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137 Cards in this Set
- Front
- Back
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Airway patency depends on
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Large airways -- cartilage
Small airways --traction from surrounding parenchyma |
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Atmospheric pressure
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760 mmHg
1000 cm H20 0 |
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Elastic recoil due to
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tissue forces from fibrous networks
surface tension from air fluid interface |
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Tissue forces of elastic recoil increased/decreased in
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Interstitial lung disease
Emphysema |
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Surface forces of elastic recoil decreased/increased
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Decreased -saline filled lungs
Increased - surfactant deficiency |
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Compliance
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Measure of elasticity of lung
change in volume/change in pressure Depends on intrinsic characteristics of the lung and lung volume |
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Normal compliance value
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100 ml/cm H20
ARDS may be <20 |
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Airflow requires
Inspiration Expiration |
Pressure difference
Inspiration-- mouth pressure has to be greater than alvelolar pressure Expiration-- alveolar pressure has to be great than mouth pressure |
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Resistance
Determinants of airway resistance |
Change in pressure/flow
Nose, pharynx, tracheobronchial tree contribute Varies w/ lung volume Small airways make SMALL contribution to resistance |
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Distending pressure
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pressure inside - pressure outside of a wall
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Conductance
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1/resistance
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Passive Expiration
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Force provided by lung elastic recoil
Driving force decreases as lung vol decreases (slowing flow) Flow stops when Palveoli = Patm |
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Flow limitation
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Increased expiratory effort produces no further increase in expiratory flow
Occurs because of airway collapse |
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Airway collapse is a fnc of
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Airway characteristics
Transmural pressure |
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Pcrit
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Critical closing pressure
Transmural pressure at which airway collapses P>0 airway tends to collapse P<0 airway has some rigidity |
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Determining Maximal Expiratory Flow
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Flow max = (Palv - Pcollapse)/Rupstream
=(Pelastic-Pcrit)/Rupstream |
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Mechanisms of expiratory flow limitation
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Decreased elastic recoil
Increase Pcrit (increased VSM tone) Increase in Rupstream |
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Air trapping
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Air left in lung despite maximal respiratory effort (increase RV)
RV reached when Pelastic = Rcrit |
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Dyspnea
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disordered breathing
breathlessness, shortness of breath best- sensation associated with increased work of breathing |
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Chemoreceptors
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Central medulla - hypercapnia
Carotid body - hypoxemia |
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Mechanoreceptors for dyspnea
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Upperairway and face -- sense lack of flow, mouthpiece
Lung-- inflation, irritants, interstitial congestion, dynamic airway compression Chest wall (joints, tendons, muscles) -- distension, alteration |
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Neurophysiologic model of dyspnea
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Efferent impulses from brain don't match the mechanical (ventilatory) response
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Two psychological responses to dyspnea
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Cognitive -- threat to health
Emotional-- distress |
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Consequence of dynamic hyperinflation of COPD
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Elastic loading
Shortening of longitudinal diaphragm fibers |
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Orthopnea
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Dyspnea in recumbent position
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Orthopnea causes
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CHF
obstructive airway disease respiratory muscle weakness increased abdominal load--(obesity/ascites) anterior mediastinal mass |
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PND
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paraoxysmal nocturnal dyspnea
awakening from sleep 2/2 dyspnea usually CHF also obstructive airway disease |
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Measuring dyspnea
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Questionnaires mostly
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Treatment of dyspnea
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Underling disease
Oxygen Pulmonary rehab Inspiratory muscle training Opiates |
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Cough
define and function |
explosive expiration
Fncs to clear airway and protect and against aspiration |
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Chronic cough causes and sites of stimulated receptors
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Asthma - large airways
GERD - lower esophagus Post Nasal Drip - Nose/sinus - CNV, oropharynx (CNIX), larynx (CNX) |
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Mechanics of cough
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Inspiratory phase
Compression phase -- closure of glottis, contraction of expiratory muscles, sudden opening of glottis Expiratory phase |
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Sputum
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Expectorated secretions from lower respiratory tract
2/2 infection (yellow/green) or inflammation (clear/gray) |
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Hemoptysis
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Expectoration of blood
Causes - infection, neoplasia, trauma, mitral stenosis, pulmonary infarction, goodpastures |
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Pain of bronchoconstriction
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Tightness retrosternally
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Spirometry
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Subject breathes into a closed system w/ recordings of volume change and time
Can measure Tital volume, inspiratory reserve, expiratory reserve Vital capacity, inspiratory capacity |
