Pathophysiology Pulmonary Infections

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54 Terms

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Upper respiratory tract infection

• Viral- Rhinovirus; adenovirus; coronaviruses; parainfluenza; respiratory syncytial virus; typically symptomatic

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Upper respiratory tract infection S/S

nasal drainage, stuffiness, sore throat, PND, headache, malaise

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Upper respiratory tract infection transmission

Contaminated surface, hand to mouth/eyes/nose

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Rhinitis

inflammation of nasal passages

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Sinusitis

inflammation of the sinuses

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Rhinosinusitis

inflammation of the nasal and paranasal sinus mucosa; Pathogen: H. influenza, S. pneumoniae, rhinovirus

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Rhinosinusitis S/S

face pain, purulent drainage, fever, HA

Rx: antibiotics, decongestants

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Rhinosinusitis Bacterial

duration about 4 weeks; severe onset (fever, purulent drainage), worsening symptoms, or >10 days with symptoms

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Rhinosinusitis Viral

duration is 5-7 days

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allergic rhinitis

Type I hypersensitivity, an allergic reaction to airborne allergens that causes an increased flow of mucus

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Allergic Rhinitis S/S

Nasal drainage (clear, watery), itching/burning eyes, nose, throat, nasal congestion

Rx: antihistamines, decongestants, nasalcorticosteroids, desensitization(immunotherapy)Allergic Rhinitis

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Influenza

Viral infection of upper/lower respiratory tract- Often epidemic, can cause death- Children: highest rate of infection- Elderly/immunocompromised: higher severity•

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Influenza

• Transmission: droplet infection• Incubation: 1-4 days• Contagious: 1 day before sx. to5 days after illness, longer for children, immunosuppressed

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Influenza A

most common- highly contagious-- also affects birds, pigs, horses

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Subtypes of Influenza A

Based on surface glycoproteins- Change antigens on cell membranes → newsubtypes

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Hemaglutinin (HA)

part of the influenza A virus that allows for attachment to the cell and subsequent endocytosis; attachment proteins

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Neuroaminidase (NA)

aids viral replication and release from host cell

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Drift

minimal/small changes antigens

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Shift

Both H and N antigens change

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URI, viral pneumonia, complicating bacterial infection

3 syndromes of seasonal influenza

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Influenza Pathophysiology

Upper airway infection- Damage ciliated/epithelial cells• Lower respiratory tract- Shedding, bronchial/alveolar cells• Secondary bacterial infection- ↓ natural defenses- ↑ bacterial adhesion

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Influenza symptoms

Abrupt onset• Fever, malaise, chills, muscle aches, HA, watery nasal discharge, sore throat, dry cough• Peak: 3-5 days

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viral pneumonia symptoms

Fever, tachypnea, cyanosis, tachycardia- Rapid progression of symptoms (within 1 day of influenza onset)- Survivors often develop acute pulmonary fibrosis

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H1N1 S/S

similar to seasonal flu, some diarrhea/vomiting, extremely high fevers

Differences- Timing- Population more serious in adults < 25years old

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Influenza prevention

Vaccine: everyone aged 6 months and older;

Especially high risk:- 6-59 months old; 50 years and older- Asthma, diabetes, chronic lung disease, HF, Pregnant women, Immunocompromised- Nursing facility & long-term care residents

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Pneumonia

inflammation and infection of bronchioles and alveoli in lung parenchyma

Risk factors:

immunocompromised, elderly, lung disease

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Pneumonia defense mechanisms

- Nasopharyngeal IgA- Cough reflex- Mucocilliary system- Alveolar macrophagesPneumonia

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community acquired pneumonia

a type of pneumonia that results from contagious infection outside of a hospital or clinic; streptococcus pneumoniae most common

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Hospital acquired pneumonia

pneumonia occurring 48 hours or longer after hospital admission and not incubating at the time of hospitalization. Not present on admission, nosocomial, usually bacterial, associated with antibiotic resistance, ventilator associated pneumonia

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Typical pneumonia

Inhalation or aspiration of virulent organism• Inflammatory/immune response- Complement activation, antibody production- Opsonization of bacteria- Release inflammatory mediators andtoxins from organism → capillarypermeability & edema- Damage to bronchial/alveoli mucous membranes- Bronchioles/alveoli fill with fluid/debris (exudate)• Consolidation of lung tissue- Problems with ventilation and oxygenation- Recovery: macrophages digest fibrin & bacteria

