Disturbance of Immune System

7/28/2019 Disturbance of Immune System

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NEPHROTOXINS

have specific, destructive effects onrenal cells

Assessment Carefully monitor renal function with

use of tests to identify nephrotoxicreactions

Diagnosis can cause acute tubular necrosis (mostcommon), defects in tubular transportsystem, interstitial nephritis, vasculitis& neprohrotic syndrome

nephrotoxic substances and renal

injuries causedo Medications all types of renal

injuries

Antibiotics longerexposure + pre-existingrenal disease

High risk

cephalosporins,sulfonamides,aminoglycosides,amphotericin B

Others tetracylcines,bacitracin, polymyxin,colistin

Analgesics salicylates,acetaminophen,phenacetin, NSAIDs acute tubular necrosis orchronic renal failure

Anesthetics reducesvasoconstrictive ability ofkidneys making it morevulnerable to effect ofshock; methoxyflurane direct nephrotoxic effect,


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associated with fatal acuterenal failure; halothane adverse effect on renalfunction

Diuretics when usedaggressively can causehypovolemia

Contrast dyes radioiodinated agents (CT) associated with acutetubular necrosis; riskfactors are age over 60yrs, pre-existing renalinsufficiency (diabeticnehropathy), dehydration,low cardiac output withpre-existing renal dse,proteinuria,hypoalbulinemia, multiplemyeloma; multiplecontrast studies within 24hr period

Other drugs probenecid,phenytoin, LMW dectran,rifampin, phenindione

o Heavy metals lead, mercury,

arsenic, copper, lithium, goldo Posions- mushrooms,

insecticides, herbicides, snakebites

o Organic solvents glycols,

gasoline, kerosene, turpentine,tetrachloroethylene

Plan/Implementation 1. Discontinue use or reduce dose ofnephrotoxic medications

2. Maintain high fluid intake dilute


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urine & prevent crystallization3. Keep patient well-hydrated through

out the test or Use of non-dyestudies, if possible ; compare

baseline and post study renalfunction tests; monitor urine outputfor several hours after test

Evaluation Outcome management??

Pyelonephritis Inflammation of the renal pelvis andparenchyma caused by bacterial infection( active or remnants of a previousinfection)

Assessment

Diagnosis acute occurs after bacterialcontamination of urethra or introductionof an instrument or device (catheter,cytoscope)

chronic occurs after chronic obstructionwith ureteral reflux or chronic disorders

Bacteria may trigger inflammatoryresponse, increase WBCs----->edema andswelling of involved tissue (papillae tocortex); if treated --->fibrosis and scartissue formation

Plan/Implementation

Evaluation


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GLOMERULONEPHRITIS

Assessment Nephrotic syndrome:clinical manifestations causedby protein wasting secondary todiffuse glomerular damage;predisposed by allergicreactions, reactions to specificdrugs, renal vein thrombosis,sickle cell disease and heartfailure

Nephritic syndromeclinical manifestations that

includes hematuria plus one ofthe ffg: oliguria (less than 400mL/24 hrs), HPN, elevated BUNor decreased GFR

Diagnosis Caused by immunologicreaction that results inproliferative andinflammatory changes inglomerular structure; can beacute or chronic usuallymanifested by either anephrotic or nephriticsyndrome

o Function filter bloodo Results from Ag-Ab

complexes trapped inthe glomerulus--->inflammatorydamage and impededglomerular function,


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reducing glomerularmembranes capacityfor selectivepermeability

o

Source of Ag exogenous (after Strepinfections) orendogenous formed inthe kidney/ antibodiesaffixed to theglomerular basementmembrane(Goodpasturessyndrome)

o Primary pathologicprocesses areproliferation andinflammation

Nephrotic syndrome- set ofclinical manifestationscaused by protein wastingsecondary to diffuse

glomerular damage;predisposed by allergicreactions, reactions tospecific drugs, renal veinthrombosis, sickle celldisease and heart failure

