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Immunology and Allergy (Pedoatrics) - Coggle Diagram
Immunology and
Allergy (Pedoatrics)
Principles
Basic Principles in Allergic Disease (Immunologic Basis)
Allergens
antigens that trigger IgE responses
Antigen-presenting cells
2 systems
Dendritic cells (DC) and Epidermal Langerhans cells (LC)
Inducers of primary T cell responses
Monocyte-macrophage system
Activates memory T cells
T- cells
TH1 – produce IL2, IFN , TNF
Activate phagocytes and production of B lymphocytes
TH2 – produce IL4, IL5, IL6, IL9, IL10 and IL13
production by B cells
activation and survival
of high amount of antibodies IgE and growth of mast cells and basophils release of leukemia inhibitory factor (LIF)
TH17 – Newest member. Produce IL17, IL22, IL17F and CCL20
autoimmune diseases and development of contact dermatitis, atopic dermatitis and asthma
Treg – IL2R
Suppresses function of TH1 or TH2 phenotypes
IgE and its receptors
High affinity to mast cells and basophil
Involved on synthesis: IL4 and IL13
Inhibit IgE synthesis: IL12, IFN
Eosinophils
Hallmark signs of helminth infection, allergy, asthma
Major Basic Protein (MBP) - >50% of granules
MAST cells
2 subtypes (secretory protease content)
Mast cell with tryptase (MCT)
Mast cell with tryptase and chymase (MCTC)
3 categories of Mediators
Preformed mediators
Newly synthesized lipid mediators
Cytokines
BASOPHILS
Granulocytes with separate lineage from mast cells
<1% of blood leukocytes
Sensitization
Host Response to foreign material
IgE- specific antibodies
Attach to mast cells and basophils
Terms
Allergy
all kinds of reaction in the skin and mucosal surfaces of the respiratory and gastrointestinal tracts
Hypersensitivity
signs and symptoms initiated by exposure to a defines stimulus
Atopy
refers to genetic predisposition to become sensitized and produce IgE antibodies upon exposure to common allergens
Allergen
protein substances capable of inciting reactions in the host eg pollens, food, dust mites, mold spores, animal danders,drugs and vaccines
Haptens
low molecular weight antigens
Mechanisms of Immune mediated Diseases
4 Types of Hypersensitivity Reaction
Type II
Antigen
Cell- or matrix associated antigen
Effector Mechanism
FcR+ cells (phagocytes, NK cells)
Immune Reactant
IgG
Examples
Some drug allergies (eg. Penicillin),Hemolytic Disease of
Newborn
Type III
Immune Reactant
IgG
Antigen
Soluble antigen
Effector Mechanism
FcR+ cells Complement
Examples
Serum sickness,Arthus reaction Lupus E,
GLomerulon ephritis
Type I
Antigen
Soluble antigen
Effector Mechanism
Mast-cell activation
Immune Reactant
IgE
Examples
Allergic Rhinitis,asthma, systemic anaphylaxis
Type IV
Immune Reactant
TH1 Cells
Antigen
Soluble Antigen
Effector Mechanism
Macrophage activation
Examples
Contact Dermatitis tuberculin reaction, leprosy, sarcoidosis
TH2 cells
Antigen
Soluble Antigen
Effector Mechanism
Eosinophil activation
Examples
Chronic Asthma,chronic rhinitis
CTL
Antigen
Cell-associated antigen
Effector Mechanism
Cytotoxicity
Examples
Contact Dermatitis,Graft rejection,Stevens Johnsons
Allergic Inflammation
Late Phase reactions
6-12 hours and resolve in 24 hours
Chronic Allergic inflammation
Acute Phase Reactions/ Immediate
Occur within 10 minutes after allergen exposure and resolve in 1-3 hours
Non – immunologic Mechanisms
increased
Acetylcholine
release>>>parasympathetic nerve fibers
Diagnostic
HISTORY
Allergic salute and nasal crease
Environmental survey
PHYSICAL EXAMINATION
MUST be thorough with emphasis on common target organs in allergic disorder: skin, eyes, nose, ears, throat and lower respiratory tract
TESTS
InVitro tests
Provocation Tests
Tests for T-cell mediated or non-IgE mediated diseases
Treatment
Patient Education
Environmental Control
Essential actions to reduce mite exposures
PharmacologicTherapy
Adrenergic Agents
Epinephrine
acute anaphylaxis
Alpha adrenergic
vasoconstriction
Pseudoephedrine, Phenylephrine, Phenylpropanolamine
Beta adrenergic ((B2))
Bronchodilatation
Salbutamol, Albuterol, Terbutaline, Formoterol, Salmeterol
Anticholinergic Agents
Ipratropium bromide
Anti-histamines
Chromes
Glucocorticosteroids
Antileukotrienes Agents
Theophylline
Mast cell stabilizers
Anti- IgE Drugs
Allergen Immunotherapy
Prevention
Primary strategies
Secondary strategies
Tertiary Prevention
Allergics
Allergic Rhinitis
Risk Factors
Exposure to indoor allergens
Presence of atopic dermatitis
Serum IgE > 100IU/ml before 6yo
Small family size lesser microbial stimulation
Family history of atopy
Clinical Manifestations
PE: Facial deformities, dental malocclusion,
“allergic Shiners”
Mouth breathing
” allergic gape”
, edema, itching tearing and redenss of conjunctiva, boggy nasal mucus membrane
Diagnosis
Allergen
Skin prick test/ prick and puncture test
