PEMBEKALAN

FARMAKOTERAPI
ROTASI KLINIK
PEDIATRI
TIM FARMAKOLOGI
FK UNISSULA

NO

DAFTAR PENYAKIT MENURUT SKDI

LoC

Gastroenteritis

4A

TB paru tanpa komplikasi

4A

Malnutrisi Energi Protein

4A

DHF / DSS

4A

Infestasi Cacing

4A

Disentri Basiler dan Amoeba

4A

Kejang Demam

4A

Anemia Defisiensi Besi

4A

Bronkopneumonia Akut

4A

10

Bronkiolitis Akut

4A

DRUGS IN INFANT AND CHILDREN

Children cannot be regarded as miniature
adults in terms of drug response, due to
differences in body constitution, drug
absorption and elimination, and sensitivity to
adverse reactions.

ABSORPTION
Gastro-intestinal absorption is slower in infancy,
but absorption from intramuscular injection is
faster. To ensure that adequate blood
concentrations reach the systemic circulation in
the sick neonate, it is common practice to use
intravenous preparations. In older and less
severely ill children, oral liquid preparations are
commonly used, resulting in less accurate dosing
and a more rapid rate of absorption. Infant skin is
thin and percutaneous absorption can cause
systemic toxicity if topical preparations (e.g. of
potent corticosteroids) are applied too
extensively.

DISTRIBUTION
Body fat content is relatively low in children,
whereas water content is greater, leading to a
lower volume of distribution of fat-soluble drugs
(e.g. diazepam) in infants. Plasma protein binding
of drugs is reduced in neonates due to a lower
plasma albumin concentration and altered
binding properties. The risk of kernicterus caused
by displacement of bilirubin from albumin by
sulphonamides is well recognized. The blood
brain barrier is more permeable in neonates and
young children, leading to an increased risk of
CNS adverse effects.

METABOLISM
At birth, the hepatic microsomal enzyme system
is relatively immature (particularly in the preterm
infant), but after the first four weeks it matures
rapidly. Chloramphenicol can produce grey baby
syndrome in neonates due to high plasma levels
secondary to inefficient elimination. Conversely,
hepatic drug metabolism can be increased once
enzyme activity has matured in older infants and
children. Drugs administered to the mother can
induce
neonatal
enzyme
activity
(e.g.
barbiturates). Phenobarbitone metabolism is
faster in children than in adults because of
greater induction of hepatic enzyme activity.

EXCRETION
All renal mechanisms (filtration, secretion and
reabsorption) are reduced in neonates, and renal
excretion of drugs is relatively reduced in the newborn.
Glomerular filtration rate (GFR) increases rapidly during
the first four weeks of life, with consequent changes in
the rate of drug elimination.

PHARMACODYNAMICS
Documented evidence of differences in receptor
sensitivity in children is lacking, and the
apparently paradoxical effects of some drugs (e.g.
hyperkinesia with phenobarbitone, sedation of
hyperactive children with amphetamine) are as
yet unexplained.
The infant should be monitored if -adrenoceptor
antagonists, carbimazole, corticosteroids or
lithium are prescribed to the mother. Adrenoceptor antagonists rarely cause significant
bradycardia in the suckling infant. In high doses,
corticosteroids can affect the infants adrenal
function and lithium may cause intoxication.

PRACTICAL ASPECTS OF
PRESCRIBING
COMPLIANCE AND ROUTE OF ADMINISTRATION
Sick neonates will usually require intravenous drug
administration. Accurate dosage and attention to fluid
balance are essential. Sophisticated syringe pumps
with awareness of dead space associated with the
apparatus are necessary. Children under the age of five
years may have difficulty in swallowing even small
tablets, and hence oral preparations which taste
pleasant are often necessary to improve compliance.
However, chronic use of sucrose containing elixirs
encourages tooth cavities and gingivitis.

 Pressurized aerosols (e.g. salbutamol inhaler) are

usually only practicable in children over the age
of ten years, as co-ordinated deep inspiration is
required unless a device such as a spacer is used.
Likewise, nebulizers may be used to enhance local
therapeutic effect and reduce systemic toxicity.
Only in unusual circumstances, i.e. extensive
areas of application (especially to inflamed or
broken skin), or in infants, does systemic
absorption of drugs (e.g. steroids, neomycin)
become significant following topical application
to the skin.