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Tidal volume
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breath size during normal quiet breathing
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TLC
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Total lung capacity
Total volume in lungs at maximal inspiration |
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RV
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Residual volume
Volume left in lung after maximal expiration |
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VC
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Vital capacity
TLC-RV -- maximum breath one can take |
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IC
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Inspiratory capacity
Breath take from FRC |
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IRV
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Inspiratory reserve
Volume of breath take from peak of tidal volume |
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FRC
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Volume at rest
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Factors decreasing expiratory flow rates
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Decreased elastic recoil
Decreased lung volume Increased airway resistance (Decreased expiratory muscle tone) |
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FEV1 in pulmonary fibrosis
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Elevated
Even though the lung has increased elastic recoil---it operates a significantly lower volume and this effect dominates |
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PFT profile for obstructive lung disease
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Decreased/normal FVC
Decreased FEV1 Decreased FEV1/FVC ratio Examples COPD, asthma |
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PFT pattern in restrictive disease
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Decreased FVC
Deceased FEV1 Normal or increased FEV1/FVC ratio ex-- weak respiratory muscles |
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Distinguishing combined from purely obstructive disease on PFTs
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All three values (FVC, FEV1, FEV1/FVC ratio)
Must be differentiated by TLC |
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Residual volume in obstructive disease
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Increased -- air trapping
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Methods for measuring TLC
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Helium dilution and boyle's law
Body plethysmography Nitrogen washout |
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Restrictive Lung Defect
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Neuromuscular disease
Chest wall problem Pleural disease Loss of lung Insterstitial lung disease |
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DC
Affected by |
Diffusing capacity
Measured as amount of CO transferred to bloodstream CO in bloodstream (smoking) Total SA for exchange Hemoglobin Thickness of the alveolar membrane Lung volume |
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Obstruction + low DLco
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Emphysema
Usually |
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Restriction + high FEV1/FVC + low DLco
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Interstitial lung disease
Usually |
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Major obstructive airway disorders
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Chronic bronchitis
Emphysema Asthma Bronchiectasis All have increased resistance and decreased expiratory pressure/flow |
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Bronchiole
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Airway of less than 1 mm diameter
Simple columnar epi, few goblets, ciliated Greatest cross sectional area of lung Spiral smooth muscle layer controls resistance |
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COPD
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Obstructive airway disease
Not fully reversible Associated with abnormal inflammatory response to inhaled particles |
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Chronic bronchitis
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Chronic persistent irritation
Recurrent infections Strongly associated with smoking |
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Chronic asthmatic bronchitis
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Chronic bronchitis plus intermittent bronchospams and wheezing
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Pathogenesis of bronchitis
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Mucus increased in vol and viscosity
Mucosal goblet cell metaplasia Cilia decreased in number and damaged Reduced ability to clear pathogens |
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Pathologic findings of chronic bronchitis
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Small airways w/ inflammatory cells
Airways w/ lymphoid folicles Thinkened bronchiole wall Luminal mucus plugs Submucosal gland hypertrophy Mucosal squamous cell metaplasia (preneoplastic) |
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Reid index
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Measuring submucosal gland hyperplasia (increased in chronic bronchitis)
Submucosa depth/epithelium--cartilage depth <0.4 is normal |
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Emphysema
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Permanent enlargement of airspaces distal to the terminal bronchioles w/ destruction of their walls
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Centrilobular emphysema
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Enlarged respiratory broncioles and spared distal acini
More severe in upper lobes Associated w/ smoking W/ progression entire acinus may become involved |
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Panacinar emphysema
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Entire acinus (from respiratory bronciole to terminal alvelolus involved)
More sever in lower lobes Associated w/ A1AT deficiency |
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Paraseptal (distal acinar) emphysema
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Distal aspect of ascinus
Upper lung fields adjacent to pleura Associated w/ bullae and spontaneous pneumothorax Unclear pathogenesis |
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Compensatory emphysema
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Not true emphysema
Overinflation of remaining lung tissue after a resection |
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Obstructive emphysema
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Not true emphysema
tumor/foreign object resulting in air trapping |
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Senile emphysema
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Not true emphysema
voluminous lungs w/ over distension, increased diameter of alveolar ducts and small alveloli --no destruction of tissue |
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Irregular emphysema
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Not true emphysema
Irregular patter of destruction and enlargment Ex scar emphysema |
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Emphysema pathogenesis
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Imbalance in protease/antiprotease
Stimulus drawing PMNs, macros will result in increase of proteases ---smoking has this effect |
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Why is panacinar associated w/ A1AT and centrilobular w/ smoking?
