This document discusses the classification and mechanisms of hypersensitivity reactions. It describes the four main types of hypersensitivity: Type I mediated by IgE antibodies; Type II mediated by IgG/IgM antibodies binding to cell surfaces; Type III occurring when antigen-antibody complexes are formed; and Type IV mediated by T cells. Examples of each type are provided along with the pathways, mediators, and time courses involved. Specific conditions like allergic contact dermatitis and allergic asthma are then summarized in more depth.
Hypersensitivity, or allergy,
* An immune response results in exaggerated reactions harmful to the host ,
* There are four types of hypersensitivity reactions ,
Type I, Type II, Type III, Type IV ,
* Types I, II and III are antibody mediated ,
* Type IV is cell mediated,
An antigen reacts with cell fixed antibody , (Ig E) ,
leading to release of soluble molecules,
An antigen (allergen) ,
soluble molecules (mediators) ,
* Soluble molecules cause the manifestation of disease,
* Systemic life threatening, anaphylactic shock ,
* Local atopic allergies , bronchial asthma,
and food allergies
Hypersensitivity, or allergy,
* An immune response results in exaggerated reactions harmful to the host ,
* There are four types of hypersensitivity reactions ,
Type I, Type II, Type III, Type IV ,
* Types I, II and III are antibody mediated ,
* Type IV is cell mediated,
An antigen reacts with cell fixed antibody , (Ig E) ,
leading to release of soluble molecules,
An antigen (allergen) ,
soluble molecules (mediators) ,
* Soluble molecules cause the manifestation of disease,
* Systemic life threatening, anaphylactic shock ,
* Local atopic allergies , bronchial asthma,
and food allergies
Normally the immune system plays an important role in protecting the body from microorganisms and other foreign substances. If the activity of the immune system is excessive or overreactive, a hypersensitivity reaction develops. The consequences of a hypersensitivity reaction may be injury to the body or death.
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
Hypersensitivity reactions for Medical StudentsNCRIMS, Meerut
Hypersensitivity (animated) for MBBS Students
Hypersensitivity refers to undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system.
Hypersensitivity reactions require a pre-sensitized state of the host.
Four types of hypersensitivity
Type I – anaphylactic
Type II – cytotoxic
Type III – immune complex mediated
Type IV – contact, tuberculin and granulomatous
Anaphylaxis is defined as a life-threatening allergic reaction set in action by a wide range of antigens and involving multiple organ systems.
The true incidence is difficult to estimate, but in 1973 the Boston Collaborative Drug Surveillance Program reported six anaphylactic reactions and 0.87 deaths from anaphylaxis per 10,000 patients.
Reactions to insect stings alone are responsible for at least 50 deaths in the United States each year.
These figures reveal the importance of continued research into the biology of anaphylaxis along with developing new (and improving existing) therapies.
Normally the immune system plays an important role in protecting the body from microorganisms and other foreign substances. If the activity of the immune system is excessive or overreactive, a hypersensitivity reaction develops. The consequences of a hypersensitivity reaction may be injury to the body or death.
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
Hypersensitivity reactions for Medical StudentsNCRIMS, Meerut
Hypersensitivity (animated) for MBBS Students
Hypersensitivity refers to undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system.
Hypersensitivity reactions require a pre-sensitized state of the host.
Four types of hypersensitivity
Type I – anaphylactic
Type II – cytotoxic
Type III – immune complex mediated
Type IV – contact, tuberculin and granulomatous
Anaphylaxis is defined as a life-threatening allergic reaction set in action by a wide range of antigens and involving multiple organ systems.
The true incidence is difficult to estimate, but in 1973 the Boston Collaborative Drug Surveillance Program reported six anaphylactic reactions and 0.87 deaths from anaphylaxis per 10,000 patients.
Reactions to insect stings alone are responsible for at least 50 deaths in the United States each year.
These figures reveal the importance of continued research into the biology of anaphylaxis along with developing new (and improving existing) therapies.
Defect in recruiting effector memory CD8+ T-cells in malignant pleural effusi...Enrique Moreno Gonzalez
Malignant pleural effusions (MPE) are a common and fatal complication in cancers including lung or breast cancers, or malignant pleural mesothelioma (MPM). MPE animal models and immunotherapy trials in MPM patients previously suggested defects of the cellular immunity in MPE. However only few observational studies of the immune response were done in MPM patients, using questionable control groups (transudate…).
Hypersensitivity reactions are exaggerated or inappropriate immunologic responses occurring in response to an antigen or allergen. Type I, II and III hypersensitivity reactions are known as immediate hypersensitivity reactions because they occur within 24 hours of exposure to the antigen or allergen.
The presentation includes an overview of hypersensitivity and type 1 hypersensitivity with certain pictures elaborating the mechanism. The presentation also talks about asthma very briefly as an example of type 1 hypersensitivity.
