NR33 Immune Dysfunction-excess2010

8/3/2019 NR33 Immune Dysfunction-excess2010

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Nursing Care of Clients

Experiencing Immune

Dysfunction

Review of immunology from H&P in 6th edchapt 19 are self study:

Slides 1-17 Identify key material to reviewfrom Fundamentals and A&P


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Chapter 19: Key Terms to review from A&P

Self-tolerance

Immunocompetent

Antigens

HLA

Stem cell/figure19-3

Chart 19-1

Leukocytes/table 19-1

Absolute neutrophil count

Left shift

Vascular leak syndrome

Sequence of inflammatoryresponses

Complement

Agglutination

Immunoglobulin

Innate native immunity

Natural active immunity

Artificial active immunity

Artificial passive immunity

Natural passive immunity

Hypersensitivity


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Overview of Immune Response

INFLAMMATION

CELL MEDIATEDANTIBODY

MEDIATED

IMMUNITY

THREE DIVISION OF IMMUNITY: FUNCTION INDEPENDENTLY

AND INTERDEPENDENTLY TO PROVIDE COMPLETE

IMMUNITY.


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FUNCTION OF THE INFLAMMATORY

RESPONSE IN IMMUNITY

I.E.: tissue macrophages and granulocytes

(neutrophils, basophils and eosinophils)

Non Specific Response Initiated By Injury OrInvasion

Self study Question:

Cite two examples of an agent that can injure or invade.


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FUNCTION OF THE INFLAMMATORY


Vasoconstriction followed by

increased capillary permeability to localize response

phagocytosis assisted by complement activation to ingestdebris

release of chemical factors that enhance

localization(vasoactive), attract factors that assist in

inflammatory response (chemotaxis) and release of factors

(cytokines) to stimulate production of granulocytes

Self study Question:

How would you explain this event to a

client in terms that they could

understand?


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Ignatavicius Figure 19-6

Steps of phagocytosis assisted by complement activation and

fixation Complement coats the

antigen


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Self study Questions:

How does complement assist in

phagocytosis?

How would complement levels be effected by

active inflammation?


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FUNCTION OF THE ANTIBODY

MEDIATED RESPO NSE IN

IMMUNITY (figure 19-8)

Known as humoral immunity (B-lymphocytesaction is predominant although assisted by T-

lymphocytes) creates two types of cells : plasma cells and

memory cells

plasma cells secrete immunoglobulins inresponse to a specific antigen

memory cells are dormant yet sensitized tothe specific antigen in case of a repeatedexposure

THE OLDER CLIENT HAS A REDUCED CAPACITY

TO RESPOND, PRODUCE, AND SUSTAIN ANIMMUNE RESPONSE USING THIS MECHANISM


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Ignatavicius Figure 19-7

Immune complex

B LYMPHOCYTES PRODUCE

ANTIBODIES SPECIFIC TO

THE ANTIGEN

ANTIBODIES BIND TO THE

ANTIGEN CREATING AN

IMMUNE COMPLEX

THE IMMUNE COMPLEX

TRIGGERS OTHER LEUKOCYTES

TO DESTROY IT

SENSITIZED B LYMPHOCYTES PRODUCE

LARGE AMOUNTS OF ANTIBODIES IF RE-

EXPOSED TO THE ANTIGEN

AN ANTIGENENTERS THE

BODY

MACROPHAGE AND T HELPER

CELLS INTRODUCE ANTIGEN

TO THE B LYMPHOCYTE

B LYMPHOCYTE IS

SENSITIZED


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Self study Questions:

What happens when antibodies and antigenscombine?

What arm of immune response is responsible

for this action?


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Types of Immunity

Innate-native immunity

genetically predisposed; not an adaptive

response

acquired immunity through humoral

response

immunity mediated by an adaptiveresponse

Active

Passive


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Active Vs. Passive Acquired

Immunity Active

natural: body responds to an antigen that is

introduced naturally artificial: acquired immunity achieved through

vaccines that have been attenuated to initiate

exposure but not develop disease

Passive natural:antibodies transferred to a fetus from

mother

artificial: injection of antibodies into a client


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Self Study Questions:

What questions would you prepare to answer before

administering a vaccine to identify what type ofimmunity the client will receive, and why?

What additional questions would you ask if you had

immune dysfunction, and why?

Classify the types of immunity:

Tetanus Toxoidoral polio vaccine

hepatitis B vaccine

post exposure protection from chicken pox

immunoglobulins passed in breast milk


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FUNCTION OF CELL MEDIATED


T helper cells, Suppressor T cells

T helper cells recognize self from non self:

facilitate B cell response through introduction of antigen

stimulate bone marrow to rapidly produce myeloid and

lymphoid stem cells

function described as a calling to arms

T suppressor cells are inhibitory.

