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76 Cards in this Set
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Pulmonary function test (PFT)
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measures parameters of lung function and describe what extent physiological function is compromised by lung disease
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PFT measures 2 mechanical properties
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1. restrictive lung disease
2. obstructive lung diseae PFT most sensitive and objective indices of presense of lung involvement and of changes in lung disease |
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Restrictive lung disease
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Dec compliance--> Stiff lungs--> Difficult to inflate --> inc work of breathing
Defined by dec (small) lung volume (Dec TLC) |
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Examples of restrictive lung disease
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pneumonia
pulmonary edema pulmonary fibrosis iterstitial peneumonitis muscular dystrophy scoliosis |
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Lung volumes reduce due to...
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intrinisic pulmonary disease
extrinsic chest wall restriction neuromuscular disorders |
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Obstructive Lung Disease
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Airway obstruction
1. Inc resistance --> 2. Airway obstruction --> 3. Narrow airways--> 4. Dec max expiratory flow --> 5. Inc work of breathing Defined by dec maximal expiratory flow rates and increased airway resistance When airways narrow--> inability to exhale rapidly |
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Obstructive lung disease due to...
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bronchospasms
airway inflammation extrinsic compression of the airway |
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Examples of airway obstruction
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asthma
COPD cystic fibrosis |
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Normal Values of PFT
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Diff lung sizes, PFT compared against expected normal values based on gender, age, height of pt
Normal range is 80-120% predicted |
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Functional Residual Capacity (FRC)
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- most stable lung volume, V we live at bc determined by physiological mechanisms (not voluntary)
- volume at end of normal expiration Equilibrium between outward chest wall recoil and inward lung recoil - Chest wall recoil springs outward INC lung volume - Elastic recoil collapses the lungs DEC lung volume |
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Total Lung Capacity (TLC)
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- total volume of air in the lungs after max inhalation
- measures lung size |
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Decrease in TLC
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is definition of restrictive lung disease
TLC dec by 1. dec lung compliance 2. ventalatory muscle weakness 3. extrinsic compression by chest wall |
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Vital Capacity (VC)
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Amt of air exhaled from a maximal inhalation (TLC) to a maximal exhalation
Usuable lung volume Volume exhaled form TLC to RV |
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Decrease in VC
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1. Dec lung compliance
2. Dec ventilatory muscle strenght 3. Extrinsic compression from chest wall abnormalities 4. Hyperinflation (Inc RV) |
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Residual Volume (RV)
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Volume of air left in the lung after complete exhalation
Prevents R-L shunt after exhalation and permits gas exchange to occur throughout resiratory cycle |
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Inability to exhale further (reduce RV) is due to..
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1. Airway closure
2. Inability of expiratory muscles to compress the outward chest wall recoil |
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Increase in RV (hyperinflation)
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seen in airway obstruction
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Measurements of FRC
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1. Nitrogen washout
2. Helium dilution 3. Body plethysmography |
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Airway obstruction characterized by
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reduction in maximal expiratory airflow
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How to measure expiratory airflow
Spirogram |
During forced exhalation from TLC, volume is plotted against time
FEV1- volume exhaled in the first second FEV 25-75%- mean flow rate in the middle half of the exhaled VC is the exhalation, reflects middle and small airways more than the FEV1 |
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Maximal expiratory Flow Volume Curve (MEFV) Curve
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measures maximal expiratory flow that can be achieved at specific lung volume
Flow is plotted against lung volume from TLC to RV |
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What does MEFV curve tell you
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tells you which airways are most obstructed: large, middle, or small
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What does normal MEFV look like
Obstructive lung disease? |
Rises to peak expiratory flow rate (PEFR) near TLC and decrease in a nearly linear fashion to zero at RV
Obstructive lung disease produces a scooped configuration curve |
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What does MEFV look like in..
Small airway obstruction Large airway obstruction |
Small airway obstruction would cause a concave appearance near RV
Large airway obstruction cause the MEFV to be truncated near TLC |
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Bronchodilator response
When a patient shows airway obstruction, PFT are repeted after inhalation |
If expiratory flow rates improve by >= 15% this suggest that the airway obstruction is acutely reversible.
