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Immune System 1.Cellular Elements T Lymph. Helper,suppressor,cytotoxic,killer 2.Humoral Elements Antibodies,complements,cytokines,other circulating p.p.

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Presentation on theme: "Immune System 1.Cellular Elements T Lymph. Helper,suppressor,cytotoxic,killer 2.Humoral Elements Antibodies,complements,cytokines,other circulating p.p."— Presentation transcript:

1 Immune System 1.Cellular Elements T Lymph. Helper,suppressor,cytotoxic,killer 2.Humoral Elements Antibodies,complements,cytokines,other circulating p.p

2 Functions AppropriateMonitor+defenseInappropriate Hypersensetive allergic reactions

3 Allergic Reactions Type I Immediate A/IgE-mast+basophils anaphylaxis,all.rhinitis,ext.asth. Type II Cytotoxic IgG or IgM/Antigens on the surface of foreign cells ABO-incompatiblity,drug induced hemolytic,heparin/thrombo. Type III Immune Complex Insoluble Ant/Ab deposit in the microvasculature Ca /neutrophils---tissue damage Type IV Delayed Antigen/T-cells—lyphocyte regulation,Macrophage activation+Mononuclear cell infiltration contact dermatitis,graft rejection

4 Definitions Anaphylasis:life-threatening allergic reactions mediated by antibodies Anaphylasis:life-threatening allergic reactions mediated by antibodies Anaphylactoid:life-threatening allergic reaction Not mediated by antibodies (unable to prove antibody involvement). Anaphylactoid:life-threatening allergic reaction Not mediated by antibodies (unable to prove antibody involvement). Antigen:Molecules capable of stimulating an immune response(AB or Lymphocyte). Antigen:Molecules capable of stimulating an immune response(AB or Lymphocyte). Heptan:small molecule bind to P.P to form macromolecule. Heptan:small molecule bind to P.P to form macromolecule. Antibodies:immunoglobulins that can recognize and bind to a specific antigen.IgG,IgA,IgM,IgD+IgE Antibodies:immunoglobulins that can recognize and bind to a specific antigen.IgG,IgA,IgM,IgD+IgE Complement:20 different protiens that bind to activated antibodies,other complement protiens and cell membranes. Series of inhibitors regulates activation(C1 esterase inhibitor deficiency) Complement:20 different protiens that bind to activated antibodies,other complement protiens and cell membranes. Series of inhibitors regulates activation(C1 esterase inhibitor deficiency)

5 Angoneurotic Edema Painless,Nonpitting,Nonpuritic,Demarcated edema of deep dermis and Sc.,usually involving face, airway,GIT and extremities. Painless,Nonpitting,Nonpuritic,Demarcated edema of deep dermis and Sc.,usually involving face, airway,GIT and extremities. Types:Hereditary deficiency or dysfunction of C1 esterase inhibitor (less than 50% of normal C1 esterase is produced). Acquired,cosumtion or autoantibodies Types:Hereditary deficiency or dysfunction of C1 esterase inhibitor (less than 50% of normal C1 esterase is produced). Acquired,cosumtion or autoantibodies ACEI-blocks metabolism of bradykinin and substance P. ACEI-blocks metabolism of bradykinin and substance P. Codeine, generation of tissue bradykinin from mast cells degranulation. Codeine, generation of tissue bradykinin from mast cells degranulation.

6 Clinical Presentation HAE:1:50,000-1:150,000 Age: by 30yr,98% of patients have S/S. Triggering factors: minor or even trivial trauma or emotional upset. Triggering factors: minor or even trivial trauma or emotional upset. AAE:less than HAE. Age: older age,associated with malignance. 96% had swelling of extremities. 93% had recurrent abdominal pain. 85% had edema of the face. 64% had oropharyngeal involvement % may die from laryngeal edema. Urticaria(erythematous,pruritic,cutaneous elevationsof the skin that blanch with pressure)can occur in some patients.

7 Drug therapies for C1 INH Deficiency 1. Antifibrinolytic:EACA,tranexamic acid.Inhibit plasminogen and plasmin activity,limiting the formation of plasmin,which can activate C1.Ache,fatigue,hypotenion,+TE. 2. Androgen,increasesC1 INH by the liver. Weight gain,headch,myalgia,so on. 3. FFP:contains C1 INH,but also contains kinins and C2,C4 that may fuel complement activation. 4. Purified C1 INH concentrate, partial resolution of symptoms within 1 h.,complete resolution within 24 h.can increaseC1 INH by 50% over 15 min. pooled plasma.

