Bod: Respiratory: Obstructive Lung Disease

Front 1

The four most common obstructive lung diseases.

Back 1

Chronic bronchitis
Emphysema
Mixed forms
Athsma ( --> COPD -- > bronchiectasis --> atelectasis)

Front 2

What is bronchiectasis?

Back 2

Dilation of airways.

Front 3

What receives the most damage in emphysema?

Back 3

Alveolar walls

Front 4

What is the definition of chronic bronchitis?

Back 4

The presence of a productive cough on most days for at least 3 consecutive months in each of two consecutive years.

Sputum production is worse in the morning.

Note that emphysema usually does not present with sputum production.

Hemoptysis can occur with chronic bronchitis, especially during "exacerbations". Emphysema, per se, does not cause hemoptysis.

Lung cancer should always be ruled out in a smoker with hemoptysis!

Chronic bronchitis is a clinical definition.

Front 5

Chronic bronchitis: gross pathology

Back 5

Reddend bronchial mucosa
Abundant secretions

Front 6

Chronic bronchitis: ciliary function

Back 6

Very impaired

Front 7

Pulmonary emphysema: definition, how different than chronic bronchitis?

Back 7

Enlargement of respiratory airways
Associated destruction and loss of tissue.

No loss of tissue in chronic bronchitis (more often hyperplasia)

Front 8

Pulmonary emphysema: Gross appearance

Back 8

Moth-eaten appearance. Large open spaces.

Front 9

Pulmonary emphysema: microscopic findings

Back 9

Enlargement of airspace
Loss of alveolar walls
Club shaped endings ("bulbous ends")
"Vanishing lung"

Front 10

What happens when an alveolar wall is broken down?

Back 10

They tend to coil and solidify and form bulbous ends (clubs)

Front 11

Pulmonary emphysema: etiology

Back 11

Cigarette smoking
Atmospheric pollution
Genetic changes

Front 12

Pulmonary emphysema: pathogensis

Back 12

Smokers have more neutrophils
Elastase levels increase
Smoking enhances elastolytic activity in macrophages

Front 13

Pulmonary emphysema: the tethering effect

Back 13

1. Material in lumen?
2. Abnormal thick mucous?
3. Smooth muscle contracted?
4. Abnormal tethering
5. Pulmonary pressures especially high?

Front 14

General attributes of the secondary lobule.

Back 14

Visceral pleura sends interlobar fibrous septae. Apex faces the inside of the lung. Can see with the naked eye.

Front 15

Empysema: types

Back 15

Centrilobular (most common)
Panlobular (primarily genetic? Rare)
Irregular
Bullous

Front 16

Panlobular

Back 16

Can be focal or widespread

Panlobular is associated with alpha-1-antitrypsin

Front 17

Centrilobular emphysema

Back 17

Affects center but may spread to periphery.
Usually worse in the upper lobes
Associated with cigarette smoking

Front 18

Centrilobular emphysema: gross pathology

Back 18

Orange with black spaces. Secondary lobule looks like Chrysler sign. Not always directly in center.

Front 19

Pleural blebs

Back 19

Can rupture and create respiratory compromise by pneumothorax.

Front 20

Bullous emphysema

Back 20

Cystic lesions 1.0 cm or greater
Not a true category
May occur in association with other types

Front 21

Bronchial athsma: definition

Back 21

Hyper-reactive airways
Episodic
Reversible bronchoconstriction

Front 22

Bronchial athsma: definition

Back 22

Paroxysmal narrowing of the small airways

Due to hyper-reactivity of the bronchial tree

Condition remits spontaneously with or without therapy.

Front 23

Bronical athsma: pathogenesis

Back 23

immflammation due to eosinophils
Trigger unknown
Hereditary

Front 24

Bronchial athsma: gross pathology

Back 24

Lungs are distended, may have small atelectic foci.
Small bronchi might be dilated and filled with vicous mucous plugs

large and voluminous lungs
Heart is obscured by the left lung
Lungs remain distended upon openin of the chest cavity

Front 25

Bronchial athsma: microscopic pathology

Back 25

Thickened basement membrane
Edema, inflammatory cells,
???
Hypertrophy of the mucous glands (similar to ch bron)
Narrowing of the lumen

Front 26

Curschmann's spirals and Charcot-Leyden crystals?

Back 26

May indicate bronchiolar athsma.

Front 27

Charcot-Leyden Crystal

Back 27

Stains red
May see in secretion in patients with athsma

Front 28

Bronchial athsma: death

Back 28

Status athsmaticus

Front 29

The term "COPD" encompasses a group of respiratory diseases whose most constant feature is what?

Back 29

Diffuse obstruction to airflow in the smaller peripheral airways, especially during expiration.

Front 30

What are the signs and symptoms of chronic bronchitis?

Back 30

- Chronic cough with expectoration (Thick yellow sputum)
- Recurrent respiratory infections (Worse during winter)
- Hypoxia (Manifested as cyanosis)
- Polycythemia (Increased RBC volume)

Front 31

What are three organisms that can cause chronic bronchitis?

