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INFLAMMATORY and IMMUNOLOGIC DISTURBANCES OBJECTIVES:at the end of 12 hours of lecture-discussion, the level 4 b students will be able to:

Describe inflammation and its signs and symptoms Discuss the process of inflammation Explain the different selected alterations related to inflammation Describe the body s general immune response Discuss the stages of immune response Differentiate between humoral and cellular immune response Explain the selected alterations related to immune functioning

INFLAMMATION INFLAMMATION: a localized, protective, reaction of tissue to injury, irritation, or infection, manifested by pain, redness, heat, swelling, and sometimes loss of function Is a defensive reaction intended to neutralize, control or eliminate the offending agent and to prepare the site for repair.

Connection to infection? infection is different from inflammation An infectious agent is only one of the several agents that triggers inflammatory response The Inflammatory Process Results in response to stress An injurious agent leading to inflammation can be physical, chemical, or infectious



ischemic change

immune reaction


Inflammatory response


VASCULAR CHANGES: Vasodilatation Capillary Permeability Blood flow Local tissue congestion _____->

CELLULAR CHANGES: Phagocytosis leukocytes Release of Chemical Mediators ( macrophage)


Local Effects: Erythema(redness) Warmth(heat) Edema(swelling) Pain Impaired functioning

Systemic Effects: fever leukocytosis malaise Anorexia Sepsis


Redness (?) Heat (?) Swelling (?) Pain (?) Loss of function

Chemical mediators of Inflammation Histamines an amine (beta-imidazolyl-ethylamine, ergamine, or ergotidime) that is a normal constituent of almost all animal body cells. In the body, it is synthesized in a type of leukocyte called a basophil or mast cell In response to certain stimuli these cells release histamine, which immediately effects a dilation of the blood vessels. Responsible for early changes in vasodilation and vascular permeability This dilation is accompanied by a lowering of blood pressure and an increased permeability of the vessel walls, so that fluids escape into the surrounding tissues.

2. Prostaglandin

an unsaturated fatty acid found in all mammals that performs a similar function to that of hormones in controlling smooth muscle contraction, blood pressure, inflammation, and body temperature Prostaglandins also promote inflammation; thus drugs that block prostaglandin synthesis are effective against arthritis and similar diseases. One of the chemical mediators suspected of causing pain 3. Bradykinins

blood chemical that dilates vessels: a chemical peptide produced in the blood when tissues are injured that plays a role in inflammation Increases vasodilatation and vascular permeability and also attracts neutrophils (the most common type of white blood cell in vertebrates, responsible for protecting the body against infection)

Systemic Response To Inflammation Fever most common sign - caused by endogenous pyrogens ( internal substances that cause fever) released from the neutrophils and macrophages (a large cell that is present in blood, lymph, and connective tissues, removing waste products, harmful microorganisms, and foreign material from the bloodstream) Leukocytosis (a marked increase in the number of white blood cells leukocytes, usually because of infection or disease) usually taking place to provide body with greater ability to fight infection

TYPES OF INFLAMMATION 1. ACUTE Characterized by local vascular and exudative changes Lasts less than 2 weeks 2. CHRONIC Develops if injurious agent persist and Symptoms presents for months or years 3. SUBACUTE ALTERATIONS IN INFLAMMATION I.RHEUMATIC HEART DISEASE(acquired heart disease) Is an infectious and inflammatory process that may affect any of the layers of the heart including heart valves, joints, connective tissues and the CNS May be caused by Acute rheumatic fever which occurs most often in school age children after an episode of group A heta hemolytic streptococcal pharyngitis Peaks in school aged children; linked to environmental factors( malnutrition, overcrowding, lower socio) and family history of disorder

Thought to be autoimmune disorder preceded by infection of group A betahemolytic streptococcus ( usually strep throat; the hart itself is not affected however Prognosis depends on heart damage Mode of transmission for streptococcal infection: Direct contact with oral or respiratory secretions

PATHOPHYSIOLOGY Rheumatic heart disease/ Endocarditis is not infectious in the sense that tissues are not invaded and directly damaged by streptococci Injury is caused by inflammatory or sensitivity reaction to streptococci when leukocytes accumulate to affected tissues and form nodules Leads to inflammation of the myocardium(leading to weaknened contractile power of the heart), pericardium leading to pericarditis With endocarditis , it leads to growth of beadlike objects along the lining of the valve leaflets leading to thickening of the leaflets causing them to shorten leading to incomplete closure of the valves - leads to valvular regurgitation where blood flows backward through the valve

ASSESSMENT FINDINGS/ LABORATORY FINDINGS I. Major symptoms: ( Jones criteria) Carditis seen in 50 of clients Aschoff nodules ( areas of inflammation around heart valves, pericardium and myocardium) Valvular insufficiency of mitral and aortic valves possible Cardiomegaly Shortness of breath, hepatomegaly, edema Polyarthritis

Migratory, therefore no contractures develop Most common in large joints, which become red, swollen, painful Chorea ( Sydenham s chorea, St. Vitus dance) : a CNS disorder characterized by abrupt, purposeless, involuntary muscular movement Gradual, insidious onset: starts w/ personality changes or clumsiness

St Vitus dance? Sydenham's chorea, named after English physician Thomas Sydenham, usually occurs following the onset of childhood rheumatic fever, with a higher incidence in girls than in boys. Sydenham's chorea is believed to be caused by the action of antibodies to the basal ganglia; these antibodies closely resemble those formed in response to the streptococcal bacteria that cause rheumatic fever. Sydenham's chorea has also been called St. Vitus's Dance. The aid of Saint Vitus is invoked by those suffering from various diseases, especially the nervous disorder Sydenham's chorea, with which his name became associated.

