NI MADE PASMIATI SETYANINGSIH LUH AYU BANGKITARYANI FITRIANA MELINDA REGI RINALDY BILLJUDIKA CINDY ANWAR RADITYA NARAYANA

PUTU SATYA PRATIWI I WAYAN SURYANATA KALAA A/P GOVINDARAJAN SURESHNAIDU A/L APPLANAIDU KAVESHA A/P KARUNAKARAN VIJAY A/L RAMACHANDRAN

(1202005003) (1202005025) (1202005051) (1202005069) (1202005083) (1202005110) (1202005169) (1202005186) (1202005213) (1202005216) (1202005220) (1202005223)

PREVIEW
Introduction

Content
Etiology, Transmission, and Pathogenesis Epidemiology Clinical Manifestation Diagnosis & Management Complication

Summary

Introduction
Plague is a systemic zoonosis caused by Yersinia pestis1

Nowadays, 200 wild rodents species Infected In Africa, Asia, and the Americas2
Can be transmitted to human / other anamial, mainly via flea Treatable, but high mortality if untreated1 Still a problem for international public health, At least 2000 cases reported annually2

The Black Death

1. Michael B. Prentice. Plague and Other Yersinia Incfections. In: Dan L. Longo, Anthony S. Fauci, Dennis L. Kasper, Stephen L. Hauser, J. Larry Jameson, Joseph Loscalzo, Eds. Harrison's Principles of Internal Medicine, 18th ed. New York: McGraw Hill;2012.p.1305-1310 . 2. Anisimov AP, Amoako KK (2006) Treatment of plague: promising alternatives to antibiotics. J. Med. Microbiol. 55(Pt 11): 14611475.

Etiology, Transmission, and Pathogenesis

ETIOLOGY
Plague: systemic zoonosis disease caused by a gram-negative bacteria Yersinia pestis from the genus of Enterobacteriaceae (gamma proteobacteria) Plague is an natural infection of rodents, but can be transsmited To human or other animal (zoonosis) via flea, animal tissue, and droplets

Yersinia pestis

Rattus rattus

Xenopsylla cheopis

Michael B. Prentice. Plague and Other Yersinia Incfections. In: Dan L. Longo, Anthony S. Fauci, Dennis L. Kasper, Stephen L. Hauser, J. Larry Jameson, Joseph Loscalzo, Eds. Harrison's Principles of Internal Medicine, 18th ed. New York: McGraw Hill;2012.p.1305-1310 .

TRANSMISSION

PATHOGENESIS
Y.pestis on rat blood Flea feeding

Bio-film on PV, make blocking

Uncontrolled septicemia, endotoxic shock , DIC, death

Infection without flea bite -> ex: primary pneumonia plague

Bite human, taken by macrophage to regional lymph node

Secondary bubo, secondary pneumonia plague, kutaneal, menigeal

Spread via blood & lymphatic sys,

Intracellular replication -> extracellular replication, make bubo

antiphagocytic systems

1. Michael B. Prentice. Plague and Other Yersinia Incfections. In: Dan L. Longo, Anthony S. Fauci, Dennis L. Kasper, Stephen L. Hauser, J. Larry Jameson, Joseph Loscalzo, Eds. Harrison's Principles of Internal Medicine, 18th ed. New York: McGraw Hill;2012.p.1305-1310 . 2. Anisimov AP, Amoako KK (2006) Treatment of plague: promising alternatives to antibiotics. J. Med. Microbiol. 55(Pt 11): 14611475.

Clinical Manifestation
Bubonic, Septicemia, Penumonia, Meningeal, and Kutaneal Plague

ETIOLOGY OF URTICARIA
Common Etiologies9,10,11:
Acute Urticaria
Medication, food, parasitic infection, insect venom, contact allergens

Chronic Urticaria
Autoimmunity Food Allergy Hereditary Hasimoto tyroiditis and Graves disease Helicobacter Pylori
9.Poonawalla T, Kelly B: Urticaria: a review. Am J Clin Dermatol 2009, 10:9-21. 10.Amin Kanani, Robert Schellenberg, Richard Warrington. Review Urticaria and Angioedema. Allergy Asthma &Clinical Immunology 2011;7(1):1-10 11.Amar SM, Dreskin SC: Urticaria. Prim Care 2008, 35:141-157.

ETIOLOGY OF ANGIOEDEMA
Alergic Angioedema
Food, Medication, Insects bite, Latex

Idiopathic Angioedema
No Identifiable cause

Drug Induced Angioedema

Medicine like Angiotensin-converting enzyme (ACE) Inhibitor

HereditaryAngioedema
Genetic mutation in C1-esterase inhibitor (C1-INH) gene
Brodell LA, Beck LA, Saini SS. Angioedema. Ann Allergy Asthma Immunol. 2008;100:291297. Santos CB, Lunn ML, Craig TJ. Shortcomings in the diagnosis of hereditary angioedema: are we adequately screening family members of affected patients? [abstract P50]. Ann Allergy Asthma Immunol. 2009;102:A38.

PATHOGENESIS

PATHOGENESIS OF URTICARIA
Underlying pathophysiolgy is mast cell activation in dermis14

Immunemediated PATHOGENESIS OF URTICARIA

IgE mediated

Complementmediated
Nonimmunemediated

C3a, C4a, C5a

Without Ig and complements

Kaplan, Allen P. Greaves, Malcolm W. Urticaria and Angioedema. Informa healthcare USA,Inc;2009.

