Unit 7 Respiration Flashcards
Name disorders of gas exchange and ventilation
Name disorder of lung inflation
Name disorders of gas exchange and ventilation
- COPD
- bronchial asthma
- bronchiectasis
- cystic fibrosis
Name disorder of lung inflation
- hydrothorax (pleural effusion)
- pneumothorax
Obstructive airway disorders
-category of respiratory disease characterized by airway obstruction. -inflamed and easily collapsible airways, obstruction to airflow, problems exhaling -Types of obstructive lung disease include; asthma, bronchiectasis, bronchitis and chronic obstructive pulmonary disease (COPD).
COPD
Chronic obstructive pulmonary disease (COPD) -chronic, acute and recurrent obstruction of airflow in the pulmonary airways, which may worsen over time -persistent inflammation of pulmonary airways, parenchyma, and vasculature is present (differs from asthma) -lung inflation occurs due to airway obstruction on expiration -2 types: emphysema and chronic bronchitis -leading cause of mortality and morbidity world wide
RF for COPD
HOST -smoking -herditary deficiency of alpha1-antitrypsin -asthma -airway hyperresponsiveness ENVIRONMENTAL FACTORS
Etiology and Pathogenesis of COPD
-inflammation and fibrosis of the bronchial wall -hypertrophy of submucosal glands -hypersection of mucus
Etiology and pathogenesis of emphysema
ETIOLOGY -smoking -hereditary deficiency in alpha1-antrypsin (an antiprotease enzyme that protects the lung from injury PATHOGENESIS -cigarette smoke stimulates movement of inflammatory cells into the lungs, -cells release elastase and proteases -if alpha -1 antitrypsin deficient then these enzymes activity is higher than normal -resulting in breakdown of elastic fibres (elastin) in lungs by proteases, decreasing elasticity -abnormal enlgment of airspaces distal to terminal bronchioles -destruction of alveolar wall and capillary beds -enlg of airspaces causes hyperinflation of lungs -results in increased total lung capacity (TLC)
Etiology and pathogenesis of chronic bronchitis
Airway inflammation and obstruction of major and small airways INCIDENCE Common in middle-aged men and associated with chronic irritation due to smoking and recurrent infections DIAGNOSIS Chronic productive cough for 3 consecutive months over two years Often gradual increase in acute exaceberations with purulent sputum ETIOLOGY -Smoking PATHOGENESIS Two primary changes are supposed to protect against smoke/irritants -In lg airways: Hypersecretion of mucus in lg areas associated with hypertrophy of submucosal glands in trachea and bronchi -In sm airways (bronchioles and sm bronchi): Increase in number of goblet cells Excess mucus production with plugging of airway lumen Inflammatory infiltration Fibrosis of bronchiolar walls COMPLICATIONS -Viral and bacterial infections are common (contribute to acute exacerbations)
Types of emphysema
-Centracinar (centrilobular) Affects bronchioles in central part of respiratory lobule Initially preserves alveolar ducts and sacs Most common type of E in male smokers Usually occur in upper parts of lung -Panacinar Initial involves peripheral alveoli and then extends to central bronchioles More common in people with alpha1-antitrypsin deficiency Also found in smokers with centracinar E Usually occurs in lower parts of lungs
Clinical features of COPD
-Insidious onset -50-60 yr -fatigue, exercise intolerance, cough, sputum production, shortness of breath -productive cough in the morning -late stages: limited activities of living, respiratory infections, respiratory failure -death EMPHYSEMA (PINK PUFFER) -lack of cyanosis -use of accessory muscles and pursed lips to breathe -barrel chest due to air remaining in lungs open expiration -dramatically decreased breathe sounds through out chest CHRONIC BRONCHITIS (BLUE BLOATERS) -Edema (associated with R sided hrt failure….edema through out body) -Barell chested -Cyanosis due to hypoxia CM -Expiration is prolonged -Expiratory wheezes and crackles can be heard -use of accessory muscles (tripod: use of sternocleidomastoid scalene and intercostal muscles) -hypercapnemia develops first and then hypoxemia indicating impaired gas exchange -low O2 levels produces vasoconstriction relfex of pulmonary vessels and further impairs gas exchange in lungs (common in CB) -hypoxemia stimulates RBC production producing mild polycythemia -increase in pulmonary vasocontriction increases work of the right ventricle, causing developement of R sided hrt failure with periphereal edema (cor pulmonale)
Restrictive lung diseases pathogenesis
Etiology -affect the collagen and elastic connective tissue in interstitium of alveolar airways -involve airways, arteries, and veins 3 impacts -diminished lung volume, - reduced diffusing capacity, - varying degrees of hypoxemia Pathogenesis -some type of injury to alveolar epithelium -inflammatory process that involves alveoli and interstitium of the lung -accumulation of inflammatory and immune cell causes cause damage to lung -build up of fibrous scar tissues -impaired gas diffusion results from alterations in the alveolar-cappilliary membrane as well as an increase in shunt resulting from unventilated regions of lung
Restrictive lung diseases CM
dyspnea tachypnea cyanosis no wheezing or signs of obstruction insidious onset of breathlessness, intially during exercise (then incapacitated) high RR and low tidal volume (maintains minute volume but reduces energy required to breath) non-productive cough clubbing of fingers and toes
What are the impacts of restrictive diseases on lung volumes?
