Your SlideShare is downloading. ×
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Altered immune part_1___2_student
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Altered immune part_1___2_student

1,296

Published on

1 Comment
2 Likes
Statistics
Notes
No Downloads
Views
Total Views
1,296
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
0
Comments
1
Likes
2
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide
  • Inflammation is always present with infection. Causes: heat radiation trauma chemicals allergens autoimmune reaction Infection is not always present with inflammation. Invasion of tissues or cells by microorganisms such as bacteria, fungi, or virus
  • Clinical manifestation of inflammation Local response Systemic response Redness Malaise Heat Nausea Pain Anorexia Swelling Increased pulse rate & resp rate Loss of function Fever Inc WBC count with shift to the left
  • Defense: The body protects against invasions by micro-organisms and prevents the development of infection by attacking the foreign antigens and pathogens Homeostasis: Damaged cellular substances are digested and removed. Through this mechanism the body’s different cell types remain uniform and unchanged. Surveillance: Mutations continually arise in the body, but are normally recognized as foreign cells and destroyed
  • Innate ( Natural ) Exists in a person without prior contact with the antigen Humans are naturally immune to some of the infectious agents that cause illness in other species. Acquired Active-results from the invasion of the body by foreign substances such as microorganisms and th subsequent development of antibodies and sensitized lymphocytes. With each reinvasion on microorganisms, the body responds more rapidly and fights off the invader. This type of immunity can result naturally (like chicken pox) or from inoculation (immunizations) Passive acquired immunity- the host receives antibodies to an antigen rather than making them. Examples-transplacental from mother to fetus and through colostrum. This type of immunity is short lived.Natural Artificial Passive Immunity- examples-serum from human y-globulin
  • Antigens Substances that elicits an immune response Composed of proteins and other large polysaccharides, lipoproteins. All the body’s cells have antigens on the surface that are unique to that person The body then become “tolerant” to it’s own molecules
  • Composed of Two types of organs Central or Primary Thymus gland and bone marrow Thymus is important in the differentiation and the maturation of the T lymphocytes During childhood the gland is large and with ageing the gland shrinks in size. Lymphocytes are produced in the bone marrow and migrate in the peripheral organs Peripheral Tonsils Gut-, genital-, bronchial-, and skin associated lymphoid tissues These two types of lymphoid tissues protect the body from external micro-organisms Lymph nodes The two important functions of the lymph node: Filtration of foreign material brought to the site Circulation of lymphocytes Spleen Is the primary site for filtration of foreign substances from the blood Two types of tissue White Pulp: Containing B & T Lymphocytes Red Pulp: Containing Erythrocytes The spleen is the major site of immune responses to blood borne antigens.
  • Mononuclear phagocytes- capturing accomplished through phagocytosis
  • B lymphocytes- the bone marrow. B cells differentiate into plasma cells when activated and they produce antibodies or immunoglobulins T lymphocytes- cells that migrate from the bone marrow to the thymus. The thymus secretes hormones that stimulate the maturation and differentiation of the T lymphocytes. T cells compose 70-80% on the circulating lymphocytes and are responsible for immunity to viruses, tumor cells, and fungi. They are categorized into T cytotoxic, T helper, and T suppressor cells. T cytotoxic cells-involved in attacking antigens on the cell membrane of foreign pathogens and releasing cytolytic substances that destroy the pathogen. T helper and T suppressor cells-involved in the regulation of cell mediated immunity and the humoral antibody response. The HIV virus invades the T helper cells and decreases their number and function. These individuals cannot mount an aggressive immune response. Natural killer cells-large lymphocytes. Involve in the recogniton and killing of virus-infected cells, tumor cells, and transplanted grafts. Mechanism not fully understood.
