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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
Functions
Appropriate
Monitor+defense
Inappropriate
Hypersensetive allergic reactions
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
Definitions
• Anaphylasis:life-threatening allergic reactions mediated by
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antibodies
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).
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
Complement:20 different protiens that bind to activated
antibodies,other complement protiens and cell membranes.
Series of inhibitors regulates activation(C1 esterase inhibitor
deficiency)
Angoneurotic Edema
• 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
• ACEI-blocks metabolism of bradykinin and
substance P .
• Codeine, generation of tissue bradykinin from
mast cells degranulation.
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.
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.
14-33% may die from laryngeal edema.
Urticaria(erythematous ,pruritic,cutaneous elevationsof
the skin that blanch with pressure)can occur in some
patients.
Drug therapies for C1 INH Deficiency
1. Antifibrinolytic:EACA,tranexamic acid.Inhibit
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plasminogen and plasmin activity,limiting the
formation of plasmin,which can activate
C1.Ache,fatigue,hypotenion,+TE.
Androgen,increasesC1 INH by the liver. Weight
gain,headch,myalgia,so on.
FFP:contains C1 INH,but also contains kinins and
C2,C4 that may fuel complement activation.
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.
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),
Secondary treatment:
1.Diphenhyramine(.5-1mg./kg.).
2.Catecholamine infusions(Ep.4-8ug/min.,Norep.48ug./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.NaHCO3,.5-1mEq/kg.with persistent hypotension or acidosis.
6.Airway evaluation ( prior to extubation).
Catecholamines
• Epinephrine
• Alpha-adrenergic--VC .
• B2 st.--bronchodilation+inhibits mast cells ,basophils mediator
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release by increasing cAMP.
Rout of administeration,dose depend on the patient's condition.
Racemic Epi.(sour white crystalline,D+L tartaric acid).
Dose:2.25% Nebulize mixure.
Child under 6 month --0.25ml.
Child above 6 month--0.5 ml.
Adolescent 0.75 ml.
Adult 1 ml.
Add 2-3.5 ml.
Onset 5-10 min.,last 90-120 min.
May be repeated in 30 min.
Norepinephrine
• May be used in refractory hypotension.
• 0.05-0.1 ug/kg/min.(4-8 ug/min.)
Isoproterenol
• May be use in refractory bronchospasm,pulmonary
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hypertension, or Rt.ventriculer dysfunction.
0. 01-0.02 ug./kg./min.(0.5-1ug/min.)
Profound B2adrenergic effects-systemic VD.
Aminophylline
• Nonspecific phosphodiesterase inhibitor-bronchodilator.
• Decrease pulmonary vascular resistance.
• Improve Rt and Lf ventricular contractility.
• Decrease histamine release from mast, and
basophilic cells
•Corticosteroids
• Decrease arachidonic acid metabolites by
inhibiting phospholipids membrane breakdown.
• 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.
• Hydrocortisone is recommended in IgEmediated reaction
• 0.25-1 g.
• Methylprednisolone is recommended for
complement mediated reaction,(30-35mg/kg)
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.
Nonimmunologic Release of Histamine
• 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.
Allergic Drug Reactions
• 5% of adult in US may be allergic to one or more
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drugs.
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 can produce anaphylaxis (Type I).
Hemolysis (type II). Serum sickness (type III).
Contact dermatitis (type IV).