UNP-MEDICINE 2021 INTERNAL MEDICINE

ALLERGIES AND ANAPHYLAXIS

LECTURER: Ma Eileen O Pascua, MD, FPCP, APRIL 8, 2020
FPSG, FPSDE
HEAD NOTES
 TITLE/EMPHASIZED
 AUDIO b) Environmental Factors
 NOTES/RECALLS/ADD-ONS  Alterations in exposure to infectious diseases
during early childhood
 Environmental pollution
ALLERGY
 Allergen levels
 Are conditions caused by hypersensitivity of the immune  Dietary changes
system to typically certain substances in the environment
They includes:
1. Hay fever (Allergic rhinitis)
2. Food allergies
3. Atopic Dermatitis
4. Allergic Asthma
5. Anaphylaxis
Allergic diseases are conditions caused by hypersensitivity of
the immune system to typically certain substances in the environment
When you say Hypersensitivity - it is also termed as ‖hypersensitivity
reaction or intolerance;
It refers to undesirable reactions produced by the normal immune
system that can be damaging, uncomfortable, or occasionally fatal to
the body host.
Allergies actually are common:
 20% of people are affected by allergic rhinitis
 6% of people have at least one food allergy
 20% have atopic dermatitis,
 18% have asthma
 and that Anaphylaxis occurs in between 0.05–2% of people.
A. The allergen enters the body.
B. an Antigen-presenting cell (APC) takes up the allergen molecule
Common substances: ―Allergens‖ and presents its epitopes, through the MHC II receptor, onto its
1. Airborn allergens: pollen, animal danders, dust mites, molds surface. The activated APC then migrates to the nearest lymph
2. Certain foods: peanuts, tree nuts, wheat, soy, fish, shellfish, node,
eggs, milk C. Where it activates T cells that recognize the allergen. They then
3. Insect stings bees or wasp give the decision for the T cell to differentiate to Th2 cell
4. Medications: Antibiotics D. And at the same time, B cells recognize the allergen and thru the
Development is due to both genetic and environmental factors activated Th2 cell
E. The B cell would be activated.
The substances that elicits the hypersensitivity reactions are called F. And differentiate into plasma cells, at which point they would
Allergens. actively synthesize antibodies of the IgE isotype.
Many allergens such as dust or pollen are airborne particles. G. The IgE antibody, that now recognizes epitopes of the allergen
In these cases, symptoms arise in areas in contact with air, such as molecule, circulates around the body thru
eyes, nose, and lungs. For instance, allergic rhinitis, causes irritation lymphatic & cardiovascular systems & finally binds to
of the nose, sneezing, itching, and redness of the eyes. Inhaled its FcεRI receptor on mast and basophil cells.
allergens can also lead to increased production of mucus in H. When the allergen re-enters the body at a later time it binds to the
the lungs, shortness of breath, coughing, and wheezing. IgE,, resulting in an aggregation of the receptor causing the cells
to release pre-formed mediators (Histamine & IL-4)
One of these mediators is . Another mediator is IL-4, which
RISK FACTORS FOR ALLERGY DEVELOPMENT affects more B cells to differentiate into plasma cells and produce
2 Categories more IgE and thus the vicious cycle
a) Host Factors:
 Heredity
 Sex
 Race  The underlying mechanism involves immunoglobulin E
 Age antibodies (IgE),
The risk of allergic sensitization and the development of allergies  Binding to an allergen
varies with age, with young children most at risk.  And then to a receptor on a mast cells or basophils,
Several studies have shown that IgE levels are highest in childhood  Where it triggers the release of inflammatory chemicals
and fall rapidly between the ages of 10 and 30 years. The peak  Such as histamine,
prevalence of hay fever is highest in children and young adults and  Which causes the 5 symptoms of allergic reaction:
the incidence of asthma is highest in children under 10.  Heat, pain, swelling, redness, and itching
Overall, boys have a higher risk of developing allergies than girls,
although for some diseases, namely asthma in young adults, females In other words, IgE is released to destroy the allergen and causes the
are more likely to be affected. These differences b/w the sexes tend production of chemicals that triggers reaction, one of w/c is
to decrease in adulthood. Histamine.
Ethnicity may play a role in some allergies; however, racial factors
have been difficult to separate from environmental influences and
changes due to migration.

