Alterations in IMMUNO

8/14/2019 Alterations in IMMUNO

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2. Autoimmunity2. Autoimmunity

or Autoantibodiesor Autoantibodies

Inappropriate reaction by the immune system inInappropriate reaction by the immune system in

which antibodies form against self antigens,which antibodies form against self antigens,

mistaken as foreign.mistaken as foreign.

E.g.E.g.

– Tissue injury ( may help the body rid itself of damagedTissue injury ( may help the body rid itself of damaged

or necrotic self component)or necrotic self component)



Etiology:Etiology:

– Altered antigensAltered antigens

– Cross reactive antibodiesCross reactive antibodies

– Viral factorsViral factors

– Hormonal factorsHormonal factors

– Genetic factorsGenetic factors



PathophysiologyPathophysiology: 3 ways of auto immune response: 3 ways of auto immune response

cause diseasecause disease

The action of antibodies on cell surfacesThe action of antibodies on cell surfaces:: byby

direct antibody-mediated cellular cytotoxicitydirect antibody-mediated cellular cytotoxicity------

interference with receptors --- or complement interference with receptors --- or complement

activation.activation.

The circulation and deposition of small immuneThe circulation and deposition of small immune

complexescomplexes :: soluble antigen-antibody complexessoluble antigen-antibody complexes

– invade and deposit in the capillaries, the– invade and deposit in the capillaries, the

synovium of joints---synovium of joints--- it causes tissue damage viait causes tissue damage via

activation of the complement system.activation of the complement system. Activation of sensitized T lymphocytes Activation of sensitized T lymphocytes: by the: by the

release of lymphokines.release of lymphokines.



– InterventionIntervention::

Anti-inflammatory agents – symptomaticAnti-inflammatory agents – symptomatic

relief.relief.



Assessment andAssessment and

Management of Patients WithManagement of Patients WithAllergic DisordersAllergic Disorders



Allergic ReactionsAllergic Reactions

AllergyAllergy

– An inappropriate, often harmful response of An inappropriate, often harmful response of

the immune system to normally harmlessthe immune system to normally harmless

substancessubstances

– Hypersensitive reaction to an allergen initiatedHypersensitive reaction to an allergen initiated

by immunological mechanisms that is usuallyby immunological mechanisms that is usually

mediated by IgE antibodiesmediated by IgE antibodies

AllergenAllergen: the substance that causes the allergic: the substance that causes the allergic

responseresponse

Atopy:Atopy: allergic reactions characterized by IgEallergic reactions characterized by IgE

antibody action and a genetic predispositionantibody action and a genetic predisposition



Immunoglobulins and AllergicImmunoglobulins and Allergic

ResponseResponse

AntibodiesAntibodies (IgE, IgD, IgG, IgM, and IgA) react(IgE, IgD, IgG, IgM, and IgA) reactwith specific effector cells and molecules, andwith specific effector cells and molecules, andfunction to protect the bodyfunction to protect the body

IgE antibodiesIgE antibodies are involved in allergic disordersare involved in allergic disorders

IgE moleculesIgE molecules bind to an allergen and triggerbind to an allergen and triggermast cells or basophilsmast cells or basophils

These cells then releaseThese cells then release chemical mediatorschemical mediators suchsuchasas histamine, serotonin, kinins, SRS-A, andhistamine, serotonin, kinins, SRS-A, and

neutrophil factorneutrophil factorThese chemical substances cause the reactionsThese chemical substances cause the reactionsseen in allergic responseseen in allergic response



Immunoglobulins and Allergic ResponseImmunoglobulins and Allergic Response

(cont.)(cont.)

Allergen triggers the B cell to make IgE antibody, whichAllergen triggers the B cell to make IgE antibody, which

attaches to the mast cell; when that allergen reappears, it bindsattaches to the mast cell; when that allergen reappears, it binds

to the IgE and triggers the mast cell to release its chemicalsto the IgE and triggers the mast cell to release its chemicals



