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Flashcards in Pneumonia and flu Deck (32):
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1. Definition and Features of Pneumonia (PNA)

A disease of the lungs that is characterized by inflammation of the parenchyma of the lung (alveolar wall) and accumulation of abnormal alveolar filling with fluid of lung tissue. Most commonly caused by infection

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Describe lung protective defenses

Lower airways usually remain organism-free due to pulmonary host defense mechanisms: Innate (Nonspecific) and Acquired (Specific).
Lower airways usually remain organism-free due to pulmonary host defense mechanisms: Innate (Nonspecific) and Acquired (Specific).

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2. Pneumonia Pathogenesis

Pneumonia is caused by: Inhalation of infectious particles, Inhalation of oropharngeal or gastric contents, Hematogenous spread, Infection from adjacent or contiguous structures, Direct inoculation or Reactivation. Pneumonia occurs when hosts ability to fight pathogens is compromised
Pneumonia is caused by: Inhalation of infectious particles, Inhalation of oropharngeal or gastric contents, Hematogenous spread, Infection from adjacent or contiguous structures, Direct inoculation or Reactivation. Pneumonia occurs when hosts ability to fight pathogens is compromised

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Clinical presentation of pneumonia

fever, chills, pleuritic chest pain, dyspnea and cough that can be productive of sputum (bacterial infections) or with minimal sputum (atypical vs viral).

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pneumonia physical exam

Fever, tachypnea, tachycardia, hypoxia, cyanosis. Lungs have crackles, rhonchi, bronchial breath sounds, egophony, dullness to percussion

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Basic Tests for all patients with suspected pneumonia pneumonia

CXR, CBC, CMP (complete metabolic profile), blood gas or pulse oximetry

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CXR results in pneumonia

NOT sufficient to pneumonia, but helps. Lobar consolidation, interstitial infiltrates and cavitation

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What can fill alveoli?

mnemonic: poor funny boy cant piss for crap: Pus, fluid, blood, cells/cancer, protein, fat, calcium

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CXR pattern and possible pathogens

Focal/ large pleural effusion: bacteria. Cavitary: bacterial abscess, fungi, acid-fast bacilli. Miliary: acid-fast bacilli, fungi. Rapid progression/ multifocal: Legionella spp, pneumococcus, staphylococcus. Interstitial: viruses, pneumocystis, mycoplasma, chlamydia. Mediastinal widening without infiltrate: inhalation anthrax

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3. Pneumonia Classifications or Types

Community Acquired Pneumonia (CAP), Hospital (Nosocomial) Acquired Pneumonia (HAP), Ventilator Associated Pneumonia (VAP), Healthcare-Associated Pneumonia (HCAP)

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Community acquired pneumonia description

Begins Outside the Hospital . Diagnosed < 48 Hrs after Hospital Admission . Patient is not a resident in a long-term facility for > 14 days or more before the onset of symptoms

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Most common causes of CAP

Bacteria: strep pneumonia, H. Influenza, M. Catarrhalis, Staph aureus, Group A strep. Less common: legionella, Mycoplasma, chlamydia

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CAP treatment

Outpatient: Macrolide or Doxycyline (60 rs or comorbid dsease). Inpatient ICU: Beta-lactam + Macrolide, Beta-lactam + Respiratory Fluoroquinolone. Inpatient non-ICU: Respiratory Fluoroquinolone , Beta-lactam + Macrolide

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Definitions of HAP, VAP and HCAP

HAP: PNA>48hrs after hospital admission. VAP: PNA > 48 - 72 Hrs after Endotracheal Tube Intubation. HCAP: PNA in a non-hospitalized patient with extensive healthcare contact (hospitalization within 90 days of infection, long term care facility,
HAP: PNA>48hrs after hospital admission. VAP: PNA > 48 - 72 Hrs after Endotracheal Tube Intubation. HCAP: PNA in a non-hospitalized patient with extensive healthcare contact (hospitalization within 90 days of infection, long term care facility,

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What is unique about HAP, VAP and HCAP organisms

•Infections are Frequently Polymicrobial in Origin and tend to be multi-drug resistant. Organisms that colonize oropharynx enter lower respiratory tract by micro/macro aspiration

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HAP, VAP and HCAP common pathogens

gram negative (SPACE): Serratia, Pseudomonas, Acinetobacter, Citrobacter, Enterobacter or Escherichia coli. Gram positive: Methicillin-Resistant Staphylococcus Aureus - MRSA

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HAP, VAP and HCAP treatment

For drug resistant strains: Antipseudomonal Agent: Cephalosporin or Carbopene.
Plus 1 of the Following: Anti-pseudomonal Fluoroquinolone or Anti-Gram Negative Aminoglycoside. Plus 1 Anti-MRSA Medication: Linezolid or Vancomycin

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4. Differential diagnosis of PNA

Airway diseases: Organizing pneumonia, Allergic Bronchopulmonary Aspergillosus (ABPA), Bronchiectasis
, Bronchopulmonary sequestration, Bronchocentric granulomatosis. Vascular disease: eosinophilic lung disease, fat emboli, vasculitis, vascular tumors. Parenchymal diseases: drug rxn, granulomatous lung disease, pulmonary edema, neoplasm, ARDS, idiopathic interstitial pneumonia.

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6. Basics of PNA Treatment

Determine severity of disease (pneumonia severity index), do further testing if severely ill or immunocompromised, or inpatient/ deteriorating

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Pneumonia severity index and mortality

class 1- 0.1% mortality. Class II: 0.6%. Class III: 2.8%. Class IV: 8.2%. Class V: 29.2%

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Which pneumonia severity classes require admission?

class IV and V

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Further testing for severely ill or immunocompromised with suspected pneumoni

Sputum gram stain/culture, blood culutre, urinary Ag testing

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Further inpatient testing

HIV serology, mycoplasma serology, chlamydia serology, fungal serology, test for TB, gram stains.

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Further testing for deteriorating patient despite therapy for pneumonia

Bronchoscopy, biopsy, bacterial serology, fungal serology, evaluate for CHF, pulm embolism, neoplasm, CT disease

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Treatment of pneumonia in patients who are not severely ill and with few risk factors

Broad spectrum empiric antibiotic therapy

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List major viral groups that cause respiratory infections

Orthomyxovirus (influenza), paramyovirus, picornaviruses, herpes viruses, adenovirus, coronavirus, papilloma virus, hantavirus

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Antigenic shift vs drift

Shift: major changes in hemagglutinin and neurominidase associated with epidemics and pandemics. Drift: minor changes in H and N associated with localized outbreaks

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•Understand Influenza (IFN) Pathogenesis

Hemagglutinin surface glycoprotein binds to sialic acid residues on respiratory epithelial cell surface glycoproteins - Infection Initiation. After viral replication, progeny virions are also bound to the host cell membrane. Neurominidase cleaves these links to liberate new virons and spread infection.

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• Know Influenza Clinical Features

Fever, lethargy, lack of appetite, coughing, wheezing, runny nose, sore throate, diarrhea, nausea, vomiting

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Complications of influenza

primary IFN pneumonia, secondary bacterial pneumonia, myositis, CNS involvement

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Diagnosis of influenza

clinical, rapid Ag tests, immunofluorescence, PCR, viral culture, serology

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Basics of IFN Prevention and Treatment

Prevention: vaccine. Treatment: Adamantanes are antivirals against IFN A. Neurominidase inhibitors are antivirals against IFN A and B. Treatment will shorten duration and severity