Immune-mediated Mast cell degranulation

Mirghani A E U. Current Concepts in the Pathogenesis and Management of Urticaria and Angioedema. Bahrain Medical Bulletin, 2005; 27( 2): 1-6 Baratawidjaja K G, Rengganis I. Imunologi Dasar 10rd edn. Badan Penerbit FK UI, 2012;369-376.

Degranulation of Mast Cell

Mirghani A E U. Current Concepts in the Pathogenesis and Management of Urticaria and Angioedema. Bahrain Medical Bulletin, 2005; 27( 2): 1-6 Baratawidjaja K G, Rengganis I. Imunologi Dasar 10rd edn. Badan Penerbit FK UI, 2012;369-376.

PATHOGENESIS OF ANGIOEDEMA
Angioedema is a result from a loss of vascular integrity23
Mastcellmediated ANGIOEDEMA Bradykininmediated Allergic reaction
Clifton O Bingham. An overview of angioedema: Pathogenesis and causes. May 2010

Associated with urticaria Generation of Bradykinin Triggered by alergen

PATHOGENESIS OF ALLERGIC ANGIOEDEMA

Clifton O Bingham. An overview of angioedema: Pathogenesis and causes. May 2010

DIAGNOSIS & MANAGEMENT

SIGN & SYMPTOM

Urticaria
1.Polymorphic, round or iregural shaped pruritic wheal 2.Develops anywhere, spread by scratching 3. Itching (may be severe) 4. Burning or stingging (rarely)

Angioedema
1. Non pitting, non pruritic, welldefined, edematous swelling in subcutaneous tissue, abdominal organs, or upper airway (larynx) 2. Last longer than hives, numb or tingling rather than pruritic
3. Burning, painful, sometimes itchy 4. Angioedema-eosinophilia syndrome

Muller, BA. Urticaria and Angioedema : A Practical Approach. American Family Physician. 2004;69(5):1123-1129. Levine, Norman. Hives and Your Skin. WebMD [Internet]. 2012 [Cited 2013 November 5] Available from: http://www.webmd.com/skin-problems-and-treatments/guide/hives-urticaria-angioedema

DIAGNOSIS
History and physical examination
Frequency, timing, duration and pattern of lesions Shape, size, site, and distribution Potential triggers (e.g food, medications, etc) Response to previous therapies used Family history

Diagnostic test
Skin prick test (SPTs) Serum-specific IgE test Other test like CBC, SPE, ASST, etc can be helpful in differential diagnosis
Greaves MW: Chronic idiopathic urticaria. Curr Opin Allergy Clin Immunol 2003;3:363-368. Snchez-Borges M, Asero R, Ansotegui IJ, Baiardini I, Bernstein JA, Canonica GW, et al. Diagnosis and treatment of urticaria and angioedema: a worldwide perspective. World Allergy Organ J. Nov 2012;5(11):125-47.

DIFFERENTIAL DIAGNOSIS

MANAGEMENT OF ACUTE URTICARIA

Avoidance triggering factor Antihistamines
First-generation: Hydroxyzine, Diphenhydramine, Cyproheptadine, Chloropherniramine, Clemastine Second-generation: Cetirizine, Desloratadine, Fexofenadine, Loratadine

Corticosteroid
Prednisone
Amin Kanani, Robert Schellenberg, Richard Warrington. Review Urticaria and Angioedema. Allergy Asthma &Clinical Immunology 2011;7(1):1-10

MANAGEMENT OF CHRONIC URTICARIA

First line treatment: Anihistamines
H1 antihistamines : Loratadine, Cetirizine, Mizolastine, Fexofenadine H2 antihistamines : Cimetidine, Ranitidine, Femotidine, Nizatadine

Second line treatment

Doxepin, Montelukast, Prednisolone, Sulfasalazine

Third line treatment

Methotrexate, Cyclosporine,Omalizumab, Mycophenolate

Kaplan, Allen P. Greaves, Malcolm W. Urticaria and Angioedema. Informa healthcare USA,Inc;2009.

MANAGEMENT OF ANGIOEDEMA
Avoidance triggering factors
Mild trauma to the face, stress, H.pylori infection, ACE inhibitors, ect

Idiopathic Angioedema treatment

Similar to urticatia

Treatment
Attenuated androgens (danazol and stanozolol, increase C4 and C1 inhibitor levels) Plasma derived C1 inhibitor replacement

Amin Kanani, Robert Schellenberg, Richard Warrington. Review Urticaria and Angioedema. Allergy Asthma &Clinical Immunology 2011;7(1):1-10

SUMMARY
Urticaria
Characterized by rapid appearance of wheals, may be accompanied by angiodema Underlying pathophysiology is mast cell activation in dermis Sign & symptoms are raised red or white welts or swelling Management with avoidance, antihistamines, corticosteroids

Angioedema
erythematous swelling of the deeper cutaneous and subcoutaneous tissue Angioedema is a result from a loss of vascular integrity that allows fluid to move into tissue Sign & symptoms are non pitting, non pruritic, well-defined, edamatous swelling that involves subcutaneous tissue Management with avoidance, antihistamines, Attenuated androgens, C1 inhibitor replacement

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