Walden University Alterations in Cellular Processes Discussion

At its core, pathology is the study of disease. Diseases occur for many reasons. But some, such as cystic fibrosis and Parkinson’s Disease, occur because of alterations that prevent cells from functioning normally.Understanding of signals and symptoms of alterations in cellular processes is a critical step in diagnosis and treatment of many diseases. For the Advanced Practice Registered Nurse (APRN), this understanding can also help educate patients and guide them through their treatment plans.

For this Discussion, you examine a case study and explain the disease that is suggested. You examine the symptoms reported and explain the cells that are involved and potential alterations and impacts.

Post an explanation of the disease highlighted in the scenario you were provided. Include the following in your explanation:

• The role genetics plays in the disease.
• Why the patient is presenting with the specific symptoms described.
• The physiologic response to the stimulus presented in the scenario and why you think this response occurred.
• The cells that are involved in this process.
• How another characteristic (e.g., gender, genetics) would change your response.

Rubric Detail – Blackboard Learn.pdf
Saved to Dropbox • Feb 25, 2022 at 6:58 AM
Rubric Detail
Select Grid View or List View to change the rubric’s layout.
Name: NURS_6501_Discussion_Rubric
Grid View
EXIT
List View
Main Posting
Excellent
Good
Fair
Poor
45 (45%) – 50
40 (40%) – 44
35 (35%) – 39
0 (0%) – 3
(50%)
(44%)
(39%)
Answers all
parts of the
Discussion
question(s) with
re!ective
critical analysis
and synthesis
of knowledge
gained from
the course
readings for the
module and
current credible
sources.
Responds to
the Discussion
question(s) and
is re!ective
with critical
analysis and
synthesis of
knowledge
gained from
the course
readings for the
module.
Responds to
some of the
Discussion
question(s).
Supported by
at least three
current,
credible
sources.
Written clearly
and concisely
with no
grammatical or
spelling errors
and fully
adheres to
current APA
manual writing
rules and style.
Main Post:
Timeliness
At least 75% of
post has
exceptional
depth and
breadth.
Supported by
at least three
credible
sources.
Written clearly
and concisely
with one or no
grammatical or
spelling errors
and fully
adheres to
current APA
manual writing
rules and style.
One or two
criteria are not
addressed or
are super”cially
addressed.
Is somewhat
lacking
re!ection and
critical analysis
and synthesis.
Somewhat
represents
knowledge
gained from the
course readings
for the module.
Post is cited
with two
credible
sources.
Written
somewhat
concisely; may
contain more
than two
spelling or
grammatical
errors.
Lacks de
super”ci
addresse
criteria.
Lacks re!
and critic
analysis
synthesis
Does not
represen
knowled
gained fr
course re
for the m
Contains
one or n
credible
sources.
Not writt
clearly or
concisely
Contains
than two
spelling o
gramma
errors.
Contains some
APA formatting
errors.
Does not
adhere t
current A
manual w
rules and
0 (0%) – 0 (0%)
0 (0%) – 0 (0%)
0 (0%) – 0
N/A
N/A
Does not
main pos
Day 3.
17 (17%) – 18
15 (15%) – 16
13 (13%) – 14
0 (0%) – 1
(18%)
(16%)
(14%)
Response
exhibits
synthesis,
critical thinking,
and application
to practice
settings.
Response
exhibits critical
thinking and
application to
practice
settings.
Response is on
topic and may
have some
depth.
10 (10%) – 10
(10%)
Posts main post
by Day 3.
First
Response
Does not
respond
Discussio
question
adequate
Provides clear,
concise
opinions and
ideas that are
supported by at
least two
scholarly
sources.
Demonstrates
synthesis and
understanding
of Learning
Objectives.
Communication
is professional
and respectful
to colleagues.
Responses to
faculty
questions are
fully answered,
if posed.
Communication
is professional
and respectful
to colleagues.
Responses to
faculty
questions are
answered, if
posed.
Provides clear,
concise
opinions and
ideas that are
supported by
two or more
credible
sources.
Responses
posted in the
Discussion may
lack e#ective
professional
communication.
Responses to
faculty
questions are
somewhat
answered, if
posed.
Respons
not be on
and lacks
depth.
Respons
posted in
Discussio
e#ective
professio
commun
Respons
faculty
question
missing.
No credi
sources a
cited.
Response may
lack clear,
concise
opinions and
ideas, and a few
or no credible
sources are
cited.
Response is
e#ectively
written in
standard,
edited English.
Response is
e#ectively
written in
standard,
edited English.
Second
Response
16 (16%) – 17
14 (14%) – 15
12 (12%) – 13
(17%)
(15%)
(13%)
Response
exhibits
synthesis,
critical thinking,
and application
to practice
settings.
Response
exhibits critical
thinking and
application to
practice
settings.
Response is on
topic and may
have some
depth.
Provides clear,
concise
opinions and
ideas that are
supported by at
least two
scholarly
sources.
Demonstrates
synthesis and
understanding
of Learning
Objectives.
Communication
is professional
and respectful
to colleagues.
Responses to
faculty
questions are
fully answered,
if posed.
Communication
is professional
and respectful
to colleagues.
Responses to
faculty
questions are
answered, if
posed.
Provides clear,
concise
opinions and
ideas that are
supported by
two or more
credible
sources.
Responses
posted in the
Discussion may
lack e#ective
professional
communication.