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PATHOGENESIS OF ANAPHYLAXIS  The frequency of a reaction to an agent partly depends on
 a simplified illustration on the Pathogenesis of anaphylaxis: the frequency of its use and partly on its intrinsic properties
mechanisms and triggers, cells, mediators, and organ  Other relatively common causes: chemotherapy, vaccines,
systems affected herbal preparations
 Some medications (vancomycin, morphine, x-ray contrast
among others) cause anaphylaxis by directly trigerring mast
cell degranulation
So be careful in giving medicines to your future patients, always ask
for any allergy history :)

VENOM AND INSECT STINGS

 Form stinging or biting insects such as Hymenoptera (ants,
bees , and wasps) or Triatomine (kissing bugs) may cause
anaphylaxis in susceptible people.
 Insects which generate allergic responses are either stinging
insects (wasps, bees, hornets and ants) or biting insects
(mosquitoes, ticks)
 Stinging insects inject venom into their victims, whilst biting
insects normally introduce anti-coagulants.
Why? What are the components in insect venom that can cause an
allergic reaction?
Histamine is found in venom, that can cause itchiness and
inflammation.
Also the proteins in the sting can cause an allergic reaction, leading to
the release of even more histamine, and possible anaphylaxis
FOOD In those who are allergic to bee stings, the venom triggers a more
 A wide variety of foods can cause allergic reactions, but severe immune system reaction by producing antibodies IgE.
90% are caused by cow’s milk, soy, eggs, wheat, peanuts, Usually, IgE protects the body from dangerous substances. However,
tree nuts, fish, and shellfish. in response to a sting, the body produces IgE that causes an
 Rates of allergies differ between adults and children. inappropriate immune responses, such as hives, swelling, and
 Peanut allergies can sometimes be out grown by children. respiratory problems, the next time a person is stung. Meaning, these
Those with tree nut allergies may be allergic to other nuts: people may not have an allergic reaction the first time they are stung
pecans, pistachios, pine nuts, walnuts. but may have an allergic reaction to a second bee sting.
 Sesame seeds and poppy seeds, contain oils in which
protein is present, which may elicit an allergic reaction GENETICS
 Egg allergies affect 1-2% of children but are outgrown by  Allergic diseases are strongly familial: identical twins are
about 2/3 of children by the age of 5. The sensitivity is likely to have the same allergic diseases about 70% of the
usually to proteins in the white, rather than eggyolk. time; the same allergic occurs about 40% of the time in
 Milk protein allergies are most common in children. non-identical twins
Approximately 60% of milk-protein reactions are IgE-  Allergic parents are more likely to have allergic children and
mediated (may also unable to tolerate dairy products, like those children’s allergies are likely to be more severe than
cheese) those in children of non-allergic parents.
Although peanut allergies are notorious for their severity, peanut It seems that the likelihood of developing allergies is inherited and
allergies are not the most common food allergy in adults or children. related to an irregularity in the immune system, but the
The use of hydrolysed milk baby formula versus standard milk baby specific allergen is not
formula does not appear to change the risk Some allergies, however, are not consistent along genealogies;
parents who are allergic to peanuts may have children who are
LATEX allergic to ragweed pollen
 Can trigger an IgE-mediated cutaneous, respiratory and
systemic reactions HYGIENE HYPOTHESIS
 The most prevalent response to latex is an allergic  It is used to explain the increase in allergic diseases that
contact dermatitis, a delayed hypersensitive reaction have been seen since industrialization, and the higher
appearing as dry, crusted lesions. incidence of allergic diseases in more developed countries
 This reaction usually last 48-96 hours.  Allergic diseases are caused by inappropriate immunological
 Sweating or rubbing the area under the glove aggravates he responses to harmless antigens driven by a TH2-mediated
lesions, possibly leading to ulcerations. immune response
Of course, higher level to the exposure of healthcare workers to areas  Many bacteria and viruses elicit a TH1-mediated immune
with significant airborne latex allergens, such as operating rooms, response, which don regulates TH2 responses, meaning
intensive-care units, and dental suites. insufficient stimulation of the TH-1 arm of the immune
But for now, we lack most available materials& you know the very system leads to an overactive TH-2 arm, which in turn leads
reason why :( to allergic disease.
 Thus, individuals living in too sterile environment are not
MEDICATIONS exposed to enough pathogens to keep the immune system
 Serious allergies only occur in about 0.03% busy. Since our bodies involved to deal with a certain level
 The most common are the Beta-lactam antibiotics (such as of such pathogens, when they are not exposed to this level,
penicillin) followed by aspirin and NSAIDs. the immune system will attack harmless antigens and thus
 Anaphylactic reactions to the NSAIDs are either agent normally benign microbial object, like pollen, will trigger an
specific or occur among those that are structurally similar immune response
meaning that those who are allergic to one NSAID can Gutworms and similar parasites are present in untreated drinking
typically tolerate a different one or different group of water in developing countries, and were present in the water of
NSAIDs. developed countries until the routine chlorination and purification of
drinking water supplies.