Mostly seen in prepubertal girls May appear months after strep infection Movements increase with excitement Lasts 1-3 months and recovers completely in 6 months Subcutaneous nodules Usually a sign of severe disease Occur with active carditis Firm, non tender nodes on bony prominence lasting for 4 weeks but usually disappears after 1-2 weeks Erythema marginatum Transient, non pruritic rash starting with central red patches that expand, results in series of irregular patches with red, raised margins and pale centers ( resembles giraffe spots) Minor symptoms

1. reliable history of RF, fever 2. Recent history of strep infection 3. Diagnostic test: ESR ( erythrocyte sedimentation rate and

anti streptolysis O ( ASO) titer increased, changes in ECG ESR(?) measures the degree of erythrocyte settling that occurs in a blood sample during a specified amount of time - increases significantly in widespread inflammatory disorders, elevation may be prolonged in localized inflammation and malignant disease REFERENCE VALUE: Normal: 0-10 mm./ hour in men 0-20 mm/ hour in women Abnormal findings: increases in pregnancy, acute or chronic inflammation, tubercolusis, rheumatic fever, rheumatoid arthritis and some cancers

PREVENTION Early and adequate treatment of oropharyngeal streptococcal infection Be aware of symptoms and signs of streptococcal pharyngitis: high fever ( 38.9 to 40 deg celcius), chills, sore throat, redness of throat with exudate, enlarged lymph node, acute rhinitis

NURSING INTERVENTONS KEY ROLE is teaching patients about the disease, preventions, treatments and its complications

After acute treatment with antibiotics, the importance of taking prophylactic antibiotics on a regular schedule CARDITIS OBJECTIVE: identify and eradicate causative organism and prevent additional complication A. ADMINISTER PENICCILIN AS ORDERED For Group A beta hemolytic strep- one time IM injection of penicillin or a 10 day course of oral penicillin Initially, patients w/ rheumatic fever are treated the same with oropharyngeal group A betahemolytic strep, then prophylactic IM of penicillin q 3-4 weeks to prevent recurrence Prophylactic antibiotics are prescribed for 5 years( or until age 21, whichever is longer) if the patient did not expereince carditis or for 10 years (or until age 40 whichever is longer) if the patient had carditis or develops valvular disease B. PROMOTE BED REST UNTIL ESR RETURNS TO NORMAL

ARTHRITIS administer aspirin as ordered, reposition child in bed frequently CHOREA Decrease stimulation Provide a safe environment; no forks with meal, assistance with mobility Provide small, frequent meals NODULES AND RASH : none ALLEVIATE CHILD S ANXIETY ABOUT THE ABILITY OF THE HEART TO CONTINUE TO FUNCTION PREVENT RECURRENT INFECTION MINIMIZE BOREDOM WITH AGE APPROPRIATE SEDENTARY PLAY PROVIDE CLIENT TEACHING AND DISCHARGE PLANNING CONCERNING

adaptation of home environment to promote bed rest ( commode, call bell, diversional activities) Importance of prophylactic medication regimen

Avoidance of reinfections

II. HERPES SIMPLEX/ ZOSTER HERPES Herpes (Greek herpein, to creep ), name applied to several types of skin eruptions characterized by formation of blisters. Herpes (Greek herpein, to creep ), name applied to several types of skin eruptions characterized by formation of blisters.

A.HERPES SIMPLEX A.DESCRIPTION: Two types of herpes simplex are known Type 1( OROLABIAL HERPES) CAUSATIVE AGENT: HSV type 1 causes cold sores or fever blisters an eruption of blisters that often occurs during the course of or after one of a variety of diseases associated with fever (most commonly colds, influenza, and pneumonia) The blisters usually appear around the mouth and on the lips (herpes labialis); about the nose, face, and ears; and in the mouth and pharynx. characterized by tiny, clear fluid- filled blister. - transmitted by kissing, sharing kitchen utensils Frequently seen in women or sharing towels.