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Pneumonia S/S

Fever, chills, ↑RR- Cough, purulent sputum- Can progress to bacteremia and sepsis

Dx: CXR

Prevention - pneumococcal vaccines

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Legionella pneumophilia

From water: Aerosolized water• Pneumonia with diarrhea, confusion, hyponatremia

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Atypical pneumonias

Damage epithelium; invade alveolar septum/wall and interstitial lung tissue

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Viral pneumonias

Frequently "interstitial", NOT alveolar; respiratory syncytial, influenza; atypical

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Fungal Pulmonary Infections

Rare and self limiting in healthy individuals• Opportunistic infection• Pneumocystis Jiroveci (PJP)• Histoplasmosis, blastomycosis, coccidiomycosis- Found in soil, rotting wood/vegetation, river valleys- Regional distribution- Granuloma formation

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Fungal pulmonary infections S/S

mild, flulike sx, productive cough, fever, night sweats, weight loss

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Tuberculosis

• Risk factors: foreign born, HIV positive, congregatesettings (prisons, shelters)• Organism mycobacterium tuberculosis- Rod shaped, acid-fast, waxy capsule- Spread by droplet nuclei- Atypical infections• m. avium intracellulare, m. avium complex

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Primary Tuberculosis

• Inhaled droplets activate inflammatory/ immune system• Macrophages and T lymphocytes seal off colony → Gohn Focus(aka: granuloma or tubercule)• Caseous necrosis: center ofgranuloma• Enter lymph → granuloma formation in lymph nodes• Gohn Complex = lung lesion and lymph node granuloma

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Latent TB

one of two things that happens after a TB infection; organism contained, no active disease, lesions calcify

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Primary progressive TB

(5%) one of two things that happens after a TB infection; organism continues to spread in lungs

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Secondary TB

Reactivation of primary lesion or reinfection• More likely if chronic disease or immunocompromised: HIV, DM, malnutrition, elderly• Reactivation: necrotic tissue liquefies and drains into bronchus secondary activeTB

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Latent TB

No symptoms of TB disease.• TB screen positive• CXR normal• Respiratory specimens are smear and culture negative.• Cannot spread TB bacteria to others.• Should consider treatment to prevent active TB disease

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Active TB

Symptomatic• TB screen positive• CXR abnormal (usually)• Respiratory specimens are usually smear or culture positive• May spread TB bacteria to others• Needs treatment for TB disease

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Tuberculosis S/S

Primary infection maybe asymptomatic• Low grade fever, sweats• Anorexia, weight loss• Cough - purulent, hemoptysis• Dyspnea• Other organ involvement- Death in 5 years if untreated

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TB difficult to treat

- Due to resistance- Waxy capsule- Bacteria can live/divide within old lesionsTB - cont.

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acute respiratory disease

-most common in infants/children

-small diameter airways

-lung maturity

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infant respiratory distress syndrome

caused by immature lungs --> too little surfactant in the alveoli; lungs collapse with each breath (atelectasis), increased work of breathing and hypoxia, hyaline membrane forms

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infant respiratory distress syndrome S/S

cyanosis, retractions, ↑ RR

Tx: O2, CPAP, surfactant,mechanical ventilation,steroids to motherduring preterm labor

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bronchopulmonary dysplasia

chronic lung disease in infants due to mechanical ventilation or prolonged O2; alveolar hypoplasia, alveolar fibrosis

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Bronchopulmonary Dysplasia S/S

Persisten hypoxia, chronic respiratory distress, retractions, tachycardia, rapid RR;

Tx: mechanical ventilation

<p>Persisten hypoxia, chronic respiratory distress, retractions, tachycardia, rapid RR;</p><p>Tx: mechanical ventilation</p>
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Viral Croup

viral infection, acute laryngotracheobronchitis, obstructive subglottic region (below vocal cords)

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Viral croup S/S

barking cough, hoarseness, inspiratory stridor

May subside with humidity, cold air

Worsen at night

Croup cough sound, can progress to airway obstruction

Tx: epinephrine, humidified O2,trach or endotracheal tube (if severe)

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Epiglottitis

Inflammation/edema epiglottis/pharynx• Common causes: H.Influenza, strep, staph• Acute onset• Edema epiglottis can cause airway obstruction

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Epiglottitis S/S

Sore throat, stridor, fever, mouth open/chin thrust forward, drooling

Tx: Abx, maintain airway withendotrachealtube or tracheostomy