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EXAMPLE: SKIN
Some common parasites, (hookworms), secrete chemicals into the gut  Substances that come into contact with the skin, causes
wall (and, hence, the bloodstream) that suppress the immune system allergic reactions, ―contact dermatitis or eczema‖
and prevent the body from attacking the parasite. This gives rise to a  Skin allergies frequently cause rashes, or swelling and
new slant on the hygiene hypothesis theory—that co-evolution of inflammation within the skin, ―wheal and flare‖ reaction
humans and parasites has led to an immune system that functions char. Of hives and angioedema
correctly only in the presence of the parasites. Without them, the  Typical symptoms: generalized hives, itchiness, flushing, or
immune system becomes unbalanced and oversensitive. swelling (angioedema) of the afflicted tissues, burning
In particular, research suggests that allergies may coincide with the sensation of the skin, swelling of the tongue or throat,
delayed establishment of gut flora in infants. runny nose, itchy eyes, cyanosis
The hygiene hypothesis has now expanded to include exposure to  With insect stings a large local reaction may occur (an area
symbiotic bacteria and parasites as important modulators of immune of skin redness greater than 10 cm size)
system development, along with infectious agents.

STRESS RESPIRATORY
 Chronic stress can aggravate allergic conditions  Shortness of breath, wheezes, or stridor
 This has been attributed to a T helper 2 (TH2)-predominant  The wheezing is typically caused by spasms of the bronchial
response driven by a suppression of interleukin 12 by both muscles while stridor is related to upper airway obstruction
autonomic nervous system and the hypothalamic-pituitary- secondary to swelling
adrenal axis  Hoarseness, painful swallowing, cough may also occur
 Stress management in highly susceptible individuals may
improve symptoms CARDIOVASCULAR
With what’s happening now days  Tachycardia, hypotension, light-headedness or loss of
Fear of contracting the COVID Virus, fear of unavailability of foods & consciousness
grocery items. Fear that classes will not resume soon and you will not  Coronary artery spasm may occur with subsequent
see yet your long time crush & love of your life. Or Fear of losing an myocardial infarction, dysrhythmia, or cardiac arrest.
internet access? Are not all these causes stress?  The coronary spasm is related to the presence of histamine-
releasing cells in the heart
Yes, when you're all stressed out, your body releases hormones &
other chemicals like histamines that lead to allergy symptoms. Or GASTROINTESTINAL
while stress doesn’t actually cause allergies, it can make an allergic  Abdominal pain, diarrhea, and vomiting
reaction worse by increasing the histamine in the bloodstream.  Loss of bladder control or pelvic pain/cramps