 Intramuscular injection should only be used when

absolutely necessary. Intravenous therapy is less
painful, but skill is required to cannulate infants
veins (and a confident colleague to keep the
target still!). Children find intravenous infusions
uncomfortable
and
restrictive.
Rectal
administration is a convenient alternative (e.g.
Metronidazole to treat anaerobic infections).
Rectal diazepam is particularly valuable in the
treatment of status epilepticus when intravenous
access is often difficult. Rectal diazepam may
also be administered by parents. Rectal
administration should also be considered if the
child is vomiting.

DOSAGE
The British National Formulary and specialist
paediatric textbooks and formularies provide
appropriate guidelines and must be consulted by
physicians who are not familiar with prescribing
to infants and children.
ADVERSE EFFECTS
With a few notable exceptions, drugs in children
generally have a similar adverse effect profile to
those in adults. Of particular significance is the
potential of chronic corticosteroid use, including
high-dose inhaled corticosteroids, to inhibit
growth.

Aspirin is avoided in children under 16 years

(except in specific indications, such as Kawasaki
syndrome) due to an association with Reyes
syndrome, a rare but often fatal illness of
unknown aetiology consisting of hepatic necrosis
and encephalopathy, often in the aftermath of a
viral illness. Tetracyclines are deposited in
growing bone and teeth, causing staining and
occasionally dental hypoplasia, and should not be
given to children. Fluoroquinolone antibacterial
drugs may damage growing cartilage. Dystonias
with metoclopramide occur more frequently in
children and young adults than in older adults.

 Valproate hepatotoxicity is increased in young

children with learning difficulties receiving
multiple anticonvulsants. Some adverse
effects cause lifelong effects as a result of
toxicity occurring at a sensitive point in
development (a critical window) during fetal
or neonatal life (programming) as with
thalidomide/phocomelia or hypothyroid
drugs/congenital hypothyroidism.

DOSIS OBAT

MACAM MACAM DOSIS

Dosis Minimal :
Dosis paling sedikit yang diberikan kepada penderita
dewasa yang memberikan efek terapi.
Dosis Terapi :
Sejumlah obat yang memberikan efek terapetik
kepada penderita.
Dosis Lazim :
Dosis yang tercantum dalam literatur telah tertera di
buku Resmi Farmakope yang lazimnya dapat
menyembuhkan.

MACAM MACAM DOSIS

Dosis Maksimal :
Dosis paling banyak yang masih bisa diberikan pada
penderita dan tidak memberikan efek toksik.
Dosis Toksik :
Dosis yang melebihi dosis terapetik yang dapat
memberikan efek keracunan pada penderita.
Dosis Letal :
Dosis yang dapat menyebabkan kematian pada
penderita.

DASAR PENGHITUNGAN DOSIS ANAK

1. Didasarkan perbandingan dengan dosis obat
untuk orang dewasa.
a) Menurut perbandingan umur
b) Menurut perbandingan berat badan (BB
dewasa = 70 Kg)
c) Menurut perbandingan luas permukaan tubuh
(LPT dewasa = 1,73 m2)
2. Didasarkan atas ukuran fisik anak secara
individual.
a) Sesuai dengan berat badan anak dalam Kg
b) Sesuai dengan LPT anak dalam meter

RUMUS RUMUS DAN CARA

PERHITUNGAN BERDASARKAN UMUR
Young (8 tahun dan < 8 tahun) :

Dilling (> 8 tahun) :

Cowling ( Tidak berlaku untuk anak diatas 12 th) :

 Fried Bayi

atau

Keterangan:
m: umur dalam bulan
n : umur dalam tahun
Da : dosis anak
Dd : dosis dewasa

RUMUS RUMUS DAN CARA

PERHITUNGAN BERDASARKAN BB
DAN LPT
CLARK :

CRAWFORD- TERRY-ROURKE :

Keterangan :
w : BB (dewasa : 70 kg)
LPT : luas permukaan tubuh (dewasa : 1,73 m2)

BB : 9 + ( n 1 ) 2
Syarat : jika diketahui umur anak dan dosisnya diberikan
(..mg/KgBB)
1.
2.
3.
4.

mg/kgBB/kali
mg/KgBB/hari
mg/th/kali
mg/th/hari

Untuk :
1 dan 2 Hitung BB terlebih dahulu
3 dan 4 Langsung hitung DT
n = umur anak

PERSENTASE DT/DM
DT/DM > 100% Dosis harus dikurangi
DT/DM < 100% Dosis bisa dipakai