  • Soluble factors secreted by WBC’s and a variety of other cells in the body Acts as messengers between the cell types Instructs cells to alter their function 100 different cytokines Interleukins: directs other cells to divide and differentiate (cell specific) Interferon: helps the body’s natural defenses attack tumors and viruses. 3 have been identifed. Tumor Necrosis Factor: activates macrophages, responsible for extensive wt loss with chronic inflammation and cancer Colony-Stimulating Factors Erythropoietin: hormone synthesized in kidneys released into blood stream in response to anoxia stimulates & regulates production of erythrocytes increase oxygen carry compposity
  • Humoral-means body fluid. 5 classes of immunoglobulins-IgG, IgA, IgM, IgD, nad IgE IgM first type of antibody formed Secondary antibody response-faster 1-3 days lasts longer than primary responseIgG is the primary antibody in secondary response Cell Mediated Protection: Fungus Viruses (Intracellular) Chronic infectious agents Tumor Cells EX: TB Fungal infections Contact dermatitis Graft infection Destruction of tumor cells
  • Thymus involution Decrease in cell-mediated immunity Decrease delayed hypersensitivity response Decreased Interleukin 1 & 2 synthesis Decreased express of IL 2 receptors Decreased proliferation response of T & B cells Decreased primary and secondary antibody responses Decreased auto antibodies
  • Infants receive passive immunity from mother in form of IgG near end of gestation Eventually produce antibodies (active acquired immunity) beginning at about 3 months of age Breastfed infants receive antibodies from breast milk protected from many infectious diseases including influenza, measles, mumps, and chickenpox
  • Type I, II, and III are humoral immunity. Type I Anaphylaxis and Atopic or inherited example- Rhinitis, Asthma Anaphylaxis occurs when mediators are released systemically. An example of a local response is the wheal and flare reaction such as a mosquito bite. Has a pale wheal containing edematous fluid surrounded by a red flare. Type II Cytotoxic Transfusion reaction, Goodpasture Syndrome Type III Immune-complex Systemic Lupus, Rheumatoid Arthritis Type IV Delayed Hypersensitivity cell mediated- Contact dermatitis, transplant rejection What kind of reaction is shown in the image? Type IV Contact dermatitis
  • Histamine Mast cells & Basophil granules: Increases permeability, constricts smooth muscle, stimulates irritant receptors, edema in the airways, bronchial constriction, urticaria, angioedema, pruritus, N/V, diarrhea, shock Leukotrienes constrict bronchial smooth muscle, increase vascular permeability, Bronchial constriction, enhanced effect of histamine on smooth muscle Prostaglandins stimulate vasoconstriction, constrict smooth muscle, Wheal and flare reaction on skin, hypotension, bronchospasm Platelet-Activating Factor Mast cells, Aggregates platelets, stimulates vasodilatation, Increase in Pulmonary artery pressure, systemic hypotension Kinins Stimulate, slow, sustained smooth muscle contraction, increase vascular permeability, stimulate secretion of mucus, stimulate pain receptors, Angioedema with painful swelling, bronchial constriction Serotonin Platelets, Increases vascular permeability, stimulates smooth muscle contraction, Mucosal edema, bronchial constriction Anaphylatoxins C3a, C4a, C5a from complement activation, stimulate histamine release, Same as histamine An allergen is introduced..the body perceives it as a threat, produces IgE that is specific which binds to Mast and Basophils. When the allergen is introduced for the second time, the Ige causes a release in histamines resulting in an allergic response. Mast cells are found throughout the body, but mostly in the skin, respiratory tract and gi system.
  • Objective data: Labs What kind of manifestations are indicative of an allergic response?
  • Who do you think would be susceptible to this kind of allergy? Two types of reaction can occur- Type IV allergic contact dermatitis nad Type I Anaphylactoid Health care workers or chronically ill patients Became more prevalent in 1987 with the introduction of universal precautions
  • Health History that covers: individual and family hx, social and environmental factors including history of treatment success and failure. Comprehensive Assessment
  • Lab Tests CBC Page 1878 Serologies page 1879 CBC Eosinophil Count is elevated with Type I hypersensitivity involving IgE Lymphocyte Count with differential Cellular immunodeficiency is Dx if the lymphocyte count is below 1200 /ul. T & B counts assist with determining the type of immuno-specific syndrome Serology Human Leukocyte (HLA)-B27 is usually present in ankylosing spondylitis and rheumatoid arthritis Radioallergosorbent test (RAST) diagnostic test for IgE antibodies to specific allergens. VERY EXPENSIVE! Helpful when confirming reactivity to allergens in histories of anaphylaxis Skin testing Can be done by scratching/pricking or sub dermal injections Patient is never to be left alone because of potential allergic reactions
  • Differential shows what stage of reaction – can help pinpoint what type of antigen B&T cell counts is used to diagnose immunodeficiency syndromes Eosinophil levels are elevated with Type 1 reactions involving IgE immunoglobulins such as exogenous pollen, food, drugs or dust reactions. Radioallergosorbent test is an in vitro diagnosistic test for IgE antibodies to specific allergens – useful to confirm reactions to various drugs or foods.
