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INTRODUCTION

Pulmonary pharmacology concerns understanding how drugs act on the lung and the pharmacological therapy of pulmonary diseases. Much of pulmonary pharmacology is concerned with the effects of drugs on the airways and the therapy of airway obstruction, particularly asthma and chronic obstructive pulmonary disease (COPD), which are among the most common diseases of the airways, although there are marked differences in inflammatory mechanisms and response to therapy between these diseases. This chapter discusses the pharmacotherapy of obstructive airways disease, particularly therapy with bronchodilators, which act mainly by reversing airway smooth muscle contraction, and anti-inflammatory drugs, which suppress the inflammatory response in the airways. This chapter focuses on the pulmonary pharmacology of β2 adrenergic agonists and corticosteroids; the basic pharmacology of these classes of agents is presented elsewhere (see Chapters 14 and 50).

This chapter also discusses other drugs used to treat obstructive airway diseases, such as mucolytics and respiratory stimulants, and covers the drug therapy of cough, the most common respiratory symptom. Drugs used in the treatment of pulmonary hypertension (see Chapter 35) or lung infections, including tuberculosis (see Chapter 65), are covered elsewhere.

ABBREVIATIONS

Abbreviations

ACh: acetylcholine

AUC: area under the curve

BDP: beclomethasone dipropionate

cAMP: 3′-5′ cyclic adenosine monophosphate, cyclic AMP

CCR: C-C chemokine receptor

COMT: catechol-O-methyl transferase

COPD: chronic obstructive pulmonary disease

CRTh2: chemokine receptor homologous molecule expressed on Th2 lymphocytes

cys-LT: cysteinyl-leukotriene

DPI: dry powder inhaler

FeNO: fractional exhaled nitric oxide

FEV1: forced expiratory volume in 1 sec

GI: gastrointestinal

GPCR: G protein-coupled receptor

GR: glucocorticoid receptor

HDAC: histone deacetylase

HFA: hydrofluoroalkane

HPA: hypothalamic-pituitary-adrenal

ICS: inhaled corticosteroid

Ig: immunoglobulin

IL: interleukin

ILC2: innate type 2 lymphocyte

IP3: inositol 1,4,5-trisphosphate

LABA: long-acting β2 agonist

LAMA: long-acting muscarinic antagonist

LTRA: leukotriene cys-LT1-receptor antagonist

5-LO: 5′-lipoxygenase

LT: leukotriene

MAO: monoamine oxidase

MAP: mitogen-activated protein

MDI: metered-dose inhaler

MMAD: mass median aerodynamic diameter

MMP: matrix metalloproteinase

NF-κB: nuclear factor kappa B

PDE: cyclic nucleotide phosphodiesterase

PG: prostaglandin

PKA: protein kinase A

pMDI: pressurized metered-dose inhaler

SABA: short-acting β2 agonists

SAMA: short-acting muscarinic antagonist

TAS2R: taste 2 receptor

Tc1 cell: cytotoxic T lymphocyte

TH17: T helper 17 cell

TH2: T helper 2 lymphocyte

TNF: tumor necrosis factor

TRP: transient receptor potential

TSLP: thymic stromal lymphopoietin

VIP: vasoactive intestinal polypeptide

MECHANISMS OF ASTHMA

Asthma is a chronic inflammatory disease of the airways that is characterized by activation of mast cells, infiltration of eosinophils, T helper 2 (TH2) lymphocytes, and innate type 2 lymphocytes (ILC2) (Figure 44–1) (Papi et al., 2018). Mast cell activation by allergens and physical stimuli releases bronchoconstrictor mediators, such as histamine, leukotriene (LT) D4, and prostaglandin (PG) D2, which cause airway smooth muscle contraction, vasodilation, microvascular leakage, and ...

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