Respiratory Flashcards
Asthma
episodic and reversible bronchoconstriction
extrinsic - Type I hypersensitivity to an inhaled (external) allergen such as pollen
Intrinsic - non-allergen medicated.
CD4 TH2 cells produce cytokines (IL-4 and IL-5) when initially stimulated by an allergen
IL-4 induces antibody isotype switch to IgE
IL-5 induces eosinophil activation
early activation
mast cells are activated by cross-linking of IgE and release immune activating substances (histamine, leukotrienes, and acetylcholine) when an allergen is presented again
histamine results in bronchoconstriction, chemotaxis for immune cells, and mucus production
acetylcholine results in bronchoconstriction (parasympathetic mediated)
leukotrienes C4, D4, and E4 induce bronchoconstriction
late activation
eosinophils are activated produce major basic protein, which causes further constriction/damage in the airways
presentation and treatment of asthma
wheezing
cough
mucus production
note: a child who is becoming sleepy and less responsive is most likely failing, retaining CO2 (case intro) and needs intubation
Physical exam
tachycardia
tachypnea with use of accessory muscles pulsus paradoxes
Histological changes
terminal bronchioles-mucus plugs
Curschmann’s spirals -the presence of trapped epithelial cells killed by eosinophil produced major basic protein
Charcot-Leyden crystals -aggregated eosinophils
increased mucus-producing cells
bronchi
thickened basement membrane
Acute exacerbation
oxygen
inhaled beta-2 agonists
short acting preferred (e.g albuterol)
appropriate for exercise induced asthma
administer before exertion in known asthmatics
systemic corticosteroids (PO or IV)
Status asthmaticus
oxygen, bronchodilators, and steroids
sympathomimetic bronchodilators(e.g. epinephrine)
intubation and mechanical ventilation
Maintenance treatment
inhaled corticosteroids (mainstay)
long-acting bronchodilators (beta-2 agonists)
in combintation with inhaled corticosteroids (increased risk of death if used without inhaled corticosteroid)
Pneumonia
Infection of lung
Classic patterns include
lobar
intra-alveolar exudate, which consolidates
may involve the entire lung or be confined to 1 lobe
4 stages
bronchopneumonia
acute inflammatory infiltrates from bronchioles into adjacent alveoli
patchy distribution
involves ≥ 1 lobe
interstitial
diffuse patchy inflammation localized to interstitial areas of alveolar walls
distribution involving ≥ 1 lobes
generally less severe than lobar or bronchopneumonia
fever, cough, and new infiltrate on CXR
Risk factors
impaired cough reflex
damage to respiratory cilia
mucus plugs
presentation and diagnosis of PNA
Symptoms
sudden-onset of
fever
productive cough
purulent yellow-green
hemoptysis
dyspnea
night sweats
pleuritic chest pain
atypical presentations are gradual in onset and flu-like
dry cough
headaches
myalgias
sore throat
Physical exam
decreased or bronchial breath sounds
crackles/rales
wheezing
egophany
with consolidation
percussion reveals
dullness over affected lobe(s)
tactile fremitus
increased with consolidation
decreased with pleural effusion
EVALUATION
CXR
may show lung opacification/consolidation in affected lobe(s)
establishes diagnosis in combination with Gram stain or culture
4 stages of lobar PNA
congestion-between 1 and 2 days. where the blood vessels and alveoli start filling with excess fluid.
red hepatization- happens between days 3 and 4. This is where exudate, which contains red blood cells, neutrophils, and fibrin starts filling the airspaces and makes them more solid.
liver-like appearance from the reddish-brown color of the exudate.
gray hepatization- happens around days 5 to 7. the lungs are still firm but the color has changed because the red blood cells in the exudate are starting to break down.
resolution- day 8 and can continue for 3 weeks. In this stage the exudate gets digested by enzymes, ingested by macrophages, or coughed up.
Tuberculosis
small droplets containing the bacteria that reaches the terminal alveoli of the uninfected person
alveolar macrophages are recruited, which eventually become infected( due to bacteria produce sulfatides, sulfatide, a surface protein that inhibits the phagosome-lysosome fusion), transporting the microbe to deeper tissues
Surface glycolipid called TB cord factor triggers an immune response where numerous cytokines are released, attracting more macrophages and helper T-cells to the area to quarantine the TB bacteria by forming granulomas and giant cells
“Ghon focus”- granuloma with bacteria, macrophage, and necrosis center
secondary TB occurs when the patient’s immune system is weakened
ghon complex is reactivated
typically manifests in the apical/posterior segments of the lung due to its increased oxygen tension
Acid-fast on Ziehl-Neelsen staining
The immune system itself causes damage
cord factor
inhibits leukocyte migration
causes characteristic serpentine growth pattern
induces TNF-α release
tuberculin
triggers cell-mediated immunity → caseation and granulomas
triggers delayed hypersensitivity reaction
a surface protein
sulfatides
prevent phagosome-lysosome fusion
findings
middle or lower lung infiltrate (suggestive of primary infection)
upper lobe infiltrate (suggestive of latent TB reactivation)
apices have higher oxygen tension and reduced perfusion/lymph clearance compared to the base
cavitary lesions
Ghon complex (lobar or perihilar lymph node involvement)
ACute respiratory distress
acute diffuse, inflammatory lung injury leading to increased vascular permeability, and loss of aerated lung tissue
Hyperactivation of coagulation and inflammation cause endothelium to become leaky (causing pulmonary edema and fluid in the alveolar)
Immune cell sticks and enters alveoli releasing proteinase, oxygen spices, and cytokines, damaging both type I and II pneumocytes and forming intra alveolar hyaline cast ( dead cell and protein-rich exudate thtas makes the gas exchange more difficult)
Damage type I pneumocyte cause decreased gas exchange.
↓ Type II pneumocytes result in ↓ surfactant production.
↓ surfactant production results in low lung compliance and subsequent atelectasis
Repair often results in interstitial fibrosis.
EVALUATION
acute severe hypoxemia on pulse oximetry and ABG
Atelectasis results in intrapulmonary shunting
diffuse, bilateral alveolar infiltrates on CXR
ground glass opacities and consolidations on chest CT
Severity graded on PaO2 / FiO2 ratio and
