Hypersensitivity Flashcards
Mast cell , basophils , eosinophils role in immunity
Inflammation in mucosa
Have a role in hypersensitivity
What is hypersensitivity?
Excess or uncontrolled reaction produced by normal immune system causes tissue damage
What cuse hypersensitivity?
Foreign Ag
1. Harmless environment Ags like food ,drug(hapten)
2. Infectious organism
Self Ag
Due to failure of tolerance–> autoimmune disease like self reactive clones
Factor determining clinical & pathological consequences
- Type of immune response
- Nature & location of the causative Ag , RT or GIT
Hypersensitivity is classified according to ______ ________ causing tissue damage
Type 1,2,3 is ____
Type 4 ____
Effort mechanism
Ab mediated
T cell mediated
Type 1 hypersensitivity is also called _____ or _____
Immediate
Anaphylctic type ( lgE mediated)
1st exposure to allergen cause
Sensitization
What are the allergen that cause hypersensitivity
Certain food
Pollen
Drugs ( penicillin )
Insect bit like bee venom
Animal serum protein
During the first exposure in hypersensitivity, allergen is taken by APCs to be presented to
Th2
In type 1 hypersensitivity why th2 is highly secreted ( هذا أفضل وصف عندي) ?
Genetic predisposition that run in families
After APCs bind with its MHC2 (that contain allergen) to TCR on th2 , what will happen
Th2 secrete lL4,13,10 that + B cell to produce lgE secretion
And lL5 to run as ADCC
After 1st exposure, Sensitization requires _____ , during that period millions of _____ molecules are synthesized, these molecules attach to ____ on thousands of mast cells and basophils
1 week
IgE
Fc epsilon receptor
In 1st exposure, mast cell and basophils secrets histamine
False , in second exposure
2nd exposure to allergen cause
Degranulation
In hypersensitivity type 1 , how Degranulation occurs?
When mast cells and basophils is attached to lgE , and FAB of lgE do crosslinking action degranulation of mast cells in tissue and basophils in blood
What are the early phase reactions to allergen
On set on 2nd exposure to Ag :
Mediators ( what is synthesis) :
Effects :
Within minutes
Physiological preformed mediators
Histamine , pAF , ECF-A (حبا في العلم جيب الفلفورم لوحدك)
1.Increase VD and capillary permeability which cause wheal and flare reaction
2. Smooth muscles contraction and Increase mucus secretion (in trachea دي جدعنة بس غالبا صح)
3. + of nerve ending in skin cause itching
Late phase reactions onset on 2nd exposure to Ag
Within hours
Late phase reactions midators
Cytokines TNF alpha , lL4,5,13
Recruitment of neutrophils , eosinophils and th2
Late phase reactions effects
Neutrophils and eosinophils that release proteases cause tissue damage
Where is clinical presentation is absorbed in hypersensitivity type 1 and name its 2 kinds
In RT , intestinal wall , skin ( site of mast cell
Systemic anaphylaxis
Localized anaphylaxis (atopy) or atopia=extraordinary
In Systemic anaphylaxis type of allergen is
Injection like penicillin, animal antitoxin
Bee venom
Mechanism of Systemic anaphylaxis
Degranulation of mast cell and basophils in blood
What are the symptoms of Systemic anaphylaxis
Edema and hypotension
Urticarial rash احمرار جلدي
Difficulties in breathing
Fatal within minutes
Localized anaphylaxis differentiate into
Airborne allergens (inhalation)استنشاق
Food drag allergens (ingestion)ابتلاع
Airborne kinds
Allergic rhinitis ( hay fever) التهاب الأنف التحسسي
Bronchial asthma الربو القصبي
Allergens of hay fever and broncil asthma is
Plant pollen
Animal dander
Fungal spores حويصلات الفطريات
