November 15 Review Quiz Flashcards

1
Q

Restrictive lung disorders cause a decrease in

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Tidal volume

A

500

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Total lung capacity

A

5-6 (Vital capacity+ reserve volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Inspiratory volume

A

2000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Expiratory volume

A

1200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Reserve volume

A

1200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Vital capacity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Exudative or inflammtory phase

A
Within 72 hours
Alveolocapillary membrane damage
Increased capillary membrane permeability
Pulmonary edema
Surfactant inactivated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Proliferative phase

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fibrotic phase

A
14-21 days
Remodeling and fibrosis
Alveoli destruction
Severe right-to-left shunting
Acute respiratory failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

FEV1 (forced expiratory volume within 1 second)/FVC

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Primary emphysema cause

A

Inherited deficiency of the enzyme α1-antitrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Secondary emphysema cause

A

Cigarette smoke: Main cause

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Centriacinar
 (Centrilobular)

A
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Panacinar (Panlobular)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acute cough

A

Resolves within 2-3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Chronic cough

A

Lasts longer than 3 weeks

18
Q

Kussmauls (hyperpnea)

A

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

19
Q

Cheyne-Stokes respirations

A

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)

20
Q

Hypoventilation leads to

A

Respiratory acidosis

21
Q

Hyperventilation leads to

A

Respiratory alkalosis

22
Q

Hypoventilation is caused by

A

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

23
Q

Hyperventilation is caused by

A

Anxiety, head injury, or severe hypoxemia

24
Q

Cyanosis develops when

A

desat of 5g/dL

25
Q

Acute respiratory failure

A

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

26
Q

Primary (spontaneous) pneumothorax

A

Occurs unexpectedly in healthy individuals

27
Q

Secondary pneumothorax

A

Is caused by disease, trauma, injury or condition

28
Q

Iatrogenic pneumothorax

A

Is caused by medical treatments, especially transthoracic needle aspiration

29
Q

Open pneumothorax

A

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

30
Q

Tension pneumothorax

A

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

31
Q

Transudative effusion

A

Watery and diffuses out of the capillaries

32
Q

Exudative effusion

A

Contains high concentrations of WBCs and plasma proteins

33
Q

Restrictive lung disorders

A
Aspiration
Atelectasis
Bronchiectasis
Pulmonary edema
Acute respiratory distress syndrome
34
Q

Obstructive pulmonary disease

A

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

35
Q

Asthma pathophys

A

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

36
Q

Ominous sign of impending death

A

PaCO2 grater than 70 mm Hg

37
Q

Chronic bronchitis

A

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

38
Q

Emphysema

A

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

39
Q

Virchow triad

A

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

40
Q

Pulmonary artery hypertension (PAH)

A

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

41
Q

Cor Pulmonale

A

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