Responses to
faculty
questions are
somewhat
answered, if
posed.
0 (0%) – 1
Respons
not be on
and lacks
depth.
Respons
posted in
Discussio
e#ective
professio
commun
Respons
faculty
question
missing.
No credi
sources a
cited.
Response may
lack clear,
concise
opinions and
ideas, and a few
or no credible
sources are
cited.
Response is
e#ectively
written in
standard,
edited English.
Response is
e#ectively
written in
standard,
edited English.
Participation
5 (5%) – 5 (5%)
0 (0%) – 0 (0%)
0 (0%) – 0 (0%)
0 (0%) – 0
Meets
requirements
for
participation by
posting on 3
di#erent days.
N/A
N/A
Does not
requirem
for partic
by postin
di#erent
Total Points: 100
Name: NURS_6501_Discussion_Rubric
EXIT
NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-.
Immediate Hypersensitivity Reactions
Authors
Angel A. Justiz Vaillant; Patrick M. Zito1.
Affiliations
1
Walden University
Last Update: June 18, 2019.
Introduction
Hypersensitivity reactions (HR) are immune responses that are exaggerated
or inappropriate against an antigen or allergen. Coombs and Gell classified
hypersensitivity reactions into four forms. Type I, type II, and type III
hypersensitivity reactions are known as immediate hypersensitivity reactions
(IHR) because occur within 24 hours. Antibodies including IgE, IgM, and
IgG mediate them.[1]
Type I or Anaphylactic Response
Anaphylactic Responseis mediated by IgE antibodies that are produced by
the immune system in response to environmental proteins (allergens) such as
pollens, animal danders or dust mites. These antibodies (IgE) bind to mast
cells and basophils, which contain histamine granules that are released in the
reaction and cause inflammation. Type I hypersensitivity reactions can be
seen in bronchial asthma, allergic rhinitis, allergic dermatitis, food allergy,
allergic conjunctivitis, and anaphylactic shock.[2][3]
Anaphylaxis
Anaphylaxis is a medical emergency because can lead to an acute, lifethreatening respiratory failure. It is an IgE-mediated process. It is the most
severe form of an allergic reaction, where mast cells suddenly release a large
amount of histamine and later on leukotrienes. In severe cases intense
bronchospasm, laryngeal edema, cyanosis, hypotension, and shock are
present.[4]
Allergic bronchial asthma
Allergic bronchial asthma is an atopic disease, characterized by
bronchospasm. It may also be a chronic inflammatory disease. In its etiology,
and environmental factors along with a genetic background play an important
role. The diagnosis is dependent on history and examination. In allergic
bronchial asthma, IgE is elevated, and sputum eosinophilia is common.
Epidemiologically, a positive skin prick test or specific IgE are risk factors
for asthma.[5]
Allergic rhinitis
Allergic rhinitis is another atopic disease where histamine and leukotrienes
are responsible for rhinorrhea, sneezing and nasal obstruction. Allergens are
similar to those found in bronchial asthma. Nasal polyps may be seen in
chronic rhinitis.[6]
Allergic conjunctivitis
Allergic conjunctivitis presents with rhinitis and is IgE-mediated. Itching and
eye problems including watering, redness, and swelling always occur.[7]
Food allergy
One must differentiate food allergy (IgE-mediated) from food intolerance that
can be cause for a variety of etiology including malabsorption and celiac
disease. It is more frequent in children as seen in cow’s milk allergy. Food
allergy symptoms mostly affect the respiratory tract, the skin, and the gut.
Skin prick tests are helpful to test for food allergens that can trigger severe
reactions, e.g., peanuts, eggs, fish, and milk.[3]
Atopic eczema
Atopic eczema is an IgE-mediated disease that affects the skin and has an
immunopathogenesis very similar to that of allergic asthma and allergic
rhinitis, which are present in more than half of the diseased.
Radioallergosorbent (RAST) may reveal the specificity of the IgE antibody
involved but has little help in management.[8]
Drug allergy
Drugs may cause allergic reactions by any mechanism of hypersensitivity.
For example, penicillin may cause anaphylaxis, which is IgE-mediated but
must responses be trivial. Penicillin cross-reacts with other semisynthetic
penicillins including monobactams and carbapenems and may also crossreact with other antibiotics such as cephalosporins.[9]
Type II or Cytotoxic-Mediated Response
IgG and IgM mediate cytotoxic-mediated response against cell surface and
extracellular matrix proteins. The immunoglobulins involved in this type of
reaction damages cells by activating the complement system or by
phagocytosis. Type II hypersensitivity reactions can be seen in immune
thrombocytopenia, autoimmune hemolytic anemia, and autoimmune
neutropenia.
Immune thrombocytopenia (ITP)
ITP is an autoimmune disorder that occurs at any age. Phagocytes destroy
sensitized platelets in the peripheral blood. Clinically, it manifests by
thrombocytopenia with shortened platelet survival and increased marrow
megakaryocytes. Sudden onset of petechiae and bleeding from the gums,
nose, bowel, and urinary tract occurs. Bleeding can accompany infections,
drug reactions, malignancy and other autoimmune disorders such as thyroid
disease and SLE.[10]
Autoimmune hemolytic anemia (AIHA)
There are two types of immune hemolytic anemia: IgG-mediated (warm
AIHA) and IgM-mediated (cold AIHA). The warm type may be idiopathic
autoimmune or secondary to other diseases such as malignancy affecting the
lymphoid tissues. The cold type may be idiopathic or secondary to infections
such as Epstein-Barr virus. The primary clinical sign of the two is jaundice.