Due to bronchospasm from asthma |
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Hyperinflation
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Airway obstruction causes airway closure, traps air in lungs during exhalation
Inc lung volume (at end of normal exhalation )--> hyperinflation Measured as inc RV |
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Airway obstruction
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most common pulmonary function abnormality in children/adults
1. asthma 2. chronic obstructive pulmonary diseases (chronic bronchitis and emphysema) 3. cystic firbosis |
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Work of breathing
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= Pressure x Volume
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Pressure to inflate the lungs (P TP)
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sum of elastic pressure (Pel to voercome volume) + resistance pressure (Pres, to overcome airflow)
PTP= V/CL +(flow X R) CL- compliance |
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PFT
Restrictive Lung diseases |
- Decreased lung volumes TLC
- Decreased compliance |
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PFT
Obstructive Lung Diseases |
- narrow and/or obstructed airways
- decrease maxmal expiratory flow rates - increased resistance |
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Compliance is dec --> lungs are stiff-->
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Pel is larger component of PTP.
More effort req to inc lung volume when lungs are stiff |
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Resistance is inc--> airway obstruction dec airflow
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Pres is larger component of PTP
More effort req to inc flow thorugh narrow airways |
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Breathing patter
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always ones that minimizes work of breathing
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Restrictive disease breathing pattern
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rapid shallow breathing patter,
do not have to inflate stiff lungs and minimize Pel |
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Airway obstruction breathing pattern
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slow deep breathing matterns-
do not have to generate high airflowa nd minimize Pres |
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Time constants
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Distribution of ventilation is affected by time takes to fill up a region of lung which depends on compliance and resistance
time constant = compliance * resistance |
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Compliance
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Volume/pressure
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Resistance
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Pressure/flow
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Which lung regions will fill first and empty first?
First in; First out |
Lung regions with Dec resistance fill rapidly due to inc flow
Lung regions with dec compliance fill rapidly de to dec volume Lung regions with dec time constant are best ventilated |
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Alveolar volume for lung regions of
1. Dec resistance 2. Inc compliance |
1. bc dec resistance fill rapidly they have inc alveolar volume
2. bc inc compliance has potential to inc volume but takes more time to fill--> they actually have dec alveolar volume bc inspiratory time is too short |
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Ptp Pleural gradient
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gradient in intrapleural pressure from base (~-2cm H2O) to the apex (~-10cm H2O) of the lung
Gradient due to gravity Elastic recoil greater at apex than base |
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Effects of gradient
Alveoli large at FRC in apex Alveoli small at FRC in base |
Alveoli large--> tidal volume is smaller
Alveoli small--> tidal volme larger Ventilation is greater at the base of the lung than at the apex |
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Two roles of elastic recoil
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1. Dec lung volume and causes exhalation to be passive
2. Supports the patency of intra-pulmonary structures when lung volume is fixed |
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Ppl gradient
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- More negative at apex and less negative at the base
- due to gravity This pressure gradient affects distribution of ventilation - Alveoli are larger in apex than the base - There is geater ventilation at the base than at the apex |
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Gravity affects distribution of ventilation in normal lungs by alterations in
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Ppl, Pel, Cl and Raw
Abnormal Cl and Raw also affect the distribution of ventilation Lung disease pathologic changes in Cl and Raw have a greater effect on distribution than gravity |
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Distribution of perfusion
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-the pulmonary vascular bed is a high compliance, low resistance circuit
- blood flow to the lung regions depend on wheater a blood vessel is open or not - the patency of pulmonary blood vessels depends primarily on intravascular pressure vs extravascular pressure |
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Distribution of perfusion
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- the gradient in Qp from apex to base of the lung is due to gravity
- there is less Qp gradient in the supine position or when gravity is minimized (outerspace) - inc in Pa like excercies will eliminate Zone 1 and make the distribution of perfusion more uniform |
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Zone 1
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Alveolar pressure > both pulmonary artery and pulmonary venous pressures.
Capillaries are compressed, and there is no flow. |
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Zone 2
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Arterial pressure > alveolar pressure
alveolar pressure > venous pressure Flow is difference between arterial and alveolar pressures, and it increases as one descends in vertical height. |
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Zone 3
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Both arterial and venous pressures > alveolar pressure.
Flow is the difference between arterial and venous pressures, and it increases slightly as one descends. |
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Distribution of V/Q
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Ventilation and perfusion are greater in the base than in the apex.
the gradient in perfusion is much steeper than that of ventilation--> V/Q is greater at the apex than at the base. |
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Pulmonary Circulation Function
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1. bring unoxygenated blood to the alveoli
2. serve as a reservoir 3. serve as a filter 4. metabolize (detoxify) some substances as they pass through the lungs. |
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Pulmonary vascular resistance (PVR)
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is extremely low
~10% of systemic vascular resistance Low PVR even when therse an increase in cardiac output (as during exercise) by: 1. highly distensible pulmonary capillaries 2. by recruitment of capillaries, which were closed at lower cardiac outputs |
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Extra-alveolar vessels
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pulmonary arteries and veins
Subjected primarily to intrapleural pressures At inc lung volume, dec Ppl distends these vessels, dec PVR. At dec lung volume, inc Ppl compresses these vessels, inc PVR. |
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Intra-alveolar vessels
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-Pulmonary capillaries
-subjected primarily to alveolar pressures -At inc lung volume, the stretch on alveolar tissues compresses capillaries, inc PVR -At dec lung volume, alveolar pressure decreases, distending pulmonary capillaries, and dec PVR. |
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Pulmonary vascular resistance (PVR)
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Intra-alveolar and extra-alveolar vessels are in series--> resistances are additive.