Back 31

- Streptococcus pneumoniae
- Haemophilus influenza
- Branhamella catarrhalis

Front 32

What are the contributing factors to chronic bronchitis?

Back 32

- Smoking
- Air/environmental pollution
- Occupational dust exposure

Front 33

Micro pathology of chronic bronchitis?

Back 33

- Hyperplasia of mucus glands.
- Goblet cell metaplasia

- Chronic inflammation, congestion, edema
- Pus and mucus in lumen of bronchioles
- Squamous metaplasia with loss of cilia
- Distortion of bronchioles
- Destruction and loss of bronchioles

Front 34

What is the characteristic histologic feature of chronic bronchitis?

Back 34

Thickening of the mucous gland layer in the bronchial wall.

Front 35

What is the Reid index?

Back 35

A system used to evaluate the degree of mucous gland hypertrophy.

Ratio of the thickness of the mucous gland layer and the thickness of the entire bronchial wall

Normal Reid index = 33-40%
Abnormal Reid index = >50%

Front 36

Emphysema: Findings

Back 36

- Lungs are hyperinflated, bases flat.
- Bullae (especially in the upper lobes)
- Increased lung volume.
- Barrel chest
- PROLONGED EXPIRATORY PHASE
- Pursed lip breathing
- Use of accessory breathing muscles.
- Digital clubbing (only in severe cases)
- Pulmonary hypertension and cor pulmonale (RVF) may be seen.

Front 37

What is the fundamental histologic change associated with emphysema?

Back 37

The enlargement of airspaces and loss of alveolar walls.

Front 38

Emphysema: male or female predominance?

Back 38

Male predominance.

Front 39

Explain the proteolytic theory.

Back 39

An imbalance between elastases (from alveolar macrophages, polys) and their inhibitors (alpha-1-antitrypsin) leads to autodigestion of the lung.

Remember, cigarette smoking leads to increased levels of larger macrophages --> elastase activity up --> digestion of lungs.

Front 40

Minute ventilation = ?

Back 40

Tidal volume * respiratory rate

Front 41

What are some of the players involved in the increased work of breathing in patients with obstructive lung disease?

Back 41

increased airway resistance --> increased minute ventilation --> air trapping --> suboptimal muscle mechanics.

Front 42

What happens when a COPDer's accessory muscles get tired?

Back 42

This is when they go into full-blown respiratory failure. They become acidotic and they go from hypoxia to hypercapnea.

Front 43

What are the most common clinical findings in those with COPD?

Back 43

Chronic cough
Expectoration
Wheezing
SOB

Front 44

What is the 4th leading cause of death in the US?

Back 44

COPD

Front 45

Typical age of those with COPD seeking medical attention?

What about the breakdown of chronic bronchitis vs. emphysema?

Approximate number of cigarette-years to develop symptom?

Back 45

COPD = 50 - 70

Chronic bronchitis 50 - 60
Emphysema = 60 - 70

Approx 25 cigarette years

Front 46

Emphysema: PFTs

Back 46

- FEV1/FVC ratio decreases
- TLC may increase, and RV increases, so VC has to decrease.
- Diffusing capacity is decreased in emphysema, generally preserved in chronic bronchitis.

Front 47

Emphysema: progression of disease and ABGs

Back 47

Hypoxemia --> severe hypoxemia --> when the FEV1 is less than one liter, hypercapnea.

Front 48

What can happen to emphysema patients with bullae?

Back 48

The bullae can rupture, causing pneumothorax.

Front 49

What is the etiology of cor pulmonale?

Back 49

COPD --> hypoxia --> pulmonary arterial vasoconstriction --> pulmonary arterial pressure rises --> right heart has to work harder --> RV failure = cor pulmonale

Front 50

COPD: treatment

Back 50

- Bronchodilators (Beta2 agonists, anticholenergics, theophyline)
- Pts who respond well to bronchodilators usually also respond well to steroids.
- Expectorants have not been proven to help.

- Exacerbation treatment usually includes some form of ABX.

- Home oxygen

Front 51

Concerning presentation of someone having an athsma attack?

Back 51

Anxious, distressed appearance, accessory muscle use, diaphoresis, bolt upright in bed, pulsus paradoxis of greater than 10 mm Hg.

Front 52

Hypoxia during an athsma attack is due to?

Back 52

V/Q mismatch. Giving O2 does help. There may be some elements of a right-to-left shunt present as well.

Front 53

What can be an "impending sign of disaster" in an asthmatic patient?

Back 53

Having a normal pH, PaCO2 with a high A-a gradient while still hyperventilating.

Front 54

What is the challenge involved with athsma attack patients treated with steroids?

Back 54

Steroids take about 4-6 hrs to work. Treating patients in the interim is the challenge. Bronchodilators (beta2 agonists, anticholinergics)