CARA PERHITUNGAN DOSIS

Bayi usia 10 tahun menderita mual dan muntah
setelah kemoterapi. Lalu dokter memberikan obat
Domperidon dengan DL 0,2-0,4 mg/kgBB/hari.
BB anak

= 9 + (n-1)2
= 9 + (10-1)2 = 27 Kg
Da = (0,2-0,4) x 27 = 5,4-10,8 mg

CONTOH SOAL
Anak umur 10 thn
Pehadoxin
DL per KgBB (5mg-15mg)/(15mg-45mg)
JAWAB :
BB anak : 9 + (10-1)2 = 27 Kg
(5mg-15mg) x 27 = (135mg 405mg)/ 1x minum
(15mg-45mg) x 27 = (405mg 1215mg)/ hari

CONTOH SOAL
Anak umur 5 thn
CTM = 40mg/tahun/hari
s.t.d.d
DT = 40 x 5 = 200 mg/hari
DT = 200/3 = 66,7 mg/kali

CONTOH SOAL
Anak BB 10 Kg
dosis dewasa asam mefenamat 500 mg

CLARK :

w anak
Da = --------------- Dd (mg)
w dewasa

Da = 10/70 x Dd = 1/7 x 500 = 71,4 mg

CONTOH SOAL
Hitunglah DT Ampicilin untuk anak usia 4
tahun, diminum 5x1 sehari selama 5 hari. DL
Ampicilin anak (oral) 1-5 tahun = 50 100
mg/kgBB/hari. DM = 4 gr.
Instruksi :
Hitung DT/ hari dan DT/kali
Hitung % DT/DM nya

 BB = 9 + (n-1).2 = 9 + (4-1).2 = 15 kg
DL = (50 100 mg/kgBB/hari) x 15 kg
= 750 1500 mg/hari
DT/hari = (750 + 1500) / 2 = 1125 mg/hari
DT/kali = 1125 mg/hari : 5 = 225 mg/kali
DM anak =
= 4 / (4+12) x 4000 mg/hari
= 1000 mg/hari
% DT/DM = (1125 mg/hari : 1000 mg/hari) x 100
% = 112,5 % > 100 %
Dosis harus dikurangi/diturunkan DM anak

DISENTRI BASILER DAN AMOEBA

DRUGS FOR AMEBIASIS
Tissue amebicides (chloroquine, emetines,
metronidazole, tindidazole) act on organisms in
the bowel wall and the liver; luminal amebicides
(diloxanide furoate, iodoquinol, paromomycin)
act only in the lumen of the bowel. The choice of
a drug depends on the form of amebiasis. For
asymptomatic disease, diloxanide furoate is the
first choice. For mild to severe intestinal infection,
metronidazole or tinidazole is used with a luminal
agent, and this regimen is recommended in
amebic hepatic abscess and other extraintestinal
disease. The mechanisms of amebicidal action of
most drugs in this subclass are unknown.

A. Diloxanide Furoate
This drug is commonly used as the sole agent
for the treatment of asymptomatic amebiasis
and is also useful in mild intestinal disease
when used with other drugs. Diloxanide
furoate is converted in the gut to the
diloxanide freebase form, which is the active
amebicide. Toxic effects are mild and are
usually
restricted
to
gastrointestinal
symptoms.

B. Emetines
Emetine and dehydroemetine inhibit protein
synthesis by blocking ribosomal movement along
messenger RNA. These drugs are used parenterally
(subcutaneously or intramuscularly) as backup drugs
for treatment of severe intestinal or hepatic
amebiasis together with a luminal agent in
hospitalized patients. The drugs may cause severe
toxicity, including gastrointestinal distress, muscle
weakness,
and
cardiovascular
dysfunction
(arrhythmias and congestive heart failure). The drugs
are restricted to use in severe amebiasis when
metronidazole cannot be used.

C. Iodoquinol
Iodoquinol, a halogenated hydroxyquinoline, is an orally
active luminal amebicide used as an alternative to
diloxanide for mild to severe intestinal infections.
Adverse gastrointestinal effects are common but usually
mild, especially when taken with meals. Systemic
absorption after high doses may lead to thyroid
enlargement, skin reactions due to iodine toxicity and
possibly neurotoxic effects, including peripheral
neuropathy and visual dysfunction.

