obstructive pulmonary disease Flashcards
increased secretions and increased spasms
asthma
increased secretions
bronchitis
loss of surrounding supporting tissue
emphysema
chronic inflammation of the airway and variable airflow obstruction; presence of intermittent symptoms
asthma
what is the cause of asthma?
immune-mediated airway inflammation caused by exposure to an allergen or an irritant
what are some symptoms of asthma
-sob
-wheezing
-coughing
-chest tightness
-feeling of breathlessness
what are some signs of a severe asthma episode
-wheezing
-orothpnea
-tachypnea
-tachycardia
-use of accessory muscles
=qgitation
-intercostal retractions
what are some common allergens
-dust mites
-smoke
-foods
-animal dander
-excersie
-pollution
true/false: type 2 inflammation involves innate and adaptive immune systems
true
type 2 inflammation: _____ induces B-cell isotope (antibody) switching to production of IgE
IL-4
type 2 inflammation: IgE, through its binding to _______ and ______ results in environmental sensitivity to allergens
basophils and mast cells
type 2 inflammation: what are the products from the cross linkage of IgE on the surface of basophils and mast cells
type II cytokines and direct activators of smooth muscle contraction and edema
type 2 inflammation: ____ has a critical role in regulating eosinophils. it controls formation, recruitment and survival of these cells
IL-5
type 2 inflammation: _____ induces airway hyperresponsivemess, mucus hyper secretion, and goblet cell metaplasia.
IL-13
type 2 inflammation: ____ can produce IL-5 and IL-13. they can be activated by epithelial cytokines known as alarming, which are produced in response to “nonallergic” epithelial exposures such as irritants, pollutants, oxidative agents, fungi or viruses.
type 2 innate lymphoid cells (ILC2)
non-type 2 inflammation: true/false: non-type 2 processes can exist either in combination which type 2 inflammation or without type 2 inflammation
true
non-type 2 inflammation: which type of inflammation is more commonly seen in severe asthma, that has not responded to the common anti-inflammatory therapies such as corticosteroids, that usually suppress type 2 inflammation
neutrophilic inflammation
these 3 cytokines are the major cytokines associated with type 2 inflammation, and have been targeted successfully in asthma therapies
Il-4,5, and 13
true/false: thymic stromal lymphopoetin (TSLP), IL-25 and IL-33 also play a role in the signalling cascade and have been targeted successfully in asthma therapies
false - actively being studied as targets for tx of asthma
these cytokines have been implicated in non-type 2 inflammation
IL-6, IL-17, TNF alpha, IL-1beta and IL-8
what are pre-disposing (risk) factors of asthma
- genetics *mutation on chromosome 17q21
- family history of asthma
- positive skin test to an allergen
- tobacco (second hand and maternal smoke)
- air pollution
- diets (vitamin D deficiency)
- obesity
- medications
- occupational exposures
this type of inflammation is eosinophilic predominant and an IgE response is common.
clinical manifestations include: elevated IgE levels, eczema, allergic rhinitis, positive fam history of allergen and attacks associated with seasonal, environmental or occupational exposure
type 2 inflammation
know the IgaE dependant pathway of the pathogenesis of asthma
an allergen is present -> mast cells and eosinophils are activated -> prostaglandins, leukotrines, interleukins and cytokines are released -> there is acute/chronic inflammation -> bronchoconstriciton, mucus and edema production, airway hyperresponsiveness
know the IgE independent pathway of the pathogenesis of asthma
cold/exercise, osmotic stimuli, irritant exposure -> mast cells and eosinophils activated -> prostaglandins, leukotrienes, interleukins and cytokines released -> acute/chronic inflammation -> bronchoconstriction, mucus & edema production and airway hyperresponsiveness
know the epithelial cell activation pathway of the pathogenesis of asthma
cyokines and chemokine are released -> mast cells and eosinophils growth, influx and proliferation of T lymphocytes, differentiation of B lymphocytes (IgE/A) and TH2 differentiations - IL production -> acute/chronic inflammation -> bronchoconstriciton, mucus and edema production and airway hyperresponsiveness
what does the activation of local inflammatory cells produce?
- acute bronchospasm
- mucosal edema
- mucus plug formation
- airway wall remodelling
what are some immunohistopathologic features of asthma
- denudation of airway epithelium ‘
- collagen deposition beneath basement membrane
- edema
- mast cell activation
- infiltration by neutrophils, eosinophils and lymphocytes
what medical conditions/findings may be associated with obstructive lung disease?
- sensitive
- GERD
- allergic rhinitis
- cough
- wheezing
- hyper inflated chest
know the mechanism of bronchial smooth muscle relaxation
- epinephrine binds to adrenergic receptors
- adenyl cyclase is stimulated
- increased cAMP production
- increased Ca2+ pump activity = Ca2+ returned to sarcoplasmic reticulum in muscle
- decreased activity of myosin light chain kinase
- dephospho rylation of myosin-P and changes to shape and binding site
- actin-myosin cross bridges are broken
- decrease in contraction of bronchial smooth muscle = smooth muscle relaxation
a term used to represent a process characterized by presence of chronic bronchitis or emphysema (usually both).
COPD
type B COPD “blue bloater” - resting hypoxemia
- chronic or recurrent cough > 3 months > 2+ successive years
- persistent, but sometimes reversible airway obstruction
- commonly caused by: cigarette smoking, repeated airway infections, genetic predisposition and inhalation of chemical irritants
chronic bronchitis
in chronic bronchitis, elevated _____ levels recruit neutrophil activation
IL-8
in chronic bronchitis, ciliated epithelium are replaced by _____- type
squamous
what are some clinical manifestations of chronic bronchitis
- sob on exertion
- cyanosis
- excessive sputum
- chronic cough
- evidence of excess body fluids
how do you know someone has bronchitis based on their pulmonary function tests (e.g. TLC, RV and FEV)
- normal total lung capacity (TLC)
- increased residual volume (RV)
- decreased FEV (forced expiratory volume) and FEV/FVC (forced expiratory volume/forced vital capacity)
how do you know someone has bronchitis based on their arterial blood gases (e.g. pCO2 and pO2)
- elevated pCO2
-decreased pO2
type A COPD “pink puffer”
- develops overtime usually > 50 years of age
- usually caused by smoking and air pollution, as well with certain occupations e.g. mining, welding, working withs asbestos
emphysema
what cells are effected in emphysema
- macrophages
- neutrophils
- epithelial cells
- lymphocytes
know the pathogenesis of emphysema
- reduction in pulmonary capillary bed: exchange of O2 and CO2 between capillary and alveoli is impaired
- loss of elastic tissue: results in a decrease in size of smaller bronchioles and results in loss of radial traction (hold airway open)
this type of emphysema is associated with chronic bronchitis and it destroys the respiratory bronchioles
centraicinar (centrilobular)
this type of emphysema destroys the alveoli and is mostly seen in smokers
panacinar (panlobular)
this type of emphysema affects the peripheral lobules
paraseptal
what are some clinical manifestations of emphysema
- pursed lip breathing
- use of accessory muscles
- thin
- cough is minimal or absent
- increased SOB for past 3-4 years
what are some clinical manifestations of emphysema
- pursed lip breathing
- use of accessory muscles
- thin
- cough is minimal or absent
- increased SOB for past 3-4 years
- barrel chest
- digital clubbing
- decrease3d breath sounds