8 Treatment of Acute Attack 1.Stop administration of suspected antigen. 2.Maintain airway with 100% oxygen. 3.I.V crystalloid/colloid. 4.Epinephrine(5-10ug.i.v,titrate as needed),

9 Secondary treatment: 1.Diphenhyramine(.5-1mg./kg.). 2.Catecholamine infusions(Ep.4-8ug/min.,Norep.4- 8ug./min.,iosproterenol.5-1ug./min). 3.Aminophylline(5-6mg./kg.over20min.inf..9-1mg/kg/h). 4.Corticosteroids(.1-1g.hydrocortisone,1-2g.methyprednisolone). 5.NaHCO 3,.5-1mEq/kg.with persistent hypotension or acidosis. 6.Airway evaluation ( prior to extubation ).

10 Catecholamines Epinephrine Epinephrine Alpha-adrenergic--VC. Alpha-adrenergic--VC. B 2 st.--bronchodilation+inhibits mast cells,basophils mediator release by increasing cAMP. B 2 st.--bronchodilation+inhibits mast cells,basophils mediator release by increasing cAMP. Rout of administeration,dose depend on the patient's condition. Rout of administeration,dose depend on the patient's condition. Racemic Epi.(sour white crystalline,D+L tartaric acid). Racemic Epi.(sour white crystalline,D+L tartaric acid). Dose:2.25% Nebulize mixure. Dose:2.25% Nebulize mixure. Child under 6 month ml. Child under 6 month ml. Child above 6 month--0.5 ml. Child above 6 month--0.5 ml. Adolescent 0.75 ml. Adolescent 0.75 ml. Adult 1 ml. Adult 1 ml. Add ml. Add ml. Onset 5-10 min.,last min. Onset 5-10 min.,last min. May be repeated in 30 min. May be repeated in 30 min.

11 Norepinephrine May be used in refractory hypotension. May be used in refractory hypotension ug/kg/min.(4-8 ug/min.) ug/kg/min.(4-8 ug/min.)Isoproterenol May be use in refractory bronchospasm,pulmonary hypertension, or Rt.ventriculer dysfunction. May be use in refractory bronchospasm,pulmonary hypertension, or Rt.ventriculer dysfunction ug./kg./min.(0.5-1ug/min.) ug./kg./min.(0.5-1ug/min.) Profound B 2 adrenergic effects-systemic VD. Profound B 2 adrenergic effects-systemic VD.

12 Aminophylline Nonspecific phosphodiesterase inhibitor-- bronchodilator. Nonspecific phosphodiesterase inhibitor-- bronchodilator. Decrease pulmonary vascular resistance. Decrease pulmonary vascular resistance. Improve Rt and Lf ventricular contractility. Improve Rt and Lf ventricular contractility. Decrease histamine release from mast, and basophilic cells Decrease histamine release from mast, and basophilic cells

13 CorticosteroidsCorticosteroids Decrease arachidonic acid metabolites by inhibiting phospholipids membrane breakdown. Decrease arachidonic acid metabolites by inhibiting phospholipids membrane breakdown. May alter the activation and migration of other inflammatory cells May alter the activation and migration of other inflammatory cells May require hours to work, but they still in practice in refractory bronchospasm or shock. May require hours to work, but they still in practice in refractory bronchospasm or shock. Hydrocortisone is recommended in IgE- mediated reaction Hydrocortisone is recommended in IgE- mediated reaction g g. Methylprednisolone is recommended for complement mediated reaction,(30-35mg/kg) Methylprednisolone is recommended for complement mediated reaction,(30-35mg/kg)

14 Special Anesthetic Consideration Avoid airway manipulation as much as possible( regional or mask inhalation). LMA,it is reasonable to assume that its large surface contact area may lead to worsened airway edema. Fiberoptic intubation,in presence of severe airway swelling and the demand for acute intervention can greatly limit the effectiveness of FO intubation. When performing emergency laryngoscopy and intubation,the attendance of an otolaryngologist is mandatory should a tracheostomy be necessary OR, is the best place for airway instrumentation, this may not always possible.

15 Nonimmunologic Release of Histamine The mechanisms appear to be noncytotoxic degranulation of mast cells, but not basophils. The mechanisms appear to be noncytotoxic degranulation of mast cells, but not basophils. Cutaneous mast cells are the only cell population that release histamine in response to drugs or endogenous neuropeptides. Cutaneous mast cells are the only cell population that release histamine in response to drugs or endogenous neuropeptides.

16 Allergic Drug Reactions 5% of adult in US may be allergic to one or more drugs. 5% of adult in US may be allergic to one or more drugs. 15% of adult in US believe,they are allergic to specific medication. They refer to adverse drug effects as being allergic in nature. 15% of adult in US believe,they are allergic to specific medication. They refer to adverse drug effects as being allergic in nature. A drug may produce different reactions in different patients or spectrum of reactions in the same patient. A drug may produce different reactions in different patients or spectrum of reactions in the same patient. A drug can produce anaphylaxis (Type I). Hemolysis (type II). Serum sickness (type III). Contact dermatitis (type IV). A drug can produce anaphylaxis (Type I). Hemolysis (type II). Serum sickness (type III). Contact dermatitis (type IV).


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