  • Antihistamines best drug to TX allergic rhinitis and urticaria, compete with H1 receptor sites, used to treat edema pruritus, ineffective in bronchoconstriction Sympathomimetic Epinephrine /Adrenalin drug of choice for anaphylactic reactions, it stimulates the alpha and beta adrenergic receptors causing vasoconstriction and relaxation of the bronchial smooth muscles Decongestants Sudafed, used to treat allergic rhinitis Corticosteroids Nasal sprays effective in treating allergic rhinitis, If reaction more severe TX course of oral corticosteroids can be used Anitprurtics applied if the skin is not broken, protect the skin and relief from itching Calamine, Coal tar solutions Mast cell stabilizing drug Nasalcrom Tilade, inhibit the release of histamines, leukotrienes and other agents from the mast cell after antigen IgE interaction Used in the treatment of asthma and allergic rhinitis, low amount of side effects Know the common side effects!!!!
  • Children usually outgrow their allergy Adults do not. Immunotherapy may need to be continued indefinitely Allergens that cause an anaphylactic response do not usually go away
  • Inappropriate reaction to self proteins Causative factors Age? Genetic Susceptibility Initiation of Auto-reactivity Virus: Multiple Sclerosis and Type I diabetes Medication: Hemolytic anemia (Aldomet, Pronestyl) Hormonal: Occurs more frequently in women, activity of disease process disappears during pregnancy, but an exacerbation occurs after delivery
  • Plasmapheresis removes whole blood separates out the unwanted components and returns the remaining to the patient. Plasma is replaced with Normal saline, LR FFP, Plasma protein fractions. When blood is manually removed only 500ml can be removed at a time, but with the dialysis machine over 4 liters can be cycles in 2-3 hours. Side effects: Hypotension Citrate toxicity Hypocalcemia: Headache, parethesia and syncope
  • Lupus Collagen disease severe vasculitis, renal involvement, lesions on skin Butterfly mask Rheumatoid Arthritis chronic inflammatory destructive deforming collagen in synovial membranes Autoimmune Hemolytic Anemia chronic premature destruction of RBC’s Multiple Sclerosis progressive disease demyelination of nerve fibers of the brain and spinal cord Guillain-Barre syndrome idiopathic peripheral polyneuritis follows viral illness symmetric pain and weakness affecting the extremities and paralysis may develop, may spread to trunk and face Myasthenia Gravis chronic fatigue, muscle fatigue in face and throat, may affect respiratory systems Addison’s disease life threatening, caused by partial or complete failure of adrenocortical function Type I Diabetes Mellitus Juvenile inability to produce adequate insulin Ulcerative Colitis large intestine and rectum, watery diarrhea with blood, mucus and pus develop mega colon which may lead to perforation of bowels Goodpasture syndrome chronic relapsing pulmonary hemosiderosis with glomerulonephritis Autoimmune Hepatitis inflammation of the liver
  • Primary- immune cells are improperly developed or absent. Involves phagocytic defects, B cell, T cell deficiencies, or combined B and T cell deficiencies. Primary disorders are rare and often serious Secondary Deficiency- more common and less severe. The deficiency is caused by illness or treatment
  • Drug induced immunodeficiency is the most common cause
  • What are some community resources for a person with compromised immune system?
