CASE 1 Respiratory System

Pharmacological Properties of Ambroxol

How does it work?
Ambroxol is a clinically proven systemically active mucolytic agent. When
administered orally onset of action occurs after about 30 minutes. The breakdown of
acid mucopolysaccharide fibers makes the sputum thinner and less viscous and
therefore more easily removed by coughing. Although sputum volume eventually
decreases, its viscosity remains low for as long as treatment is maintained.
Ambroxol is the active mucolytic agent. It makes phlegm in the airways thinner
and less sticky. It does this by increasing the body's natural production of surfactant.
This contributes to a secretomotoric effect: it helps the cilia - tiny hairs that line the
respiratory tract - to transport the phlegm out of the lungs. Here is a step-by-step
description of how Ambroxol works:
1. Ambroxol is quickly metabolised by the body. It goes straight to work at the
mucus-secreting cells, where it changes the mucus so it becomes less viscous. This
thinner, more liquid mucus helps lift the heavy, sticky phlegm off the walls of the
airways.
2. Ambroxol frees and activates the cilia. Thanks to the effect of the thinner
mucus, the cilia are no longer clogged by the thick, sticky phlegm. They are free to
move again and help to push the phlegm up and out of the respiratory tract.
Furthermore, Ambroxol enhances the movement of the cilia so they transport phlegm
out of the airways more quickly.
3. Ambroxol is not a cough suppressant. It does not interfere with the body's
natural cough response. This is important, because coughing is still needed to eject
the excess phlegm from the airways. Ambroxol makes it easier to get the phlegm
moving again.
Composition:
Each tablet contains ambroxol hydrochloride 30 mg; each 5 ml of the syrup contains
ambroxol hydrochloride 15 mg.
Indication:
All forms of tracheobronchitis, emphysema with bronchitis pneumoconiosis, chronic
inflammatory pulmonary conditions, bronchiectasis, bronchitis with bronchospasm
asthma.
Side Effect:
Occasional gastrointestinal side effects may occur but these are normally mild.
Precaution:
It is advisable to avoid use during the first trimester of pregnancy.
Dosage:

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Adults daily dose of 30 mg (one Ambroxol tablet) to 120 mg (4 Ambroxol

tablets) taken in 2 to 3 divided doses
Children up to 2 years: half a teaspoonful Ambroxol syrup twice daily
Children 2 - 5 years: half a teaspoonful Ambroxol syrup 3 times daily
Children over 5 years: One teaspoonful Ambroxol syrup 2-3 times daily

Pharmacological Properties of Ibuprofen

Class: NSAID with antipyretic and analgesic effect
Indication:

For reduction of fever in patients aged 6 months up to 2 years of age.

For relief of mild to moderate pain in patients aged 6 months up to 2 years of

age.

For relief of signs and symptoms of juvenile arthritis.

For treatment of primary dysmenorrhea.

For relief of the signs and symptoms of rheumatoid arthritis and osteoarthritis.

Pharmacodynamics - Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID)

that possesses anti-inflammatory, analgesic and antipyretic activity. Its mode of
action, like that of other NSAIDs, is not completely understood, but may be related to
prostaglandin synthetase inhibition. After absorption of the racemic ibuprofen, the
[-]R-enantiomer undergoes interconversion to the [+]S-form. The biological activities
of ibuprofen are associated with the [+]S-enantiomer.
Mechanisms of COX Inhibition by NSAIDs
All NSAIDs variably inhibit COX-1 and COX-2 and the mechanisms of inhibition fall into
three broad categories, although there are exceptions. For example, nimesulide is a
weak competitive inhibitor of COX-1 but a potent time-dependent inhibitor of COX-2,
whereas celecoxib exhibits slow competitive binding and, at higher concentrations,
binds irreversibly.The three categories are:

Category 1: rapid competitive reversible binding of COX-1 and COX-2 (e.g.,

ibuprofen, piroxicam, mefenamic acid);

Category 2: rapid, lower-affinity reversible binding followed by timedependent, higher-affinity, slowly reversible binding of COX-1 and COX-2 (e.g.,
diclofenac, flurbiprofen, indomethacin);

Category 3: rapid reversible binding followed by covalent modification of COX1 and COX-2 (e.g., aspirin)

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Drugs such as ibuprofen competitively inhibit arachidonic acid binding and dissociate
rapidly from the COX active site. By contrast, the slow tight-binding NSAIDs (e.g.,
flurbiprofen) initially compete poorly with arachidonic acid but then bind tightly in a
time-dependent manner. Both ibuprofen and flurbiprofen adopt a similar
conformation in the active site, and it is has been proposed that the kinetic
differences between category 1 and 2 NSAIDs is the speed and efficiency by which
they gain access through the narrow constriction in the COX channel created by
Arg120, Tyr355 and Glu524. The COX-2 inhibitors lack a carboxyl group and binding
of these drugs within the COX active site does not require the charged interaction
with Arg120. Instead, these larger methylsulfonylphenyl derivatives block the COX-2
channel in a time-dependent manner as the sulfonamide moiety slowly orientates
within the hydrophobic side pocket.
Dosage:
Different indication has different dosage. Further info please visit the link below guys
http://www.drugs.com/dosage/ibuprofen.html
Adverse Effect:
gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and
perforation of the stomach, small intestine, or large intestine, which can be fatal.

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