The laboratory diagnosis is made by a positive Coombs test, which identifies
immunoglobulins and C3 on red blood cells.[11]
Autoimmune neutropenia
Autoimmune neutropenia may be present with bacterial and fungal
infections, or it may occur alone or with autoimmune diseases (SLE, RA,
autoimmune hepatitis), infections and lymphoma. Bone marrow examination
is needed if neutropenia is severe. For associated autoimmune disorders, an
autoimmune antibody panel is necessary (ANA, ENA, and dsDNA).[12]
Hemolytic disease of the fetus and the newborn (erythroblastosis fetalis)
The maternal immune system suffers an initial sensitization to the fetal Rh+
red blood cells during birth, when the placenta tears away. The first child
escapes disease but the mother, now sensitized, will be capable of causing a
hemolytic reaction against a second Rh+ fetus, which develops anemia and
jaundice once the maternal IgG crosses the placenta.[13]
[14]Myasthenia gravis is an autoimmune disorder caused by antibodies to
post-synaptic acetylcholine receptors that interfere with the neuromuscular
transmission. It is characterized by extreme muscular fatigue, double vision,
bilateral ptosis, deconjugate eye movements, difficulty swallowing, and
weakness in upper arms. Babies born to myasthenic mothers can have
transient muscle weakness due to pathogenic IgG antibodies that cross the
placenta.
Goodpasture syndrome
Goodpasture syndrome is a type II hypersensitivity reaction characterized by
the presence of nephritis in association with lung hemorrhage. In most
patients, it is caused by cross-reactive autoantigens that are present in the
basement membranes of the lung and kidney. A number of patients with this
problem exhibit antibodies to collagen type IV, which is an important
component of basement membranes.[15]
Pemphigus
Pemphigus causes a severe blistering disease that affects the skin and mucous
membranes. The sera of patients with pemphigus have antibodies against
desmoglein-1 and desmoglein-3, which are components of desmosomes,
which form junctions between epidermal cells. Pemphigus is strongly linked
to HLA-DR4 (DRB1*0402), which is a molecule that presents one of the
autoantigens involved in the immunopathogenesis of this disease
(desmoglein-3).[16][17]
Type III or Immunocomplex Reactions
These are also mediated by IgM and IgG antibodies that react with soluble
antigens forming antigen-antibody complexes. The complement system
becomes activated and releases chemotactic agents that attract neutrophils
and cause inflammation and tissue damage as seen in vasculitis and
glomerulonephritis. Type III hypersensitivity reactions can classically be seen
in serum sickness and Arthus reaction.
Serum sickness
Serum sickness can be induced with massive injections of foreign antigen.
Circulating immune complexes infiltrate the blood vessel walls and tissues,
causing an increased vascular permeability and leading to inflammatory
processes such as vasculitis and arthritis. It was a complication of anti-serum
prepared in animals to which some individuals produced antibodies to the
foreign protein. It was also experienced in the treatment with antibiotics such
as penicillin.[18]
Arthus reaction
Arthus reaction is a local reaction seen when a small quantity of antigens is
injected into the skin repeatedly until detectable levels of antibodies (IgG) are
present. If the same antigen is inoculated, immune complexes develop at the
mentioned local site and in the endothelium of small vessels. This reaction is
characterized by the presence of marked edema and hemorrhage, depending
on the administered dose of the foreign antigen.[19][20]
Etiology
Multiple causes of IHR depend on the type of antigen or allergen that trigger
this inappropriate immune reactivity. In type I hypersensitivity reactions, the
allergens are proteins with a molecular weight ranging from 10 to 40 kDa.
These include cats, dust mite, German cockroaches, grass, rats, fungi, plants,
and drugs. They stimulate the IgE production. Bee and wasp venoms,
tree nuts (e.g., almond, hazelnut, walnut, and cashew), eggs, milk, latex,
antibiotics (e.g., cephalosporins), heterologous antisera, hormones (e.g.,
insulin) and others including shellfish and anesthetics can trigger
anaphylaxis.[21]
In type II hypersensitivity reactions, the antigens can be found in the
membrane of erythrocytes (e.g., A, B, O, C, c, D, d, E, e, K, k, Fy, M, and N).
In transfusion reactions, all blood groups are not equally antigenic, e.g., A or
B evoke stronger hypersensitivity reactions in an incompatible recipient than
other antigens such as Fy.[22]
In type III hypersensitivity reactions, the persistence of antigen from chronic
infection or autoimmune diseases can develop complex immune diseases,
including vasculitis and glomerulonephritis. Penicillin as an antigen can
produce any hypersensitivity reactions, e.g., anaphylactic shock, hemolytic
anemia, and serum sickness.[23]
Epidemiology
Hypersensitivity reactions are very common. Fifteen percent of the world
population will be affected by any type of allergic reaction during their lives.
In the second half of this century, allergic diseases have increased. The cause
of the increase is unknown, but it may reflect lifestyle changes, decreased
breastfeeding, and air pollution. The hygiene hypothesis proposes that since
IgE is no longer needed to protect against parasites in the Western world, the
IgE-mast cell axis has evolved in type I hypersensitivity reaction.[24][25]
European data estimate that 0.3% of the population will be troubled by
anaphylaxis at some point in their lives. In addition, 1 out of 3000 inpatients
in the United States experiences a severe allergic reaction every year.
