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SEMINAR PRESENTED BY- Dr NIKHIL SRIVASTAVA MODERATED BY- Dr ADIL SHAFATH

Seminar AnaphylaxisAnaphylaxis

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SEMINAR

PRESENTED BY- Dr NIKHIL SRIVASTAVAMODERATED BY- Dr ADIL SHAFATH

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HYPERSENSITIVITY REACTIONS

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CONTENTS•INTRODUCTION•CLASSIFICATION•Type I •Type II•Type III•Type IV•DENTAL CONSIDERATIONS•ANAPHYLAXIS & its MANAGEMENT

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INTRODUCTION•Immunity a Protective response, helping

the body to overcome infectious agents and their toxins

•Hypersensitivity an inappropriate or exagerrated response

•It is concerned with what happens to the host

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HYPERSENSITIVITY•According to Von Pirquet, Allergy meant

an altered state of reactivity to an antigen ,& included both types of immune responses protective as well as injurious

•Synonym for hypersensitivity

Ananthnarayan”s textbook of Microbiology

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COOMBS & GEL CLASSIFICATIOM (1963)

•TYPE I•TYPE II•TYPE III•TYPEIV

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TYPE I ( IgE)•ACUTEANAPHYLAXIS

•CHRONICATOPY

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Type I Hypersensitivity Reaction

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ANAPHYLAXIS•Its an acute reaction involving the smooth

muscle of the bronchi in which antigen IgE antibody complexes form on the surface of mast cells which cause sudden histamine release

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ANAPHYLAXIS•Coined by Richet•THEOBALD SMITH PHENOMENON•Sensitising Dose•Shocking Dose•‘Target Tissues’ or ‘Shock Organs’

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TYPE II HYPERSENSITIVITY REACTION•Antibody Mediated•Cytotoxic HypersensitivityAntibodies combine with host cells

recognized as foreignForeign antigens bind to host cell

membranes during induced hemolytic anemia

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•Eg-•Transfusion reaction by mismatched blood•Rhesus incompatibility•Goodpasture’s Syndrome

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TYPE III HYPERSENSITIVITY REACTIONS•Antibody Mediated through immune

complex formation•Local form is ‘Arthus Reaction’•Immune complex mediated

Hypersensitivity

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IMMUNE COMPLEX FORMATION•Hypersensitivity State: Complexes persist & lodge in blood

vessel walls, initiating inflammatory reactions

•Large complexes•Removed by neutrophils & macrophages

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• Soluble complexes (more antigen than antibody) - Most harmful - Penetrate vessel wall - Lodge in basement membrane• Complement is activated - Vascular permeability increased - Neutrophils attracted - Neutrophils release enzymes - Vasculitis results

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SENSITIVE SITES & EXAMPLES•Renal glomeruli•Synovial Membranes

•Systemic Lupus Erythematosus•Poststreptococcal glomerulonephritis

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TYPE IV HYPERSENSITIVITY REACTIONS

•Mediated by T lymphcytes•Does not involve antibodies•Delayed type hypersensitivity

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•Contact Dermatitis•Graft Rejection•Graft-versus-host reaction•Drug hypersensitivity•Autoimmune disease

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ANAPHYLACTOID REACTIONS•Anaphylaxis Like

•Hereditary Angioedema

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SIGNS & SYMPTOMS of ALLERGIC REACTION•Urticaria•Swelling •Skin Rash •Chest Tightness •Dyspnoea,shortness of breath•Rhinorrhea•Conjunctivitis

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DENTAL CONSIDERATIONS•Allergy to Local Anaesthesia•Toxic Reaction•IV Injection•Procaine•Methylparaben or Bisulfite

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TOXIC REACTION TO LA•Talkativeness•Slurred Speech•Dizziness•Euphoria•Excitement•Convulsions

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AAnesthesia

AnxietyAllergy B

BleedingBreathing

Blood Pressure

CChair Position

DDevicesDrugs

EEquipment

EmergenciesF

Follow Up

PATIENT EVALUATION

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•Diphenhydramine as a L.A.•Provocative Drug testing

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PENICILLIN•Common cause of drug allergy•5-10% population allergic• .04-.2 % develop an Anaphylactic reaction•Varies with routes

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RISK OF REACTION•History of Previous reaction•Time interval since previous reaction•Persistence of specific IgE antibodies•History of multiple drug sensitivities•Test for major & minor determinants

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•Use Alternative drug- Erythromycin or clindamycin•Cephalosporins•But can cross react