Primary infections occur in children, recurrence in adults Self limiting virus A prodrome of tingling or burning with pain may precede the appearance of vescicles by up to 24 hours triggered by sunlight exposure or increased stress

B.COMPLICATIONS Herpetic gingivostomatitis occurs in fewer than 1% of people with primary orolabial herpes Occurs more in children and young adults Onset is accompanied by high grade fever, regional lympadenopathy and generalized malaise Erythyma multiforme Acute inflammation of the skin and mucous membrane Herpes Simplex Type 1 (Blisters Around Mouth region)

Type 2( GENITAL HERPES) CAUSATIVE AGENT: HSV type 2 The second type of herpes simplex virus is the usual cause of genital herpes causes genital sores, affecting the buttocks, penis, vagina or cervix Lesions appear as grouped vesicles on an erythematous base initially involving the vagina,, rectum or penis Lesions occur 3-7 days after infection ( usually by sexual contact) and may last several weeks Lesions are symmetric and usually cause regional lympadenopathy Fever and flulike symptoms are common

As the vesicles rupture erosions and ulcerations appear When symptoms resolve, virus lies dormant in spinal root ganglia and is capable of repeatedly causing lesions Newborns can be infected during delivery Transmitted only when active lesions are present

Lesions in herpes simplex type 2

C. NURSING DX: Pain Impaired skin integrity D. THERAPEUTIC INTERVENTIONS: TYPE 1: Use of sunscreen on the lips and face Topical ointment with drying effects Administration of acyclovir ( Zovirax) 200 mg 5x daily for 5 days TYPE 2: treatment depends on severity, frequency and infectious status of sexual partner ! No cure Mild outbreak- no treatment maybe required More but infrequent outbreaks- treatment for type 1 is used More than 6 recurrences/ year- use of SUPPRESIVE THERAPY Acyclovir, valacyclovir( Valtrex) or famciclovir ( famvir) EXPECTED OUTCOME: suppresses 85% of recurrence and 20% of patients are free of recurrence during therapy 2.suppresive therapy also reduces viral shedding by 95% making the person less contagious

3. Suppresivetherapy prevents recurrent erythema multiforme ( acute eruption of macules, papules and vesicles with a multi form appearance) In pregnant women: - suppression therapy should be started during third trimester - all women with active lesion must undergo CS In immunocompromised patients: suppression therapy should be considered In severe infections of hospitalized clients: IV acyclovir is prescribed Other nursing Interventions Type 2: Teach and provide emotional support regarding incurable nature of disease Encourage increase oral fluid intake Relieve local discomfort as ordered: prescribed analgesics, sitz bath, application of heat and cold Stress the need to avoid sexual contact when lesions exist Advise client to have annual Pap smear

OUTCOMES: Reports relief of dysuria Experiences reduction in pain avoids stressful situation Exhibits intact skin without lesions or skin eruption Abstain from sexual contact when lesions are present Identifies safer sex practices

Maintains satisfying interpersonal relationship while abstaining from sexual contact

B.HERPES ZOSTER( Shingles) A. DESCRIPTION/ETIOLOGY/INCIDENCE An acute viral infection of nerve structures marked by painful vesicular skin eruptions caused by Varicella zoster (VZ) virus that also causes varicella ( chicken pox) Herpes zoster results from reactivation of latent V-Z virus that lie dormant in the nerve cells near the brain and spinal cord that travels by way of peripheral nerves to the skin where viruses multiply and create a small red rash, fluid filled blisters since a previous episode of varicella. The cause of reactivation is unknown May involve the eye leading to keratitis and blindness About 10% of adults get shingles during their lifetime usually after age 50. incidence increases to clients with weakened immune system

B. ASSESSMENT FINDINGS: Herpes zoster is marked by painful vesicular eruptions along the route of inflamed nerves pain maybe burning, lancinating ( tearing or sharply cutting), stabbing, or aching Vesicles which contain serum, later becomes purulent, rupture and form crust Inflammation is usually unilateral involving the thoracic, cervical or cranial nerves and face Blisters are usually confined to a narrow region of face and trunk Inflammation and rash on the trunk causes pain w/ slightest touch Neuralgic pain, malaise, itching

C. CLINICAL COURSE: varies from 1-3 weeks D. HEALING TIME: varies from 7-26 days

E. COMPLICATIONS Infection( encephalitis) Scarring Postherpetic neuralgia Eye complications

Note: people who have been exposed to varicella by primary infection or by vaccination are NOT at risk for infection after exposure to patients with herpes zoster Shingles..

Keratitis ( inflammation of the cornea)

E. MEDICAL MANAGEMENT: THE GOAL IS TO RELIEVE THE PAIN AND TO REDUCE OR AVOID COMPLICATIONS 1. Analgesics Control of pain by blocking nerve through injection of drugs such as lidocaine or anti inflammatory agent subcutaneously: Triamcenolone ( Aristocort, Kenacort, kenalog) 2. Cortecosteroids Use of systemic corticosteroids for patients above 50 to reduce incidence of POSTHERPETIC NEURALGIA( persistent pain of the affected nerve after healing) 3. Antiviral Oral acyclovir ( Zovirax), valacyclovir ( Valtrex), famciclovir( Famvir) are administered within 24 hours of initial eruption IV acyclovir if started early is effective in in reducing pain and halting the progression of disease

4. For opthalmic herpes zoster- considered an opthalmic emergency- refer to opthalmologist to prevent possible sequelae of keratitis, uveitis, ulceration and blindness

