Week 8 (EXAM 2) Flashcards

1
Q

Describe the structure of the lung

A

 Cone shaped with an apex, base and 3 borders (anterior, inferior and posterior)
 Apex highest point in the root of the neck, 1 inch above each clavicle
 Base is concave resting on the convex surface of the diaphragm
 Anterior border of left lung has cardiac notch
 R lung is heavier and wider than the L lung;
shorter than the L lung due to the liver
 L lung is longer and thinner than the R lung
due to the heart and pericardium

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2
Q

What are the lobes of R & L lungs

A

 3 on the right upper, middle and lower
 2 on the left upper and lower

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3
Q

What are the fissures of R & L lungs

A

 Right has horizontal fissure which separates the RUL and RML, and oblique fissure that separates the RUL/RML and RLL
 Left has oblique fissure which separates the LUL and LLL

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4
Q

What are the segments of R & L lungs

A

Segments:
 Each lobe is further subdivided into segments
 Both upper lobes have apical, anterior and posterior segments (harder to separate on the left)
 RML has medial and lateral segments

Left lung has lingual segment instead (wraps around heart)

Both lower lobes have anterior basal, posterior basal, superior basal and lateral basal segments

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5
Q

What are the muscles of inspiration?

A

Diaphragm
 Main muscle of inspiration External

Intercostal muscles
 Slope forward and downward
 Pull ribs up and outward

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6
Q

What are the ventilation mechanics

A

Resting:
1) 760 mm Hg inrapulmonic and intrapleural pressure (atmospheric pressure)

Inspiration:
1) muscles contract so the chest wall moves out
2) diaphragm descends
3) intrapulmonic pressure more negative to 758 mm Hg
4) intrapleural pressure more negative to 754 mm Hg
5) air (at atmospheric pressure 760) flows in

Expiration:
1) muscles relax so chest wall moves inward
2) diaphragm ascends
3) intrapleural pressure remains negative
4) intrapulmonary pressure becomes positive (763 mm Hg)
5) air flows out

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7
Q

What are the components of the lower respiratory tract?

A

conducting zone: (trachea and terminal bronchioles)

 Considered anatomic dead space
 air transport
 humidification
 warming
 particle filtration
 vocalization
 immunoglobulin secretion

Respiratory zone: (bronchioles, alveolar ducts, alveoli)

 gas exchange
 surfactant production
 molecule activation and inactivation
 blood clotting regulation
 endocrine function

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8
Q

What is Chronic Obstructive Pulmonary Disease (COPD)?

A

 3rd most deadly disease
 Common: global prevalence of about 174 million cases; contributes to major disability and economic/social
burdens
 Risk factors: primarily tobacco smoke inhalation
 Physical inactivity, increased age, early life events and inflammation
 Group of chronic, obstructive lung diseases
 (VIP) Affect the airways and lung parenchyma that produce obstruction to expiratory airflow
 Trouble getting air OUT
 Most individuals with COPD have a combination of chronic bronchitis, emphysema and airway hyperactivity
 Also includes cystic fibrosis, bronchiectasis and bronchopulmonary dysplasia

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9
Q

What are the types of COPD?

A

(people can have multiple or just one)

1) Emphysema
 Parenchymal alveolar disease. Destruction of alveolar walls, enlargement of airspaces distal to
the terminal bronchioles. Balance between destruction and repair of the respiratory bronchioles, alveolar ducts and alveoli.

2) Chronic bronchitis
 Small airway disease. Presence of a chronic productive cough for 3 months in each of 2 successive years. Hypersecretion of mucus in the large airways  smaller airways.

3) Asthma
 Chronic inflammatory disorder of the airways. Recurrent episodes with variable airflow obstruction
that is often reversible. Hyperresponsiveness to stimuli.

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10
Q

What is COPD etiology?

A

2 primary causes (Inhalation factors and genetics)

1) Inhalation of cigarette smoke is the primary cause
 Active or passive
 Risk for developing COPD is 30x greater in smokers than nonsmokers

2) Genetics
 Alpha1-antitrypsin deficiency (emphysema: damage to walls of alveoli)
 Primarily affects the surfactant production and integrity of the alveolar sac

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11
Q

What is the pathophysiology of COPD?

A

 Characterized by inflammation of the airway and decreased airflow to the lung caused by an irreversible
narrowing
 Ultimately disappearance of small conducting airways and bronchioles
 Cycle of tissue damage causing an inflammatory cascade and immune response  tissue damage
 Exacerbated by increased age and altered immune response

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12
Q

How does COPD present?

A

1) Obstruction can be related to any or all the following:
 Retained secretions
 Inflammation of the mucosal lining of airways
 Bronchial constriction
 Weakening of support structure of airway walls
 Air sac destruction and over-inflation

2) Episodic wheezing with a variable degree of chronic bronchitis and emphysema

3) Chest x-ray
 Hyperinflated lungs, flattened diaphragm and enlarged R ventricle

4) Incomplete emptying of the lung
 Reduced lung function as noted on PFT

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13
Q

What are common traits of COPD?

A

 Decreased activity tolerance
 Increased anxiety
 Wheezing
 Tripoding “hand on knee”
 Pursed lip breathing
 Clubbing “low O2 to finger tips”
 Cyanosis
 Secretion production
 Cough
 Dyspnea or SOB

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14
Q

Explain what’s wrong

A

R image:

Hyperinflated lungs (appear darker on x-rays due to increased amount of air vs normal tissue)

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15
Q

How is COPD diagnosed?

A

1) Spirometry
 Gold standard for diagnosis and monitoring
 Measure of airflow limitation
2) Arterial Blood Gases
3) Chest x-ray
4) Percussion “tapping body parts with fingers”
5) Auscultation “listening to sounds of body during physical examination”

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16
Q

How is lung volume affected when it is obstructed?

A

Reduced: IC, ERV, VC

Increased: RV, FRC, TLC

17
Q

What are common impairments from COPD?

A

 Reduced 6MWT duration
 Decreased strength
 Respiratory muscle weakness and fatigue
 Impaired balance
 Increased fall risk
 Dyspnea with minimal activity
 Pelvic floor dysfunction
Increased pressure on abdomen
Chronic cough

18
Q

What is COPD prognosis?

A

 With continued cigarette smoking and chronic respiratory irritation, progressive loss of lung function and
worsening of symptoms will occur
 Cessation is the only effective intervention for preventing life-threatening effects
(Inflammation an persist after cessation of smoking)
 Individuals are at risk for tissue catabolism and weight loss
(Associated with increased morbidity)
 Life-threatening complications are associated with prolonged hypoxemia
(Ischemia of organ systems)
(Most common causes of death: CHF, respiratory failure, PNA, bronchiolitis, pulmonary embolism)