Pulmonary pathophysiology - directly from west book
Is difficult to perform.
Can be used to assess the efficacy of bronchodilators.
Is unaffected by dynamic compression of the airways.
Is reduced in patients with fibrosis but not COPD.
Increases with age.
Turbulence in the trachea.
Action of the diaphragm.
Contraction of the intercostal muscles.
Power of the abdominal muscles.
Compression of the airways.
Increased FEV1.
Increased FVC.
Increased FEV1/FVC.
Decreased expiratory flow rate when related to lung volume.
Abnormally high flow rate early in expiration.
Detecting fixed upper airway obstruction.
Measuring the response to bronchodilator drugs.
Differentiating between chronic bronchitis and emphysema.
Detecting resistance in small peripheral airways.
Detecting fatigue of the diaphragm.
It is usually normal in mild COPD.
The slope of phase 3 is increased in chronic bronchitis.
In phase 3, well-ventilated units empty last.
In normal subjects the last expired gas comes from the base of the lung.
The expiratory flow rate should be as fast as possible.
Increased lung compliance.
Increase in the number of small airways.
Increased radial traction on the airways.
Increased elastic recoil of the lung.
Hypertrophy of the diaphragm
A. Decreases with age.
B. Is highly reproducible.
C. Is affected by the small, peripheral airways.
D. Is most informative in patients with severe lung disease.
E. Is normal in mild COPD.
Blood temperature is reduced.
PCO2 is reduced.
Blood pH is raised.
Concentration of 2,3-DPG in the red cell is raised.
Hydrogen ion concentration is reduced.
Arterial PO2.
Arterial oxygen saturation.
Arterial PCO2.
Plasma bicarbonate concentration.
Base excess.
6.8
7.0
7.2
7.4
7.6
Mixed respiratory and metabolic acidosis.
Uncompensated respiratory acidosis.
Fully compensated respiratory acidosis.
Uncompensated metabolic acidosis.
Fully compensated metabolic acidosis.
Hypoventilation.
Diffusion impairment.
Ventilation–perfusion inequality.
Shunt.
Residence at high altitude.
The condition is rare.
Most patients are lean.
Treatment by continuous positive airway pressure (CPAP) is often effective.
Treatment by CPAP tends to cause systemic hypertension.
Snoring is uncommon.
Increase arterial PO2 during moderate exercise.
Increase the uptake of halothane given during anesthesia.
Decrease arterial PCO2 during resting breathing.
Increase resting oxygen uptake when the subject breathes air.
Increase maximal oxygen uptake at extreme altitude.
Respiratory alkalosis with metabolic compensation.
Acute respiratory acidosis.
Metabolic acidosis with respiratory compensation.
Metabolic alkalosis with respiratory compensation.
A laboratory error.
A primary respiratory alkalosis with metabolic compensation.
A normal alveolar–arterial PO2 difference.
An arterial O2 saturation of less than 70%.
The sample was mistakenly drawn from a vein.
A partially compensated metabolic acidosis.
Can be measured with a single spirometer.
Is often larger when measured by helium dilution than with a body plethysmograph.
Is reduced during an attack of asthma.
Is determined by a balance between the elastic recoil of the lung and chest wall.
Falls with increasing age.
Is raised by increasing lung volume.
Is reduced by inhaling β2 agonists.
Is increased by destruction of alveolar walls.
Is unaffected by secretions in the airways.
Is increased by atrophy of bronchial smooth muscle.
Abnormally high levels of lactate in the blood.
Abnormally low ventilation.
Abnormally high cardiac output.
Increased lung compliance.
Reduced diffusing capacity of the lung.
Blood flow.
Ventilation.
Alveolar PCO2.
Alveolar size.
Capillary blood volume.
PCO2 of mixed venous blood.
Alveolar ventilation.
Tidal volume.
Heart rate.
Cardiac output.
Damage to pulmonary capillaries by increased alveolar pressure.
Chronic stimulation of bronchial mucous glands by cigarette smoking.
Destruction of lung elastin by excessive action of neutrophil elastase.
Excessive amounts of exercise.
Hyperventilation at high altitude.
Causes severe bronchitis with emphysema.
Results in emphysema at a relatively early age.
Is caused by infections in early childhood.
Is common in heterozygotes for the Z gene.
Tends to be most marked in the upper regions of the lung.
More cough productive of sputum.
Smaller lung volumes.
Decreased lung elastic recoil.
More hypoxemia.
Greater tendency to develop cor pulmonale.
FEV1.
FVC.
FEV1/FVC.
FEF25–75%.
None of the above.
FEV1
FEV/FVC %
FVC
FEF25–75%
FRC
β1-selective agonists are preferred to β2 agonists.
They relax airway smooth muscle by decreasing the concentration of adenyl cyclase.
They reduce the concentration of intracellular cAMP.
They reduce airway inflammation.
They are usually given as tablets by mouth.
Provides most of the structural SPport for the normal alveolar wall.
Cannot multiply.