F. NURSING MANAGEMENT 1. Administer analgesics and other meds as ordered 2. Reduce itching and protect lesions from air by application of ointments, lotions and sterile dressings as ordered 3. Protect from pressure by use of air mattress and light loose clothing 4. Use aseptic technique when caring clients with open lesions 5. Administer antibiotics as ordered 6. Encourage client to avoid scratching and to use gloves at night to limit possibility of accidental scratching 7. Assist the client to understand the basis for the rash and the itch 8. Proper diet esp rich in nutrients 9. Teach about proper hand washing to help prevent spreading of virus

G. EVALUATION/ OUTCOMES Experience an improvement in skin integrity Reports that pain and pruritus have subsided


Psoriasis Exfoliative dermatitis : a serious skin disorder characterized by progressive inflammation Pemphigus vulgaris: a serous autoimmune skin disease marked by blisters on the skin and mucous membranes Toxic epidermal necrolysis(TEN): a rare, potentially fatal skin disorder marked by epidermal erythema, necrosis and skin erosion

III. PSORIASIS A. DESCRIPTION/ ETIOLOGY/INCIDENCE A chronic inflammatory type of dermatitis that involves accelerated epidermal cell proliferation Appears to be hereditary characterized by the appearance of plaques, patches, or papules on the skin surface. The lesions are usually slightly elevated above the normal skin surface, sharply distinguishable from normal skin, and red to reddish-brown in color. characterized by the appearance of non moist plaques, patches, or papules on the skin surface. The lesions are usually slightly elevated above the normal skin surface, sharply distinguishable from normal skin, and red to reddish-brown in color covered w/ silvery scales May range in severity from cosmetic source of annoyance to a physically disabling and disfiguring disorder The extent of the disease may vary from a few tiny lesions to generalized involvement of most of the skin. Characteristically the elbows, knees, scalp, and chest are involved.

Onset may occur at any age, most common between 15-35 years old Affects about 2% of the population Uncommon in blacks PREDISPOSING: stress

Trauma Infection Changes in climate produces exacerbation familial


Primary cause unknown -Specific genetic make up and environmental stimuli triggers it. -Current evidence support immunologic basis - periods of emotional stress,anxiety aggravates situation - trauma, infection and seasonal and hormonal changes also triggers the condition Epidermal cells produces 6-9 times faster than normal - basal layer of skin divide too quickly moving too rapidly to the skin evident as scales or plaques - this psoriatic epidermal cell casts off in 3-4 days( normally- from 26-28 days) As a result, normal events of cell maturation and growth cannot take place This abnormal process does not allow the normal protective layer of skin to form

D. COMPLICATION Assymetric rheumatoid arthritis of multiple joints- 5% Erythrodermic psoriasis ( an exfoliative state involving total body surface the person is acutely ill, with fever, chills and electrolyte imbalance Usually appears in people w/ chronic psoriasis after infection, after exposure to certain medications or following of systemic corticisteroids

C. ASSESSMENT FINDING 1. Subjective: Mild pruritus ( severe if in skin folds) and sometimes pain Possible arthritic symptoms 2. Objective Bilateral symmetry Profuse Bright red(erythematous) , well demarcated plaque covered w/ silvery scales, usually on knees, scalp, elbow, genitalia Yellow discoloration of the nails, sometimes separation from the nail beds results in of patients Palmar pustular psoriasis- results if psoriasis occurs in palms and sole DIAGNOSIS: NO specific blood test, when in doubt, assess for sign of nail and scalp involvement and for positive family hx

Psoriasis of the scalp

Psoriasis of the face

Psoriasis of the hand

Psoriasis of the nails

D. MEDICAL MANAGEMENT 1. PHARMACOLOGIC THERAPY A. TOPICAL AGENT Topical Corticosteroids(Mild to severe lesions) - choose the correct strength for involved site High Potency Not for use on the face Use id limited to 4 week course 2x daily 2 week break before repeating treatment Moderate potency Used for long term therapy Low Potency used for face on long term use - occlusive dressings maybe applied to increase the effectiveness of the corticosteroids - hands with gloves, feet in plastic bags, head w/ shower cap - occlusive dressings should not remain in place longer than 8 hours - skin should be inspected w/ appearance of atrophy, hypopigmentation, striae

Current Topical Corticosteroids


Topical Non Steroidal ( FOR MILD TO SEVERE LESIONS) - used when psoriasis involve large areas of body - more potent steroids applied to large area of body potentially cause adrenal suppression thru absorption 2 Topical Non steroidal Treatments: Calcipotriene ( Dovonex) and tazarotene ( Tazorac) these agents tends to suppress EPIDERMOPOIESIS ( development of epidermal cells and cause sloughing of rapidly growing epidermal cells Not for use with elderllies and pregnant women

