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what is the primary purpose of the pulmonary system?

supplying necessary O2 to the tissues and excreting CO2
*don't need 100% O2 to fulfill purpose


what is the difference in how the respiratory system delivers O2 and CO2 molecules opposed to the circulatory system?

respiratory system delivers gas and the circulatory system delivers liquid


describe obstructive disease

-more common than restrictive
-airway resistance increased
-air trapping and obstruction impedes air flow out (extended expiration times)
-lung volumes increase (RV and TLC)
-turbulent air flow leading to wheezing
-impaired gas exchange leading to VQ mismatch
-more amendable to treatment than restrictive


describe restrictive disease

-decreased lung compliance
-lung expansion restricted, impeding air flow in
-lung volumes reduced
-air resistance NOT increased


with obstructive disease, what 3 mechanisms cause an increase in airway resistance that leads to obstructed air flow?

-excessive secretions partly blocking bronchial lumen
-airway thickening by edema, hypertrophy of mucous glands, bronchitis, or asthma
-destruction of lung parenchyma (loss of airway radial traction narrows airway)


what are pulmonary function tests?

spirometry and flow volume loops to distinguish between obstructive and restrictive conditions


describe pulmonary function tests

-FEV1: volume forcefully exhaled in one second
-FVC: total volume that can be forcefully exhaled
-FEV1/FVC: ratio used to distinguish obstructive vs. restrictive


describe pulmonary function test results with obstructive diseases

-both FEV1 and FVC are low and ratio is less than 0.7
0.6-0.7: mild
0.4-0.6: moderate
less than 0.4: severe
ex: FEV: 1.3, FVC: 3.1, ratio 42%


describe PFT results with restrictive diseases

both FEV1 and FVC are low and ratio is greater than or equal to 0.7
ex: FEV: 2.8, FVC: 3.1, ratio 90%


describe normal PFT results

-FEV: 4.0
-FVC: 5.0
-ratio: 80%


describe characteristics of asthma

-chronic airway inflammation with periodic acute severe exacerbations
-bronchial airways are hyper-reactive to stimuli
-airway narrowing at all levels with varying severity
-expiratory airflow becomes obstructed (obstructive disease)
-reversible with bronchodilators


describe extrinsic asthma

*allergic asthma
-family hx of allergic/immunologic disease
-allergic related (allergen identified)
-immune system activation
*elevation of IgE levels and serum eosinophils


describe intrinsic asthma

*non-allergic asthma
-idiosyncratic (specific to the individual)
-exacerbations with triggers
-non-immune related (no allergen identified)
*normal IgE levels


what are signs and symptoms of asthma?

-periodic acute exacerbations: mild to severe attacks; bronchospasm; mucosal edema/secretions
-mild airway obstruction lasting for weeks
-increased airway resistance to gas flow: wheezing
-productive cough, dyspnea


describe pathology of asthma

-hypertrophied airway smooth muscle contracts during an attack causing bronchoconstriction
-mucous gland hypertrophy causes increased secretions, usu. white and scant (thick, slow moving; mucous plugs leads to obstruction)
-bronchial wall edema
-infiltration of eosinophils and lymphocytes
-remodeling leads to subepithelial fibrosis


what are common etiologies of asthma attacks?

-allergy induced
-respiratory viruses (children)
-occupational and environmental irritants (adults): airborne pollens, animal danders, dust, pollutants, chemicals
-drugs: aspirin, beta2blockers, NSAIDS, drugs causing histamine release
-exertional exercise
-stress, emotional, psychological


what are inflammatory mediators associated with asthma?

-cytokines associated with Th-2 and helper T cells: IL 4, 5, 9, 13
-arachidonic acid metabolites: leukotrienes, prostaglandins
-platelet-activating factor (PAF)
-reactive oxygen species (ROS)
-kinins (bradykinin)
-chemotactic factors


describe the immune mediated process of asthma

-allergen binds to IgE on mast cell causing degranulation
-release of inflammatory mediators from mast cell
-bronchoconstriction via multiple mechanisms: decreased cAMP, increased cGMP increases PNS activity increasing cholinergic sensitivity causing vagal afferents sensitivity to histamine, noxious stimuli, cold air, irritants, and ET intubation


describe PNS role in bronchoconstriction

-balance between PNS and SNS regulates bronchial tone
-PNS stimulation via vagal activation causes activation of muscarinic receptors in bronchial smooth muscle
-muscarinic receptors cause increase in intracellular levels of cyclic guanosine monophosphate (cGMP)
-increased intracellular cGMP increases protein kinases that cause bronchoconstriction
*antimuscarinics promote dilation


what are the goals of asthma treatment?

-prevent bronchial inflammation
-maintain patent airways


what type of therapy is used for asthma treatment?

-long term control of airway narrowing
-rescue for acute bronchospasm attacks


what anti inflammatory drugs are used for asthma?

-leukotriene blockers
-mast cell-stabilizing agents


what bronchodilator drugs are used for asthma?

-beta2 agonists (rescue)
-anticholinergics (antimuscarinics)


describe glucocorticoids for asthma treatment

-not rapid acting, usu. 1-3 hours onset
-admin. IV or inhaler
-decreased bronchial hypersensitivity, inflammatory response
*most effective anti-inflammatory drugs
*effective as prophylactic pre-op drugs


what are common glucocorticoids used in asthma treatment?

-IV hydrocortisone, methylprednisolone
-fluticasone (Flovent)
-salmeterol (Advair)
-budesonide (Pulmicort)
-triamicinolone (Azmacort)
-beclomethasone (Beclovent)


describe leukotriene blockers for asthma treatment

-leukotrienes mediate inflammation in asthma
-blocker inhibit the 5-lipoxygenase enzymatic pathway (5-LO inhibitors)
-reduce the synthesis of leukotrienes
-only 50% of patients with beneficial response
*effective for aspirin-induced asthma


what are common leukotriene blockers used in asthma treatment?

-monotelukast (Singulair)
-zafirlukast (Accolate)
-pranlukast (Zyflo)
-zileuton (Ultair)


describe mast cell stabilizers for asthma treatment

*effective only with extrinisic (allergic) asthma
-block airway inflammation
-inhibits mediator release from mast cells
-stabilizes membranes inhibiting mast cell degranulation


what is a common mast cell stabilizer used in asthma treatment?



describe beta adrenergic agonists for asthma treatment

-most potent bronchodilators
-stimulation of beta 2 receptors in the lungs cause increased cyclase leading to increased cAMP which increases Ca++ promoting tracheobronchial smooth muscle relaxation
-inhibits inflammatory cell function