【Pathology】Pathophysiology of Asthma

Asthma

a chronic inflammatory condition of the respiratory passageways , particularly the mucosa

characterized by having the narrowing of the respiratory passageways which can cause difficulty breathing

sometimes it can even be extremely fatal

Content:

1. Underlying etiology
2. Molecular mechanism
3. Asthma is reversible
4. Controversial
5. Reference

1. Underlying etiology

a. Atopic triad

Genetic predisposition: with a family history of i, ii, iii.

have more allergic or hyperresponsiveness to specific types of allergens
produce massive amounts of inflammatory mediators
produce exacerbation or bronchospasm of the actual respiratory passageways

i. Asthma

ii. Atopic dermatitis

also called eczema

iii. Allergic rhinitis

b. Samters triad

three different factors that make these individuals more susceptible

Asthma
Nasal polyps
Aspirin sensitivity

Some individuals might have kind of an allergic or hypersensitive reaction to aspirin
aspirin inhibits the cyclooxygenase enzymes

which are responsible for converting arachidonic acid into prostaglandins

start tipping the balance and shunting the arachidonic acid into the leukotriene pathway
leukotriene c4, d4 and e4 responsible for bronchospasm

increased vascular permeability
cause a lot of mucus production (big morphologies)

Asthma & Nasal polyps----underlying mechanism specifically to aspirin sensitivity

so patients who have aspirin sensitivity might have nasal polyps or asthma

Arachidonic acid pathway

Arachidonic acid goes through two different pathways

cyclooxygenase pathway

a pathway which is utilized by the cox enzyme (cyclooxygenase enzyme)
leads to the formation of prostaglandin

PGE2

Dilation of the bronchilioes

PGI2

Prevent platelet aggretion

PGF2

Bronchial smooth muscle

lipo oxygenase pathway

leads to the formation of leukotrienes

leukotriene b4

a pretty good chemotactic agent

leukotriene c4
leukotriene d4
leukotriene e4

c4, d4 and e4: the culprits behind that intense bronchospasm

Prostaglandin

PGE2 & PGD2 –inflammatory responses

increase capillary permeability, enabling neutrophil and other immune cell to be extracted from particular blood capillary to the nearby tissue. It has implication in term of inflammation

c. Others

dust
pet dander / pet hair
cockroaches
cold
exercise
viral upper respiratory tract infections
emotional stress
smoke
taking aspirin, beta-blockers drug

epinephrine or the norepinephrine normally binding onto the beta2 receptors
promoting bronchodilation
When block, lead to bronchoconstriction

2. Molecular mechanism

When allergen is going to come into contact with specific types of antigen-presenting cells

antigen-presenting cells: dendritic cells, macrophages

dendritic cells have multiple different cytoplasmic extensions
dendritic cell phagocytose these allergy like particles
activate the mhc2 complexes
express that allergen with an mhc2 complex on its cell membrane
allergen bind to a t helper 2 cell
cd4 molecule is going to interact with the mhc2 molecule
produces two chemicals

interleukin four

interleukin-4 activates plasma cells
produce specific types of antibodies--IgE antibodies
a lot of IgE antibodies bind to mast cells
mast cells have a specific protein on their membrane, called an fc epsilon r1 receptor
fc epsilon r1 receptor binds with the IgE antibodies
trigger the mast cell to undergo degranulation
when it degranulates, it starts to produce massive amounts of

histamines
leukotrienes

Both are inflammatory mediators

interleukin five

interleukin 5 goes and activates a eosinophil

functions:

killing parasitic worms
plays a complex role in allergy and asthma

eosinophil has a bilobe nucleus
have the granules which stain red

because of the eosin that they apply via the right stain

eosinophil is then going to release

leukotrienes and other cytokines

attract in more white blood cells, particularly more eosinophils

specific types of proteases

*important especially in chronic cases
these proteases over time chronically can start to produce tissue damage to the respiratory tract

histamines and leukotrienes going to affect the actual bronchioles(in the submucosa)

leukotriene c4 d4 e4: the culprits behind that intense bronchospasm
histamines:

cause bronchoconstriction

hyperreactive even over time become hypertrophy and even hyperplastic

hyperplastic: make more of them
hypertrophy: the cells get bigger

bronchoconstriction is going to narrow that airway

cause dilation of the capillaries and increased capillary permeability
increased vascular permeability--- a lot of inflammation

stimulate a lot of mucus production

on top of the bronchoconstriction, patient going to get a lot of mucus buildup here

due to increase the vascular permeability &dilate capillaries

mucosa is gonna become super inflamed

fill with a lot of fluid, some eosinophils and other different types of inflammatory exudate

when inflamed
leukotrienes able to

promote bronchospasm
cause mucous buildup
cause the inflammation of the mucosa

An increase in vascular permeability

constriction
mucous buildup which is also going to be narrowing the airways

So inflammatory exudate due to the increased vascular permeability and immune cell infiltration going to narrow the airway

over time over chronic consistent exposure,
this chronic exacerbations become fibrotic
can be thickening of the basement membrane and become permanently narrow

histamines and leukotrienes going to affect the actual bronchioles(in the submucosa)

3. Asthma is reversible

Asthma is reversible, which means take away the trigger or treat them with the appropriate medication, it can be reversed they can go right back to normal

4. Controversial

Relate asthma environmentally

Hygiene hypothesis

specific for late onset asthma
people who have had reduced exposure to bacteria or viruses or pathogens, more likely or more susceptible to develop asthma later on in life

because of some type of effect on actually the maturation of our actual white blood cells

5. Reference

https://youtu.be/uQL7AYyBR-Q

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