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Pathophysiology Thorax > Module #4: Disorders of the Pulmonary System > Flashcards

Module #4: Disorders of the Pulmonary System Flashcards

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1
Q

What is hypercapnia?

A

increase PaCO2 in arterial blood

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2
Q

What are some of the causes of hypercapnia?

A

Hypoventilation of alveoli

Supression of respiration centers (DRG/VRG)

Large airway obstructions (tumors/sleep apnea)

Damage to alveoli (emphysema)

Respiratory acidosis

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3
Q

What is tissue hypoxia

A

decreased O2 in ANY tissue

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4
Q

Define Hypoxemia

A

decreased PaO2 in arterial blood

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5
Q

What are the 5 major causes of hypoxemia?

A

Decreased PO2 of inspired air (altitude/suffocation)

Hypoventilation (meds that supress DRG/VRG)

Diffusion abnormality of alveolocapillary membrane (emphysema/fibrosis/edema)

Altered V/Q perfusion ratio (low or high)

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6
Q

What does low V/Q indicative of?

A

good perfusion (blood is getting to lungs fine) but inadequate ventilation

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7
Q

What does he mean by pulmonary “right to left shunting”?

A

Low V/Q

blood travels from RIGHT side of heart and returns to LEFT side of heart w/o receiving O2

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8
Q

What are some clinical examples (diseases) of right to left shunt

A

asthma

chronic bronchitis

pneumonia

ARDS (acute respiratory distress syndrome)

ARDS of infants (hyaline membrane disease

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9
Q

What does high V/Q indicative of?

A

inadequate blood flow in a well ventilated lung

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10
Q

What is a clinical example of a high V/Q?

A

pulmonary embolism

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11
Q

What is pulmonary aspiration?

A

entry of fluids/solids into trachea and lungs

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12
Q

What is pulmonary edema?

A

excess fluid in lungs

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13
Q

What is the most common cause of pulmonary edema?

A

heart disease (increased left sided pressures)

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14
Q

What is atelectasis?

A

collapse of lung tissue

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15
Q

What are the 4 types of atelectasis?

A

Compressive

Absorptive

Surfactant Impairment

Post-Op

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16
Q

What happens to cause compressive atelectasis?

A

external pressure compresses lung

caused by tumors, fluid/air in pleural space (pneumothrorax), abdominal distention

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17
Q

What happens to cause absorptive atelectasis?

A

air from blocked or hypo ventilated alveoli gets absorbed into system

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18
Q

How does surfactant impairment causes atelectasis?

A

lack of surfactant will increase surface tension and makes lungs prone to collapse

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19
Q

How is atelectasis prevented in post-op patients?

A

post-surgical deep breathing exercise

pt positioning

early ambulation (get them up and moving ASAP)

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20
Q

Define pneumothorax

A

air accumulation w/in pleural cavity (pleural space)

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21
Q

What are the 3 types of pneumothorax?

A

Open pneumothorax

Tension pneumothorax

Spontaneous pneumothorax

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22
Q

Describe what happens during an open pneumothorax

A

air enters pleural cavity during inspiration and exits during expiration

air pressure in pleural space now = barometric pressure

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23
Q

Describe what happens during tension pneumothorax

A

air enters plueral cavity during inspiration but DOES NOT EXIT during expiration

there is a gradual build up of air pressure in pleural space, it collapses lung and compresses/displaces other structures of mediastinum (heart/vessels/etc)