HypersensitivityHypersensitivity

A reflection of excessive or aberrantA reflection of excessive or aberrant

immune responseimmune response

Sensitization: initiates the buildup of Sensitization: initiates the buildup of

antibodiesantibodies



Predisposing FactorsPredisposing Factors

Host defensesHost defenses

Nature of the allergenNature of the allergen

Concentration of the allergenConcentration of the allergenRoute of allergen entrance into theRoute of allergen entrance into the

bodybody

Exposure to the allergenExposure to the allergen



Types of hypersensitivity reactionsTypes of hypersensitivity reactions

–Anaphylactic: type IAnaphylactic: type I

–Cytotoxic: type IICytotoxic: type II

–Immune complex: type IIIImmune complex: type III

–Delayed type: type IVDelayed type: type IV



Type I—Anaphylactic ReactionType I—Anaphylactic Reaction



– Type I.Anaphylactic shockType I.Anaphylactic shock

Most severe form of type I hypersensitivityMost severe form of type I hypersensitivityClinical ManifestationsClinical Manifestations::

– ItchingItching

– EdemaEdema

– Sneezing ( wheezing, dyspnea, cyanosis,Sneezing ( wheezing, dyspnea, cyanosis,circulatory shock)circulatory shock)

– ASAP emergency treatmentASAP emergency treatment

Prevention Prevention::

– History: drugs ( antibiotics- penicilllins); FoodsHistory: drugs ( antibiotics- penicilllins); Foods

( seafoods); Insect venoms; Biologicals( seafoods); Insect venoms; Biologicals

( vaccines, hormones, enzymes, antisera); blood( vaccines, hormones, enzymes, antisera); blood

products; allergen extracts; diagnostic agentsproducts; allergen extracts; diagnostic agents

( dye)( dye)



Type II—Cytotoxic ReactionType II—Cytotoxic Reaction



– Type II Cytolytic or CytotoxicType II Cytolytic or Cytotoxic

HypersensitivityHypersensitivity

The antigen-antibody complex and complementThe antigen-antibody complex and complementattach to a cell – circulating blood cellattach to a cell – circulating blood cell cell lysis.cell lysis.

Blood transfusion - blood incompatibilityBlood transfusion - blood incompatibility cell lysiscell lysis

( transfusion reaction – of donor RBC)( transfusion reaction – of donor RBC)

Note: Blood transfusion > 100ml. incompatible –Note: Blood transfusion > 100ml. incompatible –

renal damage, circulatory shock, and death.STOPrenal damage, circulatory shock, and death.STOPTransfusion ASAP.Transfusion ASAP.

Clinical ManifestationsClinical Manifestations::

– Headache and backpainHeadache and backpain

– Chest pain- similar to anginaChest pain- similar to angina

– N& VN& V– Tachycardia and hypotensionTachycardia and hypotension

– HematuriaHematuria



Type III—Immune Complex ReactionType III—Immune Complex Reaction



Type III Immune Complex HypersensitivityType III Immune Complex Hypersensitivity

– From the formation or deposition of From the formation or deposition of

antigen-antibody complexes in tissuesantigen-antibody complexes in tissues– Molecular size – larger – rapidly clearedMolecular size – larger – rapidly cleared

by phagocytic cells.--- smaller persistsby phagocytic cells.--- smaller persists

longer in circulationlonger in circulation spleen and liverspleen and liver

Inflammation -Inflammation - acute or chronicacute or chronicdisease of the organ systemdisease of the organ system

E.g. serum sickness, urticaria,E.g. serum sickness, urticaria,

arthritis, arteritis,arthritis, arteritis,glomerulonephritis.glomerulonephritis.



Type IV—Delayed or Cellular Type IV—Delayed or Cellular

ReactionReaction



Type IV Cell Mediated DelayedType IV Cell Mediated DelayedHypersensitivityHypersensitivity

– Sensitized T cells respond to antigens by releasingSensitized T cells respond to antigens by releasinglymphokines, which direct phagocytic cell activity.lymphokines, which direct phagocytic cell activity.

– E.g.E.g.

Delayed hypersensitivity – chronic infection ( TB)Delayed hypersensitivity – chronic infection ( TB)

Graft versus host disease or transplant rejectionGraft versus host disease or transplant rejection

- Contact Dermatitis (48-72)- Contact Dermatitis (48-72)- Granuloma formation- 10-28 days, (leprosy)- Granuloma formation- 10-28 days, (leprosy)

http://pathmicro.med.sc.edu/ghaffar/tub-mont.jpg



Management of Patients WithManagement of Patients With

Allergic DisordersAllergic Disorders

History and manifestations; comprehensive allergyHistory and manifestations; comprehensive allergyhistory;history;