However, the prevalence of bronchial asthma was 1.5% in Korea. FernándezSoto et al., 2018 reported that fungal infections could be as high as 50% in
inner cities and constitute a risk factor predisposed to the development of
allergic bronchial asthma.[26] Worldwide epidemiological data of
anaphylaxis are scanty and remain unavailable in many countries.
Pathophysiology
In type I hypersensitivity reactions after a previous sensitization, the
immunoglobulin (Ig) E is produced and binds to Fc receptors on mast cells
and basophils. On encountering the allergen, it triggered cross-linking of
mast-cell cytophilic IgE, causing the activation of mast cells and their
degranulation of mediators that cause an allergic reaction. The mediators that
participate in this type of hypersensitivity reaction include histamine and
lipid mediators such as PAF, LTC4, and PGD2 that cause a vascular leak,
bronchoconstriction, inflammation, and intestinal hypermotility. Enzymes
(e.g., tryptase causes tissue damage) and TNF causes inflammation.
Eosinophils release cationic granule proteins, e.g., major basic protein
(causes killing of host cells and parasites) and enzymes (e.g., eosinophil
peroxidase, which participates in tissue remodeling).[27]
In type II hypersensitivity reaction antibodies against basement membranes
produce nephritis in Goodpasture’s syndrome. Myasthenia gravis and
Lambert-Eaton syndrome are caused by antibodies that reduce the amount of
acetylcholine at motor endplates, and autoantibodies to an intercellular
adhesion molecule cause pemphigus.
In type III hypersensitivity reactions immune-complex deposition (ICD)
causes autoimmune diseases, which is often a complication. As the disease
progresses a more accumulation of immune-complexes occurs, and when the
body becomes overloaded the complexes are deposited in the tissues and
cause inflammation as the mononuclear phagocytes, erythrocytes, and
complement system fail to remove immune complexes from the blood.
Histopathology
Human basophils present multi-lobed nuclei and distinctive granules. They
can be found in local tissues including the nose, lungs, skin or gut in response
to allergic and immune responses. The two populations of mast cells are
mucosal and connective tissue. They have morphological and
pharmacological differences. The mucosal mast cells can associate with a
parasitic infestation, and connective tissue mast cells are smaller and live
shorter. Both contain histamine and serotonin in their granules. Skin biopsy
of patients with allergic dermatitis shows inflammatory infiltrate with few
eosinophils, but their degranulation in the skin demonstrated in the biopsy
stained with antibodies against eosinophil major basic protein (MBP). In the
nasal smear of a patient with acute bronchial asthma, an infiltrate consistent
of eosinophils, and polymorphonuclear cells with a normal cytoplasm stained
with hematoxylin and eosin were shown.[28][29]
In type II hypersensitivity reactions, autoantibodies bind to desmosome
involved in cell adhesion, and autoantibodies in diabetes mellitus bind to islet
cells. They can be demonstrated in tissues by immunofluorescence. The
method that uses fluorescent antibodies has also been used in type
III hypersensitivity reactions to demonstrate the presence of immune
complexes in the intima and media of the arterial wall, as well as IgG and C3
deposits in kidney, joints, arteries, and skin. In Goodpasture syndrome, the
antibodies involved are IgG and have the capacity to fix complement.
Necrosis of the glomerulus, with fibrin deposition, is a major feature of this
syndrome.[30][31]
History and Physical
In type I hypersensitivity reactions there is a history of atopy or a patient
suffering from an allergic condition (e.g., bronchial asthma, allergic rhinitis,
or food allergy). It may associate with recurrent infections caused by viruses
and bacteria. For instance, bronchial asthma may link to recurrent bacterial
pneumonia. Clinically allergic disorders may accompany by airways
inflammation, wheezing attack, bronchial hyper-responsiveness, tachycardia,
tachypnea, intense itching of the eyes and nose, sneezing, rhinorrhea,
dermatitis, and gastrointestinal symptoms. Anaphylaxis, the most severe type
of allergy, is clinically characterized by bronchospasm, angioedema,
hypotension, loss of consciousness, generalized skin rash, nausea, vomiting,
and abdominal cramps among other symptoms.[32]
In type II hypersensitivity reactions, a patient may report multiple blood
transfusions, rhesus incompatibility, and drug history. Clinically, it may
manifest as autoimmunity, e.g., autoimmune hemolytic anemia (characterized
by jaundice), immune thrombocytopenia (characterized by bleeding
disorders), and other blood dyscrasia (autoimmune neutropenia). In this type
of hypersensitivity, drugs may attach to red blood cells and stimulate the
production of anti-red blood cell antibodies or anti-dsDNA antibody that
causes drug-induced systemic lupus erythematosus (SLE).[33][34]
Type III hypersensitivity reactions may manifest as immune complexmediated diseases including glomerulonephritis, vasculitis, serositis, arthritis,
and skin manifestations of autoimmunity such as malar rash, which is due to
photosensitivity. The prevalence of serum sickness has decreased
dramatically because animal anti-serum is rarely used to treat or prevent
infectious diseases. General manifestations of disease including anorexia,
loss of weight, and asthenia may report in IHR.[35]
Evaluation
The evaluation of immediate hypersensitivity includes complete blood cell
count, assessment of immunoglobulins, skin prick test, and detection of
autoantibodies.[4][36][37][38]
Quantitative Serum Immunoglobulins
•
IgG (involved in Type II and III HR)
•
IgM (involved in Type II and III HR)
•
IgE (elevated in allergic diseases)
Total Leukocyte Count and Differential
•
Hb (decreased in autoimmune hemolytic anemia)
•
Neutrophils (decreased in autoimmune neutropenia)
•
Lymphocytes (decreased in autoimmune lymphopenia)
•
Platelets (decreased in immune thrombocytopenia)
Autoimmunity Studies
•
Anti-nuclear antibodies (ANA, present in systemic autoimmune
disorders, such as SLE and RA)
•
Detection of specific auto-immune antibodies for systemic disorders,
e.g., anti-ds DNA, rheumatoid factor, anti-histones, anti-Smith, anti(SS-A) and anti-(SS-B)
•
Detection of anti-RBC, antiplatelet, and anti-neutrophil antibodies
•
Testing for organ-specific auto-immune antibodies, e.g., the anti-Islet
cell autoantibody that is present in diabetes mellitus
•
Coombs test (positive in autoimmune hemolytic anemia)
Allergic test
•
Skin prick tests using various allergens from animal, plants, food,
pathogens and environmental pollutants
•
Radioallergosorbent test (RAST): Use to determine specific IgE
antibodies
Treatment / Management
The treatment of immediate hypersensitivity reactions includes the
management of anaphylaxis with intramuscular adrenaline (epinephrine),
oxygen, intravenous (IV) antihistamine, support blood pressure with IV
fluids, avoid latex gloves and equipment in patients who are allergic, and
surgical procedures such as tracheotomy if there is severe laryngeal edema.