ACUTE RESPONSE DIAGNOSIS

This is how the body responds to it.  Allergic testing can help confirm or rule out allergies
In the early stages of allergy, a type I hypersensitivity reaction against  2 methods to assess the presence of allergen-specific IgE
an allergen encountered for the first time and presented by a antibodies:
professional antigen-presenting cells cause s a response in TH2  Skin Prick Test
lymphocyte, which produces cytokine, interleukin-4 (IL-4)  Allergy Blood Test
↓  Since allergy undergoes dynamic changes over time, regular
TH2 cells interact with other lymphocytes called ―B cells‖; whose role allergic testing of relevant allergens provides information on
is production of antibodies. Coupled with signals provided by IL-4, this if and how patient management can be changed, in order to
interaction stimulates the B cell to begin production of a large amount improve health and quality of life
of antibody, ―IgE.‖ Annual testing is often the practice for determining whether allergy to
↓ milk, egg, soy, and wheat have been outgrown, and some textbooks
Secreted IgE circulates in the blood and binds to an IgE-specific recommends that testing interval is extended to 2–3 years for allergy
receptor (FcεRI) on the surface immune cells (like mast cells and to peanut, tree nuts, fish, and crustacean shellfish
basophils), which are both involved in the acute inflammatory
response. Because results of follow-up testing can guide decision-making
↓ regarding whether and when it is safe to introduce or re-introduce
The IgE-coated cells, at this stage, are sensitized to the allergen allergenic food into the diet
↓
If later exposure to the same allergen occurs, the allergen can bind to SKIN TEST
the IgE molecules held on the surface of the mast cells or basophils,  “Puncture testing” and “prick testing”
and activates the sensitized cell. are series of tiny punctures or pricks made
↓ into the patient’s skin.
Activated mast cells and basophils undergo degranulation process,  Small amounts of suspected allergens
during which they release histamine and other inflammatory and/or their extracts (pollen, grass, mite
mediators (cytokines, interleukins, leukotrienes, and prostaglandins) proteins, peanut extract) are introduced to
from their granules into the surrounding tissue causing several sites on the skin marked with pen or dye
systemic effects: and this allergens are injected
↓ ―intradermally‖ into the patients skin, with
Vasodilation, mucous secretions, nerve stimulation, and smooth a needle and syringe
muscle contraction  If the patient is allergic to the substance,
↓ then a visible inflammatory reaction will usually occur within
This results in rhinorrhea, itchiness, dyspnea, and anaphylaxis 30 minutes
 This response will range from slight reddening of the skin to
MANIFESTATIONS a full-blown hive (―wheal and flare‖) in more sensitive
 Depending on the individual, allergen, and mode of patients (similar to a mosquito bite)
introduction, the symptoms can be system-wide (classical  Interpretation of the results of the skin prick test is normally
anaphylaxis), or localized to particular body systems; done by allergologists on a scale of severity
 Asthma is localized to the respiratory system and eczema is (+/- meaning borderline reactivity
localized to the dermis 4+ being a large reaction)
 Non-specific symptoms can also be observed
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Common areas for testing: forearm and the back. ANAPHYLAXIS
**** Measuring & recording the diameter of the wheal & flare  The life-threatening anaphylactic response of a sensitized
reaction human appears within minutes after systemic exposure to
specific antigen
PATCH TESTING  ―Anaphylactic Shock‖
 Used to determine if a specific  Severe, immediate, potentially fatal systemic allergic
substance causes allergic inflammation reaction that is rapid in onset and may cause death
of the skin
 Adhesive patches are usually treated PREDISPOSING FACTORS AND ETIOLOGY
with a number of common allergic
 There is no convincing evidence that age, sex, race, or
chemicals or skin sensitizers
geographic location predisposes a human to anaphylaxis
 Test for delayed reactions
except through exposure to some immunogen.
