Hypersensitivity

Hypersensitivity disorder
Done by: Sondos

Ebrahim
OBJECTIVES
• Define the hypersensitivity
• Introduce types of hypersensitivity
• Identify the causes and pathophysiology
• Identify clinical manifestation and types of
management
• Test your understanding
W H AT I S H Y P E R S E N S I T I V I T Y
• inappropriate immune response to a

substance (allergen) that is usually
harmless to most people.
TYPES OF HYPERSENSITIVITY
TYPE 1 HYPERSENSITIVITY (Anaphylactic hypersensitivity)
TYPE 2 HYPERSENSITIVITY (Cytotoxic hypersensitivity)
TYPE 3 HYPERSENSITIVITY (Immune complex

hypersensitivity )
TYPE 4 HYPERSENSITIVITY (Delayed hypersensitivity)

ANAPHYLACTIC HYPERSENSITIVITY
• Type I hypersensitivity is also known as an immediate reaction

and involves immunoglobulin E (IgE) mediated release of antibodies
against the soluble antigen. This results in mast cell degranulation
and release of histamine and other inflammatory mediators
• Unanticipated severe allergic reaction, Rapid in onset (immediate
minute when exposed to the antigen ) , Could be minor to severe
death
• Characterized by : edema in many tissues (larynx) and combined
with hypotension , bronchospasm and cardiovascular collapse in
sever cases
PAT H O P H Y S I O L O G Y
1 - I M M E D I AT E R E S P O N S E
2 - L AT E - P H A S E R E AC T I O N
1. First exposure to the allergen: Activation of T helper 2 (Th 2)
cells occurs that leads to activation of B lymphocytes to produce
large amounts of Ig-E antibodies. Ig-E antibodies bind to mast cells.
2. Re-exposure to the antigens: the antigen binds to the

antibodies cause dramatic mast cell response and release of
histamine, leukotrienes and cytokines that causes immediate
hypersensitivity reaction (within minutes) and late phase reaction
(up to 24 hours) after repeated exposure.
SYMPTOMS OF ANAPHYLACTIC
HYPERSENSITIVITY
1.Amount of
the allergen
Depends on: and the
mediator that
was released
2.The
sensitivity of 3.The route of
the target entry
organ
- may be both
local and
systemic
anaphylaxis-
EXAMPLES OF ANAPHYLACTIC HYPERSENSITIVITY
• Nasal allergic rhinitis or hay fever

• Ocular allergic conjunctivitis, potentially due to
seasonal allergens such as pollen or mold spores
• Dermatological hives, atopic eczema, or erythema
• Soft tissue angioedema
• Pulmonary reactions, such as allergic asthma or
hypoxia
• Systemic reaction, which is a life-threatening
medical emergency, and known as anaphylaxis
CYTOTOXIC HYPERSENSITIVITY
TYPE II HYPERSENSITIVITY IS ALSO KNOWN AS ENGAGES IGG AND IGM
A N T I B O D I E S , L E A D I N G T O T H E C O M P L E M E N T S Y S T E M A C T I VAT I O N A N D
C E L L D A M A G E O R LY S I S
Antibodies are directed against antigen on

the cell basement membranes of the
tissue
This reaction cause lysis and tissue
damage
May effect variety of organs and tissues
The reaction is completed in
two phases ( sensitization and
effector phase)
CYTOTOXIC
HYPERSENSIT Sensitization phase
is :production of antibodies
IVITY that recognizes the antigen on
the surface of the tissue
effector phase is: target cell
become coated with the
antibodies whitch lead to
cellular distruction
Takes 24h-48 h
1. Opsonization and phagocytosis.
• When circulating cells, such as RBCs or platelets, are coated
(opsonized) with autoantibodies, with or without complement
proteins, the cells become targets for phagocytosis by
neutrophils and macrophages.
• Examples:
a. Transfusion reactions: in incompatible blood transfusion

b. Autoimmune haemolytic anaemia, and thrombocytopenia, in
which individuals produce antibodies to their own blood cells.
2. Inflammation:
• Antibodies bound to antigens activate the
complement system by the classical pathway.
• Products of complement activation serve to recruit
neutrophils and monocytes, triggering
inflammation in tissues.
• Examples: vascular rejection in organ grafts.
Herpes zoster ???

• 3. Antibody-mediated cellular dysfunction:
a. Antibodies directed against a host protein impair or
dysregulate important functions without directly causing
cell injury or inflammation. Example: In myasthenia gravis,
antibodies against acetylcholine receptors in the motor end
plates of skeletal muscles inhibit neuromuscular transmission,
with resultant muscle weakness.
b. Antibodies also can stimulate cellular responses
excessively. In Graves disease, antibodies against the thyroid-
stimulating hormone receptor stimulate thyroid epithelial cells
to secrete thyroid hormones, resulting in hyperthyroidism.
c. Antibodies against hormones and other essential
proteins can neutralize and block the actions of these
molecules, causing functional derangements.
EXAMPLES OF CYTOTOXIC
HYPERSENSITIVITY
Hemolytic
Hemolitic Transfusio Graves disease of
anemia n reaction diseas the
newborn
IMMUNE COMPLEX HYPERSENSITIVITY
( T Y P E I I I H Y P E R S E N S I T I V I T Y ) : I N V O LV E S I G G ,
IGM, AND SOMETIMES IGA ANTIBODIES. THE
BUILD-UP OF THESE IMMUNE COMPLEXES
R E S U L T S I N C O M P L E M E N T S Y S T E M A C T I VAT I O N ,
W H I C H L E A D S T O P O LY M O R P H O N U C L E A R
L E U K O C Y T E S ( P M N S ) C H E M O TA X I S A N D
E V E N T U A L LY C A U S I N G T I S S U E D A M A G E
• Antigen–antibody (immune) complexes may deposit in
blood vessels, leading to complement activation and
acute inflammation.
• The antigens that form immune complexes may be

exogenous, such as a foreign protein, infectious
microbe, or self-antigens (autoimmunity).
• Mechanism of Type III hypersensitivity divided

into three phases:
1. Formation of Immune Complexes.
2. Deposition of Immune Complexes. Commonly

kidney (glomerulonephritis), joints (arthritis), and
small blood vessels (vasculitis)
3. Inflammation and Tissue Injury.