Allergic bronchial asthma can be treated with any of the following: inhaled
short- and long-acting bronchodilators (anticholinergics) along with inhaled
corticosteroids, leukotriene antagonists, use of disodium cromoglycate, and
environmental control. Experimentally, a low dose of methotrexate or
cyclosporin and omalizumab (a monoclonal anti-IgE antibody) has been
used. Treatment of autoimmune disorders (e.g., SLE) include one or a
combination of NSAIDs and hydroxychloroquine, azathioprine,
methotrexate, mycophenolate, cyclophosphamide, low dose IL-2, intravenous
immunoglobulins, and belimumab. Omalizumab is a monoclonal antibody
that interacts with the binding site of the high-affinity IgE receptor on mast
cells. It is an engineered, humanized recombinant immunoglobulin. Moderate
to severe allergic bronchial asthma can improve with
omalizumab.[14][32][39][40]
Differential Diagnosis
Allergic bronchial asthma must be ruled out from other classes of asthma
based on the family history of atopy and a positive skin prick test. Chronic
allergic bronchial asthma loses reversibility and is indistinguishable from
chronic obstructive pulmonary disease (COPD).
Allergic rhinitis must rule out other causes of rhinitis including vasomotor,
non-allergic rhinitis with eosinophilia, drug-induced (cocaine abuse),
mechanical (tumors, foreign body, sarcoidosis) and infectious including viral,
bacterial and leprosy. In allergic rhinitis, IgE is elevated, and prick test is
positive for similar allergens as those in allergy bronchial asthma. Also,
family predisposition to allergies may be present.
Autoimmune hemolytic anemia (AIHA) can rule out from other anemias
based on the presence of a positive direct Coombs’ test. Sometimes the AIHA
is secondary to lymphoma or autoimmune disease, especially SLE, where
other blood dyscrasias including immune thrombocytopenia and autoimmune
neutropenia may be present besides with the presence of anti-dsDNA
antibodies, and clinical signs including malar rash, nephropathy, vasculitis,
serositis, neuropathy, and among other problems.
Prognosis
The prognosis of IHR depends on the severity of the disorders, the extension
of the inflammation and tissue damage, and the available treatment and their
effectiveness to control the disease. Relapsing or slow progression
characterizes myasthenia gravis. If presents with thymoma, 68% of the
affected have a 5-year survival. In SLE, approximately 80% survive at 15
years if treated. Atopic eczema (dermatitis) is usually most severe in infancy
and improves with age in 80% of the cases. Allergic bronchial asthma that
does not respond to steroids has a reserved prognosis.[41]
The prognosis of other allergic disorders, including food allergy, drug
allergy, latex allergy, allergic conjunctivitis, and allergic rhinitis is good once
the triggers identified using skin prick test or RAST and treatment with antihistamine occurs. The use of monoclonal antibodies directed to IgE (e.g.,
omalizumab) has improved the prognosis of patients that do not respond well
to conventional therapy, although the acquisition of these biologicals is
expensive. The use of vaccines, some classic and recently experimental, is
another avenue of treatment of allergic disorders that improve the life
expectancy and quality of individuals with allergies.