 Used to help ascertain the cause of skin
1. Heterologous Proteins
contact allergy, or contact dermatitis.
a. Hormones (insulin, vasopressin, parathormone)
The skin is then examined for possible local reactions at least twice,
b. Enzymes (trypsin, chymotrypsin, penicillinase,
usually at 48 hours after application of the patch, and again two or
streptokinase)
three days later
2. a. Pollen Extracts (ragweed, grass, trees)
b. Nonpollen Allergen Extracts (dust mites, dander
BLOOD TESTING
of cats, dgs, horses, and laboratory animals
 Patient’s blood for analysis with multiple allergens
3. Food (peanuts, milk, egs, seafoods, nuts, grains, beans)
 Can be performed irrespective of age, skin condition,
4. Occupation-related Products (latex rubber products)
medication, symptom, disease activity, and pregnancy
5. Hymenoptera venom (yellow jacket, hornets, wasp,
 Measures the concentration of specific IgE antibodies in the
bee, ants)
blood (Quantitative IgE testing) using enzyme-linked
6. Polysaccharides: dextrab and thiomersal as a vaccine
immunosorbent assay (ELISA)), radioallergosorbent test
preservative
(RAST) and fluorescent enzyme immunoassay (FEIA).
7. Drugs such as protamine; antibiotics (penicillins,
Quantitative IgE test results increase the possibility of ranking how
cephalosporins, amphotericin B, nitrofurantoin,
different substances may affect symptoms.
quinolones); chemotherapy agents (carboplatin,
A rule of thumb of course is that the higher the IgE antibody value,
paclitaxel, doxorubicin); local anesthetics (procain,
the greater the likelihood of symptoms.
lidocaine); muscle relaxants (suxamethonium, gallamine,
The quantitative allergy blood result can help determine what a
pancuronium); vitamins (thiamine, folic acid); diagnostic
patient is allergic to, help predict and follow the disease development,
agents (sodium dehydrocholate, sulfobromophthalein)
estimate the risk of a severe reaction, and explain cross-reactivity.
8. Occipation-related Chemicals (ethylene oxide)
this is actually relatively safe, since the person is not exposed to any
allergens during the testing procedure
When u say immunogen, it is like antigen that are also capable of
inducing an immune response,
This is the elimination diet/food or medicine challenge test for
diagnosing allergies COOMBS AND GELL CLASSIFICATION
CHALLENGE TESTING IMMUNOLOGIC ASPECTS OF HYPERSENSITIVITY REACTIONS
 Is when small amounts of a suspected allergen are TY ALTERNATIVE ANTIBODIES IMMUNOLOGIC OFTEN
NAMES OR CELL REACTION MENTIONED
introduced to the body orally, through inhalation, or via PE
MEDIATORS DISORDER
other routes I Allergy Antibody IgE Fast response w/c Atopy
 Usually for testing food and medication allergies Immediate occurs in minutes, rather Anaphylaxis
 When this type of testing is chosen, it must be closely Anaphylactic than multiple hours or Asthma
supervised by an allergist days. Churg-Strauss
Free antigens cross link Syndrome
ELIMINATION/CHALLENGE TESTS: the IgE on mast cells
and basophils w/c
 Used most often with foods or medicines
causes a release of
 A patient with a suspected allergen is instructed to modify vasoactive biomolecules.
his diet to totally avoid that allergen for a set time. If the Testing can be done via
patient experiences significant improvement, he may then skin test for specific IgE.
be ―challenged‖ by reintroducing the allergen, to see if the II Cytotoxic Antibody IgM Antibody (IgM or IgG) Autoimmune
symptoms are reproduced. Antibody- Antibody IgG binds to antigen on a hemolytic
dependent Complement target cell, w/c is anemia
MAC actually a host cell that Rheumatic
MANAGEMENT
is perceived by the heart
 Typically involves avoiding what triggers the allergy and immune system as disease
medications to improve the symptoms. foreign, leading to Thrombocytop
cellular destruction via enia
Medicines that may block the action of allergic mediators, or to the MAC. Erythroblastos
prevent activation of the cells and degranulation processes. Testing includes both is fetalis
a. Antihistamines the direct and indirect Goodpasture's
Coombs test syndrome
b. Glucocorticoids Graves’
c. Epinephrine disease
d. Mast cell stabilizers Myasthenia
e. Antileukotriene agents gravis

