1. Respiratory Tract Infections

URTI cause

viruses such as rhinovirus, influenza, coronaviruses, adenovirus, respiratory syncytial virus

URt s/s

nasal drainage, stuffiness, sore throat, PND, headache

URT Transmission

contact with contaminated surface; and droplets

How do we prevent URT transmission?

URT treatment

symptomatic (antivirals or antibiotics not usually given)

Rhinosinusitis patho

inflammation of sinuses & nasal passages causes increased capillary permeability, swollen tissue, and edema which blocks sinus drainage (traps mucus leading to congestion, pressure, and potential infection)

Rhinosinusitis causes

mainly viral infection

Rhinosinusitis s/s

face pain, purulent discharge, fever, HA

Rhinosinusitis Difference between bacterial and viral s/s:

viral: 5-7 days, bacterial: ~4 weeks, severe onset (fever purulent discharge), worsening symptoms, or >10 days sx

Allergic rhinitis patho, hypersensitivity type

(patho of) Type 1 Hypersensitivity (IgE)

allergic rhinitis s/s

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

Influenze tranmission

droplet infection

Describe how new subtypes are created, shifts and drifts:

drift= small changes in antigens

shift= both H and N antigens change

new subtypes are made when antigens on cell membranes change

• H(hemaglutinin): attachment proteins

• N (neruoaminidase): replication proteins

3 influenza syndromes, describe why these (can) happen:

• Typical URI (rhinotracheitis): upper airway infection- inhaled virus damages ciliated/epithelial cells

• Viral pneumonia: lower respiratory tract- shredding bronchial/alveolar cells

• Complicating bacterial infection: secondary bacterial infection- decrease in natural defenses and increase in bacterial adhesion

Influenza s/s

• abrupt onset, fever, body aches + fatigue, headaches, sore throat, dry cough (unless showing pneumonia symptoms)

  • If showing pneumonia symptoms: extreme fever, shortness of breath, cyanosis, tachycardia (more resp s/s + more inflammation)

How is H1N1 different from the flu

(similar: extremely high fevers, some diarrhea/vomiting) difference: timing: can happen any time (no season), population → more serious in adults <25 years old

How do we prevent influenza?

vaccines

pneumonia definition

 inflammation and infection of the bronchioles and alveoli in lung parenchyma

pneumonia patho

inhalation/aspiration virulent organism → immune response: comp-leemtn activation + antibody opsonization of bacteria, bacteria releasing toxins causes inflammation →increased cap perm + edema → fluid starts leaking in the alveoli -buildup of pus, debris, dead cells → damaged alveoli & consolidation of thw lung tissue causing difficulty with ventilation and oxygenation to go in/CO2 out

Recovery: macrophages digest fibrin & bacteria (antibiotics help)

pneumonia Risk factors

immunocompromised, elderly, lung disease (e.g. COPD)

Describe the body’s natural defense mechanisms

nasopharyngeal IgA (antibodies that opsonize things that don’t belong), cough reflex, mucociliary system, alveolar macrophages

How is pneumonia classified? 

• Where it’s acquired (community vs healthcare acquired), 

• infectious cause (by agent) 

  • Typical: bacterial, strep-pneumoniae = most common

  • Atypical: viral mycoplasma

• by location of infection in lungs: lobar

Typical pneumonia where do you see fluid and debris build up in comparison to atypical?  

• Typical: inside the alveoli

• Atypical: in between the alveoli – can see this more on a chest x-ray

pneumonia s/s

fever, chills, increases in rr, cough with purulent sputum, can progress to bacteremia and sepsis

pneumonia diagnosis

CXR, blood & sputum culture, WBC

How do we prevent pneumonia?

vaccine

Atypical pneumonias

mycoplasma, legionella, or chlamydia attack the cells lining the airway causing inflammation in the interstitial space—fluid buildup is outside the alveoli

Who is at risk for atypical pneumonia?

tuberculosis risk factors

foreign born, HIV positive (bc they don’t have enough T lymphocytes to fight it off), congregate settings (prisons, shelters)

tuberculosis transmission

droplet

tuberculosis patho

inhaled droplets activate immune/inflammatory response: macrophages and T lymphocytes seal off colony → granuloma formation (Gohn Focus)- necrotic core (dead debris and tissue). Enter lymph → granuloma formation in lymph nodes. Gohn complex= lung lesion and lymph node granuloma

Primary TB  patho  what two things can occur? 

• Latent TB: organism contained, no active disease, lesions calcify and causes no problems 

• Primary progressive TB (5%): organism continues to spread in lungs (usually bc inadequate immune response

What is secondary TB?

Reinfection leading to active tb or reactivation of primary lesion (latent → active)

Who is at risk of this happening and TB reactivating?

People with chronic disease or are immunocompromised: HIV, DM, malnutrition, elderly

Differences between Latent and Active TB: s/s, screening results, cxr, contagiousness, treatment

• Signs/Symptoms : asymptomatic, symptomatic

• Screening results: *both screen positive 

• Chest X-ray results: normal, usually abnormal

• Sputum culture results: 

• Contagiousness: not contagious, contagious

• Treatment: recommended to prevent active TB, needs treatment

tb s/s

(primary infection may be asymptomatic), low grade fever, sweats, anorexia, weight loss, cough- purulent, hemoptysis, dyspnea, other organ involvement (death in 5 years if untreated)

tb Screening and diagnosis

skin tests, CR, sputum for AFB, new blood test for rapid diagnosis

tb treatment

latent:1-2 meds daily for 9 months, active: multidrug regime (4 for 8 weeks then 2 for 18 weeks)

Why is it difficult to treat tb?

resistance to the drugs we have, thick waxy capsule around it that makes it hard for antibiotics to break through, bacteria can live/divide within old lesions