Complications
Some of the complications of immediate hypersensitivity reactions are:
Status Asthmaticus
This is a type I hypersensitivity reaction, an acute exacerbation of bronchial
asthma that does not respond to the standard therapy with bronchodilators. It
is a medical emergency and must require aggressive treatment.[42]
Anaphylactic Shock
This is an allergic reaction, often life-threatening, triggered by an allergen to
which the immune system over-reacts.[43]
Post-Transfusion Reaction
This is a hypersensitivity reaction that occurs within 24 hours of a blood
transfusion. Hemoglobinuria that appears during or after the procedure
becomes an alarming sign. Other manifestations include back pain, fever,
chills, dizziness, and dyspnea.[44]
Serum Sickness
This is a type III hypersensitivity reaction that commences after the
administration of a drug (e.g., penicillin) or heterologous anti-serum or
plasma. Clinically, it is characterized by skin rash, fever, arthralgias, or
arthritis. Immune-complexes mediate this complication, and it may affect
many organs.[45]
Deterrence and Patient Education
Healthcare professionals can advise allergic patients about environmental
control at home and work. Every attempt to reduce high humidity and to
decrease house dust-mite exposure must do. The bedroom should be clean,
and many use mattress covers and wash bedclothes regularly. Pets, including
cats and dogs, are often the source of allergens and should not be in
convivence with the affected patient, nor should living plants and flowers,
which are “a sack of antigens.” Patients should be encouraged to
explore therapeutic options for acute or chronic desensitization for “bad
allergens.” This may be the only way to control their allergic bronchial
asthma.
Enhancing Healthcare Team Outcomes
The management of an immediate hypersensitive reaction is best done with a
multidisciplinary team that includes ICU nurses.
To improve patient outcomes, clinicians should be aware that immediate
hypersensitivity reactions are a medical emergency. No time should be
wasted with blood work or imaging studies. The treatment of immediate
hypersensitivity reactions includes the management of anaphylaxis with
intramuscular adrenaline (epinephrine), oxygen, intravenous (IV)
antihistamine, support blood pressure with IV fluids, avoid latex gloves and
equipment in patients who are allergic, and surgical procedures such as
tracheotomy if there is severe laryngeal edema. These patients are best
managed in an ICU setting.
Healthcare professionals should advise allergic patients about environmental
control at home and work. Every attempt to reduce high humidity and to
decrease house dust-mite exposure must do. The bedroom should be clean,
and many use mattress covers and wash bedclothes regularly. Pets, including
cats and dogs, are often the source of allergens and should not be in
convivence with the affected patient, nor should living plants and flowers,
which are “a sack of antigens.” Patients should be encouraged to
explore therapeutic options for acute or chronic desensitization for “bad
allergens.” This may be the only way to control their allergic bronchial
asthma.
Questions
To access free multiple choice questions on this topic, click here.
References
1. Son JH, Park SY, Cho YS, Chung BY, Kim HO, Park CW. Immediate
Hypersensitivity Reactions Induced by Triamcinolone in a Patient with
Atopic Dermatitis. J. Korean Med. Sci. 2018 Mar 19;33(12):e87. [PMC
free article: PMC5852418] [PubMed: 29542298]
2. Tomasiak-Łozowska MM, Klimek M, Lis A, Moniuszko M, BodzentaŁukaszyk A. Markers of anaphylaxis – a systematic review. Adv Med
Sci. 2018 Sep;63(2):265-277. [PubMed: 29486376]
3. Koike Y, Sato S, Yanagida N, Asaumi T, Ogura K, Ohtani K, Imai T,
Ebisawa M. Predictors of Persistent Milk Allergy in Children: A
Retrospective Cohort Study. Int. Arch. Allergy
Immunol. 2018;175(3):177-180. [PubMed: 29393170]
4. Vandervoort R. Allergy and Asthma: Anaphylaxis. FP Essent. 2018
Sep;472:20-24. [PubMed: 30152670]
5. Lee E, Kim M, Jeon K, Lee J, Lee JS, Kim HS, Kang HJ, Lee YK. Mean
Platelet Volume, Platelet Distribution Width, and Platelet Count, in
Connection with Immune Thrombocytopenic Purpura and Essential
Thrombocytopenia. Lab Med. 2019 Jul 16;50(3):279-285. [PubMed:
30726936]
6. Justiz Vaillant AA, Zito PM. StatPearls [Internet]. StatPearls Publishing;
Treasure Island (FL): Feb 22, 2019. Neutropenia. [PubMed: 29939524]
7. Leonard A, Hittson Boal L, Pary P, Mo YD, Jacquot C, Luban NL,
Darbari DS, Webb J. Identification of red blood cell antibodies in
maternal breast milk implicated in prolonged hemolytic disease of the
fetus and newborn. Transfusion. 2019 Apr;59(4):1183-1189. [PubMed:
30720868]