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A1AT deficiency leaves whole ascinus equally vulnerable to PMN damage, lower lobes are better perfused so more easily get PMNs in
Smoking bombards small airways the most, and damage starts there |
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Asthma
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Hyperresponsiveness of tracheobronchila tree to various stimuli leading to episodic reversible bronchoconstriction and inflammation
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Extrinsic asthmas
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Allergic--initiated by a type I hypersensitivitiy rxn
Genetic component, usually starts in childood Occupational Allergic pulmonobronchial aspergillus |
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Instrinic asthmas
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Non allergic
Respiratory tract infections (not genetics) Excercise, cold, ASA, stress--triggers |
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Pathologic findings in asthma
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Hypertrophic smooth muscle
Inflammatory infiltrate w/ eosinophils Submucosal hyperplasia Edema Mucus plugs |
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Mucus of asthma can contain
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Charcot Leyden crystals -- degranulated eosin membranes
Curschmann spirals--whorls of shed epis |
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Acute phase and slow phase in asthma are mediated by?
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Acute phase -- mast cells and IgE
-bronchostriction, mucus Late-- leukocyte mediated, most tissue destruction |
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Bronchiectasis
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Necrotizing bronchitis and bronciolitis w/ abnormal permanent airway dilatation
Overlaps w/ other COPD Causes--obstruction, CF, necrotizing pneumonias |
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Pathologic findings of bronchiectasis
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Peribronchial pattern
Destructive inflammation +/- microabcess, squamous metaplasia, peribronchial fibrosis |
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Two ways that PMNs and CD8s get you to airflow obstruction
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Small airway disease (airway inflammation and airway remodelling)
Parenchymal destruction (loss of alveolar attachments and decreased elastic recoil) |
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Clinical diagnosis
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Productive cough on most days for a minimum of 3 months a year for not less than two successive years
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Three mechanisms of airway obstruction in copd
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mucus hypersecretion-- luminal obstruction
mucosal and peribronchial inflammation and fibrosis -- obliterative bronchiolitis disruption of alveolar attachments -- emphysema Reduce elastic recoil Bronchial smooth muscle constriction |
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Phenotypes of COPD
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Blue bloater--
productive cough, hypoxemia/cyanosis, pulmonary htn Pink puffer-- breathless, adequate SO2, cachexic |
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Genetics and COPD
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1 in 5 smokers get COPD
Alpha-1 antitrypsin deficiency is a rare recessive condition that predisposes to COPD (its a serine protease inhibitor) |
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Effects of smoking in emphysema pathology
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Provides lung irritant for inflamatory process--attracting PMNs
Inhibiting Alpha1 antitrypsin -- decreasing the antiprotease abilities of the tissue |
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Spirometry in COPD
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Decreased force dexpiratory flow rates
FEV1/FVC - low (usuall <70%) Severity based on FEV1 % predicted Operating at higher lung volumes at rest |
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Diseases of airflow obstruction
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COPD
Asthma Cystic fibrosis |
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FRC in COPD?
