Respiratory Pathology - Obstructive And Asthmatic

Front 1

Lining of a normal bronchus

Back 1

Pseudostratified columnar epithelium

Front 2

Abnormalities of alveoli

Back 2

1. Visible endothelial cells
2. More than one layer of RBCs
3. Expansion of walls
4. Loss of room architecture
5. Visible alveolar cells
6. Anything in the lumens

Front 3

Defense mechanisms of the lung

Back 3

1. Brain
2. Free flowing body fluids
3. Mucociliary elevator
4. Phagocytosis (activation of neutrophils and macrophages, is of course, by itself a problem)
5. Immune system
6. Neurologic

Front 4

Effect of a tracheoesophageal fistula and esophageal origin of bronchus

Back 4

Cyanosis when feeding

Front 5

Bronchopulmonary sequestration

Back 5

Lobes/segments lacking normal communication with bronchial tree (abnormal vasculature is common).
2 types - extralobar and intralobar.

Front 6

Extralobar bronchopulmonary sequestration (has its own pleura because it is external to the lung)

Back 6

Congenital anomaly-diaphragmatic defect, pectus excavatum, and vascular malformations. Presents at less than 6 mos, M:F is 4:1.

Front 7

Intralobar bronchopulmonary sequestration)

Back 7

Acquired by repeated pneumonias, anyone can get it, 50% are over the ag of 20. Usually fed by systemic arterial system but dump into the pulmonary veins. 10% can have associated anomalies.

Front 8

Problems with bronchopulmonary sequestration

Back 8

1. Pneumonia/cough
2. Hypoplasia of other lung
3. Compression of normal lung
4. Abnormal x-ray
5. Cyanosis, feeding difficulty.

Front 9

Bronchogenic cysts

Back 9

Extra buds of the foregut during development.

Front 10

Problem with bronchogenic cysts

Back 10

1. Infxn
2. Rupture
3. Compression of normal lung

Front 11

Bronchial atresia

Back 11

Abnormal closure or absence of a bronchus. Causes overinflation of adjacent area. Can cause recurrent pneumonia, common in left upper lobe.

Front 12

Effects of vascular pulmonary malformations

Back 12

Dilated blood vessels due to abnormal communication. Causes cyanosis, dyspnea, failure of normal lung development, hemoptysis, hemothorax.

Front 13

Osler-Weber-Rendu syndrome

Back 13

Hereditary hemorrhagic telangiectasia. AD, many mucosal abnormal vascular connections

Front 14

Septal deviation

Back 14

Nasal blockage that can lead to infection. Congenital or acquired.

Front 15

Uncomplicated obstructive lung disease: definition

Back 15

Lung is enlarged and rate of airflow is reduced.

Front 16

Histology of emphysema

Back 16

Expanded alveoli, loss of rooms, thickened pink (hyaline) walls, and decreased vasculature.

Front 17

2 patterns of obstructive disease

Back 17

1. Hyperinflation
2. Focal alectasis with adjacent compensatory hyperinflation.

Front 18

Emphysema

Back 18

Abnormal, permanent enlargement of airspaces (alveoli) where the alveolar walls are destroyed but not fibrotic.

Front 19

Normal behavior of alveoli and bronchioles in relation to air flow

Back 19

1. Elastic network and chest pressure collapse alveoli uniformly on beginning of exhalation.
2. Due to shared walls the collapse opens bronchioles, allowing all air to escape.

Front 20

Abnormal (emphysema) behavior of alveoli and bronchioles in relation to air flow

Back 20

1. Lack of alveolar elasticity means they do not close uniformly.
2. Open alveoli crush the bronchioles closed as the chest compresses
3. Air does not escape from either the damaged portion or adjacent normal alveoli

Front 21

Is the amount of air in the lungs after expiration increased or decreased in uncomplicated emphysema?

Back 21

Increased.

Front 22

Five types of emphysema

Back 22

1. Centracinar: upper lobes, heavy smokers, chronic bronchitis
2. Panacinar: alpha-1-antitrypsin deficiency
3. Paraseptal (bullous): near pleura, causing fibrosis and pneumothorax
4. Irregular: caused by scarring
5. Interstitial: trauma, obstruction, ventilation

Front 23

How does smoking contribute to emphysema?