Compounds that may impair eosinophil chemotaxis III Immune Antibody IgG Antibody (IgG) binds to Serum
a. Anti-cholinergics complex Complement soluble antigen, forming sickness
Neutrophils a circulating immune Rheumatoid
b. Decongestants
complex. This is often arthritis
deposited in the vessel Arthus
for any kind of allergies, usually this are the basic approach :) walls of the joints and reaction
kidney, initiating a local Post
inflammatory reaction. streptococcal
glomerulone

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phritis MANIFESTATIONS
Membranous  There may be upper or lower airway obstruction or both
nephropathy
 Laryngeal edema may be experienced as a ―lump‖ in the
Reactive
arthritis throat, hoarseness, or stridor, while bronchial obstruction is
Lupus associated with a feeling of tightness in the chest and/or
nephritis audible wheezing
Systemic  Flushing with diffuse erythema and a feeling of warmth
lupus Manifested by respiratory distress due to laryngeal edema and/or
erythematos intense bronchospasm, often followed by vascular collapse, or by
us
shock without antecedent respiratory difficulty.
Extrinsic
allergic Cutaneous manifestations exemplified by pruritus and urticaria with or
alveolitis (hy without angioedema are characteristic of such systemic anaphylactic
persensitivity reactions.
pneumonitis) Gastrointestinal manifestations include nausea, vomiting, crampy
abdominal pain, and diarrhea.
IV Delayed Cell T helper Contact
Cell-mediated  T-cells cells (specifically Th1 dermatitis, Characteristic Features
immune cells) are activated by including Uru
memory an antigen presenting shiol-induced
URTICARIAL ERUPTIONS
response cell. When the antigen is contact a. Eruption of well-circumscribed, discreet cutaneous wheals
Antibody- presented again in the dermatitis (p with erythematous, raised, serpiginous borders and
independent future, the memory Th1 oison ivy blanched centers, which are inrensely pruritic and may be
cells will activate rash). localized or disseminated and may coalesce to form griant
macrophages and cause Mantoux test hives, and they seldom persist beyond 48
an inflammatory Chronic ANGIOEDEMA:
response. This ultimately transplant
can lead to tissue rejection
b. May also be present; a localized, nonpitting, deeper
damage Multiple edematous cutaneous process, that may be asymptomatic
sclerosis[6] or cause a burning or stinging sensation.
Coeliac There are 2 characteristic features of anaphylaxis
disease The angioedematous and urticarial manifestations of the anaphylactic
Hashimoto's syndrome have been attributed to the release of endogenous
thyroiditis histamine.
Granuloma
annulare
URTICARIA
V Autoimmune IgM or IgG Graves' c. Urticaria involves only the superficial portion of the dermis,
Complement disease presenting as well-circumscribed wheals with erythematous
Myasthenia raised serpinginous borders and blanched centers that may
gravis coalesce to become giant wheals
Anaphylaxis is type 1 Hypersensitivy reaction Urticaria, also known as hives, is an outbreak of swollen, pale red
Coombs & Gell classification distinguishes 4 types of immune response bumps or plaques (wheals) on the skin that appear suddenly -- either
w/c results to target organ damage as a result of the body's reaction to certain allergens, or for unknown
reasons. Hives usually cause itching, but may also burn or sting
PATHOPHYSIOLOGY
 Almost any substance can be an allergen (food, insect ANGIOEDEMA
bites/stings, etc) d. is a well-demarcated localized edema involving the deeper
 The first time body exposed to the substance, the immune layers of the skin, including the subcutaneous tissue.
system learns to recognize the foreign invader whereas, ANGIOEDEMA is an area of swelling of the lower layer of
 But with anaphylaxis, the immune system has an skin and tissue just under the skin or mucous membranes
exaggerated response when exposed to the substance
again. CLASSIFICATION OF URTICARIA and/or ANGIOEDEMA
 This response affects the whole body (life-threatening)
 Symptoms may begin within seconds and can progress 1. IgE-dependent
swiftly a. Specific antigen sensitivity (pollen, foods, drugs, fungi,
molds, Hymenoptera venom, helminths)
MECHANISM OF ANAPHYLAXIS b. Physical: dermographism, cold, solar
 Is mediated primarily by antibodies immunoglobulin E, (IgE) c. Autoimmune
class 2. Bradykinin-mediated
 These antibodies recognize the offending antigen and bind a. Hereditary angioedema: C1 inhibitor deficiency: null (type
to it 1) and dysfunctional (type 2)
 The IgE antibodies also bind to specialized receptor b. Acquired angioedema: C1 inhibitory deficiency: anti-idiotype
molecules on mast cells and basophils, causing these cells and anti-C1 inhibitor
to release their stores of inflammatory chemicals (histamine, c. Angiotensin-converting enzyme inhibitors
serotonin, leukotrienes) 3. Complement-mediated
 Effects: a. Necrotizing vasculitis
 Constriction of the smooth muscles resulting to b. Serum sickness
breathing difficulty; c. Reactions to blood products
 dilation of blood vessels, causing skin flush and 4. Nonimmunologic
hives a. Direct mast cell releasing agents (opiates, antibiotics,
 Increase in vascular permeability, resulting in curare, D-tubocurarine, radiocontrast media)
swelling and a decrease in blood pressure b. Agents that alter arachidonic acid metabolism (aspirin and
nonsteroidal anti-inflammatory agents, azo dyes, and
Mechanism is just the same with many allergic diseases benzoates)
5. Idiopathic