RV ? TLC? DC? |
FRC is increased emphysema and normal in chronic brochitis
RV is increased in all COPD (air trapping) TLC is increased in emphysema and normal in chronic bronchitis DC is normal in bronchitis and decreased in emphysema |
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Lung function over time
w/ smoking? w/ quitting? |
Lung function decreases w/ age
More rapid w/ smoking Can get back on normal slope of decline w/ quitting Disability is about 30% lung fnc |
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Exacerbation of COPD
define |
Change in baseline dyspnea/cough/sputum sufficient to warrant change in management
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Causes of exacerbations
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infections
particulates from pollution inflammation bronchioconstriction |
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Mechanisms of anticholingerics and beta-adrenergic agonists in COPD
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Anticholinergics -- block constriction via muscarinic receptors
Beta-adrenergic agonists -- increase cAMP which promotes relaxation of bronchial smooth muscle |
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COPD stages
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I: Mild: FEV1>80% predicted
II: Moderate: FEV1 50-79% III: Severe: FEV1 30-49% IV: Very severe: FEV1 <30% or 50% w/ chronic respirator failure |
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Therapy for COPD
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Risk factor reduction, flu vacc
PRN shortacting bronchodilator w/ stage II Add long term bronchodilators and repsiratory rehab w/ stage III Add inhaled glucocorticosteriods w/ Stage IV Add oxygen for respiratory failure consider surgery |
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Criteria for prescribing long term oxygen therapy
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P02 <55 mmHg
So2 < 88% |
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pH range outside of which morbidity and moralitiy rise
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6.9 to 7.7
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Arterial PCO2 determinants
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directly proportional CO2 production
inversely proportional to alveolar ventilation |
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Normal values for
pH bicarb pCO2 |
7.4
24 mmols/L 40 mmHg |
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Effect of buffers on bicarb/Co2 system in blood
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Buffers combine with H ions produced driving the equation to the H and bicarb side
Moderately acidosis/alkalosis produced by changes in CO2 Also results in larger changes bicarb than in simple system |
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Henderson Hasselbach
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pH = pk' + log [HCo3]/SxPCO2
pk= 6.1 S- solubilitiy - 0.03 mm/l/mmHg |
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Renal changes in chronic respiratory acidosis
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Retention of bicarb
Increased secretion of H Net results in less acidotic pH |
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Metabolic acidosis
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Production of a non-volatile acid by metabolic processes
Lowered pH Buffering H+ w/ HCO3 results in production of CO2 Increased ventilation b/c of chemorecetors decreases the pCO2, moderating the acidosis |
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Metabolic alkalosis
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Metabolic process increases the amount of bicarb
Increased pH Suppression of ventilation by chemoreceptors Rise in pCO2, moderation of alkalosis |
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Example of clinical setting of acute respiratory acidosis
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Underventilation like in drug overdose
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Example of clinical setting of chronic respiratory acidosis
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COPD w/ air trapping
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Example of clinical setting of Acute respiratory alkalosis
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Pyschogenic hypoventilation
Panic attack |
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Example of clinical setting of chronic respiratory alkalosis
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Not common
prolonged hypoxia ventilator induced hyperventilation |
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Example of clinical setting of metabolic acidosis
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Lactic acidosis from poor perfusion
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Example of clinical setting of metabolic alkalosis
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Extended vomitting
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Relationship of temperature at pH
Does this create problems? |
Inversely proportional
No. The measured pH changes but this does not effect neutrality as equal production of OH-. Proteins do not alter confirmation. Important in surgery. |
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Determinants of average alveolar Pco2 and Po2
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Ventilation/Metabolic rate
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Why are arterial PO2 and PC02 not exactly the same as alveolar values
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Locally equilibrium is reached during transit
Shunting and regional V/Q mismatch make arterial O2 slightly lower and CO2 slightly higher |
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Causes of hypoxemia
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Alveolar hypoventilation
Low inspired oxygen pressure Impaired diffusion Shunt V/Q mismatch |
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Alveolar hypoventilation values
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Low alveolar and arterial O2
High alveolar and arterial CO2 |
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Low inspired oxygen pressure values
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Low alveolar and arterial O2
Low alveolar and arterial CO2 (breathing stimulated by hypoxia) |
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Impaired diffusion capacity and hypoxemia
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Arterial and alveolar pressures do not reach equilibrium
Of questionable importance in causing hypoxia in lose with lung disease |
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Shunts and hypoxia
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Mixed venous blood reaches arterial circulation w/o opportunity for gas exchange
Intra or extrapulmonary Not fully corrected by increased inspired O2 |
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V/Q mismatch
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Dead space and shunt together
Often the cause of hypoxia in disease Causes hypoxia and a little hypercapnia |
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Sound of extrathoracic airway obstruction
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Inspiratory stridor
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Sound of intrathoracic airway obstruction
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Expiratory wheeze
Monophonic w/ single site of obstruction Polyphonic /muscial with multiple sits or variable degrees of obstruction |
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What type of pathology gives most tachypnea?