D. Metronidazole and Tinidazole

1.PharmacokineticsMetronidazole and tinidazole
are effective orally and distributed widely to
tissues. The half-life of metronidazole is 68 h, and
that of tinidazole 1214 h. Elimination of the drugs
requires hepatic metabolism.
2.Mechanism of actionMetronidazole undergoes
a reductive bioactivation of its nitro group by
ferredoxin (present in anaerobic parasites) to form
reactive cytotoxic products. The mechanism of
tinidazole is assumed to be similar.

3. Clinical useMetronidazole or tinidazole is the drug

of choice in severe intestinal wall disease and in
hepatic abscess and other extraintestinal amebic
disease. Both drugs are used with a luminal amebicide.
The duration of treatment required with metronidazole
is longer than with tinidazole. Metronidazole is the
drug of choice for trichomoniasis: tinidazole may be
effective against some metronidazole-resistant
organisms. Other clinical uses of metronidazole include
treatment of giardiasis (tinidazole is equally effective),
and infections caused by Gardnerella vaginalis and
anaerobic bacteria (B fragilis, C difficile).
Metronidazole is also used in combination regimens for
gastrointestinal ulcers associated with H pylori.

4. ToxicityAdverse effects of metronidazole

include gastrointestinal irritation (it is best taken
with meals), headache, paresthesias, and dark
coloration of urine. Tinidazole has a similar
adverse effect profile but may be better tolerated
than metronidazole. More serious toxicity
includes neutropenia, dizziness, and ataxia. Drug
interactions with metronidazole include a
disulfiram-like reaction with ethanol and
potentiation of coumarin anticoagulant effects.
Safety of metronidazole and tinidazole in
pregnancy and in nursing mothers has not been
established.

E. Paromomycin
This drug is an aminoglycoside antibiotic used as a
luminal amebicide and may be superior to diloxanide in
asymptomatic infection. Paromomycin may also have
some efficacy against cryptosporidiosis in the AIDS
patient. Systemic absorption in renal insufficiency may
lead to headaches, dizziness, rashes, and arthralgia.
Tetracyclines (eg, doxycycline) are sometimes used with a
luminal amebicide in mild intestinal disease.

F. Nitazoxanide
This agent has activity against various protozoans
(including Entamoeba) and helminths. It is currently
approved in the UnitedStates for treatment of
gastrointestinal infections caused by G lamblia and
Cryptosporidium parvum. Nitazoxanide appears to have
activity against metronidazole-resistant protozoal strains.

INFESTASI CACING
DRUGS THAT ACT AGAINST NEMATODES
The medically important intestinal nematodes
responsive to drug therapy include Enterobius
vermicularis
(pinworm),
Trichuris
trichiuria
(whipworm), Ascaris lumbricoides (roundworm),
Ancyclostoma and Necator species (hookworms), and
Strongyloides stercoralis (threadworm). More than 1
billion persons worldwide are estimated to be
infected by intestinal nematodes. Tissue nematodes
responsive to drug therapy include Ancyclostoma
species, which cause cutaneous larva migrans.

DRUGS THAT ACT AGAINST NEMATODES

Species of Dracunculus, Onchocerca, Toxocara, and
Wuchereria bancrofti (the cause of filariasis) all are
responsive to drug treatment. The number of
persons worldwide estimated to be infected by tissue
nematodes exceeds 0.5 billion.
A. Albendazole
1. MechanismsThe action of albendazole is thought
to involve inhibition of microtubule assembly. The
drug is larvicidal in ascariasis, cystercercosis,
hookworm, and hydatid disease and is ovicidal in
ascariasis, ancyclostomiasis, and trichuriasis.

2. Clinical useAlbendazole has a wide antihelminthic

spectrum. It is a primary drug for ascariasis, hookworm,
pinworm, and whipworm infections and an alternative
drug for treatment of threadworm infections, filariasis,
and both visceral and cutaneous larva migrans.
Albendazole is also used in hydatid disease and is active
against the pork tapeworm in the larval stage
(cysticercosis).
3. ToxicityAlbendazole has few toxic effects during short
courses of therapy (13 d). However, a reversible
leukopenia, alopecia, and elevation of liver function
enzymes can occur with more prolonged use. Long-term
animal toxicity studies have described bone marrow
suppression and fetal toxicity. The safety of the drug in
pregnancy and young children has not been established.

B. Diethylcarbamazine
1.MechanismsDiethylcarbamazine
immobilizes microfilariae by an unknown
mechanism, increasing their susceptibility to
host defense mechanisms.
2. Clinical useDiethylcarbamazine is the
drug of choice for several filarial infections
including those caused by Wucheria bancrofti
and Brugia malayi and for eye worm disease
(loa loa). The drug undergoes renal
elimination, and its half-life is increased
significantly by urinary alkalinization.

