Obstructive Diseases

Question 1

Emphysema

Answer 1

abnormal and permanent enlargement of the airspaces that are distal to the terminal bronchioles. This is accompanied by destruction of the airspace walls, without obvious fibrosis.

Question 2

Chronic bronchitis

Answer 2

chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough have been excluded.

Question 3

Bronchiectasis

Answer 3

shares many clinical features with COPD, including inflamed and easily collapsible airways and obstruction to airflow usually caused by infection. (CF)

Question 4

COPD

Answer 4

Slow, progressive irreversible airway obstruction due to chronic bronchitis and/ or emphysema
Increased dyspnea
Increased sputum (usually colorless)
Occasionally respiratory failure

Question 5

Emphysema (pink puffers)‏

Answer 5

Abnormal enlargement of the airspaces distal to the terminal bronchioles, with destruction of the alveolar walls and capillary beds
Abnormal airspaces called Bullae compress surrounding area of more normal lung
Loss of lung elasticity
pursed lip breathing

Question 6

Chronic Bronchitis (blue bloaters)

Answer 6

Defined as a persistent cough resulting in sputum production for more than 3 months in each of the past 2 years.
Goblet cell hyperplasia
Mucus plugging, excess mucus secretion
Fibrosis
Have mismatch of VQ so get more hypoxic and cyanotic, can’t over compensate with their breathing like the pink puffers

Question 7

ha-1 Antitrypsin Deficiency

Answer 7

Congenital

Should be considered in younger patients who show signs of emphysema, whether they have smoked or not.

Question 8

What is Alpha-1 Antitrypsin?

Answer 8

alpha1-antiprotease serves as a protective screen that prevents alveolar wall destruction.
Individuals with the AAT genetic defect do not release alpha1-antiprotease from the liver, and serum and alveolar levels of the protein are low. Consequently, alveoli lack antiprotease protection.

Question 9

COPD Physical signs:

Answer 9

Increased AP chest diameter (barrel chest)‏
Use of accessory muscles to breathe
Peripheral cyanosis
Clubbing of the fingernails (sign of hypoxia)‏
Decreased breath sounds
Hyperresonance on percussion
Wheezing on expiration
Prolonged expiratory phase
Low, flat diaphragm

Question 10

COPD CXR findings

Answer 10

Hyperinflation
Flattening of the diaphragm
Increased retrosternal air space
Long narrow heart shadow

Question 11

Patients with the following should have long term continuous oxygen therapy:

Answer 11

O2 sat < 90%
Decreases risk of:
Right sided heart failure
Polycythemia
Impaired mental status