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36 Cards in this Set

  • Front
  • Back
What is the most common obstructive lung disease?

**alveoli clump together
**raspberry (healthy) vs. a grape (not healthy)
What are the obstructive lung diseases?
-chronic bronchitis
What's the definition of emphysema?
the abnormal permanent enlargement of air spaces distal to the terminal bronchioles with destruction of alveolar walls and loss of lung elasticity
What's the patho of emphysema?
-tobacco smoke/air pollution/or alpha 1 antitrypsin deficiency
-breakdown of elastin in connective tissue of lungs
-emphysema: destruction of alveolar septa, airway instability
-airway obstruction, air trapping, dyspnea, frequent infections
-abnormal ventilation-perfusion ration, hypoxemia, hypoventilation, right heart failure
What are causes of emphysema?
-alpha 1 antitrypsin deficiency
-identical to bronchitis, but older onset
-smoking (main cause)
-air pollution
What's antitrypsin?

What does the deficiency mean?
-antitrypsin is a protein which inhibits action of proteolytic enzymes (that digest alveoli)
-the deficiency means tissue destruction related to circulating alveolar digesting enzymes
Clinical manifestations of emphysema
-dyspnea on exertion (shortness of breath while walking)
-barrel chest (AP diameter of chest) *upon looking at side view. looks normal looking straight on
-accessory muscle use
-chest breather
-pursed lip breathing
-weight loss
-distant heart and lung sounds (more distance between heart and lungs due to barrel chest)
-hyperresonance to percussion
-tripod stance (hunched over trying to breath)
-"pink puffer": related to increase work of breathing (use up all their energy because they're working so hard to breath)
What is restrictive pulmonary disease?
-decreased lung expansion due to alterations in lung structure
-decrease in total lung capacity (taking less air in)
-difficult in INSPIRATORY phase (breathing in phase)
what are the types of restrictive pulmonary diseases?
-intrapulmonary: atlectasis
-extrapulmonary: pleural effusions, pneumothorax
Intrapulmonary restrictive pulmonary disease
-intrapulmonary (within): atelectasis: restricitive disease that invovles collapse of previously expanded lung tissue
-airless state of alveoli
-small segment or entire lung involved
-collapse of alveoli=lower gas exchange
Types and causes of atlectasis
-most commonly seen in post-operative patients
-absorption atlectasis
-compression atlectasis
Absorption atlectasis
-results from removal of air from obstruction or hypoventiated alveoli
-obstruction of airways leading to alveoli collapse
-mucous, retained secretions

***air into alveoli, air gets stuck, gas slowly leaks out. alveoli collapse due to not refilling alveoli, gas reabsorbed by body
Compression atlectasis
-external pressure exerted by tumor, fluid, or air in pleural space or abdominal distention

**something pushing against lung causes it to collapse
Absorption atlectasis vs compression atlectasis
-atlectasis caused by airway obstruction and absorption of the air
-atelectasis caused by compression of lung tissue
Patho of atelectasis (collapse of alveoli)
1. decreased alveolar ventilation
2. lack of surfactant
3. lack of nitrogen
Patho of atlectasis
-decreased alveolar ventilation
1. trapped air diffuses into pulmonary circulation without being replaced = alveolar shrinking and collapse
Patho of atlectasis
-lack of surfactant
2. surfactant is secreted by type 2 cells in the alveolar lining.
-surfactant normally decreases surface tension which facilitates alveolar opening and ventilation (more lubricated=alveoli are more open)
-surfactant normally decreases surface tension
-lack of surfactant increases surface tension causing alveoli to collapse
Patho of atlectasis
-lack of nitrogen
-nitrogen gas maintains alveoli open at end-expiration
-lack of nitrogen = collapse of alveoli
-high O2 concentrations will decrease alveolar nitrogen levels
Clinical manifestations of atlectasis
-crackles in lungs
Extrapulmonary-pleural effusions
-presence of excess fluid within the pleural space
-not a disease, caused by a disease process
Patho extrapulmonary pleural effusions
-decreased plasma oncotic pressure, increased capillary permeability, increased plasma hydropressure
-third spacing in pleural space
-compression atlectasis, decreased ventilation but perfusion OK
Causes of pleural effusions (extrapulmonary)
-increased capillary permeability
-decreased plasma oncotic pressure (caused by proteins in the blood. draws fluid in vessel from outside)
-increased hydrostatic pressure (pushes fluid out of blood vessels into interstitial space)
Types of fluid with pleural effusions (extrapulmonary)
-exudate: high protein, cloudy, high WBC, hemothroax: bloody fluid around sac of lung, chylothorax: milky white fluid that contains lymph and fat (normally found in small intestine), gets through via fistula (small intestine fluid surrounding lung sac), emphyema: infected pleural infusion