3. ToxicityAdverse effects include headache,

malaise, weakness, and anorexia. Reactions
to proteins released by dying filariae include
fever, rashes, ocular damage, joint and muscle
pain, and lymphangitis. In onchocerciasis, the
reactions are more intense and include most
of the symptoms described as well as
hypotension, pyrexia, respiratory distress, and
prostration.

C. Ivermectin
1. MechanismsIvermectin intensifies -aminobutyric acid
(GABA)-mediated neurotransmission in nematodes and
causesimmobilization of parasites, facilitating their removal
by the reticuloendothelial system. Selective toxicity results
because in humans GABA is a neurotransmitter only in the
CNS, and ivermectin does not cross the blood-brain barrier.
2. Clinical useIvermectin is the drug of choice for
onchocerciasis, cutaneous larva migrans, strongyloidiasis,
and some forms of filariasis.
3. ToxicitySingle-dose oral treatment in onchocerciasis
results in reactions to the dying worms, including fever,
headache, dizziness, rashes, pruritus, tachycardia,
hypotension, and pain in joints, muscles, and lymph glands.
These symptoms are usually of shortduration, and most can
be controlled with antihistamines and nonsteroidal antiinflammatory drugs. Avoid other drugs that enhance GABA
activity. Ivermectin should not be used in pregnancy.

D. Mebendazole
1. MechanismMebendazole acts by selectively
inhibiting microtubule synthesis and glucose uptake
in nematodes.
2. Clinical useMebendazole is a primary drug for
treatment of ascariasis and for pinworm and
whipworm infections. Mebendazole has also been
used as a backup drug in visceral larval migrans. Less
than 10% of the drug is absorbed systemically after
oral use, and this portion is metabolized rapidly by
hepatic enzymes. Plasma levels may be decreased by
carbamazepine or phenytoin and increased by
cimetidine.

3.ToxicityMebendazole toxicity is usually limited to

gastrointestinal irritation, but at high doses
agranulocytopenia and alopecia have occurred. The
drug is teratogenic in animals and therefore
contraindicated in pregnancy.
E. Piperazine
1. MechanismPiperazine paralyzes ascaris by acting as
an agonist at GABA receptors. The paralyzed
roundworms are expelled live by normal peristalsis.
2. Clinical usePiperazine is an alternative drug for
ascariasis.
3. ToxicityMild gastrointestinal irritation is the most
common side effect. Piperazine should not be used in
pregnant patients or those with hepatic or renal
dysfunction or seizure disorders.

F. Pyrantel Pamoate
1. MechanismPyrantel pamoate stimulates nicotinic
receptors present at neuromuscular junctions of
nematodes. Contraction of muscles occurs, followed by
a depolarization-induced paralysis. The drug has no
actions on flukes or tapeworms.
2. Clinical usePyrantel pamoate has wide activity
against nematodes killing adult worms in the colon but
not the eggs. It is a drug of choice for hookworm and
roundworm infections and an alternative drug for
pinworms. The drug is poorly absorbed when given
orally.
3. ToxicityAdverse effects are minor but include
gastrointestinal distress, headache, and weakness. Use
with caution in patients with hepatic dysfunction.

G. Thiabendazole
1. MechanismThiabendazole is a structural congener of
mebendazole and has a similar action on microtubules.
2. Clinical useBecause of its adverse effects,
thiabendazole is an alternative drug in strongyloidiasis
and trichinosis (adult worms). Thiabendazole is rapidly
absorbed from the gut and is metabolized by liver
enzymes. The drug has anti-inflammatory and
immunorestorative actions in the host.
3. ToxicityThiabendazole is much more toxic than other
benzimidazoles or ivermectin, so these other drugs are
preferred. Its toxic effects include gastrointestinal
irritation, headache, dizziness, drowsiness, leukopenia,
hematuria, and allergic reactions, including intrahepatic
cholestasis.

Reactions caused by dying parasites include fever, chills,

lymphadenopathy, and skin rash. Irreversible liver failure
and fatal Stevens-Johnson syndrome have also been
reported. Avoid in pregnant patients or those with
hepatic or renal disease.
DRUGS THAT ACT AGAINST TREMATODES
The medically important trematodes include Schistosoma
species (blood flukes, estimated to affect more than 150
million persons worldwide), Clonorchis sinensis (liver
fluke, endemic in Southeast Asia), and Paragonimus
westermani (lung fluke, endemic to both Asia and the
Indian subcontinent). With few exceptions, fluke
infections respond well to praziquantel.