Nephritic syndrome set ofclinical manifestations thatincludes hematuria plus one

of the ffg: oliguria (less than400 mL/24 hrs), HPN,elevated BUN or decreasedGFR-Common includingimmunoglobulin A (IgA)nephropathy


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Plan/Implementation Interventions:

Reduce inflammationo Plasmapheresis to

remove specific

circulating Abs andmediators of theinflammatory response,in conjunction withcorticosteroids &immunosuppressiveagents (azathioprineand cyclophosphamide)

o Antibiotic therapy for

Strep organisms

Maintain fluid and electrolytebalance

o Treat volume overload

and HPN diuretics,antiHPN, restrict dietarysodium and water

o Appropriate monitoring

VS, I&O, weight;measurement of legs,

abdomen Adequate nutritional intake

high caloric, low protein diet,offer hard candies, ice chipsto quench thirst

Adequate rest physical andemotional

Prevent skin breakdown(edema) good hygiene,

massage, position changes;other prophylactic measures(mattress)

Boost clients immunedefenses; prevent RT and UTinfections


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Evaluation

Pathophysiologic Mechanisms of Glomerulonephritis:

Antibodydeposition

Cell-mediated Complementimmune activation

mechanisms

GLOMERULONEPHRITIS

Influx of Hemodynamiccirculating leukocytes alterations

On-Off

Switch

Persistent Inflammation Exit of anti-inflammatory (chronic glomerulonephritis) molecules & leukocytes

(acute glomerulonephritis)

Chronic Scarring Resolution

renal failure


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SYSTEMICLUPUSERYTHEMATOSUS

Chronic, inflammatory, autoimmunedisorder characterized by a wide arrayof clinical manifestations in vascularand connective tissue

Two types: systemic (most severe) anddiscoid (mild involving only the skinusually affecting face, neck and upperchest)

Relatively rare; seen commonly inAfrican American then Asians thenwhites; 10x more common women age15-40

Assessment Acute forms- fever, musculoskeltal aches andpains, butterfly rash on face, pleural effusion,basilar pneumonia, generalizedlymphoadenopathy, pericarditis, tachycardia,hepatosplenomegaly, nephritis, delirium,convulsions, psychosis and comaChronic forms depend on organ involvement

May include fever, malaise, weightloss, cutaneous discoid LE lesions,erythematosus of the exposed skin,

generalized lymphadenopathy, severehemolytic anemia, thrombocytopenicpurpura, hypersplenism, pericarditis,pleural effusion, tachycardia,peripheral vascular syndromes(Raynauds phenomenon, gangrene),ulceratie mucuous membrane lesions,abdominal pains, nausea, vomitin,anorexia, bloody stools, hepatic

dysfunction, focal glomerulitisprogressing to glomerulonephritis,myalgia, arthralgia, neuritis,hemiplegia, convulsions and coma

Diagnosis Cause- unknownFactors implicated:

Genetic predisposition


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Infection

Environmental irritants

Physical and emotional stress

Exposure to UV B radiation

Medications reversible formsDefinite hydralazine, procainamidePossible chlorpromazine,

ethosuximide, hydantoin, methyldopa, d-Penicillamine, oral contraceptives, practololand Quinidine

Familial tendency- incidence of 25-50% fortwins

Pathophysiology Antinuclear antibodies (ANAs) against

double (ds) DNA; formation ofautoimmune complexes triggering theinflammatory response;

Common deposition of Ag-ANAs inthe kidney --- glomerulonephritis; alsodeposited in the brain and heart

Defect in T suppressor cell --- infectiveprotective process of preventingautoantibody formation

Onset and Prognosis:

May be rapid (acute fulminant course);insidious --- chronic with remissions andexacerbations

More severe for young onset, live for 5 yrs(95% of cases)