Diagnostic testsDiagnostic tests

– CBC-eosinophil countCBC-eosinophil count

– Total serum IgETotal serum IgE

– Skin tests: note precautionsSkin tests: note precautions

Screening proceduresScreening procedures

http://pathmicro.med.sc.edu/ghaffar/skintest.jpg



MedicationMedication

Oxygen, if respiratory assistance neededOxygen, if respiratory assistance needed

Epinephrine for anaphylactic reactionsEpinephrine for anaphylactic reactions

AntiHistaminesAntiHistamines

CorticosteroidsCorticosteroids



Prevention and Treatment of AnaphylaxisPrevention and Treatment of Anaphylaxis

Screen and prevent:Screen and prevent:

Treat respiratory problems; provide oxygen,Treat respiratory problems; provide oxygen,intubation, and cardiopulmonary resuscitation asintubation, and cardiopulmonary resuscitation as

neededneeded

Epinephrine: 1:1,000Epinephrine: 1:1,000 SQSQ

Auto injection system: EpiPenAuto injection system: EpiPen

May follow with IV epinephrineMay follow with IV epinephrine

IV fluidsIV fluids



Other Allergic DisordersOther Allergic Disorders

Contact dermatitisContact dermatitis

Atopic dermatitisAtopic dermatitis

Drug reactions (dermatitis medicamentosa)Drug reactions (dermatitis medicamentosa)Urticaria and angioneurotic edemaUrticaria and angioneurotic edema

Food allergyFood allergy

Serum sicknessSerum sickness

Latex allergyLatex allergy





The round or disk shaped (discoid) rash of lupus producesThe round or disk shaped (discoid) rash of lupus produces

red, raised patches with scales. The pores (hair follicles)red, raised patches with scales. The pores (hair follicles)

may be plugged. Scarring often occurs in older lesions. Themay be plugged. Scarring often occurs in older lesions. The

majority (approximately 90%) of individuals with discoidmajority (approximately 90%) of individuals with discoid

lupus have only skin involvement as compared to morelupus have only skin involvement as compared to moregeneralized involvement in systemic lupus erythematosisgeneralized involvement in systemic lupus erythematosis

(SLE).(SLE).



Systemic Lupus Erythematous (SLE)Systemic Lupus Erythematous (SLE)

a chronic inflammatory disease of a chronic inflammatory disease of autoimmune origin.autoimmune origin.

presence of presence of autoantibodiesautoantibodies to numerousto numerousnuclear proteins, blood and nerve cells,nuclear proteins, blood and nerve cells,

and blood proteins.and blood proteins.InflammationInflammation – every organ system.– every organ system.

Lesions:Lesions: connective tissue of the vascularconnective tissue of the vascularsystem, the kidney, the dermis, thesystem, the kidney, the dermis, the

serous, synovial membranes.serous, synovial membranes.Long and chronic, with exacerbations,Long and chronic, with exacerbations,

remissions.remissions.



Etiology and IncidenceEtiology and Incidence

SLE is associated with a geneticSLE is associated with a geneticpredisposition to the disease as wellpredisposition to the disease as wellas a family history autoimmuneas a family history autoimmune

disorders.disorders.

It occurs most commonly in women,It occurs most commonly in women,

especially among those ages 20-30;especially among those ages 20-30;incidence is higher among Africanincidence is higher among AfricanAmericans than whitesAmericans than whites



PATHOPHYSIOLOGYPATHOPHYSIOLOGY(process & manifestation)(process & manifestation)

SLE is characterized by the formation of SLE is characterized by the formation of antibodies (IgE and IgM) against theantibodies (IgE and IgM) against thebody’s nucleic acids, phospholipids, whitebody’s nucleic acids, phospholipids, whiteblood cells, red blood cells, andblood cells, red blood cells, and

coagulation components.coagulation components.

Antigen-antibody complexes against hostAntigen-antibody complexes against hostDNA form and deposit in a variety of DNA form and deposit in a variety of

tissues, causing diffuse damage.tissues, causing diffuse damage.

Neutrophils attempt to phagocytize theNeutrophils attempt to phagocytize theantigen-antibody complexes, but areantigen-antibody complexes, but areineffective.ineffective.



Lysosomal enzymes are released,Lysosomal enzymes are released,further propagating the tissuefurther propagating the tissue

damage.damage.