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24
Q

Describe what happens during spontaneous pneumothorax

A

an unexpected rupture of pleura

common in 20-40 yo males

may or may not develop into tension pneumothorax

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25
What is pleural effusion?
fluid on pleural space
26
What could pleural effusion cause?
compressive atlectasis
27
What are some causes of fluid buildup?
transudate (water) exudate (protein) pus (infectious debris) blood (hemothorax) lymph fluid (chyle)
28
Define ARDS
acute respiratory distress syndrome due to acute inflammation and alveolar damage
29
Name some of the causes of ARDS
most common causes = infection (sepsis) or multiple trauma also: pneumonia burns aspiration cardiopulmonary bypass surgery pancreatitis drug OD smoke/toxic gas inhalation radiation therapy
30
What are the 3 pathophysiology phases of ARDS
Phase 1: initial injury to lung leads to massive inflammatory response, surfactant is inactivated, alveoli collapse due to less compliance and filling of inflammatory fluid Phase 2: Hyaline membrane forms into fibrous mass coating alveoli and bronchioles Phase 3: respiratory failure, secondary systemic (throughout body) inflammatory response; damage other organs which may cause death
31
What are the 3 most common obstructive pulmonary diseases?
asthma emphysema chronic bronchitis
32
What is going on in the airway with obstructive pulmonary diseases?
airway obstruction that is worse w/ expiration breath out = wheezy airway expands during inspiration but collapses (recoils) during expiration
33
Name the clinical characteristics of obstructive pulmonary disease
Dyspnea = perceived difficulty of breathing increased work of breathing (WOB) wheezing decreased FEV1/FVC ( blood can get to alveoli but lungs can't deliver O2
34
What is COPD (chronic obstructive pulmonary disease/disorder)?
syndrome describes coexisting condition of chronic bronchitis and emphysema
35
What is the primary cause of COPD?
smoking
36
What is Chronic Bronchitis?
condition of excess mucous secretion and productive cough that lasts 3+ months and occurs 2 consecutive years
37
Describe the Pathophysiology of Chronic Bronchitis
bronchial tubes are narrowed --> "traps" air in distal lungs excess mucous is produced in response to chronic exposure of irritants (smoke, pollution etc) increased mucous impairs cilia --> increased risk of infection/inflammation Low V/Q (blood is able to get to alveoli, but air can't) Hypoxemia (decreased PaO2 in arterial blood) --> increase in RBC # --> pulmonary hypertension --> cor pulmonale = hypertrophy (enlargement) and failure of right ventricle Hypercapnia (increased PaCO2)
38
What are the clinical signs/symptoms of Chronic Bronchitis?
productive/persistent cough aka smokers cough recurrent pulmonary infections reduced flow rates (decreased FEV1/FVC <70%) = prolonged expiration decreased FVC and increased RV
39
Name the treatments of Chronic Bronchitis
Expectorants Bronchodilators Physical Therapy (PT) = deep breathing exercises (pursed lip breathing) Antibiotics and steroids (usually reserved for late stage of disease b/c of side effects) Low flow O2 to address severe hypoxemia
40
What is the potential adverse effect of low flow O2 for chronic bronchitis?
Respiratory Depression central chemoreceptors (DRG/VRG) are no longer sensitive due to chronic hypercapnia peripheral receptors have taken over; these guys are sensitive to O2 pressure if you give to much O2 and PaO2 rises above 60 mmHg, the peripheral receptors will depress ventilation
41
What is emphysema?
pathological accumulation of air in the lungs --> enlargement of acini (gas exchange airways)
42
Name and describe the 2 types of emphysema
Centriacinar (centrilobar) - destruction of bronchioles/alveolar ducts; alveolar sac remains intact Panacinar (panlobular) - destruction of ENITRE acinus (terminal bronchiole, alveolar duct, alveoli)
43
Which type of emphysema is more common in chronic smokers?
Centriacinar (centrilobar) emphysema
44
Which type of emphysema is more common in the elderly?
Panacinar (panlobular) emphysema
45
Describe the pathophysiology of emphysema
lung tissue itself is damaged --> breakdown of elastin in septum of bronchioles, alveolar ducts and alveoli destruction of acinus also damages pulmonary capillary beds reduced elastin (connective tissue) limits the elastic recoil of lungs --> long slow expiration
46
What are the causes of emphysema?
Smoking
47
How does smoking effect the lungs to cause emphysema?
smoking inhibits production alpha1-antitrypsin (protease inhibitor) --> promotes the release and accumulation of elastase (enzyme that breaks down elastin (connective tissue protein) --> damages lung tissue **protease = enzyme that breaks down protein** in normal tissue alpha1-antitrypsin inhibits elastase smoking also favors the recruitment of WBC's in the lungs
48
What are the clinical signs/symptoms of emphysema?
Early sign = dyspnea on exertion (DOE) late sign = dyspnea at rest NO COUGHING/WHEEZING prolonged expiration increased WOB poor gas exchange --> hypoexmia (decreased PaO2) and hypercapnia (increased PaCO2) Barrel chest = classic sign Pts will sit leaned forward with arms extended to breath easier = classic breathing position Decreased flow rates = FEV1/FVC <70% FVC decreases RV/TLC increase End Stage = pulmonary hypertension and cor pulmonale (just like chronic bronchitis)