Potentially fatal, leading cause is renalfailure

Plan/Implementation Medical Management/Goals:1. maintenance of skin integrity2. promotion of healthy lifestyle and

reduction of stress3. maintenance of proper nutrition4. promotion of comfort


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5. increase in clients independence6. maintenance of emotional well-being

checkup every 3 months with

determination of CBC, creatinine andcholesterol levels, urinalysis, serumC3,C4 and anti-ds DNA

based on organ system involveda. cardiac with pleural effusion,

pericarditis IV pulsemethylprednisolone followed by oralprednisone

b. cutaneous antimalarial agentsc. plasmapheresis efficacy not

determinedd. risk for coronary heart disease, HPN

1. lifestyle changes2. reduce salt and fat/cholesterol

intakee. avoid sun exposure triggers

inflammatory responsef. clients on immunosuppressants

preventive/vaccines for

pneumococal pneumonia and flug. yearly assessment/checkups

dental, ophtha to monitor forsystemic infection, effects ofmedications

h. avoid sulfa antibiotics tendency tocause allergy and flares

i. Algorithm for management of clientswith SLE

Nursing Management:-depends on how client responds tocondition and/or severity/specificity ofmanifestations

Newly diagnosed knowledge deficits=advise

Follow-up =review changes,


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psychosocial assessment

During exacerbations = physiologicsupport to prevent skin breakdown,maintain nutritional and metabolic

status, minimize risk for opportunisticinfections

Grief reactions emotional support;refer for counseling

Evaluation Outcome management??

ALLERGIC

REACTIONS1. Hypersensitivity

disorders allergic

rhinitis, asthma, dermatitis


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Assessment 1. Clients history2. manifestations experienced during and

after allergen exposure3. results of allergy tests

a. skin testingb. RAST radioallergosorbent test to measureIgE levels to certain allergens in vitro;less sensitive than skin testing

c. Pulmonary function tests for asthmad. Blood assays for IgE levels, presense of

/elevated serum eosinophil levelsDiagnosis IgE formation in response to an allergen

Factors:

Air pollution

Sex, age

Exposure to second hand smokeHypersentivity rxn can be:

1. immediate humoral or antigen-antiboby;minutes after exposure

2. delayed cell mediated; prolongedresponse to the initial allergen

Types:Type Cause Patholog

icProcess

Rxn

I

II

III

Immediate/anaphylactic

Cytolytic/cytotoxic

Immunecomplex

IgE

IgGIgM

Complement

Ag-Abcomplexes

Mast celldegranualtion ---histamineandleukotrienerelease

Complement fixation ----

cell lysis

Depositionin vesselsand tissuewalls ---inflmmation

AnaphylaxisAtopic dsesSkin rxns

ABOincompatibility

Durg-inducedhemolyticanemias

Arthrus rxnSerumsicknessSLEAcute


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IV

Cell-mediated/

delayed

SensitizedT cells

Lymphokinerelease

GNephritis

TBContactdermatitis

Transplantrejection

Plan/Implementation Medical Management:1. Identify allergen detailed hx2. Avoid allergen - airborne3. Control environment

4. Administer medicationsa. Antihistamines caution for drowsiness

effectb. Decongestants limit use to 1 weekc. Steroids caution for side effectsd. Aerosols started before allergy season;

regular use with dosing of 3-4x a day(expensive)

e. Anticholinergics for common cold and

asthmaf. Bronchodilators beta-agonists to controlbronchospasm in asthma

g. Antleukotrienes to treat manifestations ofasthma and anaphylaxis

(leukotrienes contribute to airway edema,smoot muscle contraction, inflammation)5. promote desensitization for type I Ig-Emediated/immunotherapy increase IgGantibody levels (interferes with IgE binding)and may increase suppressor T-cell function

Nursing Management:1. detailed hx all current clinical

manifestations2. assess for presence of animals, presence


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of allergens in the clients environment,occupation

3. Provide appropriate health teaching

Evaluation

Relief from allergic manifestations

Disturbance of Immune System

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