Gosh this is a hard one
Overview
Asthma is a chronic inflammatory disease characterised by bronchial hypersensitivity, bronchspasm and mucous overproduction
It is a complex, multifactoral disease with genetic and environmental factors. It is also a spectrum of disease with there being multiple different subtypes and severity within a subtype. Common symptoms are asthma attacks and airway obstruction.
Types of Asthma
There are many different types of asthma:
Work related asthma
As the name states this is asthma which is related to work. This can further be divided into Occupational asthma, or work exacerbated asthma. Occupational asthma can be sensitizer induced or irritant induced, and work exacerbated asthma is just asthma which triggered at work.
T2 type vs non T2 type asthma
T2 type and non T2 type asthma refers to the
Pathogenesis
So this pathogenesis is rather complex I think, but I will do my best to detail it (This is in incredible oversimplification and is full of nuance)
- Dendritic cell presents antigen to naive T helper cell (Th-0 )
- It can either differentiate into Th-1 or Th-2 cells.
Th-1 response (IFN-γ, lymphotoxin, IL-2)
This is cell-mediated immunity and leads to neutrophilic inflammation. It is selected for with IL-12 which also inhibits the Th-2 response.
Th-2 Response
This is the other one which very complex but leads to asthma symptoms. Triggers an antiparasite type reaction,
This response provokes synthesis and release of proinflammatory cytokines to prime B lymphocyte cells, drives maturation of dendritic cells, increases numbers of inflammatory cells recruited and increases IgE levels which worsens asthma symptoms.
The released cytokines also provoke autonomic system to bronchoconstriction.
Asthma priming?
After the initial Th2 response the airways can become sensitised. This happens via B cells making IgE antibodies to an allergen. which is then attached to mast cell, eosinophils and basophils. Inflammatory response occurs upon second contact.
Clinical profile:
Clinical Signs and Symptoms:
Treatment:
Pharmacology:
Pathological profile:
Pathophysiology
Airway inflammation Bronchial hyper resposible bronchocontriciton Bronchial wall edema excess mucous secretion epithelial shedding → bronchospasm airway remodelling → more goblet cells matrix and smooth muscle\
Exacerbations
Starts with Type I hypersensitivity with ige triggered mast cells
Long term develops into type IV hypersensitivity