B. SYSTEMIC AGENT( for severe) Use of Cytotoxic preparations because of the danger of prolonged use of systemic corticosteroids a. Methotrexate inhibits DNA synthesis in the epidermal cells, thereby reducing turnover time of psoriatic epidermis - toxic to liver, kidneys and bone marrow, so labs must be monitored - teratogenic, not for pregnant b. hydroxyurea inhibits cell replication - patient monotored for bone marrow suppresion C. PHOTOCHEMOTHERAPY use of UV light exposure Or by exposure to sunlight

E. NURSING INTERVENTIONS 1. Promoting understanding Explain the etiology Explain with sensitivity that there is no cure and lifetime management is needed to control the disease Explain factors provoking: cut, injury, abrasion, sunburn, current illness, emotional stress Emphasize that repeated trauma and unfavorable environment ( cold) exacerbate the disease Explain the treatment regimen 2. Increasing skin integrity Advise not to scratch skin Measures to prevent dry skin because it worsens psoriasis Water should be warm not hot, and skin should be dried by patting not rubbing A bath oil or emollient can comfort sore and scaling skin

3. Caution client to wear dark glasses during exposure to UV light 4. Encourage diet rich in nutrient dense such as fruits, vehetables. Food rich in Vit. A

F. EVALUATION / OUTCOMES Demonstrates knowledge and understanding of disease process and its treatment Achieves smoother skin and control of lesions Develops self acceptance Absence of complication



Immune system- group of cells, molecules, and organs that act together to defend the body against foreign invaders that causes disease such as bacteria, viruses and fungi. the health of the body is dependent on the immune systems ability to recognize and then repel or destroy these invaders

Immune response the development of protective protein in response to an invasion of the body by foreign and dangerous protein substances

immunity the body s specific protective response to an invading foreign agent or organism

antigen- is a foreign protein in the body and are considered invaders

antibody- a y- shaped protein called as immunoglobulin (Ig) developed by body in response to and interacting with a specific antigen stem cell- precursors of all blood cells, found primarily in the bone marrow Complement series of enzymatic proteins in serum that, when activated destroy bacteria and other cells.

MAJOR COMPONENTS OF IMMUNE SYSTEM Bone Marrow WBCs, Lymphoid Tissues thymus gland, spleen, lymph nodes, tonslis, adenoids, tissues in GI tract (peyer s patch), respiratory and reproductive system

MAJOR COMPONENTS OF IMMUNE SYSTEM BONE MARROW: produces WBC s such as the lymphocytes B- lymphocytes ( B-cells)- mature in the bone marrow then enters the circulation T- lymphocytes ( T cells)- move from the bone marrow to thymus, where they mature into several kinds of cells with different functions LYMPH NODES distributed throughout the body connected by lymph channels and capillaries which removed foreign materials from the lymph system before it enters the bloodstream They contain immune cells that defend body against microorganism Immune functions 2 General Types of Immunity Natural or Innate- Nonspecific immunity present at birth Acquired or Adaptive- develops after birth

I. NATURAL IMMUNITY Provides rapid, non specific immunity Has a broad spectrum of defense against and resistance to infection Its basis is to defend by distinguishing between friend or foe or self and non self 2 Stages: a. immediate- generally occurring within 4 hours b. Delayed occurring 4 to 96 hours after exposure

Natural Immunity Involves the following Responses:

White Blood Cell Action participates both in natural and acquired immune response Has many types including Granulocytes and Agranulocytes Agranulocytes includes Lymphocytes, monocytes and macrophages Granulocytes include Neutrophils, basophils and eosinophils


3 types of Lymphocytes: B Cells make antibodies that bind to pathogens to enable their destruction ) B cells does not only make antibodies that bind to patthogens, but after an attack, some B cells will retain the ability to produce an antibody to serve as a memory system T cells a. CD4+ or helper T cells coordinate the immune responses and are important in the defense against intracellular bacteria. In acute HIV infection,these T cells are the main index to identify the individulas immune system activity b. CD8+ or Cytotoxic T cells are able to kill virus infected and tumor cells 3. Natural killer cells are able to kill cells of the body which are displaying a signal to kill them, as they have been infected by a virus or have been cancerous

2. Inflammatory response 3. Physical and chemical barriers physical- includes intact skin, mucous membrane and cilia of respiratory tract chemical- mucous, acidic gastric secretions, enzymes in tears and saliva, sebaceous and sweat secretions

INTERFERON- one type of biologic response, a non specific viricidal protein naturally produced by the body and is capable of activating other components of immune system

II. ACQUIRED IMMUNITY Usually develops as a result of prior to an antigen through immunization or by contracting a disease This form of immunity relies on recognition of specific foreign antigens Has 2 Types: active acquired- immunologic defenses are developed by person s own body - lasts for years or even lifetime passive acquired temporary immunity from source outside the body that has developed through immunization or previous disease

THREE MEANS OF BODY S RESPONSE TO INVASION 1. PHAGOCYTIC IMMUNE RSPONSE 2. HUMORAL OR ANTIBODY IMMUNE RESPONSE 3. CELLULAR IMMUNE RSPONSE IMMUNE RESPONSES 1. PHAGOCYTIC IMMUNE RESPONSE The 1st line of body s immune defense Involves WBC s( granulocytes and macrophages) The ability to ingest foreign particles APOPTOSIS- another process of body s way to destroy worn out cells such as blood or skin cells 2. HUMORAL IMMUNE RESPONSE/ANTIBODY RESPONSE 2ND response

