Allergic Rhinitis, Allergic Dermatitis, and Immunodeficiency: A Comprehensive Guide

Posted on May 14, 2024 in Biology

{ “*** Allergic Rhinitis: Def/ Classification /etiopathogensis:

^^ Classifciation :

^^EtioPx:

^ ^ Machanism:

(2)*** Allergic Rhitnis: Principles of Dx / Tx and Prophylaxis:
^^Dx:I-History

II-Lab

^^Tx:

(3)***Causes and CF of X induced allergy :
^^X induced allergy :

^^ CF:

1- Serum Sickness:

2- Hemolytic anemia:

3- Pulmonary Effect:

4- Renal effect:

(4) **X allery : principle of Dx and Tx
^^Dx:

1- Skin Test:

2- X provocation test:

3-Test For hematologic X reaction
4- Direct & Indirect anti-Globulin Test

NE for anaphylaxis)

(5) ***Food allergy : Clinial manigrstation & Principle of Dx:
^^Food allergy:

^^ DX:

(6)***Urticaria & angioedema: Classficaition , etiopathogensis and clinical presentation :

^^ Classification :

^^ Etiopathogensis :

^^Pathphysiology :

1-Immune mediated(+) MAst Cell:

2-Nonimmune-Mediated Mast cell (+):

^^Angioedema:

(8)***Allergic dermatitis: Principles of Dx and Tx:

(9)***Def & Classification of Immuno(-) : Causes of 2nd Immuno (-):
^^Def: 

^^ Classiciaiton :

(10) *** Principleso of Dx of Specific & non speific Immuno(-):
^^ History :

^^ Physical exam:

GRAPH  Inital later test
***Definition of autoimmunity /Classification of autoimmune disease^^ Def of autoimmunity :-Failure of organism to recognize its own components-allowing to autoimmune resposne to occur against sels^^Types of Autoimmune disease:I- Organ Specific:-Hashimotos thyroditis -specific lesion in thyroid involving infiltration of mononuclear cellsII-Disorder where lesion tends to be localized:Primary biliary cirhossism where bile duct is targetof infl cell vur Ab are not specificIII-Non organ specific:-Broadly belonging to Rheumatological disorders-SLE  ,Lesion and Ab not confined by organexaple:Hasomitoe-gRaves-Addison-SLE(lest organ speciic)(12)*** Pathogenic Mechanism & Lab Dx of autoimmune disease^^Px:I- Autoimmune  Rise by :1- BypassingTh1 cell :ab[N] modfication of the autoantigen through synthesis Breakdown as well as in combination with X -B & T Cell can be (+) directly by polyclonal activators like —————>EBV or supaerantigens:II-Bypass of Regulatory mechanism:-failure of Fas-Fast reaction which normally mediaes apoptosis  can result in survival of deleted T Cell-IL2receptor absences can also lead to autoimmunity( IL2 play importnat tole)-the desuppresion of class II gene  could give tise to expression of Class II ”Silence” btwn cellular autoantigen & Autoactive T-inducer!!III-Th1-Th2 Imbalance  result in overproduction of inflammatory cytokines(especially IL10 which antagonizes Th2  crucial for th1 deelopment—> unregulatedIL2 and IFN gamma can initiate Autoimmunity )^^ Pathological Effects(HS RXN)TABLE!!^^Laboratory Dx of autoimmn Disease:1- Serum Ab act as Diagnostic Markers2- Immunoflueorencese assay4- Agglutiation Test (Rh factos & for thyroglobulin )5-ELISA ( Ab to intrinsic factor)****Dx & Tx of immuno(-) with predominant Ab Def^^ Def :-B Cell Defect causing Ig &Ab Deficiency (50-60%)-Serum Ig & Ab Titers decrease , prdisosing to infection by encapslated g(+) bacteria^^IgA Def :-[One of most Common cause of 1 Immuno(-) ]I -CF-Many patent are Asx-Recucrent Pulmonary infection-Diahrea-allergies-Autoimmune disorder-Anaphylactic Reaction to IV immune globulin .II-Dx:1- History of : -anaphylaxis ,– Reucrent infection , -IgA def Autoimmne  disorder2-Confirmation:–  Serum IgA <10mg/dl  + normal IgG & IgM level 
III-TX:-Avoid Of Blood Products that contain IgA-Antibiotics  for needed infection-IVIG is contraindicated!^^ X linked Hyper IGM Syndrome:I-CF:-Severe Neutropenia  with Pn jirovecci-Recurrent pyogensic   Sinupulmonar infection-Lympohid tissue are small due to  Germinal centers-Many patient die before puberty , those that survive deveop cirhossi or B cell lyphoma
II-Dx:-based on clinical presentation -Elevated IGM levels ,while other Ig’s Low or abs
III-Tx:-IV immune globulin 400 mg/kg/one a month-Granulocyte colony (+) Factor is given
^^ Transient Hypogammaglobulinemia of infancy:-IgG level are low after the physiology Fall in maternal IgG at age 3-6 Month-Dx : Low Serum Ig Levels , While normal Ab production in resposne to vaccien antigen-Tx: Self limiting after Moths or years!**** Principles of Dx and Tc Primary  COMBINED! Immuno(-):^^ Primary Combined immuno(-):-combinedB+T cell Defect-Dx: Ig levels are [N[  but due to Inadequte T cell funtion AB formation are impaired^^Severe Combined Immuno(-)GX:-Cause :4 different abnormal phenotypes-T Cell are 0-B cell & NK  may be None/Low/High / Normal -but whatever the case B cell canno tfunction normal due to T cell absenceCF:-6month Infand with SCID –develop candiaisis ,-PersistantViral infection-Pn jiroveci Pn-Diahrea-Failure to thrive-ADA def  cause abnormalitiesDx:1- History of persistant infecion2- CBC and differential3-Ig level4- Mitogen Response to standard Vaccine antigen5- Test to determine tpe of SCID(ADA and purine phophorylase levels in WBC, RBCTx:-Keep Patient in isolation – IVIG & Ax-BM stem cell transplantfrom an HLA-identical sibling-ADA def injected with polyethylene glycol -Gene therapy***Ataxia -Telangiestascia:CF:-Very age of onset-ususally start when children start to walk -progression to neurological sx-Slurred speech-chroeoathoid movement-nystagmus developes-Telangiectasis may appear at age 4-6-recurrent sinupulmonary infection
Dx:-Cerebellar ataxia -Low level of IgA– High levels of serum alpha1-fetoprotienTx:-IVIG and Ax-No effective Tx for CNS abnormalities^^^Wiskott -Aldrich Sx:CF:-B & T cell function is (-)-infection with pyogenic bacteria/Pn jirovecci /oppurtunistic organism can develip-First manfiestation are hemorrhagic, -Recurrent Respiratory infection.eczema &Tpetnia
Dx:Test Show:-impaired Ab response to polysacchride antigen-cutanous anergy-Partial Tcell immuno(-)-Low IgM levels-Low or Normal IgG levels-BLOOD: small defective platlentsTX:-splenoctomy -continous ab administration -IVIG and BM transplat
*** Primary immuno(-) with predominant T cell Def:^DEF:T cell disorder make up 5-10% of 1 Immuno (-) making the person more prone to infection by virus, Pn jorivecci m fungi an other Pathogens.^^DiGeorge Syndrome:CF:-Infant have low set ears, midline facial cleft-small receding mandible-hypertoelorism-Congenital Heart disorder-Thymic and parathyroid hypoplasia or aplasia-Recurrent infection begin soon after birth , -but Degre of immu(-) caries-Hypocalcemic tetany ,24-48 hours post birth
Dx:-CF-Imune function assesent-Lateral Cehst Xray-Parathyroid function assesement-Chromosome analysis-Cardiac Defect^^Tx:-Transplation of culture thymus tissue^^Nezelof syndrome :Gx:-Autosomal Recessive congenital Immuno(-)-Cause : underdevelopment of thymus-no absence of PTG x: severe infections
Tx:-IVIG-Ax-Thymus transplant^^ X-Linked Lymphoproliferative Syndrome:CF:-ussually Asx until EB infection-ususally patient develop mononulcoeiss with Liver failureDx:-in patient that survive EBV infection:-Hypogammaglobulinemia-Decrease Ab Respons to Antigen-Impaired T Cell proliferative Response-Decrease NK -Cell function-Inverted CD4/CD8 ratio-GENETIC Dx is posible Beofre EBV infection
TX:BM transplant or 75% die