8. Jastrzębska A, Jastrzębski M, Ryniewicz B, Kostera-Pruszczyk A.
Treatment outcome in juvenile-onset myasthenia gravis. Muscle
Nerve. 2019 May;59(5):549-554. [PubMed: 30734335]
9. De A, Rajagopalan M, Sarda A, Das S, Biswas P. Drug Reaction with
Eosinophilia and Systemic Symptoms: An Update and Review of Recent
Literature. Indian J Dermatol. 2018 Jan-Feb;63(1):30-40. [PMC free
article: PMC5838752] [PubMed: 29527023]
10. Atanaskovic-Markovic M, Gomes E, Cernadas JR, du Toit G, Kidon M,
Kuyucu S, Mori F, Ponvert C, Terreehorst I, Caubet JC. Diagnosis and
management of drug-induced anaphylaxis in children: An EAACI
position paper. Pediatr Allergy Immunol. 2019 May;30(3):269276. [PubMed: 30734362]
11. Arzoo K, Sadeghi S, Liebman HA. Treatment of refractory antibody
mediated autoimmune disorders with an anti-CD20 monoclonal antibody
(rituximab). Ann. Rheum. Dis. 2002 Oct;61(10):922-4. [PMC free
article: PMC1753910] [PubMed: 12228164]
12. Horneff G, Seitz RC, Stephan V, Wahn V. Autoimmune haemolytic
anaemia in a child with MHC class II deficiency. Arch. Dis. Child. 1994
Oct;71(4):339-42. [PMC free article: PMC1030015] [PubMed: 7979529]
13. Hsiao YP, Tsai JD, Muo CH, Tsai CH, Sung FC, Liao YT, Chang YJ,
Yang JH. Atopic diseases and systemic lupus erythematosus: an
epidemiological study of the risks and correlations. Int J Environ Res
Public Health. 2014 Aug 08;11(8):8112-22. [PMC free article:
PMC4143852] [PubMed: 25111878]
14. Wang KY, Friedman DF, DaVeiga SP. Immediate hypersensitivity
reaction to human serum albumin in a child undergoing
plasmapheresis. Transfusion. 2019 Jun;59(6):1921-1923. [PubMed:
30758852]
15. Shamji MH, Thomsen I, Layhadi JA, Kappen J, Holtappels G, Sahiner
U, Switzer A, Durham SR, Pabst O, Bachert C. Broad IgG repertoire in
patients with chronic rhinosinusitis with nasal polyps regulates
proinflammatory IgE responses. J. Allergy Clin. Immunol. 2019
Jun;143(6):2086-2094.e2. [PubMed: 30763592]
16. Fauquert JL. Diagnosing and managing allergic conjunctivitis in
childhood: The allergist’s perspective. Pediatr Allergy Immunol. 2019
Jun;30(4):405-414. [PubMed: 30742722]
17. Dou J, Zeng J, Wu K, Tan W, Gao L, Lu J. Microbiosis in pathogenesis
and intervention of atopic dermatitis. Int. Immunopharmacol. 2019
Apr;69:263-269. [PubMed: 30743202]
18. Blumenthal KG, Peter JG, Trubiano JA, Phillips EJ. Antibiotic
allergy. Lancet. 2019 Jan 12;393(10167):183-198. [PMC free article:
PMC6563335] [PubMed: 30558872]
19. Li TX, Sun FT, Ji BJ. [Correlation of IgG Subclass with Blood Cell
Parameters in Patients with Autoimmune Hemolytic anemia]. Zhongguo
Shi Yan Xue Ye Xue Za Zhi. 2019 Feb;27(1):197-201. [PubMed:
30738470]
20. Vries TB, Boerma S, Doornebal J, Dikkeschei B, Stegeman C,
Veneman TF. Goodpasture’s Syndrome with Negative Anti-glomerular
Basement Membrane Antibodies. Eur J Case Rep Intern
Med. 2017;4(8):000687. [PMC free article: PMC6346855] [PubMed:
30755961]
21. Evans MS, Culton DA, Diaz LA, Googe PB, Morrell DS. Childhood
pemphigus foliaceus presenting as a polycyclic eruption: Case report and
review of the literature. Pediatr Dermatol. 2019 Mar;36(2):236241. [PubMed: 30762246]
22. Buonavoglia A, Leone P, Dammacco R, Di Lernia G, Petruzzi M,
Bonamonte D, Vacca A, Racanelli V, Dammacco F. Pemphigus and
mucous membrane pemphigoid: An update from diagnosis to
therapy. Autoimmun Rev. 2019 Apr;18(4):349-358. [PubMed:
30738958]
23. Owczarczyk-Saczonek A, Wygonowska E, Budkiewicz M, Placek W.
Serum sickness disease in a patient with alopecia areata and Meniere’
disease after PRP procedure. Dermatol Ther. 2019
Mar;32(2):e12798. [PubMed: 30511475]
24. Gershwin LJ. Adverse Reactions to Vaccination: From Anaphylaxis to
Autoimmunity. Vet. Clin. North Am. Small Anim. Pract. 2018
Mar;48(2):279-290. [PubMed: 29195924]
25. Ghazavi MK, Johnston GA. Insulin allergy. Clin. Dermatol. 2011 MayJun;29(3):300-5. [PubMed: 21496738]
26. Croote D, Darmanis S, Nadeau KC, Quake SR. High-affinity allergenspecific human antibodies cloned from single IgE B cell
transcriptomes. Science. 2018 Dec 14;362(6420):1306-1309. [PubMed:
30545888]
27. Okamoto T, Hashimoto M, Samejima H, Mori A, Wakabayashi M,
Takeda A, Nakamura H, Naruse H, Bouike Y, Araki N. Mechanisms
responsible for delayed and immediate hemolytic transfusion reactions in
a patient with anti-E + Jk(b)+ Di(b) and anti-HLA
alloantibodies. Immunopharmacol Immunotoxicol. 2004;26(4):64552. [PubMed: 15658612]
28. Kim DH, Choi YH, Kim HS, Yu JE, Koh YI. A case of serum sicknesslike reaction and anaphylaxis – induced simultaneously by
rifampin. Allergy Asthma Immunol Res. 2014 Mar;6(2):183-5. [PMC
free article: PMC3936050] [PubMed: 24587958]
29. Allaerts W, Chang TW. Skewed Exposure to Environmental Antigens
Complements Hygiene Hypothesis in Explaining the Rise of
Allergy. Acta Biotheor. 2017 Jun;65(2):117-134. [PMC free article:
PMC5418306] [PubMed: 28342137]
30. Burton OT, Epp A, Fanny ME, Miller SJ, Stranks AJ, Teague JE, Clark
RA, van de Rijn M, Oettgen HC. Tissue-Specific Expression of the LowAffinity IgG Receptor, FcγRIIb, on Human Mast Cells. Front
Immunol. 2018;9:1244. [PMC free article: PMC5997819] [PubMed:
29928276]
31. Diaferio L, Chiriac AM, Leoni MC, Castagnoli R, Caimmi S, Miniello
VL, Demoly P, Caimmi D. Skin tests are important in children with βlactam hypersensitivity, but may be reduced in number. Pediatr Allergy
Immunol. 2019 Jun;30(4):462-468. [PubMed: 30734416]
32. Beickert Z. [Classification, diagnosis, and therapy of immunological
aspects of disease according to reaction types]. Z Gesamte Inn
Med. 1975 Sep 15;30(18):589-95. [PubMed: 129967]