Back 23

1. Tobacco promotes formation of reactive oxygen species, which themselves damage tissue and recruit neutrophils via IL-8, LTB4, and TNF
2. The radicals inactivate alpha-1-antitrypsin, such that neutrophilic products are not broken down
3. The high levels of neutrophilic elastase damage tissue
4. Alveolar macrophages attempting to clear damaged tissue and foreign objects will make more elastase and metalloproteinases (remodeling proteins) that contribute to alveolar disfunction.

Front 24

What is the key ratio to consider when talking about emphysemal damage?

Back 24

The protease (elastase)-antiprotease (alpha-1-antitrypsin) ratio. Not enough antiproteases allow inflammatory proteases to continually damage tissue.

Front 25

What will the alveoli look like on gross examination of emphysema?

Back 25

Dilated. The larger the dilation, the greater the loss of surface area for gas exchange (think of how many folds there are in a deflated balloon, and then the tension in an inflated one)

Front 26

Microscopic hallmark of emphysema

Back 26

Enlarged alveolar spaces lined by slightly thickened alveolar walls with thin fibrosis and relative avascularity. INFOLDING WILL BE LOST, AND SO WILL SURFACE AREA.

Front 27

Hyperinflation

Back 27

Dilated alveoli with thin walls and NO FIBROSIS due to loss of intrinsic elasticity.

Front 28

Compensatory hyperinflation

Back 28

Caused by focal atelectasis (collapse) so that other portions must hyperinflate to compensate.

Front 29

Obstructive hyperinflation

Back 29

When the gas cannot leave. It can be congenital, there can be a blockage in the lumen, etc.

Front 30

How can you tell the difference between emphysema and hyperinflation?

Back 30

Hyperinflation does not involve an inflammatory, fibrotic process. The walls just lose their stretch, not their basic structure.

Front 31

Is there a pathologic definition for chronic bronchitis?

Back 31

No, it is clinical.

Front 32

Clinical definition of chronic bronchitis

Back 32

Persistent productive cough for at least three months in at least two years.

Front 33

How is chronic bronchitis different from emphysema?

Back 33

For one, the lung involvement is widespread and almost immediate. Chronic bronchitis is also the compensatory response against irritation, IT IS NOT A CAUSE.

Front 34

What is the disease process in chronic bronchitis?

Back 34

Resistance to airflow due to clogged bronchial tree either by inflammatory corrosion or by mechanical obstruction. Work of breathing must increase to maintain normal rate.

Front 35

Gross appearances of bronchitis

Back 35

1. Change in mucosal color
2. Mucus plugs, mucus!!
3. Thickened, narrowed lumens.

Front 36

Microscopic appearance of bronchitis

Back 36

1. Curschmann spiral: mucus shape cast in the shape of lumen .
2. Increase in size and number of mucous glands.
3. Increased goblet cells.
4. Decreased serous glands

Front 37

Etiology of bronchitis

Back 37

1. Chronic irritation
2. Infection: does NOT CAUSE, but can aggravate.

Front 38

Sequelae of chronic bronchitis

Back 38

1. COPD (when you add emphysema to the mix)
2. Cor pulmonale/cyanosis
3. Carcinoma (if smoking is a cause)
4. Bronchiectasis
5. COP
6. Fistulas
7. Chronic infection

Front 39

Bronchiestasis: definition

Back 39

Permanent abnormal dilatation of the bronchial tree. You should not be able to see bronchi close to the pleural surface. If you can, then you have this condition.

Front 40

3 types of bronchiectasis

Back 40

1. Saccular
2. Varicose
3. Cylindrical

Front 41

Clinical appearance of bronchiectasis

Back 41

Paroxysms of coughing, copious nasty pus-y sputum, hemoptysis, dyspnea.

Front 42

Etiology of bronchiectasis

Back 42

Bottom line: obstruction and infection.

Front 43

Sequelae of bronchiectasis

Back 43

1. Obstruction (bronchi are too wide!)
2. Fistulas/pleurisy
3. Cor pulmonale
4. Metastases
5. Amyloidosis
6. COPD
7. Chronic infection

Front 44

Types of asthma

Back 44

1. Atopic: don't forget aspergillus
2. Nonatopic (asthmatic bronchitis)
3. Drug-induced
4. Occupational

Front 45

Pulmonary hypoplasia

Back 45

defective development of both lungs (one may be more affected than the other) resulting in decreased weight, volume, and acini

Front 46

Foregut cysts

Back 46

abnormal detachment of primitive foregut and are most often located in the hilum or middle mediastinum

Front 47

How do you repair foregut cysts?