Opposite of helper cells

prevent over response and production of auto-antibodies

circulating volume 1/2 of T helper cells


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Neutrophil maturation: What would happen with T

helper cell action?


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FUNCTION OF CELL MEDIATED


Cytotoxic T cell, natural killer cell

Cytotoxic T cells recognize viruses and protozoa

that alter self cell antigenic surface

binding results in cell destruction

natural killer cells destroy unhealthy or abnormal

self cells

does not rely on antigenic sensitivity to initiate activation called seek and destroy cells


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Self study Questions:What are the types of T cells involved in

immunity?

The T cell arm of immunity is mostly effectedby HIV infection. What would you expect to

occur?


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Selected Stressors Associated

With Immune Dysfunction Hypersensitivity reactions

allergy

Immunodeficiency

AIDS


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Key medications to review

Beta agonists Epinephrine 1:1000 aqueous solution

Epi-pen for SQ or IM injection

Epinephrine infusion for continuous infusion Histamine antagonists

Diphenhydramine (H1 antagonists)

Ranitidine (H2 antagonists)

Alpha 1 agonists

Afrin (oxymetazoline) IV corticosteroids

Solumedrol

Inotropic agent that promotes catecholamine release Glucagon


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Nursing Care of Clients

Experiencing Hyperfunction of

the Immune Response: Allergyand Autoimmunity


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Types of hypersensitivity Table 22-1

Type 1: excess circulating IgE with mast ell releasehay fever, atopic asthma and allergic rhinitis

Type 2: IgG reacts with host cell as in Myastheniagravis, autoimmune hemolytic anemia

Type 3: immune complex formation causing damageas in SLE

Type 4: delayed reaction from T lymphocytes as in

poison ivy and PPD reaction Type 5: overreacting target cell caused by

autoantibody stimulation (graves disease)


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TYPE IV: Delayed

Hypersensitivity ReactionsA sensitized T lymphocyte responds to

an antigen

does not involve antibodies or complement

takes hours to days to take effect

characterized by edema, ischemia and

tissue destruction, pruritis a positive PPD is a TYPE IV reaction


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Collaborative management of Type

IV Hypersensitivity

Avoid offending antigen

Apply OTC topical steroids

Monitor for secondary infection

No concern about progression to

anaphylaxis since it is not a Type I

reaction


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Over View Type I

Hypersensitivity Reactions Most common type of reaction

exposure to allergen initiates inflammatory

response allergic asthma, allergic rhinitis, hay fever

route can be inhaled, ingested, injected,

contact (key point to remember every time a

client has a new drug therapy initiated)

life threatening form of Type I is called

Anaphylaxis


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Irritants associated with Type I

hypersensitivity


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Latex allergy is a TYPE I Reaction

Incidence is increasing especially for

individuals with frequent exposure

may be mixed type I and Type IV

type IV are limited to cutaneous reactions

implications for nursing practice

early identification for latex allergy

use of latex free products that can be

inhaled or in contact with vascular system


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Risk groups for latex allergy

Health care workers

Rubber industry workers

Persons with spina bifida or urogenital abnormalities

Persons who have undergone repeated or prolongedsurgeries or mucous membrane exposure to latexdevices, especially early in life

Persons with an atopic history or history of foodallergy (cross-reacting proteins, especially in banana,

avocado, passion fruit, chestnut, kiwi fruit, melon,tomato, celery)

Family history of allergy

Source: Latex Allergy @

http://www.aafp.org/afp/980101ap/reddy.html


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Pathophysiology of TYPE I

Characterized by vasodilation, increased

capillary permeability, mucosal edema


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Pathophysiology of Type I continued

First event can be local urticaria,

pruritis, watery eyes, rhinitis

Continuing events can lead to

anaphylaxis with certain types of

irritants, such as:

Latex, medications, peanut butter etc More serious adverse event is call anaphylaxis


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Clinical Manifestations/Lab

Diagnostics for low level type I Clinical Manifestations:

Sign and symptoms of allergic rhinitis, hay fever,

allergic asthma, contact dermatitis, cutaneousrash (client-specific response)

Lab tests:

elevated eosinophils, IgE

identification of specific allergens by RAST testing

Specialized tests:

skin testing

food challenge


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Collaborative care of TYPE I