  • Neutrophils Lymphocytes Eosinophils ESR level will rise above 15-20 mm/hr
  • Transcript

    • 1. NURS 1228Nursing Management ofPatients Experiencing anAltered Immune System Kathy Sims, MS, RN
    • 2. Inflammatory Response• Microorganisms invade Vas damaged tissue Basophils release histamine and kinin production occurs Vasodilation occurs along with increased capillary permeability Blood flow increases to the affected tissue, and fluid collects within it Neutrophils and monocytes flock to the invasion site to engulf and destroy microorganisms Tissue repair occurs
    • 3. Inflammatory ResponseMicroorganisms invade damaged tissue Basophils release histamine and kinin production occurs Vasodilation occurs along with increased capillary permeability Blood flow increases to the affected tissue, and fluid collects within it VASCULAR RESPONSE
    • 4. Inflammatory Response Neutrophils and monocytes flock to the invasion site to engulf and destroy microorganisms Lymphocytes arrive later. Primary role is related to humoral and cell- mediated immunity Tissue repair occursCELLULAR RESPONSE
    • 5. Inflammatory ResponseCellular Response• 5 types of white blood cells – Neutrophils – Eosinophils – Basophils – Lymphocytes – Monocytes• Elevated WBC = leukocytosis• Decreased WBC = leukopenia• Fig 13-2 Lewis, Malarky pg 680
    • 6. NeutrophilsFirst to arrive on scene – 6-12 hrsPhagocytize bacteria, foreign material and damaged cellsThey live for about 24-48hrs and then begin to accumulate as dead material/pusTo keep up with severe assault, bone marrow releases immature neutrophils (bands)This increase in bands is called shift to the left – s/s acute bacterial infections WBC Differential shows “bands”Elevated with bacterial infections, inflammatory diseases and tissue necrosisDecreased when supply is exhausted, bone marrow damage
    • 7. Monocytes & Lymphocytes2nd type phagocytic cells – 3-5 days after injuryWhen they get there, they change to macrophages and continue phagocytosisLive for weeksLymphocytes arrive following monocytes and their primary role is related to humoral and cell-mediated immunity (B&T cells)Elevated with acute infections, leukemiaDecreased with advanced cancer, deficiency related disorders (HIV)
    • 8. Eosinophils and BasophilsEosinophils & Basophils are released in large quantities during an allergic reaction ◦ They work together to mediate the effects of histamine and serotonin ◦ They are involved with phagocytosis of allergen- antibody complexes, and destruction of parasite cell surfaces so antibodies can attack ◦ Elevated during the healing phase of inflammation, food hypersensitivity, following radiation therapy and leukemia disorders ◦ Decreased values during acute infection, hyperthyroidism and stress
    • 9. Chemical Mediators• Complement system – Occur in sequential order C1-C9 – Major function • Enhanced phagocytosis • Increased vascular permeability • Chemotaxis • Cellular lysis
    • 10. Chemical MediatorsProstaglandins & Leukotrines• Stimulated by chemical mediators and phagocytosis – In general are pro-inflammatory – increased blood flow, decrease platelet clumping – NSAID medication inhibit PG synthesis • Useful in chronic inflammatory conditions to decrease pain & inflammation – Corticosteroids inhibit PG’s & leukotrines • Useful in inflammatory airway diseases because they prevent bronchoconstriction 2nd to inflammation
    • 11. REVIEW S/S INFECTION • Local or Systemic S/S Infection?• Fever______• Edema_______• Pain or Tenderness______• Malaise______• Warmth of Area ________• Increased Pulse and Resp Rate_______
    • 12. Normal Immune ResponseImmunity is a state of responsiveness to foreign substances such as foreign bodies and tumor proteins (antigen)• Serves three functions 1. Defense 2. Homeostasis 3. Surveillance
    • 13. Classifications of Immunity Innate ( Natural ) – exists in a person without prior contact to the antigen (born with) ◦ Nonspecific defense response by neutrophils and monocytes Active Acquired – results from invasion and development of specific antibodies and sensitized lymphocytes ◦ With each following attack, the body responds more vigorously ◦ Ex. Following inoculation or disease Passive Acquired – host receives antibodies to the antigen rather than synthesizing them ◦ Short lived, host cells do not retain memory
