Pneumonia and Lung abscess - DONE Flashcards

1
Q

Pneumonia def:

A

is an infection of the pulmonary parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the classification of pneumonia?

A
  1. Community-acquired pneumonia (CAP)
  2. Health care-associated pneumonia (HCAP).
    Hospital-acquired pneumonia (HAP)
    Ventilator-associated pneumonia (VAP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CAP

A

Community-acquired pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

HCAP

A

Health care-associated pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

HAP

A

Hospital-acquired pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

VAP

A

Ventilator-associated pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What results in fever in pneumonia?

A

The release of inflammatory mediators, such as interleukin-1 and tumor necrosis factor, results in fever.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What stimulate the release of neutrophils and attracts them to the lung?

A

Chemokines, such as interleukin-8 and granulocyte colony-stimulating factor, stimulate the release of neutrophils and their attraction to the lung, producing both peripheral leukocytosis and increased purulent secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the capillary leak results in?

Community-acquired pneumonia

A

The capillary leak results in a radiographic infiltrate and rales detectable on ascultation, and hypoxemia results from alveolar filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes respiratory alkalosis?

Community-acquired pneumonia

A

Increased respiratory drive in the systemic inflammatory response syndrome leads to respiratory alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Classic pneumonia evolves through a series of pathologic changes:

A
  1. Edema
  2. Red hepatization (the presence of erythrocytes in the cellular intraalveolar exudate)
  3. Gray hepatization (no new erythrocytes, those already present are lysed and degraded)
  4. Resolution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Red hepatization?

A

the presence of erythrocytes in the cellular intraalveolar exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Gray hepatization?

A

no new erythrocytes, those already present are lysed and degraded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

TYPICAL community-acquired pneumonia:

A
  • Streptococcus pneumoniae (the most common)
  • Haemophilus influenzae
  • Staphylococcus aureus
  • Klebsiella pneumoniae
  • Pseudomonas aeruginosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the most common TYPICAL community-acquired pneumonia?

A

Streptococcus pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ATYPICAL community-acquired pneumonia:

A
  • Mycoplasma pneumoniae
  • Chlamydophila pneumoniae
  • Legionella species influenza viruses, adenoviruses, human metapneumovirus respiratory syncytial viruses
17
Q

What is the etiology of community-acquired pneumonia?

A
  • Anaerobes
  • The combination of unproductive pathway (patients with alcohol or drug overdose or a seizure disorder) and significant gingivitis constitutes the major risk factor
18
Q

Anaerobic pneumonias are often complicated by…….

A

abscess formation and by significant empyemas or parapneumonic effusions

19
Q

What are the clinical manifestation of community acquired pneumonia?

A
  • Tachycardia
  • Chills and/or sweats
  • Cough (maybe either nonproductive or productive of mucoid, purulent, or blood-tinged sputum)
  • Dyspnoea
  • Pleuritic chest pain

LESS COMMON

  • Gastrointestinal symptoms (nausea, vomiting, diarrhea)
  • Fatique, headache, myalgias, arthralgias
20
Q

community-acquired pneumonia - diagnosis:

A
  • Careful history
  • Chest radiography
  • Urinary antigen tests (detect pneumococcal and Legionella antigen in urine)
21
Q

Potential etiologic agents of VAP include……

A

both MDR (multidrug-resistant) and non-MDR bacterial pathogens

*The non-MDR group is nearly identical to the pathogens found in severe CAP (Community acquired pneumonia)
22
Q

What are the clinical manifestation of ventilatory associated pneumonia?

A
  • Fever
  • Leukocytosis
  • Increase in respiratory secretions
  • Pulmonary consolidation on physical examination
  • New or changing radiographic infiltrate
  • Tachypnea
  • Tachycardia
  • Worsening oxygenation
  • Increased minute ventilation
23
Q

Ventilator-associated pneumonia (VAP) - diagnosis:

A

Ventilator-associated pneumonia is usually suspected when the individual develops a new or progressive infiltrate on chest radiograph, leukocytosis, and purulent tracheobronchial secretions.

24
Q

Ventilator-associated pneumonia (VAP) - microbiologic diagnosis:

A
  • Blood and pleural fluid cultures.
  • Non-quantitative or semiquantitative airway sampling
  • Quantitative cultures of airway specimens
25
Q

When should VAP be concidered?

A

VAP should be considered with a CPIS score of >6, or alternatively, with a new pulmonary infiltrate and at least two of the following: fever, leukocytosis, and purulent secretions.

26
Q

Lung abscess:

A
  • Lung abscess represents necrosis and cavitation of the lung following microbial infection
  • Lung abscess can be single or multiple but usually are marked by a single dominant cavity > 2 cm in diameter
27
Q

Primary lung abscess:

A
  • ~80% of cases
  • usually arise from aspiration, are often caused principally by anaerobic bacteria, and occur in the absence of an underlying pulmonary or systemic condition
28
Q

Secondary lung abscess:

A
  • arise in the setting of an underlying condition, such as a postobstructive process (e.g. HIV infection or another immunocompromising condition)
29
Q

Lung abscess - epidemiology:

A
  • In addition, patients with esophageal dismotility or esophageal lesions (structures or tumors) and those with gastric distention and/or gastroesophageal reflux, especially those who spend substantial time in the recumbent position, are at risk for aspiration.
  • It is widely thought that colonization of the gingival crevices by anaerobic bacteria or microaerophilic streptococci (especially in patients with gingivitis and periodontal disease), combined with a risk of aspiration, is important in the development of lung abscesses
30
Q

What are the primary location of primary lung abscess?

A
  • posterior upper lobes

- superior lower lobes

31
Q

Which lung is mainly affected by primary lung abscess?

A

The right lung is affected more more commonly than the left (because the right mainstem bronchus is less angulated)

32
Q

The microbiology of primary lung abscess is….

A

often polymicrobial

  • primarily including anaerobic organisms
  • as well as aerophilic streptococci
33
Q

What is the location of secondary lung abscess?

A

The location of the abscess may vary with the underlying cause

34
Q

The microbiology of secondary lung abscess is….

A

The microbiology can encompass quite a broad spectrum, with infection by Pseudomonas aeruginosa and other gram-negative rods most common

35
Q

What are the primary symptoms of lung abscess?

A
  • cough (77%)
  • sputum (65%)
  • fever and chills (40%)
36
Q

What are the imaging diagnosis of lung abscess?

A
  • chest X-ray

- CT

37
Q

What is the treatment for primary lung abscesses:

A
  • Clindamycin or IV-administeredℬ-lactam/ℬ-lactamase combination
    • Treatment duration may range from 3-4 weeks to as long as 14 weeks
38
Q

What is the treatment for secondary lung abscesses:

A
  • antibiotic coverage should be directed at the identified pathogen, and prolonged course (until resolution of the abscess is documented) is often required.
  • Treatment regiments and courses vary widely, depending on the immune state of the host and the identified pathogen.