• Large quantities of soluble antigen-antibodies form in the
blood and not removed by macrophages
• These of soluble antigen-antibodies lodge in the capillaries
between the endothelial cell and basement membrane
• Activate the classical complement pathway leading to
vasodilation
• The complement protein attract the leukocyte to the area
• Leukocyte discharge there killing agent and promote
massive inflammation this lead to tissue hemorrhage or
death
• Takes hours and days
Immune
disease (RA)
EXAMPLES OF
IMMUNE COMPLEX
HYPERSENSITIVIT PRESISTANCE
Y
INFECTION
(hepatitis
virues)
SLE
D E L AY E D H Y P E R S E N S I T I V I T Y T Y P E I V I N V O LV E S O F T- C E L L -
M E D I AT E D R E A C T I O N S . T- C E L L S O R M A C R O P H A G E S A R E A C T I VAT E D A S
A R E S U LT O F C Y T O K I N E R E L E A S E , L E A D I N G T O T I S S U E D A M A G E ,
W H I L E I T I S TA K I N G T I M E A N D D AY S F O R T H E R E A C T I O N T O D E V E L O P
HOW DOES R-CELL REACTION
WORKS?
• Cytokine-mediated inflammation, in which the cytokines are
produced mainly by CD4+ T cells. Also called delayed-type
hypersensitivity (DTH), The classic example of DTH is the tuberculin
test (PPD skin test), which is produced by the intradermal injection of
purified protein derivative (PPD), a protein-containing antigen of the
Mycobacterium tuberculosis bacillus. In a previously exposed individual,
reddening and induration of the site that reach a peak in 24 to 72 hours
(so the name delayed)
HOW DOES R-CELL REACTION
WORKS?
• Direct cell cytotoxicity, mediated by CD8+ T cells for example type
1 diabetes, graft rejection
E X A M P L E S O F D E L AY E D
HYPERSENSITIVITY
• TB (PPD TEST)
• DM TYPE 1
•
CLINICAL
M A N I F I S TAT I
ONS FOR THE
FOUR TYPES
T R E AT M E N T O F
HYPERSENSITIVITY
• The need for emergent treatment is vital with anaphylaxis, at it is usually rapid in onset and
may cause death. The recommendation is that if possible, the offending agent is removed
immediately, and patients are placed in a supine position with the elevation of lower
extremities unless there is a significant obstruction or airway inflammation. If there is
marked stridor or severe respiratory distress, immediate intubation may be required. If the
patient has a history of allergic reactions, they will be provided with emergency self-
treatment prescriptions, which include: an epinephrine, bronchodilators, antihistamines,
and/or corticosteroids. The first-line therapy that is recommended to be administered without
delay is epinephrine intramuscular (IM) injection and thereafter adjunctive therapy is utilized
for symptom control
• Epinephrine: The dose for the epinephrine is weight-based
and may be repeated every 5 to 15 minutes. Studies have
demonstrated that in about 35% of cases, a repeat dose is
required.
• Epinephrine may also be administered via slow continuous
infusion. The recommendation is to monitor blood pressure
and heart rate with its administration.
• Bronchodilators: such as albuterol, are given as either metered-
dose inhaler (MDI), dry-powder inhaler (DPI), or nebulized solution
and are usually administered when the patient is not responsive to
epinephrine for treating bronchospasm.
• Albuterol MDI or DPI dose: adults are to administer 2 to 3
inhalations as needed for symptoms relief; in severe exacerbations,
doses up to 8 inhalations every 20 minutes may be needed. Limited
in ages <4 years old.
• Antihistamines: i.e., diphenhydramine, famotidine or
ranitidine: Antihistamines are considered second-line
adjunctive therapy and can provide relief of symptoms such
as hives or pruritic. However, antihistamines should not be
used as monotherapy, as they do not mitigate upper or
lower airway obstruction, shock, or hypotension.
REFERENCES
• https://www.ncbi.nlm.nih.gov/books/NBK560561/
• Robbins basic pathology, by Vinay Kumar, Abul K. Abbas and Jon C.
Aster. Elsevier; 10 edition (March 8, 2017)

Hypersensitivity

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Hypersensitivity disorder

Done by: Sondos

• inappropriate immune response to a

TYPE 2 HYPERSENSITIVITY (Cytotoxic hypersensitivity)

TYPE 3 HYPERSENSITIVITY (Immune complex

TYPE 4 HYPERSENSITIVITY (Delayed hypersensitivity)

• Type I hypersensitivity is also known as an immediate reaction

2. Re-exposure to the antigens: the antigen binds to the

• Nasal allergic rhinitis or hay fever

Antibodies are directed against antigen on

a. Transfusion reactions: in incompatible blood transfusion

Herpes zoster ???

• The antigens that form immune complexes may be

• Mechanism of Type III hypersensitivity divided

1. Formation of Immune Complexes.

2. Deposition of Immune Complexes. Commonly

3. Inflammation and Tissue Injury.

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