The glomerular basement membraneThe glomerular basement membraneof the kidneys is particularlyof the kidneys is particularly

susceptible to complex deposition; assusceptible to complex deposition; asa result, there is a high incidence of a result, there is a high incidence of renal failure secondary to SLE.renal failure secondary to SLE.

Deposition of complex also occurs inDeposition of complex also occurs inthe brain, heart lung, GI tractthe brain, heart lung, GI tract,spleen and skin.,spleen and skin.



Clinical ManifestationsClinical Manifestations::

– Joint inflammation ( arthritis)Joint inflammation ( arthritis)– Classic butterfly rash over the cheeks andClassic butterfly rash over the cheeks and

bridge of the nose.bridge of the nose.

– PhotosensitivityPhotosensitivity

– renal, cardiac, and CNS dysfunction.renal, cardiac, and CNS dysfunction.(Raynaud’s Syndrome)(Raynaud’s Syndrome)

– GI symptoms: n&v, esophagitis, anorexiaGI symptoms: n&v, esophagitis, anorexia

Other symptomsOther symptoms::

Wt. loss; fever, malaise; lethargyWt. loss; fever, malaise; lethargy



Laboratory FindingsLaboratory Findings::

– Presence of LE cells ( autoantibodies)Presence of LE cells ( autoantibodies)– Decreased complement levelsDecreased complement levels

– Presence of immune complexes inPresence of immune complexes in

serumserum

– Presence of antibodies to DNA andPresence of antibodies to DNA and

antinuclear antibodies.antinuclear antibodies.

– Decreased levels of rbc, wbc,Decreased levels of rbc, wbc,

plateletsIncreased gamma globulinplateletsIncreased gamma globulinfraction d/t increased antibodyfraction d/t increased antibody

production.production.



Nursing DiagnosesNursing Diagnoses::– Impaires physicl mobility d/t arthritis, malaise andImpaires physicl mobility d/t arthritis, malaise and

lethargy.lethargy.

– Alt. in comfort: pain d/t inflammationAlt. in comfort: pain d/t inflammation

– Fluid volume deficit d/t vomitingFluid volume deficit d/t vomiting

– Alt. in nutrition: less than body requirements d/tAlt. in nutrition: less than body requirements d/t

anorexia, nausea, esophagitis.anorexia, nausea, esophagitis.

– Potential for infection d/t poor physical conditionPotential for infection d/t poor physical condition– Grieving d.t chronic nature of SLE and adventGrieving d.t chronic nature of SLE and advent

exacerbationsexacerbations

– Disturbance in self concept: body image d/t butterflyDisturbance in self concept: body image d/t butterfly

rash and alopeciarash and alopecia

– Alt. in tissue perfusion: renal, GI and peripheral d/tAlt. in tissue perfusion: renal, GI and peripheral d/tvasculitis.vasculitis.



Pharmacologic and Medical InterventionPharmacologic and Medical Intervention::– NSAID anti inflammatory agents e.g.NSAID anti inflammatory agents e.g.

Salicylates ( Aspirin)Salicylates ( Aspirin)– Anti malarial drugs – cutaneous and jointAnti malarial drugs – cutaneous and jointinflammation.inflammation.

– Corticosteroids – d/t systemic inflammatoryCorticosteroids – d/t systemic inflammatorymanifestations of the disease.manifestations of the disease.

– Cytotoxic agents : alkylating agentsCytotoxic agents : alkylating agents( cyclosphamide), and antifolates( cyclosphamide), and antifolates( methotrexate)( methotrexate)

– Plasmapheresis – remove circulatingPlasmapheresis – remove circulating

autoantibodies and immune complexes fromautoantibodies and immune complexes fromthe blood before organ and tissue damagethe blood before organ and tissue damageoccurs.occurs.



Other InterventionsOther Interventions

Improve airway clearanceImprove airway clearance

– Use semi-Fowler's or high-Fowler’sUse semi-Fowler's or high-Fowler’spositionposition

– Pulmonary therapy; coughing and deepPulmonary therapy; coughing and deepbreathing; postural drainage;breathing; postural drainage;percussion; and vibrationpercussion; and vibration

– Ensure adequate restEnsure adequate rest

PainPain– Administer medications as prescribedAdminister medications as prescribed

– Provide skin and perianal careProvide skin and perianal care

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Alterations in IMMUNO