Patho & Pathophis resp 2 Flashcards
How do you describe Emphysema & Bronchitis
Emphysema - Associated with destruction of tissues & alveoli, causing enlarges airspaces leading to gas trapping
Bronchitis - increased mucus production, small airway obstructions & chronic productive cough
What are the 2 main causes for Emphysema
Smoking & Inherited deficiency of alpha antitrypsin
Why are patients with Emphysema called pink puffers
This is because of the symptoms they express
Barrel chest (looking they they have always just taken a full breath.
Self Peep (pursed lips)
Shortness of Breath causing pinkish tone to their skin
Usually are very thin in appearance
What is the patho of Emphysema
Smoking and other irritants cause neutrophils to release protease enzymes (e.g. elastase)
Constant release of these enzymes are can damage the lung tissue
Alpha antitrypsin (AAT) is protease inhibitor which stops the release elastase therefore protecting the lung tissue
Some people are born with out AAT and smokers have a reduction in the amount of AAT
Leads to increased airspace size, loss of elasticity, and impaired gas exchange
Emphysema summary
Why do people get barrel chest?
Because the alveoli get trapped there is space causing the lungs to be come hyperventilated making it harder for the patient to breath out
What is a reoccurring history for Bronchitis
Chronic productive cough for 3 or more consecutive months or 2 or more consecutive years. (Generally the cough is present for years with gradual worsening)
What can cause chronic bronchitis
Smoking is the number 1 cause because of the irritant causing the immune response. Previous infections and can also lead to a patient developing chronic brochities
What is the Patho for bronchitis
The foundation for this condition is excess production of mucus from goblet cells from irritation. Hypersecretion from increased degranulation from neutrophil mediated elastase is another foundation of this condition.
Added to this the cilia are not effective and as a result there is poor removal of secretions leading to infections becoming more probable
What are the 3 elements for asthma
Bronchospasm
Mucosal oedema
Increased mucus Production/plugging
Can chronic inflammation lead to airway remodeling
YES
Airflow limitation may be only partially reversible
Long term remodeling may consequent in COPD
What are the 2 main categories for Asthma
Allergic asthma - usually begins in childhood and is a type 1 hypersensitivity IgE response
Non allergic asthma - this starts in adulthood. This is a reaction to internal factors not associates with the IgE related response
What is the difference in allgeric asthma and non allergic asthma
Allergic asthma is a IgE mediated inflammatory response
Non allergic asthma is not associated with the IgE response and it is still unclear how it occurs (it is usually more server than allergic asthma)
What are another 3 categories for asthma
Exercise-induced asthma - this is usually a mild form and most asthmatics experience some form of bronchoconstriction if they perform exercise
Aspirin induced - Intolerance to asprin and NSAIDS. causes the body to release more/become more sensitive to a type of leukotriene leading to bronchoconstriction
Chronic cough asthma - can manifest as an isolated persistent cough particularly in children
How does asthma develop
Like most type 1 hypersensitivity reactions asthma develops in 2 distinct phases:
Primary response: Vasodilation, vascular leakage, Smooth muscle contraction.
Secondary response: Intense infiltration of tissues with eosinophils & other acute/chronic inflammatory cells, Tissue destruction, Prolonged inflammation, Bronchoconstriction
What is the first stage of allergic asthma?
Inflammatory response similar to anaphylaxis.
Antigen enters
T2H cell direct plasma B cell to produce IgE
IgE binds to mast cells of mucous membranes in respiratory tract
During a subsequent exposure mast cells degranulate and release histamine
This causes (Bronchospasm, Mucosal oedema, Mucous plugging)
What are the 3 main mediators that are released in cell degranulation
Histamine - nitric oxide (vasodilation)
Leukotrienes - mucus secretion
Cytokines - attract more inflammatory mediators
What does histamine do
What is the late phase of asthma
Again this is similar to anaphylaxis
Cytokines cause while blood cells, more specifically Eosinophils to release more leukotrienes which causes prolonged inflammation, bronchoconstriction & epithelial damage. This can cause remodeling to occur which can lead to partial or total obstruction to the airways
What are some clinical manifestations of asthma?
Breathing: Narrowed bronchial lumen can expand slightly, so air reaches alveoli.
Exhalation: Bronchospasm, mucus plugging, positive intrapleural pressure decreases causing air to be trapped leading to hyperinflation.
This leads to increased intrathoracic pressure
Causes a wheeze on exhalation
Also leads to a increase in breathing effort and shortness of breath
Prolonged expiratory time
What are some clinical manifestations of life threatening asthma
Severe bronchiole obstruction leads to decreased ventilation
Sympathetic response leads to tachycardia and increase RR
Further hyperventilation causes increased use of accessory muscles due to increased thoracic pressure
Can often be identified by barrel chest
What do the vitals look like
What happens in a life threatening asthma episode
There is a miss match in the VQ. This occurs because areas of the lung are perfused but not ventilated/vice vera. This results in patients becoming hypoxemic & hypercapnic leading to acidosis
How does hyperinflation affect perfusion
The lungs are only restricted by the volume within the thorax. But as pressure starts to increase it puts pressure on the heart.
Pulmonary vascular resistance increases due to hypoxia. This causes increased pulmonary artery pressure and increased demand on the right side of the heart.
As hyperventilation worsens, pressure on the superior and inferior vena cava increases
Eventually due to the pressure these veins kink. This ofcourse decreases the amount of blood able to return to the heart.
What would the vitals look like for a status 2 -1
What are some variables that have affect on asthma severity
What is a asthma risk assessment
