Respiratory Pathology

Front 1

Describe the physical defense mechanisms of the lung.

Back 1

Filtering systems - vibrissae.

Reflexes - sneezing and coughing in the upper airway.

Mucociliary clearance - protects the conducting airways. Particles are trapped in mucus and moved upward by ciliary action and at the level of the oropharynx are either swallowed or expectorated.

Front 2

Describe the cellular defenses of the lung.

Back 2

Alveolar Machrophages - phagocytose particles and...
1. are carred to the oropharynx by ciliated cells.
2. leaves alveolar airspace, enters lymphatics to regional lymph nodes and enters blood stream.

Neutrophils function in less important role.

Lymphocytes comprise bronchus associated lymphid tissue (BALT) and lymph nodes in airspace and interstitium.

Front 3

Where are the antibodies located in the lung?

Back 3

IgA - predominates the conducting airways.

IgG - predominates in distal spaces.

Front 4

How does a respiratory viral infection predispose an individual to bacterial pneumonia?

Back 4

The virus damages the mucosa resulting in metaplasia of the epithelium with loss of cilia and inhibiting mucociliary clearance.

Front 5

The Pneumonia classes are classified on:

Back 5

1. Etiologic Agent (Most Important)

2. Type of host reaction to injury.

3. Morphologic pattern of infection.

Front 6

Morphological Pattern of Infection: Bronchopneumonia

Back 6

Shows acute inflammation with neurophils in the alveolar air space.

Starts in bronchi or bronchioles and spreads to alveoli.

Limited to patches within lobes.

Can overlap with Lobar pneumonia.

Spread through airways.

Front 7

Morphological Pattern of Infection: Lobar Pneumonia

Back 7

Shows acute inflammation with neurophils in the alveolar air space.

Starts in distal air spaces without a preceding bronchial colonization.

Spreads quickly through pore of Kohn to involve the entire lobe.

Fibrous tissue can fill the alveoli and bacteremia can develop.

Front 8

Describe Interstitial Pneumonia

Back 8

From viral and mycoplasma pneumona.

Inflammatory change confined to the alveolar septa.

Inclusion bodies in alveolar epithelial cells.

Chronic inflammatory cells (lymph and monocytes) enter and edema occurs in the alveoli.

Proteinaceous fluid may leak into the space.

Front 9

Complication of Interstitial Pneumonia

Back 9

Secondary Bacterial Pneumonia

Hematogenous spread (rare)

Front 10

Most Common Cause of Granulomatous Pneumonia

Back 10

Mycobacterium Tuberculosis.

Primary Infection - granulomas with caesous necrosis form.

Secondary Infection - reactivation of latent mycobacteria.

Front 11

Discuss ARDS

Back 11

Adult Respiratory Distress Syndrome (ARDS)

It is the final pathway to diffuse damage to the alveolar capillary walls.

Rapid onset and can result in respiratory insufficiency, cyanosis and severe hypoxia.

Front 12

Mechanism of ARDS

Back 12

An initiating event of damage to the lung and to the pneumocytes or capillary endothelium.

Fluid leaks into the interstitium and separate capillaries from the close associationo with type 1 pneumocytes.

Fluid (plasma) leaks into the alveolar space. Cell debris and fibrin covers the inner surface of the alveolus and makes a thick hyaline membrane.

Death in 50-70% of cases.

Type 1 cells cannot regenerate, fibrosis occurs.

Type 2 cells regenerate.

Front 13

Two Obstructive Lung Diseases

Back 13

1. Asthma

2. Chronic Obstructive Pulmonary Disease

Front 14

Describe the mechanisms, characteristics and microscopic changes in asthma.

Back 14

Asthma is characterized by hyper-reactive airways, reversible bronchospasms, and mucus plugs.

The plugs contain numerous esinophils and sloughed off epithelia cells.

The bronchial walls have edema and eosinophil infiltrate, increased submucosal glands and hypertrophy of muscle to do prolonged bronchoconstriction.

Front 15

Describe Extrinsic Asthma

Back 15

Type 1 Hypersensitivity Reaction due to environmental antigens.

IgE and eosinophils are elevated.

Positive family history of atopy.

Front 16

Describe Intrinsic Asthma

Back 16

idiosyncratic, non-immune mechanism.

Often viral in pathogenesis.

The inflammation of the respiratory mucosa lowers the threshold of the subepithelia vagal receptors to irritants.