Drugs used in pulmonary diseases Antiasthmatic drugs Antitussives Expectorants Yang yun×a(杨云霞)
Drugs used in pulmonary diseases Antiasthmatic drugs Antitussives Expectorants Yang yun-xia (杨云霞）
Drugs used in pulmonary diseases Coughing Wheezing Sputum(phlegm) nflammation
Drugs used in pulmonary diseases Coughing Wheezing Sputum (phlegm) Inflammation
Drugs used in pulmonary diseases Cougbigging Wheezing Sputum(phlegm nflammation
Drugs used in pulmonary diseases Coughing Wheezing Sputum (phlegm) Inflammation Coughing
Pulmonary Pharmacology: Asthma General disease characteristics increased tracheobronchial responsiveness to many stimuli physiological air passage narrowing paroxysmal dyspnea, coughing, wheezing, chest tightness
Pulmonary Pharmacology: Asthma General disease characteristics: increased tracheobronchial responsiveness to many stimuli ↓ physiological air passage narrowing ↓ paroxysmal dyspnea, coughing, wheezing, chest tightness
Prevalence Very common disorder: 4-5%affected Typically presents in early life 50%of cases developed before age 10 33% before age 40
Prevalence: Very common disorder: 4-5% affected Typically presents in early life: 50% of cases developed before age 10; 33% before age 40
Etiology two broad types a① Allergic asthma:(gE) Histamine Ag-Ab- mast cell surface Trapase mediators release Leukotrienes Prostaglandins → muscle contraction pA vascular leakage mucus hyper secretion
Etiology----- two broad types ①Allergic asthma: (IgE) • Ag-Ab → mast cell surface • → mediators release • → muscle contraction • vascular leakage • mucus hyper secretion • Histamine Trapase Leukotrienes Prostaglandins PAF
Immunopathogenesis of asthma. Exposure to allergen cause synthesis of lgE, which binds to mast cell in airway mucosa On reexposure to allergen, Ag-Ab interaction on mast cell surface triggers release of mediators of anaphylaxis: Histamine, trypase, Prostaglandin D2, leukotriene C4, and platelet-activating factor. These agent provoke contraction of airway smooth muscle, causing immediate fall in FEV1 Reexposure to allergen also causes synthesis and release of cytokines: interleukins 4&5, granulocyte macrophage colony stimulatory factors, tumor necrosis factor and tissue growth factor from Tcells and mast cells. these cytokines attract and activate eosinophil and neutrophils, whose products include eosinophil cationic protein, major basic protein, proteases, and platelet activating factors. These mediators causes edema, mucus hypersecretion, smoothmuscle contraction, and increases in bronchi reactivity associated with late asthmatic response indicated by fall in FEv1 2-8 hrs after exposure Smooth muscle Blood vesse‘ Airway wall : Cell HistaminePGD ECPhis'sarte Proteases I PAF GM-CSF MBP解的PA TNF e的 TGF IgE Mast ce Tlymphocyte ALLERGEN
Immunopathogenesis of asthma. Exposure to allergen cause synthesis of IgE, which binds to mast cell in airway mucosa. On reexposure to allergen, Ag-Ab interaction on mast cell surface triggers release of mediators of anaphylaxis: Histamine,trypase, Prostaglandin D2, leukotriene C4, and platelet-activating factor. These agent provoke contraction of airway smooth muscle, causing immediate fall in FEV1. Reexposure to allergen also causes synthesis and release of cytokines: interleukins 4 & 5, granulocyte - macrophage colony stimulatory factors, tumor necrosis factor and tissue growth factor from Tcells and mast cells. These cytokines attract and activate eosinophil and neutrophils, whose products include eosinophil cationic protein, major basic protein, proteases, and platelet activating factors. These mediators causes edema, mucus hypersecretion, smoothmuscle contraction, and increases in bronchial reactivity associated with late asthmatic response indicated by fall in FEV1 2 -8 hrs after exposure
Histamine Bronchoconstriction Prostaglandin D2 Vascular congestion Edema Platelet activating Vascular leakage factor PAF tryptase Leukotrienes
Histamine Bronchoconstriction Vascular congestion Edema Vascular leakage Prostaglandin D2 Platelet activating factor PAF trypase Leukotrienes
Etiology ② idiosyncratic asthma normal serum IgE Nonantigenic stimul ● Stimulation- induced o exercises. inhaled irritants ect
②Idiosyncratic asthma: normal serum IgE Nonantigenic stimuli ⚫ Stimulation-induced ⚫ exercises, inhaled irritants ect Etiology
CNS Vagal afferent Vagal efferent ssue response cel (mast cell or eosinophil) Sensory receptor 7g9 Mediators from Inhaled irritant response cell Mucosa Preganglionic fiber Lumen Transmitter(ACh) Postganglionic neuron Sm。 oth muscle cells