-transudate: low protein, watery, low WBC, aka hydrothorax, clear fluid around lung
Clinical maifestations of pleural effusions (enxtrapulmonary)
-mild to sever dyspnea
-pleuritic chest pain (hurts to breath due to rubbing together of spaces)
-pleural friction rub
-dull/flat percussion
-decreased or absent breath sounds
Extrapulmonary - pneumothorax
-accumulation of air or gas in the pleural space, caused by rupture in the visercal pleura or parietal pleura and chest wall
3 types of extrapulmonary pneumonthorax
1. open (communicating or primary)
2. closed (simple or secondary)
3. tension
1. open (communicating or primary): air drawn in and forced out during expiration. air pressure in pleural space = barometric (outside) pressure (causes collapse). collapse due to negative pressure. gun shot or stab wound
2. closed (simple or secondary): intact chest wall. air enters from lung into pleural space. cause-->bleb on lung (blister on lung that pops and causes a hole in the lung) **air into pleural space, only a hole in lung, not the sac
3. tension: life threatening: site of pleural rupture acts as a one way valve. air enters upon inspiration but can't escape upon expiration. clinical manifestations: mediastinal shift and tracheal deviation are life-threatening (shifts to healthy side) **air in, air trapped going out, builds up and shifts, pleural sac in injured, not the lung
Patho of pneumothorax (extrapulmonary)
-intrapleural space has a negative pressure (-5), helps to keep lung expanded
-when a break in intrapleural space occurs, air rushes in
-intrapleural space becomes positive and lung collapses = barometric pressure
Causes of pneumothorax
-spontaneous (bleb, rupture) --> young guys that are tall and skinny
-chest trauma with perforation of chest wall and/or lung (rib fracture, gunshot, stabbing)
Clinical manifestations of pneumothorax
-chest pain
-shortness of breath, hypoxemia
-decreased or absent breath sounds
-diminished chest wall movement (especially on injured side)
-hyperresonance to percussion
-type of pleural effusion
-excess blood in pleural space
-causes: chest injury and damage to blood vessels
-patho: hemorrhage into the pleural space associated with traumatic injury, surgery, or rupture of blood vessels
clinical manifestations of hemothorax
-small amount of blood (<300cc) may cause no signs and symptoms. blood is reabsorbed
-large amount (>1500cc)may be life-threatening. hypovolemia and lung compression
-dullness to percussion on affected side
-decreased to absent lung sounds
-hypotension and shock
-decreased tactile fremitus (vibrations felt while talking)
Lung abscess
-pus-containing lesion of the lung that forms a cavity
-cavity formed by necrosis of the lung tissues
-causes: most commonly, aspiration into the lung of an organism that produces infection and necrosis of the lung tissue
-clinical manifestations: foul smelling/tasting sputum, hemoptysis (blood in sputum), fever/chills, cough with purulent sputum (dark brown), pleuritic pain, dyspnea, dullness to percussion
Pulmonary embolism/infraction (PE)
-obstruction of a branch of the pulmonary artery by a clot or plug of material that travels from one blood vessel to a small blood vessel (blocking blood supply to lungs. no perfusion taking place. higher VQ ratio--> more ventilation than perfusion)
-patho: blood clots that originate in the peripheral circulation and migrate to pulmonary circulation and get lodged (right sided heart failure)

**D dimer-->higher level=blood clot indication. followed by tests like VQ scan, echo, ultrasound to see where blood isn't getting to.
Causes and clinical manifestations of pulmonary embolism (PE)
-causes: blood clot from deep vein thrombosis (biggest cause), globule of fat, septic vegetation, foreign object, air, amniotic fluid

-manifestations: pleuritic pain, dyspnea/tachypnea, cough/hemoptysis, behaviors of right sided heart failure-->edema, organ enlargement, thick sputum, upright or leaning forward, pursed lip breathing, accessory muscle use, hyperresonance with percussion, distant breath sounds, increased BP, decreased O2, increased CO2, respiratory acidosis, metabolic acidosis
Pneumonia (respiratory tract infection)
-patho: inflammation of alveoli and bronchioles
-causes: viruses, bacteria, gastric secretions via inhalation, aspiration, direct spread from infected site or blood
-manifestations: coughing, sputum production, pleuritic chest pain, chills/fever, tachypnea, SOB, orthopnea, labored breathing, dullness to percussion, decreased breath sounds (in bases of lungs where infection is), low O2 and increased CO2
Types of pneumonia (respiratory tract infection)
-community: picked up from community
-noscomial: hospital/nursing home acquired
-opportunistic: immunocompromised people (cancer patients, people on steroids)