NIC: Allergy Management chart 22-1 Treating Symptoms (chart 22-3)

decongestants (alpha adrenergics)

stimulate vasoconstriction (Neosynephrine) antihistamines

inhibit vasodilation (Diphenhydramine)

leukotriene antagonists

block leukotriene receptor (Singulair)

desensitization therapy

allergy shots

Pt teaching regarding s/s ofanaphylaxis


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Nursing Care of Clients At risk

for Experiencing Type I

Reactions Risk for Ineffective Respiratory Function

r/to Allergic Response

Health teaching

Food avoidance

allergy to molds

allergy to pollen

stinging insects

use of medication; desired and untoward

effects

s/s of anaphylaxis


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Nursing Care of Clients At risk for

Experiencing Type I Latex allergy

response

Risk for latex allergy response

Assess for history of reactions from:

dental work, tape, condom, elastic, balloons,

rubber cement

Assess for hx of:

asthma, rhinitis, conjunctivitis, eczema, etc

Assess for presence of food allergies to:

Peach banana, tomato, mango papaya etc


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Nursing Care of Clients At risk for

Experiencing Type I Latex allergy

response (continued)

Assess for frequent

instrumentation/surgical procedures

Spina bifida clients, surgery early in life

Assess for occupational exposure to

latex

Eliminate exposure to latex products

Initiate health teaching


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Life-threatening Type I hypersensitivity

reaction

Occurs rapidly, systemically

Affects multiple organs

Anaphylaxis


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Feelings of uneasiness, apprehension

Weakness, impending doom

Anxious and frightened

Generalized pruritus/urticaria (hives)

Angioedema diffuse swelling of eyes, lips and tongue

Clinical Manifestation of Anaphylaxis

(Early)


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Bronchoconstriction

Mucosal edema, excess mucus production

Crackles, wheezing, diminished breath sounds

Laryngeal edema, stridor, hypoxia, hypercapnia

Hypotension, weak, rapid, irregular pulse

Faintness, diaphoresis

Loss of consciousness

Dysrhythmias, shock

Clinical Manifestation of Anaphylaxis

(Late)


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Guidelines for care

Evidence- based practice The diagnosis and management of anaphylaxis:

an updated practice parameter. J Allergy ClinImmuno 2005 Mar;115(3 Suppl):S483-523. [232

references] Pubmed


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Shock management according to

latest guideline see chart 22-2

Assess airway, breathing, circulation,

and level of consciousness

Administer Aqueous epinephrine1:1000 dilution (1 mg/mL), 0.2 to 0.5

mL intramuscularly or subcutaneously

every 5 minutes, as necessary,

should be used to control symptoms andincrease blood pressure.


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Shock management according to

latest guideline

How should you administer Epi?

Intramuscular epinephrine injections into

the thigh have been reported to provide

more rapid absorption and higher plasmaepinephrine levels


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Place in trendelenburg

Establish airway with Endotracheal tube

Administer oxygen

Monitor HR and BP continually

Start (2) IV NS 5-10ml/kg in first 5 minutes

(may require 7 liters) and watch for fluid

overload with heart disease


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Administer epinephrine IV

can be administered intravenously overseveral minutes and repeated as

necessary in cases of anaphylaxis not

responding to epinephrine injections

and volume resuscitation. Initiate epinephrine drip

1mg epinephrine in 250 ml D5W at 4 -

10 mcg/min

Client is not responsive to SQ or

IM injection and volume

replacement


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Administer antihistamine, H2 antagonist,beta agonist nebulizers and

corticosteroids Benadryl 50 mg IVP

Ranitidine 50 mg IV

Inhaled beta-agonist for bronchospasm

Solumedrol IVP 1-2 mg/kg/day Glucagon (dose unspecified) to increase

release of Catecholamines

Vasopressors such as dopamine may berequired

Client is not responsive to SQ or

IM injection and volume

replacement


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Collaborative Management of

Anaphylaxis Transfer to ICU

Allergist/immunology consult

after recovery client/family are instructed in use of

epi-pen to self-administer when early s/s ofanaphylaxis are present


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Summary

There are five types of hypersensitivity for which we areemphasizing understanding in Type 1 and Type 4.

These types of hypersensivities both respond to irritant butfollow a different course due to their individualpathophysiologies.

Type I has the potential to be more life threatening, even if it isinnocuous in its earliest presentation.

Reduction of risk potential for anaphylaxis requires carefulscreening and analysis of high risk groups to minimizeexposure.

The life threatening reaction of anaphylaxis is managed using

NIC: shock management and vasoactive agents that stop thecapillary leaking that causes the shock condition.

A review of the emergency medications emphasizing themechanism of action, adverse effects, management side effectsand contraindications are required when providing care.

NR33 Immune Dysfunction-excess2010

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