Begins w/ B lymphocytes, that transforms into plasma cells that manufacture antibodies They are transported into bloodstream and attempt to disable invaders 3. CELLULAR IMMUNE RESPONSE 3RD immune response Involves T lymphocytes,that transforms into special cytotoxic ( or killer) T cells that can attack the pathogens Viral antigens Most immune response involve both humoral and cellular responses

4 STAGES OF IMMUNE RESPONSE 1. RECOGNITION STAGE Primary initiating event in all immune response Body must first recognize invaders as foreign before it can react to them Accomplishes recognition using lymph nodes and lymphocytes for surveillance 2. PROLIFERATION STAGE The circulating lymphocyte will be sensitized once in the node- stimulates T and B lymphocytes to enlarge, divide and proliferate T lymphocytes becomes cytotoxic or killer T cells , B lymphocytes produce and release antibodies An enlarged lymph node in the neck is an example of immune response 3. RESPONSE STAGE The lymphocytes will function as either humoral or at cellular capacity

4. EFFECTOR STAGE In this stage; either the antibody of the humoral response or the cytotoxic ( killer) T cell of the cellular response reaches and connects with the antigen on the surface of the foreign invader

Characteristics of Immunoglobulin Characteristics of Immunoglobulin COMPLEMENT Is a group of at least 20 circulating plasma proteins , made in the liver, that are sequentially activated in the presence of antigen Functions include: Cell lysis Opsonization: making antigen more susceptible to phagocytosis by coating of the antigen- antibody molecules with sticky substance) Chemotaxis- inducing phagocytes to antigen (In chemotaxis, or chemotactic sensing, cells are attracted to or repelled by a substance according to its level of concentration, or its chemical gradient.) Agglutination: clump or cause cells to clump: to cause cells such as red blood cells or bacteria to form clumps, or gather together in clumps Anaphylotoxin: stimulation of inflammatory response ASSESSING FOR IMMUNE DYSFUNCTION SIGNIFICANT ASSESSMENT FINDINGS 1. GENERAL Overall health status Recurrent infections Seasonal symptoms Weight loss Fever 2. INTEGUMENTARY SYSTEM Rashes Lesions Dermatitis

Hematoma inflammation

3. HEAD Eye: itching, burning, watering, infections Ears: recurrent infections nose: rhinitis, sneezing 4. NECK: adenopathy 5. RESPIRATORY: cough, wheeze, dyspnea, recurrent infection 6. CARDIOVASCULAR pain, palpitations, anemia, tachycardia 7. GASTRO hepatosplenomegaly, vomiting, diarrhea, colitis 8. GENITOURINARY recurrent infections, hematuria, discharge, dysuria 9. MUSCULOSKELETAL weakness, fatigue, joint pain, joint mobility, edema 10. NEUROSENSORY orientation, level of consciousness, hearing loss, headaches

Selected Tests for Evaluating Immunologic status

1. Leukocyte and lymphocyte test WBC count with differential Bone marow biopsy 2. Humoral ( Antibody- mediated) tests 3. Cellular ( Cell mediated) immunity test 4. Hypersensitivity tests Intradermal test: INTERPRETATION: based on size of wheal after 15-30 minutes Negative wheal less than 0.5 cm in diameter w/ minimal erythema Positive: 1+ wheal- wheal present( 5-8mm/0.5 cm in diameter);w/ associated erythema 2+ wheal- (7-10mm/1.0cm in diameter);w/ associated erythema 3+ 4+ - (9-15mm/1.5 cm); slight psedopodia(temporary cell protrusion) w/ associated erythema - (12mm/2.0cm) ;w/ pseudopodia and diffuse erythema

PSYCHOSOCIAL IMPLICATIONS: 1. A patient w/ immunologic problem may experience coping difficulties related to: a. the chronic, progressive of the disease b. debilitating disease effects c. loss of friends and loved ones from the disease( AIDS) d. fear of dying 2. the patient may express self concept concerns related to fears of:

a. body image changes w/ disease progression b. rejection c. loss of outlets for sexual expression d. role changes toward increased dependence 3. the patient may adjust to lifestyle changes made necessary by altered: a. physical capacity b. self care ability c. work performance, w/ potential for job loss

4. Disease related changes in social interaction patterns can lead to: a. isolation b. depression c. Hopelessness ALTERATIONS IN AUTOIMMUNITY 1. SYSTEMIC LUPUS ERYTHEMATOSUS

DESCRIPTION: chronic, noncontagious autoimmune disease in which the immune system treats the body s own tissue as a foreign substance and produces antibodies to fight it Thought to be an autoimmune disorder An estimated 1.5 million people in the United States suffer from lupus and the disease strikes women 8 to 15 times more than men and women of childbearing age are particularly susceptible ETIOLOGY As with other autoimmune diseases, the exact cause, or trigger, for lupus remains unknown. Research has shown that the disease results when a specific set of susceptible genes is exposed to a combination of environmental factors such as infectious agents, certain drugs such as anticonvulsants, some penicillins, and estrogen therapy, excessive ultraviolet light, physical trauma, or emotional stress.

