Riassunto esame Pneumologia, prof. Centanni, libro consigliato Pulmonary Infections and Pneumonia, Robbins

CLINICAL COURSE:

- Variable. Range between chest colds to severe upper resp tract infections

- Fever, headache, muscle aches, pains.

- Ventilation-perfusion mismatch can occur due to edema and exudation

- Usually mild, with low mortality (1%). Interstitial pneumonia can be more severe, give epidemics and have

greater mortality

- 2ndary infection by staph. And streptococci can occur.

INFLUENZA INFECTIONS

Influenza virus ss RNA, can be type A, Bor C.

Mucosal hyperemia (increased amount of blood flow) and swelling + lymphomonocytic and plasmacytic

infiltration + mucous secretions. Swollen mucosa can plug nasal channels.

enlargement of lymphoid tissue in Waldayer ring is frequent.

Impariment of mucociliary function secondary infections.

Plugging of airways may bring to atelectasis. Atelectasis (is defined as the collapse or closure of the lung resulting in reduced or

absent gas exchange .

HOSPITAL ACQUIRED PNEUMONIA

Pulmonary infections acquired in the course of an hospital stay. Common in pts qith severe underlying

diseases, immunesuppression, prolonged antiobiotic therapy, invasive access devices 8mechanical

ventilation).

G- rods (enterobacteriacee, and pseudomonas) and S.aureus are the most common.

ASPIRATION PNEUMONIA

In debilitated pts who aspirate gastric contents abnormal swallowing reflexes, unconsciousness or

vomiting.

Pneumonia is both chemical (irritative substances like gastic acid) and partly bacterial (oral flora).

More than one organism on culture.

Often necrotizing and fulminant clinical cause frequent cause of death. Lung abscesses are frequent in

survivors.

LUNG ABSCESSES

Pulmonary abscesses: “ local suppurative process within the lung with necrosis of lung tissue”

Any pathogen can produce abscesses but most commonly: S. Aureus and G- (or mixed infection in case of

aspriration). Anaerobic organisms found in oral cavity are exclusive isolates in 60 % of abscesses.

Mechanisms of pathogen entry:

- Aspiration of infective material(most frequent cause)

- Antecedent primary lung infection (S.aureus and K.pneumoniae)

- Septic embolism infecter emboli from venous circulation or bacterial endocarditis trapped in lung

- Neoplasia post obstructive pneumonia

- Miscellaneous

When no reasonable cause of abscess formation can be foundprimary cryptogenic lung abscesses.

MORPHOLOGY:

- Variable diameter (mm5-6cm)

- Single vs multiple

- Can affect any part of lung

- Abscesses due to aspiration are more common on the right (more vertical right bronchus). Often

single

- In couse of bronchiectasis and pneumonia multiple and basal

- Cavity may be filled with suppurative debris

- Superimposed saprophytic infection may occur

- Continuous infectionlarge cavities with poor demarcation of margins gangrene of the lung.

- Suppurative destruction of lung parenchyma within the central area of cavitation.

CLINICAL COURSE

Cough, fever, foul-smelling purulent sputum. Radiologic confirmation needed. Important: rule out carcinoma

because present in 10-15% of cases.

Complication: extension of infection to pleura, hemorrhage and development of brain abscesses or

meningitis.

CHRONIC PNEUMONIA

Often a localized lesion in immunocompetent subject inflammatory reaction is typically granulomatous.

[1]

Granuloma is a medical term for a tiny collection of immune cells known as macrophages. Granulomas form when the immune system attempts

. Granulomatous lesion can be caused by fungi

to wall off substances that it perceives as foreign but is unable to eliminate

(histoplasma), bacteria (M. tuberculosis).

histoplasmosis, blastomycosis and coccidiomycosis:

Fungal:

- Granulomatous, resembling tuberculosis

- Thermally dimorphic fungi (spore at ambient temperature and yeast at body temperature)

- Each fungus is in limited geographic areas.

TUBERCULOSIS:

M. Tuberculosisacid fast (will restain stains even on treatment with a mixture of acid and alcohol. It’s the

most frequent cause of tuberculosis. Reservoir is in infected humans.

Anti mycobacterial cell-mediated immunityconfers resistance to bacteria but also brings to hypersensitivity

to. Antigensmanifest with granulomas formation and cavitations (tissue destruction).

Macrophages are primary cell infected by M.tuberculosis:

- M. tuberculosis enters macrophages (endocytosis)

- Replication within phagosome by blocking its fusion with lysosome proliferation in alveolar macrophages.

- Bacteremia and diffusion can occur

- After 3 weeks activation of Th1 responsemacrophages become bactericidal. INF gamma production

- Macrophage differentiate into epitheliod histiocytes under INF effectgranulomas. (and form giant cells)

- TNF productionrecruitment of more monocytes. Caseation and cavitation

1mary TB ( in previously unexposed, unsensitized host) VS 2ndary TB (in previously sensitized host.

MORPHOLOGY:

- Typically in distal part of upper lobe of upper parto of lower lobe. Frequently next to pleura.

- As sensitization occurs gray-white inflammation areas (consolidations)gohn focus. In the center caseous

necrosis. [1]

Caseous necrosis is a form of cell death in which the tissue maintains a cheese-like appearance. The dead tissue appears as

When nodal involvement becomes caseous toogohn complex

a soft and white proteinaceous dead cell mass.