-vital capacity and TLC are reduced in interstitial lung disease -FEV1 is preserved -ration of FEV1 to FVC increases -arterial blood gases normal early in disease -but O2 levels decrease during exercise -advanced disease, hypoxia even at rest -late stages, hypercapnia and respiratory acidosis develop
LUNG VOLUMES Tidal volumes Inspiratory reserve volume Expiratory reserve volume Residual volume Vital capacity Inspiratory capacity Functional Residual Capacity Total lung capacity
LUNG VOLUMES Tidal volumes (Vt) - volume of air inhaled or exhaled in a normal breath (500ml in an adult; 3-5ml/kg for children) Inspiratory reserve volume (IRV) - 3000mL, maximum amount that can be inspired in addition to Vt Expiratory reserve volume (ERV) - 1100mL, maximum amount that can be exspired after expiration of Vt Residual volume (RV) - 1200mL, portion of air in lungs that cannot be exhaled ever, increased with age as more air becomes trapped in lungs at end of expiration Vital capacity - 4600mL, amount of air that can be forcibly exhaled after max inspiration (VC=Vt+IRV+ERV) Inspiratory capacity - 3500mL, amount of air that can be inhaled at normal expiratory level and distending lungs to the maximal amount (IC=Vt+IRV) Functional Residual Capacity (FRC) - 2300mL, volume of air that remains in lungs at end of normal expiration and is important to ongoing gas exchange (FRC=RV + ERV) Total lung capacity (TLC) - 5800mL, sum of all volumes in the lungs, about 20-25% less in females than males For values see page p629 table 27-1
Pulmonary embolism etiology and pathogenesis
-blook borne substance lodges itself in a pulmonary arteries and obstructs blood flow -can be a thrombus, air, fat, amniotic fluid -mortality rate is 30% (more with lg emboli). ETIOLOGY -are thrombi that arise from DVT in lower extremities -often DVT will not be suspected until presentation of PE PATHOGENESIS 2 impacts: 1) obstruction of pulmonary circulation and 2) reflexes that cause vasocontriction -obstructed blood flow causes bronchoconstriction in affected area of lung, -wasted ventilation -impaired gas exchange -loss of alveolar surfactant -pulmonary hypertension and Rsided hrt failure may result (particularly with lg embolus) -sm embolus, CM may not present CONTRIBUTING FACTORS -venous stasis and venous endothelial injury (bed rest, trauma, surgeries, childbirth, fractures of the hip and femur, MI, CHF, spinal cord injury) -hypercoagulability states (cancer cells can produce thrombin and procoagulation factors) -oral contraceptive -smoking -pregnancy -hormone replacement therapy
Pulmonary embolism CMs
-depend on size and location of PE -chest pain -dyspnea -increase resp rate PI -pleuritic pain that changes with respiration (severe on inspiration>expiration) -mod. hypoxemia -diffusion or exchange of CO2 same or increases due to hyperventilation SM PE -no CM unless in elderly/acutely ill -repeate sm PE can reduce size of pulmonary capillary bed, resulting in pulmonary hypertension MODERATE PE -breathlessness with pleuritic pain -apprehension -slight fever -cough productive of blood streaked sputum -tachycardia to compensate for decreased oxygen -breathing rapid and shallow LG PE -collapse, -crushing substernal chest pain -shock -syncope -rapid pulse -cyanotic skin and diaphoretic -fatal
Describe bronchial asthma (BA)
-more acute and intermittent that COPD -chronic inflammatory disorder of airways in which many cells play a role -in an obstructive airway disorder INCIDENCE ETIOLOGY -often occurs in response to a stimuli including allergens, noxiant, infection or exercise PATHOGENESIS - substance stimulates inflamation and immune response -activated t-lymphcytes direct further release of inflammatory mediators from eisinophils, mast cells, lymphocytes -helper T-lymphocytes produce inflammatory interleukins CM -wheezing -shortness of breath -chest tightness -cough
Extrinsic bronchial asthma (BA)
-a response caused by an extrinsic antigen such as an allergen, noxiant, or exercise Sensitization -exposure to antigen cause the production of presensitizaed IgE mast cells 1)Acute (20min) -release of chemical mediators from mast cells a) migration of inflammtory cells b) opening of intracellular junctions c) increased access of antigen to mast cells d) bronchospasm due to PS NS simulation e) edema f)increased mucus secretion 2)Late (4-8hrs) -inflamation -increase airway responsiveness -release of inflammatory mediators -produce epithelial inury -changed mucociliary funtion -reduced clearance of resp tract
Intrinsic BA
-instrinsic factors trigger asthma -infection, exercise, hyperventilation, cold air, drugs/chemicals, hormal changes, emotional upsets - exercise: pathogen. unclear, could be lack of moisture or imbalance in PS and S NS stimulation -inhaled irritants: induuce bronchospasm via irritant receptors and vagal reflex -aspirin and NSAIDs: small group have asthma, nasal polyps, and asthma,rhinitis attacks
Clinical Features of Bronchial asthma
epidsodic wheezing -tight chest -acute attacks -nocturnal asthma/clinical triad of asthma/refractory asthma -asthma attack: i)bronchospasm ii)edema iii)mucus plugging iv)expiration prolongs (forced expiratory volume and peak experiatory flow rate decrease) v)trapping of air behind occluded and narrowed airways cause hyperinflation of the lungs vi) increase in RV, decrease in IRC and FVC -more energy is required to breathe to over come the tension present in the lungs -hpoxemia and hypcapnemia -pulmonary hypertension and stress on R side of hrt
Severe asthma
Severe or refractory asthma -persistent asthma that requires continuos use of highdose corticosteriods for more thn 50% of yr -obstructive lung function -instability -need for more medication
What are the differences between COPD and BA?
collate asnwer
What are the clinical manifestations of BA?
collate asnwer
Cancer of the lung (incidence)
-second leading cause of death after CVS diseases -lung cancer death rates >prostate cancer in men -lung cancer death rates >breast cancer in women
Cancer of the lung (etiology/risk factors)
-cigarette smoking >20 times higher than non smokers -asbestos fibers -radiation -mining and exposure to heavy metals -uranium -nickel -scar cancer