Allergic rhinitis (التهاب الأنف التحسسي)
Bronchial asthma الربو القصبي
Name there mechanism
Allergic rhinitis
Degranulation of mast cells in eyes and upper RT or trachea
Bronchial asthma
Degranulation of mast cells in lower RT or lungs
Symptoms of allergic rhinitis
Red eyes
Coughing and sneezing
Symptoms of Bronchial asthma
Difficulty in breathing
كيف يسبب Degranulation of blood صعوبة في التنفس
Food and drug allergens (___) affect GIT causing _____& ______
Absorbed in blood , reach skin cause _____ , reach lung cause ____
Ingestion
Vomiting , diarrhea
Urticarial , asthmatic attack نوبة ربو
Diagnosis of type 1 hypersensitivity are 2 kinds ,name them and mechanism
- Allergy skin test –> determine causative allergen
- Allergy blood tests –> measurement of lgE in serum
Allergy skin test is a diagnosis processe that test allergen of ___,____,_____
Penicillin يستخدم قبل ما اعطي المريض الحقنه ، أتأكد اذا عنده حساسية ولا لأ
Pollens , food
Metod of allergy skin test
Pricking the skin in forearm or back with sterile lancet containing drop of allergen
يارب ما تكون نسيت شو نوع allergen إلي نحطه على المريض في حالة allergy skin test
+ve result of allergy skin test
Wheal and flare reaction within 15 to 20 min
Allergy blood tests measure lgE in serum by two ways name them
Total lgE by RIA : high in some allergic patients
Specific lgE by RAST : يستخدم ضد certain allergen
جيب الفلفورم تبعها ، والله مو صعب
Management of type 1 hypersensitivity
Identify and avoiding allergen if possible
Drugs
Immunotherapy
Name drugs that prevent release or effect of chemical mediator in type 1 hypersensitivity
- Epinephrine ( best immediate treatment for anaphylactic shock )
- Corticosteroids
- Mast cell stabilize ( prevent Degranulation)
Example for mast cell stabilizer
Na cromoglycate
العلاج بالمناعة هو
Immunotherapy
Bind to Fc of lgE prevent lgE from binding to mast cell
Monoclonal Ab or anti lgE , by this way we can prevent 1st exposure
What is the goal of allergy specific immunotherapy or desensitization
Decrease lgE and increase lgG titers
When we use desensitization?
Failure of medication to control allergy symptoms
مثل شخص كل ما يجي فصل الربيع تزيد حساسيته من pollen
Method of allergy specific immunotherapy
Repeated injection of small doses of allergen
1. Decreases th2 domination that decreases lL4,5 that decreases lgE
- Increases th1 response that increase IFN GAMA that lgG( blocking Ab)
- Increases t reg response that inhibit th2
- Tolerance in t cell specific to allergen هبد
Type 2 hypersensitivity is also called
Cytotoxic or cytolytic type (lgG,lgM mediated)
What are the mechanism of type 2 hypersensitivity
A. Formation of lgG and lgM against Ag on cell surface
B. Ab binds to Ag on cell surface
C. Mechanism of tissue damage
In type 2 hypersensitivity mechanism, Formation of lgG or IgM against Ag on self or foreign cells
Ag of self cells _____ or ______(___)
Due to failure of tolerance
_____(attach drug) or ______(exogenous)
Ag of Foreign cell (exogenous)
_______ &_______
Self protein , receptor (endogenous)
Hapten ( attach drug)
Organism
Allogenic RBC Ags
“ graft cells
Mechanism of tissue damage are _______&______
Lysis of cell by cytotoxic Abs
Interference with cell functions ومثال على ذلك Graves disease
Myasthenia Gravis
tissue damage occur in type 2 hypersensitivity
Lysis of cell by cytotoxic Abs by 3 ways name them
Complement activation , killing by Mac (c5b6789) اي الشطارة دي
Opsonization
ADCC
مش لازم اكتب امثله لأنها واضحة ومتكررة
Tissue damage in type 2 hypersensitivity is interference with cell functions , what is that ?