    • 14. Components of the Immune Response• Antigens – Elicits an immune response – Composed of proteins – Unique to that person – “Tolerant” to it’s own molecules (except in autoimmune disease)
    • 15. Lymphoid System• Central (primary) lymph organs – bone marrow and thymus gland – Lymphocytes are produced in bone marrow – Thymus gland differentiates them into B & T• Peripheral lymph organs are in the submucosa of the respiratory, gentiourinary and gastrointestinal tracts and the skin (ex. skin reactions) – Protects from external organisms (ex. Tonsils)
    • 16. Lymphoid SystemPeripheral (con’t)Lymph Nodes 1) filtration of foreign material brought to the site from the bloodstream into the lymph system 2) circulation of lymphocytes throughout the bodySpleen is primary site for filtering foreign substances and is the major site of immune responses to blood-borne antigens
    • 17. LymphoidOrgans
    • 18. Cell Involved in Immune Response • Mononuclear Phagocytes – Responsible for capturing, processing, and presenting the antigen to the lymphocyte – Present within 3-7 days of exposure – Stimulation of humoral or cell- mediated response – Capturing accomplished through phagocytosis
    • 19. Cells Involved in Immune Response• Lymphocytes – B lymphocytes – T lymphocytes • T cytotoxic cells • T helper and T suppressor cells – Natural killer cells – Dendritic Cells
    • 20. Cytokines• Soluble factors secreted by WBC’s and a variety of other cells in the body• Acts as messengers between the cell types• Instructs cells to alter their function• 100 different cytokines – Interleukins – Interferons – Tumor Necrosis Factor – Colony-Stimulating Factors – Erythropoietin
    • 21. Comparison of Humoral and Cell Mediated Immunity• Humans need BOTH humoral and cell-mediated immunity to remain healthy.• Humoral immunity – based on the development of antibodies to antigens (produced by differentiated B Cells)• Cell mediated – initiated through specific antigen recognition by T cells
    • 22. Comparison• Humoral • Cell Mediated – Antibody (B lymphocytes) – T cell recognition mediated immunity immunity – Produced in the Plasma – Primary importance in cells • Pathogens inside – Primary Response noted the cells in 4-8 days after the exposure • Fungal infections – Subsequent exposure • Rejection of results in faster transplanted tissues responses, due to • Contact memory cells hypersensitivity reactions • Tumor immunity
    • 23. Effects Across the lifespan• Hypo function in the young and old• Older populations more susceptible to infections – Bone marrow is not affected (so no big change in RBC, etc. ) – Decreased WBC response, even with infection – Thymus decreases in size and activity • T cells • B cells
    • 24. Effects Across the lifespanInfants receive passive immunity from mother inform of IgG near end of gestationEventually produce antibodies (active acquiredimmunity) beginning at about 3 months of ageBreastfed infants receive antibodies from breastmilk, protected from many infectious diseasesincluding influenza, measles, mumps, andchickenpox
    • 25. Patients with Altered Immune SystemsPrimarily an issue of lymphocyte response to conditions triggering the inflammatory response ◦ Acute infections & inflammatory conditions  Anaphylatic reactions  Exposure to new antigens & development of immunity ◦ Chronic inflammatory conditions  Long-term immunity  Chronic diseases such as asthma, COPD, chronic allergies (including latex, seasonal), autoimmune diseases such as lupus or secondary immunodeficiency disorders
    • 26. Altered Immune Response • Hypersensitivity Reactions – Immune response is over- reactive against foreign antigens or fails to maintain self-tolerance resulting in tissue damage – There are four categories
    • 27. Types of Hypersensitivity ReactionsType I AnaphylacticType II CytotoxicType III Immune-complexType IV Delayed Hypersensitivity
    • 28. Mediators of Allergic Response• Histamine• Leukotrienes• Prostaglandins• Platelet-Activating Factor• Kinins• Serotonin• Anaphylatoxins
    • 29. Anaphylactic Shock – Type 1
    • 30. Nursing Assessment• Past medical history• Current medications• Family history• External manifestations• Other objective data