brought about by some combination of genetic factors, hormonal factors ( as evidenced by usual onset during childbearing years), and environmental factors ( sunlight, thermal burns) Certain medications such as isoniazid, anticonvulsant , thorazine are also implicated

PATHOPHYSIOLOGY 1. SLE involves markedly increased B cell activity and decreased T cell production 2. there is increase in autoantibody production leads to immune complex deposition and tissue damage inflammation stimulates antigens in turn stimulates additional antibody cycle repeats PROGNOSIS: good with early detection and treatment COMPLICATIONS: Cardiovascular, Renal, Neurologic and severe bacterial infections

ASSESSMENT FINDINGS: 1. Clinical manifestations of SLE vary depending on the organs affected 2. early signs and symptoms: a. fatigue b. anorexia c. occassional fever d. joint stiffness e. skin rash

3. Disease progression typically produces: a. characteristic butterfly rash on face- acute cutaneous lesion consisting of a butterfly shaped rash across bridge of the nose and cheeks - occurs in > 50% of patients

b. alopecia c. Photosynsetivity d. skin eruptions on trunk or extremities

4. Associated manifestations: a. Symmetric arthritis b. peripheral vasculitis w/ hypertension c. Pericarditis d. Renal failure e. signs/ sx of pleuritis, COPD f. Psychosis, convulsions

MNEMONIC IN DIAGNOSTIC CRITERIA FOR SLE A person has SLE if any 4 of the following 11 symptoms are present simultaneously or on 2 separate occasions: Serositis- pleuritis / pericarditis Oral ulcers- include oral or nasopharyngeal Arthritis non erosive arthritis of 2 or more peripheral joints, w/ tenderness, swelling Photosensitivity exposure to UV light causes rash or other symptoms of SLE flare ups Blood hematologic disorders: hemolytic anemia, leukopenis, thrombocytopenia Renal disorder more than 0.5g/ day CHON in urine Antinuclear Antibody test positive Immunologic disorder Neurologic disorder seizures or psychosis Malar rash rash in cheeks Discoid rash red, scaly patches on skin that causes scarring


LABORATORY STUDIES MAY REVEAL: A. anemia, thrombocytopenia, leukocytosis or leukopenia b. proteinuria c. Increased ANA ( Anti nuclear antibodies) are produced when the bodies immune system perceive parts of its own cell nuclei as foreign Because they don t penetrate living cells, ANAs are harmless, but sometimes form antigen- antibody complexes that causes tissue damage PURPOSE: TO SCREEN SLE (The absence of ANA essentially rules out active SLE To monitor the effectiveness of immunosuppressive therapy

NURSING DIAGNOSIS Body Image disturbance Ineffective breathing pattern Decreased cardiac output Ineffective individual coping High Risk for fluid volume deficit Pain Impaired skin integrity

PLANNING AND IMPLEMENTATION Aim treatment at reducing inflammatory process Corticosteroids- single most important medication available for treatment

NSAIDS- used in an effort to minimize corticosteroid requirements Immunosuppressive agent Relieve joint pain and stiffness by applying warmpacks as needed Provide patient teachings: - basic patophysio of the disease and its progression - purpose, effects of medications - importance of follow up care and monitoring for new symptoms

- necessary lifestyle changes such as avoiding sunlight

2. MULTIPLE SCLEROSIS (MS) chronic, unpredictable, and often progressive disease of the central nervous system that attacks and destroys tissues in the brain and spinal cord. A PROGRESSIVELY DEMYELINATING DISEASE affecting nerve fibers of the brain and marked by periodic exacerbations and remissions ETIOLOGY AND INCDENCE Cause is unknown, theories include a slow growing virus, autoimmune process and an allergic response to an infectious agent Although MS can occur at almost any age, the disease usually strikes people who are between the ages of 20 and 40.

MS results from a misdirected immune-system attack leveled primarily against myelin, a white, fatty material that coats wirelike nerve fibers in the central nervous system When myelin is attacked and destroyed in MS, a process known as demyelination, nerve transmission flow is interrupted, resulting in a variety of neurological problems. ASSESSMENT FINDINGS:

PRIMARY SYMPTOMS: Fatigue, weakness, numbness, poor coordination and loss of balance


DIAGNOSTIC STUDIES: Lumbar puncture reveals elevated CSF protein and gamma globulin MRI reveals presence of 3-4 lesions of greater than 3mm in diameter on the brain

PATTERNS OF MS: Exacerbations: new symptoms appear and the existing ones worsen Relapsing remitting: periods of neurological dysfunction followed by partial or full recovery Secondary progressive : initial pattern of relapse and recovery, which becomes steadily progressive over time Progressive relapsing : progressive from onset with clear exacerbations