Is formed when a type I epithelial cell divides.
Secretes surfactant.
Is metabolically inactive.
Infiltration of the alveolar wall with lymphocytes and plasma cells.
Breakdown of many alveolar walls.
Mucous gland hypertrophy in the bronchi.
Mucous plugging of airways.
Increased volume of the pulmonary capillary bed.
Cough productive of copious sputum.
Hemoptysis.
Rhonchi in both lungs.
Dyspnea especially on exercise.
Depressed diaphragms on the radiograph.
Increased FEV1.
Increased FVC.
Increased FEV1/FVC %.
Increased TLC.
Increased airway resistance when related to lung volume.
Typically worsens on exercise.
Is chiefly caused by diffusion impairment.
Is associated with a large increase in diffusing capacity during exercise.
Is usually associated with carbon dioxide retention.
Is improved during exercise because of the abnormally large increase in cardiac output.
Expiratory muscles have a large mechanical advantage.
Airways have a small diameter.
Dynamic compression of the airways is more likely than in a normal subject.
Radial traction on the airways is increased.
Airway resistance is increased.
Is typically substantially increased.
Shows an abnormally large increase during exercise.
Is unaffected by thickening of the blood-gas barrier.
Is reduced in part because of obliteration of pulmonary capillaries.
Falls only late in the disease.
It reduces the volume of the chest wall on the affected side.
It causes an increased blood flow in the affected lung.
When present in the tension form it is a medical emergency.
Spontaneous pneumothorax is mainly seen in older women.
The FVC is increased
Increased permeability of the alveolar epithelial cells.
Reduced capillary hydrostatic pressure.
Reduced colloid osmotic pressure of the blood.
Increased hydrostatic pressure in the interstitial space.
Reduced colloid osmotic pressure of the interstitial fluid.
Fluid can drain through the interstitium of the thick side of the blood-gas barrier.
The alveolar epithelium has a high permeability for water.
The strength of the barrier on the thin side is mainly attributable to the endothelial cells.
No protein normally crosses the capillary endothelium.
Water is actively transported into the alveolar spaces by alveolar epithelial cells.
Fluid tracks through the interstitium of the thin side of the blood-gas barrier to the perivascular and peribronchial spaces.
There is no increase in lung lymph flow.
Fluid floods the alveoli one by one.
The hydrostatic pressure in the interstitium probably falls.
Cuffs of fluid collect around the small arteries and veins.
Septal lines on the chest radiograph.
Increased lung compliance.
Reduced lymph flow from the lungs.
Severe hypoxemia.
Fluffy shadowing on the chest radiograph.
Carbon dioxide retention typically occurs.
The alveoli that contain fluid become overexpanded.
The fluid is free of red blood cells.
During positive pressure ventilation the fluid is moved peripherally.
No changes are seen on the chest radiograph.
The hypoxia directly increases capillary permeability.
Pulmonary venous pressure is increased.
The best treatment is to give diuretics.
Dyspnea is not a feature
It is related to the high pulmonary artery pressures caused by hypoxic vasoconstriction.
Lung compliance is increased.
Airway resistance is not affected.
The arterial hypoxemia cannot be abolished by breathing 100% oxygen.
Respiration is deep and labored.
The alveolar edema causes chest pain.
Overtransfusion.
Walking.
Anemia.
Use of oral contraceptives.
Leg exercises.
CO2 retention.
Increased physiologic dead space.
Pulmonary hypotension.
Decreased lung elastic recoil.
Reduced airway resistance.
May complicate long-standing COPD.
Always causes a reduced cardiac output.
Does not occur in diffuse interstitial pulmonary fibrosis.
Cannot cause neck vein engorgement.
Cannot cause ankle edema.
Hydrocarbons.
Sulfur oxides.
Nitrogen oxides.
Carbon monoxide.
Ozone.
Ozone is mainly produced in automobile engines.
A temperature inversion occurs when the air near the ground is hotter than the air above.
The main source of sulfur oxides is the automobile.
Nitrogen oxides can cause inflammation of the upper respiratory tract.
Scrubbing flue gases is ineffective in removing particulates
Inhaled smoke contains negligible amounts of carbon monoxide.
Cigarette smokers can have enough carboxyhemoglobin level in their blood to impair mental skills.
Nicotine is not addictive.
The risk of coronary heart disease is not affected by smoking.
The concentration of pollutants in cigarette smoke is less than in the air of a large city on a smoggy day.
Most particles less than 5 µm in diameter are filtered by the nose during resting breathing.
Many inhaled particles are deposited in the region of the terminal and respiratory bronchioles.
Astronauts who are weightless have the same particle deposition as when they are on earth.
Particles 0.5 µm wide diffuse almost as fast as gas molecules.
Many particles larger than 10 µm wide are not deposited in the lung but are exhaled with the next breath.
Frequent coughing.
Exercise.
Mining operations that produce very small dust particles.
Rapid deep breathing.
Nose breathing, as opposed to mouth breathing.
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