49
What are some of the acute treatments for emphysema?
O2 therapy bronchodilators corticosteroids/antibiotics
50
What are some of the chronic treatments for emphysema?
QUIT SMOKING pulmonary PT --> pursed lipped breathing exercises and safe exercise strategies O2 therapy (for hypoxemia Beta agonist (dilate airways) anticholinergic meds (prevent constriction of airways)
51
What is asthma?
reversible obstructive lung disease caused by increased reax of airways to various stimuli (hypersensitive)
52
Describe the pathophysiology of Asthma
Initial Attack: Hyper responsiveness of the airways stimulus (allergen) triggers massive inflammatory immune response --> inflammation and epithelial damage 3 classic pathological changes: bronchial smooth muscle spasm; mucous production (impair cilia function); vascular congestion Late asthma response = secondary attack 4-12 hrs after due to infiltration of WBCs; can be more severe than initial attack
53
What are the clinical signs/symptoms of an asthma attack?
Audible high pitched wheezing (on either both inspiration and expiration or just expiration) shortness of breath (SOB) decreased flow rates (FEV1/FVC <70%) increased respiration rate (tachypnea) apprehension/anxiousness (dyspnea, tachycardia, sensation of chest constriction) early on will have non-productive cough later on will have productive cough (removes mucous)
54
What are some of the triggers of Asthma attacks?
Foods (wines) Pollen smoke dust mold animals pollutants some are aspirin sensitive (NSAIDs) Occupational hazards (wood dust, cotton dust, animals, etc)
55
Describe Exercise Induced Asthma (EIA) symptoms triggers duration
onset 5 - 15 min after strenuous exercise triggered especially in dry cold air (late fall) lasts for 15-60 minutes can just feel like you're out of shape could have "classic" asthma symptoms (SOB, wheezing, chest tightness, anxiety) worse in "long duration endurace sports" swimming is better (warm moist air)
56
What are the clinical signs/symptoms of restrictive pulmonary conditions?
short shallow breathing patterns increased or no change in FEV1/FVC (>90%) Decreased FVC, RV, TLC dyspnea upon exercise progresses to dyspnea at rest
57
Name the 4 Restrictive Parenchymal Conditions
Sarcoidosis Idiopathic pulmonary fibrosis Pneumoconiosis Drug or Radiation-induced interstitial lung disease
58
What is sarcoidosis?
inflammation that produces tiny lumps of cells in various organs throughout the body microscopic lumps = granulomas
59
What are the 7 Restrictive Extraparenchymal Conditions?
Myasthenia gravis Guillain-Barre syndrome Muscular Dystrophies C-spine Injuries Kyphoscoliosis Obesity Ankylosing spondylitis
60
What is Pulmonary Fibrosis?
excessive fibrosis proliferation in the lungs
61
What are the causes of Pulmonary Fibrosis?
secondary complication from disease (TB/ARDS) inhalation of environmental hazards (pneumoconiosis) idiopathic pulmonary fibrosis
62
Describe the pathology of pulmonary fibrosis
Altered repair process leads to fibrosis and poor lung compliance chronic inflammation alveoli are invaded by fibroblasts --> shrink and lose elasticity
63
What is Pneumoconiosis?
lung pathology due to inhalation of inorganic environmental hazards (usually chronic exposure)
64
What are the most common inorganic environmental hazards that cause of Pneumoconiosis?
Silica --> mining Asbestos Coal Miner lung = combo of coal, silica, quartz
65
What causes TB?
mycobacterium tuberculosis
66
Describe the pathology of TB
inflammatory process is secondary to bacteria immune response leads to formation of granulomatous lesions (tubercle) tissue w/in tubercle becomes necrotic (caseous) scar tissue forms around tubercle m. tuberculosis remains dormant unless disrupted or if immune system becomes compromised (HIV)
67
What is the single greatest risk factor to reactive TB?
HIV
68
How would you diagnose TB?
Positive skin test- will indicated pt had disease or was vaccinated Chest films - see calcifications/nodules in upper lobes of lungs sputum culture - can take up to 6 wks
69
What is a pulmonary embolism?
blood clot
70
How are pulmonary emboli formed?
occlusion of pulmonary vascular/capillary supply
71
What happens to V/Q in pt w/ pulmonary embolism and what does that mean?
high V/Q ratio lungs can deliver O2, but blood can't get to alveoli
72
What is the most common pulmonary embolism?
Deep Vein Thrombosis (DVT)
73
What are the pathologic risk factors of pulmonary embolism?
Venous stasis - immobility (post-op/being old/travel/obesity), pregnancy, CHF Hypercoagulation - congenital, oral contraceptives, malignancy Damage to endothelium of blood vessels - trauma, surgery, CVA (stroke)
74
Describe the Pathology of pulmonary emboli
clots, fats, air can form emboli (big old clot) emboli lodges in lungs secondary response causes further vasoconstriction --> increase hypoxemia, increase pulmonary blood pressures --> right sided heart failure vasoconstriction --> decreased surfactant production --> atelectasis --> hypoxemia if massive enough can lead to cardiac arrhythmias, shock and death

Pathophysiology Thorax (5 decks)

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