Hypersensitivity - medical information ( a detailed study )martinshaji
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
There is no cure for hypersensitivity vasculitis itself. The main goal of treatment will be to relieve your symptoms.
this chart is all about hypersensitivity , i made this for my academic purpose .
please comment
thank u
CNS Introduction, Neurons, Type of Neurons and functions, Neuroglia and types, Receptors and their types, Synapse, Neurotransmitters and their functions
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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3. Classification
Type I – Immediate, Atopic,
Anaphylactic
Type II – Antibody Dependent
Type III – Immune Complex
Type IV – Cell Mediated / Delayed
Type Of Hypersensitivity
4. TYPE I. Immediate OR Anaphylactic
Hypersensitivity
Type I hypersensitivity is also known as
immediate
or anaphylactic hypersensitivity.
The reaction may involve skin (urticaria
and eczema), eyes (conjunctivitis),
nasopharynx (rhinorrhea, rhinitis),
bronchopulmonary tissues (asthma) and
gastrointestinal tract (gastroenteritis).
5. Mediated by IgE antibody to specific
antigens
The primary cellular component in this
hypersensitivity is the mast cell or
basophil.
The reaction is amplified and/or
modified by platelets, neutrophils and
eosinophils.
Mast cells stimulated and release
histamine.
6. Most of the IgE in the body is bound
with high affinity receptors (Fc
epsilonRI), found on mast cells and
basophils.
The cells are activated by cross-linking
of Fc epsilonRI receptors via antigen
binding to the bound IgE molecules.
7.
8. Such cross-linking leads to rapid
degranulation of the mast cells and the
release of primary inflammatory
mediators stored in the granules.
Mast cell activation via Fc epsilonRI also
leads to the production of two other
types of mediators. These secondary
mediators.
9. Molecules SOME SPACES Effects
Primary mediators
Histamine
Vascular permeability,
sm contraction
Serotonin
vascular permeability,
sm contraction
Secondary mediators
Leukotrienes
vascular permeability,
sm contraction
Prostaglandins
vasodilation, sm
contraction, platelet
activation
Bradykinin
vascular permeability,
sm contraction
12. Type II Hypersensitivity
The second class of damaging reactions
is caused by specific antibody binding to
cells or tissue antigens.
The antibodies are of the IgM or IgG
classes and cause cell destruction.
It involves binding of antibodies (IgG or
IgM) to cell surface antigen or
extracellular matrix molecules.
Antibody directed to cell surface
antigens can activate complement to
damage the cells.
13. Red Blood cell
with Ag on cell
membrane
IgG binds to Ag
on membrane
Membrane attack
complex of
compliment lysis red
cell (cell death)
14. The result may be complement
mediated lysis as occurs in
Haemolytic Anemia
ABO Transfusion Reactions.
Pencillin allergy also belong to this
class.
15. Type III (Immune-Complex Mediated)
Hypersensitivity
Due to the formation of antigen-antibody
complexes, also called immune-
complexes.
Type III hypersensitivity is mediated by
immune complexes essentially of IgG
antibodies.
When antibody combines with specific
antigen, immune complexes are formed.
Normally they are promptly removed by
reticulo-endothelial system.
16. Occasionally, they persist and deposit in
tissues resulting in disorders.
In persistent microbial or viral infections,
immune complexes may be deposited in
organs eg. Kidneys - resulting in
dysfunction, in joints – arthirits, in BV –
Vasculitis.
Wherever the immune complexes are
deposited, they cause inflammation and
tissue injury.
17.
18. Type IV Hypersensitivity
This is the only class of hypersensitive
reactions to be triggered by antigen -
specific T lymphocyte cells (not
antibodies).
Cell mediated hypersensivity is induced
mainly in skin.
When skin again comes in contact with
those agents, the sensitized person
develops erythema, itching, eczema or
necrosis within 12 – 48 hours.
19. The Langerhans cell in the epidermis
interacts with CD4 T cells to cause
contact sensitivity.
It occurs after sensitisation with simple
chemicals, (e.g nickel & formaldehyde),
plant materials (Ivy poison, Oak poison),
topically applied drugs (sulfonamides &
neomycin), some cosmetics and soaps.
20.
21. (a) In the sensitization phase after initial
contact with antigen (e.g., peptides
derived from intracellular bacteria), TH
cells proliferate and differentiate into
TH1 cells. Cytokines secreted by these
T cells are indicated by the dark blue
balls.
22.
23. (b) In the effector phase after subsequent
exposure of sensitized TH1 cells to
antigen, the TH1 cells secrete a variety
of cytokines and chemokines. These
factors attract and activate macrophages
and other nonspecific inflammatory cells.
