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Lung Clin Med > Tyler Clin Med > Flashcards

Tyler Clin Med Flashcards

1
Q

Typical Community acquired pneumonia NOT associated with co morbidity

A

i. Strep pneumo

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2
Q

Atypical Community acquired pneumonia NOT associated with co morbidity

A
  1. Chlamydophila pneumonia
  2. C. psittaci
  3. Legionella
  4. M. Pneumo
  5. Coxiella
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3
Q

CAP CAUSE in individual with alcoholism comorbidity

A
  1. Strep pneumo
  2. oral anaerobes
  3. klebsiella
  4. acinetobacter
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4
Q

CAP source with COPD comorbidity

A
  1. S. pneumo
  2. Moraxella Catarrhalis
  3. H. flu
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5
Q

CAP source post CVA aspiration

A
  1. Oral flora

2. S. pneumo

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6
Q

Post Bronchi obstruction CAP cause

A

Anaerobe

strep pneumo

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7
Q

CAP from post flu

A
  1. Strep Pneumo

2. Staph aureus

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8
Q

CAP in someone with neutropenia or immunocompromised

A

Pseudomonnas

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9
Q

Community acquired pneumonia from injection drug use

A

staph aureaus

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10
Q

How do you determine Community acquired pneumonia tx?

A

History and comorbidities

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11
Q

How is community acquired pneumonia treated in hospital setting? (not in ICU)

A

if not in ICU receive IV ceftriaxone 1 gm daily with 500 mg of azithromycin 500 mg daily

-levofloxacin can also be used

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12
Q

What abx is starting to see resistance patterns?

A

azithromycin

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13
Q

Treatment considerations for ventilator acquired pneumonia are the same as?

A

Hospital acquired pneumonia

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14
Q

What patients are at risk for multi drug resistant pneumonia?

A

Hospital acquired pneumonia and ventilator acquired pneumonia

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15
Q

When is a thoracocentesis indicated for pleural effusion

A

all effusions that have more than 1 cm layering in the decubitus view

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16
Q

How do you treat pleural effusion related to Heart failure?

A
  1. try diuretics

2. Do thoracentesis if effusions are asymmetrical, fever, chest pain, or effusion doesn’t resolve

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17
Q

How do you treat pleural effusion related to infections?

A

Thoracentesis ASAP

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18
Q

What is Light’s Criteria used for?

A

Transudative vs Exudative source of effusion

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19
Q

Exudates fulfill at least 1 of which 3 criteria in lights criteria?

A
  1. High pleural fluid protein/serum protein ratio
  2. Pleural fluid LDH greater than 2/3 upper limit of normal
  3. Pleural/serum LDH ratio >0.6
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20
Q

What are the transudate criteria?

A

They DO NOT HAVE ANY OF THESES

  1. High pleural fluid/serum protein ratio (greater than .5)
  2. Pleural fluid LDH greater than 2/3 upper limit of normal
  3. Pleural/serum LDH ratio >0.6

because of this ~25% transudates are diagnosed as exudates

21
Q

What lab tests should you do for an exudative effusion?

A
  1. pH
  2. glucose
  3. white blood cell count with Dif
  4. microbiologic studies
  5. cytology
22
Q

Acute respiratory distress syndrome develops rapidly and patient will present with …? (3)

A
  1. Severe Dyspnea
  2. Diffuse pulmonary infiltrate
  3. hypoxemia
23
Q

What are the key diagnostic criteria for ARDs?

A
  1. Diffuse bilateral pulmonary infiltrate on CXR
  2. PaO2/FiO2 <300 mmHg
  3. Absence of elevated left atrial pressure
  4. Acute onset within 1 week of clinical insult or new or worsening respiratory sx (respiratory failure within 7 days)

PaO2= arterial partial pressure of oxygen in mmHg

FiO2= inspired O2 fraction

24
Q

What would you see in the clinical case and pathophysiology of ARDs?

A
  1. Alveolar edema and neutrophil inflammation
  2. hyaline membrane development from diffuse alveolar damage
  3. Alveolar edema causes atelectasis and reduced lung compliance
  4. Hypoxemia, tachypnea, progressive dyspnea, hypercarbia ( from loss of alveolar exchange)
  5. CXR shows bilateral lung opacities
25
Q

What are the phases of ARDS?

A
  1. Proliferative phase –> day 7-21, could recover or
    - develop progressive lung injury
    - evidence of pulmonary fibrosis
    - often have dyspnea and hypoxemia
  2. Fibrotic phase –> set up for chronic respiratory failure
    • decreased lung compliance, greater pneumothorax risk
26
Q

What can produce or exacerbate lung injury causing or worsening ARDs?

