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In this paper I will be discussing                 the pathogenesis of several hypersensitivity
reactions which are

further classified as one of four types: type I, type II,
type III, and type IV. The topics discussed will be

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allergic rhinitis, arthus reaction, contact dermatitis, and hypersensitivity
pneumonitis. To begin it is first

important to define pathogenesis; not to be confused with the
term etiology. Pathogenesis refers to

“the sequence of cellular and tissue events that take place
from the time of initial contact with an

etiologic agent until tlhe ultimate expression of a disease”
Grossman and Porth (2014). A great example

used in our text to explain etiology is the following,
“atherosclerosis often is cited as the etiology (or

cause) of coronary artery disease.”

                Allergic
rhinitis is a very common hypersensitivity affecting childrens and adults
alike. Allergic

rhinitis is considered to be a type I hypersensitivity
disorder. The hypersensitivity occurs in the nasal

mucosa when allergens are inhaled. Once inhaled, the
allergens are deposited on the nasal mucosa and

presented to T cells by antigen presenting cells. In the
presence of cellular cytokines, B lymphocyte cells

begin switching class, which result in an increase in IgE
production. IgE antibodies are needed in order

for a hypersensitivity reaction to occur. IgE production, triggers
the release of mediators like histamine,

which is responsible for the common symptoms of rhinorrhea,
sneezing, nasal itching, and watery eyes

that is associated with allergic rhinitis.

                The
Arthus reaction is a localized immune complex reaction classified as a type
III, immune

complex-mediated disorder. Arthus reaction is associated
with tissue necrosis. This reaction occurs due

to repeated exposure to an antigen where there are increased
levels of preformed antibodies, such as a

vaccine. Symptoms usually begin within one hour of an
exposure and is accompanied by localized pain,

inflammation, redness and sometimes tissue destruction. Lesions
may develop and are usually red,

raised, and inflammed. Ulcers often form at the center of
the lesion due to the release of cytokines. The

Arthus reaction mechanism is not completely understood but
is believed to be the result of localized

contact of injected antigen with circulating IgG antibody.

                Allergic
contact dermatitis is a type IV hypersensitivity reaction. This inflammatory
response

has two phases, sensitization and elicitation. The reaction
is typically localized to areas on the skin that

have come in direct contact with the agent. During the
sensitization phase, the substance is captured by

dendritic cells, which travel to regional lymph nodes and
stimulate T cell production. Reexposure

to the specific substance results in rapid activation of
memory-specific T cells. The most common, is the

dermatitis manifested by a triggered reaction.

                Hypersensitivity
pneumonitis is a form of inflammatory lung disease, resulting from a

magnified immune response after exposure to large quantities
of inhaled organic particles or 

occupational antigens. Initially it was termed “farmer’s
lung.” The exact pathophysiology of

hypersensitivity pneumonitis remains unclear, but evidence
supports a role for both type III and type IV

immune responses.

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