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Asthmatic

s
Drugs
Fadel Muhammad Garishah
Diponegoro University
School of Medicine

Diponegoro University
School of Medicine Pharmacology and Therapy I
Case I
A 56-year-old man presents to ED with the history of
shortness of breath for 45 minutes. He reports that he was
feeling well and in his usual state of health until about an
hour ago, when he smelled something burning. Twenty
minutes later, he began to fell short of breath and was
wheezing. He tried using his albuterol inhaler without
success, so he proceeded to the ED. At the ED, he was
tachycardia, tachypnea, wheezing and hypertensive. His
O2 sats on RA were 87% to 88%. His last admission for an
asthma attack was 2 months ago.
What is his acute asthma management?
Long term managements?

Diponegoro University, School of Medicine


Bronchial Asthma
Asthma
Asthma is defined as recurrent reversible airway obstruction,
with attacks of wheeze, shortness of breath and often
nocturnal cough. Severe attacks cause hypoxaemia and are
life-threatening.
Asthmatic patients experience intermittent attacks of
wheezing, shortness of breath-with difficulty
especially in breathing out-and sometimes cough.
Essential features include:
airways inflammation, which causes
bronchial hyper-responsiveness, which in turn results in
recurrent reversible airway obstruction.

Diponegoro University, School of Medicine


Pathogenesis involves exposure of genetically
disposed individuals to allergens; activation of Th2
lymphocytes and cytokine generation promote:
differentiation and activation of eosinophils
IgE production and release
expression of IgE receptors on mast cells and eosinophils.
Important mediators include leukotriene B4 and
cysteinyl leukotrienes (C4 and D4); interleukins IL-4,
IL-5, IL-13; and tissue-damaging eosinophil proteins.

Diponegoro University, School of Medicine


Inflammatory cells releasing Growth factors act
on smooth muscle cells
causing hypertrophy and hyperplasia, and the
smooth muscle can itself release proinflammatory
mediators and autocrine growth factors schematically
the changes that take place in the bronchioles.
Epithelial cell loss means that irritant receptors and C
fibres are more accessible to irritant stimuli-an
important mechanism of bronchial hyper-reactivity.

Diponegoro University, School of Medicine


Asthma Pathogenesis

IgE

cysteinyl leukotrienes

Diponegoro University, School of Medicine


Airway Narrowing: Acute Asthmatic Attacks

1. Contraction of airway smooth muscle


2. Inspissation of viscid mucus plugs in the airway lumen
3. Thickening of bronchial mucosa from edema, cellular
infiltration, and hyperplasia of secretory, vascular, and
smooth muscle cells.
Which is easily reversed? Requires sustained treatment?
- Easily reversed : Contraction of Airway Smooth Muscle
by giving Bronchodilator drugs
- Sustained treatment? Mucus Hypersecretion and
Thickening mucosa due to immune cells infiltration
maintained with antiinflammatory drugs

Diponegoro University, School of Medicine


Diponegoro University, School of Medicine
Antiasthmatic drugs include:
bronchodilators
anti-inflammatory agents.
Treatment is monitored by measuring forced
expiratory volume in 1 second (FEV1) or peak
expiratory flow rate and, in acute severe disease,
oxygen saturation and arterial blood gases.

Diponegoro University, School of Medicine


Bronchodilators

Antiinflammatory drugs

Antiinflammatory drugs
Severe acute asthma is a medical emergency
requiring hospitalisation.
Treatment includes (Bronchodilators reverse the
bronchospasm of the immediate phase; anti-
inflammatory agents inhibit or prevent the
inflammatory components of both phases )
oxygen (in high concentration, usually 60%),
inhalation of nebulised salbutamol, and
intravenous hydrocortisone followed by a course of
oral prednisolone.
Additional measures occasionally used include nebulised
ipratropium,
intravenous salbutamol or aminophylline,
and antibiotics (if bacterial infection is present).
Monitoring is by PEFR or FEV1, and by measurement of
arterial blood gases and oxygen saturation.

Diponegoro University, School of Medicine


Oxygen
Salbutamol: 2-Adrenoceptor agonists act as
physiological antagonists of the spasmogenic
mediators but have little or no effect on the bronchial
hyper-reactivity
Glucocorticoids: These reduce the inflammatory
component in chronic asthma and are life-saving in
status asthmaticus (acute severe asthma).
Theophylline (often formulated as aminophyllin)
relaxant effect on smooth muscle has been attributed
to inhibition of phosphodiesterase (PDE) isoenzymes,
with resultant increase in cAMP and/or cGMP
ipratropium: Muscarinic receptor antagonists
Cysteinyl leukotriene receptor antagonists
Histamine H1-receptor antagonists

Diponegoro University, School of Medicine


Cromoglicate and nedocromil: Given
prophylactically, they reduce both the immediate-
and late-phase asthmatic responses and reduce
bronchial hyper-reactivity.
Omalizumab is a humanised monoclonal anti-IgE
antibody. It is effective in patients with allergic
asthma as well as in allergic rhinitis. It is of
considerable theoretical interest (see review by
Holgate et al., 2005), but it is expensive and its
place in therapeutics is unclear

Diponegoro University, School of Medicine

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