At inc lung volume, PVR is inc in intra-alveolar vessels and dec in extra-alveolar vessels. At dec lung volume, PVR is inc in extra-alveolar vessels and dec in intra-alveolar vessels. Therefore, PVR is lowest at FRC, the volume at which lungs exist most of the time. |
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What affects PVR
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PAO2 is the most important regulator of pulmonary vascular tone.
Hypoxia causes local pulmonary vasoconstriction --> protective reflex--> directs blood flow away from hypoxic regions of lung. This preserves V/Q matching. Acidosis and Inc PAco2 exacerbate the effect of hypoxia on PVR. |
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Fluid exchange in pulmonary capillary
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alveolar-capillary membrane is porous
fluid needs to stay in cap not in alveolus |
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What forces keep fluid in capillary
Moving fluid into the Capillary Moving fluid into the Alveolus |
Into the Cap:
- Inc colloid osmotic pressure - Inc alveolar P Into the Alveolus -Inc capilarry hydrostatic P - Inc Alveolar surface tension |
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What happens in heart failure
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Large increases in capillary hydrostatic pressure push fluid into the alveoli--> pulmonary edema
Lesser increases in capillary hydrostatic pressure -> push fluid into interstitial space dec compliance |
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Pulmonary Lymphatics
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clears fluid from interstitial space
drain through the hilum to the thoracic duct into the superior vena cava |
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Heart failure and pulmonary edema
Left heart failure |
blood backs up from the L ventricle to the lungs
Inc cap pressure--> pulmonary edema |
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Heart failure and pulmonary edema
Right heart failure |
blood backs up from the R ventricle into systemic veins
Dec throacic duct flow Dec pulmonary fluid clearance--> pulmonary edema |
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Host defense mechanisms
Larger particles (>10u) |
move in a straight line, do not follow airways
impact upper airway and do not reach lungs |
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Host defense mechanisms
Middle size particles (2-10u) |
carried in turbulent flow in large airways
Sediment out in turbulent eddies 5-10u Deposit in trachea and are removed by cough 2-5u deposit in bronchi removed by mucocilary activity |
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Host defense mechanisms
Small sized particles (<2u) |
carried in airflow to respiratory bronchioles and alveoli
deposited by diffusion removed by alveolar macrophages very small ones are exhaled back out |
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Cough
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clears the airways of secretions
Large airways mechanisms is high airflow velocity (85% of speed of sound) Cough is primary mechanism for removing secretions when cilia are damaged from inflammation |
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Cough receptors
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located in upper airway, nasopharyns, oropharyns, large airways and esophagus
NOT located in small airways or alveoli |
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Deposition of B2 particles in lung
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deposition of inhaled paricles in large airway is greater for larger particles
bronchodilator effect (Inc FEV1) is greater for larger inhaled particles Deposition in the periphery is greater for small inhaled particles Deposition is greater for all particles with slower inspiratory flow rates |
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Ineffective cough result from
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-Abnormalities or alterations in the cough reflex
-unresponsive to repeated stimulation -receptor not present in alveoli or lung parenchyma -suppressed by CNS depressant medications -neuromuscular diseases or abdominal wall muscle weakness -laryngeal abnormalities preventing glottic closure |
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Mucocillary clearance
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Mucous layer traps inhaled materials and propels them toward large airways by cilia
cilia beat 600-900 times per minutes (10-15Hz) D 0.25um and L 5-8um Cilia beat in serous layer below mucous blanket |
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Cilia
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have microscopic hooks, attach to underside of mucous blanket to propel it
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Mucocillary action damanged
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1. Cilia can be abnormal (genetic mutation of contractile structure of cilia--> primary cilary dyskinesia)
2. Substances can affect cilary activity 3. Mucous can be too thick--> bc of chronic infection, difficult to remove 4. Cystic fibrosis 5. # of substances can affect viscosity of mucous 6. Respiratory viral infections can inactivate mucocilary clearance |
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Cystic fibrosis
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where fluid layer under mucous blanket is dehydrated--> inability to propel mucous
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mucous in large areas
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then removed by cough
Absence of mucociliary activity--> moves mucous in the airway is gravity |