November 15 Review Quiz

Question 1

Restrictive lung disorders cause a decrease in

Answer 1

Tidal volume (TV) and Force vital capacity (FVC)

Question 2

Tidal volume

Answer 2

500

Question 3

Total lung capacity

Answer 3

5-6 (Vital capacity+ reserve volume)

Question 4

Inspiratory volume

Answer 4

2000

Question 5

Expiratory volume

Answer 5

1200

Question 6

Reserve volume

Answer 6

1200

Question 7

Vital capacity

Answer 7

Inspiratory volume (2000)+ Expiratory volume (1200)+ tidal volume (500)

Question 8

Exudative or inflammtory phase

Answer 8

Within 72 hours
Alveolocapillary membrane damage
Increased capillary membrane permeability
Pulmonary edema
Surfactant inactivated

Question 9

Proliferative phase

Answer 9

4-21 days
Resolution of the pulmonary edema and proliferation of type II pneumocytes, fibroblasts, and myofibroblasts
Hyaline membranes
Hypoxemia

Question 10

Fibrotic phase

Answer 10

14-21 days
Remodeling and fibrosis
Alveoli destruction
Severe right-to-left shunting
Acute respiratory failure

Question 11

FEV1 (forced expiratory volume within 1 second)/FVC

Answer 11

Normal: greater than or equal to 80%
COPD: < 80%

Question 12

Primary emphysema cause

Answer 12

Inherited deficiency of the enzyme α1-antitrypsin

Question 13

Secondary emphysema cause

Answer 13

Cigarette smoke: Main cause

Air pollution, occupational exposures, and childhood respiratory infections: Possible contributors

Question 14

Centriacinar
 (Centrilobular)

Answer 14

Septal destruction occurs in the respiratory BRONCHIOLES and alveolar ducts, usually in the UPPER lobes.
Alveolar sac (alveoli distal to the respiratory bronchiole) remains intact.
Tends to occur in SMOKERS with chronic bronchitis.

Question 15

Panacinar (Panlobular)

Answer 15

Involves the entire ACINUS.
Damage is more randomly distributed.
Involves LOWER lobes 
of the lung.
Occurs in those with inherited deficiency of the enzyme α1-antitrypsin

Question 16

Acute cough

Answer 16

Resolves within 2-3 weeks

Question 17

Chronic cough

Answer 17

Lasts longer than 3 weeks

Question 18

Kussmauls (hyperpnea)

Answer 18

Slightly increased ventilatory rate, very large tidal volume, and no expiratory pause

Question 19

Cheyne-Stokes respirations

Answer 19

Alternating periods of deep and shallow breathing; apnea lasting 15-60 seconds, followed by ventilations that increase in volume until a peak is reached, after which ventilation decreases again to apnea (e.g. CHF, sleep apnea)

Question 20

Hypoventilation leads to

Answer 20

Respiratory acidosis

Question 21

Hyperventilation leads to

Answer 21

Respiratory alkalosis

Question 22

Hypoventilation is caused by

Answer 22

Airway obstruction, chest wall restriction or altered neurologic control of breathing

Question 23

Hyperventilation is caused by

Answer 23

Anxiety, head injury, or severe hypoxemia

Question 24

Cyanosis develops when

Answer 24

desat of 5g/dL

Question 25

Acute respiratory failure

Answer 25

PaO2 = 50 mm Hg PaCO2 >/= 50 mm Hg pH = 7.25

Question 26

Primary (spontaneous) pneumothorax

Answer 26

Occurs unexpectedly in healthy individuals

Question 27

Secondary pneumothorax

Answer 27

Is caused by disease, trauma, injury or condition

Question 28

Iatrogenic pneumothorax

Answer 28

Is caused by medical treatments, especially transthoracic needle aspiration

Question 29

Open pneumothorax

Answer 29

Air pressure in the pleural space equals barometric pressure, because air that is drawn into the pleural space during inspiration is forced back out during expiration

Question 30

Tension pneumothorax

Answer 30

Site of pleural rupture acts as a one-way valve. Life threatening

Question 31

Transudative effusion

Answer 31

Watery and diffuses out of the capillaries

Question 32

Exudative effusion

Answer 32

Contains high concentrations of WBCs and plasma proteins

Question 33

Restrictive lung disorders

Answer 33

``` Aspiration Atelectasis Bronchiectasis Pulmonary edema Acute respiratory distress syndrome ```

Question 34

Obstructive pulmonary disease

Answer 34

Asthma Chronic bronchitis Emphysema (inherited a1 antitrypsin deficiency) Chronic bronchitis plus emphysema equals COPD

Question 35

Asthma pathophys

Answer 35

IgE causes mast cells to degranulate, releasing a large number of inflammatory mediators: vasodilation, incr capillary permeability, mucosal edema, bronchospasm, tenacious mucous secretion Early: antigen activates dendritic cells to present antigen to CD4 T cells. IL 4 stimulates B cell activation and the production of IgE. IL 5 stimulates the activation of eosinophils Late: 4-8 hours after early response. Chemotactic recruitment of lymphocytes, eosinophils and neutrophils

Question 36

Ominous sign of impending death

Answer 36

PaCO2 grater than 70 mm Hg

Question 37

Chronic bronchitis

Answer 37

Hypersecretion of mucus and chronic productive cough that lasts at least 3 months of the year and for at least 2 consecutive years

Question 38

Emphysema

Answer 38

Destruction of alveoli through the breakdown of elastin in the septa as a result of an imbalance between proteases and antiproteases, oxidative stress, and apoptosis of the lung's structural cells

Question 39

Virchow triad

Answer 39

Venous stasis, hypercoagulability, and injuries to the endothelial cells that line the vessels

Question 40

Pulmonary artery hypertension (PAH)

Answer 40

Mean pulmonary artery pressure above 25 mm Hg Caused by left ventricular pressure, incr blood flow through the pulmonary circulation, obliteration or obstruction of the vascular bed, active constriction of the vascular bed produced by hypoxemia or acidosis Pathophys: overproduction of vasoconstrictors and decreased production of vasodilators, remodeling, resistance to pulmonary artery blood flow, thus increasing the pressure in the pulmonary arteries, workload of the right ventricle increases and subsequent right ventricular hypertrophy, may be followed by failure and eventually death

Question 41

Cor Pulmonale

Answer 41

Secondary to PAH, creates chornic pressure overload in the right ventricle Right ventricular enlargement