***Chronc -MC- Candiasis-Perisistnat Candidial ifneciton due to T cell-defectCF:-thrush is common-infection of scalp skin nails Gi and Vaginal mucosa-Thickened nails-Edema & erythma of periungal  tissue-Skin lesion crusted , ertyramatous
Dx:-basedon presence of recurrent candida infection -muosal lesion in absence of know cause of candida infection -Conformed by KOH examTx:-Topical antifunal -Long Temr : systemic Antigfunal-Immunomodulators (16)****Phagocytic Cell Def:Clincial symtpomns , Principles of Treatment^^Def:-10-15% of Primary immuno(-)-the abiltty to kill pathogens in impaired-cutaneous staphylocci and gram (-) infection are characteriszed^^ Chronic Granolmatous tissue:CF:-CGD begin with recuring abscess during early childhood-x granulomal lesiosn occurs in lungs ,liver ,LN , GI & GU-Suppurative lymphadenitis
TX:-Continous prophylactic Ax(TMP-SMX) with cephalexin-Oral antigundal as prophylaxis-Granulocyte transfusion can be live saving-HLA indetical sigbling BM trnasplant^^Chediak Higashi syndrome:-Giant lysosomal granules develop in neutrophil CF:-oculocutanous albinism -Recurent Resp Infection-Fever/ Jaunidce/ hepatosplenomagly/ LNpathy
Principle of Tx:-Transplantation of   unfractionated HLA-Identical Bone Marrow-cytoreductive chemotherapy maybe Curaive^^Hyper-Ige Syndrome:-coarse facial feaues, delayed shedding of tetth , osteopenia , reccurent fracture–Dx: CF and Serum IgE level >1000 IU/ml-Tx: Lifelong antistaphlococi AxComplement System Defiency :Clinical Sx , Principles of Tx^^Complement Def :-def of complement compoenets or inhibitors  coudl be heredetary / acquired-Hereditary: autosomal Revessive except for Deficienies of C1 (-)  which is autosomal Dominant– Def Result in  Defective: Opsonization , phagocytocis and pathogen lysisDef:1-C1—–>Angioedema Sx with progression2-C1q,C4,c2 ——>increase in predispositon for immune complex disease SLE3-MBL def ———->increase risk in infection with yeast sacchomycoses4-Alternative pathway(factor D,B properdin) are associated with decreased opsoniation 5-C3 ———->Defective Opsonization , Leukocyte chemotaxis,decreased bactericidal killing6-MAC def——->increase risk of Infection  esp N.meningitidis!^^ Tx:-replacing missng component of the cascade , through direct infusion or Gene therapy because this isnt available we do manage Sequelae of particualr complement deficiency-Eradicating particular infection-Immunosuppresive X is the Sx are Related to Autoimmune Disease(18)***MHC complex: Principle of structure ,relevance of organ transplantation disease^^ Principle Structure:HLA system MHC system are controlled by genes located on chromosome 6 , Encondes cell surface molecules specilaized to preent antigenic peptide to TCR on T CellsMHC molecules  :Class 1Class 2-Heavy chain bound to B microglobulin molecule-Heavy chain :1-3 globular doman 2-Hydrophobic section3-cytoplasmic Tail-Alpha 1 and alpha 2 domain most distant-CD8+ react to class 1 MHC—->Cytotoxix function -On antigen presenting cell,tymic epithelium /acitvated T cell-Consist of:1-2 polypeptide  chains 2-Hydrophobic transmembrane region3-Cytoplasmic tail-Express to Cd4 molecule which are T helper CellClass 2Class 2-On antigen presenting cell,tymic epithelium /acitvated T cell-Consist of:1-2 polypeptide  chains 2-Hydrophobic transmembrane region3-Cytoplasmic tail-Express to Cd4 molecule which are T helper Cell^^ Relevance of Organ transplantation and disease :-Depends on MHCMHC class 1——->stimulate Cd8+ T cellMHC classII ————-when Lymphocute from indicidual of different MHC class II join lyphocuyte react with MHC class II -Fever Naemia .Weight loss, rash .  diahprea splenomegaly are obeserved-the greater the transplatation antigen difference the more severe he Rxn^^ Relevance for disease:-many HLA linked disease are autoimune -mostly associatd with MHC class II —>Resulting in presentation of uatoantifent -HLA natigen might affect the susceptiblity of a cell to viral attachment or infection  , therby influencing the development of autoimmunity!****Transplatation : Def, Forms, Main requirment :^^DEf : Transfer of living rissue or cell from Donot to a receiptien , with intention of maintaining the functional integrity of transplanted  Tissue^^Forms:***Immuno(-) Post transplation : Principles & complication :^^Principles:-immuno(-) 2nd ImmunoDef that accompany organ failure-make transplant patient more vunerable toinfection-most common sign is fever with localizing sign-the greatest concern with early infection is that organism can infect the gradt or its vascular supply causing mycotic aneurysm^^ Complication :-opportunistic infection occur 1-6 Months after transplantation .-infection can be : Bacteria / viral/ Funal /parasite-Infection risk return to basrline  in most patients in around 6 Months-other can develop chronic rejection , needing high dose of immuno(-)!I-Orthotopic: transplant into its normal anatomical positonII-heterotopoic: …not into normal anatomical positonsIII-Autogragy :…. Back to the original DonorIV- Isograft:… btwn individual of identical genetic Constiution V- allograft: …Allogenic individual members of same psecies  but different geneitc contistionV- Xenogradt: …Xenogenic indivifuals(Dif species)^^ Main requirment for organ donation :1-Brain death :-pupil no light response-corneal reflex absenct-No resposne to pain-No cough or vommit reflex-No Spontanous resiration2- Absence of :-intoxcation ,sedating X  -hypothermia-electrolye abnormalities3-Dx should be made by 3 doctos …Organ should not be damaged oor traumatices4-…Permission of Donor and his family      ****ReactionTypes , Causes, And Clinical Symptomns:^^ Rejection:Hyperacute-less then 24-48 H-Cause:by prexisting complement fixing Ab to graft HLA or ABO antigens-Morphology :small vessel thrombosis & graft infarctionAccelerated Rejection-occut 3-5 days after-cause:prexisting non complement fixing -b-Morphologyhistopathological cellular infiltrate with or without vascular changes—>Fever graft failure & edemaAcute6-90 Days-Cause:T cell mediatd Delayed HS -Morphology :Mononucealr cellular infiltration  with soem hemorhange ,edema, necrosisChronic Rejection ->60 days -x causes  include early Ab mediated Rejection / delayed HS /Celular response….-Proliferation of neointima on SM and extracellar matrix^^Graftvs Host :-when Donor T cell react agaisnt Recipient self antigens-Sx are : Fever, Anemia. Weight loss rash diharea splenomegaly-the greater the Antigen difference the  more severe the Sx