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Flashcards in The Lungs 1 Deck (73)
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1

What three things do primary lung diseases effect?

1. The airways
2. The interstitium
3. The pulmonary vascular system

2

What is atelectasis aka pulmonary collapse?

Loss of lung volume caused by inadequate expansion of airspaces

3

Is atelectasis reversible? What does treatment aim to do?

Yes (except for contraction atelectasis). Tx helps to prevent hypoxemia and infection of the collapsed lung.

4

What is resorption atelectasis?

When alveoli distal to an obstruction collapse because the air that was present prior to the obstruction event was eventually absorbed.

5

What is compression aka passive aka relaxation atelectasis? Name five causes.

Alveolar collapse due to external pressure such as from: 1) pleural effusion (from CHF), 2) hemothorax, 3) pneumothorax, 4) neoplasm, or 5) from being bedridden (diaphragm moves superiorly when lying flat)

6

What is contraction aka cicatrization atelectasis? Is it reversible?

Fibrotic changes that increase the elastic recoil, causing decreased lung compliance and an inability to fill. Not reversible.

7

What are the four clinical indicators of an acute lung injury?

1. Acute onset of dyspnea
2. Decreased O2 sats
3. Bilateral pulmonary infiltrates on CXR
4. No evidence of left heart failure

8

What can untreated acute lung injury potentially progress to?

Acute respiratory distress syndrome (ARDS)

9

Acute respiratory distress syndrome (ARDS) is caused by diffuse _______ damage involving the pulmonary capillaries and endothelium.

alveolar

10

Name five common causes of ARDS.

1. Shock
2. Pneumonia with sepsis
3. Endotoxins
4. Ishemia
5. Aspiration of gastric contents

11

Name five less common causes of ARDS.

1. Inhalation of toxic gas or very hot air.
2. Radiation.
3. Near drowning.
4. Metabolic disorders.
5. Drugs

12

How serious is ARDS aka "shock lung" and what are some clinical manifestations?

Respiratory failure is rapid and life threatening. Patients are cyanotic with severe arterial hypoxemia. O2 treatment doesn't work. Can progress to organ failure.

13

Describe the pathogenesis of acute respiratory distress syndrome (7 steps).

1. Alveolar damage (epithelial, endothelial, or commonly both).
2. Pro-inflammatory imbalance caused by nuclear factor kB.
3. Cytokine release within 30 minutes: IL-8, IL-1, TNF.
4. The cytokines activate endothelial cells and NEUTROPHILS.
5. Neutrophils release factors that maintain the inflammatory cascade.
6. Endothelial and epithelial injury leads to loss of surfactant.
7. Alveolar collapse.

14

What is nuclear factor kB?

Pro-inflammatory thing that plays a role in ARDS!

15

Name three anti-inflammatory factors that play a role in ARDS.

1. Endogenous anti-proteases
2. Antioxidants
3. Anti-inflammatory cytokines

16

What is the #1 factor that determines the degree of tissue injury in ARDS?

The balance between pro and anti-inflammatory factors in the lungs.

17

What are the two phases of ARDS?

1. Initial (acute) exudative phase
2. Organizing phase

18

Name five morphological features of the acute exudative phase of ARDS.

1. Lungs are dark red, firm, airless, and heavy.
2. Alveolar edema.
3. Epithelial necrosis.
4. Accumulation of neutrophils.
5. HYALINE MEMBRANES lining the alveolar ducts.

19

When does the organizing phase of ARDS begin?

A week after the initial injury.

20

Describe five morphological changes of the organizing phase of ARDS.

1. Fibroblast proliferation.
2. Type II pneumocyte proliferation.
3. Alveolar macrophages trying to digest the hyaline crap.
4. Fibrin organization --> intra-alveolar fibrosis and thickening of the septa.
5. Unusual resolution.

21

Within 72 hours of the initiating insult, _____% of patients develop the clinical signs of ARDS; the mortality rate is _____%.

85% develop clinical signs. 40% mortality rate

22

For those who have an uncomplicated outcome following ARDS, normal respiratory function returns within ____ to ____ months.

6 to 12 months

23

What does the term "wet lung" refer to?

ARDS lung

24

Obstructive pulmonary disease is a disease of the airways characterized by a ________ of airflow resulting from a ________ in resistance of the lung tissue.

limitation of airflow due to an increase of resistance.

25

Name two examples of obstructive pulmonary diseases.

1. Chronic bronchitis
2. Emphysema

26

What are the differences between pure chronic bronchitis and pure emphysema?

Pure chronic bronchitis includes hypersecretion of mucus and inflammation of the upper large airways, peribronchiolar fibrosis and obstruction of the small airways (bonchioles).

Pure emphysema is loss of elastic recoil and overinflation of the ACINI (respiratory bronchiole, alveolar ducts, and alveoli).

27

COPD is characterized by ________ airflow obstruction, whereas asthma is characterized by _______ airflow obstruction.

irreversible (COPD)

asthma is reversible

28

Is fibrosis present in the acini of a emphysematous lung? What is the major cause of emphysema?

There is NOT obvious fibrosis. Major cause is cigarette smoking.

29

Centriacinar emphysema is characterized by loss of elasticity and overinflation of the ________ ________, whereas panacinar emphysema is characterized by loss of elasticity and overinflation of the ________ ________, and ________.

Centriacinar: overinflation of the respiratory bronchioles (just proximal to the alveolar ducts).

Panacinar is overinflation of the alveolar ducts and alveoli.

30

With centriacinar aka centrilobular emphysema, are both normal and emphysematous airspaces present in the same acini and lobules? How does this differ from panacinar emphysema?

Yeah. Different than panacinar emphysema, in which there is UNIFORM enlargement of the structures distal to the respiratory bronchiole.