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The classification of urticaria-angioedema focuses on the different DIFFERENTIAL DIAGNOSIS
mechanisms for eliciting clinical disease and can be useful for  Urticaria and angioedema can be differentiated from
differential diagnosis; contact sensitivity, a vesicular eruption that progress to
Nonetheless, most cases of chronic urticaria are idiopathic. chronic thickening of the skin with continued allergic
exposure
DERMOGRAPHISM  They can also be differentiated from atopic dermatitis, a
 Literally means ―writing in the skin‖ condition that may present as erythema, edema, papules,
 Occurs in 1-4% of the population vesiculation, and oozing proceeding to a subacute and
 Is defined by the appearance of a linear chronic stage in which vesiculation is less marked or absent
wheal at the site of a brisk stroke with a and scaling, fissuring, and lichenification predominate in a
firm object or by any configuration distribution that characteristically involves the flexor
appropriate to the eliciting event surfaces.
 Firm stroking of the skin produces an initial  In cutaneous mastocytosis, the reddish brown macules
red line (capillary dilatation), followed by an and papules, characteristic of urticarial pigmentosa, urticate
axon-reflex flare with broadening erythema with pruritus upon trauma; and in systemic mastocytosis,
(arteriolar dilation) and the formation of a without or with urticarial pigmentosa, there is episodic
linear wheal (transudation of fluid/edema); systemic flushing with or without urtication but no
- events are collectively termed the triple response angioedema.
of Lewis The rapid onset and self-limited nature of urticarial and
angioedematous eruptions are distinguishing features of both urticaria
and angioedema how-ever there are also other differentials such as
Other forms of urticaria are as follows

PRAUSNITZ-KÜSTNER REACTION

PATHOPHYSIOLOGY AND MANIFESTATION The diagnosis of an anaphylactic reaction depends on a history