A. Praziquantel
1. MechanismPraziquantel increases membrane
permeability to calcium, causing marked
contraction initially and then paralysis of
trematode and cestode muscles; this is followed
by vacuolization and parasite death.
2. Clinical usePraziquantel has a wide
antihelminthic spectrum that includes activity in
both trematode and cestode infections. It is the
drug of choice in schistosomiasis (all species),
clonorchiasis, and paragonimiasis and for
infections caused by small and large intestinal
flukes.

The drug is active against immature and adult

schistosomal forms. Praziquantel is also 1 of 2
drugs of choice (with niclosamide) for infections
caused by cestodes (all common tapeworms) and
an alternative agent (to albendazole) in the
treatment of cysticercosis.
3.PharmacokineticsAbsorption from the gut is
rapid, and the drug is metabolized by the liver to
inactive products.
4. ToxicityCommon adverse effects include
headache, dizziness and drowsiness, malaise,
and less frequently, gastrointestinal irritation,
skin rash, and fever.

Neurologic effects can occur in the treatment of

neurocyticercosis
including
intracranial
hypertension and seizures. Corticosteroid therapy
reduces the risk of the more serious reactions.
Praziquantel is contraindicated in ocular
cysticercosis. In animal studies, the drug
increased abortion rate.

B. Bithionol
1. Clinical useBithionol is a codrug of choice
(with triclabendazole) for treatment of
fascioliasis (sheep liver fluke) and analternative
agent in paragonimiasis. The mechanism of
action of the drug is unknown. Bithionol is orally
effective and is eliminated in the urine.

2. ToxicityCommon adverse effects of bithionol

include nausea and vomiting, diarrhea and
abdominal cramps, dizziness, headache, skin rash
(possibly a reaction to dying worms), and
phototoxicity. Less frequently, pyrexia, tinnitus,
proteinuria, and leukopenia may occur.
C. Metrifonate
Metrifonate is an organophosphate prodrug that
is converted in the body to the cholinesterase
inhibitor dichlorvos. The active metabolite acts
solely against Schistosoma haematobium (the
cause of bilharziasis). Toxic effects occur from
excess cholinergic stimulation. The drug is
contraindicated in pregnancy.

D. Oxamniquine
Oxamniquine is effective solely in Schistosoma
mansoni infections (intestinal bilharziasis), acting on
male immature forms and adult schistosomal forms.
The drug causes paralysis of the worms, but its
precise mechanism is unknown. Dizziness is a
common adverse effect (no driving for 24 h);
headache, gastrointestinal irritation, and pruritus
may also occur. Reactions to dying parasites include
eosinophilia, urticaria, and pulmonary infiltrates. It is
not advisable to use the drug in pregnancy or in
patients with a history of seizure disorders.

DRUGS THAT ACT AGAINST CESTODES (TAPEWORMS)

The 4 medically important cestodes are Taenia
saginata (beef tapeworm), Taenia solium (pork
tapeworm, which can cause cysticerci in the brain
and the eyes), Diphyllobothrium latum (fish
tapeworm), and Echinococcus granulosus (dog
tapeworm, which can cause hydatid cysts in the liver,
lungs, and brain). The primary drugs for treatment of
cestode infections are praziquantel (see prior
discussion) and niclosamide.
A. Niclosamide
1. MechanismNiclosamide may act by uncoupling
oxidativephosphorylation or by activating ATPases.

2.Clinical useNiclosamide is an alternative drug to

praziquantel for infections caused by beef, pork, and
fish tapeworm. It is not effective in cysticercosis (for
which albendazole or praziquantel is used) or hydatid
disease caused by Echinococcus granulosus (for which
albendazole is used). Scoleces and cestode segments
are killed, but ova are not. Niclosamide is effective in
the treatment of infections from small and large
intestinal flukes.
3. ToxicityToxic effects are usually mild but include
gastrointestinal distress, headache, rash, and fever.
Some of these effects may result from systemic
absorption of antigens from disintegrating parasites.
Ethanol consumption should be avoided for 2448 h.

VIRAL CROUP

PNEUMONIA DAN
BRONKOPNEUMONIA

TERIMA KASIH
SELAMAT BELAJAR