Activated macrophages are more
effective in presenting antigen, thus
perpetuating the DTH response, and
function as the primary effector cells in
this reaction.
24.
25. A prolonged DTH response can lead to
formation of a granuloma, a nodule-
like mass. Lytic enzymes released
from activated macrophages in a
granuloma can cause extensive tissue
damage.
29. Allergic Contact Dermatitis
ACD accounts for approximately 20% of all
contact dermatitis
ACD is a type IV, delayed or
cell-mediated immune reaction
that is elicited when the skin
comes in contact with a chemical
to which an individual has been
previously sensitized
Synonyms include contact dermatitis and
contact eczema
31. Pathogenesis
ACD is a type IV hypersensitivity
response
Requires prior sensitization to the
chemical
Once sensitized a low concentration of
causative chemical elicits a response
32. Clinical Features of ACD
Acute blistering
Scaly plaques
Patchy and diffuse distributions may be
seen with body washes and shampoos
33. Treatment of ACD
Involves identification of causative
allergens
Clear the dermatitis with topical, or if
necessary systemic corticosteroids
Complete and prolonged clearing can
take up to 6 weeks or more, even when
allergens are being avoided
34.
35. Nickel
Most common allergen
tested by the NACDG,
with 14% of patients
Reacting to it.
Commonly used in jewelry,
Buckles and other metal
containing objects.
36. Individuals with
nickel allergy should
avoid custom jewelry
and can usually wear
stainless steel or gold.
37. Neomycin Sulphate
Most commonly used
topical antibiotic used
with other antibacterial
Agent e.g Bacitracina &
Polymixin, as well as
Corticosteriods.
Co-reactivity is commonly seen with
neomycin and bacitracin
38. Thimerosal
Thimerosal is used as a preservative.
Most sensitization may be due to its use
as a preservative in vaccines.
Other exposures include:
o Contact lens solution
o Otic and opthalmic solutions
o Antiseptics and
o Cosmetics
39. Systemic Contact Dermatitis
Systemic exposure to a chemical may
result in a diffuse dermatitis
Patient has had a prior contact allergy
and then becomes exposed through a
systemic route, such as injection, oral,
intravenous, or intranasal administration
40. One of most
common examples
is patient with
ethylenediamine
allergy and
Subsequent reaction
to aminophylline.
43. Asthma
Asthma is a condition characterized by
reversible bronchospasm and chronic
inflammation of airway passages.
44. Individuals with asthma appear to
produce large amounts of the Antibody
IgE that attach to the mast cells present
in many tissues.
Exposure to a trigger such as pollen
will result in the allergen-binding mast
cell-bound IgE, which in turn causes the
release of inflammatory mediators such
as Histamine and Leukotrienes.
45. The response of a patient with asthma
to these triggers can be divided into
an ―early phase‖ and a ―late phase.‖
46. Early Phase of Asthma
The early phase of asthma is characterized by:
a. Marked constriction of bronchial airways
(bronchospasm)
b. Difficulty in breathing
c. Production of excess mucus.
The bronchospasm that occurs may be the
result of the increased release of certain
inflammatory mediators such as histamine,
prostaglandins and bradykinin that, in the early
stages of asthmatic response, promote
bronchoconstriction rather than inflammation.
49. Late Phase of Asthma
The late phase of asthma can occur several hours
after the initial onset of symptoms and manifests
mainly as an inflammatory response.
The primary mediators of inflammation during the
asthmatic response are the white blood cells
Eosinophils that stimulate mast cell degranulation
and release substances that attract other white cells
to the area.
Subsequent infiltration of the airway tissues with
white blood cells such as Neutrophils and
lymphocytes also contributes to the overall
inflammatory response of the late phase of asthma.
50. Some Potential Asthma Triggers..
Allergens — Pollen, pet dander, fungi,
dust mites
Perfumes
Pollutants
Cigarette smoke
Respiratory tract infections
51. Sign and Symptoms
Early Phase:
Shortness of breath
Cough
Chest tightness and pain
Wheezing
Cyanosis
53. Staging of Severity
Type Day Attacks Night Attacks
Mild Intermittant < 2 times in a week < twice in a month
Mild Persistant > 2 times in a week > Twice in a month
Moderate
Persistant
> 3 times in a week
or Daily
> 4 times in a
month
Severe Persistant Continous or At
any time
Daily
54. Treatment
Type Quicker Relief Long Term
Mild Intermittant Short Acting B2
Agonist
Short Acting B2
Agonist
Mild Persistant Short Acting B2
Agonist
Low Dose Inhaled
Steroid OR
SR Theophylline OR
Leukotriene
Antagonist
Moderate
Persistant
Short Acting B2
Agonist
High Dose Inhaled
Steroid OR
Low Dose Inhaled
Steroid + Short
Acting B2 Agonist