Binding of Ab to cellular receptors –> stimulation or blocking of receptor
في مثال جميل على دا هو Graves disease و myasthenia Gravis
Clinical presentation of type 2 hypersensitivity are
Allohemolysis
Autoimmune hemolysis , thrombocytopenia, granulocytopenia
How Interference with cell functions occur ?
Binding of Ab to cellular receptors causing stimulation or blocking of receptors
What is the meaning of allogenic ?
Different Ag from an individual in the same species , his Ag could be blood or even stem cells
Allohemolysis is a clinical presentation of type 2 hypersensitivity, name its kinds
ABO incompatibility
Rh incompatibility(Rh factor or D Ag)
What is ABO incompatibility?
Comments why for transfusion reaction
If a person with A+ve is tranfused(نقل إليه) with B+ve RBCs preexisting (natural) antiB lgM rapidly hemolyse( تقتل او انحلال الدم) RBCs in circulation by complement activation
What is the mechanism of Rh incompatibility?
Fetal Rh +ve( ليش البيبي عنده ار اش موجب ، لأن ورثه من ابوه) leak into Rh -ve mother circulation(قصدو الدورة الدموية) during birth of 1st child —> this reaction sensitive mother to produce lgG ام شريرة
–> ln second pregnancies lgG that was produced in first pregnancy cross placenta and destroy fetal RBCs
–> still birth or erythroblastosis or jaundice
How we prevent lgG killing RBCs of fetal?
Anti D or anti RH+ve injection is given to the mother within 72 hour of 1st delivery of Rh+ baby (الممرضة البطلة رح تعطي الجرعة للأم أو ما تولد البيبي)
–> neutralize or destroy any leaking fetal RBCs in mother circulation during baby delivery
–> no + of mother immune system
How we can treat a mother with rh-ve and her fetal with rh+ve RBCs
By exchange transfusion ( it also may happen in uterus)
Autoimmune hemolysis destruction of
Hemolysis of self RBCs
Throm’bo-cyto-penia is the destruction of
Self platelets
Granu-lo-cyto-penia I the destruction of
Self granulocytes
How auto immune against RBCs , platelets, granules (وهذه كلها self cells) occur ?
Abs called acto Abs attack patient own Ags
Autoimmune hemolysis , thrombocytopenia, granulocytopenia , e.g for drug(happten)
Drags like penicillin may bind to Ags on RBCs or platelets –> production of cytotoxic Abs to cell-frug complex
E.g hemolytic anemia by penicillin
Name other clinical presentation of type 2 hypersensitivity
Disease due to affection of cell receptor [ type 5 hypersensitivity]
Good pasture syndrome
Rheumatic fever
Hyperacute & acute graft rejection
E.g for disease due to affection of cell receptor
+ of receptor Graves disease
- of receptor Myasthenia Gravis
What is Graves disease?
When pituitary gland produces TSH to stimulate thyroid gland , thyroid gland associated with TSH receptor will coat with TSH and the thyroid gland will be + and secrete T3 and T4
But when immune system produces Abs in excess way (بطريقة مفرطة) that bind to TSH receptor that + thyroid gland to produce more and more T3,T4
—> hyperthyroidism إفراط الغدة الدرقية
What is Myasthenia Gravis الوهن العضلي?
At nerve ending, nerve produce ACh(اسيتاي كولين) that bind to receptors on muscles called ACh receptors .
But when immune system produce lgG that bind to ACh receptors and - it paralysis الشلل occur
When lgG and lgM is non cytotoxic Abs ?
وهن العضلات القاتل و Gravis disease
good pasture مثال على مريض
يتعذب في دنيتو بسبب Renal failur and RT failure
What is good pasture syndrome
IgG auto Abs ( failure of tolerance) bind to non collagenous proteins(dr: لازم تكونوا اخذتوه في الفسيولوجي) in basement members ( احفظو كده) of lung alveoli and kidney glomeruli ( شوف الشعر ده)
What is heterophile Abs ?
Specific for one or epitope on different Ags