Immunoassays
Nasal eosinophillia
Treatment (Example)
FIRST-GENERATION H1 ANTAGONISTS
Chlorpheniramine
SECOND-GENERATION H1 ANTAGONISTS
Cetirizine
Loratadine
Childhood Asthma
Clinical Manifestations
Intermittent cough and episodic expiratory wheeze
Diagnosis
Clinical history
Asthma symptoms
Measurement of lung function
5yo –use of spirometry or PEF
Allergy skin test
Differential diagnostic possibilities
UpperAirway disease
Obstruction involving large airways
Obstruction involving the smaller airways
TREATMENT
4 Components of Care
Assessment and monitoring
Education
Control of environmental factors
Pharmacotherapy
SABA
Atopic Dermatitis(AD)
Diagnosis
Based on findings of pruritus, typical morphology
Family history
Treatment
Non-pharmacologic treatment
Eliminating rough clothing, irritating soap,food allergens,dust mites
Pharmacologic
Topical anti-inflammatory
Sedating H1 blockers
Treatment and prevention of Staphylococcal
Asthma and AR
Prevention
maternal avoidance of allergenic foods
Use ; hydrolyzed cow milk formula for who cannot breastfed
Probiotics
Urticaria ad Angioedema
Acute
skin lesions < 6 weeks
causes
Histamine
Radiocontrast agents
Viruses
Hep B, EBV
NSAIDS
Parasitic infestations
Chronic
skin lesion > 6 weeks
cause
Autoantibodies to IgE or to high affinity receptor for IgE
Papular Urticaria (Acute Prurigo)
Human, dog, cat ,bird fleas,Mosquitoes and live bedbugs
Physical Urticaria
Weather changes
Cold-dependent Urticaria
Laboratory: cryoproteins eg. Cold agglutinins cryoglobulin
Cholinergic Urticaria and Heat Urticaria
Dermatographism
Pressure Urticaria/ Angioedema
Solar Urticaria
sun/ light
Aguagenic Urticaria
water
Psychogenic Urticaria
emotional stress
Diagnosis
Vasculitis syndrome
skin lesions persist in the same location for more than 24 hours
pigmented or purpuric,or burn more than itch
Outline
History and PE
Chest radiograph
Blood tests – CBC, ESR, ANA
Stool exam
Skin biopsy
Treatment
Acute urticaria
DOC: Diphenhydramine and Hydroxyzine or 2nd generation drugs
Loratadine
Cetirizine
Chronic urticaria
Anti histamine (Hydroxyzine)
oral corticosteroids
Cold urticaria
DOC: Cyproheptadine
Anaphylaxis
Clinical Manifestations
urticaria and angioedema
Treatment
Medications
IM Epinephrine
IM H1 and H2 antihistamines
Oxygen
Inhaled B2 agonist
Systemic corticosteroids
Other Allergic Disorders
Adverse Reaction to Drugs
Allergic Conjunctivitis
Adverse Reaction to Food
Immonology
Basic Immunology
Innate Immunity
COMPONENTS AND FUNCTIONS OF INNATE IMMUNE SYSTEM
BARRIERS
Epithelial cells
Prevent microbial entry
Intra-epithelial lymphocytes
Microbial killing
Defensins/ cathelicidins
Microbial killing
Circulating Effector Cells
Macrophages
Efficient phagocytosis and killing of microbes; Secretion of cytokines
B1-B cells
Secretion of natural antibodies
Neutrophils
Early phagocytosis and killing of microbes
NK cells
Lysis of infected cells, activation of macrophages
Circulating effector proteins
Mannose-binding lectin (collectin)
Opsonization of microbes, activation of complement- lectin pathway
C-reactive protein (pentraxin)
Opsonization of microbes, activation of complement
Complement
Killing of microbes, Opsonization of microbes, activation of leukocytes
Cytokines
INF gamma
Macrophage activation
IL-12
INF gamma production by NK and T cells
INF alpha and beta
Resistance of viral infection
IL-15
Proliferation of NK cells
TNF, IL-1, chemokines
Inflammation
IL-10, TGF beta
Control of inflammation
Adaptive Immunity
Activation of specific immune system
Initiated by monocyte-macrophage as antigen-presenting cells,providing a link between innate immune response and adaptive immunity
Dominant effector cells in the 1st 1-2 days of infection and produce cytokines which activates the NK cells and T cells (IL-1, TNF,IL-12)
Tissues and Organs of Immune
Primary lymphoid organs
Bone marrow and the thymus
Secondary organs
Lymph nodes, the lymphatics, the spleen
Immunity to Microbes
Immunity to Extracellular Bacteria
Immunity to Viruses
Cytotoxic T cells – eliminate them inside the cells
Immunity to Fungi and Ectoparasites
Neutrophils – important phagocytic cells
Immunity to Protozoa
immunity mediated by macrophages and CD4T cells
Immunity to Worms
mediated by eosinophils and IgE antibody
Immuno deficiency Diseases
CLASSIFICATION
Primary Immunodeficiency
Classified according to the host defense system
Combined T and B cell deficiency
Phagocytic defects
T cell deficiency (cellular deficiency)
Complement defects
B cell deficiency (antibody deficiency)
Secondary Immunodeficiency
more common
Causes
Post-organ transplant
Prolonged corticosteroid therapy
Use of chemotherapeutic agents
Autoimmune disease
Infectious
HIV
Congenital rubella
Varicella
Rubeola
Malnutrition
Medical History-taking and Physical Examination