    • 31. Clinical ManifestationsDepend on local vs systemic accessLocal – wheal and flare at application or bite site, edema and itching at site of exposureSystemic – local reaction + s/s shock ◦ Rapid weak pulse ◦ Hypotension ◦ Dilated pupils ◦ Bronchial edema = bronchoconstriction = dyspnea and cyanosis
    • 32. Anaphylactic Shock• Find out the causative factor• Insure patent airway• Epinephrine SQ/IV• Administer high flow O2• Recumbent position with legs elevated• Keep warm• Administer H1 blocker (Benadryl)• Administer H2 blocker (Tagamet)• Maintain blood pressure – Fluids – Vasopressors (Dopamine) – Norepinephrine bitartrate (Levophed)
    • 33. Atopic Reactions• 20% pop – inherited sensitivity to environmental allergens – Allergic rhinitis, asthma, atopic dermatitis, uticaria and angioedmea• Review s/s of each
    • 34. Type II Cytotoxic/Cycolytic Reactions• Cellular tissue is destroyed by activation of the complement system – causes mass phagocytosis and cytolysis• Target cells are usually erythrocytes, platelets and leukocytes• EX: Blood incompatibilities, Rh factor and drug reactions
    • 35. Type III: Immune-Complex Reactions• Tissue damage secondary to antigen-antibody complexes that are too small to be effectively removed by phagocytosis and deposit themselves in the tissue and small vessels• Associated with diseases such as SLE (lupus), acute glomerulonephritis and rheumatoid arthritis
    • 36. Type IV: Delayed Hypersensitivity Reactions• Cell mediated response where sensitized T lymphocytes attack antigens and release large amounts of cytokines which attract macrophages to the area• Takes 24-48 hours for a response to occur• Ex. Contact dermatitis, transplant reactions and some drug reactions (topical usually)
    • 37. Latex Allergy – 2 types anaphylacticand type 4 delayed hypersensitivityIdentification is crucialRisk factors ◦ Long-term multiple exposures ◦ History of: Hay fever, Asthma, and certain food allergies (avocados, guava, kiwi, bananas, water chestnuts, hazelnuts, tomatoes, potatoes, peaches, grapes, apricots)
    • 38. Teaching to prevent latex allergy• Use non latex gloves whenever possible• Use powder free gloves• DO NOT use oil based creams or lotions in association with glove use• Know symptoms• Wear medi-alert bracelet & carry epi pen• Avoid latex equipment with pts with chronic illnesses – especially children
    • 39. General Assessment for Allergic Disorders• Comprehensive health history – Individual and family – Environmental factors – THINK PQRST – Weekly food/med diary – Level of stress & lifestyle• Comprehensive physical exam• Review table 14-2
    • 40. Diagnostic Exams
    • 41. Diagnostic Tests• CBC with WBC differential – why?• What about B & T cell counts?• What does an elevated eosinophil level tell you?• RAST test – what is the purpose?• Sputum, bronchial secretions and nasal swabs may be done to look for eosinophils – looking for allergies• If asthma – PFT testing
    • 42. Skin testing• Used to confirm specific sensitivity in patients with atopic disease (a type 1 reaction)• Cannot be performed on patients who are medications to suppress the immune system• Done by scratch method or intracutanous injection with control site• + reaction will occur in min and last 8-12hrs• + reaction is wheal and flare response – size does not correlate with severity• Always an anaphylactic risk – pt should never be left alone, anti-inflammatory cream may be used – prepared with tourniquet and epinephrine
    • 43. Nursing Teaching for Chronic Allergens• Allergen recognition and control• Lifestyle adjustments• Elimination diet• Avoidance of stress• Environmental allergens – air conditioned room, damp dusting daily, hypoallergenic covers, mask outdoors• Communicate drug allergies• Insect – carry kits with epi & bracelet
    • 44. Drug Therapy• Antihistamines – Take when s/s appear – usually short term• Sympathomimetic/Decongestants – Review differences – relaxation of bronchial muscles, short term• Corticosteroids – Nasal sprays – no more than 3 days or 3 times a day• Anitprurtics – Non-broken skin, short-term use• Mast cell stabilizing drug – Inhibit immune response, used long-term, low side effects• Leukotriene – Used long-term, take same dose daily for effect – Ex: Singulair
