Module 3 - Gas exchange & immunity Flashcards
When do Type 2 alveolar cells begin to produce surfactant?
~28-30 weeks gestation
What are the 4 types of hypersensitivity
Type 1 - IgE mediated allergies
Type 2 - IgM/IgG auto antibodies
Type 3 - antibody complexes
Type 4 - T-cell mediated –> macrophages/cytotoxic T-cells
What is bronchiolitis
acute lower respiratory tract infection
targets lung EPITHELIUM (not affected by bronchodilators)
Which virus typically causes bronchiolitis?
respiratory synctycial virus
other viruses: parainfluenza, mycoplasma, adenovirus
What age is bronchiolitis most common?
<2 years old
Respiratory anatomy of infants/children
narrow airway (funnel shaped, anterior facing)
narrowest part = cricoid making intubation difficult
immature intercostal muscles –> diaphragm primary mode of breathing
horizontal intercostal muscles –> rib cage moves up/down vs. up/out
abdominal breathing
obligate nose breathing until 6 months
shorter airway –> higher risk of lower respiratory infections
narrower lumen –> higher risk of obstruction
Types of retractions
tracheal tug
substernal
suprasternal
supraclavicular
intercostal
subcostal
Infant ventilation
extrathoracic airway narrow during inspiration and widen during expiration
inthrathoracic airway widens on inhalation and narrows on expiratoin
asymmetrical movement helps move air towards lungs
Extrathoracic definition
trachea
Intrathoracic
below trachea
Functional residual capacity
volume remaining in lungs after exhalation
Infant sleep & breathing
reduced gas exchange
reduced muscle tone –> narrower airway
shorter exhalations = increased functional residual capacity (reduced G/E)r
reduced intercostal activity
Intermittent breathing
normal for infants to stop breathing for up to 15 seconds
True infant apnea
no breathing for >20 seconds
Restrictive lung disorders
pulmonary edema
respiratory distress syndroem
Obstructive lung disorders
asthma
allergies?
Croup sounds
stridor on inspiration
Asthma sounds
prolonged expiration, wheezing
Cortisol and surfactant
increase maturation of Type 2 alveolar cells & increase surfactant production
Insulin and surfactant
decrease production fo surfactant
URTI
inflammation of upper airway –> impacts inspiration
LRTI
inflammation of lower airways –> impacts expiration
*air trapping, prolonged expiration
URT anatomy
nose
mouth
sinuses
larynx
LRT anatomy
trachea
bronchi
bronchioles -> alveoli
lungs
S/S impending respiratory failure
increased WOB
retractions
grunting
reduced chest movement
cyanosis not relieved by O2 therapy
HR >150 OR increasing/decreasing bradycardia
tachypnea or bradypnea
extreme anxiety/agitation
fatigue
reduced LOC
Bronchiolitis Treatment
1)O2 therapy (humidifed)
2)hydration (IV, NG)
other:
positioning (elevate head)
reduce fatigue
nasal suction (infants)
epinephrine/dexamethasone
Syncytia
merging of epithelial cells d/t RSV
CD8 T-cells
differentiate into cytotoxic T-cells
CD4 T-helper cells
TH1 –> stimulate cytotoxic T-cells
TH2 –> stimulate B-cells to differentiate into plasma cells. Promote class switching
Which T-helper cell is more commonly associated to allergies?
TH2
*TH2 shift occurs in pregnancy –> more prone to developing allergies
Mechanism of TH1 hypersensitivity
APC presents antigen to TH2 –> TH2 cells rls mediators that cause B-cells to differentiate into IgE producing cells
IgE antibodies bind to allergen
IgE antibodies bind to mast cells via Fc region –> PRIMING
on secondary exposure, allergen crosslinks IgE antibodies on mast cell surface cause mast cell degranulation –> allergic symptoms
Where are mast cells located?
connective tissue
skin
mucous membranes
adjacent to blood/lymph vessels
Where are basophils located?
bloodstream
Type 1 phases
Primary/immediate –> mast cells
Secondary/late –> inflammatory cells sustain inflammation
Mechanism of Type 2 hypersensitivity
IgG or IgM antibodies target endogenous/exogenous antigens located on cell surface
1) complement/antibody mediated cell destuction
2) “ inflammation
3) antibody-mediated cellular dysfunction
Mechanism of Type 2 hypersensitivity
IgG or IgM antibodies target endogenous/exogenous antigens located on cell surface
1) complement/antibody mediated cell destuction
2) “ inflammation
3) antibody-mediated cellular dysfunction
Types of T2 hypersensitivity reactions
blood transfusion reactions
hemolytic disease of newborn
Virus components
genetic material –> DNA or RNA
protein capsid
envelope (cell membrane attached to virus –> OPTIONAL)
What type of virus evolves more rapidly?
RNA
Bronchiolitis patho
epithelial inflammation
pulmonary edema
increased mucus production —> mucus plug
tissue necrosis
What is asthma?
chronic obstructive respiratory disease that causes airway inflammation, edema, mucus production and bronchospasm
Common asthma triggers in children
viral RTI
allergens
air pollution
seasonal changes
reduced medication compliance
PRAM
pediatric respiratory assessment measure
Asthma treatment
bronchodilators
anticholinergics
systemic corticosteroids
O2 therapy
magnesium sulfate (relax smooth muscle)
IV drugs
intubation/ventilation
Bipap/CPAP
Asthma & breathing
a lack of wheezing/silent chest can indicate the airway was completely closed and respiratory failure is imminent
PRAM scores
mild 0-3
moderate 4-7
severe 8-12
Asthma symptoms
1) dyspnea, chest tightness, wheezing, sputum production, and cough,
2) airflow obstruction (s/t inflammation)
3) bronchial hyperresponsiveness (IgE mast cells)
4) underlying airway inflammation
Types of asthma
atopic
non-atopic
Atopic asthma
type 1 hypersensitivity reaction
caused by IgE antibodies responding to allergens
Non-atopic asthma
non-allergenic asthma. caused by triggers such as viral infection, stress, pollution, exercise, etc.
Systemic effects of corticosteroids
adrenal suppression
growth impairment
decreased bone density
myopathy
weight gain
Layers of respiratory tract
mucosa (epithelium + lamina propria)
submucosa
basement membrane
cartilage/smooth muscle/adventitia
How does aspirin promote asthma?
aspirin = nsaid
inhibition of COX pathway leads to increased LOX activation
increased LOX = increased immune response –> hyperreactivity
Long-term effects of asthma
smooth muscle & goblet cell hypertrophy
injury to epithelium
blood vessel proliferation
Asthma phases
Early phase 10-20 onset caused by IgE antibodies
Late phase 4-8 hrs post exposure -> inflammatory cells rls mediators prolonging inflammation
Leukotrienes & inflammation
bronchoconstriction
increased bronchial reactivity
mucosal edema
mucous hypersecretion
How do infants breath
extrathoracic airway narrows on inspiration, widens on expiration
intrathoracic airway widens on inhalation, narrows on expiration
Incubation of RSV
2-8 days
Stages of extrinsic asthma
1) sensitization
2) provocation
Phases of an asthma attack
early (within minutes d/t IgE antibodies)
late (hours d/t rls of inflammatory cells/mediators)