Back 47

Surgical resection is curative.

Front 48

Pulmonary sequestration

Back 48

a discrete mass of lung tissue without any normal connection to the airway system

Front 49

Atelectasis

Back 49

incomplete expansion of the lungs (neonatal atelectasis) or to the collapse of previously inflated lung
3 types: resorption (or obstruction), compression, and contraction atelectasis

Front 50

Resorption atelectasis

Back 50

1. consequence of complete obstruction of an airway,
2. mediastinum shifts toward the atelectatic lung
3. caused principally by excessive secretions

Front 51

Compression atelectasis

Back 51

1. Something in the pleural cavity compresses the lung
2. Can be due to pneumothorax
3.most commonly encountered in patients with cardiac failure
4. Mediastinum shifts away from atelectic lung

Front 52

Contraction atelectasis

Back 52

local or generalized fibrotic changes prevent full expansion of the lung

Front 53

Is atelectasis reversible?

Back 53

Yes. Bronchiectasis is not.

Front 54

Cytokine mediators of acute lung injury

Back 54

tumor necrosis factor (TNF), interleukin (IL)-1, IL-6, IL-10, and transforming growth factor (TGF)-β

Front 55

Progression of acute lung injury

Back 55

acute respiratory distress syndrome or acute interstitial pneumonia

Front 56

Examples of hemodynamic edema

Back 56

Left-sided heart failure, increased hydrostatic pressure, pulmonary vein obstruction

Front 57

The major diffuse obstructive disorders

Back 57

emphysema, chronic bronchitis, hyperinflation, bronchiectasis, and asthma

Front 58

Two major causes of obstructive lung disorders and their related diseases

Back 58

1. Narrowing of the airway (asthma)
2. Loss of alveolar elasticity (emphysema)

Front 59

COPD

Back 59

Emphysema w/chronic bronchitis

Front 60

Major difference between centroacinar and panacinar emphysemal changes.

Back 60

Front 61

Associated causes of panacinar emphysema

Back 61

Alpha-1-antitrypsin deficiency

Front 62

Pathogenesis of emphysema (image)

Back 62

Front 63

Classic presentation of emphysema

Back 63

Classically, the patient is barrel-chested and dyspneic, with obviously prolonged expiration, sits forward in a hunched-over position, and breathes through pursed lips

Front 64

How do you diagnose emphysema?

Back 64

Expiratory airflow limitation, best measured through spirometry, is the key to diagnosis.

Front 65

Blue bloaters vs. pink puffers

Back 65

Chronic bronchitis vs. emphysema

Front 66

Histologic study of the airways in chronic bronchitis reveals

Back 66

(1) goblet cell metaplasia with mucus plugging of the lumen, (2) clustering of pigmented alveolar macrophages, (3) inflammatory infiltration, and (4) fibrosis of the bronchiolar wall

Front 67

the ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and the cartilage

Back 67

The Reid Index, increased in chronic bronchitis.

Front 68

Proposed mechanistic malfunction in asthma

Back 68

The inhibitory interferon-gamma from TH1 cells fails to stop overproduction of TH2, which in turn continue the asthmatic formation of reactive memory cells.

Front 69

A busy pictorial representation of atopic asthma

Back 69

Front 70

Major chemokines implicated in causality of asthma

Back 70

(1) leukotrienes C4, D4, and E4
(2) acetylcholine
Minor:
(1) histamine
(2) prostaglandin D2

Front 71

primary ciliary dyskinesia

Back 71

poorly functioning cilia contribute to the retention of secretions and recurrent infections that in turn lead to bronchiectasis

Front 72

Kartagener syndrome

Back 72

bronchiectasis, sinusitis, and situs inversus or partial lateralizing abnormality

Front 73

Usual flora cultured from bronchiectasis

Back 73

Haemophilus influenzae and Pseudomonas aeruginosa specifically, and then a whole mix of everyone else.