A

mechanical ventilator-related over distention of normal lung units with positive pressure

27
Q

How is alveolar collapse in ARDs on a ventilator prevented?

A
  • low tidal volumes with positive end-expiratory pressure (PEEP) at levels to minimize alveolar collapse
  • lowers required FiO2 used to achieve adequate oxygenation
  • place patient in prone position
28
Q

What can increased pulmonary vascular permeability in ARDs lead to?

A

interstitial and alveolar edema

29
Q

When should ARDs patients receive fluids?

A

Only as needed to achieve adequate cardiac output and tissue O2 delivery

30
Q

What could potentially reduce the mortality in severe ARDs?

A
  • neuromuscular blockage with cisatracurium for 48 hrs

- Most patients will REQUIRE sedation and paralytic agens

31
Q

What should NOT be given and has no clinical evidence to treat ARDs?

A
  • glucocorticoids

- nitric oxide

32
Q

What is the tx of influenza? How soon should they be started?

A
  1. Neuraminidase inhibitors- limit virus escaping host cell

- give within 48 hours for symptoms stopping 1-2 days sooner

33
Q
  1. prior isolation on culture
  2. Recent hospitalization and receptor of parental abx

are risk for what 2 organisms?

A

MRSA and Pseudommnas

34
Q
  1. Compromised immune system
  2. Recent prior antibiotic use
  3. Structural lung abnormalities such as cystic fibrosis or bronchiectasis
  4. Repeated exacerbations of chronic obstructive pulmonary disease requiring frequent glucocorticoid and/or antibiotic
    use

are risk factors for what?

A

Pseudomonas with CAP

35
Q

What is risk for pseudomonas in Hospital acquired pneumonia

A
  1. Increased age, length of mechanical ventilation, antibiotics at admission, transfer from a medical unit or ICU, and admission in a ward with higher incidence of patients with P. aeruginosa infections.
  2. A lower probability of P. aeruginosa was associated with trauma and admission in a ward with high patient turnover
36
Q

Hospital acquired pneumonia and ventilator acquired pneumonia have risk for what?

A
  1. Increased mortality
  2. MDR pathogens and MRSA
  3. MDR pathogens without MRSA
  4. MRSA alone
37
Q

What is MDR

A

nonsusceptibility to at least one agent in three different antimicrobial classes.

38
Q

What is Extensivly drug resistant?

A

nonsusceptibility to at least one agent in all but two antimicrobial classes.

39
Q

What is pan drug resistant?

A

nonsusceptibility to all antimicrobial agents that can be used for treatment.

40
Q
  • Difficult to wean from the ventilator
  • Persistent lack of improvement overall
  • New infiltrates on chest x-ray
  • Newf evers
  • New changes in baseline data:CBC,CMP,etc.

Are clues to what?

A

Ventilator associated pneumonia

41
Q

Early onset VAP and HAP (less than 5 days in hospital) with no other risk factors for MDR organism is likely what?

A
  1. Step pneumonia
  2. H. flu
  3. Enteric gram neg bacilli
42
Q

Late onset HAP or VAP with more than 5 days in hospital is likely caused by what?

A
  1. Staph aureus or ESKAPE

(E. coli, serrate, klebsiella, actinetobacter, pseudomonas, enterobacter

43
Q

-Cefepime
-piperacillin-tazobactam
-meropenem or ertapenem
-levofloxin
should be used when?

A

Ventilator associated pneumonia with low risk of MRSA and no risk of MDR

44
Q
  • Cefepime
  • piperacillin-tazobactam
  • meropenem
  • levofloxin

+VANCOMYCIN
should be used when?

A

suspected MRSA

45
Q

When should vancomycin be used?

A

MRSA/MDR risk, sepsis, hypotension, rapid progression of infiltrates on chest radiograph

46
Q

Vancomycin + levofloxacin or azithromycin should be used when?

A

Leginella suspected

47
Q

Ciprofloxacin or levofloxacin + vancomycin should be used to treat what?

A

Pseudomonas

48
Q

What can be substituted for vancomycin?

A

linezolid

49
Q
  1. Alveolar edema and neutrophil inflammation
  2. hyaline membrane development from diffuse alveolar damage
  3. Alveolar edema causes atelectasis and reduced lung compliance
  4. Hypoxemia, tachypnea, progressive dyspnea, hypercarbia ( from loss of alveolar exchange)
  5. CXR shows bilateral lung opacities

is what?

A

Pathophysiology of ARDs

Lung Clin Med (6 decks)

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