Asthma

d. Brief and Related Anatomy and Physiology

ANATOMY
 The airways of the lungs consist of the cartilaginous bronchi, membranous bronchi, and gas-
exchanging bronchi termed the respiratory bronchioles and alveolar ducts.

(Sembulingam & Sembulingam, 2012)

- While the first 2 types function mostly as anatomic dead space, they also contribute to
airway resistance. The smallest non-gas-exchanging airways, the terminal bronchioles, are
approximately 0.5 mm in diameter; airways are considered small if they are less than 2 mm
in diameter (Morris & Pearson, 2019).
o ANATOMIC DEAD SPACE
 This is the volume of the conducting airways.
 The normal value is about 150 ml, and it increases with large inspirations
because of the traction or pull exerted on the bronchi by the surrounding lung
parenchyma.
 The dead space also depends on the size and posture of the subject
 can be measured by Fowler’s method.
(West, 2016)

 Airway structure consists of the following:

- Mucosa, which is composed of epithelial cells that are capable of specialized mucous
production and a transport apparatus
- Basement membrane
- A smooth-muscle matrix extending to the alveolar entrances
 - Predominantly fibrocartilaginous or fibroelastic-
supporting connective tissue (Morris & Pearson, 2019).

 Cellular elements include mast cells, which are involved in

the complex control of releasing histamine and other
mediators.
 Basophils, eosinophils, neutrophils, and macrophages also
are responsible for extensive mediator release in the early
and late stages of bronchial asthma.
 Stretch and irritant receptors reside in the airways, as do
cholinergic motor nerves, which innervate the smooth
muscle and glandular units.
 In bronchial asthma, smooth muscle contraction in an
airway is greater than that expected for its size if it were
functioning normally, and this contraction varies in its
distribution
(Morris & Pearson, 2019).

(Davies & Moores, 2010)

PHYSIOLOGY
 Airway narrowing, which is the principal feature of asthma, is brought about by the
contraction of smooth muscle in the walls of the airways.
 Bronchial smooth muscle can contract in all individuals and hence the diameter of the airways
changes, but the effect on ventilation is usually negligible.
 In asthmatics, the changes in airways diameter are exaggerated and the airways respond to
stimuli which in non-asthmatics would be innocuous.
- These two effects are together called BRONCHIAL HYPERREACTIVITY.
o is related to an underlying inflammation of the bronchial mucosa
o mucosa of asthmatics is thickened and infiltrated with inflammatory cells.
(Davies & Moores, 2010)

e. Pathophysiology
 (Kumar, Abbas & Aster, 2013)

 The major etiologic factors of asthma are genetic predisposition to type I hypersensitivity
(atopy), acute and chronic airway inflammation, and bronchial hyperresponsiveness to a
variety of stimuli.
  The inflammation involves many cell types and numerous inflammatory mediators, but the
role of type 2 helper T (TH2) cells may be critical to the pathogenesis of asthma.
1) The classic atopic form of asthma is associated with an excessive TH2 reaction against
environmental antigens.
- Cytokines produced by TH2 cells account for most of the features of asthma
o IL-4 stimulates IgE production
o IL-5 activates eosinophils, and
o IL-13 stimulates mucus production and also promotes IgE production by B
cells.
o IgE coats submucosal mast cells, which, on exposure to allergen, release
granule contents.
- This induces two waves of reaction:
o an early (immediate) phase and;
o a late phase (Fig. 12-11).
 The early reaction is dominated by bronchoconstriction, increased mucus
production and variable vasodilation.
 Bronchoconstriction is triggered by direct stimulation of subepithelial vagal receptors.
 The late-phase reaction consists of :
- inflammation, with activation of eosinophils, neutrophils, and T cells.
- In addition, epithelial cells are activated to produce chemokines that promote
recruitment of more TH2 cells and eosinophils (including eotaxin, a potent
chemoattractant and activator of eosinophils), as well as other leukocytes, thus
amplifying the inflammatory reaction.
 Repeated bouts of inflammation lead to structural changes in the bronchial wall, collectively
referred to as airway remodeling.
- These changes include hypertrophy of bronchial smooth muscle and mucus glands, and
increased vascularity and deposition of subepithelial collagen, which may occur as
early as several years before initiation of symptoms.
(Kumar, Abbas & Aster, 2013)

n. REFERENCES:
Davies, A., & Moores, C. (2010). Systems of the Body: The Respiratory System (2nd ed., pp. 49-51).
Philadelphia: Elsevier.
Kumar, V., Abbas, A., & Aster, J. (2013). Robbins Basic Pathology E-Book (9th ed., pp. 468-469).
Philadelphia: Elsevier.
Morris, M., & Pearson, D. (2019). Asthma: Practice Essentials, Background, Anatomy. Retrieved 16
March 2020, from https://emedicine.medscape.com/article/296301-overview#a3
Sembulingam, K., & Sembulingam, P. (2012). Essentials of Medical Physiology (6th ed., p. 675). New
Delhi, India: Jaypee Brothers Medical Publishers (P) Ltd.
West, J. (2016). West’s Respiratory Physiology : The Essentials (10th ed., pp. 22-23). Philadelphia, PA:
Wolters Kluwer.