Hypersensitivity Reactions Flashcards
Which type of hypersensitivty is called allergy
Type 1
Type 1 hypersentivity is mediated by
Binding of an allergen to IgE on the surface of mast cells
Th2 cells, IgE ab dependent activation of mast cells and leukocytes
Type 1 hypersensitivity releases
Vasoactive and spasmogenic subs which act on the vessels,smooth muscles and inflammatory cytokine recruit inflammatory cells
What are the phases of type 1 hypersensitivity
Immediate response= vasodilation, vascular leakage , smooth muscle spasm, glandular secretion—minutes after— VASODILATION, CONGESTION, EDEMA.
Late phase reaction= eosinophil, neutrophil, basophil, CD4+T cell infiltration, tissue destruction — 2 to 24 hours later— INFLAMMATORY INFILTRATE, RICH IN EOSINOPHILS, NEUTROPHILS and T CELLS
Which hypersensitivity type has high serum levels of IgE
Type 1
What is systemic anaphylaxis
Vascular shock
Widespread edema
Difficulty in breathing
Laryngeal edema
Vomiting
Abdominals cramps
Diarrhea
Laryngeal obstruction
Shock and die
Atopic allergy
Type 1
Urticaria
Angioedema
Allergic rhinitis hay fever
Bronchial asthma
What are the mechanisms of type 2 hypersensitivity
1-Opsonization and phagocytosis
2- Inflammation
3-Cellular Dysfunction
What is a Goodpasture syndrome
Type 2 hypersensitivity disease
Ab goes to kidney and lung basement membrane causing inflammation.
Nephritis and lung hemorrhages
Bulbous pemphigoid
Type 2 hypersensitivity disease
Vesicle formation in skin
Pernicious anemia
Type 2 hypersensitivity disease
Ab against the GIS
Megaloblastic anemia
Acute rheumatic fever
Type 2 hypersensitivity disease
Ab of streptococcal goes to heart muscle and cause distraction bc they lookalike
Carditis
Graves’ disease
Ab against the TSH receptor activate thyroid cells
Type 2 hypersensitivity disease
Myasthenia gravis
Ach receptor ab impair neuromuscular transmission
Type 2 hypersensitivity disease
Type 3 hypersensitivity
Mediated by antigen-antibody aggregates called ‘immune compexes’ which commonly occur in renal glomeruli,joint,skin,heart,serosal surface, small BV.
These complexes produce tissue damage mainly by inflammation.
Fever, urticaria,joint pain, vasculitis , glomerulonephritis, arthritis.
Acute necrotising vasculitis with necrosis of vessel wall and neutrophil is infiltration
Diseases that caused by type 3 hypersensitivity
Systemic lupus erythemotosis
Poststreptococcal GN
Polyarthritis Nodosa
Arthur’s reaction: localized tissue necrosis
Which type of hypersensitivity disease doesn’t involve ab
Type 4
Which type of hypersensitivity is mediated by T cells
Type 4
How does type 4 hypersensitivity initiated
Ag activated T lymphocytes — delayed type hypersensitivity CD4+
— T cell mediated cytotoxicity CD8+
What does CD4+ T cell mediated HS type 4 causes
Chronic inflammatory disease/autoimmune diseases)
Which type of hypersensitivity reactions has a response to intracellular microbiologyical agents
Type 4
What are the reactions of type 4 hypersensitivity
1- Proliferation and differentiation of CD4+ T cells= naive CD4 T cell recognize ag and differentiation of CD4+T cell to TH1,TH17 cell. Some of TH1, TH17 cells may remain in the memory pool of T cells
2- responses of differentiated effector T cells= repeat exposure to ag — memory T cell recognize ag and activated ,secrete cytokines ; TH1 activate macrophage, TH17 recruit neutrophils and monocytes
Which type of hypersensitivity reactions is the major mechanism of defense against intracellular pathogens
Type 4 (mycobacteria, fungi, parasites, transplant rejection)
Granuloma formation
Type 4 hypersensitivity
with persistent ag such as tbc colonizing lungs, peri vascular macrophage ,infiltration.
Activated macrophages cause morphological transformation into epi-like cells, epithelioid cells
Aggregation of cells surrounded by lymphocytes.
Type 4 hypersensitivity diseases
Graft rejection
Viral disease
Type 1 DM
Multiple Sclerosis
Crohn Disease
Contact dermatitis
Rheumatoid arthritis
Delayed type of type 4 hypersensitivity
Tuberculin reaction
What happens in Cellular Dysfunction
Type 2
antireceptor ab impair or dysregulate normal function of receptors.Graves’ disease, myasthenia gravis
Inflammation in type 2 hypersensitivity
Deposited ab activate complement, generating by product, causing recruit of neutrophils and release of enzymes
Glomerulonephritis
Vascular rejection
Opsonization and phagocytosis
Type 2
Opsonization of cells by ab and complement components and ingestion by phagocytes
Transfusion reaction
Erytroblastosis fetalis
Autoimmune hemolytic anemia
