CERELYN E.
DACULA, MD
Far Eastern University – Nicanor Reyes Medical Foundation
January 5, 2016
 Hyperreactivity of the immune system.
 Exaggerated or inappropriate immune response
that is harmful to the host.
 Most of the time, there is a need of an initial
contact of the host to the allergen.
 Reactions typically occur after the second
contact with a specific antigen (allergen).
 First contact is necessary preliminary event that
induces sensitization to that allergen.
In hypersensitivity, there is the hyperreactivity of
the immune system. Most of the time, there is a
need of an initial contact of the host to the
allergen, and then the hypersensitivity manifests
after the second contact of the host to the
allergen.
MEDIATORS
HISTAMINE:
ANTIBODY MEDIATED:
 TYPE 1: Immediate Hypersensitivity
(Allergy/Anaphylaxis)
 TYPE 2: Antibody Mediated Hypersensitivity
 TYPE 3: Immune Complex Hypersensitivity
T-CELL MEDIATED:
 TYPE 4: Cell Mediated (Delayed)
Hypersensitivity
- Type 1 – Allergic reactions, and the most dreadful
of which is your anaphylaxis because it can lead to
death if it is not reversed immediately.
- Type 2 – Cytotoxic type of Hypersensitivity
 Manifests itself in tissue reactions occurring
within seconds after the antigen combines with
the matching antibody
 Systemic anaphylaxis
 Local reaction
The antibody that is involved here is mainly the IgE.
The antigen induces the production of the IgE. The
second contact by the same antigen results in the
fixation of your antigen to the IgE. If the IgE is
bound to your antigen, it releases your so called
mediators from the cells within second to minutes.
For example, you have the allergen, the APCs take
up the allergens to the T-helper cells, and the T-
helper cells activate the T-cells to release your IgE.
Once the IgE binds to the phagocytes (i.e.
Basophils/Eosinophils), it can now activate the
release of the mediators. The mediators are the
once that later on produce the clinical effects or the
clinical manifestations. The most commonly
associated mediator on your type 1 hypersensitivity
is your HISTAMINE.
 Histamine is one of the primary mediators
 Histamine exists in a preformed state in
platelets and in granules in mast cells,
basophils, and eosinophils
 Causes vasodilation, increased capillary
permeability, and smooth muscle contraction
(eg. Bronchospasm)
The vasodilation is the reason why the area of the
allergy is warm and erythematous, this may also
be due to increased capillary permeability. It may
also cause smooth muscle contraction which
causes bronchospasm, and that’s the reason why
patients with allergies manifests with difficulty in
breathing.
CERELYN E. DACULA, MD
Far Eastern University – Nicanor Reyes Medical Foundation
January 5, 2016

PROSTAGLANDINS AND LEUKOTRIENES: COMMON CLINICAL MANIFESTATIONS INCLUDE:

 Derived from arachidonic acid via the  Hay fever

Cyclooxygenase Pathway  Asthma
 Prostaglandins: Bronchoconstriction  Eczema
 Leukotrienes: Increased permeability of  Urticaria
capillaries

Aside from the Histamine, the Prostaglandins may

also contribute to the
bronchospasm/bronchoconstriction.  Involves the binding of IgG antibodies to cell

With all the mediators combined, there will be surface antigens or extracellular matrix
swelling of the airway, no wind will enter the the molecules
lungs, there will also be difficulty in breathing;  Antibody directed at cell surface antigens can
there is now an anaphylactic reaction which may
cause death. It needs to be reversed immediately activate complement (or other effectors) to
to avoid death. damage the cells (cell damage - because IgG is
an opsoniser, it may activate the complement
TREATMENT AIMS TO REVERSE THE ACTION OF which can damage the cells)
MEDIATORS BY:
 The result may be complement-mediated lysis,
as occurs in:
 Maintaining the airway
- Hemolytic Anemias
 Providing artificial ventilation if necessary
- ABO Transfusion Reactions
 Supporting cardiac function
- Rh Hemolytic Disease
ONE OF THE FOLLOWING MAY BE GIVEN: - G6PD - Recording
Recording Example: The mommy is type O then her
 Epinephrine – The fastest anti-inflammatory baby is type B or type A, the baby has still circulating
mediator, a bronchodilator that acts on beta 2 type O blood from the mother, that’s why upon
delivery, there is jaundice due to ABO Incompatibility
receptors. This is the first drug of choice given
causing RBC lysis.
in the emergency room.
 Drugs such as PENICILLIN can attach to surface
 Antihistamines – can be given later
proteins on RBC and initiate antibody
 Corticosteroids - can be given later
formation, that is why in patients with G6PD, we

- Atopic hypersensitivity disorders exhibit a strong give patients a list drugs and foods to avoid, so

familial predisposition ( that’s why you ask for allergies that we will not trigger the G6PD reactions,

in the family history) and are associated with elevated thus, to avoid immune complex formation.