33. Kotur G, Kotur G, Horvatić I, Galešić D, Jubanović L, Galešić K.
[GOODPASTURE’S SYNDROME–CASE REPORTS]. Lijec
Vjesn. 2015 May-Jun;137(5-6):171-6. [PubMed: 26380476]
34. Agulló-García A, Cubero Saldaña JL, Colás Sanz C. Series of 12 cases
of wheat-dependent exercise-induced allergy in Aragon, Spain. Rev Clin
Esp. 2019 May;219(4):184-188. [PubMed: 30651196]
35. Mori F, Liccioli G, Piccorossi A, Sarti L, Barni S, Giovannini M, Azzari
C, Manfredi M, Novembre E. The Diagnosis of Ceftriaxone
Hypersensitivity in a Paediatric Population. Int. Arch. Allergy
Immunol. 2019;178(3):272-276. [PubMed: 30605910]
36. Braun V, Darrigade AS, Milpied B. Positive patch test reaction to
carbamazepine after a very long delay. Contact Derm. 2018
Oct;79(4):240-241. [PubMed: 29799125]
37. Iordache AM, Docea AO, Buga AM, Mitrut R, Albulescu D, Zlatian O,
Ianosi S, Ianosi G, Neagoe D, Sifaki M, Rogoveanu OC, Branisteanu
DE, Calina D. The incidence of skin lesions in contrast media-induced
chemical hypersensitivity. Exp Ther Med. 2019 Feb;17(2):11131124. [PMC free article: PMC6327547] [PubMed: 30679982]
38. Seremet T, Haccuria A, Lienard D, Del Marmol V, Neyns B.
Anaphylaxis-like reaction to anti-BRAF inhibitor dabrafenib confirmed
by drug provocation test. Melanoma Res. 2019 Feb;29(1):9598. [PubMed: 30383722]
39. Liao B, Zeng M, Liu JX. [The assessment value of peripheral blood
eosinophils for treatment prognosis of chronic rhinosinusitis]. Lin Chung
Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2019 Jan;33(1):5-8. [PubMed:
30669190]
40. Khedher A, Meddeb K, Sma N, Azouzi A, Fraj N, Boussarsar M.
Pulmonary Barotrauma Including Huge Pulmonary Interstitial
Emphysema in an Adult with Status Asthmaticus: Diagnostic and
Therapeutic Challenges. Eur J Case Rep Intern
Med. 2018;5(5):000823. [PMC free article: PMC6346923] [PubMed:
30756032]
41. Kim TH, Yoon SH, Hong H, Kang HR, Cho SH, Lee SY. Duration of
Observation for Detecting a Biphasic Reaction in Anaphylaxis: A MetaAnalysis. Int. Arch. Allergy Immunol. 2019;179(1):31-36. [PubMed:
30763927]
42. Yoon U, Abdullah M, Elia E, Herman J. Intraoperative Diagnosis and
Management of Acute Hypotensive Blood Transfusion Reaction
(AHTR): A Report of Two Cases. Am J Case Rep. 2018 Oct
29;19:1283-1287. [PMC free article: PMC6223195] [PubMed:
30369594]
43. Patterson-Fortin J, Harris CM, Niranjan-Azadi A, Melia M. Serum
sickness-like reaction after the treatment of cellulitis with
amoxicillin/clavulanate. BMJ Case Rep. 2016 Oct 18;2016 [PMC free
article: PMC5073577] [PubMed: 27756758]
44. Tanno LK, Bierrenbach AL, Simons FER, Cardona V, Thong BY,
Molinari N, Calderon MA, Worm M, Chang YS, Papadopoulos NG,
Casale T, Demoly P., on behalf the Joint Allergy Academies. Critical
view of anaphylaxis epidemiology: open questions and new
perspectives. Allergy Asthma Clin Immunol. 2018;14:12. [PMC free
article: PMC5883526] [PubMed: 29632547]
45. Fernández-Soto R, Navarrete-Rodríguez EM, Del-Rio-Navarro BE,
Sienra-Monge JJL, Meneses-Sánchez NA, Saucedo-Ramírez OJ. Fungal
Allergy: Pattern of sensitization over the past 11 years. Allergol
Immunopathol (Madr). 2018 Nov – Dec;46(6):557-564. [PubMed:
29739683]
Copyright © 2019, StatPearls Publishing LLC.
This book is distributed under the terms of the Creative Commons Attribution 4.0 International License
(http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution, and reproduction in
any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to
the Creative Commons license, and any changes made are indicated.
Bookshelf ID: NBK513315PMID: 30020687