    • 45. Immunotherapy• Recommended for control of allergic symptoms, when the allergen can not be avoided or tx ineffective• Small titers given to develop immunity• Useful if allergic to insects, not for food or ezcema allergies• Must be observed for a minimum of 20 minutes for anaphylactic response – done in an area with ER equipment
    • 46. Autoimmunity Conditions• Inappropriate reaction to self proteins• Causative factors – Age? – Genetic Susceptibility – Initiation of Auto-reactivity • Virus • Medication • Hormonal
    • 47. Treatment• Apheresis – Use of a procedure to separate the components of the blood followed by the removal of one or more of the components – Complications can include hypotension and citrate toxicity- causes hypocalcemia
    • 48. Examples of Autoimmune Diseases• Lupus • Addison’s disease• Rheumatoid Arthritis • Type I Diabetes Mellitus• Autoimmune Hemolytic • Ulcerative Colitis Anemia • Goodpasture syndrome• Multiple Sclerosis• Guillain-Barre syndrome • Autoimmune Hepatitis• Myasthenia Gravis• Table 14-16
    • 49. Immunodeficiency disorders• Definition- the immune system does not adequately protect the body• Involves impairment of one or more immune mechanisms• Can be primary or secondary disorders• Patients are at HIGH RISK for infection – NDX-Ineffective Protection
    • 50. Primary Immunodeficiency• Primary- immune cells are improperly developed or absent. Involves phagocytic defects, B cell, T cell deficiencies, or combined B and T cell deficiencies. Primary disorders are rare and often serious
    • 51. Secondary Immunodeficiency• Most common is Drug • Surgery induced immunodeficiency • Anesthesia – Chemotherapy • Burns – Corticosteroids • Disease Processes• Stress – AIDS• Age – Alcoholic Cirrhosis – Infants – Chronic Renal Disease – Older Adults – Diabetes Mellitus• Malnutrition – Cancer• Radiation – Systemic Lupus Erythematous
    • 52. Graft-versus-Host DiseaseOccurs when an immunoincompetent patient is transfused or transplanted with immunoincompetent cellsResponse may result from the infusion of blood products containing viable lymphocytesIn most transplant cases, there is a concern for the Host to reject the Graft, in Graft versus Host it is reversed
    • 53. GVH Disease• Response in 7-30 days • Target organs• Once the reaction starts – Skin there is little that can be – GI tract done – Liver• Mechanism not completely • There is no adequate understood, it is thought treatment that the donor T cells are – Corticosteroids attacking the and – Immunosuppressive agents destroying the host cells – Radiation of blood products
    • 54. Immunosuppressive Therapy• Goal is to adequately suppress the immune response to prevent rejection of the transplanted organ while maintaining sufficient immunity to prevent an overwhelming infection• Aseptic technique and infection prevention is a priority
    • 55. Nursing Diagnosis• Risk for Infection• Ineffective Protection• Pain• Hyperthermia• Fatigue• When do you use which one?• What are the r/t?• What are the AMB?
    • 56. Nursing Interventions• Aseptic technique is a priority• Handle and collect specimens appropriately• Patient will be on reverse isolation• Limit visitors• Teach about decreasing stress• Avoid public areas, if possible• Teach about proper diet• Teach about proper hygienic practices• Refer to community resources• Do you remember the different types of precautions? (Airborne, Contact etc.)?
    • 57. Associated diagnostic tests – Lewis page 677-683• RBC, HGB & HCT• ESR• Lymph Node Assessment• Lymph Node Biopsy• Bone Marrow• CT, PET & MRI scans
    • 58. REVIEW• Which type of WBC are the first cells to respond to a bacterial infection? _____• Which type of WBC responds primarily to viral infections (may be elevated with mono or TB which are bacterial)?_____• Which type of WBC are elevated with allergic reactions?________________• What happens to a patient’s ESR level when there is an active inflammatory process or infection? ____________
    • 59. Questions?• Do questions at end of chapter• Review main bullets of reading• Focus on nursing care/teaching• ATI Med Surg BookUnit 13 Chapter 98• Review notes from 1117 class on Infection

    ×