IgE levels.  Such autoimmune antibodies may combine with

the cell surface with resulting hemolysis.
- Antigens are TYPICALLY ENVIRONMENTAL:
EXAMPLES:
 Respiratory allergy to pollens, ragweed, or
house dust.  Goodpasture Syndrome – Antibody forms

 Foods (eg. Intestinal allergy to shellfish, against basement membranes of kidney and

seafoods) lung, resulting in severe damage to the

membranes through activity of complement-
attracted leukocytes
CERELYN E. DACULA, MD
Far Eastern University – Nicanor Reyes Medical Foundation
January 5, 2016

EXAMPLES:
 Graves Disease – Antibodies to cell surface
receptors alter function without cell injury | eg.: 1. ARTHUS REACTION
autoantibody binds to the thyroid stimulating
hormone (TSH) receptor and by stimulating the  Typically elicited in the skin when a low dose of
thyroid causes hyperthyroidism. antigen is injected and immune complexes form
locally
 IgG antibodies are involved, and the resulting
activation of complement – activation of mast
 When antibody combines with its specific cells and neutrophils – enhanced vascular
antigen, immune complexes are formed. permeability
 Normally, they are promptly removed, but  Occurs in about 12 hours
occasionally they persist and are deposited in
2. SYSTEMIC IMMUNE COMPLEX
tissues, resulting in several disorders.
ACUTE POST-STREPTOCOCCAL
EXAMPLE: GLOMERULONEPHRITIS – STREP
GLOMERULONEPHRITIS
There is an antigen-antibody complex that will
lodge in the glomerulus causing antigen-antibody  Onset occurs several weeks after a group A-
interaction interaction. If there is antigen antibody hemolytic streptococcal infection
interaction, there will be an activation of the
 Lumpy deposits of immunoglobulin and
complement, causing damage to the glomerulus. If
there is damage to the glomerulus, the kidneys complement component. C3 are seen along
cannot filter the cells –> Urine w/ RBCs  glomerular basement membranes suggesting
Hematuria
antigen antibody complexes; That’s why in
 Persistent MICROBIAL or VIRAL infections, Glomerulonephritis, we also check for the level
immune complexes may be deposited in organs of C3.
(eg. Kidneys), resulting in dysfunction  Inflammatory process damage the kidneys
 Autoimmune disorders, “self” antigens may
elicit antibodies that bind to organ antigens or
are deposited in organs especially in
- Joints (Arthritis)  Cell mediated hypersensitivity is a function not
- Kidneys (Nephritis) of antibody but specifically sensitized T-
- Blood Vessels (Vasculitis) lymphocytes that activate macrophages to
 Environmental antigens such as fungal spores cause an inflammatory response
and certain drugs can cause immune complex  The response is delayed, usually starts 2-3 days
formation with disease. after contact with the antigen and often lasts
for days.
WHENEVER IMMUNE COMPLEXES ARE DEPOSITED:
EXAMPLES:
 They activate the complement system and
macrophages, and neutrophils are attracted to 1. CONTACT HYPERSENSITIVITY
the site.  May cause damage to normal tissues
that has the complex  Occurs after sensitization of:

 Cause inflammation and tissue injury. - Previous chemicals

- Plant materials
CERELYN E. DACULA, MD
Far Eastern University – Nicanor Reyes Medical Foundation
January 5, 2016

PRACTICE!!
- Topically applied drugs
- Some cosmetics
1. SLE - Type 3 Hypersensitivity
- Soaps
2. Allergic Rhinitis – Type 1 Hypersensitivity
- Others
3. Multiple Sclerosis - Type 3 Hypersensitivity
 Small molecules enter the skin and then, acting
4. Hashimotos Thyroiditis - Type 3 Hypersensitivity
as haptens, attach to the body proteins to serve
5. PPD - Type 4 Hypersensitivity
as complete antigen
6. Hemolytic Anemia - Type 2 Hypersensitivity
 When the skin again comes in contact with the 7. Eczema - Type 4 Hypersensitivity
offending agent, the sensitized person develops
the following within 12-48 hours: FROM THE OTHER TRANS: (Sorry if I stole dis lol)
- Erythema
1. Wegener’s granulomatosis – IV
- Itching
2. Polyarteritis nodosa – III
- Vesication
3. Contact dermatitis – IV
- Eczema or necrosis of the skin
4. Poison ivy – IV
 Patch testing on a small area of the skin can
5. Metal allergy – IV
sometimes identify the offending agent.
6. Drug allergy – I
 Subsequent avoidance of the material will
7. Penicillin - II
prevent recurrences.
OBLIGATORY MESSAGE: SASAYANGIN KO INK NYO
EXAMPLE: ALLERGY TO RUBBER SLIPPERS
MUAHAHAHAHAHA
Initially – Will not manifest, after 2-3 days, the
Di ko alam kung ano yung nakain ko, di ko alam kung bakit ako
hypersensitivity will manifest.
gumawa ng trans. Kaloka. HAHA. Pero wala din kasing trans for
this. HAHAHA. Tawag ng kabaklaan ata ‘to.

2. TUBERCULIN TYPE HYPERSENSITIVITY

 When a small amount of tuberculin is injected
into the epidermis of the patient previously
exposed to Mycobacterium tuberculosis, there
is little immediate action – due to the formation
of memory T-cells to the Mycobacterium.
 Gradually, however, induration and redness
develops and reaches peak in 24-72 hours
 A positive skin test indicates that the person
Wag niyo akong ijujudge. Medyo bingi din ako kaya double
check yung mga voice notes, yung mga naka box na blue yung
voice notes pero inincorporate ko na din sa ibang bullets. USE
AT YOUR OWN RISK!
TY BUNNY SA RECORDINGZZ. Muaks. <3
TY JESSICA QUE FOR THE SLIDES!! <3
I dedicate this trans to you Cel Lucero. <3 Sabi ko sayo,
gagawa ako e. HAHAHA! Love you po. <3

has been infected with the agent but does not

I also dedicate this sa mga walang hiya kong seatmates na sina
imply the presence of current disease.
Faye Hipolito at Dani Hernandez. Luvyu ghurLz. <3

And dinidedicate ko din ‘to kay Mico Raphael na nagjudge

sakin kasi kailangan ko ng “study buddy”. HAHAHA. Muah.
Luvyu po.

I LOVE YOU JED DE GUZMAN! HAHA! <3 (As

requested)
CERELYN E. DACULA, MD
Far Eastern University – Nicanor Reyes Medical Foundation
January 5, 2016