) , Salad dressings ,
Candies and other snacks , Mixes for
pancakes, biscuits, and cookies

Suggestion
We suggest Rosas mother, Mrs. Melati,
to return to exclusive breastfeeding
and to stop giving cows milk formula
for Rosa.
Further diagnostic investigations are
needed to confirm our diagnostics.

Conclusion
According to the case, we can
conclude that Rosa is having
gastrointestinal disorder.
Our major tendencies are lactose
intolerance and cows milk protein
allergy.

References
www.aafp.org/afp/20070701/afp20070701p76
-f1.gif
www.neocate.com
www.i.ehow.com/.../5245469/294354-main_Fu
ll.jpg
www.mayoclinic.com
Wyllie R. The digestive system, In: Kliegman
RM, Berhman RE, Jenson HB, Stanson BF.
Nelsons textbook of pediatrics. 18th ed.
Philadelphia: WB Saunders Co, 2007:1521645
Sherwood L. Human physiology. 5th ed.
Belmont: Thomson Learning, 2004.