NURSING DX: Anxiety Body image disturbance Bowel incontinence Fatigue High risk for injury Impaired physical mobility

MEDICAL MANAGEMENT: NO KNOWN CURE : goal of treatment is to delay the progression,manage the symptoms and treat acute exacerbations Immunotherapy: corticosteroids Antispasmodics amantadine Ataxia: beta adrenergic blockers, anticonvulsants and benzodizepines

NURSING MANAGEMENT: Minimize spasticity and contractures by applying warm packs and encouraging swimming and stationary biking Avoid hot baths because sensory loss might lead to burn Discourage strenuous physical exercises as this may lead to paresis, numbness or incoordination Instruct the patient to walk with feet apart and to watch feet while wlaking to prevent falling Encourage use of eye patch or eyeglasses to block visual impulse in diplopia Assist patient and partner in exploring alternative methods of sexual expression.

3. GUILLAIN BARRE SYNDROME An acute, rapidly progressive form of polyneuritis producing muscle weakness and mild sensory disturbances May be autoimmune or caused by other illness ETIOLOGY AND INCIDENCE GBS is a post infectious polyneuritis of unknown origin that commonly follows febrile illness: most often viral- cytomegalovirus, Epstein Barr virus, mycoplasma pneumoniea and HIV

It can develop in any illness but more common in males between ages 16-25; and 45-60 60-75% recover completely; 20-25% with residual deficits seen in patients with rapid disease progression, those requiring mechanical vent, and above 60 s. Death rate is 5% PATHOPHYSIOLOGY: Segmental demyelination of peripheral nerves causing inflammatory and degenerative changes in sensory and motor nerve roots and some cranial nerves producing ascending weakness dyskinesia, hyporeflexia and paresthesias

2. GBS is a result of a cell mediated and humoral immune attack on peripheral nerve myelin sheath proteins that causes inflammatory demyelination 3. molecular mimicry immune system cannot distinguish between the two proteins and attacks and destroys its own peripheral nerve myelin(autoimmune attack) influx of macrophages and other immune mediated agents attack myelin inflammation axon unable to support nerve conduction ASSESSMENT FINDINGS: 1. common signs and symptoms: a. Paresis in the legs ( usually the initial) b. motor weakness progressing upward to involve entire peripheral nervous system, including respiratory muscles c. paresthesias of hand and feet d. optic nerve demyelination- blindness e. vagus nerves : inability to swallow or clear secretions : autonomic dysfunction nstability of cardiovascular system: tachycardia, baradycardia, hypertension, or orthostatic hypotention

DIAGNOSTIC: A history of viral illness in the previous two weeks Lumbar puncture may reveal elevated CSF proteins but not conclusive

NURSING DX Ineffective breathing pattern and impaired gas exchange related to rapidly progressive weakness and impending respiratory failure Impaired bed and physical mobility related to paralysis Imbalanced nutrition, less than body requirements r/t to inability to swallow Impaired verbal communication r/t cranial nerve dysfunction Fear and anxiety r/t loss of control and paralysis

NURSING INTERVENTIONS: 1. Maintaining respiratory function: suctioning, oxygen therapy, monitor respiratory status Parameters to begin mechanical vent: a. vital capacity of less than 15 ml/kg b. partial pressure of oxygen (PaO2) < 70mmhg progressive bulbar( glossopharyngeal , vagal nerve) weakness 2. enhancing physical mobility frequent position change every 2 hours Passive range of motion Padding over bony prominence 3. Providing adequate nutrition Paralytic ileus results from insufficient parasympathetic activity- IV fluids and parenteral nutrition as prescribed Monitor bowel sounds Gastrostomy tube if patient cannot swallow due to bulbar paralysis 4. Improving communication 5. Monitoring and managing complications Respiratory failure is the major cause of mortality

Other complications: cardiac dysrrhytmias ( ECG monitoring); transient hypertension, hypotension, urinary retention, DVT,

HYPERSENSITIVTY REACTIONS Represents immune response to allergens that results in tissue destruction A reflection of excessive or abberant ( deviating from what is normal) immune response Usually does not occur with 1st exposure to allergen, rather the reaction follows a re exposure after sensitization in a certain person FACTORS THAT DETERMINE A HYPERSENSITIVTY RESPONSE 1. Responsiveness of the host to allergen 2. Amount of allergen 3. Nature of allergen any foreign protein can serve as allergen when coupled w/ normal tissue protein carrier( pollen, foods, dust ) 4. Route of entrance to the body- allergen may gain entry via respi, epidermal or mucousal, by injection, or through digestive tract

5. Timing of exposure to allergen if the host s contact with allergen are widely separated by time, the immunologic mediators maybe so dilute that little response occurs. Conversely, if frequent contacts is made w/ allergen, reactions are likely to occur 6. Site of the allergen- immune mediator reaction a reaction can occur in the tissues with little consequence, however, the same reaction occurring in the bloodstream can lead to severe reaction 7. host s threshold of reaction its immune system can be changed by factors such as stress, fatigue, or infection all of which can decrease the immune system s responsiveness to potential allergens.