 Urticarial eruptions are distinctly pruritic, may involve any revealing the onset of symptoms and signs within minutes after the
area of the body from the scalp to the soles of the feet, and responsible material is encountered.
appear in crops of 12- to 36-hour duration, with old lesions In current clinical practice, immunoassays using purified antigens can
fading demonstrate the presence of specific IgE in the serum of patients with
 Most of the physical urticarias (cold, cholinergic, anaphylactic reactions, and intracutaneous skin testing may be
dermatographism) are an exception, with individual lesions performed after the patient has recovered to elicit a local wheal and
lasting less than 2 hours. flare in response to the putative antigen
 The most common sites for urticarial are the extremities
and face, with angioedema often being periorbital and in TREATMENT
the lips  Identification of the etiologic factor(s) and subsequent
 No residual discoloration occurs with either urticarial or elimination provide the most satisfactory therapeutic
angioedema unless there is an underlying process leading to program
superimposed extravasation of erythrocytes  For most forms of urticarial, H1 antihistamines such as
chlorpheniramine or diphenhydramine effectively attenuate
both urtication and pruritus, but because of their side
effects, nonsedating agents such as loratadine,
PATHOLOGY desloratadine, and fexofenadine, or low-sedating agents
 Characterized by edema of the superficial dermis in such as cetirizine or levocetirizine generally are used first.
urticarial and of the subcutaneous tissue and deep  Cyproheptadine in dosages beginning at 8 mg and ranging
dermis in angioedema up to 32 mg daily and especially hydroxyzine in dosages
 Collagen bundles in affected areas are widely separated, beginning at 40 mg and ranging up to 200 mg daily have
and the venules are sometimes dilated. Any perivenular proven effective when H1 antihistamines fail.
infiltrate consists of lymphocytes, monocytes, eosinophils,  The addition of an H2 antagonists such as cimetidine,
and neutrophils that are present in varying combination and ranitidine, or famotidine in conventional dosages may add
numbers benefit when H1 antihistamines are inadequate.
angioedema and urticaria - may appear separately or together as  Early recognition of an anaphylactic reaction is mandatory,
cutaneous manifestations of localized nonpitting edema; a similar since death occurs within minutes to hours after the first
process may occur at mucosal surfaces of the upper respiratory or symptoms
gastrointestinal tract. o Mild symptoms like pruritus and urticarial
 Epinephrine 0.3 to 0.5 mL of 1:1000 (1
mg/mL)SQ or IM
o Severe Reactions
 May repeat above doses of Epinephrine
as required at 5- to 20-min intervals
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 UNP-MEDICINE 2021 INTERNAL MEDICINE
o Minor adverse effects from epinephrine include PROGNOSIS
tremors, anxiety, headaches, and palpitations.  In those in whom the cause is known and prompt treatment
 Epinephrine provides both a- and –adrenergic effects, is available, the prognosis is good
resulting in vasoconstriction, bronchial smooth-muscle  Even if the cause is unknown, if appropriate preventive
relaxation, and attenuation of enhanced venular medication is available, the prognosis is generally good
permeability.  Cause of death in delayed treatment of anaphylactic
 Ancillary agents Antihistamine, diphenhydramine, 50-100 reactions is usually due to either respiratory (typically
mg IM or IV, and Aminophylline, 0.25-05 g IV, are asphyxia) or cardiovascular causes (shock), with 0.7-20% of
appropriate for urticarial-angioedema and bronchospasm cases causing decease
 Intravenous glucocorticoids, 0.5-1 mg/kg of Medrol, are not And lastly, prognosis is generally good, and in severe allergic reaction
effective for the acute events but alleviate later recurrence (anaphylaxis), it must be addressed immediately
of bronchospasm, hypotension, or urticaria.
When epinephrine fails to control the anaphylactic reaction, hypoxia
due to airway obstruction or related to a cardiac arrhythmia, or both,
must be considered

Oxygen alone via a nasal catheter or with nebulized albuterol may be

helpful, but either endotracheal intubation or a tracheostomy is
mandatory for oxygen delivery if progressive hypoxia develops.

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