extrathoracic? Intrathoracic? parenchymal |
Parencyal
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Differentiate between fine and course crackles
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Fine - high pitched, low amplitude, short duration
Coarse --low pitched, high amplitude, long duration |
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Vascular ring
Definition and presentation |
Abnormal branching of aortic arch involves both trachea and esophagus
Infants w/ intermittent respiratory distress, dysphagia Less sever do not present until later |
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Types of vascular rings (aortic arch variations -- 5)
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1. Double aortic arch -- causes tracheal and esophageal compression
2. Right aortic arch w/ PDA - tracheal and esophageal compression 3. Left aortic arch w/ PDA - tracheal and esophageal compression 4. Aberrant brachiocephalic -tracheal copression 5. Aberrant subclavian artery - esophageal compression |
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Most common tracheoesphageal fistula?
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Esophageal atresia with distal fistula
80% of cases Presents as inability to swallow Stomach contents refluxing into lungs Emergency |
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What type of trachesophageal fistula sometimes goes undiagnosed?
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H-type
Esophagus intact with fistula Often presents as chronic bronchitis |
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Bronchiogenic cysts
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Abnormal budding of bronchial tissues
Early (central) or late (peripheral) in gestation Epithelium or epithelial components Water dense on CT Risk of infection |
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Congenital Cystic Adenomatoid Malformation
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Overgrowth of terminal bronchioles
Cysts communicate with airway Firm mass with deranged structure Neonatal distress, infections Increasing chance of malignant transformation with increase in solid vs cystic components |
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Mixed cystic and adenomatous tissue in a congenital cystic adenomatoid malformation?
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Associated with other congenital defects
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Pulmonary sequestration
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Non-functional pulmonary tissue with systemic vascular supply, potential for infection
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Extralobar pulmonary sequestration vs intralobar pulmonary sequestration
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Intra - more common, more likely to have pulmonary vasculature, not connected to respiratory system, infections
Extra -- associated with other abnormalities, systemic vasculature, might be connected to respiratory tree, more common in males, respiratory difficulties |
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Congenital lobar emphysema
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Overinflation of a lobe
Secondary to obstruction -- malacias, pulmonary artery sling, many causes If compresses normal lung--respiratory distress--surgery |
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Congenital diaphragmatic hernia
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Guts in thorax, risk of pulmonary hypoplasia
Mostly left sided (Bockdalek) Girls twice as likely as boys Usually happens if diaphragm is not formed when guts come back in from umbilical sac |
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Foreign body in airway presentation
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New wheeze or stridor
Stridor if extrathoracic, wheeze if intra Associated with coughing/respiratory distress |
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Brochiolitis
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Viral infection causing diffuse small airway inflammation
Usually RSV in kids May have significant oxygen desaturation, obstruction -wheeze Hyperinflation on chest xray |
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Croup
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Tracheal/laryngeal inflammation caused by infection
Inspiratory stridor H. influenza was frequent cause pre-vaccination |
