Exam 1 Respiratory Flashcards
Airway smooth muscle extends to
distal terminal bronchioles
Airway smooth muscles are influence by
PSNS and SNS
Thoracic ganglia of the SNS innervate
smooth muscles of bronchi and pulmonary blood vessels
tracheobronchial blood vessels and glands
Sympathetic tone is
bronchodilation via beta 2 receptors
Vagus nerve of the PSNS system innervates
smooth muscles of bronchi
Beta adrenergic receptors located in the
smooth muscle of the blood vessels, skin muscle mesentary and bronchial smooth muscle
B2 adrenoreceptors cause
widening of airways (bronchodilation)
increase intracellular cyclic AMP
Nonadrenergic non-cholinergic nerves (NANC)
influences on inflammation and smooth muscle tone
M3
mediate bronchoconstriction via the activation of IP3 which increases the intracellular Ca2+ concentrations
Asthma causes recurrent episodes of
wheezing breathlessness chest tightness cough (night and early am) tachypnea prolonged expiration phase of respiration fatigue
Asthma is
a chronic inflammatory disorder of the airways characterized by increase responsiveness of the tracheobronchial tree to a variety of stimuli
Asthma creates airways that are
inflammed, edematous
bronchial hypersensitivity/reactivity to irritant stimuli
difficult with air outflow
Degree of airway hyper-responsiveness and bronchoconstriction parallels
the extent of inflammation
Asthma is characterized by
inflammation
hyperreactivity
reversible airway obstruction
airway hyper-responsiveness and inflammation from allergen in bronchial mucosa leads to
activation of T2 lyphmocytes and cytokine release
Asthma medications are aimed
at flattening the response to the mediators
Asthma mediators
eosinophils mast cells neutrophils macrophages basophils T lymphocytes
Probably mediators of acute bronchoconstriction
cytokines, interleukins
arachiddonic acid metabolites, leukotrienes and prostraglandins
histamine, adenosine and platelet activating factor
Atopic Extrinisic asthama
produced by an allergen and IgE synthesis
COPD Factors
genes smoking age/gender lung growth/development exposure to particles: cigarette smoke, occupational dust and fumes, indoor air pollution socioeconomic status asthma/bronchial hyperactivity chronic bronchitis infections
Neutrophils/marcophages
COPD
Esinophils/ mast cells
asthma
COPD/Emphysema/Bronchitis
cell death of destruction of the alveoli, thickening of membrane air gas exchange over inflated alveoli
Obstruction is either
not reversible or incompletely reversible by bronchodilators
Cell death is caused by
desctruction of alveoli due to lung parenchyma, degraded matrix and toxic actions of inflammatory cells
COPD
results in enlargement of air spaces, fibrosis, and increase mucous production
Steroids have
limited effect on inflammation process
Inhaled corticosteroids help
reduce frequency of excerbations
Bronchodilators in COPD
best for patients with chronic breathlessness “worsened by exertion”
Steps of Airway Outflow Disorders
step 1: short acting bronchodilators step 2: regular inhaled corticosteroids step 3: long acting bronchodilators step 4: PDE inhibitors, methyxanthines, leukotriene inhbitor Step 5: oral corticosteroid other- cromolyns
Bronchdilators
B2 agonist
anticholinergics
methylxanthines
Receptor selectivity to B2 is ____ more times more strongly than B1
200-400
Short acting Beta agonist
terbutaline, albuterol, levalbuterol, salbutamol
Long acting beta agonist
salmeterol
MOA of Beta Agonist
Coupled to stimluatory G proteins
activate adenlyl cyclase which increases the production of cAMP which leads to bronchodilation, reduced Ca release and alters membrane conductance
inhibits mediator release from mast cells
increases mucous clearance by action of the cilia
Pharmacokinetics of B adrenergic agonist
rapid onset of action (within minutes) short DOA (4-6 hours) good for use as a rescue inhaler given: inhalation/aerosol powder or nebulized orally or injected (SC) short or long acting