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PREVENTION OF PENICILLIN REACTION• Emergency Kit• Medical History• Not use penicillin in patient with history of

reactions to drugs• Tell Patient• No topical preparations• Don’t use penicillinase-resistant penicillins

unless infection caused by specific bacteria

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•Oral penicillin•Disposable syringes•Ask patient to wait for 30 min after Ist

dose given•Inform about signs & symptoms of

allergic reaction

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MANAGEMENT OF SEVERE TYPE I REACTIONS•Within MinutesHead Down positionAirway patentSupport respiration & circulationNote the rate & depth of Respiration

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ANGIOEDEMA•Edema of tongue•Pharyngeal tissues•larynx

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•Activate EMS•Inject 0.3 to 0.5 ml 1:1000 epinephrine IM

into tongue or SC•Supplement with IV diphenhydramine

50mg – 100 mg•Support Respiration•Carotid or femoral pulse

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ANAPHYLAXIS• Both respiratory & circulatory components of depression occur

early• Two symposia have been held by the National Institute of Allergy

and Infectious Diseases (NIAID) and the Food Allergy and Anaphylaxis Network (FAAN) to review knowledge and to discuss a definition of anaphylaxis.

• The following definition was recommended: “Anaphylaxis is a serious allergic reaction that is rapid in onset and may cause death.”

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PATHOPHYSIOLOGY• Ist contact with antigen results in formation of antibodies

by plasma cells• Antibodies circulate in IgE• Antibodies attach to target tissue• Next contact with antigen may result in combination of

antigen with antibody• Degranulation of mast cells• Smooth muscle contracts, vessels lose fluid• Acute respiratory distress and cardiovascular collapse

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SIGNS & SYMPTOMS• Itching of palate• Nausea,vomitting• Substernal Pressure• Shortness of Breath• Hypotension• Pruritus• Urticaria• Laryngeal Edema• Bronchospasm • Cardiac Arhytmmias

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MANAGEMENT• Call for help• Supine position• Open airway• Administer O2• Check pulse, B.P.,respiration• Inject 0.5 ml of epinephrine into tongue• Provide CPR• Repeat IM injection if no response

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Ref: The prevention andmanagement of anaphylaxis

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SYSTEMIC LUPUS ERYTHEMATOSUS

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CONTENTS•DEFINITION•INCIDENCE•ETIOLOGY•PATHOPHYSIOLOGY•CLINICAL PRESENTATION•LABORATORY FINDINGS•MEDICAL MANAGEMENT•COMPLICATIONS•DENTAL MANGEMENT

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DEFINITION•Classical example of systemic

autoimmune or collagen disease•‘lupus’•It’s a generalised form of lupus

erythematosus which affects multiple organ systems

•It is a more serious form•DLE predominantly affects the skin &

course tends to be benign

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INCIDENCE & PREVALENCE•Autoimmune disease•Female to Male ratio-5:1•Presence of Antibodies directed against

components of cell nuclei•Antinuclear antibodies

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ETIOLOGY•Unknown•Autoimmune Disease•Familial Aggregation•Triggering Exogenous & Endogenous

factors•Infectious agents,stress,diet,toxins, drugs & sunlight

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PATHOPHYSIOLOGY•Production of pathogenic antibodies &

immune complexes & their deposition with resultant inflammation & vasculopathy

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CLINICAL PRESENTATION• Polyarthritis• Butterfly-shaped rash across the nose & cheek• Renal failure• Neuropsychiatric Symptoms• Pulmonary manifestations• Cardiac involvement with clinically detectable

heart murmur• Libman-Sacks endocarditis

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LABORATORY FINDINGS• Antinuclear

antibody test• Hematologic

Abnormalities• Clotting

abnormalities-Lupus Anticoagulant, elevated PTT

• ESR• Proteinuria,

Haematuria

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MEDICAL MANAGEMENT•Symptomatic or Palliative t/t•Avoid Sun exposure•Aspirin & NSAIDs for mild disease•Antimalarials•Glucocorticoids•Cytotoxic agents

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•Plasmaphersis•Lymph node irradiation•Cyclosporine injection•Sex hormone therapy•Immune gamma globulin

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COMPLICATIONS•Neurologic or psychiatric involvement•Infection•Coronary Artery Disease•Osteonecrosis

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ORAL MANIFESTATIONS• Oral lesions of lip &

Mucous membrane• Erythematous with

white spots or radiating lines

• On lip, a silvery,scaly margin develops

• Xerostomia, dysguesia & hyposalivation

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DENTAL MANAGEMENT•Physician Consultation•Drug considerations•Haematologic considerations•Infective endocarditis-But no Antibiotic

Prophylaxis•Establishment & Maintainence of Optimal

Oral Health Care

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BIBLIOGRAPHY•Little & Fallace’s Dental Management of

the Medically Compromised Patient•Ananthanarayan’s Textbook of

Microbiology•Kuby’s Immunology•Prevention & Management of

Anaphylaxis: A Symposium on Allergy

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THANK YOU